{
    "Contributors": "MIMIC",
    "Source": "MIMIC-IV",
    "URL": "https://www.physionet.org/content/mimic-iv-note/2.2/",
    "Categories": [
        "Summarization"
    ],
    "Definition": [
        "Summarize the MRI imaging diagnostics' detailed findings for the Head_and_neck into a concise conclusion."
    ],
    "Reasoning": [],
    "Input_language": [
        "English"
    ],
    "Output_language": [
        "English"
    ],
    "Instruction_language": [
        "English"
    ],
    "Domains": [
        "Medicine",
        "Clinical Reports",
        "MRI",
        "Head_and_neck"
    ],
    "Positive Examples": [],
    "Negative Examples": [],
    "Instances": [
        {
            "input": "Diffusion images demonstrate no evidence of an acute infarct.  Right-sided\npostsurgical changes and encephalomalacia are again noted.  Hyperintensities\nin the white matter in the periventricular region as well as in the pons\nindicate moderate changes of small vessel disease.  There is no midline shift\nor hydrocephalus.  Suprasellar and craniocervical regions are unremarkable. \nMajor vascular flow voids are maintained.",
            "output": "No acute infarcts are identified.  Encephalomalacia in the right temporal\nregion and small vessel disease are noted."
        },
        {
            "input": "There is no evidence of intracranial hemorrhage, edema, masses, mass effect,\nmidline shift or territorial infarction.  The ventricles and sulci are normal\nin caliber and configuration.  Wispy enhancement is seen in the pons,\nconsistent with a small vascular malformation.",
            "output": "1. There is no evidence of acute intracranial process or hemorrhage.\n2. Wispy enhancement in the pons is suggestive of a small vascular\nmalformation such as a capillary telangiectasia or a small developmental\nvenous anomaly."
        },
        {
            "input": "Within the superficial lobe of the left parotid gland there  is a 1.9 cm T2\nhyperintense well-circumscribed enhancing lesion. The remaining salivary\nglands and thyroid appear normal.\n\nThere is no evidence of mucosal masse or abnormal lymph nodes.  The neck\nvessels appear patent.\n\nThe visualized portions of the brain demonstrate prominence of the ventricles\nand cerebral sulci, likely age related.  There are extensive periventricular\nand subcortical white matter T2 hyperintensities likely representing chronic\nsmall vessel disease changes.  Within the left maxillary sinus is a 1.1 cm\nmucosal retention cyst.  There is a mild amount of nonspecific fluid within\nthe left mastoid air cells.  Status post left lens replacement.",
            "output": "Circumscribed T2 hyperintense enhancing lesion within the superficial lobe of\nthe left parotid gland measuring up to 1.9 cm.  Primary differential\nconsiderations include benign entities such is pleomorphic adenoma or\nWarthin's tumor given the patient's age.  Although, malignant differential\nconsiderations cannot be entirely excluded."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.\n\nThere are extensive foci of periventricular and subcortical white matter FLAIR\nhyperintensities, relatively unchanged since the prior MRI allowing for the\ndifferences in technique, nonspecific.  None of these lesions demonstrate\nenhancement or slow diffusion.\n\nThe orbits are unremarkable.  The visualized paranasal sinuses and mastoid air\ncells are clear.  Intracranial flow voids are maintained.",
            "output": "1. Several relatively stable nonspecific T2/FLAIR hyperintense lesions in the\nperiventricular, subcortical white matter.  The differential diagnosis is\nbroad and includes sequelae of demyelinating disease, sequela of prior\ninfection/inflammatory process, chronic hypertension, chronic migraines,\nmicrovascular ischemic changes among other potential etiologies.\n2. No acute intracranial abnormality."
        },
        {
            "input": "There is no evidence of infarction, hemorrhage, edema, mass, or mass effect.\n\n The ventricles and sulci are normal in caliber and configuration.\n\nA few small FLAIR hyperintensities in the supratentorial white matter, for\nexample see series 10, images 16 and 13) are nonspecific but compatible with\nearly changes of chronic white matter microangiopathy.  No diffusion\nabnormalities are detected.\n\n The visualized paranasal sinuses and mastoids appear clear.\n\n Major intracranial vascular flow voids are preserved.",
            "output": "No acute intracranial abnormality.  No evidence of infarction."
        },
        {
            "input": "There is no evidence of acute infarction.  No intracranial hemorrhage.  No\nmass, mass effect, edema or midline shift.\n\nThe ventricles and sulci are normal, without evidence of hydrocephalus. The\nbasal cisterns are patent.  There is no evidence of impending, downward\nherniation.  There is gross preservation of the principal intracranial\nvascular flow voids.\n\nFollowing the administration of intravenous contrast material, there is no\nabnormal enhancement.  The dural venous sinuses appear patent on MP-RAGE\nimagine sequences.\n\nThe visualized paranasal sinuses, middle ear cavities, and mastoid air cells\nare well aerated and clear.  The orbits are within normal limits bilaterally. \nThere is an unchanged partially calcified 8 mm subcutaneous nodule within the\nleft frontal scalp, likely consistent with a sebaceous cyst (image 23, series\n12).",
            "output": "1. Unremarkable MRI examination of the brain.  Specifically, no evidence for\nabnormal FLAIR/T2 signal or enhancement to suggest encephalitis."
        },
        {
            "input": "There is no evidence for an enhancing mass, edema, acute infarction, blood\nproducts.  Ventricles, sulci, and basal cisterns are normal in size.\n\nThere is diffuse supratentorial sulcal FLAIR signal hyperintensity, without\nclear evidence for leptomeningeal contrast enhancement on postcontrast T1\nweighted or MP RAGE images, which only demonstrate prominent leptomeningeal\nblood vessels.\n\nMajor arterial and dural venous sinus flow voids appear grossly preserved.",
            "output": "Diffuse hyperintensity on FLAIR images without clear evidence for\nleptomeningeal enhancement on postcontrast T1 weighted or MP RAGE images. \nThis appearance is nonspecific but occasionally can be seen in the setting of\nrecent lumbar puncture, or following administration of high fraction of\nsupplemental oxygen; please correlate with any recent intervention.  Other\ndiagnostic considerations include subtle leptomeningeal carcinomatosis.  The\npatient does not appear to have symptoms of infectious meningitis according to\nthe ED and hospitalist notes.\n\nIf there has been no recent lumbar puncture, then CSF sampling could be\nconsidered to assess for leptomeningeal carcinomatosis."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, or infarction.\nThe ventricles and sulci are normal in caliber and configuration. There is no\nabnormal enhancement after contrast administration. The dural venous sinuses\nare patent. The intracranial vascular flow voids are preserved. The paranasal\nsinus and mastoid air cells are clear. The orbits are unremarkable.  Posterior\ndisc bulge at C3-C4 level seen on the sagittal view is unchanged since ___.",
            "output": "Normal brain MRI without evidence of metastatic disease."
        },
        {
            "input": "MR BRAIN:\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline\nshiftorinfarction.  Severe brain parenchymal atrophy, most prominent at the\ntemporal lobes, consider neuro degenerative process, similar to prior. \nFindings consistent with severe chronic small vessel ischemic changes. \nDegenerative changes cervical spine, probably moderate central canal\nnarrowing.  Minimal mucosal thickening paranasal sinuses, clear mastoids. \nPreserved vascular flow voids.\n\nMRA brain:\nLateral projecting aneurysm cavernous segment left ICA, measuring 2.5 mm from\nneck to dome, 1.8 mm at the neck.  Adjacent ICA measures 4.2 mm diameter.\n\n\nOtherwise the intracranial vertebral and internal carotid arteries and their\nmajor branches appear normal without evidence of stenosis, occlusion. d",
            "output": "1. No acute findings.\n2. Advanced brain parenchymal atrophy, most prominent at temporal lobes,\nconsider neuro degenerative process.\n3. Chronic small vessel ischemic changes.\n4. Laterally projecting 2.5 mm aneurysm cavernous segment left ICA."
        },
        {
            "input": "A 3 mm focus of slow diffusion in the right centrum semiovale (series 502,\nimage 22) does not have a definite correlate on the ADC map and suggests a\nsubacute infarct.  Focus of high signal on diffusion-weighted imaging in the\ncortical right parietal lobe (series 502, image 23) is likely artifactual.\n\nProminence of the ventricles and sulci, likely represent age related atrophy.\n\nDeep white matter and periventricular FLAIR hyperintensities are nonspecific\nbut likely represent sequela of chronic small vessel ischemic disease.\n\nThere is mild layering the gas in the maxillary sinuses, bilaterally. \nOtherwise the paranasal sinuses and the mastoid air cells are clear.  The\norbits are unremarkable.\n\nPreviously questioned asymmetry in the left fossa of ___ is not\napparent on the MR.\n\n___ pannus along the posterior dens results in mild crowding at\nthe cervicomedullary junction.",
            "output": "1. 3 mm focus of slow diffusion in the right centrum semiovale, compatible\nwith a subacute infarct.\n2. Periventricular and deep white matter FLAIR hyperintensities are\nnonspecific, but likely represent sequela of chronic small vessel ischemic\ndisease.\n3. Previously questioned asymmetry in the left fossa of ___ is not\napparent on the current MR\n4. Degenerative pannus along the posterior dens again results in mild crowding\nat the cervicomedullary junction."
        },
        {
            "input": "There is increased signal on T1 fat saturated images as well as lack of flow\nvoid on contrast imaging, from just beyond the origin of the left vertebral\nartery, to the C2/3 level, similar in overall extent compared to recent CTA\nhead and neck, allowing for differences in imaging technique.  Acute fractures\nof the left C5 and C6 transverse foramina suggest acute injury to the\nvertebral artery as the etiology for the thrombosis.\n\nThe common, internal and external carotid arteries appear normal.  There is no\nevidence of stenosis by NASCET criteria. The origins of the great vessels,\nsubclavian, andthe right vertebral arteries appear normal bilaterally.\n\nThe common carotid bifurcations appear normal.",
            "output": "1. Thrombosis of the left vertebral artery from just beyond its origin off the\nsubclavian, to the C2/3 level, similar in overall extent compared to recent\nCTA.\n2. No imaging findings to confirm that dissection as the cause of the\nthrombosis.  However, the acute transverse foramina fractures on the left\nsuggests this is the likely etiology.\n3. Remaining major vasculature in the neck is normal.\n\nNOTIFICATION:  The findings were discussed with ___, M.D. by ___\n___, M.D. on the telephone on ___ at 10:57 am, 5 minutes after\ndiscovery of the findings."
        },
        {
            "input": "There is mild periventricular white matter FLAIR signal hyperintensity likely\nrepresenting chronic microangiopathy.  There is no evidence infarct,\nhemorrhage, mass, mass effect.  The ventricles and cortical sulci are\nprominent consistent with volume loss.  There is a 2.2 AP by 3.8 TD by 2.4 SI\ncm anterior left middle cranial fossa arachnoid cyst mildly displaces the\nadjacent cortex.  The vascular flow voids are preserved.  The extra-axial\nspaces are unremarkable.  The bilateral lenses are absent.  The paranasal\nsinuses and mastoid air cells are clear.  The soft tissues the soft tissues\nand calvarium are unremarkable.",
            "output": "1. No acute intracranial abnormality without evidence of stroke.\n2. Mild periventricular white FLAIR signal hyperintensity is nonspecific but\nlikely represents sequela of chronic microangiopathy."
        },
        {
            "input": "Left parietal encephalomalacia with small amount of surrounding gliosis, which\nextends into the left frontal opercular region is unchanged from ___\nand compatible with prior infarct.  Periventricular, deep white matter and\npontine FLAIR signal hyperintensities (series 10, image 8), likely represents\nsequela of microangiopathy.  There is no evidence of acute infarct.\n\nAtrophy and subtle increase T2 signal intensity within the left hippocampus is\nunchanged from ___ (series 101, image 85).\n\nEx vacuo dilatation of the temporal horn of the left lateral ventricle, is\nunchanged from ___.  Otherwise, mild prominence of the sulci and ventricles,\nlikely represents age-related involutional changes.\n\nThe orbits are unremarkable.  There is moderate mucosal thickening and an\nair-fluid level in the left maxillary sinus, suggestive of active sinusitis. \nThe ethmoid air cells demonstrate mild mucosal thickening.  Mastoid air cells\nare clear.\n\nRight parietal T2 hypointense, T1 hyperintense scalp lesion measuring 8 mm\n(series 8, image 22) is moderately increased from ___ (previously 4 mm) and\nlikely represents a sebaceous cyst.",
            "output": "1. No acute intracranial abnormality.  Left parietal encephalomalacia and\nadjacent gliosis, unchanged from ___.  There is no acute infarct.\n2. Atrophy and subtle increased T2 signal hyperintensity within the left\nhippocampus, is unchanged from ___ and again suggestive of mesial temporal\nsclerosis.\n3. Additional nonspecific FLAIR hyperintensities likely represent sequelae of\nmicroangiopathy.\n4. Paranasal sinus disease, worse in the left maxillary sinus, where there is\nsuggestion of acute sinusitis.\n5. Right parietal scalp lesion is moderately increased from ___ and likely\nrepresents a sebaceous cyst, but direction inspection is recommended."
        },
        {
            "input": "The study is mildly degraded by motion artifact.\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  Findings consistent with severe chronic small vessel ischemic\nchanges.  Brain parenchymal atrophy.  Preserved vascular flow voids.\n\nThe paranasal sinuses and mastoid air cells are clear.  The orbits appear\nunremarkable.",
            "output": "1. No infarct..\n2. Findings consistent with chronic small vessel ischemic changes, brain\nparenchymal atrophy.."
        },
        {
            "input": "Ventricles appear normal. There is no evidence for an acute infarction.  There\nis no mass lesion or abnormal enhancement.\n\nThe major vascular flow voids are preserved.\n\nThe orbits appear normal.\n\nThere is a small amount of fluid layering within the sphenoid sinuses and\nlikely fluid within the left mastoid, similar to the ___ CT.",
            "output": "1. No intracranial mass lesion or abnormal enhancement is identified.\n2. Small amount of fluid within the sphenoid sinuses appear similar to the ___ CT sinus."
        },
        {
            "input": "Low signal on GRE within the left occipital lobe and mild associated vasogenic\nedema and local mass effect appear similar to the prior head CT.  There is\nfaint peripheral enhancement, however no nodular lesion is identified.  There\nis no slow diffusion.\n\nThere is a small focus of low signal intensity on GRE within the right lateral\ncerebellar hemisphere, likely a chronic microhemorrhage.\n\nThere is mild global parenchymal volume loss.  Confluent areas of hyperintense\nsignal on T2/FLAIR within the subcortical and periventricular white matter,\nand pons are nonspecific, but likely reflect the sequela of moderate chronic\nsmall vessel disease.  The major vascular flow voids are preserved.  The major\ncortical veins and dural venous sinuses are patent.\n\nThe orbits are unremarkable.  Endotracheal tube is noted.",
            "output": "1. Acute to subacute left occipital intraparenchymal hemorrhage with mild\nassociated vasogenic edema and local mass effect, similar to the prior CT.  No\nunderlying mass is identified.  Recommend follow-up address enhanced MR head\nin ___ months to ensure resolution.\n2. Probable moderate chronic small vessel disease.\n3. Additional findings described above."
        },
        {
            "input": "There is a focus of slow diffusion in the left pons (series 3 and 4:11) with\nassociated T2 and FLAIR hyperintense signal (series 9 and 10:10) compatible\nwith a acute to subacute infarct..  There is no intracranial hemorrhage, mass,\nmass effect, or midline shift.  Prominent ventricles and sulci are compatible\nwith age-related involutional changes.  Periventricular and subcortical T2 and\nFLAIR hyperintense signal are no-nspecific but likely represent chronic small\nvessel ischemic disease given the patient's age\n\nThere is mucosal thickening in the bilateral ethmoid air cells.  Remaining\nparanasal sinuses are clear.  Mastoid air cells and middle ear cavities are\npatent.  There is no acute fracture.",
            "output": "Focus of slow diffusion in the left pons (series 3 and 4: image 11) with\nassociated T2 and FLAIR hyperintense signal compatible with an acute to early\nsubacute infarct.\n\nNOTIFICATION:  The findings were discussed by Dr. ___ with Dr. ___\n___ on the telephone on ___ at 11:13 am, 5 minutes after discovery of\nthe findings."
        },
        {
            "input": "There is no intracranial mass, mass effect, or midline shift.  There is no\nfocal parenchymal signal abnormality besides two subcortical white-matter\nT2/FLAIR hyperintensities which are entirely nonspecific.  Ventricles and\nsulci are age-appropriate.  There is no restricted diffusion to suggest acute\ninfarct. No abnormal susceptibility artifact identified. Major intravascular\nflow voids are preserved including within the major dural venous sinuses.\n\nVisualized paranasal sinuses demonstrate no abnormal signal besides mild\nmucosal thickening in the maxillary sinuses.  Fluid signal noted within the\nright mastoids.",
            "output": "Essentially normal MRI of the brain."
        },
        {
            "input": "MRI Brain:  There is no evidence of hemorrhage, edema, masses or infarction. \nThere is mild prominence of the ventricles and sulci most likely reflecting\nmild parenchymal volume loss. The orbits are unremarkable. There is extensive\nparanasal sinusitis. There is almost complete opacification of the ethmoid air\ncells. There is fluid signal and aerosolized secretions in the sphenoid\nsinuses. There is mucosal thickening and a mucous retention cyst in the right\nmaxillary sinus and mucosal thickening with secretions in the left maxillary\nsinus. There is mild mucosal thickening of the frontal sinus.\n\nMRA brain: The intracranial vertebral and internal carotid arteries and their\nmajor branches appear normal without evidence of stenosis, occlusion, or\naneurysm formation.  There is a fetal type right PCA incidentally noted.\n\nMRA neck:  There is narrowing and irregularity of left internal carotid artery\njust distal to the bifurcation (image 10, series 105b). The right common and\ninternal carotid arteries appears normal without evidence of narrowing or\nstenosis.",
            "output": "1.  No evidence of acute hemorrhage, stroke, or mass effect.\n\n2.  Unremarkable MRA of the head without evidence of aneurysm, vascular\nmalformation, or stenosis.\n\n3.  Irregularity and narrowing of the left internal carotid artery. An\nultrasound of the carotid arteries or a CTA of the neck could be performed to\nfurther evaluate."
        },
        {
            "input": "There is mild asymmetric prominence of the right palatine tonsil which does\nnot appear masslike.  Otherwise, the aero digestive tract appears normal with\nno evidence of a mass lesion.\n\nThere are mildly prominent nonspecific right level 2A lymph nodes underlying\nmarked symptomatic site.  However, there are similar appearing left level 2\nlymph nodes.  There is no lymphadenopathy by size criteria.\n\nThe major salivary glands and thyroid appear normal.\n\nThe major vascular flow voids are preserved.  The imaged portions of the brain\nare unremarkable.  There is mild mucosal thickening in the left maxillary\nsinus.",
            "output": "1. Nonspecific asymmetric prominence of the right palatine tonsil, which can\nbe correlated with direct inspection in context of right-sided pharyngeal\nsymptoms.  No fluid collection.\n2. Nonspecific mildly prominent level 2 lymph nodes, right greater than left,\nbut which are not pathologically enlarged by size criteria."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.  There are several small foci of subcortical white matter\nintensity on the FLAIR images.  These are of doubtful clinical significance,\nbut the differential diagnosis includes demyelinating disease, chronic small\nvessel ischemia, infectious processes such as Lyme disease and white matter\nabnormalities associated with chronic headaches.",
            "output": "1. Scattered subcortical white matter hyperintensities as discussed above. \nOtherwise normal study."
        },
        {
            "input": "A small developmental venous anomaly is again seen in the right gyrus rectus.\nOtherwise, there is no abnormal parenchymal, pachymeningeal or leptomeningeal\ncontrast enhancment to suggest CNS vasculitis.  There is no evidence for\nedema, abnormal diffusion or blood products.  Sulci, ventricles and cisterns\nare normal in size. There are 2 small foci of high T2 signal in the right\nfrontal deep white matter and left frontal periventricular white matter,\nnonspecific findings, unchanged from ___.  FLAIR images demonstrate\nsymmetric hyperintensity in the sulci inferior to the bilateral rectus gyri,\nwhich likely represents incomplete suppression of CSF signal.\nMild mucosal thickening of the ethmoid air cells and mucous retention cysts in\nthe bilateral maxillary sinuses. The remainder the paranasal sinuses are\nclear. The orbits are unremarkable. The mastoid air cells are clear.",
            "output": "1. Two nonspecific small foci of high T2 signal in bifrontal white matter,\nstable since   ___, which are nonspecific but not likely to be\nrelated to vasculitis. No parenchymal or meningeal contrast enhancement to\nsuggest active vasculitis.\n2. Stable small developmental venous anomaly in the right gyrus rectus.\n3.  Hyperintensity on FLAIR images in the sulci inferior to the bilateral\nrectus gyri, likely artifacts related to incomplete CSF signal suppression.\nSuggest follow up MRI in several months."
        },
        {
            "input": "MR BRAIN:\nRedemonstrated postsurgical changes related to remote endoscopic endonasal\nresection of large pituitary macroadenoma, with expected postsurgical changes.\nAs imaged, the sella appears unchanged, with osseous expansion and a small\namount of residual tissue along the left inferolateral aspect of the sella, as\ndescribed on the recent MRI.\n\nThere is patchy ill-defined enhancement within the bilateral parahippocampal\nand inferior temporal gyri with corresponding T2/FLAIR hyperintense signal,\nleft greater than right, as noted on the recent MRI from ___, new in\ncomparison to prior MRI from ___.\n\nMR ___: Evaluation of the areas of concern on MR contrast for\nfusion imaging is significantly limited by artifact from the adjacent sinuses.\nNo definite increased blood volume or blood flow is noted in the medial\ntemporal lobes.\n\nASL Perfusion: ASL perfusion imaging is limited by artifact overlying the left\ngreater than right medial temporal lobes.  There is no evidence of increased\nperfusion in the bilateral medial temporal lobes.\n\nMR Spectroscopy: Single and multi voxel MR spectroscopy of the enhancing FLAIR\nhyperintense foci at the bilateral medial temporal lobes demonstrates\ndecreased NAA with evidence of lipid and lactate peaks, findings which are\ncompatible with radiation necrosis.",
            "output": "1. Redemonstrated postsurgical changes related to remote EEA resection of\nlarge pituitary macroadenoma, with expected postsurgical changes and unchanged\nappearance of the sella since the ___ MRI.\n2. Again noted is patchy ill-defined enhancement with T2/FLAIR hyperintensity\nin the bilateral parahippocampal and medial temporal gyri, left greater than\nright.\n3. MR contrast perfusion and ASL perfusion of the medial temporal lobes is\nlimited by artifact, however no definite increased perfusion is noted in these\nregions.\n4. MR spectroscopy demonstrates decreased NAA with evidence of lipid and\nlactate peaks within the bilateral medial temporal lobes.  Although\nnonspecific, findings are compatible with post treatment changes/radiation\nnecrosis.  Continued attention on follow up scans is recommended."
        },
        {
            "input": "Again seen are postsurgical changes related to remote endoscopic endonasal\nresection of a large pituitary macroadenoma, with expected postsurgical\nchanges, stable since prior study.  The sella appears unchanged, with osseous\nexpansion and a small amount of residual tissue along the floor of the sella\non the left.\n\nThere is redemonstration of patchy ill-defined enhancement  with corresponding\nT2/FLAIR hyperintense signal and mild cortical expansion within the left\ngreater than right hippocampal and inferior temporal gyri.  These findings are\nstable in comparison to MRI examinations from 2 months prior, dated ___ and ___.\n\nThere is no evidence of hemorrhage or mass effect.  There is prominence of the\nventricles and sulci suggestive of involutional changes.  Mild periventricular\nand subcortical T2 and FLAIR hyperintensities are noted which are nonspecific\nbut compatible with chronic small vessel ischemic changes.\n\nThere are mild ethmoid and sphenoid sinus mucosal thickening.  Is trace\nnonspecific fluid in the bilateral mastoid air cells.  The orbits and globes\nappear unremarkable, noting bilateral lens replacements.",
            "output": "1. Stable postsurgical changes related to EEA resection of large pituitary\nmacroadenoma, with an unchanged appearance of the sella.\n2. Redemonstrated T2 FLAIR hyperintense signal, cortical expansion and patchy\nheterogeneous enhancement within the left greater than right hippocampal and\ninferior temporal gyri, which appears unchanged comparison to MRI exams from\n___ and ___. In the setting of known radiation\ntreatment for cavernous sinus involvement of the large pituitary macroadenoma,\nfindings could reflect post-radiation changes.  Encephalitis is an alternate\nconsideration.\n3. No evidence of hemorrhage or mass effect."
        },
        {
            "input": "MRI brain:\n\nThe MP rage images are limited by motion.  A few FLAIR hyperintensities in the\nwhite matter are seen including a chronic appearing right frontal cortical\ninfarct (5: 6), unchanged from the prior study.  The previously noted\nenhancement in the medial temporal lobe structures is only assessed on the T1\npost-contrast images and appears to have decreased since the previous study. \nThe FLAIR hyperintensities have also considerably decreased (5:15 compared to\n15:10 of ___ examination).  Postoperative changes are again\nidentified with in both frontal regions.\n\nMRI sella:\n\nPostoperative changes are identified within the sella with deviation of the\ninfundibulum to the left side.  The posterior pituitary signal is identified\nwithin the left side of the pituitary gland at the junction of the\ninfundibulum and the pituitary fossa.  There is no significant interval change\nand no new soft tissue changes are identified to indicate recurrent adenoma.\n\nSubtle bilateral medial temporal lobe enhancement is identified (11:11) which\nhas considerably decreased compared to the previous sella MRI of ___ (18:11).",
            "output": "1. Postoperative changes are seen within the sella without signs of recurrent\nadenoma.\n2. Considerable decrease in enhancement and signal changes within both medial\ntemporal lobes since the previous MRI examinations.  The FLAIR signal\nintensities have almost resolved and subtle enhancement persist in the\nregions.\n3. No new signal abnormalities, acute infarcts or abnormal enhancement."
        },
        {
            "input": "Left basal ganglia intraparenchymal hemorrhage in the ___\n@ ___ ___: And globus pallidus is identified. There is mild surrounding\nedema seen. There is slowed diffusion at the margin of the hematoma. Extensive\nsmall vessel disease is identified. Moderate brain and medial temporal atrophy\nis seen. There are no chronic micro hemorrhages.",
            "output": "Left basal ganglia hemorrhage. Marginal signal diffusion could be related to\ncompression of brain parenchyma from hematoma or associated infarct.\nSmall-vessel disease and brain atrophy."
        },
        {
            "input": "Slow diffusion of the left insular cortex, left middle frontal gyrus, left\ntemporal opercula, posterior aspect of the head left basal ganglia as well as\nmore punctate regions of slow diffusion involving the left parietal occipital\nlobe demonstrates associated FLAIR hyperintense signal compatible with late\nacute to subacute infarct.\n\nThere is no gradient echo susceptibility to suggest hemorrhagic\ntransformation.  The major intracranial flow voids are preserved.  There is no\nevidence of intra or extra-axial mass effect.\n\nMyelomalacia and FLAIR hyperintense signal of the posterior body and splenium\nof the corpus callosum is compatible with prior infarct.\n\nThere is global cerebral volume loss, greater than would be expected for the\npatient's age.\n\nMild mucosal thickening of the maxillary sinuses is identified.  The remainder\nthe paranasal sinuses are clear.  The orbits are unremarkable.  The mastoid\nair cells are clear.",
            "output": "1. Late acute to subacute infarct of the left frontal lobe, left insula and\nbasal ganglia and left temporal lobe.  Additional punctate regions of subacute\nto late acute infarct of the left parietal occipital lobe.  The pattern is\nsuggestive of embolic infarcts.\n2. Myelomalacia and FLAIR hyperintensity of the posterior body and splenium\nthe corpus callosum is compatible with remote infarct.\n3. There is global cerebral volume loss, greater than would be expected for\nthe patient's age.  Clinical correlation is recommended.\n\nNOTIFICATION:   The findings were discussed by Dr. ___ with Dr.\n___ on the telephone on ___ at 9:33 AM, 5 minutes after discovery\nof the findings."
        },
        {
            "input": "Volumetric 3D  T1 weighted images were not obtained.\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift,\nacute infarction.  There is tiny chronic subcortical infarct involving\nanterior left parietal lobe.  There are mild to moderate chronic small vessel\nischemic changes there are mild benign perivascular spaces at the level of the\nbasal ganglia bilaterally.  There are no foci of chronic parenchymal\nmicrohemorrhage on gradient images.  There is generalized brain parenchymal\natrophy, involving frontal, parietal, temporal lobes, without disproportionate\ninvolvement of anteromedial temporal lobes.\nIncidentally seen are degenerative changes in the partially seen upper\ncervical spine, with probably moderate central canal narrowing at C3-C4 level\nfrom right paramedian disc osteophyte complex.  Minimal opacification of\nbilateral mastoid air cells is seen.  Trace mucosal thickening of paranasal\nsinuses.  Intracranial vascular flow voids are preserved",
            "output": "1. Generalized brain parenchymal atrophy.\n2. Mild to moderate chronic small vessel ischemic changes.\n3. Single small focus of chronic subcortical infarct."
        },
        {
            "input": "There is interval increase in size of an enhancing lesion within the left\ncerebellar hemisphere, which measures 0.8 x 0.7 cm, previously 0.6 x 0.4 cm\n(2:6), with corresponding flow voids.  There is an adjacent  prominent\nvascular branch that appears to communicate with the left sigmoid/ jugular\nbulb (3:37, 33), which may represent a venous draining branch.\n\nThere is slight increase in T1 hypointense signal adjacent to this enhancing\nfocus, which is difficult to further assess given the lack of additional\nsequences, but may represent associated edema, and is felt less likely to\nrepresent hemorrhage.\n\nOtherwise, there is no enhancing mass or abnormal enhancement.  The ventricles\nare normal in size without midline shift.  The visualized paranasal sinuses\nand bilateral mastoid air cells appear clear.  The orbits and visualized soft\ntissues appear unremarkable.  The dural venous sinuses otherwise appear\nunremarkable.",
            "output": "1. Interval increase in size of a left cerebellar hemisphere enhancing lesion,\nmeasuring 0.8 x 0.7 cm, previously 0.6 x 0.4 cm, likely representing the nidus\nof arteriovenous malformation with a prominent adjacent vasculature, likely a\ndraining vein.\n2. Slight increase in adjacent T1 hypointensity, which may represent\nincreasing edema."
        },
        {
            "input": "There is no intracranial mass, mass effect, or midline shift.  There is no\nacute hemorrhage or acute infarction.\nThere is moderate dilatation of the lateral and the third ventricles, somewhat\nout of proportion to generalized sulcal prominence.  The cerebral aqueduct is\npatent.\nThere is mild nonspecific periventricular, subcortical, and deep white matter\nT2/FLAIR hyperintensity. There is no pathologic intracranial enhancement.\nIntracranial flow voids are maintained.  Subtle prominence of anterior\ncommunicating artery can relate to branching point.  Left fetal PCA pattern.\nThe orbits are unremarkable. Visualized paranasal sinuses and mastoid air\ncells are clear.",
            "output": "1. Multiple nonenhancing T2/FLAIR signal hyperintense lesions in the\nperiventricular subcortical and deep white matter which are nonspecific.\nCorrelation with CSF analysis is recommended.\n\n2.  Dilatation of the ventricular system which is out of proportion to the\ndegree of generalized sulcal prominence.  These findings could be due to\ncentral parenchymal volume loss or communicating hydrocephalus such as NPH,\netc.\nClinical correlation given the h/o dysequilibrium and close followup is\nrecommended.  No priors."
        },
        {
            "input": "Please note the study is mildly degraded by motion.\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, or midline\nshift.  There are 2 punctate foci of questionable mild low diffusion in the\nright frontal lobe, series 4, image 27.  There is a stable focus of chronic\nhemorrhage in the right parietal lobe,.  There is prominence of the ventricles\nand sulci suggestive involutional changes.  There are chronic lacunar the\nmajor vascular flow voids infarctions in the pons and left basal ganglia. \nEncephalomalacia in the bifrontal lobes is seen.  The major vascular flow\nvoids are preserved.  Periventricular and subcortical T2 and FLAIR\nhyperintensities are noted.\n\nThe orbits, paranasal sinuses and mastoids are normal.",
            "output": "1. 2 punctate foci of low diffusion in the right frontal lobe, near the\nconvexity, which may represent small acute infarcts versus artifact.\n2. Stable bifrontal encephalomalacia with a background of senescent volume\nloss."
        },
        {
            "input": "There is a new area of slow diffusion involving the right ACA distribution in\nthe superior parasagittal frontal cortex extending into the right cingulate\ngyrus and posteriorly into the right parietal lobe near the vertex.\n\nThere are stable areas of encephalomalacia in bilateral anterior frontal\nlobes, right greater than left.  There is stable surrounding FLAIR signal\nabnormality.\n\nUnchanged susceptibility foci identified in the parietal lobes, suggesting\nchronic micro hemorrhagic changes (image 17, series 13 and image 21, series\n13).\n\nThe ventricles and sulci are patent and prominent in keeping with age-related\nvolume loss.\n\nThe orbits are unremarkable.  There is mild mucosal thickening in bilateral\nethmoid air cells.  The remaining visualized paranasal sinuses and mastoid air\ncells are clear.",
            "output": "1. New acute infarct in the right anterior cerebral artery distribution\ninvolving the superior parasagittal frontal lobe, right cingulate gyrus and\nareas of right superior parietal lobe near the vertex, there is no evidence of\nacute hemorrhagic transformation.\n2. Stable encephalomalacia in bilateral anterior frontal lobes, right greater\nthan left.\n\nNOTIFICATION:  The findings were discussed by Dr. ___ with Dr. ___\n___ on the telephoneon ___ at 10:18 AM, 5 minutes after\ndiscovery of the findings."
        },
        {
            "input": "The patient is status post stent-mediated coil embolization of an anterior\ncommunicating artery aneurysm, with susceptibility artifact from the stent is\nseen surrounding the A1 segment and proximal A2 segment of the right ACA.  At\nthe site of the prior aneurysm there is a stable rounded focus of low signal\nfrom the coil pack. There is evidence of minimal flow within the aneurysmal\nsac, more prominent along the posterior and right portion of the coil pack\nwhich is unchanged from ___ (series 4 image 68). There is no interval\nincrease in size of the aneurysmal sac. The internal carotids, vertebral ane\nbasilar arteries appear unremarkable. The vessels of the circle of ___ and\nits main branches, including the bilateral ACA's are patent, without evidence\nof stenosis or new aneurysm",
            "output": "Stable size and appearance of the coil embolized AComm artery aneurysm, with\nminimal flow within the aneurysmal sac also unchanged from prior MRA performed\nin ___."
        },
        {
            "input": "MRI BRAIN:  Again in comparison with the prior exam, numerous calvarial,\nmandibular and left temporomandibular T1/T2 hyperintense enhancing lesions are\nre- demonstrated, there is persistent expansion in the clivus with\nheterogeneous enhancing mass lesion as demonstrated in the images with fat\nsuppression and gadolinium technique, extending towards the petrous segments\nand clivus bilaterally (Image 1 through 9, series 10).  No diffusion\nabnormalities are detected to indicate acute or subacute ischemic changes.\n\nMRI OF THE ORBITS:  In the coronal fat suppression technique with gadolinium\ncontrast, the multiple bone metastatic lesions are better depicted including\nthe orbital regions, in comparison with the prior exam, the previously noted\nlobulated T1 hypointense, T2 hyperintense heterogeneous enhancing lesion and a\nleft superior orbit appears slightly smaller, measuring approximately 10 x 10\nmm in coronal projection and previously 14 by 15 mm.  , with persistent mass\neffect in the left optic nerve, better depicted in the coronal images (image\n10, series 11).  There is a small area of enhancement adjacent to the right\nsphenoidal fissure, probably causing mass effect in the right optic nerve\n(image 11, series 10), also suspicious for metastatic disease.\nPersistent mucosal thickening is seen in the maxillary sinuses bilaterally.",
            "output": "1. Numerous unchanged calvarial enhancing lesions, as described in detail\nabove, including left orbital lesion, which apparently is slightly smaller in\ncomparison with the prior study, however with persistent mass effect and mild\ndisplacing the left optic nerve inferiorly, and likely consistent with\nplasmacytoma from multiple myeloma.\n2. Small unchanged area of enhancement is identified in the right sphenoidal\nfissure adjacent to the optic nerve, also suspicious for metastatic disease.\n3. There is no evidence of acute intracranial process."
        },
        {
            "input": "The small left-sided frontoparietal subdural hematoma measuring 5 mm is\nidentified with minimal indentation on the adjacent brain.  There is no\nmidline shift or hydrocephalus. Chronic blood products identified along the\ncerebellum indicating superficial siderosis and chronic micro hemorrhages are\nseen in both medial occipital lobes. Mild brain atrophy seen. No evidence of\nsignificant subcortical white matter ischemic disease seen. The suprasellar\nand craniocervical regions are unremarkable.",
            "output": "Small 5 mm subacute to chronic left-sided subdural hematoma and frontoparietal\nregion without significant mass effect or midline shift. Minimal indentation\nand obliteration of adjacent sulci seen.  Findings of chronic micro\nhemorrhages and superficial siderosis identified indicating prior hemorrhage\nfrom amyloid angiopathy or other etiology."
        },
        {
            "input": "The left middle cerebral peduncle demonstrates a focus of slow diffusion with\ncorresponding FLAIR hyperintensity.  There is no hemorrhage.  There is diffuse\nparenchymal volume loss without midline shift.  There are nonspecific\nperiventricular and subcortical FLAIR hyperintensities, likely a sequela of\nchronic small vessel microangiopathy.  The visualized arterial vascular flow\nvoids are preserved; please refer to recent CTA for additional details.  There\nis partial bilateral maxillary, and ethmoid air cell opacification.",
            "output": "1. Left middle cerebral peduncle acute to early subacute infarction, without\nhemorrhage.\n2. Diffuse parenchymal volume loss with commensurate prominence of the\nventricles, sulci, and cisterns.\n\nNOTIFICATION:  The findings were discussed with ___, M.D. by\n___, M.D. on the telephone on ___ at 09:50, 2 minutes\nafter discovery of the findings."
        },
        {
            "input": "Redemonstrated are postsurgical changes related to right frontal craniotomy,\nwith stable appearance of the nodular enhancement along the medial aspect of\nthe surgical bed.  The dominant hemorrhagic lesion within the left parietal\nlobe, measures approximately 24 mm x 13 mm, not significantly changed in size\ncompared to the prior exam (9; 121).  The extent of FLAIR hyperintensities\nsurrounding this lesion also appears grossly unchanged compared to the prior\nexam.\n-the previously seen enhancing lesion adjacent to the left lateral ventricle\nis not definitively seen on the current exam.\n-there has been interval improvement of the now 1 mm lesion within the left\nsuperior paramedian parietal lobe (9; 97).\n-the previously seen metastases within the right frontal lobe near the vertex,\nare not seen on the current exam.\n-the previously seen enhancing focus along the lateral aspect of the right\nfrontal lobe is not seen on the current exam.\n-the previously seen 8 mm lesion along the right temporal lobe, now\ndemonstrates a small remnant ring-enhancing lesion measuring approximately 3\nmm (9; 81.)\n\nVentricles and sulci are age appropriate.  Mucous retention cyst is seen\nwithin the right maxillary sinus.",
            "output": "1. Overall, significant interval improvement in the burden of disease compared\nto the prior exam from ___.\n2. The dominant hemorrhagic lesion within the left parietal lobe measuring up\nto 24 mm, has not significantly changed in size."
        },
        {
            "input": "Study is mildly degraded by motion.\n\nGrossly stable postsurgical changes related to right frontal craniotomy and\nmass resection again seen, including blood products grossly stable T2/FLAIR\nhyperintensity.  Surgical bed again demonstrates nodular enhancement along the\nmedial aspect, grossly unchanged.\n\nLeft parietal hemorrhagic peripherally enhancing lesion with associated T1\nhyperintensity and increase susceptibility is grossly unchanged, again\nmeasuring approximately 2.4 x 1.3 cm.  Grossly stable T2 and FLAIR\nhyperintensity surrounding this lesion is again seen.\n\nNew punctate right temporal enhancing lesion is seen (see 16:56).\n\nNew punctate left medial occipital enhancing lesions are seen (see 16:77,\n102).\n\nNew punctate left temporal enhancing lesion is seen (see 16:74).\n\nNew punctate right frontal enhancing lesion inferior to surgical bed is seen\n(see 16:24).\n\nNew punctate right parietal enhancing lesion is seen (see 16:37).\n\nNew punctate right parasagittal precentral gyrus enhancing lesion is noted\n(see 16:144).\n\nThere has been interval progression of right cerebellar nodular enhancement,\nnow measuring approximately 7 mm, previously having measured approximately 4 x\n1 mm (see 19:7 on current study and 10:5 on prior exam).\n\nThere is interval progression left superior frontal gyrus approximately 2 mm\nlesion, previously approximately 1 mm on prior exam (see 16:151).\n\nGrossly stable punctate medial left occipital enhancing lesion is again seen\n(see 16:101 on current study and 9:97 prior study).\n\n\nGrossly stable approximately 2 mm left frontal focus of increased\nsusceptibility with peripheral enhancement is grossly unchanged (see 16:144;\n14:22 on current study and 9:113 on prior exam).\n\nGrossly stable left frontal punctate focus of chronic blood products versus\nmineralization without definite associated enhancement is again seen (see\n14:17 and 16:110 on current study and 6:15 on prior study).  Additional\ngrossly stable nonenhancing right medial occipital focus of increased\nsusceptibility is again seen (see 14:13 and 16:85 on current study and 6:12 on\nprior study).\n\nRight lateral temporal nonenhancing lesion is grossly unchanged (see 16:7 on\ncurrent study and 9:81 on prior exam).\n\nA new punctate focus of increased susceptibility without definite associated\nenhancement of the posterior right cingulate gyrus is seen (see 14:19 and\n16:125 on current study and 6:18 on prior exam).\n\nThere is no evidence of midline shift or acute infarction.  The ventricles and\nsulci are grossly stable in caliber and configuration.\n\nRight maxillary sinus mucosal thickening is present.  Bilateral maxillary\nsinus probable mucosal retention cysts are seen.",
            "output": "1. Study is mildly degraded by motion.\n2. Multiple new punctate enhancing lesions as described, concerning for tumor\nprogression.\n3. Grossly stable postsurgical changes related to right frontal craniotomy and\nmass resection with nonspecific nodular enhancement.  While enhancement may\nrepresent postsurgical change, residual tumor is not excluded on the basis of\nthis examination.  Recommend attention on follow-up imaging.\n4. Interval progression of right cerebellar and left frontal enhancing\nlesions, as described.\n5. Additional grossly stable intracranial lesions as described.\n6. New nonenhancing posterior right cingulate gyrus focus of chronic blood\nproducts versus mineralization compared to ___ prior exam.\n7.  Paranasal sinus disease, as"
        },
        {
            "input": "The patient is status post right frontal craniotomy with essentially unchanged\npostoperative changes.\n\nThere is numerous intra-axial enhancing abnormalities as follows:\n\n-Questionable minimal interval enlargement of left thalamic enhancing focus of\nless than 2 mm (series 17, image 95).\n-Interval stability of multifocal right frontal surgical margin nodular\nenhancement (series 17, image 141).\n-Interval stability of left frontal (series 17, image 139) and left parietal\n(series 17, image 130) parenchymal enhancing abnormalities.\n-Mild interval decrease in size of left occipital (series 17, image 86) and\nright cerebellar (series 17, image 32) enhancing abnormalities.\n-There is resolution of previously identified multiple left frontal, right\nparietal, bilateral temporal enhancing abnormalities.\n-Interval stability of right frontal intrinsic T1 hyperintensity (series 16,\nimage 16) with corresponding signal void at T2 star images and questionable\ncorresponding abnormal enhancement which may be related to hemorrhagic\nmetastasis.\n\nThere are supratentorial multifocal signal void at T2 star images; not\nsignificantly changed since the previous examination.  However; there is only\n1 newly developed right frontal microhemorrhages on T2 star sequence is\nidentified (series 14, image 16).  There is redemonstration of areas of\nincreased DWI signal intensity at left parietal and right frontal regions;\nunchanged.\n\nThere is no evidence of midline shift or acute infarction.  The ventricles and\nsulci are normal in caliber and configuration.  Both orbits are normal.  There\nare bilateral mucous retention cyst at both maxillary sinuses with mild\nmucosal thickening involving ethmoid air cells.  Paranasal sinuses and mastoid\nair cells otherwise are clear.  There is no definite aggressive osseous\nprocess identified.",
            "output": "1. Either interval stability or interval decrease of previously identified\nnumerous brain parenchymal enhancing abnormalities as detailed.  About 10\nsupra and infratentorial enhancing abnormalities identified in this\nexamination.\n2. There is no definite convincing newly developed abnormal intracranial\nenhancement.\n3. No acute intracranial abnormality."
        },
        {
            "input": "Study is degraded by motion.  The patient is status post right frontal\ncraniotomy. There is stable susceptibility deep to the surgical site,\ncompatible with chronic blood products and/or mineralization related to\nresection.\n\nThere are multiple enhancing parenchymal cerebral nodules which appear stable\nor improved as described below.\n\n-In the right frontal superior and middle gyri, deep to the craniotomy, there\nis parenchymal enhancement which is stable from prior.\n-In the right inferior frontal gyrus, there is a stable region of enhancement\nmeasuring 3 mm (series 17, image 120).\n-In the left middle frontal gyrus, there is a stable, 4 mm ring enhancing\nlesion (series 17, image 146).\n-In the white matter adjacent to the atrium of the left lateral ventricle,\nthere is a stable appearing 3 mm enhancing nodule (series 17, image 97).\n-In the left parietal lobe, there is a 19 x 10 x 13 mm (AP by transverse by\nSI) peripherally enhancing lesion which demonstrates slow diffusion and is\nstable in size from prior examination (series 17, image 124).  This lesion\nagain demonstrates minimal intrinsic T1 hyperintensity, concerning for\nsubacute blood products (see 12:20 on current study and 12:20 on ___\nprior exam).\n-Right posterior cingulate gyrus focus of increased susceptibility with T1\nhypointensity and adjacent minimal curvilinear hyperintensity versus adjacent\nvasculature is grossly unchanged (see 14:19; 17:118; 19:43; 18:29 on current\nstudy and 14:18; 17:118; 18:28 on prior exam).\n-Previously described subtle left occipital enhancement is not visualized on\ntoday's examination.\n-Previously described right cerebellar lesion can questionably be seen on\nseries 17, image 27.  The degree of enhancement is less conspicuous on today's\nimaging.\n\nThere are foci of susceptibility in the bilateral frontal lobes and medial\nright parietal lobe which are stable from prior, and likely represents old\nhemorrhage or mineralization.\n\nThe ventricles and sulci are grossly stable in caliber and configuration.\n\nThere bilateral maxillary retention cysts versus polyps are noted.",
            "output": "1. Multiple enhancing foci in bilateral cerebral and right cerebellar\nhemispheres appear stable or improved as compared to prior examination.\n2.  Within limits of study, no definite new intracranial enhancing lesions.\n3.  Paranasal sinus disease , as described.\n4.  Additional findings as described above."
        },
        {
            "input": "Seen in the high right frontal region, there is a lobulated relatively well\ndefined and circumscribed, 2.4 x 2.2 x 1.5 cm (SI by AP by TV) T2/FLAIR\nhyperintense mass with internal foci of susceptibility artifact and intrinsic\nT1 hyperintensity likely representing trace intralesional hemorrhage, which\ndemonstrates relatively homogeneous enhancement following the administration\nof contrast. The mass demonstrates slight high signal on diffusion-weighted\nimages without clear low ADC value, likely T2 shine through. It is difficult\nto ascertain whether the lesion is parenchymal, based within the cortex or\nsubcortical white matter, or extra-axial with an imperceptible dural tail; the\nmass abuts and is inseparable but is not clearly contiguous with the overlying\ndura (for example see series 901, image 67).  There is no adjacent parenchymal\nedema. There is minimal mass effect on the adjacent brain parenchyma, slight\neffacement of the regional sulci.  No shift of midline structures.\n\nElsewhere, there is no evidence of infarction, hemorrhage, or extra-axial\ncollection.  No mass effect.\n\nThe ventricles and sulci are normal in caliber and configuration.\n\nThere are mucous retention cysts in the maxillary sinuses bilaterally. \nRemaining visualized paranasal sinuses, mastoids, appear clear.\n\nThe globes and orbits are unremarkable.\n\nMajor intracranial vascular flow voids are preserved.  Major dural venous\nsinuses are patent.",
            "output": "2.4 cm right frontal region enhancing mass with trace foci of intralesional\nhemorrhage.  It is unclear whether the mass is parenchymal or extra-axial;\nalthough the enhancement pattern and signal characteristics suggest\nmeningioma, there is no clear dural tail.  If intraparenchymal, a cortically\nbased lesion such as oligodendroglioma should be considered.  Metastasis\ncannot be excluded, although a metastasis of this size without parenchymal\nedema would be unusual."
        },
        {
            "input": "The patient's previously noted 2.4 cm probably extra-axial mass occupying a\nportion of the right superior frontal sulcus is again seen.  There is no\nmidline shift and mild mass effect.  No additional enhancing lesions\nidentified.  No evidence of acute intracranial hemorrhage or infarction.\nUnchanged right maxillary sinus mucous retention cyst.",
            "output": "Unchanged 2.4 cm right frontal mass.  Examination performed for surgical\nplanning with surface markers."
        },
        {
            "input": "Status post right frontal craniotomy for mass resection.  Expected\npostsurgical changes are noted, including pneumocephalus, blood products, and\npachymeningeal thickening overlying the right cerebral hemisphere.  Restricted\ndiffusion surrounding the surgical site likely represents post manipulation\nischemia.  Small amount marginal enhancement may be reactive in etiology. \nFLAIR signal hyperintensity likely represents postoperative edema.  No\ndefinite abnormal enhancement to suggest residual tumor.\n\nSmall mucous retention cysts seen in bilateral maxillary sinuses.  The\nremaining of the paranasal sinuses and maxillary air cells clear.",
            "output": "Status post right frontal craniotomy and resection with expected appropriate\npostsurgical changes."
        },
        {
            "input": "Patient is status post right frontal craniotomy and resection of the right\nfrontal tumor.  Compared to the exam from ___, the postcontrast\nimages demonstrate interval increase in hyperintensity within and peripherally\nsurrounding the surgical bed, measuring approximately 25 mm x 17 mm, series\n12, image 150.  Dural thickening and likely enhancement underlying the right\nfrontal surgical bed also appears slightly progressed compared to the prior\nexam.  Heterogeneous areas of slow diffusion within the right frontal surgical\nbed appears slightly increased compared to the prior exam.\n\nThere is no evidence of a large territorial infarction.  The dural venous\nsinuses are patent.  A mucous retention cyst is seen along the floor of the\nright maxillary sinus.  The globes are grossly unremarkable.  Mild mucosal\nsinus thickening is seen involving the ethmoid air cells.",
            "output": "1. Status post right frontal craniotomy and resection of the right frontal\ntumor.  Overall, interval increase in hyperintensity on the postcontrast\nimages within and peripherally surrounding the right frontal surgical bed\nspanning approximately 25 mm x 17 mm compared to the exam from ___\ncould be secondary to evolution of the blood products and associated reactive\nchanges, although progressive neoplastic process cannot definitively be\nexcluded on these limited sequences.\n2. No evidence of a large territorial infarction.\n3. Mild paranasal sinus disease."
        },
        {
            "input": "Right frontal vertex craniotomy is again seen.  Subjacent small extra-axial\nfluid collection is stable to minimally decreased compared to ___.\nSubjacent linear dural enhancement is unchanged.  There is minimal residual\nmarginal T1 hyperintensity in the right frontal surgical bed. There is thin\nlinear contrast enhancement along the surgical bed margins without evidence\nfor nodular components, with a rim enhancing area now measuring 2.1 x 1.3 cm\non images ___, compared to 2.5 x 1.7 cm on ___.  There is\nminimal T2/FLAIR hyperintensity along the inferomedial margin of the surgical\nbed.  There is no shift of midline structures.  Ventricles and basal cisterns\nare normal in size.\n\nNo new enhancing lesion is identified.  No new edema, acute infarction, or\nevidence for new unexpected blood products.\n\nMajor arterial flow voids are grossly preserved.  Dural venous sinuses are\npatent on postcontrast MP RAGE images.\n\nThere are mucous retention cysts in the maxillary sinuses, right greater than\nleft, similar to prior.  Minimal mucosal thickening is also again seen in the\nethmoid air cells.",
            "output": "1. Right frontal vertex surgical cavity has decreased in size compared to ___, demonstrating thin marginal contrast enhancement without\nevidence for nodular components.\n2. No evidence for new enhancing lesions."
        },
        {
            "input": "The patient is status post right frontal vertex craniotomy.  A small\nextra-axial fluid collection overlying the right frontal lobe has decreased\ncompared to prior.  There is thin rim enhancement surrounding the right\nfrontal resection cavity measuring 2.1 x 1.3 cm, unchanged (17; 145, 146). \nFLAIR hyperintensity and a small amount of chronic blood product are again\nseen within the resection cavity.  Overlying dural enhancement is unchanged.\nThere is no evidence of new lesion, acute hemorrhage, mass effect, midline\nshift or infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.\nThe major intracranial vascular flow voids maintained.  The dural venous\nsinuses are patent.\nSubmucosal retention cysts are seen in bilateral maxillary sinuses.  There is\nminimal mucosal thickening of the ethmoid air cells and moderate mucosal\nthickening of the right sphenoid sinus.  The orbits are unremarkable.",
            "output": "Stable appearance of a right frontal resection cavity with persistent thin rim\nenhancement without new nodularity .  No evidence of new metastatic lesions."
        },
        {
            "input": "The patient is status post right frontal vertex craniotomy.  The small\nextra-axial fluid collection has near completely resolved.  The area of thin\nrim enhancement in the right frontal resection cavity appears slightly\nimproved, measuring 1.5 x 1.1 cm, previously 2.1 x 1.3 cm (series 8, image\n116).  FLAIR hyperintensities and small amount of blood products within the\nresection bed are stable to slightly improved.  Overlying dural enhancement is\nslightly improved.  There is increased enhancement in the burr hole site, more\nconspicuous from prior (series 8, image 126).\n\nThere is no definite evidence of new lesion, acute hemorrhage, infarction,\nmass effect or midline shift.  The dural venous sinuses are patent.  The major\nvascular flow voids are preserved.  Mucous retention cysts are seen within the\nmaxillary sinuses.  There is mild mucosal thickening of the ethmoidal air\ncells.  The orbits are unremarkable.",
            "output": "1. Similar appearance of right frontal resection cavity with persistent but\nslightly decreased amount of rim enhancement.  No new nodularity.  No definite\nevidence of new metastatic lesions.\n2. Enhancement at the burr hole site is more conspicuous from prior. \nRecommend attention to this area on follow-up examinations\n3. Findings consistent with sinus disease."
        },
        {
            "input": "Postsurgical changes are again demonstrated from right superior frontal\ncraniotomy.  Dural thickening and enhancement subjacent to the craniotomy site\nis again demonstrate.  Trace extra-axial fluid at the craniotomy site is\nnoted, almost entirely resolved.\n\nThere is continued although improved thin rim enhancement at the frontal\nresection cavity, which again shows decreased compared to the previous\nexamination enhancement at the burr hole site is again demonstrated an appears\nslightly decreased compared to the previous exam.  There are no definite new\nlesions.  Blood products noted at the resection site.\n\nThere is no evidence of new hemorrhage, edema, masses, mass effect, midline\nshift or infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.\n\nThe major intracranial vascular flow voids are preserved.  Orbits are\nunremarkable.  There are mucous retention cysts in the bilateral maxillary\nsinuses and there is mild scattered mucosal thickening in the ethmoid air\ncells, sphenoid sinus, and maxillary sinuses",
            "output": "Decrease in enhancement at the right frontal resection cavity.  No new\nnodularity.  No new enhancement elsewhere to suggest new metastatic disease.\n\nEnhancement at the right frontal burr hole site is again demonstrated and\nappears slightly decreased from the previous exam."
        },
        {
            "input": "There is a new intra-axial mass in the left parietal lobe, likely in the\npostcentral gyrus, measuring approximately 3.1 x 3.1 x 3.0 cm (AP, transverse,\nSI).  The mass demonstrate peripheral intrinsic T1 hyperintensity, with\ncentral T1 hypointensity, as well as predominantly T2/FLAIR hyperintensity. \nThere is associated surrounding vasogenic edema resulting in mild mass effect\non the adjacent parenchyma.  Additionally, the mass demonstrate diffusion\nrestriction.  The intrinsic T1 hyperintensity limits the evaluation of with\nthe mass demonstrates enhancement are not.\n\nThere is also a new small lesion in the body of the left corpus callosum that\ndemonstrate T1 hypointensity, T2 and FLAIR hyperintensity, and diffusion\nrestriction.  It measures approximately 8 x 8 x 11 mm.\n\nThere is is a new small enhancing lesion in left superior parietal lobule\n(10:99).  This lesion also demonstrates T2/FLAIR hyperintensity and\nisointensity on T1 weighted images.\n\nThere is stable redemonstration of postsurgical changes of right frontal\ncraniotomy.\n\nThere is no evidence of midline shift.  The ventricles and sulci are normal in\ncaliber and configuration.  The vascular flow voids are grossly unremarkable. \nThe dural venous sinuses are patent.  Stable mucous retention cyst in the\nbilateral maxillary sinuses with associated mucosal thickening in the\nbilateral ethmoid air cells.  The bilateral mastoid air cells are clear.  No\nabnormal marrow signal.",
            "output": "1. New large hemorrhagic lesion with surrounding vasogenic edema in the left\nparietal lobe, and additional enhancing lesions in the a body of the left\ncorpus callosum and left superior parietal lobules, raises concern for new\nmetastatic disease, in keeping with patient history of sarcoma.\n2. Stable postsurgical changes of right frontal craniotomy.\n3. Moderate paranasal sinus disease as described above.\n\nNOTIFICATION:  The impression and recommendation above was entered by Dr.\n___ on ___ at 13:03 into the Department of Radiology\ncritical communications system for direct communication to the referring\nprovider."
        },
        {
            "input": "There is redemonstration of postsurgical changes related to right frontal\ncraniotomy with slightly increased amount of nodular contrast enhancement\nalong the medial aspect of the surgical bed (10:276).  There has been interval\ndecreased size of the  intra-axial enhancing mass along the left parietal lobe\ncentered in the left postcentral gyrus now measuring 2.6 x 1.7 x 2.5 cm,\npreviously 3.1 x 3.1 x 3 cm.  This mass appears intrinsically T1 hyperintens. \nThere is decreased regional FLAIR hyperintensity surrounding the adjacent\nparenchyma.\n\nThere is decreased size of the additional smaller lesions including:\n6 x 4 mm enhancing focus adjacent to the left lateral ventricle, possibly in\nthe body of the corpus callosum (10:189), decreased in size previously 8 x 8 x\n11 mm in maximal dimension.\n2 mm enhancing lesion in the left superior paramedian parietal lobe (10:197),\ndecreased in size previously 6 mm.\n\nMultiple new punctate enhancing lesions with the majority demonstrating FLAIR\nhyperintensity included:\nTwo 2 mm enhancing FLAIR hyperintense lesions in the right frontal lobe near\nthe vertex ___: 253).\n4 mm enhancing focus along the lateral aspect of the right frontal lobe and 2\nmm enhancing focus along the right parietal lobe (10:209)\n1 mm punctate focus in the left parietal lobe (10:207)\n8 x 7 mm enhancing lesion along the right temporal lobe (10:170).\n3 mm enhancing focus in the left cerebellar hemisphere (10:87).\n\nThere is no evidence of acute hemorrhage, midline shift or acute infarction. \nThe ventricles and sulci are normal in caliber and configuration.  The major\nintracranial flow voids are maintained.  The dural venous sinuses are patent.\n\nThere is mucosal thickening within the right frontoethmoidal recess, multiple\nethmoid air cells and bilateral maxillary sinuses with near complete\nopacification of the left maxillary sinus.  No significant fluid signal is\nseen in the mastoid air cells.  The visualized orbital structures and soft\ntissues are within normal limits.",
            "output": "1. Multiple new scattered subcentimeter enhancing lesions in the right\nfrontal, right temporal and bilateral parietal lobes as well as the left\ncerebellar hemisphere with the largest measuring  8 x 7 mm in the right\ntemporal lobe concerning for new metastatic disease.\n2. Postsurgical changes related to a right frontal craniotomy with slightly\nincreased nodular enhancement along the resection cavity.\n3. Decreased size of the dominant hemorrhagic lesion in the left parietal lobe\ncentered in the postcentral gyrus and smaller enhancing lesions in the body of\nthe left corpus callosum and left superior parietal lobe near midline, likely\nrelated to positive treatment response.\n4. Reduced FLAIR hyperintensity surrounding the hemorrhagic lesion in the left\nparietal lobe, possibly representing edema.\n5. Persistent moderate paranasal sinus disease as described above."
        },
        {
            "input": "The patient is status post left frontal craniectomy and resection of a left\nfrontal lobe mass. A 5 mm T2 hypointense nodule along the posterior medial\nportion of the resection cavity demonstrating mild enhancement, is essentially\nunchanged in size and configuration from prior exam. Previously noted layering\nof fluid/ hemorrhage products in the resection cavity has resolved.\n\nWhen compared to the prior exam, cortical thickening with gyriform enhancement\nalong the lateral margin of the resection cavity within the lateral left\nfrontal lobe has now resolved. There remains mild cortical thickening with\nenhancement along the medial frontal cortex, which demonstrates interval\ndecrease in conspicuity and size from prior exam. The waxing and waning nature\nof this finding would suggest epileptic foci rather than tumor recurrence. No\nnew foci of abnormal enhancement. The arterial spin labeling sequences are\ntechnically limited and nondiagnostic.\n\nNo evidence of acute infarct. No new intra or extra-axial hemorrhage or mass.\nSulci, ventricles and cisterns are within expected limits, noting mild ex\nvacuo dilatation of the anterior horn and body of the left lateral ventricles\nsecondary to ex vacuo dilatation. Periventricular and subcortical nonspecific\nT2/FLAIR hyperintensities are noted, which are commonly seen in setting of\nsmall vessel ischemic disease. Gliosis surrounding the resection bed is noted.\nThe major flow voids are preserved. There is a mucous retention cyst in the\nleft maxillary sinus. Otherwise the paranasal sinuses are clear. The orbits\nare unremarkable. The mastoid air cells are clear.",
            "output": "1. Interval resolution of cortical thickening and enhancement along the\nlateral margin of the left frontal lobe resection cavity, with significant\ndecrease residual cortical thickening and enhancement of the left medial\nfrontal cortex. The waxing and waning nature of this finding would suggest\nepileptic activity rather than tumor recurrence.\n\n2. Unchanged appearance of the resection bed with stable T2 hypodense nodule\nalong the posterior medial portion of the resection cavity.  No new enhancing\nlesions."
        },
        {
            "input": "There are postoperative changes of a prior left frontal craniotomy with\nunderlying left frontal resection cavity and associated encephalomalacia.\nThere is no evidence of acute intracranial hemorrhage or mass effect.\n\nThere is no evidence of acute ischemia based on diffusion-weighted imaging.\nThere are normal vascular flow voids. There is confluent T2/FLAIR signal\nhyperintensity surrounding the resection cavity which is presumably on the\nbasis of prior radiation therapy. This appears unchanged when compared to\nprior exam. There are additional punctate in confluent subcortical and\nperiventricular white matter T2/FLAIR signal hyperintensity which may relate\nto sequelae of chronic small vessel ischemic disease. The ventricles appear\nprominent which is likely on the basis of brain volume loss.\n\nWhen compared to prior exam, the enhancement within the medial aspect of the\nright frontal lobe, adjacent to the resection cavity has resolved. Minimal\nresidual left subdural enhancement likely reflects normal postoperative change\nand appears similar to prior exam.",
            "output": "1. Postoperative change of prior left frontal craniotomy with left frontal\nresection cavity.\n2. Left frontal T2/FLAIR signal hyperintensity surrounding the resection\ncavity which is presumably on the basis of prior radiation therapy.\n3. Resolution of enhancement within the medial aspect of the right frontal\nlobe, adjacent to the resection cavity.\n4. No evidence of new abnormal enhancement, acute intracranial hemorrhage,\nmass effect, or acute ischemia."
        },
        {
            "input": "Please note the study is degraded by motion. There are postoperative changes\nof a prior left frontal craniotomy with subjacent cystic resection cavity,\nassociated volume loss with ex vacuo dilatation of the left lateral ventricle,\nand surrounding T2/FLAIR signal hyperintensity.  There is unchanged dural\nenhancement at the resection site which is likely on a postoperative basis.\nThere are no new areas of nodular enhancement surrounding the resection site.\nThere are no new lesions or new areas of abnormal brain parenchymal or\nleptomeningeal enhancement.\n\nThere are gradient signal hypointense foci are within the resection site,\nlikely on the basis of old postoperative blood products, with additional\nscattered punctate foci of gradient signal hypointensity within the left basal\nganglia and left frontal lobe which also likely represent chronic\nmicrohemorrhages.\n\nThere are normal vascular flow voids. There is no evidence of acute infarct\nbased on diffusion-weighted imaging. There is diffuse brain parenchymal volume\nloss. There is additional punctate in confluent subcortical/periventricular\nT2/FLAIR signal hyperintensity which may be on the basis of chronic\nmicroangiopathy.\n\nThere is a left maxillary sinus mucosal retention cyst. The orbits, mastoid\nair cells, and remaining paranasal sinuses are unremarkable.",
            "output": "1.  Study is degraded by motion.\n2. Postoperative changes related to patient's prior left frontal anaplastic\noligodendroglioma resection as described.\n3. Within limits of study, no definite evidence of residual or recurrent\ndisease.\n4. No evidence of acute intracranial hemorrhage or acute infarct.\n5. Atrophy and probable small vessel ischemic changes as described.\n6. Paranasal sinus disease as described."
        },
        {
            "input": "Images are limited by motion artifact.  However, both postcontrast axial T1\nweighted and postcontrast MP RAGE images demonstrate a 3 x 1 mm enhancing\nfocus in the left genu of the corpus callosum abutting the left lateral\nventricle, images 16:17, 19:77, 18:49, which is not seen on prior exams.  This\nis not contiguous with the left frontal surgical cavity.  The left frontal\nsurgical cavity margins demonstrate persistent linear high signal on pre and\npostcontrast T1 weighted images without evidence for new contrast enhancement.\n\nThere is high T2 signal surrounding the left frontal surgical cavity and\nextending into the left frontal white matter, including the internal and\nexternal capsules.  This is contiguous with high T2 signal in the genu, body,\nand splenium of the corpus callosum bilaterally, as well as along the frontal\nhorn and body of the right lateral ventricle.\n\nDiffuse ventriculomegaly, with superimposed ex vacuo enlargement of the\nfrontal horn and anterior body of the left lateral ventricle, are unchanged\ncompared to ___ and ___.  Enlargement of the sylvian fissures,\nand to a lesser extent of the cerebral sulci, is also unchanged.  Marked\nthinning of the corpus callosum is unchanged.\n\nChronic blood products are again seen along the left frontal surgical cavity\nmargins.  Foci of chronic blood products are also again seen within the left\nlentiform nucleus and left external capsule.\n\nThere is no acute diffusion abnormality.\n\nMajor arterial flow voids appear grossly preserved.  Major dural venous\nsinuses appear patent on postcontrast MP RAGE images.\n\nThere is severe mucosal thickening is with the maxillary sinuses, right\ngreater than left, with near-complete opacification on the right.  There is\nsevere mucosal thickening in the right ethmoid air cells and mild mucosal\nthickening in the left ethmoid air cells.  There is moderate mucosal\nthickening in the right sphenoid sinus.  These findings are new since ___.",
            "output": "1. Motion limited exam.\n2. New 3 x 1 mm enhancing focus in the left genu of the corpus callosum\nabutting the left lateral ventricle, which is not contiguous with the left\nfrontal surgical cavity.  This area is encompassed by unchanged high T2 signal\nthroughout the genu, body, and splenium of the corpus callosum bilaterally,\nwhich is contiguous with unchanged right periventricular high T2 signal and\nwith unchanged extensive high T2 signal in the left frontal white matter.  The\nnew enhancing lesion is concerning for active tumor.\n3. No new contrast enhancement along the left frontal surgical cavity margins.\n4. Extensive inflammation of bilateral maxillary sinuses, right ethmoid air\ncells, and right sphenoid sinus, new compared to ___.\n\nNOTIFICATION:  The impression above was entered by Dr. ___ on\n___ at approximately 15:45 into the Department of Radiology critical\ncommunications system for direct communication to the referring provider."
        },
        {
            "input": "MR BRAIN:  The patient is status post left frontal craniotomy with stable\npostoperative persistent mild left hemispheric dural thickening and\nenhancement.  Hemorrhage products within the resection cavity is also stable. \nPreviously described new left genu of the corpus callosum enhancing focus has\nsignificantly decreased in size and is barely perceptible when compared to the\nprior exam.  The left frontal surgical cavity demonstrates persistent mild\nlinear T1 hyperintense intrinsic signal without definitive postcontrast\nenhancement.  Speckled left basal ganglia and enhancement is unchanged.  There\nis no new abnormal enhancement.  Ex vacuo dilatation of the frontal horn of\nthe left lateral ventricle is unchanged in configuration from prior exam. \nFLAIR white matter left frontal and corpus callosal hyperintense signal is\nunchanged in configuration from the prior examination.\n\nSuperimposed periventricular and subcortical nonspecific white matter T2/FLAIR\nhyperintense signal is compatible with chronic microangiopathy in a patient of\nthis age.  There is no acute intracranial hemorrhage or infarct.  There is\nmild ventriculomegaly, compatible with an does signal changes, unchanged from\nprior exam.  The major intracranial flow voids are preserved.  The dural\nvenous sinuses are patent.  The paranasal sinuses are essentially clear.  The\norbits are unremarkable.  The mastoid air cells are clear.\n\nMR ___: There is decreased blood flow and blood volume to the\nleft frontal lobe compatible with postsurgical changes encephalomalacia. \nThere is no increased perfusion to the FLAIR hyperintense left left frontal\nlobe and anterior corpus callosum.\n\nASL Perfusion: There is no increased perfusion on ASL.\n\nMR Spectroscopy: Single voxel spectroscopy centered in the FLAIR hyperintense\nleft frontal white matter above the resection cavity demonstrates mildly\nincreased choline to NAA of approximately 1.1, essentially unchanged from\nprior examinations dating to ___.  Multi voxel spectroscopy centered\nover the resection cavity and the contralateral normal-appearing right frontal\nlobe demonstrates overall paucity of metabolites and increased lactate\ncompatible with posttreatment changes.",
            "output": "1. Near-complete interval resolution of previously described new left genu of\nthe corpus callosum enhancement.  On multi voxel spectroscopy centered within\nthe resection cavity, there is no evidence of increased choline to NAA ratio. \nThere is no increase perfusion.  No new enhancement.\n2. Single voxel straw sclerae centered over the FLAIR hyperintense white\nmatter superior to the resection cavity demonstrates unchanged minimally\nincreased choline to NAA ratio over approximately 1.1.  This likely represents\nposttreatment changes and is not concerning for disease progression at this\ntime.  However close attention on followup is recommended.\n3. Chronic findings as described above."
        },
        {
            "input": "MR BRAIN:  The patient is status post remote left frontal craniotomy and\nresection of a left frontal lobe mass with expected mild dural thickening and\nenhancement overlying the resection site.  Hemorrhage product within the\nresection cavity is stable.  There is no evidence of enhancement or nodularity\nwithin the resection cavity.  Previously described enhancement along the left\ngenu of the corpus callosum has resolved.  Speckled left greater than right\nbasal ganglia postcontrast enhancement, presumably vascular nature is\nunchanged.  No new enhancing lesions are identified.\n\nLeft frontal encephalomalacia and white matter FLAIR hyperintense edema\npattern is stable.  Superimposed periventricular and subcortical T2/FLAIR\nwhite matter hyperintensities are nonspecific and likely represent a\ncombination of treatment changes and small vessel ischemia.  Allowing for ex\nvacuo dilatation of the frontal horn of the left lateral ventricle, the\nremainder of the sulci, ventricles and cisterns are within expected limits\ngiven the degree of the patient's global cerebral volume loss.  The major\nintracranial flow voids are preserved.  The paranasal sinuses are essentially\nclear.  The orbits are unremarkable.  The mastoid air cells are clear.\n\nMR ___: Decreased perfusion within the resection cavity is\nnoted.  There is no evidence of increase perfusion along the margins of the\nresection site.\n\nASL Perfusion: No increased perfusion is identified..\n\nMR Spectroscopy: Single voxel spectroscopy centered over the superior margins\nof the left frontal lobe resection cavity demonstrates mildly increased\ncholine to NAA ratio of approximately 1.1, unchanged from prior exam.  Multi\nvoxel spectroscopy centered over the medial posterior aspects of the resection\ncavity and the contralateral normal-appearing white matter demonstrates\nexpected paucity of metabolites within the resection cavity itself compatible\nwith posttreatment changes, however evaluation is limited secondary to\npronounced technical artifacts.",
            "output": "1. Resolution of previously described enhancement along the left genu of the\ncorpus callosum seen on ___.  There is no increased enhancement or\nnodularity along the left frontal resection cavities to suggest disease\nprogression.  No new lesions.\n2. Single voxel spectroscopy centered over the superior margins of the\nresection cavity demonstrates mildly increased choline to NAA ratio of\napproximately 1.1, unchanged from prior exam, compatible with posttreatment\nchanges.  Multi voxel spectroscopy is technically limited.\n3. Additional chronic findings as described above."
        },
        {
            "input": "Left frontal craniotomy changes are seen.  Stable small amount of chronic\nblood products are noted in the resection cavity.  There are multiple stable\npunctate foci of low signal in the bifrontal lobes, likely secondary to\nposttreatment changes.  There is FLAIR hyperintense signal surrounding the\nresection cavity, extending into the bilateral gyrus recti and along the right\nperiventricular and subcortical white matter, stable since ___.  Stable left\nfrontal parenchymal volume loss is seen with asymmetric ex vacuo dilatation of\nthe left frontal horn.  There is stable enlargement of the lateral and third\nventricles with prominence of the sulci diffusely.  There is a new focus of\nFLAIR hyperintensity in the medial right thalamus, series 15, image 11, which\ndemonstrates questionable contrast enhancement, series 16, image 11.  No\ndefinite restricted diffusion is seen at this site.  The previously seen focus\nof enhancement in the left genu of the corpus callosum on MRI from ___\nis no longer visualized.  No new abnormal contrast enhancement is identified.\n\nThere is no evidence of hemorrhage, mass effect, midline shift or infarction. \nThe major vascular flow voids are preserved.\n\nStable abnormal T1 hypo intense signal is noted in the visualized upper\ncervical spine and throughout the calvarium.  The orbits, visualized soft\ntissues, mastoid air cells and paranasal sinuses are normal.",
            "output": "1. Stable postsurgical changes to the left frontal lobes with complete\nresolution of the previously seen focus of enhancement in the left genu of the\ncorpus callosum and stable surrounding high signal, likely reflecting\nposttreatment changes.\n2. New focus of high signal in the medial right thalamus with questionable\nfaint contrast enhancement and no restricted diffusion, which may represent a\nlate subacute infarction or a new  additional site of disease.  Recommend a\nshort-term follow-up MRI in ___ months to evaluate interval change.\n3. Stable diffusely abnormal bone marrow signal throughout the calvarium and\nvisualized upper cervical spine, likely secondary to anemia, smoking or any\nprocess resulting in reconversion of hematopoietic marrow.  Recommend clinical\ncorrelation.\n\nRECOMMENDATION(S):  Short-term follow-up MRI in ___ months is recommended."
        },
        {
            "input": "Study is mildly degraded by motion.  The patient has had prior left frontal\ncraniotomy to resect a left frontal anaplastic oligodendroglioma with stable\npost-treatment changes.  Ex vacuo dilation of the left lateral ventricle,\nparticularly the anterior horn appears stable, secondary to encephalomalacia. \nAreas of susceptibility artifact surrounding the resection bed on gradient\necho images most likely represents blood products from prior surgery, similar\nthe prior exam.  Surrounding FLAIR/T2 signal prolongation in the white matter\nsurrounding the resection bed and extending to the bilateral gyrus tract the\nas well as right periventricular and subcortical white matter are unchanged. \nA small area of focal signal prolongation on FLAIR sequences in the medial\nright thalamus which was new on the prior exam persists and is overall\nunchanged (series 7, image 11); however, equivocal enhancement on the prior\nexam is less conspicuous today (series 10, image 11).  No evidence of\ndiffusion signal abnormalities.\n\nBilateral prominence of the ventricles and sulci in general is similar to the\nprior exam, consistent with cortical atrophy.  No shift of normally midline\nstructures.\n\nThe sella turcica is within normal limits.  A small left maxillary sinus\nmucous retention cyst is unchanged.  Bilateral ethmoid air cell and frontal\nsinus mucosal thickening is noted.  Mastoid air cells are clear.  The orbits\nare within normal limits.\n\nHeterogeneous appearance of the partially imaged upper cervical spine with\nareas of focal decreased signal intensity and T1 weighted images as well as in\nthe calvarium is overall similar the prior exam (e.g., series 3, image 12).",
            "output": "1. Study is mildly degraded by motion.\n2. Stable-post treatment changes centered around the left frontal resection\nbed.\n3. Small focus of FLAIR signal prolongation the right medial thalamus is\nunchanged; equivocal enhancement on the prior exam is less conspicuous on\ntoday's exam.  Close attention on follow-up is recommended.\n4. Within limits of study, no definite new foci of FLAIR signal abnormality or\nenhancement identified.\n5. Decreased signal intensity within the partially imaged upper cervical spine\nis unchanged but could indicate sequelae of marrow reconversion suggests\nanemia.  If clinically indicated, consider dedicated cervical spine MRI\nfurther evaluation.\n6.  Paranasal sinus disease as described."
        },
        {
            "input": "There are small acute infarcts in the right ACA territory, involving the right\nparafalcine frontal lobe, anterior cingulate gyrus, and the right superior\nfrontal gyrus (series 500 and 502:26, as well as images ___.\n\nDiffuse, patchy calvarial marrow signal hypointensity is unchanged from prior.\n\nThere are stable, expected post treatment changes in the left frontal lobe,\nvolume loss.\n\nThere is no evidence of extra-axial collection, or mass-effect.\n\nAdvanced brain parenchymal atrophy..  Chronic lacunar infarcts basal ganglia,\nstable.\n\nThere is trace bilateral maxillary sinus and ethmoid air cell mucosal\nthickening.  The remaining visualized paranasal sinuses and the mastoids,\nappear clear.  Major intracranial vascular flow voids are preserved.  The\nglobes and orbits are unremarkable.",
            "output": "Limited study, patient did not complete exam.\nRight ACA distribution acute infarct.\nPosttreatment changes, volume loss left frontal lobe.\nDiffuse brain parenchymal atrophy.\nStable marrow changes, may be reactive, or infiltrative process.."
        },
        {
            "input": "Study is moderately degraded by motion.  Within these confines:\n\nMRI BRAIN:\n\nAgain seen are multiple small acute infarction the right ACA territory\ninvolving the right parafalcine frontal lobe, as well as the anterior\ncingulate gyrus and right superior frontal gyrus, without interval change from\nprior.\n\nThere are stable post treatment changes in the left frontal lobe related to\nremote left frontal mass resection.  FLAIR abnormality surrounding the\nresection site in the left frontal lobe parenchyma is stable.  Scattered foci\nof left supratentorial chronic blood products are unchanged.  There is no\ndefinite evidence of intracranial enhancing mass.\n\nThere is no new acute infarct since the recent prior study from ___. \nThere is no evidence of new hemorrhage, extra-axial collection, or mass\neffect.\n\n Bilateral periventricular and deep white matter foci of T2/FLAIR signal\nhyperintensity are nonspecific but compatible with moderate changes of chronic\nwhite matter microangiopathy and/or treatment related effects.\n\nThird and lateral ventriculomegaly is chronic and stable.  Additionally,\nventricular and sulcal caliber is globally prominent, compatible with global\nparenchymal volume loss, advanced for this patient's age.  There is unchanged\nex vacuo dilatation of the frontal horn of left lateral ventricle.\n\nThere is bilateral maxillary sinus mucosal thickening.  The globes and orbits\nare grossly preserved.  Major dural venous sinuses are grossly patent.\n\nMRA BRAIN:\n\nWidely patent vertebrobasilar system.  Conventional bilateral PCA anatomy. \nPatent bilateral posterior cerebral arteries with preserved distal runoff. \nLeft PCOM is diminutive but patent.  Right PCOM is not well seen, either\ndiminutive or absent.\n\nWidely patent bilateral intracranial internal carotid arteries and bilateral\nmiddle cerebral arteries.  The A1 ACAs are grossly preserved bilaterally, and\nthe anterior communicating artery complex is grossly preserved.  The proximal\nA 2 ACA is are patent.  There is moderate left and severe right A2/A3 ACA\nluminal narrowing which may at least in part due to artifact, however\nunderlying atheromatous disease could also produce this appearance and cause\nnarrowing at this location (400:7, 4:116).  Additionally, given hyperdensity\nseen in this location in the region of the right ACA on recent head CT, this\ncould reflect thrombus formation.  The left and right ACA suggested to be\ndistal to this.  Nonocclusive irregularity of bilateral cavernous segment\ninternal carotid arteries suggestive atherosclerotic changes are noted.\n\nNo large vessel occlusion.  No aneurysm formation.\n\nThe intracranial vertebral and internal carotid arteries and their major\nbranches appear normal without evidence of stenosis,occlusion,or aneurysm\nformation.\n\nMRA NECK:\n\nThe extracranial vertebral and internal carotid arteries are tortuous; but\nwidely patent.  Otherwise, the origins of the great vessels, subclavian and\nvertebral arteries appear normal bilaterally.  The common, internal and\nexternal carotid arteries appear normal.  There is no evidence of internal\ncarotid artery stenosis by NASCET criteria.\n\n OTHER:\nLimited imaging of cervical spine demonstrates diffuse nonspecific marrow\nhypointensity (see 03:13).  Limited imaging of the thyroid gland demonstrates\napproximately 6 mm left and 6 mm right thyroid nodules (see 1502: 82, 90),\nsuggested to be present on ___ prior neck CT (see 2: ___ on\nprior contrast neck CT).",
            "output": "1. Study is moderately degraded by motion.\n2. Grossly stable right ACA distribution acute infarcts.\n3. Focal severe luminal narrowing of the right A2/A3 ACA corresponds to\nhyperdense vessel seen on recent CT, likely severe stenosis or occlusion\npossibly due to thrombus formation/embolism versus underlying atheromatous\nplaque, with resulting right ACA territory infarct.  The right ACA is grossly\npatent distal to this.\n4. Moderate luminal narrowing, left A2/A3 ACA, patent distally.\n5. Additional nonocclusive probable atherosclerotic changes of circle of\n___ as described.\n6. Otherwise, grossly patent circle of ___ without definite evidence of\nstenosis,occlusion,or aneurysm.\n7. Grossly patent bilateral cervical carotid and vertebral arteries without\ndefinite evidence of stenosis, occlusion, or dissection.\n8. Grossly stable left frontal post treatment changes, with no definite\nevidence of new enhancing intracranial mass.\n9. Limited imaging of cervical spine demonstrates diffuse nonspecific marrow\nsignal abnormality.  If concern for cervical spine metastatic disease,\nconsider contrast cervical spine MRI for further evaluation.\n10. Limited imaging of the thyroid gland demonstrates approximately 6 mm\nbilateral thyroid nodules."
        },
        {
            "input": "The examination is motion degraded.\n\nAllowing for these limitations however, there is no evidence of\ndiffusion-weighted hyperintense signal to suggest acute infarct. Grossly,\nthere is no intra or extra-axial mass effect or acute hemorrhage.  Right\nfrontal encephalomalacia is noted. Sulci, ventricles and cisterns are within\nexpected limits for the patient's age appropriate global cerebral volume loss.\nThere appears to be confluent subcortical and periventricular white matter\nFLAIR hyperintensities, which are nonspecific, but compatible small-vessel\nischemic disease in a patient of this age. The major intracranial flow voids\nare preserved. Mucosal thickening of the ethmoid air cells is noted.",
            "output": "1. The study is motion degraded.\n2. Allowing for this, there is no evidence of acute infarct."
        },
        {
            "input": "Please note the study is substantially degraded by motion. There is\nredemonstration of bilateral fat stranding of the subcutaneous fat in the\nneck, though more prominent on the right.  There is unchanged asymmetric\nthickening of the right platysma muscle.  There is again suggestion of\ninduration of the fat within the right greater than left deep cervical fascia\nadjacent to the platysma (see series 6, image 26).  No retropharyngeal\nextension of inflammatory, although evaluation of the chest is limited by\nmotion.  Scattered subcentimeter nonspecific lymph nodes are noted throughout\nthe visualized portion the neck bilaterally. There are no pathologically\nenlarged lymph nodes. Evaluation of the aerodigestive tract demonstrate no\nexophytic mucosal mass or mass effect.   The salivary glands are normal\nbilaterally.  The thyroid gland is normal.\n\nMarrow signal in the cervical spine appear unremarkable.  The left vertebral\nartery is hypoplastic, unchanged compared to prior exam, again likely\ncongenital in nature.",
            "output": "1. Please note the study is substantially degraded by motion.\n2. Redemonstration of subcutaneous fat stranding of right greater than left\nneck soft tissues, not significantly changed compared to ___ contrast\nenhanced CT neck study, consistent with patient's reported cellulitis.\n3. Redemonstration of fat induration of right greater than left deep cervical\nfascia adjacent to platysma, without abnormal fluid collection.  Recommend\nclinical correlation and attention on followup imaging.\n4. Within limits of this motion degraded study, no definite soft tissue\ncollection identified."
        },
        {
            "input": "1.6 cm left frontal coronal radiata diffusion-weighted hyperintense focus with\ncorresponding FLAIR hyperintense and ADC hypointense signal is compatible with\nlate acute to subacute infarct.  There are superimposed periventricular and\nsubcortical T2/FLAIR white matter hyperintensities, which are nonspecific, but\ncompatible with chronic microangiopathy in a patient of this age. Sulci,\nventricles and cisterns are within expected limits for the patient's age. \nThere is no intra or extra-axial mass effect or acute hemorrhage.  The\nintracranial flow voids are preserved. A sphenoid sinus mucous retention cyst\nand very minimal by maxillary mucosal thickening is identified, otherwise the\nparanasal sinuses are essentially clear. The orbits are unremarkable. The\nmastoid air cells are clear.",
            "output": "1. Left frontal coronal radiata subacute to late acute infarct.\n2. Nonspecific T2/FLAIR subcortical and periventricular white matter\nhyperintensities, commonly seen with chronic microangiopathy in a patient of\nthis age.\n\nNOTIFICATION:   The findings were discussed by Dr. ___ with Dr. ___\n___ on the telephone on ___ at 12:52 ___, 50 minutes after discovery\nof the findings."
        },
        {
            "input": "MRI BRAIN:\nThere is no evidence of acute infarction or intracranial hemorrhage.  Small\nchronic infarct in the left corona radiata.  Patchy to confluent areas of T2\nand FLAIR hyperintense signal abnormalities in the periventricular and\nsubcortical white matter are nonspecific, but likely reflect chronic small\nvessel ischemic changes. Mild prominence of the ventricles and sulci is\nsuggestive of involutional changes.  No mass effect or midline shift.\n\nThere is mild mucosal thickening of the paranasal sinuses.  The mastoid air\ncells are clear.  Unremarkable intraorbital contents.\n\nMRA BRAIN:\nThe intracranial vertebral and internal carotid arteries and their major\nbranches appear normal without evidence of stenosis, occlusion, or aneurysm\nformation.\n\nMRA NECK:\nThere is common origin of the right brachiocephalic and left common carotid\narteries, a normal anatomic variant.  Signal, contour, and luminal\nirregularity of the bilateral carotid bifurcations likely relates to minimal\natherosclerotic disease.  Otherwise, the common, internal and external carotid\narteries appear normal.  There is no evidence of internal carotid artery\nstenosis by NASCET criteria.  The origins of the great vessels, subclavian and\nvertebral arteries appear normal bilaterally.",
            "output": "1. No evidence of acute infarction or intracranial hemorrhage.\n2. Small chronic infarct in left corona radiata.\n3. Patent circle of ___ with no focal stenosis or evidence of aneurysm\nformation.\n4. Minimal atherosclerotic calcifications of the common carotid bifurcations. \nOtherwise, patent cervical carotid and vertebral arteries with no focal\nstenosis or evidence of aneurysm formation."
        },
        {
            "input": "Study is mildly degraded by motion.  no acute intracranial infarct or\nhemorrhage.  The intracranial arteries demonstrate normal T2 flow voids. There\nis moderate generalized cerebral atrophy with ex vacuo dilatation of the\nventricular system. Mild periventricular deep white matter T2 and FLAIR\nhyperintense changes are most likely sequela of microangiopathy. \nApproximately 5 mm left CP angle area of increase susceptibility and\nisointense T2 signal is again noted (see 4, 5: 6), corresponding to area of\ncalcification on prior noncontrast head CT (see 2:6 on prior head CT).\n Partially empty sella. The orbits are preserved.  There is mild mucosal\nthickening involving the paranasal sinuses.",
            "output": "1. Study is mildly degraded by motion.\n2. No acute infarct or acute intracranial hemorrhage.\n3. 5 mm calcific density in the left cerebellar pontine angle is nonspecific\nand may represent a calcified meningioma or dural calcification.  If\nclinically indicated, consider contrast brain MRI for further evaluation.\n4.  Paranasal sinus disease , as described."
        },
        {
            "input": "Examination is mildly degraded by motion.  Within this confine:\n\nThere is a small focus of left posterior frontal cortical based slowed\ndiffusion with subtle increased gyriform FLAIR signal and a subtle post\ngadolinium enhancement (502:24, 900:112, 7:19).\n\nThere is no evidence of hemorrhage, space-occupying mass, mass effect, or\nmidline shift.   The ventricles and sulci are normal in caliber and\nconfiguration.  Areas of FLAIR hyperintensity and high signal on diffusion\nwithin the bilateral choroid plexus are compatible with benign\nxanthogranulomas.  The major intracranial vascular flow voids are preserved.\n\nThe visualized paranasal sinuses and mastoid air cells are grossly clear.  The\norbits are unremarkable.",
            "output": "1. Examination is mildly motion degraded.\n2. Punctate focus of left posterior frontal slowed diffusion with associated\ninsure form FLAIR hyperintensity and subtle post gadolinium enhancement,\nlikely reflecting a small embolic infarct, possibly septic given history as\nwell as enhancement pattern.\n3. No acute hemorrhage.\n\nNOTIFICATION:  The findings were discussed with ___, M.D. by\n___, M.D. on the telephone on ___ at 11:16 AM, 2 minutes after\ndiscovery of the findings."
        },
        {
            "input": "Seen again is acute hemorrhage within the right thalamus, grossly unchanged in\nsize as compared to the most recent head CT examination.  Small volume\nintraventricular hemorrhage layering within the occipital horns is also\nsimilar to the previous examination.\n\nMild surrounding vasogenic edema is noted extending into the posterior limb of\nthe right internal capsule and into the right cerebral peduncle.  Mild\nassociated mass effect is also seen with partial effacement of the right\nlateral ventricle.  There is no appreciable midline shift.\n\nSeveral areas of internal enhancement are seen within the intraparenchymal\nhemorrhage, unlikely to be reactive and worrisome for MR ___ sign or possible\nunderlying vascular malformation.  No additional areas of abnormal enhancement\nare identified intracranially.\n\nAreas of high signal on DWI surrounding the right thalamic hemorrhage are\nartifactual in nature.  Allowing for this, no evidence of acute infarction. \nThe dural venous sinuses appear patent.\n\nThe ventricles and sulci are prominent compatible with global parenchymal\nvolume loss.  An area of encephalomalacia and gliosis seen in the left frontal\nlobe, likely secondary to prior/chronic infarction.  Periventricular and\nsubcortical white matter FLAIR hyperintensities are noted, a nonspecific\nfinding that most likely represents the sequelae of chronic small vessel\nischemic disease.\n\nMild mucosal thickening is seen in scattered ethmoid air cells.  The remainder\nof the visualized paranasal sinuses, middle ear cavities, and mastoid air\ncells are well aerated and clear.  The orbits are within normal limits\nbilaterally.",
            "output": "1. Intraparenchymal hemorrhage centered in the right thalamus with mild\nsurrounding edema and local mass effect.  Mild bilateral intraventricular\nhemorrhages is also seen.  No midline shift.\n2. No evidence for acute infarction or additional site of intracranial\nhemorrhage.\n3. Several foci of enhancement are seen within the intraparenchymal\nhemorrhage, which may represent MR ___ sign suggestive active hemorrhage\nversus underlying vascular malformation such as AVM. Recommend continued\nimaging follow-up and, if clinically indicated, a catheter angiogram could be\nconsidered.\n4. Background mild-to-moderate global parenchymal volume loss, chronic left\nfrontal infarction associated encephalomalacia/gliosis, and evidence of\nchronic small vessel ischemic disease."
        },
        {
            "input": "Examination is moderately motion degraded.\n\nMRI BRAIN:\nRe-identified is a 21 x 18 mm intraparenchymal hemorrhage centered in the\nright thalamus/posterior limb of the internal capsule, unchanged in size\ncompared to prior examination given difference of modality.  There is\nsurrounding rim of vasogenic edema with associated localized mass effect and\nminimal effacement of the adjacent right lateral ventricle.  Thin rim of\nenhancement surrounding the hemorrhage is likely due to hemorrhage itself. \nOtherwise no definite underlying lesion is identified.  Rim of high signal on\ndiffusion images is attributable to hemorrhage.  No new hemorrhage is\nidentified.\n\nThere is no evidence of masses, midline shift or infarction.   There is\nmoderate prominence of the ventricles and sulci suggestive of involutional\nchange.  Background periventricular, subcortical and deep white matter\nT2/FLAIR hyperintensities are in a configuration most suggestive of chronic\nsmall vessel ischemic disease.  There is no other abnormal enhancement after\ncontrast administration.  There is otherwise no abnormal focus of slowed\ndiffusion.\n\n The visualized paranasal sinuses are grossly clear.  The orbits are grossly\nunremarkable.  The mastoid air cells are clear.\n\nMRA brain: There is loss of flow related signal in the distal V4 segment of a\nhypoplastic right vertebral artery, secondary to hypoplasia, with patency\ndemonstrated on the recent prior CT examination.  There is normal variant\nfetal type origin of the left PCA.  The remainder of the intracranial\nvertebral and internal carotid arteries and their major branches appear patent\nwithout evidence of significant stenosis, occlusion, or aneurysm formation. \nThe central circle of ___ vasculature appears mildly prominent, which can\nbe seen in the setting of chronic hypertension.",
            "output": "1. Unchanged 21 x 18 mm right thalamic/internal capsule intraparenchymal\nhemorrhage with surrounding vasogenic edema, likely hypertensive in etiology. \nThin rim of surrounding enhancement is likely secondary to hemorrhage itself,\nand no definite underlying lesion is identified.\n2. Otherwise no new hemorrhage or infarct.\n3. Loss of flow related signal of the distal V4 segment of the right vertebral\nartery, secondary to slow flow in the setting of hypoplasia, with patency\ndemonstrated on recent prior CT examination.  Otherwise patent intracranial\narterial vasculature without significant stenosis, occlusion, or aneurysm\nformation.\n4. Mild prominence of the central circle of ___ vasculature which can be\nseen in the setting of hypertension.\n5. Moderate global atrophy and areas of white matter signal abnormality in a\nconfiguration most suggestive of chronic small vessel ischemic disease."
        },
        {
            "input": "Allowing for differences in imaging plane, a large, heterogeneous right\nparieto-occipital lobe intraparenchymal hemorrhage is minimally changed,\nmeasuring 7.4 x 3.2 cm in the axial plane.  Inferior to the dominant component\nof hemorrhage, there is a relatively linear region of enhancement which\nappears to correspond to the left occipitotemporal sulcus, enhancement likely\nmeningeal in origin.  A rim of restricted diffusion likely corresponds to\nassociated ischemia.  Internal restricted diffusion corresponds to blood\nproducts.  Adjacent vasogenic edema is similar to the prior CT. 5 mm of\nmidline shift, ipsilateral sulcal effacement, and ipsilateral lateral\nventricle effacement are unchanged.  A small adjacent extra-axial hematoma is\nalso unchanged.  The basilar cisterns are patent.  Extensive periventricular\nand subcortical white matter T2/FLAIR hyperintensities are nonspecific but\nlikely sequelae of chronic small vessel ischemic disease.\n\nNo evidence of new hemorrhage. Bilateral maxillary sinus and ethmoid air cell\nmucosal thickening is again noted.",
            "output": "1. A large right parieto-occipital intraparenchymal hematoma minimally changed\nwith approximately 5 mm of midline shift.  A small amount of adjacent subdural\nand subarachnoid hemorrhage is unchanged.\n2. Somewhat linear enhancement appearing to extend into the left\noccipitotemporal sulcus is likely meningeal in origin and raises the\npossibility of amyloid related inflammation.  However, this finding is\nsomewhat nonspecific.  Recommend follow-up imaging upon hematoma resolution."
        },
        {
            "input": "There has been evolution of the right occipital hematoma since the prior\nexaminations.  There is largely resolution of mass effect and now a large\ncavity within the right occipital lobe.  Small amounts of blood products\npersist around the periphery and at the occipital pole.  There is minimal\nenhancement around the margins of the hematoma.  Again seen is white matter\nhyperintensity on FLAIR, likely edema.\nAgain seen and unchanged are extensive white matter hyper intensities on\nFLAIR.  No new lesions are identified.  There is no evidence of new\nhemorrhage.  There is no other abnormal enhancement after contrast\nadministration.",
            "output": "1. Evolution of right occipital hematoma without evidence of new hemorrhage.\n2. Expected enhancement of the peripheral of the hematoma with no other\nabnormal enhancement identified.\n3. Unchanged extensive white matter hyperintensity on FLAIR"
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.\n\n There are scattered predominantly subcortical T2/FLAIR hyperintensities in\nthe cerebral hemispheres bilaterally, a nonspecific finding which could\nrepresent migraine related white matter changes or early small vessel ischemic\nchanges/microangiopathic changes.  Alternatively, these white matter lesions\ncould represent at an autoimmune/inflammatory process.  Distribution pattern\nof the white matter lesions does not suggest an underlying demyelinating\ncondition.  These are not in a distribution compatible with HIV\nencephalopathy.\n\nThe ventricles and sulci are normal in caliber and configuration.\nMajor vascular flow voids are preserved.\n\nThere is mild mucosal thickening of the ethmoid air cells.  The remainder of\nthe paranasal sinuses and mastoid air cells is clear.  The orbits are normal.",
            "output": "1. Scattered predominantly subcortical white matter changes could be migraine\nrelated or represent early small-vessel ischemic changes/microangiopathic\nchanges.  Alternatively the lesions may represent an autoimmune/inflammatory\nprocess.  Distribution pattern does not suggest an underlying demyelinating\ncondition or HIV encephalopathy.\n2. No acute hemorrhage, intracranial mass or acute infarction.\n3. Mild paranasal sinus disease as described above."
        },
        {
            "input": "Study is mildly degraded by motion.  New bifrontal nonenhancing white matter\nlesions with no associated T1 hypointensity, restricted diffusion, or\nsusceptibility are noted.  Additional numerous nonenhancing periventricular\nand subcortical supratentorial white matter lesions, some which are associated\nwith T1 hypointensity, but none of which have associated restricted diffusion\nor susceptibility are again seen.\n\nThere is no evidence of hemorrhage,  mass effect, midline shift or infarction.\nThe ventricles and sulci are normal in caliber and configuration.  There is no\nabnormal enhancement after contrast administration.",
            "output": "1. Study is mildly degraded by motion.\n2. New numerous nonenhancing bifrontal white matter lesions, with additional\nmultiple stable bilateral supratentorial white matter lesions, compatible with\npatient's history of multiple sclerosis."
        },
        {
            "input": "There are multiple foci of T2/FLAIR hyperintensities scattered throughout the\nwhite matter of both centrum semiovale and in the subcortical regions\n(representative images 6: 13, 14, 15, 17) without DWI correlate. Although\nthese lesions are non-specific and could be seen in migraine, the largest of\nthese adjacent to the frontal horn of the left lateral ventricle is unusually\nlarge for migraine related changes. There is also marked prominence of the\nlateral ventricles and sulci, noteworthy in a patient of this age group.\n\nOtherwise, there is no evidence of acute intracranial hemorrhage, mass, mass\neffect or shifting of the normally midline structures. No diffusion\nabnormalities are detected to indicate acute or subacute ischemic changes. The\nmajor vascular flow voids are present and demonstrate normal distribution. The\norbits, the paranasal sinuses and the mastoid air cells are clear.",
            "output": "1. Multiple foci of T2/FLAIR hyperintensities scattered throughout the white\nmatter of both hemispheres without restricted diffusion are non-specific but\ncan be seen in the setting of migraine. However, the largest of these lesions\nis unusually large and raises concern for atypical demyelinating disease.\nRepeat exam with gadolinium enhancement is recommended for full assessment.\n2. Marked prominence of the lateral ventricles and sulci suggestive of\ninvolutional changes of the brain is noteworthy in a patient of this age\ngroup."
        },
        {
            "input": "There are bilateral T2/FLAIR signal hyperintense lesions in the\nperiventricular and subcortical white matter predominantly in the left greater\nthan right frontal and parietal lobes. Compared to recent prior study, these\nhave not significantly changed in number or configuration. There is no\nevidence of restricted diffusion or enhancement within these lesions.\n\nThere is no acute infarction, intracranial hemorrhage, extracerebral fluid\ncollection, midline shift or mass effect.  No diffusion abnormalities are\ndetected.  The ventricles and sulci are unchanged.  The major vascular flow\nvoids are maintained. There is no evidence of abnormal enhancement. The orbits\nare unremarkable. The paranasal sinuses and mastoid air cells are clear",
            "output": "Stable foci of non-specific T2/FLAIR signal hyperintense in the\nperiventricular and subcortical white matter of the bilateral frontal and\nparietal lobes.  No abnormal enhancement or restricted diffusion. These\nfindings are nonspecific and can be seen in the setting of various etiologies\nincluding migraine and demyelinating disease."
        },
        {
            "input": "There are bilateral T2/FLAIR signal hyperintense lesions in the\nperiventricular and subcortical white matter predominantly in the frontal and\nparietal lobes, left greater than right. Compared to recent prior study, these\nhave not significantly changed in number or configuration. There is no\nevidence of restricted diffusion or enhancement within these lesions.\n\nThere is no acute infarction, intracranial hemorrhage, extracerebral fluid\ncollection, midline shift or mass effect. No diffusion abnormalities are\ndetected. The ventricles and sulci are unchanged. The major vascular flow\nvoids are maintained. There is no evidence of abnormal enhancement. The orbits\nare unremarkable. The paranasal sinuses and mastoid air cells are clear.",
            "output": "1. Stable periventricular and subcortical white matter parenchymal signal\nintensity abnormalities of bilateral frontal and parietal lobes without\nassociated enhancement of diffusion abnormality. These lesions are nonspecific\nand can be seen in various etiologies including migraine and demyelinating\ndisease.\n2. No new lesions identified."
        },
        {
            "input": "MRI Brain without contrast:\nThere is no evidence of acute infarction, hemorrhage, edema, masses, mass\neffect, or midline shift.  The ventricles and sulci are normal in caliber and\nconfiguration..  Chronic lacunar infarct right thalamus.  Mild-to-moderate\nchronic small vessel ischemic changes.  Mild paranasal sinus disease.  Mild\nbilateral mastoid opacification.\n\nMRA brain without contrast:\nMild narrowing distal bilateral V4 segments vertebral arteries and proximal\nbasilar artery.  Moderate narrowing left P3 segment PCA.  Mild-to-moderate\nnarrowing bilateral cavernous segments ICA..  Probable left supraclinoid ICA\nsmall infundibulum.  The intracranial vertebral and internal carotid arteries\nand their major branches otherwise appear normal without evidence of\nhigh-grade stenosis, occlusion, or aneurysm formation.\n\nMRA neck without contrast:\nMild narrowing right P1 segment.  Otherwise, normal neck arteries, there is\ntime-of-flight in her artifact present.  The common, internal and external\ncarotid arteries appear normal.  There is no evidence of internal carotid\nartery stenosis by NASCET criteria.  1.8 cm left thyroid nodule, ultrasound\nsuggested.",
            "output": "1. No acute intracranial findings.\n2. Moderate chronic small vessel ischemic changes, chronic lacunar infarct.\n3. Origin of great vessels are suboptimally evaluated secondary to motion.\n4. Probable mild narrowing right V1 segment vertebral artery.\n5. Narrowed bilateral cavernous carotid, left PCA P3 segment.\n6. 1.8 cm thyroid nodule, ultrasound recommended according to guidelines."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are prominent for the patient's age,\nsuggesting mild cortical volume loss, this finding is nonspecific, however has\nbeen described in patients with chronic use of steroid therapy, please\ncorrelate.  A slightly prominent perivascular spaces noted on the right basal\nganglia (image 15, series 7).  No diffusion abnormalities are detected.  Major\nintracranial vascular flow voids are preserved.  There is a trace amount of\nfluid in the right ethmoid air cells.  Otherwise, the visualized paranasal\nsinuses and mastoid air cells are clear.  The globes and intraorbital\nstructures are normal.",
            "output": "1.  Slightly prominent ventricles and sulci for the patient's age, this\nfinding is nonspecific, however may reflect mild cortical volume loss.\n\n2.  There is no evidence of acute or subacute intracranial process."
        },
        {
            "input": "In comparison to the prior study of ___, there is interval\ndevelopment of widespread T2/ FLAIR abnormalities in bilateral frontal,\nposterior parietal, occipital, and temporal lobes predominantly involving the\nsubcortical white matter.  These are associated with fast diffusion and siplay\nno abnormal enhancement.  These findings and at the time course since a normal\nbrain MRI on ___ most suggest posterior reversible encephalopathy\nsyndrome.  Although the anatomic distribution would be appropriate for\nwatershed infarction, the predominant involvement of subcortical white matter,\nrather than cortex, and the fast diffusion argue against this diagnosis.\n\nThe ventricles and sulci are mildly prominent for age, but stable from the\nprior examination.  There is no enhancing mass or mass effect.  There is no\nhemorrhage.  Major intracranial vascular flow voids are preserved.  The circle\n___ and its major branches and the dural venous sinuses enhance\nappropriately on postcontrast sequences.",
            "output": "Interval development of widespread bilateral relatively symmetric T2/FLAIR\nabnormalities in the subcortical white matter most likely represents PRES."
        },
        {
            "input": "The study is moderately degraded by motion artifact with the postcontrast T1\nweighted sequences being extremely motion limited.  There is no focus of slow\ndiffusion to suggest acute infarction.  Widespread relatively symmetric\nbilateral T2/ FLAIR hyperintensities in bilateral frontal, posterior parietal,\noccipital, and temporal lobes predominantly involving the subcortical white\nmatter have progressed compared to prior study.  There is also involvement of\nthe bilateral cerebellar hemispheres, much more prominent when compared to\nprior examination.  There is no associated enhancement or diffusion\nabnormality.  There is no mass or mass effect.  Ventricles are stable in size\nand configuration, but remain prominent for age.  Principal intracranial\nvascular flow voids are preserved.  In the right ethmoid air cells are\npartially opacified.  The orbits are unremarkable.",
            "output": "1. Moderately motion degraded study, particularly affecting the postcontrast\nT1 weighted images.\n2. Widespread bilateral relatively symmetric areas of T2/FLAIR signal\nhyperintensity involving the frontal, parietal, occipital, and temporal\nsubcortical white matter and the bilateral cerebellar hemispheres without\nassociated slow diffusion or enhancement have progressed compared to prior\nexamination and likely represent worsening PRES.\n3. No evidence of hemorrhage or acute infarction."
        },
        {
            "input": "The extensive areas of high signal intensity on the T2 and FLAIR images\nsuggesting posterior reversible encephalopathy syndrome have completely\nresolved.  There is no evidence of hemorrhage, edema, masses, mass effect, or\ninfarction. The ventricles and sulci are normal in caliber and configuration.\nThere is no abnormal enhancement after contrast administration.",
            "output": "Resolution of findings suggestPRES since ___.\nThe study now appears normal."
        },
        {
            "input": "MR:\nThere is no intracranial mass, mass effect, or midline shift.  There is no\nfocal parenchymal signal abnormality. Ventricles and sulci are\nage-appropriate. There is no restricted diffusion to suggest acute infarct. No\nabnormal susceptibility artifact identified. Major intravascular flow voids\nare preserved including within the major dural venous sinuses.\n\nVisualized paranasal sinuses and mastoid air cells demonstrate no abnormal\nsignal.\n\nMRV head: Normal flow signal is demonstrated within the superior sagittal\nsinus, straight sinus, transverse sinuses, and sigmoid sinuses. The jugular\nbulbs and proximal jugular veins are patent. Evaluation of the deep venous\nsystems reveals normal flow signal in the internal cerebral veins. The vein of\n___ is also unremarkable.\n\nMRA neck:  The common, internal and external carotid arteries appear normal. \nThere is no evidence of stenosis by NASCET criteria. The origins of the great\nvessels, subclavian, and vertebral arteries appear normal bilaterally.  Of\nnote, the left vertebral artery is hypoplastic, is better appreciated on the\ntime-of-flight images, and arises proximally from the subclavian artery.  The\ncommon carotid bifurcations appear normal.",
            "output": "Normal MRI and MRV of the brain.  Normal MRA of the neck."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.\n There are patchy T2/FLAIR hyperintensities in the cerebral hemispheres\nbilaterally, left more than right, as well as in the pons, a nonspecific\nfinding and likely related to chronic small vessel ischemic changes.\nThere is no abnormal enhancement after contrast administration.\n\nThe ventricles and sulci are age appropriate.\nMajor vascular flow voids are preserved.  Major dural venous sinuses patent.\n\nThe paranasal sinuses and mastoid air cells appear centrally clear.  The\norbits appear unremarkable.",
            "output": "1. No evidence of intracranial metastatic disease, acute infarction,\nhemorrhage or intracranial mass.\n2. Nonspecific patchy white matter changes in the cerebral hemispheres\nbilaterally and in the pons, likely sequela of chronic small vessel ischemic\nchanges."
        },
        {
            "input": "There are 2 new ring-enhancing lesions in the right and left inferior\ncerebellar hemispheres measuring approximately 2.0 x 1.8 x 1.4 cm (AP, TRV,\nSI) and 1.4 x 1.7 x 1.0 cm) respectively, with mild surrounding white matter\nedema pattern.  The right cerebellar lesion abuts the right sigmoid sinus\n(series 11, image 56) without evidence of invasion.  No other enhancing\nlesions are identified.\n\nThere are moderate periventricular and subcortical T2/FLAIR white matter\nhyperintensities, nonspecific, but compatible with chronic microangiopathy in\na patient of this age.  This is unchanged from prior examination.\n\nThe sulci, ventricles and cisterns are within expected limits for the\npatient's age.  There is no evidence of acute infarct or intracranial\nhemorrhage.\n\nThe major intracranial flow voids are preserved.  The dural venous sinuses are\npatent.\n\nNo suspicious marrow signal.  The visualized paranasal sinuses are essentially\nclear.  The orbits are unremarkable.  No significant fluid signal is seen in\nthe mastoid air cells.",
            "output": "1. Two new ring-enhancing lesions in the right and left cerebellar hemispheres\nmeasuring up to 2 cm in greatest dimension.\n2. Additional findings described above.\n\nRECOMMENDATION(S):  The findings were discussed with Dr. ___. by\n___, M.D. on the telephone on ___ at 10:01 am, 5 minutes after\ndiscovery of the findings."
        },
        {
            "input": "Rim enhancing right cerebellar metastatic lesion now measures approximately\n1.7 x 1.6 x 1.2 cm (AP by transverse by SI), decreased in size.  Left\ncerebellar rim enhancing metastatic lesion now measures approximately 1.5 x\n1.4 x 0.9 cm  (AP by transverse by SI), decreased in size.  There continues to\nbe surrounding edema, which appears increased from the previous examination,\nbut there is no significant mass effect, and the enhancement appears thicker\nand more irregular than on the previous exam.  No other enhancing lesions are\ndemonstrated.  There are scattered nonspecific T2/FLAIR hyperintensities in\nthe white matter which are nonspecific but likely reflect chronic small vessel\ndisease in this age group.  No evidence of hemorrhage or infarction.\n\nStable ventricular size and configuration.  No evidence of hydrocephalus.  No\nshift of the midline structures are basal cistern effacement.\n\nThe major intracranial vascular flow voids are preserved.  Orbits and\nvisualized extracranial soft tissues are unremarkable.",
            "output": "1. The rim enhancing lesions in the left and right cerebellar hemispheres have\ndecreased in size in the previous exam, although surrounding edema has\nincreased and the degree of enhancement has increased, possibly reflecting\npost treatment change."
        },
        {
            "input": "There is redemonstration of two peripherally enhancing cerebellar lesions. \nWhen compared to most recent MRI dated ___, the lesion in the\nright lateral cerebellum is stable in size measuring 17 mm x 18 mm x 11 mm\n(AP, TR, SI), whereas the lesion in the left cerebellum slightly increased in\nsize, measuring approximately 17 mm x 15 mm x 12 mm, as compared to 14 mm by\n15 mm x 10 mm.  These 2 lesions appear smaller when compared to MRI ___.  Additionally, the lesion appear to have more nodular peripheral\nenhancement compared to prior MRI.  There is no significant interval change of\nthe surrounding vasogenic edema.\n\nNo new lesions or new areas of abnormal enhancement are identified.\n\nThere is no evidence of hemorrhage, midline shift or infarction.  Stable size\nand configuration of the ventricles.  There are unchanged T2/FLAIR\nhyperintensity in the periventricular and subcortical white matter, which are\nnonspecific, but likely reflecting chronic microangiopathy.\n\nThere is mild mucosal thickening of the ethmoid air cells and small mucous\nretention cyst in the right maxillary sinus, otherwise the paranasal sinuses\nare clear.  The globes and orbits are unremarkable.  The bilateral mastoid air\ncells are clear.  There is no abnormal marrow signal.",
            "output": "1. Redemonstration of two peripherally enhancing cerebellar lesions with\nstable size of the right sellar lesion, and slight interval increase in size\nof the left cerebellar lesion when compared to most recent MRI.  However,\nthese two lesions demonstrate interval decrease in size when compared to MRI\ndated ___.  Additionally, the surrounding vasogenic edema is\ngrossly unchanged.\n2. No new lesions are identified.\n3. Unchanged supratentorial T2/FLAIR hyperintensity in the periventricular and\nsubcortical white matter, which are nonspecific, but likely reflecting chronic\nmicroangiopathy."
        },
        {
            "input": "The previously described two peripherally enhancing cerebellar lesions are\nagain seen, the lesion on the right side adjacent to the right transverse\nsinus remains relatively stable in size and configuration measuring\napproximately 18 x 17 mm in size (12: 98), which is similar to the prior exam.\nThe lesion on the left cerebellar hemisphere appears slightly larger,\nmeasuring approximately 20 x 18 mm in transverse dimension (12:108), and\npreviously 18 x 10 mm.  Please note that there is increased pattern of\nvasogenic edema surrounding this lesions, which is more evident on the axial\nFLAIR and axial T2 weighted images (8:8, 9:8).\n\nThe cerebellar pontine angles and perimesencephalic cisterns are preserved,\nthere is no evidence of tonsillar herniation.  Unchanged pontine areas of\nFLAIR high-signal intensity are nonspecific and may reflect changes due to\nchronic small vessel disease.  Supratentorially subcortical and\nperiventricular areas of T2/FLAIR high-signal intensity are again seen and may\nrepresent a combination of posttreatment changes and chronic small vessel\ndisease.\n\nNo diffusion abnormalities are detected, there is no evidence of territorial\ninfarction, no new areas with abnormal enhancement or new lesions are seen. \nThe ventricles and sulci remain unchanged and appear slightly prominent\nsuggesting mild cortical volume loss, likely involutional.\n\nThe major vascular flow voids are present and demonstrate normal distribution.\nThe major dural sinuses are patent and enhance normally.  The orbits are\nunremarkable, the paranasal sinuses demonstrate an unchanged mucous retention\ncysts in the right maxillary sinus, the bony structures and soft tissues are\ngrossly unremarkable.",
            "output": "1.  The previously described two peripherally enhancing cerebellar lesions are\nagain seen, the lesion on the right cerebellar hemisphere remains grossly\nunchanged, measuring approximately 18 x 17 mm in transverse dimension, the\nlesion in the left cerebellar hemisphere appears slightly larger and measures\napproximately 20 x 18 mm in transverse dimension and previously 18 x 10 mm.\n\n2.  The pattern of vasogenic edema and T2/FLAIR high signal intensity has\nincreased surrounding the cerebellar enhancing lesions, probably related with\nposttreatment changes versus tumoral edema.\n\n3.  Unchanged pontine, subcortical periventricular T2/FLAIR hyperintensity\nRDS, which may represent changes due to chronic small vessel disease and\nposttreatment changes.\n\n4.  No diffusion abnormalities are detected, there is no evidence of acute\nintracranial hemorrhage or territorial infarction..\n\n5.  No new lesions or new areas with abnormal enhancement are seen."
        },
        {
            "input": "Interval increase size of right and left cerebellar lesions with nodular\nperipheral enhancement measuring 1.7 x 2.1 cm (AP, TRV) and 2.7 x 2.6 cm (AP,\nTRV) respectively.  The degree of associated parenchymal FLAIR edema pattern\nhas also significantly increased with mild effacement of the fourth ventricle\n(series 8, image 8) when compared to prior exam.  There is no increasing\ndiffusion-weighted signal abnormality.  No tonsillar herniation or\nhydrocephalus.\n\nThere is no evidence of acute infarct or intracranial hemorrhage.  The sulci,\nventricles and cisterns are otherwise within expected limits for the patient's\nage.  Prominent periventricular and subcortical T2/FLAIR white matter\nhyperintensities are nonspecific and unchanged from prior examinations,\ncommonly seen in the setting chronic small vessel ischemic disease.\n\nThe major intracranial flow voids are preserved.  The dural venous sinuses are\npatent.  There is mild mucosal thickening of the visualized paranasal sinuses.\nThe orbits are unremarkable.  No significant fluid signal seen in the mastoid\nair cells.  No suspicious marrow signal.",
            "output": "1. Interval increase size of bilateral cerebellar hemisphere lesions with\nincreased associated parenchymal FLAIR edema pattern, resulting in mild\neffacement of the fourth ventricle.  The findings could represent\nposttreatment effect, however close follow-up is recommended to exclude\nprogression and to evaluate the degree of fourth ventricular effacement.\n2. There is no cerebellar tonsillar herniation or hydrocephalus.\n3. No acute infarct or intracranial hemorrhage.\n4. Additional findings described above.\n\nNOTIFICATION:  The impression and recommendation above was entered by Dr.\n___ on ___ at 10:43 into the Department of Radiology critical\ncommunications system for direct communication to the referring provider."
        },
        {
            "input": "There are 2 new enhancing lesions measuring up to 2 mm in the left medial\nfrontal lobe vertex (series 6, image 21) and left mid cingulate gyrus (series\n6, image 19).\n\nMultiple regions of T1 spin echo hyperintense signal involving the right\norbitofrontal lobe (series 6, image 14 and bilateral anterior temporal lobes\nand right hippocampal formation as well as left occipital lobe (series 6,\nimage 10) are without corresponding enhancement on MPRAGE in felt to be most\ncompatible with pulsation artifact.\n\nMinimal increase size of peripherally enhancing and centrally hypoenhancing\nleft cerebellar lesion measuring approximately 3.3 x 2.8 cm (TRV, AP; series\n6, image 8) and right cerebellar hemisphere lesion measuring approximately 2.3\nx 2.2 cm.  There remains mass effect on the fourth ventricle without evidence\nof hydrocephalus.\n\nNo acute infarct.  The dural venous sinuses appear patent.",
            "output": "1. 2 new enhancing lesions measuring up to 2 mm in the left medial frontal\nlobe vertex and left mid cingulate gyrus.\n2. Mild interval increase size of known left cerebellar and right cerebellar\nperipherally enhancing lesions without evidence of aggressive hydrocephalus.\n3. Multiple regions of T1 spin echo hyperintense signal of the right\norbitofrontal lobe, bilateral anterior temporal lobes, right information and\nleft occipital lobe are without definitive corresponding lesions on MP rage,\nlikely pulsation artifact.  However close attention on follow-up is\nrecommended.\n\nNOTIFICATION:  The impression and recommendation above was entered by Dr.\n___ on ___ at 12:33 into the Department of Radiology critical\ncommunications system for direct communication to the referring provider."
        },
        {
            "input": "Study is degraded by motion.  Within these confines:\n\nThe patient is status post left suboccipital craniotomy for resection of the\nleft cerebellar mass.  Postsurgical changes are noted with intrinsic T1\nhyperintensity and low signal intensity on the gradient echo sequence in the\nleft cerebellar resection cavity, suggestive of post surgical blood products. \nThere is thin peripheral enhancement at the anteromedial and lateral aspects\nof the surgical resection cavity, without intrinsic T1 hyperintensity,\nsuggestive of residual tumor.  There is slow diffusion at the periphery of the\nsurgical resection cavity, suggestive of postsurgical devitalized tissue. \nThere is grossly stable surrounding edema in the left cerebellar hemisphere,\nextending into the cerebellar vermis and left middle cerebral peduncle.\n\nThe peripherally enhancing, irregular right cerebellar lesion abutting the\nright transverse sinus is grossly stable in size and appearance, measuring 2.1\ncm (AP) by 1.9 cm (TV).  There is unchanged surrounding edema in the right\ncerebellar hemisphere.  There is unchanged partial effacement of the fourth\nventricle, without evidence of hydrocephalus.\n\nSmall enhancing lesion, measuring 3 mm, parasagittal in the left posterior\nfrontal lobe (14:20; 13:144; 101:78; 100:54), unchanged compared with the\nprior MR head.\n\nGrossly stable left corpus callosum body approximately 2 mm enhancing lesion\nis again seen (see 14:17; 13:126; 101:58; 100:53).\n\nAdditional approximately 4 mm right frontal parafalcine extra-axial enhancing\nstructure is grossly unchanged compared to ___ prior exam (see\n100:57 9:20; 101:38; 13:145 on current study and 900:87 on ___\nprior exam).\n\nThe ventricles are otherwise grossly stable in caliber and configuration.\n\nThere is no evidence of venous sinus thrombosis.  There are nonspecific\nbilateral supratentorial and pontine T2/FLAIR white matter hyperintensities,\nwhich may represent the sequelae of chronic microangiopathy.  There is a trace\nof fluid in the mastoid air cells.  Right posterior occipital calvarial\nprobable hemangioma is noted (see 101:128; 9:15; 100:67).  An approximately 2\nmm pineal cyst is noted.",
            "output": "1.  Study is degraded by motion.\n2. Status post left suboccipital craniotomy for resection of the left\ncerebellar mass.\n3. Thin peripheral enhancement at the anterior, medial and lateral aspects of\nthe surgical resection cavity, without intrinsic T1 hyperintensity, concerning\nfor residual tumor.\n4. Postsurgical changes are noted in relation to the surgical resection cavity\nanteriorly, in keeping with blood products.  Slow diffusion at the periphery\nof the surgical resection cavity, in keeping with postsurgical devitalized\ntissue.\n5. Grossly stable right cerebellar, 3 mm left frontal and approximately 2 mm\nleft corpus callosum enhancing lesions as described.\n6. Additional approximately 4 mm right frontal parafalcine extra-axial\nenhancing lesion, grossly unchanged compared to ___ prior exam,\nsuggestive of meningioma.\n7. Unchanged edema surrounding the left surgical resection cavity and the\nright cerebellar lesion, causing partial effacement of the fourth ventricle,\nwithout hydrocephalus.\n8. Nonspecific bilateral supratentorial and pontine T2/FLAIR white matter\nhyperintensities, which may represent the sequelae of chronic microangiopathy."
        },
        {
            "input": "There are multiple intra axial supra and infratentorial enhancing\nabnormalities as follows:\n\n-Left frontal parasagittal enhancing abnormality measuring about 4 mm (series\n4, image 284); not significantly changed since previous examination.\n-Left middle orbital gyrus enhancing abnormality measuring less than 3 mm\n(series 4, image 282); more conspicuous in this examination.\n-Left frontal anterior body/undulate gyrus junction focal enhancing\nabnormality measuring 4 mm (series 4, image 257); unchanged since previous\nexamination.\n-Right cerebellar hemisphere peripherally enhancing abnormality measuring 21 x\n17 mm; unchanged since previous examination.\n-Left cerebral hemisphere surgical bed irregular nodular enhancement measuring\nabout 25 x 27 mm; unchanged since previous examination.\n\n\nThere is no midline shift and or significant mass effect.  There is no acute\nintracranial hemorrhage or acute infarction.",
            "output": "1. Multiple supra and infratentorial enhancing abnormalities (about 5)\nsuggestive of metastatic disease."
        },
        {
            "input": "Study is moderately degraded by motion, especially on postcontrast imaging.\n\nCorresponding to the calcified lesion seen on CT, there is a 42 x 38 x 36 mm\n(1001:90, 1000:129) homogeneously enhancing left frontal vertex, dural-based\nmass with slowed diffusion, with suggestion of adjacent dural tail with slowed\ndiffusion, most consistent with meningioma.  Areas of internal susceptibility\nartifact correspond to the areas of calcification as seen on CT.  There is no\nadjacent parenchymal edema.  There is mild localized mass effect with\neffacement of the adjacent sulci and minimal effacement of the left lateral\nventricle.\n\nThere is an additional 9 x 9 mm homogeneously enhancing dural based right\nparietal extra-axial mass, also likely consistent with meningioma (1000:129),\ncorresponding to calcified lesion on prior CT with corresponding\nsusceptibility artifact.  There is no significant mass effect from this second\nlesion.\n\nThere is no evidence of acute hemorrhage, edema, midline shift or infarction. \nThere is mild asymmetric prominence of the left lateral ventricle, likely a\ncongenital variant.  There is mild background prominence of the ventricles and\nsulci suggestive of involutional changes.  Areas of mild periventricular,\nsubcortical and deep white matter T2/FLAIR hyperintensities are in a\nconfiguration most suggestive of chronic small vessel ischemic disease.  The\nprincipal intracranial vascular flow voids are preserved.  There is no other\nfocus of abnormal slowed diffusion.\n\nThere is a tiny mucous retention cyst in the right maxillary sinus.  The\nremainder of the visualized paranasal sinuses are grossly clear.  The orbits\nare grossly unremarkable.  There is no abnormal fluid signal within the\nmastoid air cells.",
            "output": "1. Study is moderately degraded by motion.\n2. 42 x 38 x 36 mm left frontal vertex extra-axial homogeneously enhancing\nmass with calcifications with associated localized mass effect but no definite\nadjacent edema, most consistent with meningioma.\n3. Additional 9 x 9 mm homogeneously enhancing, calcified extra-axial right\nparietal mass, also most consistent with meningioma.  No significant mass\neffect or adjacent parenchymal edema.\n4. Mild global atrophy and areas white matter signal abnormality in a\nconfiguration most suggestive of chronic small vessel ischemic disease.\n5. Minimal paranasal sinus disease as described."
        },
        {
            "input": "A dominant, 4.6 x 4.0 cm extra-axial dural-based homogeneously enhancing mass\nat the left frontal vertex demonstrating restricted diffusion is minimally\nchanged from the previous examination.  Multiple foci of internal\nsusceptibility artifact correspond with known calcifications as seen on prior\nCT.  Mild local mass effect with partial effacement of the adjacent sulci and\nminimal effacement of the left lateral ventricle is unchanged.  No parenchymal\nedema is seen.\n\nA second, smaller, right parietal dural-based extra-axial enhancing mass is\nalso unchanged, measuring 0.9 x 0.8 cm on today's examination, previously 0.9\nx 0.9 cm.  No appreciable mass effect is seen.\n\n\nThere is no evidence of acute infarction.  No acute intracranial hemorrhage.\n\nThe ventricles and sulci are mildly prominent, compatible with age related\nparenchymal changes.  Periventricular and subcortical white matter FLAIR\nhyperintensities are noted, likely the sequelae of chronic small vessel\nischemic disease.   The basal cisterns are patent.  There is gross\npreservation of the principal intracranial vascular flow voids.\n\n  The dural venous sinuses appear patent on MP-RAGE imagine sequences.\n\nA mucous retention cyst is seen in a left anterior ethmoid air cell.  The\nremainder of the visualized paranasal sinuses, middle ear cavities, and\nmastoid air cells are well aerated and clear.  The orbits are within normal\nlimits bilaterally.",
            "output": "1. Stable appearance of a dominant 4.6 x 4.0 cm dural-based, extra-axial,\nhomogeneously enhancing mass at the left vertex, compatible with a meningioma.\nAllowing for differences in measurement technique, the mass appears similar in\nsize compared to the prior examination.  Mild local mass effect without\nparenchymal edema is unchanged.\n2. Stable, second, smaller right parietal dural-based extra-axial\nhomogeneously enhancing mass, compatible with a secondary site of meningioma.\n3. Chronic findings of global cerebral parenchymal volume loss and small\nvessel ischemic disease."
        },
        {
            "input": "Examination is mildly degraded by motion.\n\nThere are postsurgical changes of left frontal craniotomy for resection of an\nunderlying left front meningioma.  Hyperintense signal abnormality on the\ndiffusion images in the left frontal lobe near the vertex are favored to be\nartifactual.  Chronic blood products are identified in the resection bed. \nThere is a small confluent area of T2 FLAIR signal abnormality in the deep\nleft frontal lobe near the vertex likely related to evolving postsurgical\nchanges.  There is dural thickening and enhancement along the superior\nresection cavity, best demonstrated on the sagittal MPRAGE images.  Otherwise,\nthere is no evidence of abnormal enhancement in the resection bed to suggest\nresidual tumor.\n\nA 9 mm right parietal enhancing dural-based extra-axial mass with associated\nminimal mass effect on the adjacent right parietal lobe is unchanged dating\nback to ___.\n\nThe previously identified nonspecific extra-axial fluid collections along the\nbifrontal convexities have resolved.\n\nThere is no evidence of acute intracranial hemorrhage or infarction.  The\nventricles and sulci are stable in size and configuration with no mass effect\nor midline shift.\n\nThe major intracranial arterial flow voids are preserved.  The dural venous\nsinuses, including the superior sagittal sinus, are patent.  There is minimal\nmucosal thickening of the ethmoid sinuses.  Mild-to-moderate right mastoid air\ncell effusion is present.  The intraorbital contents are preserved.",
            "output": "1. Examination is mildly degraded by motion.\n2. Evolving postsurgical changes of left frontal craniotomy for resection of\nunderlying left frontal meningioma.\n3. Dural thickening and enhancement along the superior resection cavity. \nWhile finding may be postoperative in nature, recurrent residual tumor is not\nexcluded on the basis examination.  Recommend attention on follow-up imaging.\n4. Otherwise, no definite evidence of recurrent or residual tumor.\n5. Stable 9 mm right parietal extra-axial mass, most suggestive of meningioma.\n\nRECOMMENDATION(S):  Dural thickening and enhancement along the superior\nresection cavity. While finding may be postoperative in nature, recurrent\nresidual tumor is not excluded on the basis examination. Recommend attention\non follow-up imaging."
        },
        {
            "input": "Study is moderately degraded by motion, especially on postcontrast imaging. \nWithin these confines:\n\nPostsurgical changes related to patient's known left frontal meningioma\nresection are noted, including minimal restricted diffusion with T2 and FLAIR\nhyperintensity and blood products along resection cavity bed.  Minimal\nbilateral nonspecific extra-axial collections are noted on FLAIR imaging (see\nseries 11).  Minimal enhancement along the anterior (see 03:21; 13:137) and\nposterior (see 13:143; 03:22) resection cavity margin is noted.  The venous\nsinuses, including the superior sagittal sinus are grossly preserved.  Grossly\nstable\n\nGrossly stable approximately 9 mm right parietal enhancing dural-based\nextra-axial mass with minimal mass effect on adjacent parietal lobe is grossly\nunchanged (see 13:140).\n\nThere is no evidence of midline shift.  The ventricles and sulci are grossly\nstable in caliber and configuration.  Trace bilateral mastoid fluid is noted. \nMinimal bilateral ethmoid air cell mucosal thickening is present.",
            "output": "1. Study is moderately degraded by motion.\n2. Postsurgical changes related to patient's left frontal meningioma resection\nas described.  Minimal restricted diffusion around resection cavity may\nrepresent postoperative changes.\n3. Minimal enhancement along anterior and posterior margins of resection\ncavity concerning for residual tumor, with differential consideration of\npostoperative changes.\n4. Grossly stable approximately 9 mm right parietal extra-axial mass\nsuggestive of meningioma."
        },
        {
            "input": "Postoperative changes are again seen in the left frontoparietal region. \nPachymeningeal enhancement seen previously has slightly decreased.  No\ndefinite new nodular area of enhancement is identified.  There is\nencephalomalacia in the left frontoparietal region unchanged from the previous\nstudy.  Mild-to-moderate changes of small vessel disease seen.  No new areas\nof parenchymal enhancement are identified.  A small right parietal extra-axial\nlesion is unchanged.  No acute infarcts are identified..",
            "output": "1. Postsurgical changes are seen in the left parietal region with slightly\ndecreased pachymeningeal enhancement.  No new nodular areas of enhancement.\n2. Unchanged small right parietal extra-axial lesion."
        },
        {
            "input": "In the right parietal lobe, there is a 2.9 x 2.3 x 2.1 cm predominantly rim\nenhancing, tri-lobed lesion or aggregate of 3 abutting lesions with slow\ndiffusion and hemorrhage.  In the right parietal corona radiata, there is a\n1.6 x 1.3 x 1.3 cm predominantly rim enhancing, bi-lobed lesion or aggregate\nof 2 abutting lesions with slow diffusion and hemorrhage.  The lesions are\nassociated with vasogenic edema resulting in mild effacement of the adjacent\nsulci and right lateral ventricle.  A component of fast diffusion extends into\nthe splenium of the corpus callosum but does not cross to the contralateral\nhemisphere.  There is cortical involvement, best seen on series 8, images 16\nand 17.\nThese findings strongly suggest a malignant neoplasm.  This could represent\nmetastatic disease or a malignant glioma.\nNo hydrocephalus or midline shift.  The basal cisterns are patent.  No\nadditional lesions identified.\n\nThere is no evidence of infarction.  Mild periventricular and subcortical\nwhite matter T2/FLAIR hyperintensities are nonspecific but likely sequelae of\nchronic small vessel ischemic disease.  The major intracranial flow voids are\npreserved.",
            "output": "Right parietal lobe lesions measuring up to 2.9 cm with evidence of prior\nhemorrhage likely represent a malignant neoplasm, metastatic or primary\nglioma."
        },
        {
            "input": "Study is moderately degraded by motion.  Within these confines:\nThe patient's previously noted right parietal peripherally enhancing lesions\nwith adjacent edema and mass effect on the right lateral ventricle are again\nseen, overall increased compared to ___ prior exam.  The larger\nmass now measures approximately 3.9 (AP) x 3.5 (TV) x 3.9 (SI) cm and the\nsmaller more anterior lesion measures approximately 2.4 (AP) x 2.4 (TV) x 2.5\n(SI) cm.  These lesions again demonstrate associated areas of slow diffusion. \n3 mm right to left midline shift is noted, slightly progressed compared to\nprior exam.",
            "output": "1. Study is moderately degraded by motion.\n2. Interval progression in size of previously noted right parietal enhancing\nlesions, with increased adjacent edema and mass effect on right lateral\nventricle.\n3. Approximate 3 mm right to left midline shift, slightly increased compared\nto prior exam.\n\nNOTIFICATION:  The impression and recommendation above was entered by Dr.\n___ on ___ at 15:01 into the Department of Radiology critical\ncommunications system for direct communication to the referring provider."
        },
        {
            "input": "Slight increase in size of the right parietal peripherally enhancing lesion\nmeasuring approximately 4.7 x 4.0 x 4.0 cm (AP X TR X SI) from previously 3.9\nx 3.5 x 3.9 cm.\n\nA smaller anterior lesion is similar in size measuring approximately 2.5 x 2.4\nx 2.5 cm (AP X TR X SI).  The lesions again demonstrate associated areas of\nslow diffusion and surrounding edema.\n\nThere is mild increase in leftward midline shift now measuring approximately 5\nmm from previously 3 mm.",
            "output": "1. Slight increase in size of right parietal lesion as detailed above.\n2. Stable smaller lesion anteriorly.\n3. Mild increase in leftward midline shift now measuring 5 mm from previously\n3 mm."
        },
        {
            "input": "The patient is status post right parietal craniotomy for resection of the\nright parietal lobe masses with susceptibility artifacts noted in the surgical\nbed and along the right parietal lobe convexity consistent with a combination\nof hemorrhage and air as noted on head CT from ___.  Allowing for\nmodality and technique differences, these findings are not substantially\ndifferent.  Peripheral curvilinear enhancement in the surgical bed may\nrepresent postoperative changes.  No other foci of abnormal enhancement in the\nbrain.  The surrounding vasogenic edema is similar to CT performed 1 day prior\nand MRI from ___.  Associated local mass effect including right\nlateral ventricular effacement and 3 mm left for midline shift have improved. \nBifrontal pneumocephalus is grossly unchanged.  Major intracranial flow voids\nare preserved.  Slow diffusion along the margin of the resection cavity is\nlikely secondary to marginal ischemia - consistent with appropriate\npost-procedural changes.  The dural venous sinuses are patent.\n\nThere is mild mucosal thickening ethmoid air cells and small amount of fluid\nin the bilateral mastoid air cells.  Otherwise the remaining visualized\nparanasal sinuses are unremarkable.  The orbits are unremarkable. \nSubcutaneous soft tissue edema and emphysema are grossly unchanged.",
            "output": "1. Status post resection of the right parietal lobe mass with appropriate\npostoperative changes in the surgical bed and along the right parietal lobe\nconvexity.  Peripheral curvilinear enhancement in the surgical bed may\nrepresent postoperative changes.  Continued attention on follow-up imaging is\nrecommended.\n2. Stable postoperative bifrontal pneumocephalus and subcutaneous emphysema\nedema along the right parietal craniotomy site.\n3. Unchanged right parietal lobe vasogenic edema with improved local mass\neffect."
        },
        {
            "input": "Evaluation is suboptimal due to motion artifact.  Within this confine:\n\nPostoperative changes are seen secondary to a right parietal craniotomy for\nresection of a right parietal mass, including blood products. There is\nresolution of the bifrontal pneumocephalus. A new subdural hygroma is seen\noverlying the right frontal region, measuring 2 8 mm..  A 4 mm leftward\nmidline shift is seen, relatively unchanged.\n\nA resection cavity in the right parasagittal parietal lobe appears larger,\nmeasuring 4.3 cm x 2.9 cm x 4.1 cm (AP x TV x SI), previously measuring 1.1 cm\nx 1.0 cm (AP x TV).  This demonstrates internal T1 moderately intense signal,\nlikely representing proteinaceous fluid.  Additionally, there is thin\ncurvilinear peripheral enhancement, most likely representing postoperative\nchange.  No definitive nodular enhancement is seen.  The degree of surrounding\ndiffusion-weighted hyperintense signal has slightly improved.  The adjacent\nsuperior sagittal sinus appears patent.  The degree of surrounding T2 signal\nabnormality is slightly improved.  There is unchanged mild effacement of the\nright occipital horn without ventriculomegaly.  No new enhancing lesion.\n\n The paranasal sinuses are clear.  Moderate bilateral mastoid effusions are\nunchanged.  The intraorbital contents are normal.",
            "output": "1. Postoperative changes secondary to right parietal craniotomy for resection\nof a right parietal mass, including a new subdural hygroma overlying the right\nfrontal region, measuring up to 8 mm.\n2. Larger right parasagittal parietal lobe resection cavity with thin\ncurvilinear peripheral enhancement, most consistent with postoperative change.\nNo definite nodular enhancement.  The resection cavity does appear slightly\nincreased in size from prior examination but is now filled with presumed\nproteinaceous/hemorrhagic fluid.\n3. Slight improvement in the degree of surrounding T2 signal abnormality.\n4. No new enhancing lesions within confines of motion degraded exam.\n5. Unchanged moderate sized bilateral mastoid effusions."
        },
        {
            "input": "There is diffuse age-appropriate parenchymal volume loss with commensurate\nprominence of the ventricles, sulci, and cisterns.  There are nonspecific\nscattered areas of increased T2/FLAIR hyperintense signal within the\nperiventricular and subcortical white matter, which is likely a sequela of\nchronic small vessel microangiopathy in a patient of this age.  There is no\ndisproportionate temporal lobe or hippocampal atrophy.\n\nThere is no evidence of hemorrhage, infarction, mass effect or midline shift. \nNo intra or extra-axial fluid collections are seen.\n\nThe paranasal sinuses and mastoid air cells appear clear.  Expected voids are\nvisualized within the larger intracranial vasculature.",
            "output": "1. Diffuse parenchymal volume loss with nonspecific white matter changes,\nlikely a sequela of chronic small vessel microangiopathy in a patient of this\nage.  Otherwise, unremarkable brain MRI without hemorrhage, infarction, or\nmass effect."
        },
        {
            "input": "Aero digestive tract:\n\nThere is no mass.\nIf there is a mass, please insert field choice -->\n\nNeck lymph nodes:\nThere is no adenopathy involving bilateral levels ___.\nThere is no retropharyngeal adenopathy.\n\nExtra nodal tumor spread:\nNot applicable.\n\nDeep neck muscles, masticator space:\nUnremarkable.\n\nBones, skull base:\nThere is no bone involvement.\nThere are no findings suggestive of perineural tumor extension.\nJugular foramen, carotid canal,pterygopalatine fossa,infraorbital\nforamen,other skull base foramina are not involved.\nThere is mild reversal lordosis of the cervical spine.  There is 4 mm\nretrolisthesis of C5 on C6.  There is mild to moderate multilevel degenerative\nchanges of the cervical spine with spinal canal stenosis most significant at\nC5-6 and C6-7.\nThere is a mucous retention cyst in the right maxillary sinus.\n\nVessels:\nUnremarkable.\n\nBrachial Plexus:\nUnremarkable.\n\nThyroid, salivary glands:\nThere are subcentimeter lesions in the thyroid.\n\nMild asymmetric enhancement and FLAIR hyperintense signal of the left\nsubmandibular gland and sublingual glands.  Re-identified is dilatation of the\nleft submandibular duct measuring up to 6 mm in diameter.  There is no\nevidence of abnormal focal mass involving the left submandibular and\nsublingual gland.  No evidence of abnormal filling defect within the left\nsubmandibular duct.\n\nThe right submandibular and sublingual glands appear unremarkable.  There is\nno dilatation of the right submandibular duct.\n\nThe parotid glands appear unremarkable.\n\nOther findings:\nVisualized brain parenchyma is grossly unremarkable.",
            "output": "1. Re-identified is dilatation of the left submandibular duct measuring up to\n6 mm in diameter.  There does appear to be mild increased enhancement of the\nleft submandibular and sublingual gland without evidence of surrounding fatty\ninflammatory stranding.  No evidence of focal mass lesion within the\nsubmandibular or sublingual gland.  No evidence of mass lesion at the level of\nthe root of tongue.\n2. This could represent stenosis/scarring of the left submandibular caruncle\nsecondary to previously passed stone.  No definite mass lesion is identified\nat the root of the tongue however clinical correlation and direct\nvisualization is recommended.  This could represent inflammatory or autoimmune\ndisorder.\n3. Mild to moderate degenerative changes of the cervical spine most\nsignificant at C5-6.   4 mm retrolisthesis of C5 on C6.\n4. Additional findings described above."
        },
        {
            "input": "There is no hemorrhage, infarction, mass, mass effect, or edema.  There are no\nabnormal foci of restricted diffusion.  Scattered T2/FLAIR signal hyperintense\nfoci predominantly in the periventricular, deep and left-greater-than-right\nparietal subcortical white matter (for example see series 11, image 18) are\nunchanged in comparison to MR from ___, non-specific however\ncompatible with sequelae of chronic small vessel ischemic change.  The\nventricles and sulci are normal in caliber and configuration.  The major\nintracranial vascular flow voids are preserved.  The major dural venous\nsinuses are patent.  There is minimal right maxillary sinus mucosal\nthickening; otherwise, the imaged paranasal sinuses and mastoid air cells\nappear clear.  The globes are intact and unremarkable",
            "output": "Scattered small T2/FLAIR signal hyperintense foci in the periventricular,\nsubcortical and deep white matter, unchanged in appearance since ___.  These findings are nonspecific, a upper compatible with sequelae of\nmild chronic white matter small vessel ischemic change.  Overall, no\nsignificant interval change since ___."
        },
        {
            "input": "There are few punctate foci of slow diffusion involving the\ncortical/subcortical right hippocampus (04:11) without definite corresponding\nsignal abnormality on T2 weighted FLAIR images.  No edema or mass effect.  A\nsmall focus of blooming artifact along the left paracentral lobule on image\n11:17 corresponds to a dural calcification on the preceding head CT.  Small\nfocus of low signal on gradient echo images over the left temporal cortex,\nimage 11:13, may represent a chronic microhemorrhage versus a prominent sulcal\nblood vessel.  Ventricles and sulci are age-appropriate. The major\nintracranial vascular flow voids are maintained.\n\nThere is mild mucosal thickening in the ethmoid sinuses.  There is trace\nmucosal thickening plus/minus fluid in left greater than right mastoid air\ncells.",
            "output": "Several punctate punctate acute cortical and/or subcortical infarcts of the\nright hippocampus.\n\nNOTIFICATION:  The findings were discussed with ___, M.D. by ___\n___, M.D. on the telephone on ___ at 9:12 am, 10 minutes after\ndiscovery of the findings."
        },
        {
            "input": "A few small foci of increased DWI signal are noted in the cerebral white\nmatter in the right frontal lobe, right thalamus and in the right middle\ncerebellar peduncle.\nHowever, these do not of demonstrates low ADC signal.\nA punctate focus of increased DWI signal adjacent to the left lateral\nventricle has slightly low ADC signal- series 4 and 3, image 19.\nThis may represent a tiny acute-subacute infarct.  However, is too small to be\naccurately characterized.  Presence of mineralization can also give this\nappearance.\n\nPunctate foci of negative susceptibility are noted in the pons and left\nfrontal lobe which can relate to foci of mineralization or micro hemorrhage.\nBasal ganglia mineralization noted.\n\nThere is moderate dilation of the lateral and the third ventricles left more\nthan right along with prominent Sylvian fissures and cerebral sulci related to\ndiffuse parenchymal volume loss.\nThere are periventricular and subcortical T2 FLAIR hyperintense foci noted, in\nthe frontal parietal and the  left temporal lobe nonspecific in appearance and\ncan relate to small vessel ischemic changes, etc.\nThe major intracranial arterial flow voids are noted, the right vertebral\nartery is dominant and tortuous.\n\nFluid noted in the mastoid air cells diffusely.\nFluid with dense contents noted in the right side of the sphenoid sinus.\nMild to moderate ethmoidal mucosal thickening.\nSmall 1 cm node/ nodule in the right parotid.\n\nStudy somewhat limited due to motion artifacts.",
            "output": "Punctate focus of slow diffusion, in the left frontal periventricular\nlocation-\n-?Tiny acute -subacute infarct or focus of minerlization or microhemorrhage;\ntoo small to be accurately characterized.\nFluid in the mastoid air cells on both sides, and in the right side of the\nsphenoid sinus correlate clinically for etiology and significance.\nOther details as above.\n\nRECOMMENDATION(S):  Correlate clinically and consider followup to assess for\nany interval change.\n\nNOTIFICATION:  D/w Dr. ___ by Dr. ___ phone on ___ at 6.58pm\n5 min after discovery."
        },
        {
            "input": "MRI BRAIN:\nThere is an acute infarct with restricted diffusion centered in the left\nposterior limb of the internal capsule with involvement of adjacent left basal\nganglia globus pallidus and left thalamus.  There are additional scattered\nperiventricular and subcortical T2/FLAIR white matter hyperintensities, which\nare nonspecific, but suggestive of chronic small vessel disease.  There is no\nevidence of hemorrhage,edema,masses, mass effect or midline shift.  The\nventricles and sulci are normal in caliber and configuration.  There is no\nabnormal enhancement after contrast administration.\n\nMRA BRAIN:\nThe intracranial vertebral and internal carotid arteries and their major\nbranches appear normal without evidence of stenosis,occlusion,or aneurysm\nformation.\n\nMRA NECK:\nEvaluation of neck vessels on time-of-flight is limited due to\nmotion/pulsation.  Limited evaluation of the origins of the great vessels,\nsubclavian and vertebral arteries.  There is flow signal within the proximal\ncommon carotid arteries and vertebral arteries bilaterally. The common,\ninternal and external carotid arteries appear normal.  There is no evidence of\ninternal carotid artery stenosis by NASCET criteria.",
            "output": "1. Acute stroke centers within the left posterior limb of the internal capsule\nwith involvement of the adjacent left lobes pallidus and left thalamus.\n2. Location of restricted diffusion is suggestive of a left lateral\nlenticulostriate stroke.\n3. The ___ remains patent without evidence of\nstenosis,occlusion,or aneurysm.\n4. Patent bilateral cervical carotid and vertebral arteries without evidence\nof stenosis, occlusion, or dissection.\n\nNOTIFICATION:  These findings were communicated to Dr. ___ by Dr.\n___ at 8:55 AM on ___."
        },
        {
            "input": "Images through the internal auditory canal demonstrates symmetric appearance\nof the seventh eighth nerve complexes.  There is no evidence of abnormal\nenhancement or mass lesion within the internal auditory canals,\ncerebellopontine angles or membranous labyrinth. No other mass lesions are\nseen within the posterior fossa.",
            "output": "1. Normal MRI of the IACs."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  No thalamic or hippocampal infarcts.  Findings consistent with\nmild chronic small vessel ischemic changes. The ventricles and sulci are age\nappropriate.  No abnormal enhancement.\nMajor vascular flow voids appear preserved, major dural venous sinuses are\npatent.\n\nThere is mild mucosal thickening along the ethmoid air cells.  There is\npartial opacification of the right mastoid air cells.  Note is made of\nbilateral lens replacement surgery.  The orbits appear otherwise unremarkable.",
            "output": "1. No acute findings intracranially.\n2. Findings consistent with mild chronic small vessel ischemic changes."
        },
        {
            "input": "Examination is mildly degraded by motion.\n\nThere are multiple small foci of restricted diffusion in the right frontal\nlobe, predominately involving the right frontal lobe cortex anteriorly and\nright postcentral gyrus (images 17, ___ of series 302).\n\nThere is also a small focus of restricted diffusion in the right parietal lobe\n(image 19 of series 302).\n\nAdditionally, there are curvilinear areas of FLAIR hyperintense signal\nabnormality in the right superior frontal gyrus and sulcus (image 18 of series\n6).  There is a corresponding curvilinear area of intrinsic T1 hyperintense\nsignal (image 14 of series 4) compatible with cortical laminar necrosis.\n\nThere is no evidence of mass.\n\nMild prominence of the ventricles and sulci is suggestive of involutional\nchanges.  There is also prominence of the bifrontal extra-axial CSF spaces. \nThere is no mass effect or midline shift.  Periventricular and subcortical T2\nand FLAIR hyperintensities are noted which may represent small vessel ischemic\nchanges.\n\nFocal fat within the falx is again seen (see 06:18; 04:11 on current study and\n02:22 on prior exam).\n\nThere is a partially empty sella.  There are postsurgical changes of bilateral\nlens replacement.  There is mild mucosal thickening of the ethmoid sinuses.\nThe mastoid air cells appear clear.",
            "output": "1. Examination is mildly degraded by motion.\n2. Multiple punctate foci of acute to subacute infarction in the right frontal\nlobe.\n3. Small focus of acute to subacute infarction in the right parietal lobe.\n4. Small curvilinear area of cortical laminar necrosis in the right superior\nfrontal gyrus with adjacent probable subacute blood products in the right\nsuperior frontal sulcus."
        },
        {
            "input": "There is no evidence of hemorrhage or mass effect. The ventricles and basal\ncisterns appear normal.\n\nThere are normal vascular flow voids. There is no evidence of acute infarct\nbased on diffusion-weighted imaging. The brain parenchymal volume is within\nnormal limits. There is extensive subcortical and periventricular white matter\nT2/FLAIR signal hyperintensity, the findings of which are nonspecific although\ncan be seen with sequelae of chronic small vessel ischemic disease\n\nThe orbits, mastoid air cells, and paranasal sinuses are unremarkable.",
            "output": "1. No hemorrhage, mass effect, or acute infarct.\n2. Extensive subcortical white matter signal abnormality, a nonspecific\nfinding though may be on the basis of sequelae of chronic small vessel\nischemic disease."
        },
        {
            "input": "MRI Brain:\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.  Again seen is opacification of the left sphenoid sinus and\nleft ethmoid air cells.\n\nMRV brain:  The dural venous sinuses appear normal.  Limited view of the\nintracranial arteries raises a possibility of narrowing of the proximal M1\nsegments of the middle cerebral artery on the left.  However, this is a\nlimited evaluation.  There is a similar possible narrowing of the proximal M2\nbranches of the right middle cerebral artery.\n\nMRA neck:  The common, internal and external carotid arteries appear normal. \nThere is no evidence of internal carotid artery stenosis by NASCET criteria. \nThe origins of the great vessels, subclavian and vertebral arteries appear\nnormal bilaterally.",
            "output": "1. No evidence of hemorrhage, edema or infarction.\n\nNormal appearance of the dural venous sinuses.\n\nPossible bilateral middle cerebral artery narrowing.\n\nNormal appearance of the neck arteries.\n\nParanasal sinus fluid similar to the CTA of ___"
        },
        {
            "input": "No significant change in the multiple scattered juxta cortical FLAIR white\nmatter hyperintensities in the left greater than right frontal lobes.  There\nare no new or enhancing lesions.  There is no evidence of hemorrhage, edema,\nmasses, mass effect, midline shift or infarction.\nThere is no abnormal enhancement after contrast administration.\nThe major intracranial vascular flow voids are maintained.  The ventricles and\nsulci are normal in caliber and configuration.  The paranasal sinuses, orbits\nand mastoid air cells are normal.",
            "output": "1. Unchanged multiple scattered juxta cortical FLAIR white matter\nhyperintensities, which are nonspecific but can be seen with demyelinating\ndisease as well as other differential considerations including sequela of\nchronic migraine headaches, prior trauma, infection/inflammation and less\nlikely chronic small vessel ischemic disease given the patient's age.\n2. No evidence of any new or enhancing lesions."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There are a few scattered juxtacortical FLAIR hyperintensities\nseen in the left greater than right frontal lobes (series 100 a, image 73, 66,\n58).  These are not associated with enhancement.  Intracranial flow voids are\npreserved.  The orbits are unremarkable.  The paranasal sinuses are clear.",
            "output": "Scattered Juxtacortical FLAIR hyperintensities in the left greater than right\nfrontal lobe without associated enhancement.  While findings are nonspecific,\nthey can be seen in the setting of  demyelinating disease.  Other\ndifferentials include chronic headaches or much less likely chronic small\nvessel microvascular disease, given young patient age."
        },
        {
            "input": "Postoperative changes are seen secondary to a right suboccipital craniotomy\nfor resection of a right cerebellar mass, including slight pneumocephalus,\nfocal pachymeningeal thickening, blood products, surround edema without mass\neffect and thin curvilinear enhancement around the resection cavity.  No\nnodular-appearing enhancement to suggest residual tumor is seen.  The adjacent\ntransverse sinus is patent.\n\nA 1.3 x 1.2 cm heterogeneously enhancing lesion is seen in the anteromedial\nleft thalamus without surrounding T2 signal abnormality.  This encroaches on\nthe third ventricle without evidence of ventriculomegaly.\n\nThere is asymmetric bulging of the right pons without abnormal signal or\nenhancement (11:9 and 14:72).\n\n The ventricles and sulci are prominent, consistent with global cerebral\nvolume loss.  Patchy periventricular T2 hyperintensities are most consistent\nwith chronic microvascular angiopathy. The paranasal sinuses, mastoid air\ncells and middle ear cavities are clear.  The intraorbital contents are\nnormal.",
            "output": "1. Status post right suboccipital craniotomy for resection of a right\ncerebellar mass with expected postsurgical changes.\n2. No nodular-appearing enhancement suggest residual tumor.  Unremarkable\nadjacent transverse sinus.\n3. 1.3 cm enhancing lesion in the anteromedial left thalamus likely represents\na metastatic focus.  Encroachment of the third ventricle is seen without\nevidence of ventriculomegaly.\n4. Asymmetric bulging of the right pons without abnormal signal or\nenhancement; attention on follow up with close imaging monitoring is\nrecommended for underlying lesion."
        },
        {
            "input": "Again seen thalamic mass invaginating into the third ventricle.  This is high\nsignal intensity on the postcontrast T1 weighted and MP rage images,\ncorresponding to the enhancement demonstrated on the prior brain MR study. \nThe lesion appears unchanged.\nAgain seen are postoperative findings after suboccipital craniectomy minimal\nperipheral enhancement has decreased slightly since the prior study. \nSurrounding right cerebellar hemisphere mass-effect has markedly improved\nsince the previous examination.",
            "output": "1. Left thalamic enhancing mass unchanged.\n2. Decreasing postoperative changes after suboccipital craniectomy for right\ncerebellar hemisphere mass resection."
        },
        {
            "input": "There is no acute infarct mass effect midline shift or hydrocephalus.  Mild to\nmoderate brain atrophy seen with early changes of small vessel disease.  No\nmicro hemorrhages are identified.  There are no definite lacunar infarcts in\nthe basal ganglia region.  Following gadolinium administration, there is no\nabnormal parenchymal vascular or meningeal enhancement seen.\n\nFlow signal is visualized within the clivus and upper cervical vertebral\nmarrow.  This a nonspecific finding and could be related to marrow\nhyperplasia.  Clinical correlation recommended.",
            "output": "No acute infarct, mass effect or abnormal enhancement."
        },
        {
            "input": "Diffuse restricted diffusion is seen along the parietal lobes, occipital\nlobes, basal ganglia and cerebral cortices as well as superior landed cortex\nconsistent with global hypoxic ischemic brain injury.  Subtle increased FLAIR\nsignal is also seen involving the basal ganglia bilaterally.  Increased\nrestricted diffusion is also seen involving the midbrain and hippocampi by\nbilaterally consistent with patient's injury.\n\nNo hemorrhage is identified.  The principal vascular flow voids appear to be\nwell preserved.  No marrow signal abnormalities are seen.  Extensive fluid is\nseen within the frontal sinuses, maxillary sinuses sphenoid sinuses and\nethmoid air cells.  The globes are unremarkable.",
            "output": "1. Diffuse restricted diffusion is seen along the bilateral parietal lobes,\noccipital lobes, basal ganglia, midbrain, hippocampi by and perirolandic\ncerebral cortices consistent with global hypoxic ischemic brain injury.\n2. Extensive fluid is seen within all of the sinuses, also consistent with\ndrowning injury."
        },
        {
            "input": "Images of the pituitary appear normal. The pituitary signal intensity appears\nnormal before and after contrast administration. No masses are identified. The\nsuprasellar cistern and cavernous sinuses appear normal. On limited evaluation\nof the whole-brain: There is no evidence of edema, or mass effect.  The\nventricles and sulci are mildly prominent consistent with global involutional\nchanges.  Periventricular and a few scattered deep white matter foci of\nT2/FLAIR signal hyperintensity bilaterally are nonspecific but compatible with\nmild changes of chronic white matter microangiopathy.  No abnormal enhancement\nwithin the brain.  The major intracranial vascular flow voids are preserved. \nThere is a small mucous retention cyst in the left maxillary sinus.  The\nglobes and orbits are within normal limits.",
            "output": "1. Unremarkable MR appearance of the pituitary gland.\n2. No evidence of acute intracranial abnormality on limited evaluation of the\nbrain."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.  No demyelination.  Submucosal retention cysts bilateral\nmaxillary sinuses, similar to prior, which trace mucosal thickening.  No\nfluid.  Patent mastoids on the left, trace opacification right mastoids. \nIntracranial vascular flow voids are preserved.  Patent dural venous sinuses.",
            "output": "1. Normal intracranial contents.  No demyelination.\n2. Paranasal sinus disease."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  There is a partially empty sella, unchanged since MRI on ___ and likely of no clinical significance.  Subcortical and\nperiventricular white matter lesions displaying high signal on FLAIR are new\ncompared with prior MRI head in ___ and are nonspecific, however likely\nrepresent sequela of chronic small vessel ischemic disease.  There is CSF\npulsation artifact in the lateral ventricles.    The ventricles and sulci are\nnormal in caliber and configuration for patient's age.  There is no abnormal\nenhancement after contrast administration.",
            "output": "1. No evidence of intracranial mass.\n2. Subcortical and periventricular white matter changes are nonspecific,\nhowever likely represent sequela of chronic small vessel ischemic disease.\n3. Incidental note is made of a partially empty sella, unchanged since ___\nand likely of no clinical significance."
        },
        {
            "input": "Diffusion-weighted signal hyperintensity with correlatives ADC map\nhypointensity involving the anterior superior right temporal lobe extending\ninto the posterior aspect of the insula and basal ganglia with scattered\ngyriform foci of slow diffusion of the precentral gyrus on the right is\nidentified with associated FLAIR hyperintense signal, compatible with more\nlate acute infarct. Additional punctate focus of slow diffusion with too small\nto correlate with definite ADC abnormality of the posterior parietal occipital\nlobe (series 6, image 20) is also seen, and also likely represents a late\nacute infarct.\n\nSubtle blush of enhancement of the right frontal convexity (series 13, image\n19) corresponding to a focus of prior infarct seen on examination of ___ is noted, consistent with evolving sequela. There is a rounded\nsubcortical FLAIR hyperintense focus of the left frontal convexity (series 11,\nage image 18) which is nonspecific.\n\nOverlying area of the anterior left frontal lobe is a cyst homogeneously\nenhancing extra-axial dural-based lesion measuring approximately 2.7 by 1.6 cm\n(TRV, AP) consistent with a meningioma. This lesion is unchanged in appearance\nfrom prior exam and exerts mass effect on the underlying brain parenchyma\nwithout evidence of signal abnormality.\n\nThe major flow voids are preserved. Sulci, ventricles and cisterns are within\nexpected limits for the patient's age. The paranasal sinuses are clear. The\norbits are unremarkable. The mastoid air cells are clear.",
            "output": "1. Geographic region of late acute infarct in the right MCA distribution\nfollowing the temporal lobe, posterior insula extending to the posterior basal\nganglia. Smaller focus of late acute infarct involving the pre central gyrus\non the right.  In addition, there is a punctate focus of slow diffusion of the\nleft parietal occipital lobe, which also likely represents late acute infarct.\nThe distribution of these infarcts would suggest embolic etiology. Clinical\ncorrelation with outside hospital CTA and MRI is recommended. Repeat CTA or\nMRA of the head and neck may yield additional information if clinically\nindicated.\n2. Faint blush of contrast seen in the right frontal convexity, consistent\nwith evolving sequela of recent infarct involving the right MCA distribution\nseen on examination of ___.\n3. Left frontal meningioma is unchanged from prior exam.\n\nNOTIFICATION:   The findings were discussed by Dr. ___ with Dr.\n___ on the telephone on ___ at 8:26 AM, at the time of\ndiscovery of the findings."
        },
        {
            "input": "There is motion artifact which degrades spatial resolution.\n\nThe parenchymal signal is unremarkable without acute infarct, hemorrhage,\nmass, or mass effect.  The ventricles and cortical sulci are normal in caliber\nand configuration.  The vasculature is patent.\n\nThe orbits, calvarium, and soft tissues are unremarkable.  There is mild\nmucosal thickening within bilateral maxillary sinuses with inferior mucous\nretention cysts.  The mastoid air cells and middle ears are clear.\n\nWithin the limitations of the motion artifact, the bilateral hippocampal\nformations and mammillary bodies are preserved in signal and configuration.\nThere is no disproportionate medial temporal atrophy. There is no focal lobar\nencephalomalacia. There are no focal cortical dysplasias or gray matter\nheterotopia noted.",
            "output": "1. Motion artifact which degrades spatial resolution.\n2. No acute intracranial abnormality without of seizure focus.\n3. Mild maxillary sinus disease."
        },
        {
            "input": "Study is mildly degraded by motion.\n\nBRAIN MRA:\nBilateral approximately 2 mm proximal cavernous internal carotid artery\nprobable infundibula are noted.  Otherwise, the intracranial vertebral and\ninternal carotid arteries and their major branches appear normal without\nevidence of stenosis, occlusion, oraneurysm formation.  Fenestration of\nproximal right PCA is noted.\n\nBRAIN MRI:\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  Scatter bifrontal and biparietal punctate FLAIR and T2\nperiventricular deep white matter hyperintensities are noted, and may\nrepresent microangiopathic changes..  Mucosal thickening is noted in left\nfrontal and ethmoid sinuses.",
            "output": "1.  Study is mildly degraded by motion.\n2.  Patent circle of ___ without definite evidence of aneurysm, occlusion,\nor stenosis.\n3.  No acute intracranial abnormality, with no definite evidence of acute\ninfarct.\n4.  Paranasal sinus disease, as described.\n5. Probable microangiopathic changes, as described."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.\n\nThere are few scattered foci of T2/FLAIR hyperintensity in the subcortical and\nperiventricular white matter, nonspecific, likely secondary to small vessel\nischemic disease.\n\nThere is an old lacunar infarct in the left basal ganglia.\n\nThere is T1 hyperintensity in bilateral globus pallidus, nonspecific, can be\nsecondary to patient's underlying liver failure.\n\nThere is a 5 mm pineal cyst.\n\nThe orbits are unremarkable.  There is mucosal thickening in left maxillary\nsinus, bilateral ethmoid air cells, and bilateral frontal sinuses.  Bilateral\nsphenoid air cells are clear.  Not minimal nonspecific fluid opacification in\nbilateral mastoid air cells.",
            "output": "1. Intrinsic T1 hyperintensity in bilateral globus pallidi, non specific,\nlikely secondary to underlying liver failure.\n2. Findings of small vessel ischemic diseas and old lacunar infarct in the\nleft basal ganglia.\n3. Otherwise, unremarkable MRI of the brain without any abnormal enhancement\nor findings suggestive of intracranial Nocardiasis."
        },
        {
            "input": "There is no evidence of intracranial hemorrhage, edema, masses, mass effect,\nmidline shift infection, or acute infarction.  The ventricles and sulci are\nslightly more prominent than in ___, suggestive of increased\natrophy.  Again noted is a T2/FLAIR hyperintensity in the left basal ganglia\nwhich is consistent with a chronic infarct (series 11, image 14).  There is no\nabnormal enhancement after contrast administration.\nMajor intracranial flow voids are preserved.  The dural venous sinuses are\npatent.",
            "output": "1. Chronic infarct in the left basal ganglia.  Otherwise, unremarkable MRI\nwithout evidence of acute infarction, hemorrhage, mass, edema, or signs of\ninfection.\n2. Atrophy slightly greater than in ___."
        },
        {
            "input": "T2 and FLAIR hyperintensities in the white matter in the supratentorial region\nboth involving the periventricular and subcortical white matter are unchanged\nexcept there is now a T1 hypointensity in the right periventricular region. \nThere are no definite new or enhancing lesions seen including FLAIR\nabnormality in the right cerebellum which is also unchanged.  There is no mass\neffect midline shift or hydrocephalus.",
            "output": "Evolution of previously seen FLAIR hyperintensities consistent with history of\nmultiple sclerosis without definite new abnormalities or enhancing lesions."
        },
        {
            "input": "MR BRAIN:\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  Mild mucosal thickening of the bilateral maxillary sinuses and\nbilateral ethmoid air cells, right greater than left.  The visualized portion\nof the remaining paranasal sinuses and mastoid air cells are clear.  The\nvisualized orbits are unremarkable.\n\nMRV: Normal flow signal is demonstrated within the superior sagittal sinus,\nstraight sinus, transverse sinuses, and sigmoid sinuses. The jugular bulbs and\nproximal jugular veins are patent. Evaluation of the deep venous systems\nreveals normal flow signal in the internal cerebral veins. The vein ___\nis also unremarkable.",
            "output": "1. No evidence of dural venous sinus thrombosis.\n2. Normal brain MRI, without evidence of intracranial hemorrhage or\ninfarction.\n3. Mild paranasal sinus disease."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  Paranasal sinuses, middle ear cavities, and mastoids are\nclear.  Visualized orbits are unremarkable.",
            "output": "Normal brain MRI.  No evidence of infarction or hemorrhage."
        },
        {
            "input": "Study is mildly degraded by motion.  There is no evidence of hemorrhage,\nedema, masses, mass effect, midline shift or infarction.   The ventricles and\nsulci are normal in caliber and configuration.  There is no abnormal\nenhancement after contrast administration.  Partially empty sella is noted.\n\n The major intracranial vascular flow voids are maintained.  Nonspecific\nbilateral mastoid fluid.  The paranasal sinuses and orbits are normal. \nScattered subcentimeter nonspecific lymph nodes are noted throughout the\nvisualized portion of the neck bilaterally, without definite enlargement by CT\nsize criteria.",
            "output": "1. Study is mildly degraded by motion.\n2.  No acute intracranial abnormality, with no definite evidence of acute\ninfarct.\n3. Scattered subcentimeter nonspecific lymph nodes as described, which may be\nreactive.\n4. Nonspecific bilateral mastoid fluid.  Please note evaluation of middle ear\ncavities is limited on this examination.  If clinically indicated, consider\nnoncontrast head CT for further evaluation."
        },
        {
            "input": "MRI IAC:\n\nImages are mild limited by motion artifact.\n\nThere is an AICA loop in the right porus acusticus, best seen on image 5:29. \nFLAIR images demonstrate an asymmetric focus of intermediate signal intensity\nin the right porus acusticus on image 3:7, which probably corresponds to the\nAICA loop.  No definite lesion is seen in either internal auditory canal on\nthe high-resolution T2 weighted images.  Evaluation for leptomeningeal\ncontrast enhancement is not possible in the absence of intravenous contrast.\n\nFoci of high T2 signal in the periventricular, deep, and subcortical white\nmatter of the cerebral hemispheres are nonspecific though most likely sequela\nof chronic small vessel ischemic disease in this age group.  They appear\nsimilar to ___.  There is no abnormal diffusion.\n\nThe ventricles and sulci appear slightly larger than in ___, indicating mild\ninterim parenchymal volume loss.\n\nMRA BRAIN:\n\nThe images are moderately limited by motion artifact.  Allowing for the\nartifact, no evidence for flow-limiting stenosis or aneurysm greater than 3 mm\nis seen in the major intracranial arteries.",
            "output": "1. Mildly motion limited noncontrast MRI of the internal auditory canals\ndemonstrates an AICA loop in the right porus acusticus.  Asymmetric focus of\nintermediate signal intensity in the right porus acusticus on FLAIR images is\nmost likely related to the AICA loop, as no other lesion is seen on the\nhigh-resolution T2 weighted images.\n2. Mild parenchymal volume loss has progressed since ___.\n3. T2 hyperintense foci in the supratentorial white matter are similar to\n___, nonspecific but likely sequela of chronic small vessel ischemic disease\nin this age group.\n4. Moderately motion limited brain MRA demonstrates no evidence for a\nflow-limiting stenosis or an aneurysm greater than 3 mm.\n\nRECOMMENDATION(S):  Repeated exam with intravenous contrast, as well as\npremedication to reduce motion, should be considered for exclusion of an\nenhancing mass or leptomeningeal enhancement, particular given the history of\nbreast cancer."
        },
        {
            "input": "MRI IAC:\n\nImages are mild limited by motion artifact.\n\nThere is an AICA loop in the right porus acusticus, best seen on image 5:29. \nFLAIR images demonstrate an asymmetric focus of intermediate signal intensity\nin the right porus acusticus on image 3:7, which probably corresponds to the\nAICA loop.  No definite lesion is seen in either internal auditory canal on\nthe high-resolution T2 weighted images.  Evaluation for leptomeningeal\ncontrast enhancement is not possible in the absence of intravenous contrast.\n\nFoci of high T2 signal in the periventricular, deep, and subcortical white\nmatter of the cerebral hemispheres are nonspecific though most likely sequela\nof chronic small vessel ischemic disease in this age group.  They appear\nsimilar to ___.  There is no abnormal diffusion.\n\nThe ventricles and sulci appear slightly larger than in ___, indicating mild\ninterim parenchymal volume loss.\n\nMRA BRAIN:\n\nThe images are moderately limited by motion artifact.  Allowing for the\nartifact, no evidence for flow-limiting stenosis or aneurysm greater than 3 mm\nis seen in the major intracranial arteries.",
            "output": "1. Mildly motion limited noncontrast MRI of the internal auditory canals\ndemonstrates an AICA loop in the right porus acusticus.  Asymmetric focus of\nintermediate signal intensity in the right porus acusticus on FLAIR images is\nmost likely related to the AICA loop, as no other lesion is seen on the\nhigh-resolution T2 weighted images.\n2. Mild parenchymal volume loss has progressed since ___.\n3. T2 hyperintense foci in the supratentorial white matter are similar to\n___, nonspecific but likely sequela of chronic small vessel ischemic disease\nin this age group.\n4. Moderately motion limited brain MRA demonstrates no evidence for a\nflow-limiting stenosis or an aneurysm greater than 3 mm.\n\nRECOMMENDATION(S):  Repeated exam with intravenous contrast, as well as\npremedication to reduce motion, should be considered for exclusion of an\nenhancing mass or leptomeningeal enhancement, particular given the history of\nbreast cancer."
        },
        {
            "input": "Again is re- demonstrated the vascular loop extending into the porous\nacoustics of the right internal auditory canal.  Otherwise, images through the\ninternal auditory canal demonstrates symmetric appearance of the seventh\neighth nerve complexes.  There is no evidence of abnormal enhancement or mass\nlesion within the internal auditory canals, cerebellopontine angles or\nmembranous labyrinth. No other mass lesions are seen within the posterior\nfossa.\n\nLimited included imaging of the remainder of the brain demonstrates no\nevidence of hemorrhage, edema, masses, mass effect, midline shift or\ninfarction. There is prominence of the ventricles and sulci suggestive\ninvolutional changes.  Periventricular and subcortical T2 and FLAIR\nhyperintensities are noted, likely secondary to chronic microvascular ischemic\nchanges.  There is no abnormal enhancement after contrast administration.\n\nNo osseous abnormalities are seen. The paranasal sinuses, mastoid air cells,\nand middle ear cavitiesare clear. The orbits are unremarkable. The visualized\nportion of the principle vascular flow voids are preserved.",
            "output": "1. Re- demonstration of the vascular loop extending into the porous acoustics\nof the right internal auditory canal.  Otherwise, no evidence of IAC or\ncerebellopontine angle mass.\n2. No evidence of intracranial metastatic disease."
        },
        {
            "input": "There is no evidence of intracranial hemorrhage, mass, mass effect or shifting\nof the normally midline structures.  The ventricles and sulci abnormal in size\nand configuration for the patient's age.  Pontine, subcortical, and\nperiventricular areas of FLAIR high-signal intensity are seen, which are\nnonspecific and may reflect changes due to small vessel disease.  No diffusion\nabnormalities are detected to indicate acute or subacute ischemic changes.\n\nThe major vascular flow voids are present and demonstrate normal distribution.\nThe orbits are unremarkable, paranasal sinuses, middle ear cavities and\nmastoid air cells are clear.",
            "output": "1.  There is no evidence of acute intracranial process or hemorrhage.\n\n2.  Subcortical and periventricular areas of FLAIR high-signal intensity are\nnonspecific, and may reflect changes due to small vessel disease.\n\n3.  Grossly, there is no evidence of intracranial metastatic disease, however,\nplease note that this examination is limited without contrast due to early\ntermination of the exam and claustrophobia."
        },
        {
            "input": "The obtained MP RAGE images are severely degraded by motion artifact.  There\nis also severe susceptibility artifact from the right frontal VP shunt\napparatus.  Diffuse ventriculomegaly is again seen.  The temporal and\noccipital horns of the lateral ventricles do not appear any larger than on ___.  Evaluation of the remainder the ventricular system is limited by\nartifacts.  Basal cisterns do not appear compressed, and cerebellar tonsils\nare normally positioned.  No other diagnostic information can be discerned.",
            "output": "Incomplete exam.  The single obtained MP RAGE sequence is severely motion\ndegraded and further limited by susceptibility artifact from right frontal VP\nshunt apparatus.  Ventriculomegaly is again seen, as detailed above."
        },
        {
            "input": "Study is moderately degraded by motion.  Within these confines:\n\nThere is susceptibility artifact at the right frontal calvarium secondary to\nventriculostomy hardware which obscures adjacent structures particularly on\nthe gradient echo and diffusion-weighted sequences.\n\nThere is a right frontal approach ventriculostomy catheter with tip\nterminating in the left lateral ventricle (08:17).  There is extensive\nperiventricular, pontine and subcortical white matter FLAIR hyperintensity\nlikely reflecting sequela of advanced chronic microangiopathy.  There is a\nchronic right cerebral peduncle infarct (see 04:14).\n\nThere is no definite acute infarct, hemorrhage, mass, or mass effect.  There\nis unchanged dilatation of the ventricles and mild prominence of the cortical\nsulci.  There is sulcal FLAIR hyperintensity at the right frontal convexity\nwith no definite corresponding abnormality on all imaging sequences,\nsuggestive of susceptibility artifact.\n\nThe orbits are unremarkable.  There is catheter traversing the right lateral\nand posterior inferior neck soft tissues, otherwise the soft tissues are\nunremarkable.  The mastoid air cells do not demonstrate fluid signal.  Minimal\nbilateral ethmoid and frontal sinus mucosal thickening is present.",
            "output": "1.  Study is moderately degraded by motion and limited secondary to\nprogrammable shunt artifact and lack of administration of intravenous\ncontrast, limiting evaluation for possible meningitis.\n2. Within limits of study, no acute intracranial abnormality, with no definite\nfindings of posterior reversible encephalopathy syndrome.\n3. Nonspecific right frontal convexity sulcal signal intensity abnormalities\nas described, suggested to be artifact.  If concern for subarachnoid\nhemorrhage, consider noncontrast head CT further evaluation.\n4. Stable ventricular dilatation.\n5. Extensive white matter parenchymal signal intensity abnormalities as\ndescribed, again suggestive of microangiopathic changes.  Please note that\ntransependymal CSF flow is not excluded on the basis examination."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, or infarction.\nThe ventricles and sulci are normal in caliber and configuration.\nThere are a few foci of T2/FLAIR signal hyperintensity noted in the\nsubcortical and deep white matter of the bifrontal lobes which are\nnonspecific.  There is no abnormal enhancement after contrast administration.\nThe orbits are unremarkable; limited assessment of the optic nerves.\nThere is minimal mucosal thickening within the ethmoid air cells.  There is a\nmucous retention cyst in the right maxillary sinus.  Minimal fluid in the\nmastoid air cells.\nMajor vascular flow voids are preserved.  There is prominent adenoidal tissue\nnoted.\nSlightly hypointense marrow signal.",
            "output": "1.  No acute infarction, hemorrhage, or enhancing mass lesion.\n\n2.  Few nonspecific foci of T2/FLAIR signal hyperintensity in the bifrontal\nwhite matter.  This is above unclear etiology at also unclear clinical\nsignificance.  Differential diagnosis includes migraine headache,\ndemyelinating process, prior infection inflammation, , Lyme disease, and early\nchronic small vessel ischemic disease.\n\nRECOMMENDATION(S):  Correlate clinically and followup if needed."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  No pituitary gland, no empty sella..  No sagging brainstem. \nNormal optic nerves, sheaths, posterior globes.",
            "output": "1. Normal brain MRI."
        },
        {
            "input": "The examination is severely degraded by patient motion, and other than\ndiffusion-weighted imaging, portions of the examination are nearly\nnondiagnostic.  Allowing for this:\n\nNumerous scattered and small foci of restricted diffusion are seen throughout\nthe brain, involving the bilateral frontal lobes, right parietal lobe, left\noccipital lobe, posterior right temporal lobe, right cerebellum, bilateral\nbasal ganglia, and bilateral centrum semiovale.  These findings suggests small\nembolic infarcts.\n\nThe ventricles and sulci also appear diffusely enlarged compatible global\nparenchymal volume loss.  Periventricular and subcortical white matter FLAIR\nhyperintensities are noted, a nonspecific finding that most likely represents\nthe sequelae of chronic small vessel ischemic disease.  There is no evidence\nfor overt intracranial hemorrhage.\n\nWithin the confines of a motion grade examination, the paranasal sinuses\nappear grossly clear.  Equivocal mastoid fluid is seen bilaterally.  The\nglobes are not well assessed.",
            "output": "1. Severely motion degraded examination.\n2. Multiple tiny punctate areas of restricted diffusion seen throughout the\nbrain, as detailed above.  These findings are compatible with a central\nembolic source.  In the acute setting, both bland and septic emboli which have\na similar imaging appearance.\n3. No obvious intracranial hemorrhage.\n4. Background global parenchymal volume loss and evidence of chronic small\nvessel ischemic disease.\n\nNOTIFICATION:  The findings were discussed with ___, M.D. by\n___, M.D. on the telephone on ___ at 9:30 pm, 2 minutes after\ndiscovery of the findings."
        },
        {
            "input": "There is no intracranial mass, mass effect, or midline shift. Ventricles and\nsulci are age-appropriate. There is no focal parenchymal signal abnormality.\nThere is no region of restricted diffusion or abnormal susceptibility\nartifact. Major intravascular flow voids are preserved.\n\nPost contrast images demonstrate no abnormal parenchymal or meningeal\nenhancement.\n\nVisualized paranasal sinuses and mastoid air cells are clear.",
            "output": "Normal MRI of the brain."
        },
        {
            "input": "The examination is slightly motion degraded.  Within these confines:\n\nThere is a right cerebellar hemisphere punctate enhancing lesion (series 101b,\nimage 27; series 13, image 7), which may represent a vascular structure versus\npunctate metastatic focus.  No other enhancing lesions are identified.  Right\nfrontal and occipital encephalomalacia is similar in configuration from prior\nCT examination of ___ allowing for technical differences.\n\nThere is superimposed mild periventricular and subcortical T2/FLAIR\nnonspecific white matter hyperintensities, commonly seen in setting chronic\nmicroangiopathy in a patient of this age.  There is no acute infarct or\nintracranial hemorrhage.  Sulci, ventricles and cisterns are within expected\nlimits given the degree of age related global cerebral volume loss.  The dural\nvenous sinuses are patent.  The major intracranial flow voids are preserved. \nThe paranasal sinuses are essentially clear.  The orbits are unremarkable. \nThe mastoid air cells are clear.",
            "output": "1. An equivocal punctate enhancing right cerebellar focus.  This may represent\na vessel versus metastatic disease.  Recommend continued followup.\n2. Right frontal and occipital encephalomalacia is similar in configuration\nfrom prior CT examination allowing for technical differences.  No new infarct\nor intracranial hemorrhage."
        },
        {
            "input": "Study is mildly degraded by motion.  The previously identified enhancing focus\nin the right cerebellar hemisphere is minimally more conspicuous in comparison\nto prior from ___, currently 3 mm (series 4, image 37 and series\n400b, image 97).  No additional foci of abnormal enhancement are identified. \nThere are no abnormal areas of restricted diffusion seen.  Right frontal\nencephalomalacia is unchanged (series 4, image 75).  There is no evidence of\nacute infarction, hemorrhage, mass-effect, or edema.  The ventricles and sulci\nare normal in size and configuration.  The globes are intact.",
            "output": "Mild interval increase in conspicuity of a 2-3 mm right cerebellar hemispheric\nfocus of enhancement, concerning for metastasis.  No additional foci of\nenhancement identified.  Otherwise, unremarkable limited brain MR."
        },
        {
            "input": "2 mm right cerebellar hemisphere enhancing lesion is re-identified (series 19,\nimage 34).  In addition, the following new lesions are identified with\nassociated FLAIR hyperintense signal:  A 5 mm left cerebellar floccular lesion\n(series 19, image 35) and a 3 mm left medial temporal lobe lesion (series 19,\nimage 38).\n\nRight frontal and parietal encephalomalacia is similar in appearance to prior\nexam.  Otherwise, sulci, ventricles and cisterns are within expected limits\nfor the degree of the patient's age related global cerebral volume loss.  The\nmajor intracranial flow voids are preserved.  The dural venous sinuses are\npatent.  The paranasal sinuses are clear.  The orbits are unremarkable.  Fluid\nsignal is seen in the bilateral mastoid air cells.",
            "output": "1. Previously described 2 mm right cerebellar hemisphere enhancing lesion is\nre-identified.\n2. New 5 mm left cerebellar floccular lesion and 3 mm left medial temporal\nlobe lesion with associated FLAIR hyperintense signal.\n\nNOTIFICATION:  The impression and recommendation above was entered by Dr.\n___ on ___ at 15:46 into the Department of Radiology critical\ncommunications system for direct communication to the referring provider."
        },
        {
            "input": "The examination is mildly motion degraded, particularly the postcontrast MP\nRAGE sequences.  Within these confines:\n\nInterval enlargement of a 7 mm left cerebellar floccular lesion,, previously\nmeasuring approximately 5 mm (series 19, image 51).  A 2-3 mm posterior medial\ntemporal lobe lesion is unchanged (series 19, image 56).  These lesions are\nassociated with FLAIR hyperintense signal.\n\nAdditional previously described 2 mm right cerebellar hemisphere lesion is not\nseen on the current exam although this may be secondary to the degree of\nmotion artifact.\n\nWithin the confines of a motion degraded examination no definitive new lesions\nare identified.\n\nRight frontal and parietal encephalomalacia is unchanged from prior\nexamination.  Otherwise, the sulci, ventricles cisterns are within expected\nlimits given the degree of the patient's global cerebral age related volume\nloss.  There is no acute infarct or intracranial hemorrhage.  Superimposed\nperiventricular and subcortical T2/FLAIR white matter hyperintensities are\nnonspecific, but commonly seen in the setting of chronic microangiopathy in a\npatient this age.  The major intracranial flow voids are preserved.  The dural\nvenous sinuses are patent.  The paranasal sinuses are clear.  The orbits are\nunremarkable.  The mastoid air cells are clear.",
            "output": "1. Mild interval enlargement of a left cerebellar floccular lesion, now\nmeasuring 7 mm from previously described 5 mm.\n2. Unchanged appearance of a left medial posterior temporal lobe 3 mm lesion.\n3. Previously described 2 mm right cerebellar hemisphere lesion is not seen on\nthe current exam, although this may be secondary to motion artifact.\n4. Within the confines of a motion degraded examination, no definitive new\nlesions."
        },
        {
            "input": "Multiple enhancing lesions are noted, consistent with metastatic disease. \nNone of the lesions demonstrate associated edema or blood products.\nThe largest is in the left cerebellar flocculus, and appears slightly smaller\nin size compared to the most recent prior study, now measuring 4 x 3 mm,\ncompared with 7 x 5 mm previously (series 19, image 40).\nThe previously noted lesion in the posterior left temporal lobe is stable in\nsize and appearance, measuring 2 mm (series 19, image 45).\nA punctate right cerebellar lesion was seen on earlier exams, but not the most\nrecent study from ___, and 1 on the present study.\nThere is a new small lesion in the left posterior inferior cerebellar\nhemisphere measuring 2 mm (series 19, image 30).\nA new lesion in the anterior right temporal lobe measures 3 mm (series 19,\nimage 50).\nThere is a new 1 mm lesion in the left frontal lobe (series 17, image 73).\nThere is also a 1 mm lesion in the right superior cerebellar hemisphere,\nlateral to the the location of the right cerebellar hemisphere lesion seen on\nmore remote studies (series 19, image 40).\n\nThere is no evidence of blood products or acute diffusion abnormality. \nScattered periventricular and subcortical FLAIR hyperintensities are\nnonspecific in appearance but may represent a sequela of chronic small vessel\nischemic changes.  Right frontal and parietal areas of encephalomalacia are\nagain noted. The ventricles and sulci are otherwise age appropriate.  The\nmajor intracranial flow voids are preserved.  The major dural venous sinuses\nare patent.",
            "output": "1. Interval development of at least 4 new small enhancing lesions in bilateral\ncerebellum, anterior right temporal lobe, and left frontal lobe, indicating\nprogression of disease.\n2. Decreased size of the largest preexisting lesion in the left cerebellar\nflocculus, now 4 mm.  Stable 2 mm left posterior temporal lesion.\n\nNOTIFICATION:  Review of the ___ medical record indicates that the\nreferring physician ___ is already aware of the findings."
        },
        {
            "input": "Multiple enhancing supratentorial and infratentorial lesions are again\ncompatible with metastases.\n\nThere is a tiny focus enhancement in the right frontal lobe (900b:79) which is\nnew.  No additional new lesions identified.\n\nFaint residual enhancement seen in the posterior left temporal lesion\n(900b:47) which is decreased in the interval.\n\nTiny foci of enhancement in the right cerebellar hemisphere (900b:46) is\nunchanged, as well as on the left (900b:52).  A stable focus of enhancement in\nthe anterior right temporal lobe (900b:53)\n\nPreviously described additional lesions the including within the left\ncerebellar flocculus, additional lesions in the vermis, and within the left\ncerebellar hemisphere inferiorly.\n\nRight frontal and parietal encephalomalacia is unchanged.  Scattered white\nmatter FLAIR hyperintensities are also stable, potentially from chronic small\nvessel disease.  Please note that FLAIR sequences somewhat motion degraded. \nThere is no acute infarct.  Major intravascular flow voids are preserved.",
            "output": "Multiple enhancing lesions compatible with metastases.  Multiple prior\ninfratentorial enhancing lesions have resolved including the dominant lesion\non the left and interval decrease in size of the posterior left temporal\nlesion.  Several stable lesions including two within the cerebellum and one\nwithin the anterior right temporal lobe.  Single new enhancing lesion in the\nright frontal lobe, as detailed above."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There are nonspecific bilateral supratentorial T2/FLAIR white\nmatter hyperintensities, which may represent the sequelae of chronic\nmicroangiopathy. Note is made of moderate narrowing at the craniocervical\njunction secondary to atlantoaxial degenerative change.",
            "output": "1.   No acute intracranial abnormality is identified.\n2. Nonspecific bilateral supratentorial T2/FLAIR white matter\nhyperintensities, which may represent the sequelae of chronic microangiopathy.\n3. Moderate narrowing at the craniocervical junction secondary to atlantoaxial\ndegenerative change."
        },
        {
            "input": "In the right cerebellar hemisphere, there is a 4.5 x 4.1 cm, predominantly T2\nand FLAIR hyperintense lesion with poorly defined central T1 and T2\nisointensity, heterogeneous internal and continuous at peripheral enhancement,\nand adjacent vasogenic edema exerting mass effect on the fourth ventricle. \nThere is no associated diffusion restriction.  In the left cerebellar\nhemisphere, there is a 0.8 x 0.7 cm lesion with similar imaging\ncharacteristics, but no significant adjacent vasogenic edema (series 10, image\n4).  In the right frontal lobe, near the precentral sulcus, there is a 2 mm T2\nhyperintense, enhancing lesion with no appreciable adjacent vasogenic edema\n(series 7, image 16; series 10, image 16; series 9 100, image 116).  In the\npons, there is patchy T2 and FLAIR signal hyperintensity without T1, T1\npostcontrast, or diffusion correlates, possibly the sequela of ischemic\ndisease.\n\nThere is no evidence of hemorrhage or infarction.   The ventricles and sulci\nare normal in caliber and configuration.  The major vascular flow voids are\npreserved.  An ACA aneurysm is better appreciated on the same day head and\nneck CTA.  The dural venous sinuses are patent on post-contrast MP rage\nsequences.  There is mild paranasal sinus mucosal thickening.",
            "output": "1. A dominant right cerebellar hemisphere lesion measures 4.5 x 4.1 cm with\nadjacent vasogenic edema exerting mass effect on the fourth ventricle.  No\nhydrocephalus.  Smaller lesions in the left cerebellar hemisphere and right\nfrontal lobe demonstrate similar imaging characteristics.  Given the presence\nof a lung mass identified on chest CT 1 day prior, metastasis is the\noverwhelmingly likely etiology.\n2. No evidence of infarction or hemorrhage.\n3. Nonspecific patchy T2 signal hyperintensity in the pons enhancement,\npossibly chronic ischemic disease.\n4. An ACA aneurysm is better appreciated on the same day head and neck CTA.\n5. Mild paranasal sinus mucosal thickening."
        },
        {
            "input": "Patient has undergone right occipital craniotomy for resection of rim\nenhancing lesion seen on the previous study.  Restricted diffusion on the\nmedial aspect could indicate postsurgical change.  Blood products are seen in\nthis region with air.  On postcontrast images small area of enhancement is\nseen at the medial aspect of the blood products (13:7).  The mass effect on\nthe fourth ventricle is decreased.  Small amount of fluid is seen in the\nsubcutaneous scalp region related to surgery.  No hydrocephalus is seen.\n\nPreviously seen left cerebellar and right frontal lobe enhancing lesions are\nunchanged.",
            "output": "Status post resection of right cerebellar lesion.  Blood products and expected\npostsurgical changes are seen with small area of residual enhancement on the\nmedial aspect.  Previously seen small lesions in the left cerebellum frontal\nlobe are unchanged."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  A couple of left frontal deep white matter millimetric T2 and\nFLAIR hyperintensities are nonspecific.  The intracranial arteries demonstrate\nnormal T2 flow voids.  The paranasal sinuses are clear.  The orbits are\nnormal.  The craniocervical junction appears normal.  The pituitary appears\nnormal.",
            "output": "No infarct.  Essentially normal MRI brain."
        },
        {
            "input": "No abnormal enhancing lesions post contrast.  The left CPA signal seen on the\nFLAIR imaging represents pulsation artifact and a true lesion.",
            "output": "1. Normal brain MRI."
        },
        {
            "input": "Again seen is a right frontal extra-axial 1 cm enhancing mass, unchanged since\nthe prior studies.  This minimally indents the adjacent brain. The appearance\nremains most typical of a meningioma.\nAgain seen is fluid in the left mastoid air cells, slightly increased since\nthe prior study.  There is mucosal thickening in the maxillary sinuses and\nthickening and loculated fluid in the ethmoid air cells bilaterally.  There is\nminimal mucosal thickening in the frontal and sphenoid sinuses.\nThere is no evidence of hemorrhage, edema, other masses, mass effect, midline\nshift or infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no other abnormal enhancement after contrast\nadministration.",
            "output": "1. Unchanged right frontal extra-axial enhancing mass, most likely a\nmeningioma.\n2. Otherwise normal study."
        },
        {
            "input": "The 10 x 11 x 11 mm (TR x AP x SI) extra-axial, dural-based, enhancing lesion\nalong the right frontal convexity is not significantly changed compared to\nmultiple prior studies dating back to ___.  There is mild mass effect\non the underlying right superior and middle frontal gyri without evidence of\nunderlying signal abnormality.\n\nThere is no evidence of acute infarction or intracranial hemorrhage.\n\nThere is global parenchymal volume loss with increased prominence of the\nsulci, ventricles and cisterns.  There are minimal T2/FLAIR hyperintensities\nin the periventricular white matter, which are nonspecific but most likely\nrepresent chronic microangiopathic changes.\n\nThere is no evidence of hydrocephalus.\n\nThe orbits are unremarkable.\n\nThere is mild mucosal thickening in the right maxillary and sphenoid sinus. \nThere is partial opacification of the left mastoid air cells.  The remaining\nparanasal sinuses and right mastoid air cells are clear.\n\nThe major intracranial flow voids are preserved.  A developmental venous\nanomaly in the right cerebellar hemisphere is noted.\n\nThe marrow signal is within normal limits and the extracranial soft tissues\nare unremarkable.",
            "output": "Stable appearance of extra-axial lesion along the right frontal convexity,\nwhich most likely represents a meningioma.  Unchanged mild mass-effect on the\nright frontal lobe without evidence of underlying signal abnormality."
        },
        {
            "input": "MRI BRAIN:\nNo evidence of acute infarction, blood products, edema, mass effect, or other\nsignal abnormalities.  Major intracranial flow voids are preserved.  The sulci\nand ventricles are normal in size and configuration.  Cerebellar tonsils are\nnormally positioned.\n\nThere is complete opacification of the ethmoid air cells.  There is extensive\npolypoid mucosal thickening with mucous retention cysts in the maxillary\nsinuses, as well as fluid in the right maxillary sinus.  There is fluid nearly\nopacifying the left sphenoid sinus, with mucosal thickening in bilateral\nsphenoid sinuses, and a mucous retention cyst in the right sphenoid sinus. \nThere is mucosal thickening in right greater than left frontal sinuses.\n\nMRV BRAIN:\nNormal flow signal is demonstrated within the superior sagittal sinus,\nstraight sinus, transverse sinuses, and sigmoid sinuses.  No evidence for\ndural venous sinus thrombosis.\n\nMRA NECK:\nFat-suppressed axial T1 weighted images demonstrate no evidence for intramural\nhematoma or dissection.  On the 2D time-of-flight MRA of the neck, evaluation\nof the non dominant left vertebral artery for subtle irregularities is limited\ndue to its small caliber.  Dominant right vertebral artery, as well as\nbilateral common carotid and cervical internal carotid arteries, appear patent\nwithout evidence for flow-limiting stenosis.  Specifically, no internal\ncarotid stenosis is seen by NASCET criteria.",
            "output": "1. Normal noncontrast brain MRI.\n2. No evidence of dural venous sinus thrombosis.\n3. No evidence for cervical carotid or vertebral dissection.  Evaluation of\nthe non dominant left vertebral artery for subtle irregularities on the 2D  \ntime-of-flight neck MRA is limited.  Dominant right vertebral artery, as well\nas bilateral common carotid and cervical internal carotid arteries, appear\nunremarkable.\n4. Extensive paranasal sinus disease."
        },
        {
            "input": "MRI BRAIN:\nThere is a 4 mm focus of FLAIR hyperintense signal centered in the right\ncerebral peduncle (series 26, image 12), demonstrating diffusion-weighted\nhyperintensity without corresponding ADC hypointensity.  There is subtle\npostcontrast enhancement on spin echo sequence (series 28, image 12) without\ncorresponding enhancement on MPRAGE.  The findings would suggest subacute\ninfarct.\n\nNo evidence for acute infarct.  No focal lobar encephalomalacia.  Minimal\nperiventricular and subcortical T2/FLAIR white matter hyperintensities are\nnonspecific, but compatible with chronic microangiopathy in a patient of this\nage.\n\nThe major intracranial flow voids are preserved.  The dural venous sinuses are\npatent.  There is mild mucosal thickening of the right frontal sinus and\nopacification of the right frontal ethmoidal recess.  The orbits are\nunremarkable.  Trace fluid signal is seen in the mastoid tips.  No suspicious\nmarrow signal..\n\nMRA BRAIN:\nMild loss of flow related signal of the right paraclinoid ICA corresponds to\nknown flow diverting stent.  No evidence of right paraclinoid aneurysm.\n\nThe remainder of the intracranial ICA, MCA, ACA and their major branches are\nunremarkable.  The posterior circulation is also unremarkable.  No evidence of\nnew aneurysm, high-grade stenosis or occlusion.\n\nMRA NECK:\nA dissection flap of the distal right cervical internal carotid artery (series\n4, image 24) is new since examination of ___, with pseudoaneurysm\nmeasuring approximately 5 mm in diameter..  There is no T1 hyperintense signal\non axial T1 fat saturated sequences suggest acute mural thrombus.\n\nRe-identified is mild irregularity of the bilateral V3 segments, which may\nrepresent previously described dissections, unchanged since examination of ___.\n\nThe right brachiocephalic, bilateral common carotid, subclavian and vertebral\narteries are otherwise unremarkable.  There is no stenosis of the cervical\ninternal carotid arteries by NASCET criteria.",
            "output": "1. 4 mm FLAIR hyperintense lesion centered in the right cerebral peduncle,\ndemonstrating trace enhancement on T1 postcontrast spin echo sequence, which\nlikely represent subacute infarct.  Of note, no enhancement is definitively\nseen on MPRAGE.  Recommend follow-up examination in ___ months to document\nresolution of the enhancement.\n2. No evidence of acute infarct.  No intracranial hemorrhage, mass or other\nabnormal enhancement.\n3. The patient is status post right paraclinoid ICA flow diverting stent\nplacement, with no residual aneurysm identified.  Otherwise, patent circle of\n___ without evidence of stenosis,occlusion,or aneurysm.\n4. There is a dissection flap of the distal right cervical internal carotid\nartery new since examination of ___, with pseudoaneurysm measuring\napproximately 5 mm in diameter.  No T1 hyperintense mural signal to suggest\nacute thrombus.  Unchanged mild irregularity of the bilateral V3 segments,\nwhich may represent previously described dissections.\n5. Remainder of the MRA neck is unremarkable.  There is no stenosis of the\ncervical internal carotid arteries by NASCET criteria.\n6. Additional findings described above."
        },
        {
            "input": "MRI BRAIN:\nThere is no evidence of hemorrhage,edema,masses, mass effect, midline shift or\ninfarction.  No diffusion abnormalities are detected the ventricles and sulci\nare normal in caliber and configuration.  There is no abnormal enhancement\nafter contrast administration.  The orbits are unremarkable, paranasal\nsinuses, middle ear cavities and mastoid air cells are clear\n\nMRA BRAIN:\nThe intracranial internal carotid arteries and their major branches appear\nnormal without evidence of stenosis,occlusion.  There is severe focal\nnarrowing involving the right intradural V4 segment.  Otherwise the remainder\nof the vertebral artery are widely patent.  No evidence of aneurysm.\n\nMRA NECK:\nThe origins of the great vessels, subclavian and vertebral arteries appear\nnormal bilaterally.  The common, internal and external carotid arteries appear\nnormal.  There is no evidence of internal carotid artery stenosis by NASCET\ncriteria.",
            "output": "1. No acute intracranial abnormality.  No evidence of an acute infarct,\nintracranial mass, or hemorrhage.\n2. Severe focal narrowing of the right intradural V4 segment of the vertebral\nartery.\n3. Otherwise unremarkable MRA of the head and neck."
        },
        {
            "input": "MRI BRAIN:\nThere is no evidence for a mass, edema, acute infarction, or blood products. \nThere is a developmental venous anomaly in the right cerebellar hemisphere,\nfor example image 1700:36.  Minimal hyperintensity along the frontal and\noccipital horns of the lateral ventricles is a nonspecific finding which may\nbe seen in asymptomatic patients.  Ventricles, sulci, and basal cisterns are\nnormal in size.  Cerebellar tonsils are normally positioned.  Major dural\nvenous sinuses are patent.\n\nA right anterior ethmoid air cell is opacified.  There is mild mucosal\nthickening in some of the other anterior ethmoid air cells, right greater than\nleft, and in the right frontal sinus.\n\nMRA NECK:\nThere is a 3 vessel aortic arch.  Common carotid and cervical internal carotid\narteries are widely patent without stenosis by NASCET criteria.  V3 segments\nof bilateral vertebral arteries appear irregular, with mild narrowing on the\nright, with but without significant narrowing on the left.  Remaining portions\nof bilateral vertebral arteries appear widely patent.\n\nMRA BRAIN:\nImages are technically limited.  The intracranial vertebral arteries and ___\n___ are better assessed on the gadolinium enhanced neck MRA.  There is no\nevidence for flow-limiting stenosis in the major intracranial arteries.  There\nis a bilobed, posteriorly projecting aneurysm of the right internal carotid\nartery opposite the ophthalmic artery origin, which measures 6 x 3 mm on image\n5:125.  There is a questionable 1 mm aneurysm projecting anteriorly at the\nleft ophthalmic artery origin, versus tortuosity of the proximal left\nophthalmic artery, not well assessed due to artifacts (image 5:127).",
            "output": "1. Irregularity of bilateral V3 segments of the vertebral arteries, with mild\nnarrowing on the right, but without significant narrowing on the left.  This\nmay represent sequela of the reported prior vertebral dissection, though\nevaluation for intramural hematoma is limited in the absence of fat-suppressed\naxial T1 weighted images.  Fibromuscular dysplasia may have a similar\nappearance.\n2. 6 x 3 mm bilobed, posteriorly projecting aneurysm of the right internal\ncarotid artery opposite the stomach artery origin.\n3. Questionable 1 mm aneurysm projecting anteriorly at the left ophthalmic\nartery origin, versus tortuosity of the proximal left ophthalmic artery, not\nwell assessed due to artifacts.\n4. No concerning abnormalities in the brain parenchyma.  A developmental\nvenous anomaly is incidentally noted in the right cerebellar hemisphere.\n\nRECOMMENDATION(S):  Comparison with prior studies would be helpful.  CTA could\nbetter assess whether there is a small aneurysm at the left ophthalmic artery\norigin, if clinically indicated.\n\nNOTIFICATION:  The impression and recommendations above were entered by Dr.\n___ on ___ at 12:05 into the Department of Radiology critical\ncommunications system for direct communication to the referring provider."
        },
        {
            "input": "There is no evidence of intracranial hemorrhage, mass, mass effect or shifting\nof the normally midline structures. The ventricles and sulci are slightly\nprominent for the patient's age, however, this finding is nonspecific. No\ndiffusion abnormalities are detected to suggest acute or subacute ischemic\nchanges. The major arterial vascular flow voids are present and demonstrate\nnormal distribution. The orbits are remarkable for left ocular prosthesis,\nprobably related with phthisis bulbi. The paranasal sinuses demonstrate\nmucosal thickening in the left frontal ethmoidal recess, ethmoidal air cells\nand opacification of the sphenoid sinus, more significant on the left,\nbilateral mucosal thickening is noted in the mastoid air cells, suggesting an\nongoing inflammatory process.",
            "output": "1. There is no evidence of acute or subacute intracranial process. Slightly\nprominent ventricles and sulci for the patient's age, this finding is\nnonspecific.\n\n2. Mucosal thickening identified in the paranasal sinuses and mastoid air\ncells as described above, suggesting an ongoing inflammatory process."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  The ventricles and sulci are prominent, consistent global\ncerebral volume loss.  Patchy periventricular T2 hyperintensities are most\nconsistent with chronic microvascular ischemic disease.  No diffusion\nabnormalities are detected.\n\nCurvilinear FLAIR hyperintensities are seen in the cortex of the right\nparietal lobe (images 22 and 26 series 11).  These are likely sequela of prior\ninfarcts.\n\nThere is mild mucosal thickening of the left ethmoid sinus.  The mastoid air\ncells and middle ear cavities are clear.\n\nLymphadenopathy is seen in the right level 2 cervical neck region, with the\nlargest measuring 2.7 x 1.5 cm (image 21 series 8).  These were seen on the\nCTA dated ___.\n\nThe major vascular flow voids are present and demonstrate normal distribution.\nThe orbits are unremarkable, the paranasal sinuses and mastoid air cells are\nclear.",
            "output": "1. Curvilinear FLAIR hyperintensities in the cortex of the right parietal lobe\nlikely represent sequela of prior infarcts.\n2. Right level 2 cervical lymphadenopathy, as seen on the recent CTA."
        },
        {
            "input": "Some of the images are mildly limited by motion artifact.\n\nNo evidence for an enhancing intracranial mass or other pathologic contrast\nenhancement.  No evidence for acute infarction, edema, or blood products. \nScattered small T2/FLAIR hyperintense foci are seen in the periventricular,\ndeep, and subcortical white matter of the cerebral hemispheres, nonspecific in\nthis age group.  No evidence for infratentorial signal abnormalities.\n\nVentricles, sulci, and basal cisterns are normal in size for age.  Cerebellar\ntonsils are normally positioned.\n\nDural venous sinuses appear patent on postcontrast MP RAGE images.  Major\nvascular flow voids appear preserved allowing for hypoplasia of the non\ndominant intracranial left vertebral artery distal to the left ___.",
            "output": "1. No evidence for an intracranial mass or acute intracranial abnormalities.\n2. Scattered small T2/FLAIR hyperintense, nonenhancing foci in the\nsupratentorial white matter are nonspecific.  Diagnostic considerations given\nthe patient's history include a combination of sequela of lupus cerebritis,\nmigraine associated lesions, and sequela of chronic small vessel ischemic\ndisease given the known diabetes."
        },
        {
            "input": "There is mild asymmetric prominence of the right earlobe with possible mild \ncontrast enhancement.  There is no evidence of underlying lesion, or fluid\ncollection.\n\nThe visualized intracranial structures are unremarkable.  The vascular flow\nvoids are preserved.  The orbits and calvarium are unremarkable.  There is no\nfluid signal within the paranasal sinuses or mastoid air cells.  The\nmasticator and parapharyngeal spaces are unremarkable.  The salivary glands\nare unremarkable.  The nasal and oral pharynx are unremarkable.  The unchanged\nchronic leftward angulation of the larynx and vocal cords.  There are no\nabnormal lymph nodes by size, morphology, or signal.  There are multilevel\ndegenerative changes of the cervical spine with heterogeneous degenerative\nendplate changes.  There is no focal lesion.",
            "output": "1. Mild asymmetric prominence of the right ear lobe with possible mild\nenhancement.  No evidence of underlying lesion or fluid collection."
        },
        {
            "input": "Patient is status post partial resection of an enhancing mass arising from the\npituitary fossa with suprasellar extension, with associated postsurgical\nchanges.  The residual mass measures approximately 2.3 cm TRV by 2.1 cm AP by\n2.8 cm CC, decreased in size compared to the prior exam at which time this\nmass measured up to 3.3 cm CC.  The heterogeneously solid and cystic mass is\nnot distinguishable from pituitary gland and superiorly displaces the optic\nchiasm.  The mass abuts the floor of the third ventricle, however there is no\nevidence of ventriculomegaly.  The mass abuts bilateral posterior cerebral\narteries along the posterior margin, the A1 segments of the anterior cerebral\narteries anteriorly, and cavernous segments of the bilateral internal carotid\narteries.\n\nNo new enhancing lesions are seen.\n\nNew postsurgical change related to patient's posterior nasal septectomy and\nbilateral sphenoidotomies are noted.  Moderate mucosal sinus thickening is\nseen involving the right maxillary sinus.  Mild maxillary sinus mucosal\nthickening is seen involving the left maxillary sinus, with an air-fluid\nlevel.  There is near complete opacification of the ethmoid air cells.  The\nmastoid air cells, and middle ear cavities are clear.  The globes are\nunremarkable.  No definite marrow signal abnormalities are identified.",
            "output": "1. Status post partial resection of an enhancing suprasellar mass, now\nmeasuring 2.8 cm in craniocaudal dimension, previously measuring up to 3.3 cm,\nconsistent with patient's known craniopharyngioma.  Again seen is obliteration\nof the pituitary gland as well as superior displacement of the optic chiasm. \nThe mass abuts the bilateral posterior cerebral arteries, A1 segments of the\nanterior cerebral arteries and cavernous segments of the bilateral internal\ncarotid arteries.\n2. Moderate to severe sinus disease involving the maxillary sinuses and\nethmoid air cells, progressed compared to the prior exam from ___.\n3. Postsurgical changes related to posterior nasal septectomy and bilateral\nsphenoidotomies."
        },
        {
            "input": "The post-contrast MP rage sequences are severely degraded by motion artifact.\n\nPostsurgical changes related to recent craniotomy and transsphenoidal surgery\nare noted.  High T2/FLAIR signal and hemorrhagic products in the right frontal\nlobe is in keeping with postsurgical change.  Evolving right parieto-occipital\nintraparenchymal hemorrhages with extensive surrounding vasogenic edema and 8\nmm shift of normally midline structures to the left are grossly unchanged\ncompared to the prior CT of ___.  A right frontal extra-axial\nhemorrhagic collection measuring 9 mm in maximum dimension from the inner\ntable appears slightly more prominent compared to the prior examination but is\nprobably stable allowing for changes in technique and positioning (09:16). \nThere is no new hemorrhage.  There is right-sided uncal herniation which is\nunchanged from the prior CT.\n\nThere is a new focus of high T2/FLAIR signal in the right basal ganglia that\nis hyperintense on the diffusion-weighted images that is isointense on the ADC\nmap and shows postcontrast enhancement, likely representing a subacute\ninfarct.\n\nAccurate evaluation of the suprasellar region is difficult as the postcontrast\nMPRAGE sequences are severely degraded by motion.  An area of T1 and T2\nhyperintensity in the suprasellar region and inferior frontal lobe\ndemonstrating slow diffusion and heterogeneous low-level enhancement may\nrepresent postsurgical changes.  Similarly, there is T2 heterogeneous material\nwith thick rim enhancement and central fluid signal in the sella turcica that\nshows peripheral slow diffusion and may represent postsurgical change, however\nresidual tumor cannot be excluded.",
            "output": "1. Stable postsurgical changes related to recent craniotomy and\ntranssphenoidal surgery for resection of a sellar/suprasellar mass including\nhigh T2/FLAIR signal and hemorrhagic products in the right frontal lobe.\n2. Stable evolving right parieto-occipital intraparenchymal hemorrhages with\nextensive surrounding vasogenic edema and 8 mm shift of normally midline\nstructures to the left.\n3. Stable right frontal extra-axial hemorrhagic collection measuring 9 mm in\nmaximum dimension from the inner table.\n4. New subacute right basal ganglia infarct.\n5. Accurate evaluation of the suprasellar region is difficult as the\npostcontrast MPRAGE sequences are severely degraded by motion.  Postsurgical\nchanges are seen but evaluation for residual tumor is limited."
        },
        {
            "input": "MRI BRAIN:\nThere are postsurgical changes related to prior craniotomy and transsphenoidal\nsurgery for craniopharyngioma resection.  There remains extra-axial hemorrhage\nproduct, dural thickening and enhancement overlying the right frontal lobe,\nimproved from prior examination.\n\nThere is a lobulated and heterogeneously enhancing mass involving the sella\nand suprasellar region, measuring 1.8 x 2.6 x 1.4 cm TV x AP x CC (111a: 70,\n27:98). Areas of T2 hyperintensity are consistent with cystic foci. Limited\ncomparison to the recent MRI performed on ___ due to substantial\nmotion during the post-contrast MPRAGE images.  However, the mass has\ndecreased in size compared to ___, after which stage II\ncraniopharyngioma resection was performed.\n\nTwo foci of signal abnormality within the right occipital lobe demonstrate\ncentral T2 hyperintensity, with a surrounding rim of T2 hypointensity and\nassociated susceptibility artifact; these correspond to areas of prior\nintraparenchymal hemorrhage.\n\nNo evidence of infarction or midline shift.  Ventricles and sulci are normal\nin caliber and configuration.\n\nMRA BRAIN:\nThe left A1 segment is hypoplastic.  The intracranial vertebral and internal\ncarotid arteries and their major branches appear normal without evidence of\nstenosis, occlusion, or aneurysm formation.\n\nMRA NECK:\nThe common, internal and external carotid arteries appear normal.  There is no\nevidence of internal carotid artery stenosis by NASCET criteria.  The origins\nof the great vessels, subclavian and vertebral arteries appear normal\nbilaterally.",
            "output": "1. No acute infarct.\n2. Heterogeneously enhancing cystic sellar and suprasellar mass measuring 1.8\nx 2.6 x 1.4 cm, consistent with residual craniopharyngioma.  This has\ndecreased compared to ___, but comparison to the recent\npost-operative scan on ___ is limited.\n3. Two foci of signal abnormality with surrounding hemosiderin rim in the\nright occipital lobe, consistent with prior hemorrhage.\n4. Unremarkable MRA of the brain and neck."
        },
        {
            "input": "Postoperative changes of right frontal craniotomy and transsphenoidal approach\nfor sellar lesion resection are again noted with associated underlying dural\nenhancement.\n\nSince ___, there has been interval enlargement of the lesion centered\nat the sella with progressive suprasellar extension.  Specifically, a larger\nT2 hyperintense peripherally enhancing cystic component is seen at the\nanterior aspect of the sella extending superiorly.  Overall, the lesion now\nmeasures 2.5 cm AP x 2.0 cm AP, previously 1.4 x 1.8 cm in similar ___.\nThere is presumed mass effect on the optic nerves, left greater than right\nthough they are not definitively identified nor is the optic chiasm clearly\nseen.\n\nEncephalomalacia noted within the anterior right frontal lobe.  Sequela of\nprior hemorrhage noted in the right parieto-occipital region.  There is no\nacute infarct.  No new areas of abnormal enhancement.\n\nVisualized paranasal sinuses and mastoid air cells are clear.",
            "output": "Interval enlargement of the enhancing and partially cystic lesion at the sella\nwith larger suprasellar extension when compared to ___."
        },
        {
            "input": "Again seen are postoperative changes after partial resection of a\ncraniopharyngioma.  There is an enlarged sella turcica containing in\nhomogeneously enhancing material along with a large cystic component,\nunchanged since the study of ___.  The walls of the cyst enhance and\nthe posterior portion, although containing numerous small cysts, includes most\nof the solid component of the tumor.  The mass extends into the suprasellar\ncistern, elevating the optic chiasm, which is closely adherent to the superior\nmargin of the cyst.  The anterior cerebral arteries are also elevated by the\ncyst.",
            "output": "1. Unchanged appearance of mixed solid and cystic enhancing lesion arising\nfrom the sella turcica and extending into the suprasellar cistern."
        },
        {
            "input": "The patient's previously noted 2.6 x 2.8 x 2.9 cm mixed solid and cystic\nlesion in the suprasellar region with peripheral and internal enhancement is\nagain seen.  There is no midline shift and local mass effect on the A1 segment\nof the right anterior cerebral artery, the optic chiasm and left optic nerve.\n\nPost surgical changes in the right frontotemporal calvarium is noted.  The\nparanasal sinuses, middle ear and left mastoid air cells are clear. There is\npartial opacification of the right mastoid air cells.",
            "output": "1. Unchanged size and morphology of 2.6 x 2.8 x 2.9 cm mixed solid and cystic\nlesion in the suprasellar region with peripheral and internal enhancement.\n2. Unchanged local mass effect as noted.\n3. No evidence of new abnormal enhancement."
        },
        {
            "input": "The patient is status post right pterional craniotomy with stable postsurgical\nsequela including dural thickening and enhancement.\n\nA sellar and suprasellar lobulated partially cystic 2.7 x 2.4 x 2.4 cm (SI,\nAP, TRV) mass with 1.4 x 1.5 x 2.0 cm more solid component is identified. \nOverall the cystic component has increased in size from prior exam where it\nmeasured approximately 2.3 x 1.9 x 1.5  cm.  The solid component is similar in\nappearance.  The mass continues to exert mass effect on the optic chiasm and\nrectus gyri, slightly increased from prior examination.  The lesion also\nexerts lateral mass effect on the left optic nerve, slightly increased from\nprior exam.  There is superior mass effect on the right A1 segment.\n\nNo acute infarct or new intracranial hemorrhage is noted.  Minimal right\nfrontal encephalomalacia (series 11, image 12) is unchanged.  Chronic\nhemorrhage product along the right parietal temporal lobe is unchanged from\nprior examination.\n\nThe major intracranial flow voids are preserved.  The dural venous sinuses are\npatent on postcontrast MP-RAGE there is mild mucosal thickening of the\nparanasal sinuses.  The orbits are unremarkable.  Trace fluid signal is noted\nin the right mastoid tip.",
            "output": "1. Interval increased cystic component of a sellar and suprasellar lobulated\ncystic and solid mass measuring approximately 2.7 cm in SI dimension,\npreviously measuring approximately 2.3.  The lesion exerts increased mild mass\neffect on the optic chiasm, left optic nerve and anterior cerebral arteries. \nThe solid component of the lesion is overall similar.\n2. No evidence of dural venous thrombosis on postcontrast MP-RAGE.\n3. No acute infarct or intracranial hemorrhage.  No new lesions identified."
        },
        {
            "input": "The patient is status post right frontal craniotomy and transsphenoidal\nsurgery, with expected and stable postsurgical changes.\n\nA known, mixed solid and cystic mass within the suprasellar cistern is again\nvisualized, heterogeneous in demonstrating mixed peripheral and internal\ncontrast enhancement.  The overall ___ of the mass measured 2.6 x 2.7 x\n3.2 cm (TRV x AP x SI), previously measuring 2.5 x 2.7 x 3.1 cm (TRV x AP x\nSI).  The mass continues to exert unchanged mass effect on the A1 segment of\nthe right anterior cerebral artery, the optic chiasm, and mild lateral\nmass-effect on the left optic nerve.\n\nThere is no evidence for infarction on diffusion-weighted images.  Evaluation\nof parenchymal edema is limited secondary to the lack of T2 or FLAIR\nsequences.\n\nParanasal sinuses, middle ear cavities, and mastoid air cells appear grossly\nwell aerated.  The orbits are unremarkable bilaterally.  The dural venous\nsinuses are patent on MP-RAGE sequences.",
            "output": "1.  Unchanged size and morphology of a 2.6 x 2.7 x 3.2 cm mixed solid and\ncystic enhancing heterogeneous lesion within the suprasellar cistern.\n2.  Stable, local mass effect on the A1 segment of the right anterior cerebral\nartery, the optic chiasm, and the proximal left optic nerve.\n3.  No evidence for additional sites of abnormal, intracranial enhancement."
        },
        {
            "input": "Sellar and suprasellar cystic and peripherally enhancing lesion is again\ndemonstrated for CyberKnife radiosurgery planning.  On this postcontrast\nimages the lesion demonstrate low signal intensity areas with peripheral\nenhancement with overall size of the anterosuperior cyst minimally decreased\noverall but with better defined peripheral enhancement seen on the current\nstudy.  Right frontal approach shunt catheter extends to the anterior horn of\nthe right lateral ventricle.  Peripheral pachymeningeal enhancement is likely\nrelated to the shunt catheter.  No acute infarcts are identified.  Previously\nseen hypointense areas within the right parietal region on susceptibility\nimages are again noted on MP rage images.",
            "output": "CyberKnife radiosurgery planning study demonstrates multi cystic sellar and\nsuprasellar mass with peripheral enhancement slightly decreased from the prior\nstudy in size particularly in the suprasellar region."
        },
        {
            "input": "The patient is status post remote previous transsphenoidal resection of a\ncraniopharyngioma, with recent aspiration of a recurrent cyst within the\nsuprasellar cistern.  \"Right frontal craniotomy changes are also unchanged. \nExpected postoperative changes are identified.  The dominant residual T2\nhyperintense cyst with a mildly enhancing peripheral rim now measures 2.0 x\n1.1 cm, previously 2.8 x 2.6 cm.  Additional heterogeneously T2 hyperintense\nan septated cystic lesion within the suprasellar cistern is noted inferior to\nthis, it appears similar to the previous examination.\n\nA right frontal approach external ventriculostomy catheter extends through the\nright lateral ventricle, and terminates at the margin of the residual cystic\nlesion (11:117), unchanged in appearance from postoperative CT of ___, allowing for technical differences.\n\nAreas of encephalomalacia within the right frontal, temporal, occipital lobes\nare noted, with susceptibility artifact adjacent to these areas of\nencephalomalacia within the right occipital and temporal lobes (for example,\n8: 12, 10).  These findings appear similar to the previous MRI dated ___\n___, but are new from ___.\n\nOtherwise, no evidence for extra-axial fluid collection.  No abnormal\nparenchymal enhancement. There is no evidence of acute infarction.  No\nintracranial hemorrhage.\n\nThe ventricles and sulci are normal, without evidence of hydrocephalus. The\nbasal cisterns are patent.  There is no evidence of impending, downward\nherniation.  There is gross preservation of the principal intracranial\nvascular flow voids.\n\nFluid is noted within several right mastoid air cells.  The remainder of the\nvisualized paranasal sinuses, middle ear cavities, and mastoid air cells are\nwell aerated and clear.  The orbits are within normal limits bilaterally.",
            "output": "1. No evidence for new intracranial hemorrhage or acute infarction.\n2. Decreased size of a now 2.0 x 1.1 cm dominant cystic lesion with mild\nperipheral enhancement again seen extending superiorly from the suprasellar\ncistern.\n3. Interval placement of a right frontal approach transventricular drainage\ncatheter with the tip terminating along the superior margin of the patient's\ndominant suprasellar cystic lesion.\n4. Expected postoperative changes status post transsphenoidal and right\nfrontal craniotomy partial resection of a suprasellar mass, with an unchanged\nappearance to residual complex cystic material within the suprasellar cistern.\n5. Several areas encephalomalacia with adjacent susceptibility artifact\npredominantly noted in the right temporal and occipital lobes.  These findings\nare incompletely imaged on prior limited MRI examinations, but appear similar\nfrom at least ___.\n6. Additional findings described above."
        },
        {
            "input": "Right frontal craniotomy changes are noted.  A right frontal approach\nventriculostomy catheter is noted terminating at midline just above the level\nof the suprasellar lesion.  Re-demonstrated is dural enhancement and\nthickening overlying the right frontal lobe, similar in appearance to the\nprior study, likely related to surgery.  There is no evidence of h midline\nshift or infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.\n\nWithin the sella T1 hyperintense areas are identified which extends slightly\nto the suprasellar region.  The previously seen cystic area has decreased in\nsize and there is no longer extension to the region of optic chiasm.  There is\nno discrete solid component seen adjacent to the suprasellar or sellar region.\nChronic blood products are identified in the right occipital region.  There is\nno hydrocephalus.",
            "output": "1. The previously seen cystic area within the sella and suprasellar region has\ndecreased in size a but demonstrates the T1 hyperintensity and T2\nhypointensity which may be secondary to proteinaceous material within the\ncyst.  No definite solid component is identified.\n2. Please consider focused MRI of the sella for of follow-up examination of\nbetter evaluation of the sellar and suprasellar abnormality.\n3. No enhancing brain lesion but mild pachymeningeal enhancement is identified\nlikely secondary to postoperative change.\n4. A drainage catheter is seen from the right frontal region extends to the\nsuprasellar region as before."
        },
        {
            "input": "Again seen is a a cystic lesion in the sella turscica and supraseller cistern.\nThis measures approximately 20 mm cranial caudal, 15 mm left to right and 25\nmm in the AP dimension.  This appears unchanged since the prior study.  The\nlesion is mildly hyperintense to CSF on the precontrast T1 weighted images and\ndemonstrates no contrast enhancement.  The mass again extends into the\nsuprasellar cistern, contacting the optic nerves, unchanged.\nAgain seen are postsurgical findings after right frontal craniotomy for tumor\nresection.  A ventriculostomy is again seen extending through the frontal horn\nof the right lateral ventricle.  There is tissue loss associated with the\nprior surgery, unchanged since the previous examination.\nThere are no findings to suggest tumor progression.  No new abnormalities are\ndetected.",
            "output": "1. Status post partial resection of a craniopharyngioma with residual cystic\nmaterial.\n2. No evidence of tumor progression."
        },
        {
            "input": "Right trans frontal ventriculostomy catheter with tip terminating near the\nsuprasellar cistern is unchanged in position from prior exam.  The patient is\nstatus post right pterional craniotomy for resection of a sellar mass. \nResidual multi-septated cystic lesion within the sella extending into the\nsuprasellar cistern without definitive nodular enhancing component has\nincreased in size from prior exam, measuring 2.1 x 2.1 x 1.5 cm, particularly\ninvolving the suprasellar component.\n\nRight orbital frontal encephalomalacia is unchanged.  Superficial siderosis\nand encephalomalacia of the right posterior temporal lobe is unchanged.  There\nis no acute infarct.  No new intracranial hemorrhage.  The sulci, ventricles\nand cisterns are otherwise within expected limits for the patient's age.  The\nmajor intracranial flow voids are preserved.  The dural venous sinuses are\npatent.\n\nThe paranasal sinuses are essentially clear.  The orbits are unremarkable.  No\nsignificant fluid signal is seen the mastoid air cells.\n\nMultiple lesions in the left parotid gland appears slightly enlarged compared\nto prior examination, felt to likely represent parotid lymph nodes.  The\nadenoids also appear enlarged.  This may be reactive and clinical correlation\nis recommended.",
            "output": "1. Residual multi-septated cystic lesion in the sella extending into the\nsuprasellar cistern without definitive enhancing nodular component appears\nslightly increased in size, particularly along the suprasellar component.\n2. There is no new enhancing intracranial lesion.\n3. There are multiple left parotid lesions which appears slightly increased in\nsize compared to prior exam, felt likely to represent parotid lymph nodes. \nThe adenoids are also enlarged compared to prior exam.  This could be reactive\nand clinical correlation is recommended.\n4. Additional findings as described above.  No acute infarct or additional new\nintracranial hemorrhage."
        },
        {
            "input": "A large right anterior frontal and temporal craniotomy is re-identified, with\na residual right-sided frontal ventricular shunt catheter extending to the\nfrontal horn of the right lateral ventricle.\n\nEncephalomalacia in the right frontal region and chronic blood products in the\nright temporal occipital region are unchanged.  There is no hydrocephalus or\nmidline shift.\n\nBilobed T1 hyperintense lesion is identified within the sella and extending to\nthe suprasellar region.  The lesion demonstrate increased T1 hyperintensity on\npre contrast images since the previous study but this signal intensities which\ncould be secondary to increased protein content within the lesion.  Some of\nthe changes could also be secondary to the current MRI performed on a higher\nfield strength 3 tesla magnet.  The overall size of the lesion and suprasellar\nextent is not significantly changed to minimally increased but within the\nmargin differences in slice selection.\n\nThere is no hydrocephalus or midline shift.  No new areas of abnormal\nenhancement identified.",
            "output": "1. Again noted is sellar and suprasellar lesion and postoperative changes. \nThe intrinsic signal characteristics of the lesion have slightly changed from\nthe prior study which could be due to increased protein content of the lesion.\n2. The overall extent of the lesion is unchanged to minimally increased in the\nsuprasellar component but within the margin of measurement differences and\nslice selection.\n3. The size of the lesion can be further monitored on the follow-up\nexamination.\n4. No new enhancing lesion, hydrocephalus or signal abnormality.\n\n1. ."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.\n\nThe orbits are unremarkable.  The visualized paranasal sinuses and mastoid air\ncells are clear.  Intracranial flow voids are maintained.",
            "output": "No acute intracranial abnormality.  Unremarkable MRI of the brain."
        },
        {
            "input": "Study is mildly degraded by motion.  There is no evidence of hemorrhage,\nedema, masses, mass effect, midline shift or infarction.  Allowing for\ndifference in technique, there is grossly stable prominence of the ventricles,\nsulci and extra-axial spaces suggestive involutional changes.  There is been\ninterval progression of periventricular, pontine and subcortical T2 and FLAIR\nhyperintensities are noted, which may represent small vessel ischemic changes.\nApproximately 3 mm pineal cyst is again noted.",
            "output": "1.  Study is mildly degraded by motion.\n2. Grossly stable global volume loss.\n3. Interval progression of microangiopathic changes compared to ___ prior\nexam.\n4. No evidence of acute infarct."
        },
        {
            "input": "MR BRAIN:\n There is no evidence of acute infarction.  No intracranial hemorrhage.  No\nmass, mass effect, edema or midline shift.\n\nThe ventricles and sulci are normal, without evidence of hydronephrosis. \nPeriventricular and subcortical white matter T2/FLAIR hyperintensities are\nsuggestive of mild chronic small vessel ischemic disease.  Several punctate T2\nhyperintense foci within the inferior bilateral cerebellar hemispheres (8:3,\n2) are hypointense on FLAIR imaging, and may represent prominent CSF spaces\nversus tiny chronic infarctions.  The basal cisterns are patent.\n\nA mucous retention cyst is noted in the left maxillary sinus.  There is mild\nmucosal thickening of the right maxillary sinus.  The remainder of the\nvisualized paranasal sinuses, middle ear cavities, and mastoid air cells are\nwell aerated and clear.  The orbits are within normal limits bilaterally.\n\nMRA brain: There is mild atherosclerotic irregularity narrowing of the right\ncavernous segment ICA.  Otherwise, the intracranial vertebral and internal\ncarotid arteries and their major branches appear normal without evidence of\nstenosis, occlusion, or aneurysm formation.",
            "output": "1.  No evidence for acute intracranial infarction or hemorrhage.\n2.  Mild atherosclerotic these cavernous segment right ICA.  Otherwise, patent\nintracranial vasculature.\n3.  Evidence of mild chronic small vessel ischemic disease.\n4.  Mild paranasal sinus disease."
        },
        {
            "input": "There is no acute infarct. There is no evidence of hemorrhage, mass, mass\neffect, or midline shift. Ventricles and sulci are age-appropriate. There is\nno abnormal enhancement.  There are multiple foci of FLAIR hyperintensity in\nthe subcortical, deep, and periventricular white matter. These do not appear\nsignificantly changed from MRI on ___ and are likely the sequelae of\nchronic small vessel ischemic diseas.\n\nThe calvarium is intact. Intracranial flow voids are maintained. There is\nmucosal thickening of the paranasal sinuses. The mastoid air cells are clear.\nThe orbits are normal.",
            "output": "1. No evidence hemorrhage or infarction.\n2. Multiple foci of FLAIR hyperintensity in the white matter, nonspecific but\ncommonly seen at this age due to chronic small vessel ischemic disease."
        },
        {
            "input": "There is diffusion abnormality involving the left pontomedullary junction with\nassociated FLAIR/T2 increased signal, consistent with early subacute infarct.\n\nChronic lacunar infarcts lower pons.  Focal FLAIR abnormality right midbrain,\nlikely chronic infarct.  Findings consistent with moderate chronic small\nvessel ischemic changes.  No evidence of hemorrhage.  No mass effect.  Mild\nparanasal sinus disease.  Patient is status post bilateral lens replacements.",
            "output": "1. Early subacute infarct left pontomedullary junction\n2. Chronic lacunar infarcts brainstem.\n3. Moderate chronic small vessel ischemic change."
        },
        {
            "input": "Images are degraded by artifact from dental hardware.  The frontal lobes and\nanterior temporal lobes cannot be evaluated due to artifact.\n\nOtherwise, there are a few subcortical foci of T2/FLAIR hyperintense signal. \nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  There is no abnormal enhancement after contrast administration\nin the partially visualized brain.\n\nThere is marked hypointensity on T1 weighted imaging of the marrow of the\nskull and cervical spine, likely representing patient's sickle cell status.",
            "output": "1. The frontal lobes and anterior temporal lobes cannot be evaluated due to\nartifact from dental amalgam.  Otherwise, no evidence of CNS infection.\n2. A few subcortical foci of T2 FLAIR hyperintense signal, a nonspecific\nfinding.\n3. There is low signal on T1 weighted imaging of the bone marrow of the skull\nand partially visualized cervical spine, presumably reflecting the patient's\nsickle cell status."
        },
        {
            "input": "Please note study is limited due to lack of administration of intravenous\ncontrast, which was not administered due to patient refusal of contrast.\n\nWithin limits noncontrast study, images through the internal auditory canal\ndemonstrates symmetric appearance of the seventh eighth nerve complexes. There\nis no evidence of mass lesion within the internal auditory canals,\ncerebellopontine angles or membranous labyrinth. No other mass lesions are\nseen within the posterior fossa.\n\nLimited included imaging of the remainder of the brain demonstrates no\nevidence of hemorrhage, edema, masses, mass effect, midline shift or\ninfarction. The ventricles and sulci are normal in caliber and configuration. \nPeriventricular and subcortical T2 and FLAIR hyperintensities are noted, which\nmay represent small vessel ischemic changes, some of which were present on\n___ since prior exam, and some which are new.\n\nScout images again demonstrate patient's known type 1 anterior malformation,\nwith cerebellar tonsils suggested to extend approximately 1 cm inferior to\nforamen magnum (see 18:12).",
            "output": "1. Within limits of this noncontrast examination, no evidence of IAC or\ncerebellopontine angle mass.\n2. Scout imaging again demonstrates patient's known Chiari 1 malformation,\nwith suggested approximately 1 cm extension of cerebellar tonsils inferior for\nmagnum."
        },
        {
            "input": "The majority of the numerous metastatic lesions involving the bilateral\ncerebral and cerebellar hemispheres have decreased in size when compared to\nthe examination of ___.\n\nA few scattered lesions do appear slightly increased in size or demonstrates\nincreased enhancement.  For example:\n\n4 mm left frontal vertex lesion (series 10, image 142)\n3 mm right middle frontal gyrus lesion (series 10, image 92), previously 2 mm\n2-3 mm left rectus gyrus lesion (series 10, image 70), previously measuring\n1-2 mm.\nA punctate right temporal lobe lesion (series 10, image 46), which is barely\nperceptible on previous exam although this could be secondary to artifact.\nPunctate right parietal lesion (series 10, image 122), is not definitively\nseen on prior exam\nPunctate left parietal lobe lesion (series 10, image 93), is not definitively\nseen on prior exam.\nRight thalamic 3 mm lesion (series 10, image 74).\n\nSurrounding white matter edema pattern associated with the left frontal lobe\ndominant lesions have improved from prior exam.  Minimally increased edema\npattern surrounding the right frontal vertex lesions.\n\nThere is no acute infarct or intracranial hemorrhage.  The sulci, ventricles\nand cisterns are within expected limits for the patient's age.  The major\nintracranial flow voids are preserved.  The dural venous sinuses are patent. \nThe orbits are unremarkable.  There is mild mucosal thickening of the\nparanasal sinuses.  No significant fluid signal is seen in the mastoid air\ncells.  No suspicious osseous lesions.  Midline frontal subgaleal lipoma\nmeasuring 3-4 mm in greatest thickness is unchanged.  Scattered sebaceous\ncysts are also noted.",
            "output": "1. Mixed response.  The majority of the numerous metastatic lesions involving\nthe bilateral cerebral and cerebellar hemispheres have decreased in size. \nHowever, a few lesions appears slightly increased in size or demonstrates\nenhancement.  At least 2 punctate lesions were not definitively seen on prior\nexamination involving the right parietal and left parietal lobes.\n2. No acute hemorrhage or infarct.\n3. Additional findings as described above."
        },
        {
            "input": "Numerous infratentorial and supratentorial peripherally enhancing lesions are\nseen with apparently good treatment response, given the interval resolution of\nmany lesions, and diminution of the remaining lesions.  No new or larger\nenhancing lesions are seen.\n\nThere is no evidence of acute intracranial hemorrhage or new infarction.  An\nold infarct is seen in the body of the right caudate.  The ventricles and\nsulci are prominent, consistent with global cerebral volume loss.   The\nintracranial flow voids are maintained. A 4 mm subgaleal lipoma is\nre-demonstrated in the left frontal region, unchanged.\n\nNew fluid is seen in the bilateral mastoid air cells.  The paranasal sinuses\nare clear.  The intraorbital contents are normal.",
            "output": "1. Treatment response, with interval improvement and resolution of many\nlesions, and diminution of the remaining lesions.  There is no evidence of new\nor larger enhancing lesions.\n2. New mild bilateral mastoid effusions.\n3. No acute infarct or intracranial hemorrhage."
        },
        {
            "input": "There are numerous enhancing metastasis (at least 19 supratentorial and at\nleast 13 infratentorial), as demonstrated previously.  Most of the lesions are\nsmaller than on the previous examination.  A some of the tiny punctate\nenhancing lesion appear stable.  Some of them which were previously rim\nenhancing node demonstrating more solid enhancement pattern, but this could be\ndue to contraction of the lesions and decrease in size there are no definite\nnew or enlarging lesions.  The lesions do not cause significant mass effect.\n\nThere is a new subdural collection overlying the right hemisphere which\nmeasures up to 1 cm.  It mostly follow CSF signal although there is a layering\nposterior component which is enhancing and T1 slightly intermediate signal. \nThis causes mild mass effect and crowding of the underlying sulci, with slight\neffacement of the right lateral ventricle relative to the left side and a\nminimal degree of leftward midline shift measuring approximately 2 mm.  There\nis no evidence of recent infarction.\n\nGlobal prominence of the ventricles and sulci reflecting volume loss is again\nnoted.  Chronic lacunar infarcts in the bilateral basal ganglia.\n\nThe major intracranial vascular flow voids are preserved.  Orbits are grossly\nunremarkable.  There is patchy fluid signal in the bilateral mastoid air\ncells.  There is a mucous retention cyst in the right maxillary sinus.  Left\nfrontal subgaleal lipoma is again demonstrated, and there are also multiple\nlow signal subcutaneous structures most conspicuously in the superior left\nfrontal scalp which probably reflects epidermal inclusion cysts.",
            "output": "1. Treatment response, with decrease in size of many of the lesion numerous\nmetastatic lesions, and some unchanged punctate enhancing lesions.\n2. There is a new right 1 cm subdural collection most of which follow CSF\nsignal, with a layering enhancing component suggesting subdural hygroma and\ncomponent of subacute to chronic subdural hematoma, with local mass effect and\nminimal leftward midline shift of approximately 2 mm.  This finding is already\nknown on review of Neuro-Oncology clinical note dated ___."
        },
        {
            "input": "Re demonstrated are multiple enhancing nodules scattered throughout the brain\nand skull.  Metastasis in the skull and scalp appear unchanged in size. \nScattered enhancing lesions in the cerebellum in cerebrum are overall\ndecreased in size and conspicuity, for example series 16, image 13, 19, 8 and\n5.\n\nRe demonstrated is a evolving right-sided frontoparietal subdural hematoma\nmeasuring approximately 1.5 cm, unchanged from prior.  There is effacement of\nthe right ventricle with 3 mm of left-sided shift, unchanged from prior.  No\nevidence of new hemorrhage.\n\nProminent ventricles and sulci consistent with age-related involutional\nchange.  Increased focal FLAIR hyperintensity of the bilateral basal ganglia\nand periventricular white matter.  FLAIR intensity is consistent with chronic\nsmall vessel ischemic changes.  The intracranial flow voids are preserved.  No\nevidence of infarction.\n\nRight maxillary mucous retention cyst.  Partial opacification of the bilateral\nmastoid air cells.  Otherwise the paranasal sinuses are patent.",
            "output": "1. Demonstrated are multiple metastases scattered through the head. \nIntracranial metastases are less conspicuous and decreased in size. \nMetastases in the scalp and skull are overall unchanged in appearance.  No\nevidence of new suspicious enhancement soft tissue mass.\n2. Evolving right-sided subdural hematoma measuring up to 1.5 cm.  No new\nregions of hemorrhage.  3 mm of left-sided shift is unchanged\n3. Unchanged opacification of the bilateral mastoid air cells."
        },
        {
            "input": "Study is degraded by motion.  Within these confines:\n\nMR BRAIN:\nThere are redemonstration of multiple enhancing nodules scattered throughout\nthe skull and soft tissue with significant restricted diffusion, some of which\nare interval increase in size (series 17, image 76).  There are scattered\nenhancing lesions with mild restricted diffusion throughout the brain interval\nless conspicuous or decreasing size from previous study (for example, series\n17, image 152, 136, 71, 53 and 60).  However there is a new metastatic lesion\nadjacent to the left lateral ventricle in the left frontal lobe (series 17,\nimage 127) measuring 7 mm) in the callosum.  Some of these metastases have\nsusceptibility artifact on gradient echo sequence which may represent chronic\nblood products versus mineralization.\n\nThere is interval improved evolving right-sided frontal parietal subdural\nhematoma measuring up to 1.5 cm in maximum thickness (previously measuring 2.2\ncm in maximal thickness.)  There is interval improved 3 mm midline shift to\nthe left (previously 4 mm midline shift to the left).  There are also\nscattered new restricted diffusion along the parenchymal underneath the\nsubdural hematoma concerning for new metastatic lesions, which are obscured on\nother sequence secondary to subdural hematoma.\n\nModerate periventricular and subcortical white matter T2/FLAIR\nhyperintensities are nonspecific but likely sequelae of chronic small vessel\nischemic disease.  There are chronic lacunar infarcts involving bilateral\nbasal ganglia and cerebellum.  There is prominence of the ventricles and sulci\nsuggestive of involutional changes.\n\nThere are scattered opacification of bilateral ethmoid air cells.  There is\nredemonstration of a mucous retention cyst in the right maxillary sinus.",
            "output": "1.  Study is degraded by motion.\n2. New 7 mm enhancing lesion adjacent to the left lateral ventricle in the\nfrontal lobe callosum concerning for new metastatic lesion.\n3. Interval decrease in size of other multiple intracranial metastasis as\ndescribed.\n4. Grossly stable to slightly increase in size of the scalp and skull\nmetastasis.\n5. Interval decrease in size of right frontoparietal subdural hematoma and\nmidline shift as described.\n6. Nonspecific new restricted diffusion underlying right frontoparietal\nsubdural hematoma.  While findings may represent blood products, new\nmetastatic lesion is not excluded on the basis examination.  Recommend\nattention on follow-up imaging.\n7.  Additional findings as described above.\n\nNOTIFICATION:  The impression and recommendation above was entered by Dr.\n___ on ___ at 16:12 into the Department of Radiology critical\ncommunications system for direct communication to the referring provider."
        },
        {
            "input": "Again noted are multiple enhancing parenchymal lesions, predominantly\nsuperficial, reflecting multiple metastases.  The largest lesion, in the\ncorpus callosum on the left, best seen on image 121 of series 5, is clearly\nlarger than on the study of ___.  Most of the other lesions\nappear unchanged in size, or smaller than on the prior study.\nLesions demonstrated include a 2 mm enhancing focus in the right cerebellar\nhemisphere seen on image 47 of series 5,\nA linear appearance of enhancement superficially over the cerebellum best seen\non image 64 of series 5 and perhaps reflecting leptomeningeal involvement, and\napproximately 1 mm focus in the left cerebellar hemisphere seen on image 52 of\nseries 5,\nA 2 mm focus in the left frontal lobe seen on image 107 of series 5, a 4 mm\ncortical focus on image 130 of series 5 is in the left frontal lobe,\nA 1 mm focus superficially in the left frontal lobe best seen on image 145 of\nseries 2, a 3 mm focus seen on image 148 of series 5 in the right frontal lobe\nA 2 mm focus seen on image 158 of series 5 in the right frontal lobe.\n\nA 12 mm cystic appearing left frontal scalp lesion appears unchanged.\nAgain seen and unchanged is right hemispheric subdural hematoma.",
            "output": "1. Multiple enhancing lesion supra and infratentorially compatible with\nmetastases.\n2. Enlargement of the left corpus callosum lesion."
        },
        {
            "input": "Study is degraded by motion.  Within these confines:\n\nWhen compared to most recent MRI dated ___, there has been\nsignificant interval increase in size of the nodular peripherally enhancing\nlesion in the genu of the corpus callosum, now measuring 20 mm x 25 mm x 13 mm\n(AP, TV, SI), previously measured 6.5 mm.  This lesion demonstrate diffusion\nrestriction with T2 hypointensity, suggestive of hypercellular nature.  The\nmass appears to cross the midline.  It is difficult to assess the perilesional\nvasogenic edema due to extensive pre-existing FLAIR hyperintensity in the\nbilateral corona radiata, which is increased compared to prior exam.\n\nSimilarly, there is increase in size of metastatic lesions along the body of\nthe left lateral ventricles (13: 109).  The remainder of metastatic lesion are\ngrossly stable in size, such as lesions in the left frontal lobes (13:131\nthrough 139), right frontal operculum (13:104), right frontal gyrus (13:150),\nleft cerebellum (13:63), and right cerebellar tonsil (13: 39, 45, and 13:38).\n\nThere is interval decrease of right cerebral convexity subdural fluid\ncollection.\n\nThere is no evidence of new hemorrhage, midline shift or infarction.   The\nventricles and sulci are stable in caliber and configuration.  Stable several\ncystic appearing lesion in the bilateral frontal scalp, likely representing\nsebaceous cysts.\n\nThere is mild mucosal thickening of the ethmoid air cells and bilateral\nmaxillary sinuses.\n\n Limited imaging of the parotid glands demonstrate left subcentimeter\nnonspecific probable lymph nodes.",
            "output": "1.  Study is degraded by motion.\n2. Interval increase in size of nodular peripherally enhancing lesion in the\ngenu of the corpus callosum with associated diffusion restriction compatible\nwith progression of metastatic disease.  Superimposed infection can not be\nexcluded due to presence of diffusion restriction, suggest clinical\ncorrelation.\n3. Redemonstration of numerous metastatic disease in the supra and\ninfratentorial brain, some of which demonstrate interval increase in size,\nsuch as the lesions along the body of the left lateral ventricle (13:109).\n4. Interval increase of FLAIR hyperintensity in the bilateral corona radiata. \nWhile findings may represent treatment related changes, edema is not excluded\non the basis examination.\n5. Interval decrease of right cerebral convexity subdural hematoma compared to\n___ prior MRI exam."
        },
        {
            "input": "MR BRAIN:\nCompared to most recent MRI dated ___, there is no significant\nincrease in size of the nodular peripheral enhancing lesion in the genu of the\ncorpus callosum, measuring 21 mm x 26 mm x 12 mm (AP, TV, SI).  There has been\nslight interval decrease in the thickening of the rind of the lesion.  The\nlesion continues to demonstrate T2 hypointensity with associated diffusion\nrestricting, suggestive of hypocellularity.  The perilesional vasogenic edema\nis unchanged, although this is difficult to assess due to extensive\npre-existing FLAIR hyperintensity in the bilateral corona radiata, likely\nrelated to posttreatment changes and superimposed sequelae of chronic\nmicroangiopathy.\n\nAdditionally, there is unchanged metastatic lesion along the subependymal\nsurface of the body of the left lateral ventricle.  The remainder of\nmetastatic lesion in the left frontal lobe, right operculum (11:184), left\ncerebellum, and right cerebellar tonsil.  Overall, no new lesions are\nidentified.\n\nThere is stable right cerebral convexity subdural fluid collection there is no\nevidence of new hemorrhage, midline shift or infarction.   The ventricles and\nsulci are stable in caliber and configuration.  The visualized major vascular\nflow voids are grossly preserved.  There is no evidence of dural sinus\nthrombosis.\n.\nMR ___ perfusion: There is no significant increase in perfusion of\nthe corpus callosum lesion.\n\n Perfusion: There is no significant increased perfusion.\n\nMR Spectroscopy: Overall, the single and multiple voxel evaluation\ndemonstrates decreased choline:creatinine ratio with elevation of the lactate\npeak.  However, the anterior medial voxel shows elevated choline:creatine\nratio, with a lower lactate peak.",
            "output": "1. Stable size of nodular peripherally enhancing lesion the genu of the corpus\ncallosum without evidence of elevatedcholine:creatinine ratio or increased\nperfusion abnormality.  Findings compatible with radiation necrosis, and less\nlikely progression of metastatic disease.  The peripheral rind of the dominant\nlesion demonstrates slight interval decrease in the extent of\nthickening/enhancement.\n2. Stable redemonstration of numerous metastatic disease in the supratentorial\nand infratentorial brain.\n3. Stable confluent FLAIR hyperintensity in the bilateral corona radiata, most\nlikely related to posttreatment changes.\n4. Stable right cerebral convexity subdural hematoma.\n5. Additional findings as described above."
        },
        {
            "input": "Motion artifact mildly limits evaluation.\n\nThere are numerous predominantly ring-enhancing supratentorial and\ninfratentorial lesions consistent with diffuse metastatic disease.\n\nIn the infratentorial compartment, the largest lesion is centered in the left\nsuperior vermis, 2.1 x 1.7 cm on image 14:55, with a second largest adjacent\nlesion in the superior left cerebellar hemisphere abutting the tentorium, 1.4\nx 1.1 cm on image 14:62.  There is edema in the left cerebellar hemisphere\nwith partial effacement and rightward displacement of the fourth ventricle. \nThere are small areas of edema in the right cerebellar hemisphere associated\nwith some of the metastases, without significant mass effect.\n\nIn the supratentorial compartment, the largest lesion involves the left\nparacentral lobule, centered within the the precentral gyrus, 1.8 x 1.2 cm on\nimage 14:128.  There is moderate associated edema with sulcal effacement, but\nno effacement of the lateral ventricle or shift of midline structures. \nRemaining supratentorial lesions demonstrate minimal or no edema.\n\nGradient echo images suggest subtle blood products within the enhancing rims\nof the above-described largest lesions in the left superior cerebellar and\nleft precentral gyrus.\n\nThere is no acute infarction.  There are small chronic infarcts within\nbilateral basal ganglia.\n\nProminence of the lateral and third ventricles is, commensurate with\nprominence of the cerebral sulci, consistent with global parenchymal volume. \nThere is no evidence for hydrocephalus.  The fourth ventricle is only\npartially effaced.\n\nMajor vascular flow voids appear preserved.  Major dural venous sinuses are\npatent.\n\nThere is complete opacification of the left maxillary sinus, with osseous\nremodeling demonstrated on the preceding same-day CT, consistent with chronic\nsinusitis.  The medial wall of the left maxillary sinus bulges into the nasal\ncavity.  The left ostiomeatal unit is occluded.  There is a mucous retention\ncyst in the contralateral right maxillary sinus, along with minimal mucosal\nthickening.  There is mild mucosal thickening within bilateral ethmoid air\ncells.\n\nMidline nasopharyngeal soft tissues are abnormally enlarged for age.",
            "output": "1. Innumerable supratentorial and infratentorial metastases.  The largest\nlesions in the left superior cerebellum are associated with edema, causing\npartial effacement and rightward shift of the fourth ventricle.  The largest\nlesion in the left precentral gyrus is associated with moderate edema but no\neffacement of the left lateral ventricle or shift of midline structures.\n2. No evidence for supratentorial hydrocephalus.  Enlargement of the lateral\nand third ventricles is commensurate with enlargement of the sulci, consistent\nwith global parenchymal volume loss.\n3. Small chronic infarcts within bilateral basal ganglia.  No acute infarction\n4. Chronic left maxillary sinusitis with occlusion of the left ostiomeatal\nunit.\n5. Enlarged midline nasopharyngeal soft tissues, which may be reactive, but\ncould be further evaluated by direct visualization if clinically warranted."
        },
        {
            "input": "Motion artifact mildly limits evaluation.\n\nThere is subtle mild FLAIR hyperintensity along the sulci of the left frontal\nlobe (7:13 and 15) with associated curvilinear enhancement versus hyperemia\n(9: 150-162) And a small focus of intrinsic T1 hyperintensity (5:13).  There\nno additional areas of abnormal enhancement, and no enhancing mass lesion. \nThere is no evidence of acute infarction.  The ventricles and sulci are normal\nin size.  Basal cisterns are preserved.  Cerebellar tonsils are normally\npositioned.\n\nThe dural venous sinuses appear patent on the postcontrast MP RAGE images. \nMajor arterial flow voids appear grossly preserved.\n\nThere is trace mucosal thickening in the ethmoid air cells.",
            "output": "1. Mildly motion limited exam.\n2. FLAIR and T1 signal abnormalities in several left frontal sulci, with\nassociated hyperemia versus leptomeningeal enhancement.  These findings are\ncompatible with subarachnoid hemorrhage, but superimposed leptomeningeal\nmalignancy cannot be excluded.\n\nNOTIFICATION:  The impression above was entered by Dr. ___ on\n___ at 15:57 into the Department of Radiology critical communications\nsystem for direct communication to the referring provider."
        },
        {
            "input": "There is interval resolution of previously identified left frontal sulcal\nFLAIR hyperintensity likely related to left frontal convexal subarachnoid\nhemorrhage.  There is residual increased susceptibility on T2 star sequence\nalong same left frontal region related to hemosiderin deposition (series 10,\nimage 17 and 16).\n\nThere is no evidence of acute hemorrhage, edema, masses, mass effect, midline\nshift or infarction.  There are essentially unchanged few small punctate\nbilateral frontal and parietal white matter nonenhancing T2 FLAIR\nhyperintensities; nonspecific in appearance.  The ventricles and sulci are\nnormal in caliber and configuration.  There is no abnormal enhancement after\ncontrast administration.\n\nBoth orbits are normal.  Paranasal sinuses and mastoid air cells are\nessentially clear.",
            "output": "1. No acute intracranial abnormality or abnormal intracranial enhancement.\n2. Interval resolution of previously identified left frontal sulcal FLAIR\nhyperintensity likely related to left frontal convexity subarachnoid\nhemorrhage with subtle residual changes as described."
        },
        {
            "input": "The study is severely limited by motion.  Within these confines, there is no\nevidence acute infarct, intracranial hemorrhage or midline shift.\n\nExtensive calvarial enhancing lesions, including a left sphenoid expansile\nlesion, measuring up to 1.4 cm in the left posterior vertex (series 10, image\n155) are replacing the normal bone, including the skullbase.  There is\nextension of tumor from the skullbase into the sella (series 10, image 60). \nThese lesions are new compared to prior.  No evidence of enhancing mass lesion\nwithin brain. No leptomeningeal enhancement.  The dural venous sinuses are\npatent.  There is fluid in the left maxillary sinus.  There is bilateral\nopacification of the mastoid air cells.",
            "output": "1. Severely motion degraded study.  Within these confines, widespread\ncalvarial enhancing lesions, consistent with myeloma infiltration of the bone\nmarrow.  No intracranial enhancing mass.\n2. No acute infarct or hemorrhage."
        },
        {
            "input": "Study is moderately degraded by motion.\n\nThe gray-white matter signal is unremarkable without acute infarct,\nhemorrhage, mass, or mass effect.  The ventricles and cortical sulci\ndemonstrate normal caliber and configuration.  The vascular flow voids are\npreserved.\n\nThe orbits, calvarium, and soft tissues are unremarkable.  The paranasal\nsinuses and mastoid air cells are clear.",
            "output": "1.  Study is moderately degraded by motion.\n2. Within limits of this motion degraded noncontrast study, no acute\nintracranial abnormality."
        },
        {
            "input": "Study is mildly degraded by motion.\n\nThere is restricted diffusion in the left superior temporal gyrus (302:18,\n300:18), compatible with an acute infarction.  This is new compared to ___, but unchanged compared to the prior CTA performed earlier on\nthe same date.  Within the left supplemental motor area, there is an\nadditional curvilinear focus of high DWI signal without a definite ADC\ncorrelate (302:23), suggesting a late acute/early subacute infarction.  No\nevidence of hemorrhagic transformation.  There is encephalomalacia in the left\ncerebellum (5:4, 6:5).  No shift of midline structures.\n\nThere is prominence of the ventricles and sulci suggestive involutional\nchanges.  Bilateral scattered T2/FLAIR hyperintensities are nonspecific, but\nlikely represent a sequela of chronic small vessel disease.  Principal\nintracranial vascular flow voids are preserved.\n\nThere is a mucous retention cyst in the left maxillary sinus.  Mild mucosal\nthickening is also noted within the ethmoid air cells bilaterally.  The orbits\nare unremarkable.  Left parietal skull osteoma is noted.",
            "output": "1. Acute infarction in Wernicke's area, and late acute/early subacute\ninfarction in the left supplemental motor area, suggesting an embolic source. \nNo evidence of hemorrhagic transformation.\n2. Atrophy and probable chronic small vessel disease.\n\nNOTIFICATION:   The findings were discussed by Dr. ___ with Dr. ___\n___ on the telephoneon ___ at 3:39 ___, 2 minutes after discovery of the\nfindings."
        },
        {
            "input": "There is no midline shift.  There is no mass or mass effect.  There\nis no evidence for restricted diffusion.  There is a 0.3 cm round focus of\nsusceptibility in the left cerebellum (s7, i6). There is no associated edema.\nThe ventricles and sulci appear appropriate for the patient's age. The midline\nstructures are unremarkable. There are normal flow voids seen at the base of\nthe brain. There is no abnormal signal intensity within the orbits. The\nvisualized paranasal sinuses and mastoid air cells are clear.",
            "output": "0.3 cm foci of magnetic susceptibility in the left cerebellum.\nThis could represent a small punctate foci of hemorrhage or cavernoma or\ncalcification. Recommend follow up examination."
        },
        {
            "input": "Study is mildly degraded by motion.  Question minimal right basal ganglia T1\nhyperintensity versus artifact (see 04:14).  Periventricular and subcortical\nT2 and FLAIR hyperintensities without definite associated T1 hypointensity,\nincrease susceptibility, are noted.  There is no evidence of hemorrhage,\nedema, masses, mass effect, midline shift or infarction.   The ventricles and\nsulci are normal in caliber and configuration.  Limited imaging of the orbits\ndemonstrates right-sided coloboma.",
            "output": "1. Study is mildly degraded by motion.\n2. No definite evidence of acute infarct.\n3. Within limits of this motion degraded noncontrast study, no definite\nevidence of mass.\n4. Nonspecific supratentorial white matter lesions as described.  Differential\nconsiderations include sequela of prior trauma or infection, history of\nmigraine headaches, inflammatory or demyelinating process, and\nmicroangiopathic changes.  If concern for active demyelinating process,\nconsider contrast enhanced brain MRI for further evaluation.\n5. Right coloboma.\n6. Right basal ganglia signal abnormality versus artifact.  If not\nartifactual, finding may represent physiologic calcification or history of\nneurofibromatosis with differential considerations of hepatic encephalopathy\nor history of hyperalimentation.\n7. Please note evaluation of neck and skull base is limited on this\nexamination."
        },
        {
            "input": "There are multiple subacute cortical infarctions scattered throughout the\nposterior circulation, occipital lobes, bilateral temporal lobes, and\nadditionally within bilateral frontal lobes. There is no mass, edema, or mass\neffect identified. Ventricles appear unremarkable. Intracranial flow voids are\npreserved. Basal cisterns are patent. Insults of note is made of diffuse\ncervical vertebral body and clivus bone marrow T1 hypo intensit.",
            "output": "Diffuse subacute cortical infarcts involving bilateral temporal, frontal, and\npredominantly posterior circulation territories con likely reflective of\nemboli, probably from a proximal source.\n\nDiffuse bone marrow T1 hypo intensity which may reflect infiltrate or process\nversus chronic disease."
        },
        {
            "input": "There is no evidence of acute intracranial hemorrhage, mass, mass effect or\nshifting of the normally midline structures.  The ventricles and sulci normal\nin size and configuration the patient's age.  No diffusion abnormalities are\ndetected.  There is no evidence of abnormal enhancement.  The major vascular\nstructures are patent and demonstrate normal distribution.  The orbits are\nunremarkable, the paranasal sinuses and the mastoid air cells are clear.",
            "output": "Essentially normal MRI of the brain with and without contrast, there is no\nevidence of acute or subacute intracranial process"
        },
        {
            "input": "The ventricles and extra-axial spaces are normal in size. There is no evidence\nof midline shift, mass effect or hydrocephalus. There are no acute infarcts.\nThere is no evidence of focal abnormalities.  The vascular flow voids are\nmaintained. The visualized paranasal sinuses are clear. Following gadolinium\nadministration there is no evidence of abnormal parenchymal, vascular and\nmeningeal enhancement seen.  A partial empty sella is incidentally noted.",
            "output": "No significant abnormalities are seen on MRI of the brain with and without\ngadolinium.  No evidence of age inappropriate brain or medial temporal atrophy\nor significant subcortical white matter ischemic disease."
        },
        {
            "input": "There is no parenchymal signal abnormality. Prominence of the ventricles and\nsulci is suggestive of global volume loss. There is no region of restricted\ndiffusion.  No abnormal susceptibility artifact. Major intravascular flow\nvoids are preserved.\n\nWithin the left masseter muscle is a structure measuring just over 1 cm with a\nfluid fluid level. This is incompletely characterized postoperative changes of\nleft parotidectomy again seen. Some fluid signal seen within the petrous all\nair cells bilaterally.",
            "output": "No intracranial abnormality to explain patient's symptoms. Focal lesion in the\nleft masseter which is incompletely characterized on this exam but where seen\nis not definitely changed since ___ suggesting benign etiology."
        },
        {
            "input": "The postcontrast MPRAGE sequences are moderately degraded by motion.\n\nA lobulated intraparenchymal hematoma in the right thalamus measures 1.3 x 1.1\ncm, unchanged in size from the prior examination.  This hematoma is T1/T2\nhypointense with a thin rim of T1 hyperintense signal.  This hematoma\ndemonstrates susceptibility.  No new hemorrhages are identified.  A small\namount of surrounding T2/FLAIR hyperintense signal in the right thalamus\nrepresents edema without mass effect.  This hematoma has a thin rim of slow\ndiffusion.\n\nThere is a chronic lacunar infarction in the left corona radiata.\n\nThere is no evidence of midline shift or acute infarction.   The ventricles\nand sulci are normal in caliber and configuration.  There is no abnormal\nenhancement after contrast administration.  Scattered foci of T2/FLAIR\nhyperintensities in the periventricular and subcortical white matter are\nnonspecific, but may represent the sequela of chronic small vessel ischemic\ndisease.  Susceptibility in the left lateral ventricle atrium is due to\ncalcified choroid plexus.\n\nThe paranasal sinuses and mastoid air cells are clear.  The patient is status\npost bilateral cataract surgery.  The major intracranial flow voids are\npreserved.",
            "output": "1. Unchanged, acute intraparenchymal hematoma in the right thalamus with no\nevidence of enhancement to suggest an underlying mass.  Follow-up is\nrecommended in 4 weeks to ensure resolution.\n2. No acute infarction.\n3. No new hemorrhages.  No micro hemorrhages."
        },
        {
            "input": "There is a homogeneously enhancing extra-axial, dural-based mass along the\nleft tentorium near the incisura, which has low signal on the ADC map without\nhigh signal on diffusion tracer images.  It measures 1.9 cm AP, 1.0 cm\ntransverse, 1.8 cm craniocaudad (100:40, 101:85).  The medial aspect of the\nmass is inseparable from the trigeminal nerve, but the mass extends\nposteriorly and inferiorly below the level of the trigeminal nerve.  The\ninferior aspect of the mass extends to the upper margin of the left internal\nauditory canal, but does not extend into the left internal auditory canal. \nAnteriorly, the mass extends into the Meckel's cave (image 100:38).\n\nThe left midbrain and pons are mildly remodeled.  There is minimal high signal\nin the left pons on FLAIR images, image 15:8.  There are scattered small foci\nof high T2 signal in the supratentorial white matter, nonspecific but likely\nsequela of mild chronic small vessel ischemic disease in this age group. The\nventricles are age-appropriate.\n\nThere is a developmental venous anomaly in the right cerebellar hemisphere\nwith associated low signal on gradient echo images.  There is no clear\nevidence for an associated cavernous malformation.  Dural venous sinuses\nappear patent on postcontrast MP RAGE images.\n\nThere is mucosal thickening in the bilateral ethmoid air cells and right\nmaxillary sinus.  Remaining paranasal sinuses are patent.",
            "output": "1. Homogeneously enhancing dural-based mass along the left tentorium near the\nincisura is most suggestive of a meningioma.  However, the medial aspect of\nthe mass is associated with the left trigeminal nerve, and the mass extends\ninto the left Meckel cave anteriorly.  Therefore, a trigeminal schwannoma\ncannot be definitively excluded.\n2. The left midbrain and pons are mildly remodeled.  Minimal high signal in\nthe left pons may represent mild edema, versus chronic small vessel ischemic\nchanges.\n3. Scattered nonspecific supratentorial white matter signal abnormalities,\nlikely sequela of mild chronic small vessel ischemic disease in this age\ngroup.\n4. Developmental venous anomaly in the right cerebellar hemisphere."
        },
        {
            "input": "Patient is status post resection of the left cerebral pontine angle meningioma\nresection, including pneumocephalus along the frontal lobes, left greater than\nright.  Multiple susceptibility artifacts near the cerebellum are most\nconsistent with foci of air.  Trace amount of layering material in the lateral\noccipital horns of the lateral ventricles on GRE sequences is most consistent\nwith blood products.\n\nIn the surgical bed, there is mild dural thickening but no residual nodular\nenhancement.  There is no new or enlarging mass in the region.  Asymmetrically\nhyperintense appearance of the dura on the left hemisphere on FLAIR sequences\nmay represent postsurgical changes.\n\nThere is no evidence of acute infarction.\nThe paranasal sinuses are grossly clear, aside from mild mucosal thickening of\nthe ethmoid air cells and frontal sinuses.  The middle ear cavities and\nmastoid air cells are clear.\nThe intracranial flow voids are maintained.  Dural venous sinuses enhance\nnormally.",
            "output": "1. Status post resection of left cerebral pontine angle meningioma.  No\nevidence of residual mass.  Mild dural thickening in the surgical bed is\nlikely postsurgical changes.\n2. Pneumocephalus and trace amount of layering blood products in the bilateral\nposterior horn of the lateral ventricles."
        },
        {
            "input": "Again seen are postoperative changes after posterior fossa meningioma\nresection.  There is no evidence of residual or recurrent tumor.  There is no\nevidence of hemorrhage, edema, masses, mass effect, midline shift or\ninfarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.",
            "output": "1. Postoperative changes after tumor resection.  No evidence of residual or\nrecurrent neoplasm.."
        },
        {
            "input": "There has been no significant interval change.  Postoperative changes are seen\nin the left side of the posterior fossa.  There is no residual or recurrent\nenhancement seen.  There is no acute infarct mass effect midline shift or\nhydrocephalus identified.  An incidental developmental venous anomaly in the\nright cerebellum is again noted.  Mild mucosal thickening is seen in the\nethmoid air cells.",
            "output": "Stable postoperative appearance without signs of recurrent mass or\nenhancement."
        },
        {
            "input": "There is no evidence of hemorrhage, masses, mass effect, midline shift or\ninfarction.  Moderate brain parenchymal atrophy.  Vascular flow voids are\npreserved.  Dural venous sinuses are patent.  No abnormal intracranial\nenhancement.  No meningeal enhancement.\n\nThere is edema and enhancement involving the mucosal surface of the oropharynx\nand nasopharynx, may be reactive from intubation, inflammatory process, or\nother etiology cannot be excluded.\n\nExtensive opacification paranasal sinuses, mastoids, likely from intubation.. \nAbnormal left globe, may be from prior surgery, vitreous hemorrhage,\nclinically correlate.",
            "output": "1. No acute intracranial contents.  Parenchymal atrophy.\n2. Symmetric mucosal enhancement, stranding oropharynx, may be reactive,\ninflammatory, or other etiology, incompletely visualized.\n3. Abnormal left globe, see above."
        },
        {
            "input": "There is no evidence of hemorrhage, masses, mass effect, midline shift or\ninfarction.  Moderate brain parenchymal atrophy.  Vascular flow voids are\npreserved.  Dural venous sinuses are patent.  No abnormal intracranial\nenhancement.  No meningeal enhancement.\n\nThere is edema and enhancement involving the mucosal surface of the oropharynx\nand nasopharynx, may be reactive from intubation, inflammatory process, or\nother etiology cannot be excluded.\n\nExtensive opacification paranasal sinuses, mastoids, likely from intubation.. \nAbnormal left globe, may be from prior surgery, vitreous hemorrhage,\nclinically correlate.",
            "output": "1. No acute intracranial contents.  Parenchymal atrophy.\n2. Symmetric mucosal enhancement, stranding oropharynx, may be reactive,\ninflammatory, or other etiology, incompletely visualized.\n3. Abnormal left globe, see above."
        },
        {
            "input": "No evidence for an enhancing mass, acute infarction, edema, or blood products.\nMild global parenchymal volume loss is again seen with prominent ventricles\nand sulci.  Major arterial flow voids are grossly preserved.  Dural venous\nsinuses appear patent on postcontrast MP RAGE images.\n\nPostsurgical changes are again seen in the left globe.  There is mild mucosal\nthickening in the left greater than right maxillary sinuses, as well as in the\nbilateral ethmoid air cells and left frontal sinus.  There is also mild\nmucosal thickening in the underdeveloped sphenoid sinuses.  There is fluid in\nthe nasopharynx, bilateral middle ear cavities, and bilateral mastoid antra. \nThere is bilateral paucity of pneumatized mastoid air cells, and they are also\nopacified with fluid.  The fluid may be secondary to prolonged supine\npositioning in the inpatient setting.",
            "output": "1. No evidence for an enhancing mass or acute intracranial abnormalities.  No\nchange compared to the MRI from ___.\n2. Fluid within bilateral mastoid antra and middle ear cavities may be\nsecondary to prolonged supine positioning in the inpatient setting, but please\ncorrelate with any associated acute infectious/inflammatory symptoms."
        },
        {
            "input": "There is no acute infarct, hemorrhage, edema, or mass effect.  There is very\nslight asymmetric prominence of all components of the left lateral ventricle,\nlikely congenital/developmental.  The ventricles and sulci are otherwise\nnormal in size and configuration. There is no focus of abnormal enhancement\nafter administration of IV contrast. Intracranial flow voids are preserved. \nSeen only on one image (5:10) is a tiny focus of increased T1 signal in the\nright paramedian pons, at the level of the right middle cerebellar peduncle,\nwithout corresponding FLAIR-signal abnormality or enhancement.  The cochleae,\nvestibules, and IACs are unremarkable bilaterally.",
            "output": "1.  No evidence of acute ischemia in the medulla or elsewhere.\n2.  Normal, symmetric appearance of the ___ and ___ cranial nerve complexes,\nwithout pathologic enhancement or mass.\n3.  The fluid-signal structures of the otic capsule are unremarkable."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  Again seen is an ill-defined focus of enhancement in the right\ntemporal lobe.  This has not changed since the prior studies.  It is hypo\nintense on the gradient echo images and slightly hyperintense on the FLAIR\nimages.  The appearance remains most suggestive of a capillary telangiectasia.\nAgain seen are multiple areas of white matter hyperintensity on the FLAIR\nimages.  Although nonspecific, these are often attributed to chronic small\nvessel ischemia.  There is no other abnormal enhancement after contrast\nadministration.\n\nThere is partial opacification of the sphenoid sinus on the right.  This\nappears unchanged since the study of ___.",
            "output": "1. Unchanged enhancing focus in the right temporal lobe.  This remains most\nsuggestive of a capillary telangiectasia.  ."
        },
        {
            "input": "Again noted is a brush like 1.2 cm focus of postcontrast enhancement along the\nposterior right temporal lobe, unchanged in size from prior exam without\nevidence of corresponding T2/FLAIR with diffusion-weighted signal abnormality.\nThe findings are consistent with a capillary telangiectasia. No new enhancing\nlesions. There are scattered periventricular and subcortical white matter\nT2/FLAIR nonspecific hyperintensities, which may be seen in setting of small\nvessel ischemic disease.\nThere is mild global cerebral volume loss, within expected limits for the\npatient's age. Sulci, ventricles and cisterns are within expected limits given\nthe degree of volume loss. No evidence of intra or extra-axial mass, acute\nhemorrhage or infarct. The major flow voids are preserved. Incidental note is\nmade of a partial empty sella.\n\nIncidental note is made of a prominent left concha bullosa. Mild mucosal\nthickening of the paranasal sinuses. The mastoid air cells are essentially\nclear. The orbits are unremarkable.",
            "output": "1. Unchanged appearance of right temporal  capillary telangiectasia without\nnew abnormal lesions identified.\n2. Nonspecific white matter changes, as described above, which may be seen in\nthe setting of small vessel ischemic disease."
        },
        {
            "input": "Study is moderately degraded by motion.  Within these confines:\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  There is prominence of the ventricles and sulci suggestive\ninvolutional changes.  There is no abnormal enhancement after contrast\nadministration.  Partially empty sella is noted.  Bilateral maxillary and\nfrontal sinus and ethmoid air cell mucosal thickening is present.\n\nQuestion nonspecific low marrow signal versus artifact (see 11:12).  Scattered\nsubcentimeter nonspecific lymph nodes are noted throughout the visualized\nportion of the neck bilaterally, without definite enlargement by size\ncriteria.",
            "output": "1. Study is moderately degraded by motion.\n2. No acute intracranial abnormality.\n3. Within limits of study, no definite evidence of intracranial mass.\n4. Question nonspecific low marrow signal as described.  If not artifactual,\ndifferential considerations include anemia and infiltrative process.  If\nclinically indicated, consider correlation with CBC.\n5. Nonspecific subcentimeter lymph nodes as described.\n6. Mild paranasal sinus disease, as described.\n\nNOTIFICATION:  The impression and recommendation above was entered by Dr.\n___ on ___ at 16:47 into the Department of Radiology critical\ncommunications system for direct communication to the referring provider."
        },
        {
            "input": "There is no evidence of acute infarction.  No intracranial hemorrhage. No\nmass, mass effect, edema or midline shift.\n\nThe ventricles and sulci are mildly prominent compatible with age related\nglobal parenchymal volume loss.  Mild enlargement of the bilateral temporal\nhorns may reflect minimal to mild medial temporal lobe atrophy.\n\n Periventricular and subcortical white matter FLAIR hyperintensities are\nnoted, a nonspecific finding that most likely represents the sequelae of\nchronic small vessel ischemic disease.   There is gross preservation of the\nprincipal intracranial vascular flow voids.\n\nMucosal thickening is seen in scattered ethmoid air cells and within the\nbilateral maxillary and left sphenoid sinuses.  The remainder of the\nvisualized paranasal sinuses, middle ear cavities, and mastoid air cells are\nwell aerated and clear.  The orbits are within normal limits bilaterally.",
            "output": "1. No evidence for acute infarction or intracranial hemorrhage.\n2. Mild-to-moderate global parenchymal volume loss and evidence of minimal to\nmild bilateral medial temporal lobe atrophy.\n3.  Periventricular and subcortical white matter FLAIR hyperintensities are\nnoted, a nonspecific finding that most likely represents the sequelae of\nmoderate chronic small vessel ischemic disease.  Mild-to-moderate changes of\nsmall vessel disease are also seen within the pons."
        },
        {
            "input": "There is no acute infarct or intra or extra-axial mass.\n\nWhen compared to the prior examination of ___, there are new foci of gradient\necho susceptibility in the left thalamus (series 11, image 13 and series 11,\nimage 12).  In addition, gradient echo susceptibility foci in the pons are\nmuch more prominent when compared to the prior exam, likely secondary to\ndifferences in technique.  Additional diffuse foci of gradient echo\nsusceptibility artifact are similar appearance to prior exam.\n\nAgain noted are diffuse periventricular and subcortical as well deep and\npontine white matter confluent T2/FLAIR hyperintensities, which are\nnonspecific, more prominent when compared to examination of ___. \nThere is diffuse global cerebral and cerebellar volume loss, more prominent\nwhen compared to prior exam of ___.  The sulci, ventricles and cisterns are\nprominent but within expected limits given the degree of volume loss.\n\nThe paranasal sinuses are essentially clear.  The orbits are unremarkable.",
            "output": "1. There are new foci of gradient echo susceptibility in the left thalamus\nsince ___, likely representing micro-hemorrhages.  Gradient echo\nsusceptibility within the pons are more prominent when compared to the prior\nexam but this is likely secondary to differences in technique.  Additional\npreviously seen susceptibility foci are similar appearance.\n2. Nonspecific diffuse confluent periventricular and subcortical, deep and\npontine white matter T2/FLAIR hyperintensities, have increased since\nexamination of ___, likely representing sequela of chronic microangiopathy\nand superimposed infarcts.\n3. Interval increase in involutional changes.\n4. No acute infarct."
        },
        {
            "input": "The study is partially degraded due to motion artifact.\n\nThere are punctate foci of diffusion signal abnormality within the left\nparietal and left frontal lobes.  There is corresponding isointensity to gray\nmatter on the ADC map.  Confluent bilateral subcortical, deep and\nperiventricular white matter T2/FLAIR hyperintensity is nonspecific but\ncompatible with chronic small vessel ischemic disease given the patient's age.\n\nThere is a small old lacunar infarct within the left putamen.  Foci of\nsusceptibility artifact within the bilateral thalami (left greater than right)\nand pons are compatible with old micro hemorrhages.  There is no evidence of\nacute hemorrhage, edema, masses, mass effect or midline shift.  Prominence of\nthe ventricles and cerebral sulci likely relate to age related involutional\nchanges.\n\nThe major intracranial vascular flow voids are maintained.  The paranasal\nsinuses, mastoid air cells and orbits are normal.",
            "output": "1. Motion degraded study.\n2. Evidence of punctate subacute infarcts involving the left frontal and left\nparietal lobes.\n3. Confluent white matter T2/FLAIR hyperintensity is nonspecific but\ncompatible with chronic small vessel ischemic disease given the patient's age.\n4. Small old lacunar infarct in the left putamen.\n5. Focus of susceptibility artifact within the bilateral thalami (left greater\nthan right) and pons are compatible with old micro hemorrhages.\n\nNOTIFICATION:   The findings were discussed with ___, M.D. by ___\n___, M.D. on the telephone on ___ at 10:14 pm, 5 minutes\nafter discovery of the findings."
        },
        {
            "input": "The patient is status post left frontal craniotomy and resection of a left\nfrontal parafalcine meningioma.  The T1 weighted images without contrast\ndemonstrate gyriform pattern of high-signal intensity in the cortex of the\nleft frontal lobe, likely consistent with cortical pseudo-laminar necrosis,\nthere is mild pattern of enhancement surrounding the surgical cavity, with no\nfrank evidence of enhancement to indicate residual or recurrent meningioma.\n\nFLAIR hyperintensity signal is identified surrounding the surgical cavity in\nthe left frontal lobe, extending towards the genu of the corpus callosum,\nlikely consistent with posttreatment changes.  Additional punctate areas of\nFLAIR high-signal intensity in the subcortical white matter are nonspecific\nand may reflect changes due to chronic small vessel disease.  No diffusion\nabnormalities are detected.  The ventricles and sulci are prominent, there is\nex vacuo dilatation of the left frontal ventricular horn, consistent with\npostsurgical change.\n\nThe major vascular flow voids are present and demonstrate normal distribution.\nThe major dural venous sinuses enhance normally.\n\nThe orbits are unremarkable, the paranasal sinuses, middle ear cavities and\nmastoid air cells are clear.",
            "output": "1. The patient is status post left frontal craniotomy and resection of a left\nfrontal parafalcine meningioma, producing ex vacuo dilatation of the left\nfrontal ventricular horn.\n\n2.  Gyriform pattern of intrinsic T1 high-signal intensity in the cortex of\nthe left frontal lobe, likely consistent with cortical pseudo-laminar\nnecrosis.\n\n3.  Mild pattern of enhancement surrounding the surgical cavity, with no frank\nevidence of enhancement to indicate or suggest residual or recurrent\nmeningioma.\n\n4 FLAIR hyperintensity signal surrounding the surgical cavity in the left\nfrontal lobe, extending towards the genu of the corpus callosum, likely\nconsistent with posttreatment changes.\n\n5.  Punctate areas of FLAIR high-signal intensity in the subcortical white\nmatter are nonspecific and may reflect changes due to chronic small vessel\ndisease."
        },
        {
            "input": "Evaluation is mildly limited by motion.  Corresponding to findings on prior\nhead CT, a left frontal extra-axial parafalcine mass measures approximately\n5.7 x 4.6 cm demonstrating heterogeneous hyperintense signal on T2 weighted\nimages with area of focal cystic change anteriorly and marked fairly uniform\nhyperenhancement after contrast administration.  This abuts the falx with\nsuggestion of a dural tail (series 9, image 15; series 10, image 10).  No\nadditional lesions identified there is marked surrounding vasogenic edema\nwhich extends posteriorly to the middle of occipital horn left lateral\nventricle.  There is marked mass effect on the frontal horns, subfalcine\nherniation, and approximately 1.3 cm of rightward midline shift.  Basal\ncisterns remain patent.  The lesion abuts the anterior superior sagittal\nsinus, without definitive invasion.  No evidence of intracranial hemorrhage or\ninfarction.",
            "output": "1. 5.7 cm left frontal parafalcine mass suggestive of a meningioma.\n2. Marked surrounding edema and mass effect on the frontal horns of the\nlateral ventricles with subfalcine herniation and approximately 1.3 cm of\nrightward midline shift.  Patent basal cisterns.\n3. No evidence of infarct or intracranial hemorrhage."
        },
        {
            "input": "Study is degraded by motion.\n\nThere are postsurgical changes from left frontal craniotomy and resection of\nleft frontal parafalcine meningioma.  Nonspecific slowed diffusion is noted\nthroughout the left frontal lobe adjacent to the surgical bed.  Evolving blood\nproducts are noted along the falx in the surgical bed and along the lateral\nsurgical tract in the left frontal lobe.  Susceptibility artifact within the\nsurgical bed likely can be attributed to a combination of blood products and\npneumocephalus.  Minimal linear enhancement is seen along the resection bed\n(see 3, ___.\n\nThere is extensive left frontal lobe vasogenic edema, not substantially\nchanged from prior.  There is grossly stable rightward midline shift measuring\napproximately 6 mm, with rightward subfalcine herniation.\n\nThe ventricles and sulci are grossly stable in caliber and configuration. \nMinimal layering intraventricular hemorrhage is again seen within the left and\nright lateral ventricle occipital horns.",
            "output": "1. Study is degraded by motion.\n2. Postsurgical changes related to interval left parafalcine meningioma\nresection as described.\n3. Minimal nonspecific enhancement along resection bed.  While finding may\nrepresent postoperative change, residual tumor is not excluded on the basis of\nthis examination.  Recommend attention on follow-up imaging.\n4. Grossly stable left frontal probable vasogenic edema and approximately 6 mm\nleft to right midline shift.\n\nRECOMMENDATION(S):  Minimal nonspecific enhancement along resection bed. While\nfinding may represent postoperative change, residual tumor is not excluded on\nthe basis of this examination. Recommend attention on follow-up imaging."
        },
        {
            "input": "There is a left cerebellar early subacute hematoma again seen which is similar\nin size to most recent prior study measuring approximately 2.5 x 1.9 cm. \nThere is minimal surrounding T2/FLAIR signal hyperintensity and mild mass\neffect on the left dorsal aspect of the fourth ventricle. There is no\nhydrocephalus. There is no significant enhancement on post-contrast images.\nThere are no new regions of hemorrhage.\n\nThe ventricles and sulci are normal in caliber and configuration.  There is no\nevidence of acute infarction. There is no extra-axial collection. There is no\nshift of midline. There is T2/FLAIR signal hyperintensity in the\nperiventricular, deep, and subcortical white matter which is nonspecific but\nlikely on the basis of chronic small vessel ischemic disease.  There are small\nlacunar infarcts in the left aspect of the corpus callosum and periventricular\nwhite matter in the left frontal lobe. There is no abnormal enhancement after\ncontrast administration.  Vascular flow voids are preserved. The orbits are\nunremarkable. There is mild mucosal thickening within the ethmoid and\nmaxillary sinuses. There is mucous retention cyst in the right maxillary\nsinus. The mastoid air cells are clear.",
            "output": "1. No significant interval change in early subacute left cerebellar hematoma.\nNo significant enhancement is seen.  No new regions of hemorrhage are\nidentified. Followup to resolution is recommended.\n\n2.  T2/FLAIR signal hyperintensity in the periventricular, deep, and\nsubcortical white matter which is nonspecific but likely on the basis of\nchronic small vessel ischemic disease."
        },
        {
            "input": "There is continued interval evolution of the left cerebellar hematoma, with\nsignificant decrease in the size of the hematoma; only a small focus of\naltered signal intensity noted in the medial aspect of the left cerebellar\nhemisphere, related to subacute -chronic blood products with associated\nnegative susceptibility. On the postcontrast images, there is no significant\nabnormal enhancement noted within this focus. A small normal-appearing venous\ntributary is  noted medially.\nOn the gradient echo sequence, a few small scattered foci of negative\nsusceptibility are noted in the left caudate head and left thalamus; a\npossible small focus each in the left sub insular location and right temporal\nlobe series 15, image 11 and 12 versus end on appearance of vessel.\n\nNo acute infarct, new suspicious focus of intracranial hemorrhage, mass\neffect, shift of normally midline structures or hydrocephalus.\nThere are multiple small T2 FLAIR hyperintense foci in the cerebral white\nmatter in the frontal and parietal lobes, nonspecific in appearance.\nThe ventricles, extra-axial CSF spaces, cerebral sulci and cerebellar folia\nare normal.\nThe major intracranial arterial flow voids are noted.\nVenous sinuses are unremarkable\nSella, pineal gland, craniocervical junction regions are unremarkable.\n\nThe imaged paranasal sinuses and the mastoid air cells are grossly clear.\nThe imaged orbits are unremarkable.\nA small retention cyst in the right maxillary sinus.\nBone marrow signal is unremarkable.\nMild degenerative changes are noted in the upper cervical spine included.",
            "output": "1.  Continued interval evolution of the left cerebellar hematoma. Only a small\nresidual focus of altered signal intensity noted without significant abnormal\nenhancement; however, a small slow flow vascular malformation such as\ncavernoma, cannot be completely excluded. Continued followup as needed.\n2.  A few small scattered foci of negative susceptibility related to micro\nhemorrhages as described above, can relate to hypertension, early amyloid\nangiopathy, etc.  Corelate for risk factors.\nOther details as above."
        },
        {
            "input": "Slow diffusion of the left frontal lobe, including the insula, basal ganglia\nand anterior left temporal lobe, as well as smaller regions of the left pre\nand postcentral gyrus corresponds to known left MCA territory infarct. \nAssociated gradient echo susceptibility, corresponds to known hemorrhagic\ntransformation with mild associated subarachnoid hemorrhage along the\nconvexity.  There is diffusion-weighted hyperintense signal of the left\noccipital lobe without evidence of associated ADC hypointensity.  There is\ngradient echo susceptibility in this region and the finding may represent a\ncombination of subacute infarct and subarachnoid hemorrhage.  Allowing for\ndifferences in technique, there is no evidence of superimposed new infarct.\n\nSuperimposed confluent periventricular and subcortical T2/FLAIR white matter\nhyperintensities are nonspecific, but compatible with chronic microangiopathy\nin a patient of this age.  Allowing for mild left ventricular sulcal\neffacement secondary to mass effect from the left MCA territory infarct, the\nsulci, ventricles cisterns are within expected limits for the degree of\npatient's age related global cerebral volume loss.  The major intracranial\nflow voids are preserved.  There is near complete opacification of the\nsphenoid sinus.  Atelectasis and mucosal thickening of the left maxillary\nsinus is identified.  The orbits are unremarkable, noting right lens\nreplacement.  The mastoid air cells demonstrate mild fluid signal at the tips.",
            "output": "1. Left frontal lobe infarct with hemorrhagic transformation is essentially\nunchanged in size and configuration from prior CT examination, allowing for\ntechnical differences.  Left frontal convexity subarachnoid hemorrhages also\nre-identified.\n2. Left occipital likely subacute infarct with superimposed subarachnoid\nhemorrhage is re-identified.\n3. No superimposed acute hemorrhage or infarct since prior exam.\n4. No change in ventricular configuration."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.\n\n The major intracranial vascular flow voids are maintained.  The paranasal\nsinuses, mastoid air cells and orbits are normal.",
            "output": "1. No acute intracranial abnormality.\n2. No abnormality identified to account for the patient's headaches."
        },
        {
            "input": "There are multiple-several small foci of subcortical and periventricular\nT2/FLAIR signal hyperintensity, in the frontal and the parietal lobes of both\ncerebral hemispheres without abnormal enhancement or slow diffusion.  No focal\nlesions are noted in the corpus callosum or brainstem on the FLAIR sequence.\nThese are greater than expected for age, and can be seen with chronic small\nvessel ischemia, vasculitis, demyelinating disease, prior infectious or\ninflammatory insult, chronic headaches, or autoimmune disorders.\nThe brain parenchymal volume is within normal limits.\n There is no evident of acute infarct based on diffusion-weighted imaging.\nThere is no abnormal brain parenchymal or leptomeningeal enhancement.\nThere is no evidence of acute hemorrhage or mass effect.\nThe ventricles and basal cisterns appear normal.\n\nThere are normal vascular flow voids.\nThe orbits and left mastoid air cells appear normal.\nThere is mild bilateral maxillary and ethmoid sinus mucosal thickening.\nVery minimal fluid in the right mastoid air cells.\nMultiple prominent bilateral cervical lymph nodes are seen, incompletely\nassessed.",
            "output": "1. Multiple-several small foci of subcortical and periventricular T2/FLAIR\nsignal hyperintensity, in the frontal and the parietal lobes of both cerebral\nhemispheres without abnormal enhancement or slow diffusion, greater than\nexpected for age,  and can be seen with chronic small vessel ischemia,\nvasculitis, demyelinating disease, prior infectious or inflammatory insult,\nchronic migraine headaches, or autoimmune disorders.  Correlate clinically and\nwith labs and consider a close followup as needed to assess for any interval\nchange.\n2. No evidence of acute hemorrhage, mass effect, or acute infarct.\n\nCOMPARISON:\nCTA head/ neck ___ and outside hospital CT head ___."
        },
        {
            "input": "There is no acute infarct identified. Mild to moderate brain atrophy seen.\nSeveral hyperintensities in the white matter indicate moderate changes of\nsmall vessel disease.  There is no mass effect midline shift or hydrocephalus\nseen. The suprasellar and craniocervical regions are unremarkable. Vascular\nflow voids are maintained. No microhemorrhages are identified.",
            "output": "Moderate small vessel disease and mild to moderate brain atrophy. No acute\ninfarcts mass effect or hydrocephalus."
        },
        {
            "input": "There are multiple enhancing metastases within the supratentorial and\ninfratentorial brain. The largest metastasis is a 11 mm right cerebellar\nenhancing mass that demonstrates slowed diffusion (best seen on the diffusion\nseries 502, image 6 and post-contrast series 3L, image 6). The next largest\nmetastases are as follows: a 7 mm enhancing metastasis in the right frontal\nlobe white matter that demonstrates slowed diffusion (series 3L, image 14) and\na 5 mm enhancing metastasis in the left occipital lobe white matter that also\ndemonstrates slowed diffusion (series 3L, image 11). There is a 3 mm enhancing\nmetastasis in the peripheral right frontal lobe subcortical white matter that\nmay be near the motor strip (series 3L, image 18). There is no hemorrhage or\nsignificant edema associated with any of these metastases. No metastases are\nidentified within the brainstem. There is no midline shift. Ventricles, sulci,\nand cisterns are age-appropriate. These metastases are unchanged from recent\nMRI on ___.\n\nMajor intravascular flow voids are preserved. There is normal enhancement of\nthe major intracranial arteries and dural venous sinuses following contrast\nadministration.\n\nThere is an approximately 2.3 cm enhancing lesion of the right frontal bone,\nconsistent with an osseous metastasis (series 401b image 96). The paranasal\nsinuses and mastoid air cells are clear. The orbits are normal.",
            "output": "1.  Multiple enhancing metastases in the cerebrum and cerebellum, all\nunchanged from recent MRI on ___. The largest metastasis is a 11\nmm right cerebellar enhancing mass.  Also of particular clinical significance\ngiven the history of left arm weakness is a 3 mm enhancing metastasis in the\nright frontal lobe near the arm area of the motor strip (series 3L, image 11).\nNo hemorrhage or significant edema associated with any metastases.\n2.  Right frontal bone 2.3 cm osseous metastasis.\n3.  Slow diffusion at the site of presumed metastasis could not be verified on\nADC due to small size but the appearance is more likely suggestive of\nmetastasis than small subacute infarcts."
        },
        {
            "input": "Previously seen multiple supra and infratentorial regions are considerably\ndecreased in size and are not apparent. There are no new enhancing lesions\nseen. No new areas of brain edema identified. There is no mass effect midline\nshift or hydrocephalus. No acute infarcts seen. No evidence of chronic micro\nhemorrhages. Developmental venous anomaly seen in the right posterior temporal\nregion.",
            "output": "Considerable resolution of previously seen enhancing lesion. None of the\nlesions are not apparent on the current study.  No new lesions are seen."
        },
        {
            "input": "Enhancing lesions seen on the MRI of ___ are no longer visible. \nHowever, there are several FLAIR hyperintensity seen in the centrum semiovale\nbilaterally best visualized on series 15 image 17 image ___ since the\nprevious MRI examination and demonstrates subtle enhancement following\ngadolinium administration, series 16, image 17. Although the enhancement is\nsubtle, the appearance of new FLAIR lesions at the site is suspicious for new\nmetastatic lesions.  There is no mass effect midline shift or hydrocephalus.",
            "output": "Several new small signal abnormalities ( <3-mm) on FLAIR images in the centrum\nsemi ovale of both cerebral hemispheres with subtle enhancement suspicious for\nnew metastatic lesions.\n\nNOTIFICATION:  Critical communication dashboard."
        },
        {
            "input": "There are scattered enhancing lesions in the supratentorial brain, some of\nwhich are new, concerning for progression of metastatic disease.  A new 5 mm\nenhancing lesion is seen in the in the right anterior temporal lobe (900:24). \nScattered enhancing foci measuring up to 4 mm in the bilateral subependymal\nregions are also new (900: 55, 900:62, 10:16).  The biggest cluster is seen\nadjacent to the occipital horn of the right lateral ventricle. The previously\nnoted T2/FLAIR hyperintensities in the bilateral centrum semiovale with subtle\nenhancement are more conspicuous on today's study (10:17). There are several\nnon-enhancing lesions in the right frontal lobe which demonstrate increased\nsignal on diffusion-weighted images (502:18, 502:21) but due to their small\nsize, are difficult to evaluate on ADC.\n\nThere is no evidence of acute hemorrhage or mass affect. The ventricles are\nunchanged in size and configuration. The dural venous sinuses are patent.\nMajor intracranial vascular flow voids are preserved. The paranasal sinuses\nand mastoid air cells are clear. The globes are unremarkable.",
            "output": "1.  New enhancing lesions in the supratentorial brain concerning for\nprogression of metastatic disease as described above.\n\n2.  Previously seen T2/FLAIR hyperintensity in the bilateral centrum semiovale\nwith subtle enhancement are more conspicuous on today's study and remain\nconcerning for metastatic disease.\n\n3.  Punctate foci of increased signal on diffusion-weighted images in the\nright frontal lobe without correlation on other sequences are too small to\ncharacterize and non-specific.  Attention on follow-up imaging is recommended."
        },
        {
            "input": "There is interval decrease in the number and size of previously seen scattered\nsub- 5 mm enhancing lesions in the supratentorial brain, suggestive of\ntreatment response and metastatic disease from patient's known lung cancer. \nRepresentative lesions include:\n- previously seen 5 mm enhancing lesion in the right temporal lobe now\nmeasures 3 mm on image ___.\n- previously seen scattered foci of sub- 5 mm lesions adjacent to the\noccipital horn of right lateral ventricle are no longer better visualized on\ntoday's study.\n- previously-seen enhancing 4 mm lesion adjacent to the anterior horn of the\nleft lateral ventricle now measures 3 mm on image 84/___ B.  No new lesions\nare seen.\n\nThere is interval increase in size and number of T2/FLAIR/DWI hyperintensity\nwithin bilateral centrum semiovale and periventricular region which do not\ndemonstrate enhancement on postcontrast images, nonspecific, could be\nsecondary to a combination of post treatment changes and small vessel ischemic\nchanges.\n\nNo evidence of acute hemorrhage or mass effect.  The ventricles are normal in\nsize and configuration.  The dural venous sinuses are patent.  The major\nvascular  flow voids are preserved.\n\nThe orbits are unremarkable.\n\nMild mucosal thickening in bilateral ethmoid air cells.  The remaining\nvisualized paranasal sinuses and mastoid air cells are clear.",
            "output": "1. Interval decrease in the size and number of previously seen enhancing sub 5\nmm lesions in bilateral supratentorial brain, likely in keeping with treatment\nresponse to metastasis.  No new enhancing lesions are seen.\n2. Interval increase in the size and number of scattered foci of nonenhancing\nT2/FLAIR hyperintensity, nonspecific, could be secondary to a combination of\npost treatment changes and small vessel ischemic changes.\nRECOMMENDATION(S):"
        },
        {
            "input": "There is a persistent and unchanged enhancing right pericallosal lesion\nmeasuring 2 mm (10:15).  The lesion is not causing mass effect or vasogenic\nedema.  There are periventricular and deep cortical T2/FLAIR hyperintensities,\nunchanged, nonenhancing.  These lesions are nonspecific and may represent the\nsequelae of chronic small vessel disease.\n\nThere are no areas of hemorrhage. Decreased GRE signal in the bilateral basal\nganglia is due to calcifications as seen on prior head CT.\n\nThe ventricles and sulci are not significantly changed from ___. \nThere is no shift of normally midline structures.  The globes, paranasal\nsinuses, mastoid air cells are unremarkable.",
            "output": "1. Stable right pericallosal 2 mm enhancing lesion.  No mass effect or edema.\n2. No new enhancing lesions.\n3. Periventricular and deep white matter T2/FLAIR hyperintensities,\nnonspecific, may represent the sequelae of chronic small vessel disease.\n4. No infarction or hemorrhage."
        },
        {
            "input": "The sagittal T1 weighted images are severely degraded by motion artifact.\n\nModerate prominence of the ventricles and sulci is unchanged and consistent\nwith global atrophy.  There is no evidence of hemorrhage, edema, mass, mass\neffect, or acute infarction.  Confluent and scattered punctate periventricular\nand subcortical white matter FLAIR hyperintensities are nonspecific but likely\nsequelae of chronic microangiopathy in a patient this age.  A cluster of small\nT2 hyperintense foci in the basal ganglia bilaterally following the signal\nintensity of CSF on all sequences likely represent prominent perivascular\nspaces.  Lack of flow related signal of the left V3 segment and portions of\nthe left V4 segment corresponding to findings on CTA of ___.  The\nremainder of the principal intracranial vascular flow voids are preserved. \nThere is fluid signal in a few left mastoid air cells.  The orbits are\nunremarkable.",
            "output": "1.  No evidence of hemorrhage, edema, mass, mass effect, or acute infarction.\n\n2.  Moderate global atrophy and chronic white matter changes likely\nrepresenting small vessel ischemic disease."
        },
        {
            "input": "MRI brain:  There are foci of mild slow diffusion within the right posterior\nlimb internal capsule an just posterior laterally within the periventricular\nwhite matter (08:14), with correlate FLAIR hyperintensity, consistent with\nsites of subacute infarction.  There is no evidence of associated hemorrhage.\n\nThere is background confluent periventricular and subcortical white matter\nFLAIR hyperintensity in addition to central and dorsal pontine FLAIR\nhyperintensity, likely representing sequela of advanced chronic\nmicroangiopathy.  There is linear gradient echo hypointensity in the right\nmidline central mid upper pons, consistent with site of remote hemorrhage\n(18:8).  There is prominence of the ventricles and cortical sulci consistent\nwith a moderate degree of volume loss.  The vascular flow voids are preserved.\nThe extra-axial spaces are unremarkable.\n\nThe bilateral native lenses are absent, otherwise the orbits are unremarkable.\nThe soft tissues and calvarium are unremarkable.  There is no abnormal fluid\nsignal within the paranasal sinuses, mastoid air cells, or middle ears.\n\nMRA head:  The bilateral intracranial internal carotid arteries are patent. \nThere is a 2 mm posterior medially projecting outpouching from the left\nanterior cavernous segment internal carotid artery (13:112).  There is a 2 mm\nsuperiorly projecting outpouching from the left communicating segment internal\ncarotid artery (13:129).  The anterior and bilateral posterior communicating\narteries are not definitively seen.  There is mild right dominance of the\nvertebral arteries.  There is a mildly beaded appearance of the basilar artery\nand V4 segment vertebral arteries, likely reflecting intracranial\natherosclerosis.  There is low signal within the left V3 segment vertebral\nartery with slightly diminished signal at the corresponding right V3 segment\nvertebral artery.  There is abrupt reconstitution of the V4 segment and\npreserved flow void on the T2 sequence, which favors artifact rather then\nocclusion.\n\nMRA neck:  There is artifact at the thoracic inlet which obscures diagnostic\nvisualization of the aortic arch and great vessel origins (21:165).  The right\ninterna carotid artery is patent without stenosis by NASCET criteria.  There\nis atheroma at the left carotid bulb with proximal ulceration causing ___\nstenosis by NASCET criteria (21:82).  There is a mildly beaded appearance of\nthe left vertebral artery, likely reflecting atherosclerosis.  There is absent\nflow enhancement within the left V3 segment vertebral artery with abrupt\npreserved flow proximally within V2 and cranially within V4.  Additionally\nthere is preserved flow void on the axial T2 sequence, which favors artifact\nrather then occlusion.  The right vertebral artery is patent.",
            "output": "1. Small subacute infarcts at the posterior limb right internal capsule and\nwithin the right periatrial white matter.  No associated hemorrhage.\n2. Extensive background sequela of chronic advanced microangiopathy.\n3. Small linear chronic blood products at the right midline pons.\n4. 2 mm posterior and medially projecting outpouching from the left cavernous\nsegment internal carotid artery, which may represent a small aneurysm versus\ninfundibulum at a nonvisualized vessel origin.\n5. 2 mm superiorly projecting outpouching from the left communicating segment\ninternal carotid artery, likely representing a small aneurysm.\n6. Mild beaded stenosis of the basilar and bilateral vertebral arteries,\nlikely reflecting atherosclerosis.\n7. Atheroma at the left carotid bulb with proximal ulceration causing ___\nstenosis by NASCET criteria\n8. Artifact at the thoracic inlet which obscures the aortic arch and origin of\nthe great vessels.\n9. Absent flow enhancement within the left V3 segment vertebral artery with\nabrupt preserved flow proximally within V2 and cranially within the V4\nsegments, in addition to preserved flow void on the spin echo sequence, which\nfavors artifact rather than occlusion.  This may be a consequence of slow flow\nor, potentially related to vertebral artery origin stenoses not demonstrated\non this examination.\n10. Given the artifact at the thoracic inlet and the left V3 segment vertebral\nartery, consider CTA or contrast MRA imaging to further characterize these\nareas.  characterized with a dedicated CTA.\n\nRECOMMENDATION(S):  Given the artifact at the thoracic inlet and the left V3\nsegment vertebral artery, consider CTA or contrast MRA imaging to further\ncharacterize these areas.  characterized with a dedicated CTA."
        },
        {
            "input": "There is redemonstation of two foci of slow diffusion with corresponding T2/\nFLAIR hyperintensity in the posterior limb of the right internal capsule and\nposterolaterally within the periventricular white matter, consistent with\nknown sites of subacute ischemia (series 302, image 14; series 300, image 14;\nseries 6, image 12 and series 7, image 12).  Confluent T2/FLAIR\nhyperintensities involving the subcortical, periventricular and deep white\nmatter as well as the central and dorsal pons are stable and likely the\nsequelae of chronic small vessel ischemic disease.  A focus of gradient echo\nhypointensity in the right mid pons is likely related to prior hemorrhage.\n\nThere is no evidence of new hemorrhage, edema, masses, mass effect, midline\nshift or acute infarction.  There is prominence of the ventricles and sulci\nsuggestive involutional changes. The vascular flow voids are preserved. \nVisualized paranasal sinuses and mastoid air cells are clear.  The orbits are\nunremarkable.",
            "output": "1. No acute intracranial abnormality.\n2. Stable small subacute infarcts involving the posterior limb of the right\ninternal capsule and right periventricular white matter.\n3. Stable white matter changes, likely secondary to the sequela of chronic\nsmall vessel ischemic disease.\n4. Stable chronic blood products in the right mid pons."
        },
        {
            "input": "There is a focus of slow diffusionin the right parietal white matter (series\n300: Image 23 and series 3 are 2:  Image 23), compatible with acute\ninfarction.  There is no evidence of hemorrhage, edema, masses, mass effect,\nor midline shift There is prominence of the ventricles and sulci in an\natrophic pattern.  Ill-defined periventricular subcortical white matter FLAIR\nhyperintensities likely represent the chronic sequela of small-vessel ischemic\ndisease.  The basilar cisterns appear patent.  The major intracranial flow\nvoids are preserved.  The dural venous sinuses appear patent.\n\nA punctate focus of blooming artifact is seen in the left cerebellar folia,\nlikely representing an old punctate microhemorrhage.  Mild mucosal thickening\nis seen in the bilateral ethmoid air cells and bilateral maxillary sinuses,\nleft greater than right.  Otherwise, the remaining visualized paranasal\nsinuses, mastoid air cells, and middle ear cavities appear clear.  The orbits\nare unremarkable.",
            "output": "1. Focus of subacute infarct is noted in the right frontoparietal region.\n2. Age related involutional changes and chronic sequela of small-vessel\nischemic disease.\n3. Paranasal sinus disease, as described in detail above."
        },
        {
            "input": "1 cm late acute right thalamic infarct (series 6, image 16) is identified.  No\nevidence of hemorrhagic transformation.  There are very mild periventricular\nand subcortical scattered T2/FLAIR white matter hyperintensities, nonspecific,\nbut compatible with chronic microangiopathy in a patient this age.  The sulci,\nventricles and cisterns are within expected limits for the degree of mild\nsenescent related global cerebral volume loss.\n\nThere is a well-circumscribed right parietal 4.1 by 1.9 cm (TRV, AP)\nextra-axial dural-based lesion compatible with a calcified meningioma,\nexerting minimal mass effect on the underlying brain parenchyma.  No evidence\nof associated parenchymal FLAIR hyperintense edema pattern.  No other\nintracranial mass lesions are identified.\n\nThe major intracranial flow voids are preserved.  The dural venous sinuses are\npatent.  The paranasal sinuses are essentially clear.  The orbits are\nunremarkable.  The mastoid air cells appear clear.  No suspicious osseous\nsignal.",
            "output": "1. Late acute right thalamic infarct without evidence of hemorrhagic\ntransformation.\n2. Right parietal 4.1 cm calcified meningioma, with mild mass effect on the\nunderlying brain parenchyma.  No evidence of associated parenchymal FLAIR\nhyperintense edema pattern.\n3. Additional findings described above.\n\nNOTIFICATION:  The findings were discussed with ___, NP by ___\n___, M.D. on the telephone on ___ at 8:04 am, 5 minutes after\ndiscovery of the findings."
        },
        {
            "input": "There is a 6-7 mm area of slow diffusion in the left cerebellum without\ndefinite hypointensity on the corresponding ADC map.  This may reflect a\nsubacute infarction.  There is a corresponding FLAIR signal abnormality.\n\nThere is a punctate focus of hypointensity on the gradient recalled echo\nimages in the left parietal lobe white matter (in 15 of series 7).  This may\nreflect a tiny focus of microhemorrhage.  Otherwise, there is no evidence of\nhemorrhage, edema, or masses.\n\nMild prominence of the ventricles and sulci is suggestive of involutional\nchanges.  No mass effect or midline shift.  Multiple scattered T2 and FLAIR\nhyperintense foci in the periventricular and subcortical white matter are\nnonspecific, but may reflect chronic small vessel ischemic changes.\n\nMinimal mucosal thickening of the ethmoid sinuses.  Moderate right mastoid air\ncell effusion.  Unremarkable intraorbital contents.",
            "output": "1. Subacute infarct in the left cerebellum.\n2. Solitary left parietal microbleed.  No evidence of new hemorrhage.\n3. Mild cerebral atrophy and chronic small vessel ischemic disease."
        },
        {
            "input": "There are postoperative changes in the left frontal lobe with stable mild\ndural thickening and gliosis. FLAIR hyperintensity is slightly increased and\nrecommend attention on followup imaging.  Blood products is seen in the\noperative bed.  No evidence for meningioma recurrence.\n\nThere is no intracranial mass, mass effect, or midline shift.There is no\npathologic intracranial enhancement.  Ventricles and sulci are\nage-appropriate.  There is no hydrocephalus or acute ischemia. Intracranial\nflow voids are maintained. Visualized paranasal sinuses and mastoid air cells\nare clear.  Bilateral maxillary sinus retention cysts are noted.",
            "output": "No evidence of meningioma recurrence. Slight increase in FLAIR hyperintensity.\nThis could represent progressive postoperative gliosis but recommend attention\non followup imaging."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, mass effect, midline shift or\ninfarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There are few periventricular and subcortical T2 and FLAIR\nhyperintensities are noted.  There is no abnormal intracranial enhancement\nafter contrast administration.  The major vascular flow voids are preserved.\n\nThere is a 1.8 cm TR x 1.1 cm AP spiculated mass in the right suboccipital\nsoft tissues.  A 1.6 cm AP x 1.3 cm TR soft tissue mass in the superior left\nparotid gland and a 3 cm AP x 1.1 cm TR ill-defined postauricular mass are\nseen.   There is a 0.6 cm enhancing lesion in the posterior left parotid gland\nand a 1.7 cm TR x 1.6 cm AP mass in the inferior left parotid gland. There is\na partially visualized 1.7 cm AP x 2.1 cm TR right tonsillar mass.  Multiple\npartially visualized enlarged right level IIa lymph nodes are seen, with the\nconglomerate of lymph nodes measuring 2.9 cm AP x 1.8 cm TR.  In addition,\nasymmetric thickening and contrast enhancement of the superior left temporalis\nmuscle is seen.\n\nThe left lacrimal gland is enlarged, enhancing and demonstrates restricted\ndiffusion, compatible with lymphomatous infiltration.\n\nThe pituitary gland demonstrates a convex superior margin, slightly greater\nthan would be expected for the patient's age measuring approximately 7 mm in\nSI dimension.  No abnormal nodularity is identified however close attention on\nfollowup examination is recommended.\n\nThere is partial opacification of the right mastoid air cells.  The right\norbit is unremarkable.  Minimal mucosal thickening in the ethmoid and left\nfrontal sinus is seen.  A T2 hypo intense lesion is noted in the left frontal\nsinus, consistent with an osteoma as seen on prior CT.  An additional T2 hypo\nintense lesion is noted in the lateral left frontal calvarium, series 8, image\n11, which is sclerotic on the prior CT and likely also represents an osteoma\nversus bone island.\n\nPartially visualized degenerative changes are noted in the upper cervical\nspine.",
            "output": "1. No definite evidence for intracranial metastatic disease.\n2. The left lacrimal gland is enlarged, enhancing and demonstrates slow\ndiffusion, concerning for lymphomatous involvement.\n3. Multiple left parotid, right level IIa, left postauricular, right sub\noccipital and right tonsillar masses, as described above, likely secondary to\nlymphadenopathy from provided history of lymphoma.  Recommend a dedicated CT\nof the neck for further evaluation.\n4. Asymmetric thickening and enhancement in the superior left temporalis\nmuscle, likely secondary to lymphomatous involvement.\n5. The pituitary gland measures approximately 7 mm in SI dimension with convex\nsuperior margin, slightly larger than would be expected for the patient's age.\nAlthough there is no focal enhancing nodularity associated with this\nenlargement, close attention on followup examination is recommended."
        },
        {
            "input": "There are two nonspecific foci of T2/FLAIR hyperintensity, anteriorly in the\nleft external capsule and in the white matter adjacent to the head of the\nright caudate nucleus.  No periventricular or posterior fossa lesions are\nidentified.  There is no evidence of demyelination.  There is no evidence of\nhemorrhage, edema, masses, mass effect, midline shift or infarction.   The\nventricles and sulci are normal in caliber and configuration.  There is no\nabnormal enhancement after contrast administration.\n\nMild secretions are noted posteriorly in the left ethmoid air cells.  There is\na small mucous retention cyst in the right maxillary sinus.\n\nThere is prominent symmetric enlargement of the tonsillar pillars bilaterally\nand prominent level 2 nodes.  The largest node measures approximately 14 mm in\ndiameter.",
            "output": "1. There is no evidence of demyelination.\n2. Two nonspecific foci of T2/FLAIR hyperintensity, anteriorly in the left\nexternal capsule and in the white matter adjacent to the head of the right\ncaudate nucleus.  No periventricular or posterior fossa lesions are\nidentified.\n3. Prominent tonsillar pillars and level 2 lymph nodes bilaterally."
        },
        {
            "input": "Study is mildly degraded by motion.\n\nThere is no evidence of hemorrhage, edema, enhancing masses, mass effect,\nmidline shift or infarction.  Minimal asymmetry of the lateral ventricles is\nnoted, with the right lateral ventricle noted to be slightly larger than left,\nwithout definite evidence of ventriculomegaly, likely congenital.  Otherwise,\nthe ventricles and sulci are grossly preserved in caliber and configuration.\n\nThere is no abnormal enhancement after contrast administration.\n\nLeft maxillary sinus probable mucous retention cyst is noted.  Minimal\nnonspecific low-lying cerebellar tonsils with approximately 2 mm extension\ninferior to foramen magnum is noted.\n\nLimited imaging of the pituitary gland, question 3 mm hypoenhancing lesion\nversus volume averaging artifact (see 13:264).",
            "output": "1. Study is mildly degraded by motion.\n2. No acute intracranial abnormality.\n3. Within limits of study, no definite evidence of intracranial lesion or\nenhancing mass.\n4. Limited imaging of the pituitary gland, question 3 mm hypoenhancing lesion\nversus volume averaging artifact.  If concern for pituitary mass, consider\ncorrelation with endocrine function testing and dedicated pituitary MRI.\n5. Minimal nonspecific low-lying cerebellar tonsils with approximately 2 mm\nextension inferior to foramen magnum.\n6. Paranasal sinus disease , as described."
        },
        {
            "input": "The ventricles and extra-axial spaces are normal in size without midline shift\nmass effect or hydrocephalus. .  A few scattered foci of FLAIR hyperintensity\nindicate early changes of small vessel disease.  On FLAIR images the\nevaluation of posterior fossa is limited due to pulsation artifacts but these\nareas better visualized and T2 coronal images appears normal.  Following\ngadolinium administration no abnormal parenchymal vascular or meningeal\nenhancement seen.  Coronal images through the temporal lobes demonstrate no\nevidence of asymmetry or atrophy of the hippocampal formations or other medial\ntemporal lobe structures.  The vascular flow voids are maintained.  No acute\ninfarcts are seen.  Suprasellar and craniocervical regions are unremarkable. \nMild soft tissue changes are seen in ethmoid air cells and right mastoid air\ncells.",
            "output": "Except for early changes of small vessel disease, no significant abnormalities\non MRI of the brain with and without gadolinium including coronal images\nthrough the temporal lobes.  No enhancing brain lesions or focal abnormalities\nare identified."
        },
        {
            "input": "There is tiny focus of mildly increased signal on diffusion images involving\nsubcortical white matter of the left pars triangularis  series 502, image 18,,\nwith normalized ADC values, without enhancement, may represent subacute\ninfarct approximately 10 to 15-days old.  There is no evidence of hemorrhage,\nedema, masses, mass effect, midline shift.  There is mild generalized brain\nparenchymal atrophy, similar compared to prior.  There is suggestion 2.7 mm\ninferolaterally directed aneurysm arising from the right M2 MCA branch coronal\nimage 73, sagittal image 169, MRA brain without contrast recommended in\nfurther evaluation.  There are moderate chronic small vessel ischemic changes,\nmildly worsened since ___.\n\nThere are degenerative changes in the partially visualized cervical spine,\nwith probably moderate central canal narrowing at C3-C4 level, suboptimally\nevaluated.  There is submucosal retention cyst in the right maxillary sinus,\nand mild mucosal thickening remaining paranasal sinuses, without fluid. \nMastoid air cells, middle ear cavities are clear.  There is an area of\nabnormal T2 signal involving cervicomedullary junction, seen on one view only,\nhas configuration most consistent with artifact, also seen on FLAIR images\nimage 3.  Dural venous sinuses are patent.  Intracranial of vascular flow\nvoids are preserved.",
            "output": "Suggestion of subacute infarct subcortical white matter left pars\ntriangularis, 10 to 15-day-old.\nSuggestion of 2.7 mm right M2 aneurysm, MRA brain recommended.\nThere are moderate chronic small vessel ischemic changes, and generalized mild\nbrain parenchymal atrophy.\nProbably moderate central canal narrowing at C3-C4 level, partially seen.\nRemainder as above\n\nRECOMMENDATION(S):  MRA brain without contrast\n\nNOTIFICATION:  The impression and recommendation above was entered by Dr.\n___ on ___ at 14:57 into the Department of Radiology\ncritical communications system for direct communication to the referring\nprovider."
        },
        {
            "input": "There is mild irregularity of the bilateral cavernous and supraclinoid\nsegments of the internal carotid arteries, likely representing atherosclerotic\ndisease, without significant narrowing.  There is a 2 mm inferolaterally\ndirected outpouching of the cavernous segment of the right internal carotid\nartery (3:102, 306:9).  There is a 3 mm inferiorly directed outpouching at the\nright M2 bifurcation, corresponding to finding on prior MR, compatible with\naneurysm (3:113, 3 of 6:1).  The intracranial vertebral and internal carotid\narteries and their major branches otherwise appear patent without evidence of\nsignificant stenosis,occlusion,orother aneurysm formation.",
            "output": "1. 3 mm aneurysm at the right M2 bifurcation, corresponding to abnormality on\nprior MR.\n2. 2 mm inferolaterally directed outpouching of the cavernous right internal\ncarotid artery, likely reflecting an additional aneurysm versus infundibulum.\n3. Otherwise patent intracranial arterial vasculature without significant\nstenosis, or occlusion."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  There is prominence of the ventricles and sulci suggestive\ninvolutional changes.  Periventricular and subcortical white matter\nhypodensities are noted, likely the sequelae of chronic small vessel ischemic\ndisease.  There is preservation of gray-white matter differentiation.  The\nbasal cisterns remain patent.\n\nNo osseous lesion is identified.  The paranasal sinuses, middle ear cavities,\nand mastoid air cells are clear.  The bilateral orbits are unremarkable in\nappearance.  The major intracranial flow voids are preserved.",
            "output": "1. No evidence of hemorrhage or infarction.\n2. Mild global cerebral atrophy and evidence for chronic small vessel ischemic\ndisease."
        },
        {
            "input": "There is no evidence of intracranial hemorrhage, edema, masses, mass effect,\nmidline shift or infarction.  There is prominence of the ventricles and sulci\nsuggesting cortical volume loss.  No diffusion abnormalities are detected. \nThe mamillary bodies appear normal with no abnormal T2 or FLAIR hyperintensity\nto suggest Wernicke's encephalopathy.  The major vascular flow voids are\npatent and demonstrate normal distribution.  The orbits are unremarkable, the\nparanasal sinuses are clear, mild bilateral patchy mucosal thickening is noted\nin the mastoid air cells.",
            "output": "1. Involutional changes out of proportion to patient's age, with prominent\nsulci, suggesting cortical volume loss.\n2. No evidence of Wernicke's encephalopathy, although evaluation for mild\ndisease is somewhat limited without the use of intravenous contrast."
        },
        {
            "input": "There is no intra or extra-axial mass, acute hemorrhage or infarct. There are\nprominent bifrontal convexity extra-axial CSF spaces, presumably subarachnoid\nin nature as bridging veins are seen extending to the dural surface.  The\nsulci, ventricles cisterns are otherwise within expected limits for the\npatient's age.  There is no abnormal enhancement.  The major intracranial flow\nvoids are preserved.  The major intracranial flow voids are preserved.  The\nparanasal sinuses are clear.  The orbits are unremarkable.  The mastoid air\ncells are clear.\n\nThere are multiple nonenhancing cutaneous lesions demonstrating T1 and T2\nintermediate intensity signal measuring up to 9 mm of the right frontal and\nparietal vertex (series 2, image 12) and of the left occipital skull (series\n12, image 6).",
            "output": "1. No evidence of intra cranial metastatic disease.  There is no abnormal\nenhancement or signal.  No acute infarct or intracranial hemorrhage.\n2. Prominent bifrontal convexity extra-axial CSF spaces, presumably\nsubarachnoid in nature as bridging veins are seen extending to the dural\nsurface.\n3. Multiple nonenhancing subcutaneous lesions demonstrating T1 and T2\nintermediate intensity measuring up to 9 mm these presumably represent\nsebaceous cysts, however clinical correlation is recommended."
        },
        {
            "input": "There is no intra or extra-axial mass, acute hemorrhage or infarct. The sulci,\nventricles and cisterns are within expected limits for the patient's age. \nThere are scattered rounded subcortical and periventricular T2/FLAIR white\nmatter hyperintensities, which are nonspecific.  The major intracranial flow\nvoids are preserved.  There is mild mucosal thickening of the ethmoid air\ncells and a small mucous retention cyst in the left maxillary sinus.  The\norbits are unremarkable.  The mastoid air cells are clear.",
            "output": "1. No acute intracranial abnormality on noncontrast MRI head.  Specifically no\nintracranial mass, acute hemorrhage or infarct.\n2. There are scattered T2/FLAIR subcortical and periventricular white matter\nhyperintensities, nonspecific.  The differential consideration in a patient of\nthis age is broad and may be seen in the setting of chronic headache such as\nmigraine.  Sequela of prior infectious/inflammatory or traumatic etiology as\nwell as small vessel ischemic disease are also considerations.  These are not\nin a distribution typical for demyelinating process."
        },
        {
            "input": "MRA BRAIN:\nStatus post coiling of a left MCA bifurcation aneurysm with associated\nsusceptibility artifact.  There is no evidence of flow related signal or\nenhancement within the coil pack to suggest recanalization.  The right ACA A1\nsegment is hypoplastic, likely congenital.  There is a persistent fetal origin\nof the left PCA.  There is a 1-2 mm infundibulum versus small aneurysm at the\norigin of the left superior cerebellar artery.  The intracranial vertebral and\ninternal carotid arteries and their major branches appear otherwise normal.\n\nOTHER:\nThere is evidence of a partially visualized right frontal approach\nventriculostomy with the tip of the catheter terminating anterior to the third\nventricle. The ventricles and sulci are grossly preserved in caliber and\nconfiguration, decreased compared to prior head neck CTA exam.  There is no\ndefinite abnormal enhancement after contrast administration.",
            "output": "1. Status post coiling of a left MCA bifurcation aneurysm without evidence of\nflow related signal or enhancement within the coil pack to suggest\nrecanalization.\n2. A 1-2 mm infundibulum versus small aneurysm at the origin of the left\nsuperior cerebellar artery not definitely seen on ___ prior.\n3. Partially visualized ventricles and right frontal approach ventriculostomy\ncatheter with interval decrease of ventricle size compared to ___\nhead and neck CTA.  If clinically indicated, consider dedicated noncontrast\nhead CT for further evaluation."
        },
        {
            "input": "There is artifact over the left vertex, which is present on all sequences,\npossibly related to an external device.  This mildly limits the examination.\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.\n\nBilateral hippocampal formations and mammillary bodies are preserved in signal\nand configuration. There is no disproportionate medial temporal atrophy. There\nis no focal lobar encephalomalacia. There are no focal cortical dysplasias or\ngray matter heterotopia noted.\n\nTrace mucosal thickening is present in the anterior ethmoid air cells. \nMastoid air cells and middle ear cavities are clear.  Orbits are unremarkable.",
            "output": "Normal brain MRI."
        },
        {
            "input": "There is a 5.2 x 2.7 cm intraparenchymal hematoma in the right frontal lobe\ninvolving the superior frontal gyrus, with surrounding white matter edema. \nMass-effect is mild and includes right frontal cerebral sulcal effacement.  No\nventricular entrapment.\n\nThere is a small left-sided subdural hematoma measuring up to 0.7 cm in\nthickness along the left convexity unchanged in size and extent compared with\nprior CT, layering along the left tentorial leaflet and posterior falx.\n\nThere is a 4.0 x 2.8 cm left temporal intraparenchymal hematoma with\nsurrounding white matter edema.  Minimal mass effect includes left temporal\nsulcal effacement and minimal effacement of the temporal horn of left lateral\nventricle without entrapment.  No herniation.\n\nThere is small volume intraventricular hemorrhage layering in the fourth\nventricle as well as in the occipital horns of the lateral ventricles.  There\nare also scattered foci of biparietal subarachnoid hemorrhage, small volume\n(see series 10 and 11 images ___.\n\nNo midline shift herniation.  Outside of the areas of hematoma, there is no\nevidence of parenchymal restricted diffusion to suggest acute infarct.  There\nis no focal or nodular enhancement within the left temporal or the right\nfrontal hematomas to suggest underlying mass.  No other abnormal enhancement\nelsewhere.\n\nThere are a few foci of of supratentorial chronic microhemorrhage, for example\nin the right parietal white matter (10:16), and in the right temporal lobe\nwhite matter (10:10).\n\n The ventricles and sulci are prominent, compatible with global parenchymal\nvolume loss.  Bilateral periventricular and deep white matter foci of T2/FLAIR\nsignal hyperintensity are nonspecific but compatible with mild-to-moderate\nchanges of chronic white matter microangiopathy.\n\nAside from bilateral lens extraction, the globes and orbits are within normal\nlimits.  Major intracranial vascular flow voids are preserved.  Major dural\nvenous sinuses are patent.  There is layering fluid in the sphenoid sinus. \nThere is trace layering fluid in the right maxillary sinus.  Remaining\nvisualized paranasal sinuses and the mastoids appear clear.",
            "output": "1. 5.2 cm right frontal lobe and 4.0 cm left temporal lobe intraparenchymal\nhematomas with surrounding edema and minimal mass effect.  No evidence of\nunderlying mass.\n2. 0.7 cm thick left subdural hematoma, similar.\n3. Small volume layering intraventricular hemorrhage in the lateral and fourth\nventricles.\n4. Trace bilateral foci of biparietal small volume subarachnoid hemorrhage.\n5. No evidence of acute infarction.  No significant intracranial mass effect.\n6. Mild global parenchymal volume loss.  Mild-to-moderate changes of chronic\nwhite matter microangiopathy."
        },
        {
            "input": "The patient's previously noted enhancing left posterior frontal mass is again\nseen measuring 60 mm x 40 mm by 46 mm.  There is rightward midline shift of\napproximately 1 cm, unchanged compared to the prior exam.",
            "output": "1. Re-demonstrated is patient's enhancing left posterior frontal mass,\nunchanged compared to prior exam from ___."
        },
        {
            "input": "The patient is status post left frontal craniotomy with resection of the\npreviously noted high left posterior frontal extra-axial mass.  Surgical skin\nstaples overlie the craniotomy clefts.  Blood products are noted in the\nsurgical cavity.  Residual vasogenic edema involving the left frontal and\nparietal lobes appears grossly unchanged.  Apparent thickening and enhancement\nof the adjacent falx may be reactive in nature, however residual tumor cannot\nbe excluded.  There is slow diffusion surrounding the surgical cavity, likely\nsecondary to surgical manipulation.  There has been interval decrease in\nleft-to-right midline shift, previously measuring up to 1 cm, now measuring\napproximately 4 mm.  There is decreased effacement of the left lateral\nventricle and third ventricle.  The basilar cisterns remain patent.\n\nMajor arterial flow voids are grossly preserved.  The dural venous sinuses are\npatent on post-contrast MP rage images.\n\nSinus mucosal inflammatory changes and small volume mastoid effusions appear\nunchanged.",
            "output": "1. Status post left frontal craniotomy with resection of previously noted high\nleft posterior frontal extra-axial mass.  Apparent thickening and enhancement\nof the adjacent falx may be reactive in nature, however residual tumor cannot\nbe excluded.\n2. While there is persistent vasogenic edema involving the left frontal and\nparietal lobes, there is decreased mass effect with improvement in left to\nright midline shift and decreased effacement of the left lateral and third\nventricles.  The basilar cisterns remain patent."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are prominent in a mild atrophic\npattern well within the range of normal for a patient of this age.  There is\nno abnormal intracranial enhancement after contrast administration.  There is\npartial opacification of the sphenoid sinus with peripheral enhancement after\ncontrast administration.",
            "output": "1. Paranasal sinus inflammatory changes.  Otherwise normal study."
        },
        {
            "input": "MRI BRAIN:\nThere is no evidence of hemorrhage,edema,masses, mass effect, midline shift or\ninfarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.  There is minimal mucosal thickening of the anterior ethmoid\nair cells with small mucous retention cyst in the right maxillary sinus,\notherwise the paranasal sinuses and mastoid air cells are clear.  Hyperostosis\nfrontalis interna noted, otherwise no abnormal marrow signals.  Prominent\nbilateral intraparotid lymph nodes are seen.\n\nMRA BRAIN:\nThe intracranial vertebral and internal carotid arteries and their major\nbranches appear normal without evidence of stenosis,occlusion,or aneurysm\nformation.  The left vertebral artery is dominant, and the right vertebral\nartery is diminutive.  The right A1 segment is hypoplastic, normal variant.\n\nMRA NECK:\nThere is a moderate narrowing at the junction of the right cervical and\npetrous ICA (101:19) likely artifactual.  Otherwise the origin of the great\nvessels, subclavian and vertebral arteries appear normal bilaterally.  The\ncommon, internal and external carotid arteries appear normal.  There is no\nevidence of internal carotid artery stenosis by NASCET criteria.",
            "output": "1. No acute intracranial abnormality.  No evidence of an acute stroke,\nhemorrhage, or intracranial mass.\n2. Patent circle of ___ without evidence of stenosis,occlusion,or aneurysm.\n3. Limited evaluation without contrast enhanced MRI but within this\nlimitation, patent bilateral cervical carotid and vertebral arteries without\nevidence of stenosis, occlusion, or dissection."
        },
        {
            "input": "Redemonstrated is an acute/subacute infarction involving the right insula,\nright MCA territory and scattered punctate subcortical white matter foci,\nconsistent with known right frontoparietal infarct as demonstrated by\nhyperintense signal on diffusion restriction and corresponding ADC\nhypointensity (4:20).  There is mild surrounding FLAIR signal hyperintensity,\nmost consistent with cytotoxic edema.\n\nThere is no evidence of hemorrhagic transformation, or evidence of masses,\nmass effect, or midline shift.  The ventricles and sulci are prominent, likely\nrelated involutional changes. Periventricular and subcortical white matter\nT2/FLAIR hyperintensities are nonspecific but likely sequelae of chronic small\nvessel ischemic disease.\n\nThe orbits are unremarkable.  There is mild mucosal thickening of the ethmoid\nair cells.  Otherwise, the paranasal sinuses are clear.  Major intravascular\nflow voids are preserved.",
            "output": "1. Re-identified is an acute/subacute infarction involving the right\nfrontoparietal region with mild surrounding cytotoxic edema.\n2. There is no evidence of hemorrhagic transformation."
        },
        {
            "input": "There is no acute infarct, hemorrhage, intracranial mass, mass effect, or\nshift of normally midline structures.  The ventricles and sulci are prominent,\nsuggestive of age-related involutional changes.  Numerous scattered\nperiventricular and subcortical white matter T2 FLAIR hyperintensities are\nnonspecific, but likely represent sequela of chronic small vessel ischemic\ndisease.  Additional bilateral T2, FLAIR and DWI  hyperintensities in the\ncortical spinal tracts are also seen (image 10, series 5, image 12, series 6\nand image 17, series 402). Normal intracranial flow voids are preserved. \nThere is no diffusion abnormality to indicate acute or subacute ischemic\nchanges. The soft tissues of the face and scalp are unremarkable.",
            "output": "1. T2 and FLAIR hyperintensities in the corticospinal tracts suggesting the\npossibility of ALS, please correlate clinically.\n2. Multiple T2 and FLAIR foci distributed in the periventricular and\nsubcortical white matter are nonspecific, and may represent changes due to\nchronic small vessel ischemic disease."
        },
        {
            "input": "Multiple foci of slow diffusion are identified in the right caudate head,\nputamen, centrum semiovale, consistent with early subacute infarcts. Small\nfocus of hemorrhagic transformation within right caudate head infarct. There\nwas no parenchymal hemorrhage on head CT from earlier today at 11:08.\n\n4.2 x 3.7 x 6.5 cm (AP by TV by SI) multilobulated enhancing mass is\nidentified in the sella and suprasellar regions.  Tumor has figure-of-eight\nappearance.  There is intermediate T2 signal within the tumor.  Heterogeneous\nlow signal on gradient images is identified within the mass, consistent with\ninternal hemorrhages.  Tumor extends in the suprasellar cistern, extending\nsuperiorly to the level of the foramina ___, obliterating significant\nportion of the third ventricle, posteriorly displacing anterior commissure.  2\nmilli completely fill sphenoid sinus, largely from osseous remodeling, with\nareas of soft tumor extension into the sphenoid sinus that is going through\nthe sphenoid sinus wall.  Separate pituitary gland cannot be identified. \nLarge component of the tumor extends into the superior prepontine, anterior\nperimesencephalic cistern, with mass effect on the brainstem.  Anterior margin\nof the tumor contacts upper basilar artery, left superior cerebellar artery\nwhich is posterior displaced, and bilateral posterior cerebral arteries. \nTumor exerts mass effect on bilateral cavernous sinuses in there is cavernous\nsinus extent bilaterally, right greater than left.  Bilateral ICA narrowing is\nbetter seen on CTA from today broad area of contact with bilateral cavernous\nsegment, supraclinoid ICA, measuring approximately 180 degrees on the right,\nand less than 180 degrees on the left.  Distal petrous segments of bilateral\nICA are encircle by tumor, narrowing right greater than left.  Tumor contacts\nright supraclinoid ICA, and posterior margin of bilateral A1, A-comm.  Tumor\ninvolves nearly replaces entire clivus extending into the epidural space in\nthe prepontine cistern.\nTumor extent abutting posterior nasopharyngeal mucosa secondary to osseous\nexpansion and possible component of tumor extending through the bone.  Tumor\ncrosses bilateral petroclival synchondrosis and extends into the tips of both\npetrous apex.\n\nUpper, heterogeneous component of the suprasellar tumor there is hemorrhagic\nhas heterogeneous enhancement, with some areas of no enhancement..\n\nIntracranial portions of the bilateral optic nerves cannot be separately\nidentified from the overlapping mass.  Intraorbital portions of the bilateral\noptic nerves are atrophic.\n\nFindings consistent with mild-to-moderate chronic small vessel ischemic\nchanges.  Generalized brain parenchymal atrophy.",
            "output": "1. There are right frontal lobe, basal ganglia subacute infarcts.  Small focus\nof hemorrhagic transformation right caudate head.\n2. Large sellar, suprasellar, middle skullbase mass,, most consistent with\ngiant pituitary macroadenoma.  Morphology and T2 characteristics make other\netiologies, such as meningioma or chordoma less likely.\n3. Blood products, heterogeneous enhancement within suprasellar tumor\ncomponent,, of indeterminate acuity, consider component of pituitary apoplexy\nif appropriate.\n4. Description of local involvement as above.\n\nRECOMMENDATION(S):  Follow-up head CT without contrast.\n\nNOTIFICATION:   The findings were discussed with ___, M.D. by ___,\nM.D. on the telephone on ___ at 5:24 pm, 5 minutes after discovery of\nthe findings."
        },
        {
            "input": "MRI head:  There is no intra or extra-axial mass, acute hemorrhage or infarct.\nThere are very few scattered punctate periventricular and subcortical T2/FLAIR\nwhite matter hyperintensities, which are nonspecific in a patient this age. \nThe major intracranial flow voids are preserved.  The paranasal sinuses are\nclear.  The orbits are unremarkable.  The mastoid air cells are clear.\n\nMRV: There is lack of flow related signal of the left transverse sinus. The\nleft sigmoid sinus and visualized internal jugular vein are diminutive but\npatent.  Normal flow signal is demonstrated within the superior sagittal\nsinus, straight sinus, right transverse sinuses, and right sigmoid sinuses.\nThe jugular bulbs and proximal jugular veins are patent. Evaluation of the\ndeep venous systems reveals normal flow signal in the internal cerebral veins.\nThe vein ___ is also unremarkable.",
            "output": "1. Lack of flow related signal of the left transverse sinus.  No associated\nsecondary signs such as T2 or T1 hyperintense signal within the transverse\nsinus to definitively establish the presence of thrombus.  The finding may\nrepresent slow flow, however, to completely exclude thrombosis repeat MRV with\nslower VENC or CT venogram may be performed.\n2. A very few scattered periventricular subcortical T2/FLAIR white matter\nhyperintensities are nonspecific in a patient of this age.  However, the\ndifferential considerations include, but not limited to sequela of chronic\nheadache such as migraine, prior trauma or infectious/ inflammatory etiology.\n3. No acute infarct or intracranial hemorrhage.\n\nRECOMMENDATION(S):  Repeat MRV with slower VENC or CTV could be performed to\nfurther evaluate lack of flow related signal in the left transverse sinus.\n\nNOTIFICATION:  The findings were discussed with Dr. ___. by ___\n___, M.D. on the telephone on ___ at 11:53 AM, 60 minutes after\ndiscovery of the findings."
        },
        {
            "input": "MRV:  After adjusting the VENC settings, there is now flow related signal\nnoted in the left transverse sinus.  Normal flow signal is demonstrated within\nthe superior sagittal sinus, straight sinus, right transverse sinuses, and\nsigmoid sinuses. The jugular bulbs and proximal jugular veins are patent.\nEvaluation of the deep venous systems reveals normal flow signal in the\ninternal cerebral veins. The vein ___ is also unremarkable.",
            "output": "1. After adjustment of VENC settings, there is now flow related signal noted\nin the left transverse sinus.\n\nNOTIFICATION:  The findings were discussed with Dr. ___. by ___\n___, M.D. on the telephone on ___ at 2:03 ___, 15 minutes after\ndiscovery of the findings."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are patent and prominent in keeping\nwith age-related volume loss.  There is no abnormal enhancement after contrast\nadministration.\n\nThere are extensive areas of T2/FLAIR hyperintensity in the subcortical,\nperiventricular and deep white matter, nonspecific, likely secondary to small\nvessel ischemic changes.\n\nThe orbits are unremarkable noting prior left cataract surgery.  Mucosal\nthickening in bilateral ethmoid air cells.  The remaining visualized paranasal\nsinuses and mastoid air cells are clear.  Intracranial flow voids are\nmaintained.",
            "output": "1. No acute intracranial abnormality.  No abnormal focus of enhancement to\nsuggest metastatic disease."
        },
        {
            "input": "Please note the study is mildly degraded by motion.\n\nMRI Brain:  There is no evidence of acute intracranial hemorrhage, edema,\nmasses or acute infarction.  Ventricles and sulci are normal in caliber and\nconfiguration.  Scattered areas of T2/FLAIR hyperintensities in the\nperiventricular, subcortical and deep white matter (Series 12: Images 14, 15,\n16, 19) are nonspecific, but unchanged from prior study and may represent a\nsequela of chronic small vessel ischemic disease.  Small punctate foci of\nsusceptibility within the right cerebellum (13:7), right temporal lobe (13:9)\nand left precentral gyrus (13:21) are again noted, compatible with chronic\nmicrohemorrhage.  No new foci of blood products are noted.\n\nThere is mucosal thickening within the right maxillary sinus, with areas of\nlow T2 signal posteriorly (11:2) that correspond to a calcified focus on the\nrecent CT from ___ (2a:1, prior study) and may represent an osteoma. \nThis is unchanged from the prior MRI.  There is also mild mucosal thickening\nwithin the ethmoid air cells.  Minimal opacification of the right mastoid air\ncells is noted (11:7).  The orbits are unremarkable.\n\nMRA brain: The intracranial vertebral and internal carotid arteries and their\nmajor branches appear normal without evidence of stenosis, occlusion, or\naneurysm formation.  Dominant left vertebral artery, a normal variant. \nQuestion minimal irregularity of right petrous segment of internal carotid\nartery suggestive of atherosclerotic disease.\n\nMRA neck:  There is a normal 3-vessel arch. The common, internal and external\ncarotid arteries appear normal.  There is no evidence of internal carotid\nartery stenosis by NASCET criteria.  The origins of the great vessels,\nsubclavian and vertebral arteries appear normal bilaterally.",
            "output": "1. Mildly motion degraded study.\n2. No evidence of acute ischemia.\n3. Question minimal irregularity of right petrous segment of internal carotid\nartery suggestive of atherosclerotic disease.\n4. No evidence of dissection, stenosis or aneurysm greater than 3 mm in the\nmajor head and neck vessels.\n5. Chronic changes including probable small vessel ischemic disease and\nscattered punctate microhemorrhagic changes as described above.  No new\nhemorrhage.\n6. Paranasal sinus disease as described above, with redemonstrated right\nmaxillary osteoma."
        },
        {
            "input": "There is no evidence of enhancing mass or abnormal enhancement to suggest\nmetastatic disease.  There is no infarction, hemorrhage, edema, mass effect,\nor midline shift.  The ventricles are normal in size and configuration.  The\nparanasal sinuses bilateral mastoid air cells appear clear.  The orbits and\nvisualized soft tissues appear unremarkable.",
            "output": "1. Unremarkable brain MRI without evidence of metastatic disease."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  Moderately prominent perivascular spaces cerebral hemispheres.\nMild diffuse brain parenchymal atrophy.  Preserved vascular flow voids.  Mild\nparanasal sinus disease, most prominent at the ethmoid sinus.  Clear mastoids.\nDominant patent left transverse, sigmoid sinus..  Severe narrowing very\ndistal, already hypoplastic, right transverse sinus, with inhomogeneous\ncontrast opacification of the right sigmoid sinus proximal jugular vein, which\nis likely secondary to suboptimal opacification and contrast mixing.  No\nabnormality on FLAIR, T2, gradient on diffusion images to suggest thrombus. \nFindings consistent with moderate chronic small vessel ischemic changes.",
            "output": "No metastases.\nMild paranasal sinus disease."
        },
        {
            "input": "What appears to be surface electrodes are noted. Artifact from the electrode\nlimits evaluation of the posterior midline brain at the vertex on\ndiffusion-weighted sequences.\n\nAgain noted is an ossified nonenhancing extra-axial focus overlying the left\ntemporal lobe (series 701b, image 63), measuring approximately a 1.1 x 1.3 cm\n(TRV, CC), which may be seen on prior exams dating back to ___, likely\nrepresenting a dural ossification versus ossified meningioma. No adjacent\nparenchymal edema pattern is noted.\n\nNo intra-axial mass, acute infarct or hemorrhage.\nSulci, ventricles cisterns are prominent, within expected limits for the\npatient's age and volume loss. There are periventricular and subcortical white\nmatter T2/FLAIR nonspecific hyperintensities, commonly seen in setting of\nsmall vessel ischemic disease in a patient of this age.\nSmall foci of increased signal intensity in the insular cortex/ subcortical\nlocation on both sides, can be nonspecific or related to inflammatory changes.\nSlightly small hippocampi on both sides, with prominent temporal horns.\n\nThe dural venous sinuses are patent.\nThe major intracranial flow voids are preserved.  Right vertebral artery is\ndominant and left is diminutive.\nProminent pituitary, for the age, no abnormally enlarged, however.\n\nThe paranasal sinuses are clear.\nThe patient is status post bilateral lens replacements. Otherwise orbits are\nunremarkable.\nThe mastoid air cells are clear.",
            "output": "1. No evidence of acute infarct. No parenchymal mass.\n2. Extra-axial ossified lesion overlying the left temporal lobe is noted,\nsimilar appearance to prior exams from presumably representing a meningioma\nversus dural or ossification.\n3. Subcortical and periventricular White matter changes compatible with small\nvessel ischemic disease in a patient of this age.\n4. Small foci of increased signal intensity in the insular cortex/ subcortical\nlocation on both sides, can be nonspecific or related to inflammatory changes.\nCorrelate clinically and with the chain consider followup to assess for any\ninterval change."
        },
        {
            "input": "FLAIR images demonstrate hyperintensity throughout the cerebral sulci, more\nextensive in appearance than on ___, but this could be related to\ntechnical differences.  Postcontrast T1 weighted images demonstrate mild\ndiffuse leptomeningeal enhancement without nodularity.  There is no\nparenchymal signal abnormality to suggest cerebritis.  There is no\nsusceptibility artifact on gradient echo images to suggest blood products. \nThere is no acute diffusion abnormality.\n\nThere is a developmental venous anomaly extending from the anterior left\ncerebellar hemisphere through the left middle cerebellar peduncle and into the\nvein of ___.  There is no evidence for a cavernous malformation in the brain\nparenchyma.\n\nVentricles, sulci, and basal cisterns are normal in size.  Major arterial flow\nvoids are grossly preserved.\n\nThere is a small mucous retention cyst in the left maxillary sinus.",
            "output": "1. Diffuse sulcal hyperintensity on FLAIR images with non nodular\nleptomeningeal enhancement on postcontrast T1 weighted images, compatible with\nmeningitis.  Signal abnormality on FLAIR images appears more extensive than on\n___ study dated ___, but this could be related to differences in\ntechnique.\n2. No evidence for cerebritis.\n3. Developmental venous anomaly in the left cerebellar hemisphere and left\nmiddle cerebellar peduncle."
        },
        {
            "input": "In the right frontal lobe, magnetic susceptibility changes are seen with a 12\nmm by 11 mm in transverse dimension, heterogeneous lesion with vague pattern\nof enhancement after contrast administration consistent with a cavernous\nmalformation, with no significant mass effect or vasogenic edema, there is a\nsmaller but similar lesion in the left cerebellar hemisphere, also consistent\nwith cavernoma (series 10, image 5).\n\nExtensive subcortical punctate, periventricular areas of T2 FLAIR high-signal\nintensity which are nonspecific and may reflect changes due to chronic small\nvessel disease, lacunar ischemic changes are seen in the pons and bilateral\nbasal ganglia.  There is no evidence of acute intracranial hemorrhage, edema,\nmasses, mass effect, midline shift or large territorial infarction.  No\ndiffusion abnormalities are detected.  The major vascular flow voids are\npresent.  The ventricles and sulci are normal in caliber and configuration.\n\nThe orbits demonstrate bilateral lens replacement, the paranasal sinuses and\nmastoid air cells are clear.  No osseous lesions are seen.",
            "output": "1. Extensive areas of T2/FLAIR high-signal intensity identified in the\nsubcortical and periventricular white matter, which are nonspecific and may\nreflect changes due to chronic small vessel disease.\n2. Chronic lacunar infarcts identified in the pons and basal ganglia.\n3. Right frontal and smaller left cerebellar cavernomas, with no evidence of\nsignificant mass effect or vasogenic edema.\n4. No acute intracranial abnormality.  There is no evidence of acute\nintracranial process."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor acute infarction.  2 areas of chronic cortical infarct anterior lateral\nleft temporal lobe, and inferolateral left occipital lobe.  Chronic lacunar\ninfarct right caudate head,, adjacent deep matter with mild ex vacuo\ndilatation right lateral ventricle.  . Chronic lacunar infarct posterior\nmargin right internal capsule.  Wallerian degeneration with atrophy right\nmidbrain.  Moderate chronic small vessel ischemic changes elsewhere.  No\nchronic microhemorrhage.  Advanced brain atrophy.\nAbnormal right globe, likely a chronic retinal detachment ; patient has known\nright eye blindness.\nMinimal opacification bilateral mastoid air cells.\nPreserved vascular flow voids",
            "output": "1. No evidence of hemorrhage or recent infarct.\n2. Multiple chronic cortical and lacunar infarcts.\n3. Atrophy."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  There are patchy and confluent T2/FLAIR hyperintensity\nthroughout the subcortical and periventricular white matter, nonspecific, but\nmost likely reflecting chronic microvascular disease in this age group. \nSimilar signal changes are seen in the pons.  A punctate focus of\nsusceptibility in the right cerebellar hemisphere on image 5 of series 11\ncould reflect a focus of chronic microhemorrhage the ventricles and sulci are\nmildly prominent reflecting involutional changes.  Partially empty sella\nconfiguration is noted.\n\nThe major intracranial vascular flow voids are preserved.  There is mild\npatchy fluid signal in the right mastoid air cells.  Orbits are grossly\nunremarkable.  Degenerative changes are noted in the imaged upper cervical\nspine.",
            "output": "1. No acute intracranial abnormality.  No evidence of acute or subacute\ninfarction.\n2. Nonspecific white matter signal changes which most likely reflect chronic\nmicroangiopathy in this age group.\n3. Focus of probable chronic microhemorrhage in the right cerebellar\nhemisphere."
        },
        {
            "input": "MRI BRAIN:\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.  Intracranial flow voids are preserved.  There is no\nabnormality corresponding to hyperdensity in the right posterior fossa seen on\nprior CT.\n\nMRA BRAIN:\nThe intracranial vertebral and internal carotid arteries and their major\nbranches appear normal without evidence of stenosis, occlusion, or aneurysm\nformation.\n\nMRA NECK:\nThe common, internal and external carotid arteries appear normal.  There is no\nevidence of internal carotid artery stenosis by NASCET criteria.  The origins\nof the great vessels, subclavian and vertebral arteries appear normal\nbilaterally.  .",
            "output": "1. No acute intracranial process.\n2. Unremarkable head and neck MRA.\n3. No abnormality corresponding to hyperdensity in the right posterior fossa\non CT."
        },
        {
            "input": "There is no evidence of infarction or hemorrhage.  There is no mass or\nabnormal enhancement.  The dural venous sinuses appear patent on the\npostcontrast images.  There is mild prominence of the sulci related to\ninvolutional changes.  There is minimal nonspecific periventricular and\nsubcortical FLAIR hyperintensity, likely sequela of chronic small vessel\nischemic disease.\n\nThere is no edema, mass effect or midline shift.  The visualized principal\nintracranial vascular flow voids are preserved.  There is mild mucosal\nthickening of the bilateral ethmoid air cells.  The right maxillary sinus is\nrelatively smaller in size with mild circumferential mucosal thickening.  The\nvisualized soft tissues appear unremarkable.\n\nSubtle increased signal is seen at the anterior aspect of the lower fourth\nventricle on FLAIR images and subtle postcontrast high signal is also seen in\nthis region (11:4 and 14:4)  is which appears artifactual as the enhancement\nis not visualized on the MP rage images.",
            "output": "1. No evidence of infarction, hemorrhage, mass, or abnormal enhancement.\n2. Subtle signal and enhancement near the foramina of image in the which\nappears artifactual."
        },
        {
            "input": "Postcontrast MP RAGE and spin echo T1 weighted images are substantially\ndegraded by motion artifact.  Axial gradient echo images are moderately\nlimited by motion artifact.  Axial FLAIR and T2 weighted images were repeated\nwith motion reducing technique, series 15 and series 16.\n\nThere is abnormal high T2 signal throughout the medulla, more extensive on the\nright than left extending into the visualized upper cervical spinal cord, best\nseen on axial T2 weighted series 16, images ___.  There appears to be\nassociated slow diffusion, series 5 and 6, images ___.  Evaluation for any\nassociated contrast enhancement is markedly limited.  Of note, sagittal images\ndemonstrate degenerative changes in the included cervical spine, with moderate\nto severe spinal canal stenosis at C3-C4 and at least moderate spinal canal\nstenosis at C4-C5, not adequately assessed.  While this may contribute to\nsignal abnormality in the cervical spinal cord, this does not explain the\nsignal abnormality in the medulla.\n\nThere is no evidence for intracranial blood products allowing for bilateral\nglobus pallidus calcifications. Allowing for motion artifact on postcontrast\nT1 weighted and MP RAGE images, there is no evidence for an enhancing mass.\nThe ventricles and sulci are prominent, compatible with global cerebral\natrophy.  There is gross preservation of the principal intracranial vascular\nflow voids.  The dural venous sinuses appear patent on MP-RAGE imagine\nsequences.\n\nMucosal thickening is noted in the bilateral maxillary sinuses and ethmoid air\ncells.",
            "output": "1. Motion degraded examination.\n2. High T2 signal and slow diffusion throughout the medulla, right greater\nthan left, extending into the visualized upper cervical spinal cord. \nEvaluation for any associated contrast enhancement is markedly limited by\nmotion artifact.  While sagittal images demonstrate upper cervical spinal\nstenosis, which may contribute to signal abnormality in the cervical spinal\ncord, this does not explain signal abnormality in the medulla.  Demyelination,\nsequela of infection/inflammation, and a neoplasm should be considered.  Since\nthe patient has longstanding neurologic symptoms, acute infarction is\nunlikely.\n\nRECOMMENDATION(S):  Cervical spine MRI with and without contrast.\n\nNOTIFICATION:  The findings were discussed with ___, M.D. by\n___, M.D. on the telephone on ___ at 2:38 pm, 5 minutes after\ndiscovery of the findings."
        },
        {
            "input": "Incompletely visualized slow diffusion and T2 and FLAIR hyperintense changes\nin the medulla and upper cervical cord appears fairly similar compared to\nprior.  Mild enhancement of the medullary and cervical lesions are now\napparent on cervical spine imaging (not clearly evident on brain imaging). \nEnhancement of the cervical myelopathy will be described on the cervical spine\nMR. ___ new areas of slow diffusion.  The FLAIR and T2 hyperintense changes\nsurrounding the temporal horn of the right lateral ventricle appears fairly\nsimilar compared to prior.  Ventricular profile is normal.  Small area of\nsignal abnormality in the left facial colliculus is also unchanged compared to\nthe prior study.  Multiple periventricular and deep white matter T2 and FLAIR\nhyperintensities appear relatively similar compared to prior (large amount of\nmotion artifact on prior study).  Mild mucosal thickening involving the\nparanasal sinuses.  The orbits appear normal.  Difficult to comment on optic\nnerve demyelination on this nondedicated axial imaging.  The major\nintracranial vessels appear patent.",
            "output": "Stable intracranial findings.\n\nThe suspected demyelinating changes surrounding the temporal horn of the right\nlateral ventricle, medulla and upper cervical cord appears fairly similar\ncompared to prior.  There is  mild enhancement of these lesions better seen on\nthe cervical spine imaging suggesting breakdown of the blood brain barrier. \n___ new intracranial lesions.\n\nFindings are suggestive of neuromyelitis optica and correlation with an \nantibodies advised.  In the differential diagnosis consider other\ndemyelinating conditions.\nIschemia, infective and neoplastic etiologies are considered less likely.\n\nThe enhancement involving the cervical cord myelopathy would be fully\ndescribed on the cervical spine MR report."
        },
        {
            "input": "No significant change in the T2/FLAIR hyperintense changes surrounding the\ntemporal horn of the right lateral ventricle.  The unchanged is T2/FLAIR\nsignal abnormality corresponding to the left facial colliculus.  Multiple\nadditional superimposed periventricular to is and deep white matter T2/FLAIR\nhyperintensity is are unchanged.  There is no evidence of hemorrhage, edema,\nmasses, mass effect, midline shift or infarction.\n\nThe major intracranial vascular flow voids are maintained.  The ventricles and\nsulci are normal in caliber and configuration.  The paranasal sinuses, mastoid\nair cells and orbits are normal.  There is no definite abnormal enhancement\nafter contrast administration.\n\nFor details of the cervicomedullary junction please refer to the concurrently\nperformed MR cervical spine study.",
            "output": "1. No significant change in suspected demyelinative changes surrounding the\ntemporal horn of the right lateral ventricle and left facial colliculus. \nThese findings in combination with the described findings on the concurrently\nperformed MRI cervical spine study are suspicious for neuromyelitis optica.\n2. Superimposed scattered T2/FLAIR white matter hyperintensities are unchanged\nand may represent chronic small vessel ischemic changes.\n3. For details of the cervicomedullary junction please refer to the\nconcurrently performed MRI cervical spine."
        },
        {
            "input": "Study is mildly degraded by motion.  Confluent area of periventricular FLAIR\nhyperintensity along the right temple horn is stable compared to ___.  FLAIR hyperintense lesions in left facial colliculus and medulla are\nalso unchanged. Multiple scattered foci of FLAIR hyperintensity in\nperiventricular, deep, and subcortical white matter are unchanged.  No lesions\ndemonstrate associated restricted diffusion or increase susceptibility.\n\nThere is no evidence of hemorrhage, midline shift or infarction.   The\nventricles and sulci are stable in caliber and configuration.  There is no\nabnormal enhancement after contrast administration.  Bilateral ethmoid air\ncell, maxillary sinus, and sphenoid sinus mucosal thickening is present.",
            "output": "1. Study is mildly degraded by motion.\n2. Grossly stable nonspecific nonenhancing white matter lesions as described,\ncompatible provided history of chronic demyelinating disease.\n3. Paranasal disease as described.\n4. No evidence of acute infarct."
        },
        {
            "input": "Irregular heterogeneously enhancing left cerebellar hemisphere mass measuring\n25 x 18 mm has significantly increased in size compared to the prior\nexamination where it measured 7 x 7 mm (900:75).  There has been prominent\nincrease in surrounding vasogenic edema and mass effect, with mild effacement\nof the adjacent fourth ventricle there is apparent extension of this mass past\nthe tentorium into the left posterior temporal lobe with heterogeneous,\nirregular enhancing mass in this region measuring 42 x 29 mm, also\nsignificantly increased compared the prior examination where it measured 13 x\n11 mm (900:87).  Minimal increased gradient echo susceptibility within the\ntemporal lobe aspect of the enhancement, compatible with micro hemorrhage\n(series 6, image 10).  There has also been prominent increase in surrounding\nvasogenic edema, extending into the left temporal, parietal, and occipital\nlobes.  There has been significant increase in associated mass effect and\nthere is now a up to 5 mm of rightward midline shift.  There is increasing\neffacement of the occipital horn of the left lateral ventricle.  These lesions\ndemonstrate areas of central slowed diffusion.\n\nThere is no evidence of acute infarct.   The ventricles and sulci are\notherwise age appropriate in caliber and configuration.  Background areas of\nperiventricular and subcortical white matter T2/FLAIR hyperintensity are\nunchanged, and likely represent the sequela of chronic small vessel ischemic\ndisease.  The principal intracranial vascular flow voids are preserved.  The\ndural venous sinuses are patent on MP-RAGE images.\n\nThere is a small mucous retention cyst in the right maxillary sinus.  The\nremainder of the paranasal sinuses are grossly clear.  The orbits are grossly\nunremarkable.",
            "output": "1. Prominent interval increase in size of heterogeneously enhancing left\ncerebellar and left temporal lesions with central hypo enhancement, which\nappear contiguous, with i extension past the tentorium with extravagant\ninterval increase in associated vasogenic edema with increasing mass effect\nand 5 mm rightward midline shift.  This may represent radiation necrosis,\nhowever close interval followup is recommended to exclude progression.\n2. No new enhancing mass.\n\nNOTIFICATION:  The impression above was entered by Dr. ___ on\n___ at 17:34 into the Department of Radiology critical communications\nsystem for direct communication to the referring provider."
        },
        {
            "input": "24 x 22 mm left cerebellar lesion is unchanged in size, with interval decrease\nenhancement, now with only minimal heterogeneous rim enhancement.  This again\nappears in contiguity with a left medial posterior temporal lesion, which\ncrosses the falx measuring up to 29 x 24 mm, decreased compared to the prior\nexamination where it measured 42 x 29 mm, and demonstrates decreased areas of\nrim heterogeneous enhancement.  Surrounding FLAIR hyperintensity has markedly\nimproved compared to the prior examination.  These lesions demonstrate areas\nof slowed diffusion.\n\nThere is no evidence of hemorrhage, worsening edema, new masses, mass effect,\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There are few, unchanged areas of periventricular and\nsubcortical white matter T2/FLAIR hyperintensity reflecting either\nposttreatment change or chronic small vessel ischemic disease.  The principal\nintracranial vascular flow voids are preserved.\n\nThere is a small mucous retention cyst in the right maxillary sinus.  The\nremainder the visualized paranasal sinuses are grossly clear.  The orbits are\ngrossly unremarkable.  There is partial opacification of a few left-sided\nmastoid air cells, unchanged.",
            "output": "1. No interval change in size of a left cerebellar lesion and interval\ndecrease in size of a contiguous left medial posterior temporal lesion,\ncrossing the falx, though the degree of surrounding heterogeneous rim\nenhancement and adjacent edema has markedly improved.  Given these changes,\nthese areas most likely reflect radiation necrosis.  Residual disease cannot\nbe excluded, and continued attention on followup is advised.\n2. No new enhancing mass."
        },
        {
            "input": "A 2.3 x 2.2 cm left cerebellar lesion is not significantly changed in size,\nand again demonstrates mild rim enhancement, not significantly changed since\n___, however decreased compared with ___ (10:7).  This lesion\nagain appears contiguous with a 2.9 x 2.2 cm left medial posterior temporal\nlesion which crosses the left falx, not significantly changed in size\n(900:72).  This lesion again demonstrates heterogeneous rim enhancement, not\nsignificantly changed from prior, however decreased compared with ___.\nFLAIR hyperintensity surrounding the left cerebellar lesion appears slightly\nincreased compared with ___.  FLAIR hyperintensity surrounding the\nleft posterior temporal lesion is not significantly changed.  These lesions\nagain demonstrate areas of slow diffusion.  These lesions also demonstrate\nintrinsic T1 hyperintense signal likely representing hemorrhage product.\n\nThere is no evidence of hemorrhage, new masses, mass effect, midline shift or\ninfarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There are scattered subcortical white matter T2/ FLAIR\nhyperintensities, likely reflecting either post treatment change or chronic\nsmall vessel ischemic disease.  The major intracranial vascular flow voids are\npreserved.\n\nThere is a mucosal retention cyst in the right maxillary sinus.  There is\npartial opacification a few left mastoid air cells, unchanged.  Remainder of\nthe paranasal sinuses are clear.  The orbits are grossly unremarkable.",
            "output": "1. No significant interval change in size of peripherally enhancing left\ncerebellar lesion, which appears contiguous with a left medial posterior\ntemporal lobe lesion, which crosses the left falx.\n2. There may be minimally increased surrounding FLAIR hyperintense signal\nassociated with the left cerebellar lesion.  FLAIR hyperintense signal\nassociated with the left temporal lobe lesion is unchanged.\n3. No new enhancing lesions."
        },
        {
            "input": "Intrinsically T1 hyperintense lesions of the left temporal lobe and brachium\npontis is overall unchanged from prior examinations dating back to ___ demonstrating very minimal peripheral enhancement.  The degree of white\nmatter edema pattern is stable.  The lesions demonstrates associated\ndiffusion-weighted hyperintense signal, overall also unchanged.  No new\nlesions.  No evidence of acute infarct or intracranial hemorrhage.  The sulci,\nventricles and cisterns are otherwise within expected limits for the patient's\nage. Incidental note is made of a partial empty sella. The major intracranial\nflow voids are preserved.  The dural venous sinuses are patent on postcontrast\nMP-RAGE.  There is mild mucosal thickening of the ethmoid air cells as well as\na right maxillary sinus small mucous retention cyst.  The orbits are\nunremarkable.  Fluid signal is noted in the bilateral mastoid air cells.",
            "output": "1. Essentially unchanged intrinsic T1 hyperintense lesions of the left medial\ntemporal lobe and brachium pontis with subtle peripheral enhancement.  No new\nlesions.\n2. No interval change in degree of surrounding FLAIR hyperintense signal.\n3. Additional findings as described above."
        },
        {
            "input": "Within the inferomedial left temporal lobe, there is lesion measuring 2.7 x\n2.6 cm (900:83), previously 2.7 x 2.5 cm.  Within the superior left cerebellar\nhemisphere and left middle cerebellar peduncle, there is an additional lesion\nmeasuring 2.7 x 2.2 cm (900:74), previously measuring 2.4 x 2.0 cm.  Areas of\nrestricted diffusion within the lesions are stable since prior, may represent\nposttreatment change.  Both lesions have intrinsic bright T1 signal, and mild\nperipheral enhancement.  Intrinsic bright T1 signal has mildly decreased in\nthe cerebellar lesion.  Mildly more prominent enhancement involving lateral\nmargin of the cerebellar lesion, may represent posttreatment change, follow-up\nrecommended.  Adjacent T2 hyperintense signal within the surrounding\nparenchyma appears stable.  There is mild local mass effect, without evidence\nfor midline shift or ventricular effacement.  There is atrophy adjacent to the\nlesions, and ex vacuo dilatation of the left margin of the fourth ventricle,\nand left temporal horn and atrium of the lateral ventricle.  There is\nasymmetric parenchymal atrophy of the left margin of cerebellum, likely\nposttreatment change, stable.\n\nThere is no evidence of acute infarction.  No intracranial hemorrhage. The\nventricles and sulci are prominent relative to the patient's age.  Mild\nchronic small vessel ischemic changes.  The basal cisterns are patent.  There\nis no evidence of impending, downward herniation.  The sella turcica is within\nnormal limits.\n\nA mucous retention cyst is noted within the right maxillary sinus.  The\nremainder of the visualized paranasal sinuses, middle ear cavities, and\nmastoid air cells are well aerated and clear.  The orbits are within normal\nlimits bilaterally.",
            "output": "1.  No significant change in the size of the left inferior temporal lobe and\nleft cerebellar lesions, with treatment related changes, and mild peripheral\nenhancement.  Small area of mildly more prominent enhancement within left\ncerebellar lesion may represent posttreatment change, continued follow-up\nrecommended.\n2.  No evidence for new or additional intracranial metastatic lesions.\n3.  Mild to moderate age advanced global cerebral atrophy."
        },
        {
            "input": "Re-identified in the medial temporal lobe extending to the subependymal\nsurface of the temporal and occipital horn of the left lateral ventricle\nmeasuring approximately 2.1 x 1.8 cm in greatest dimension is overall similar\nin size to prior examination with intrinsic T1 hyperintense signal as well as\nsuperimposed peripheral nodular enhancement.  However, diffusion-weighted\nhyperintense signal and enhancement of the subependymal component of the\nlesion appears slightly more prominent when compared to the prior examination\n(series 502, image 13 and 14; series 10, image 9 and 10).\n\nIn the left middle cerebellar peduncle extending to the left cerebellar\nhemisphere is an additional peripherally enhancing lesion measuring\napproximately 2.6 x 2.3 cm, also overall similar in appearance to prior\nexamination.  Re-identified is very minimal intrinsic T1 hyperintense signal\nwithin the cerebellar lesion, potentially slightly decreased.\n\nAssociated diffusion-weighted hyperintense signal with these lesions is also\nsimilar.  Surrounding FLAIR edema pattern is similar to slightly more\nprominent.\n\nNo new enhancing lesions are identified.  There are superimposed\nperiventricular and subcortical T2/FLAIR white matter hyperintensities, which\nare nonspecific in a patient this age and may represent posttreatment change.\n\nAtrophy and ex vacuo dilatation of the occipital horn of the left lateral\nventricle and volume loss of the left cerebellum are unchanged.\n\nThere is no evidence for acute infarct or intracranial hemorrhage.  The sulci,\nventricles cisterns are mildly prominent, greater than would be expected for\nthe patient's age.  The major intracranial flow voids are preserved.  The\ndural venous sinuses are patent.  A mucous retention cyst in the right\nmaxillary sinus is slightly more prominent compared to prior exam.  There is\nmild mucosal thickening of the frontal sinuses and ethmoid air cells.  The\norbits are unremarkable.  Fluid signal is noted in the bilateral mastoid air\ncells.",
            "output": "1. No definite interval change in size of left medial temporal lobe and left\ncerebellar lesions, with mild peripheral enhancement.  However, there does\nappear to be mildly increased weighted signal and prominence of left occipital\nand temporal horn dependent mole enhancement associated with the temporal lobe\nlesion as well as equivocal associated mildly increased FLAIR hyperintense\nwhite matter edema pattern.  While findings could represent posttreatment\nchange, apparent increased nodularity and enhancement along the ependymal\nsurface does raise the suspicion for progression.  Close attention on\nfollow-up is recommended.\n2. No new enhancing lesions are identified.\n3. No evidence for acute infarct or intracranial hemorrhage.  Additional\nfindings as described above."
        },
        {
            "input": "Again seen are ring enhancing masses in the left cerebellar hemisphere and\nleft temporal lobe.  Both are surrounded by edema.  The cerebellar hemispheric\nedema appears greater than on the prior study.  No new lesions are identified.\nGradient echo images demonstrate signal loss in both lesions, suggesting\nchronic hemorrhage.  There is a micro bleed adjacent to the occipital horn of\nthe right lateral ventricle, unchanged since the prior study.  There is no\nevidence of new hemorrhage.\nNo other masses are identified.  There is no evidence of infarction.  The\nventricles and sulci are mildly prominent in an atrophic pattern.",
            "output": "Left cerebellar and left temporal lobe ring-enhancing lesions compatible with\nmetastatic disease appear unchanged.\nMild increase in edema in the left cerebellar hemisphere.\nNo evidence of new lesions."
        },
        {
            "input": "No significant change in size of the enhancing masses in the left cerebellar\nhemisphere and left temporal lobe with a similar degree of surrounding edema. \nHemosiderin staining within both lesions are compatible with old hemorrhages.\n\nRedemonstrated is a small focus of susceptibility adjacent to the occipital\nhorn of the right lateral ventricle compatible with an old microbleed.\n\nNo new lesions are identified.\n\nThere is no evidence of a new intracranial hemorrhage.  There is no evidence\nof acute infarction.  Mild periventricular white matter T2/FLAIR\nhyperintensities are again noted.\n\nThe major intracranial vascular flow voids are maintained.  Prominence of the\nventricles and cerebral sulci are compatible with age related involutional\nchanges.  There is a 1.3 cm mucous retention cyst within the right maxillary\nsinus.  Mild mucosal thickening of the ethmoid air cells.  There is a mild\namount of nonspecific fluid within the bilateral mastoid air cells.  The\norbits are normal.",
            "output": "1. Grossly stable size of the enhancing masses in the left cerebellar\nhemisphere and left temporal lobe with grossly stable surrounding edema.\n2.  Within limits of study, no definite new enhancing lesion identified.\n3. Treatment and/or microangiopathic changes as described.\n4.  Paranasal sinus disease and nonspecific bilateral mastoid fluid, as\ndescribed."
        },
        {
            "input": "Study is mildly degraded by motion.\n\nAgain is noted left temporal and cerebellar hemisphere peripherally enhancing\nstructure with extension to left lateral ventricle margin.  Nonspecific areas\nof increased nodular enhancement along this structure are noted.  The\nstructure again demonstrates slow diffusion along its inferior cerebellar\nmargin (see 550, 552:8).  Overall size and configuration of this structure is\ngrossly unchanged.  Again is noted nonspecific foci of blood products versus\nmineralization within the structure and within the adjacent left temporal\nlobe.  Grossly stable T2 and FLAIR hyperintensities within the left middle\ncerebellar peduncle and left temporal lobe are grossly unchanged.\n\nGrossly stable right occipital focus of blood products versus mineralization\nis again seen (see 06:12 on current study and 14:11 on ___ prior MRI exam).\n\nThere is no evidence of midline shift or infarction.   The ventricles and\nsulci are stable in caliber and configuration.  Additional few T2 FLAIR\nperivertebral subcortical hyperintensities are grossly unchanged.  Partially\nempty sella is again noted.  Right maxillary sinus probable mucous retention\ncyst is noted.  Bilateral ethmoid air cell mucosal thickening is present. \nMinimal nonspecific bilateral mastoid fluid is noted.",
            "output": "1. Study is mildly degraded by motion.\n2. Left temporal bone cerebellar peripherally enhancing parenchymal signal\nabnormality abutting left lateral ventricle as described, grossly stable in\nsize.  Question interval increase of peripheral nodular enhancement of mass\nversus artifact related to differences in technique.  Differential\nconsiderations again include tumor and radiation necrosis.\n3. Grossly stable left temporal and cerebellar edema versus treatment effects\nadjacent to parenchymal signal intensity abnormality.\n4. Within limits of study, no definite new enhancing intracranial lesions\nidentified.\n5.  Paranasal sinus disease and nonspecific mastoid fluid, as described."
        },
        {
            "input": "A lesion in the left cerebellar hemisphere, extending into the left temporal\nlobe appears mildly increased in size and demonstrates increased internal\nnodular enhancement, in areas which were largely cystic on the prior study. \nThe largest cerebellar component measures 2.8 x 2.6 cm (previously 2.5 x 2.4\ncm) and the largest temporal component measures 2.6 x 2.4 cm (Previously 2.4 x\n2.4 cm).  Extension along the lateral aspect of the left lateral ventricle is\nunchanged.  No new enhancing lesions identified.  Susceptibility within the\nlesion likely representing blood products or mineralization appears slightly\nincreased.\n\nA focus of susceptibility in the right occipital lobe (series 14, image 11) is\nunchanged.\n\nSurrounding vasogenic edema is not significantly changed.  There is no\nsignificant mass effect.\n\nMild prominence of the ventricles and sulci, likely represent age related\ninvolutional change.  Additional periventricular and deep white matter FLAIR\nhyperintensities, likely represent sequela of chronic small vessel ischemic\ndisease.\n\nThe dural venous sinuses are patent.  No intracranial hemorrhage, edema, mass\neffect or infarction.\n\nThe orbits are unremarkable.  There is a small mucous retention cyst in the\nright maxillary sinus.  Otherwise the paranasal sinuses are clear.  There is\nmild opacification of mastoid air cells, bilaterally.",
            "output": "1. The heterogeneously enhancing lesion in the left temporal lobe and\ncerebellar hemisphere is mildly increased in size and demonstrates increased\ninternal nodular enhancing components raising suspicion for possible\nprogression.  No new lesions identified.  No worsening mass effect or midline\nshift.\n2. Periventricular and deep white matter FLAIR hyperintensities likely\nrepresent sequela of chronic small vessel ischemic disease.\n3. Additional findings described above."
        },
        {
            "input": "A lesion demonstrating internal and peripheral irregular enhancement, with\nsomewhat stellate appearance, is seen involving the left cerebellar hemisphere\nand the adjacent inferior left temporal lobe across tentorium, with linear\nband of enhancement extending into the left peritrigonal area.  There are\ninternal foci of GRE hypointensity, and very dark T2 signal, which may\nrepresent blood products or mineralization, unchanged.  The cerebellar\ncomponent measures 2.6 x 2.1 cm, previously measuring 2.5 x 2.5 cm.  The left\ntemporal lobe component measures 2.2 x 2.2 cm, previously measuring 2.3 x 2.4\ncm.\n\nStable punctate foci of subcortical enhancement posterior right parietal lobe\nseries 12, image 242.  1.5 mm focus of subcortical enhancement anterior right\nfrontal lobe, series 12, image 156, stable since ___..  More\nprominent subcortical 2 mm focus of enhancement inferior left parietal lobe\nseries 12, image 188.\n\nNo new lesion is seen.\n\nThe previously seen focus of microhemorrhage in the right occipital lobe is\nunchanged.\n\nBrain parenchymal atrophy.  Confluent periventricular T2 signal abnormalities\nconsistent with posttreatment change.  Stable left cerebellar, temporal lobe\nT2 signal abnormalities.  A small mucous retention cyst is seen in the right\nmaxillary sinus, unchanged.  There is mild opacification of the bilateral\nmastoid air cells.  The intraorbital contents are normal.",
            "output": "1. Minimal decrease in the size of enhancement involving left temporal lobe\nand adjacent left cerebellum, across tentorium, suggestive of radiation\nnecrosis.  ASL would be helpful in further follow-up, if clinically indicated.\n2. More prominent 2 mm focus of enhancement left parietal lobe.  Few\nadditional punctate foci of stable enhancement."
        },
        {
            "input": "Irregular, spiculated enhancement in the left cerebellar hemisphere extending\nacross the tentorium into the inferomedial left temporal lobe and along the\nlateral subependymal surface of the left lateral ventricle is unchanged since\nthe prior examination.  The left temporal lobe component measures\napproximately 2.2 x 2.2 cm.  The cerebellar component measures approximately\n2.6 x 2.2 cm.  Associated susceptibility artifact is not appreciably changed,\nindicating mineralization or chronic sequela of hemorrhage.  The T2/FLAIR\nsignal hyperintensity surrounding the dominant areas of enhancement is not\nsignificantly changed.\n\nScattered punctate foci of enhancement more posteriorly located in the left\ncerebellar hemisphere are new (series 17, images 54-68).  There is also\nincreased T2/FLAIR hyperintense signal associated with these foci of\nenhancement.\n\nAn enhancing lesion in left midbrain has increased in size since the prior\nexamination and measures 4 x 3 mm, previously 3 x 1 mm (series 17, image 85). \nThe T2/FLAIR hyperintense signal associated with the lesion is also increased\n\nPunctate foci of enhancement in the subcortical right parietal lobe (series\n17, image 143) and right frontal lobe (series 17, images 96 and 102) are\nunchanged.  A previously seen punctate focus of enhancement in the inferior\nleft parietal lobe is not appreciated.  Enhancement of the canalicular and\nlabyrinthine segments of the left seventh cranial nerve is unchanged.\n\nNo evidence of acute intracranial hemorrhage or infarction.  Periventricular\nand subcortical white matter T2/FLAIR hyperintensities are nonspecific but\nlikely sequelae of chronic small vessel ischemic disease.  Incidental\npartially empty sella.  The ventricles and sulci are enlarged, most\nsignificantly at the level of the left lateral ventricle trigone and fourth\nventricle, reflecting volume loss.  The major intracranial flow voids are\npreserved.",
            "output": "1. The dominant area of irregular, spiculated enhancement involving the left\ncerebellar hemisphere and adjacent inferior left temporal lobe is stable in\nappearance.\n2. An enhancing lesion in the left mid brain has increased in size. Scattered\nfoci of enhancement in the posterior left cerebellar hemisphere are new. \nDifferential considerations include evolving postradiation changes or\nprogression of metastatic disease.  Attention to these areas and evaluation\nwith MR spectroscopy and ASL perfusion on subsequent studies is recommended.\n3. Additional punctate foci of supratentorial enhancement are unchanged.\n4. Enhancement of the canalicular and labyrinthine segments of the left\nseventh cranial nerve likely reflects postradiation changes."
        },
        {
            "input": "Similar to slightly less conspicuous appearance of the lobulated left\ncerebella lesion adjacent to the tentorium measuring 2.6 x 2.4 x 1.7 cm (AP X\nTR X SI).  There is unchanged tissue loss and encephalomalacia involving the\nleft cerebellar hemisphere.\nThe lesion as previously crossed the tentorium into the inferior medial left\ntemporal lobe, this portion has however increased in size now measuring 2.4 x\n2.6 x 1.7 cm (AP X TR X SI) from previously 2.2 x 2.2 x 1.5 mm.  There is also\nmild increase of the surrounding FLAIR edema.\nThere is stable susceptibility artifact associated with these 2 lesions,\nconsistent with calcifications previously identified on the CT.\nThe previously seen foci of nodular enhancement along the left inferior\ncerebellar hemisphere are no longer appreciated.\n\nStable appearance of the 4 x 3 mm (AP X TR) lesion in the left mid brain\n(series 17, image 74).  There has been resolution of the previously seen edema\nassociated with this lesion.\nNo significant change of punctate foci of enhancement in the subcortical right\nparietal lobe (series 17, image 131) and in the right frontal lobe (series 17,\nimage 95 and 98).  Note is made of a new subependymal 3 mm focus of\nenhancement along the frontal horn of the right lateral ventricle (series 17,\nimage 104).\n\nEnhancement of the canalicular and labyrinth venous segment of the left facial\nnerve is unchanged (series 17, image 53).\n\nThere is no evidence of acute intracranial hemorrhage or infarction.\n\nNonspecific periventricular and subcortical white matter changes are again\nidentified, similar to prior and likely reflect sequela of chronic small\nvessel ischemic changes.  There is a stable partially empty sella.\n\nThere is unchanged generalized parenchymal volume loss, slightly more than\nexpected for patient's age but possibly treatment and disease related.  There\nis stable prominence of the ventricular system which is consistent with the\npreviously mentioned parenchymal volume loss.\nThe major intracranial flow voids are preserved.  Major dural venous sinuses\nare patent.\n\nThere is mild mucosal thickening along the ethmoid air cells.  A mucous\nretention cyst is seen in the right maxillary sinus.  There is partial\nopacification of the bilateral inferior mastoid air cells.  The orbits appear\nunremarkable.\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.",
            "output": "1. New 3 mm subependymal enhancing lesion along the frontal horn of the right\nlateral ventricle.\n2. Increase in size of the left medial temporal lobe lesion with mildly\nworsening surrounding FLAIR edema.\n3. Stable spiculated left cerebellar lesion, left mid brain lesion and small\npunctate foci of enhancement in the right parietal and frontal lobes.\n4. Unchanged nonspecific white matter changes in the cerebral hemispheres\nbilaterally, likely sequela of chronic small vessel ischemic changes."
        },
        {
            "input": "Again seen are enhancing lesions in the left cerebellar hemisphere with\ninvolvement of the cerebellar peduncle and in the left medial temporal lobe. \nBoth lesions demonstrate ring-like patterns suggestive of necrosis.  There has\nbeen a marked increase in left temporal lobe edema since the prior studies. \nThis is been progressive since ___.  There has also been an increase\nin the solid enhancing component of the left temporal lobe lesion.\nThe volume of enhancement in the posterior fossa lesion has decreased since\n___.  These changes are superimposed on left cerebellar hemisphere\nand peduncle tissue loss, which does not appear to have progressed over this\ntime.  Again seen is chronic hemorrhage associated with the left temporal and\ncerebellar lesions.  There is no evidence of new hemorrhage\nEnhancing foci in the right parietal white matter and right frontal white\nmatter are no longer detectable.  There is a 2 mm focus of enhancement in the\nright inferior frontal lobe subcortical white matter best seen on image 83 of\nseries 17, not previously detected.  A focus previously seen adjacent to the\nfrontal horn of the right lateral ventricle is no longer detected. \nEnhancement in the left internal auditory canal, likely the facial nerve, is\nunchanged.\nAgain seen and unchanged is enlargement of the ventricle size and sulci in an\natrophic pattern along with periventricular white matter hyperintensity.",
            "output": "1. The left temporal lobe component of the ring-enhancing lesion demonstrates\nan increase in the volume of solid enhancement as well as a dramatic increase\nin surrounding edema.  This potentially could relate to radiation necrosis or\ntumor progression.\n2. The cerebellar component of the lesion appears somewhat smaller than on the\nprior studies.\n3. Several tiny enhancing parenchymal lesions previously noted are no longer\ndetectable.\n4. There is a new enhancing focus in the right inferior frontal subcortical\nwhite matter.  This presumably represents another metastasis."
        },
        {
            "input": "MR BRAIN: A peripherally enhancing cystic component of the left temporal lobe\nlesion measuring 2.4 x 2.2 cm is essentially unchanged compared to ___ but increased compared to ___. The more solid, heterogeneously\nenhancing component in the left temporal lobe is similar in size, measuring\n3.0 x 2.4 cm.  There remains T1 hyperintense material within the lesion,\nprobably reflecting blood products.  Extensive FLAIR hyperintensity\nsurrounding the lesion in the left temporoparietal lobes is unchanged.  \nBlooming artifact in the left temporal lobe lesion and left cerebral\nhemisphere is similar, consistent with blood products.\n\nIrregular enhancement, encephalomalacia, and blooming artifact in the left\ncerebellar hemisphere and middle cerebellar peduncle is also unchanged. \nEpendymal enhancement in the temporal horn and trigone of the left lateral\nventricle is unchanged. The previously seen 2 mm focus of enhancement in the\nmedial right frontal lobe white matter is stable (13:147).\n\nThere are no definite new foci of enhancement identified.  Prominence of the\nlateral ventricles is unchanged. There is no evidence of acute infarction or\nacute hemorrhage.\n\nThe visualized intracranial flow voids are preserved.  The dural venous\nsinuses are patent.\n\nThere is mild mucosal thickening in the anterior ethmoid air cells and a right\nmaxillary mucous retention cyst.  The orbits are unremarkable.\n\nMR ___: There is generally increased mean transit time and\ndecreased blood flow to the left temporal lobe lesion, with the exception of\nmildly increased blood flow along the anterolateral margin, as seen on ASL\nperfusion.\n\nASL Perfusion: There is focal increased perfusion along the anterolateral\naspect of the left temporal lobe lesion (4:10), however most of the lesion\ndemonstrates hypoperfusion.\n\nMR Spectroscopy: There is incomplete water suppression on single voxel\nspectroscopy, which is therefore nondiagnostic.  On multi voxel spectroscopy,\nthere is a general paucity of metabolite within the lesion, although voxels\noverlying the lesion demonstrate increased choline to NAA ratio.",
            "output": "1. The left temporal lobe lesion is stable in comparison with ___,\nincluding heterogeneously enhancing component and adjacent cystic component. \nThe majority of this lesion demonstrates overall decreased perfusion and a\npaucity of metabolite, which is favorable for radiation necrosis.  There is\nhowever a focal region of nodular enhancement along the anterolateral margin\nof the lesion that demonstrates increased perfusion and should be observed on\nfollow-up studies as residual lesion/progression remains a possibility given\nincreased perfusion.\n2. Unchanged enhancement encephalomalacia of the left cerebellar hemisphere\nand middle cerebellar peduncle.\n3. Unchanged 2 mm focus of enhancement in the medial right frontal lobe white\nmatter.\n4. No acute infarction, acute hemorrhage, or new lesions."
        },
        {
            "input": "Heterogeneous lesion within the left temporal lobe with a predominantly solid\nanterior component and predominately cystic posterior component measuring\napproximately 33 mm in maximal AP dimension has slightly decreased in size\nover the interval.  On ___, it measured approximately 36 mm in\nmaximal AP dimension.  The predominately solid component now measures\napproximately 30 AP x 20 TRV mm. This measured approximately 38 AP x 24 TRV\nmm.  The cystic component now measures approximately 21 AP x 17 TRV mm.  This\npreviously measured approximately 22 AP x 24 TRV cm on ___. \nPeripheral enhancement of the cystic component is re-identified.  There is\nalso similar associated probable hemorrhage.  Enhancement is again noted\nextending into the subjacent left cerebellar peduncle and left cerebellar\ncerebellum where there are postsurgical changes.  Enhancement is less\nconfluent.  Previously described subtle enhancement in the right inferior\nparasagittal frontal lobe (series 10; image 126) is less conspicuous.  No\nconvincing new lesions are evident.  Few punctate foci of susceptibility\nabnormality noted in the right temporal, and bilateral frontal lobes are\nsimilar.\n\nApproaching moderate prominence of the lateral ventricles and moderate to\nsevere prominence of the fourth ventricle appears similar.  No acute\ninfarction is seen.\n\nMajor vascular flow voids at the skull base are preserved. Small probable\nretention cyst in the right maxillary sinus is similar.",
            "output": "1. Dominant partially solid, partially cystic left temporal lobe lesion may\nhave minimally decreased in size over the interval.  Subjacent enhancement\nwithin the left cerebellar peduncle and left cerebellum is less confluent.  No\nnew lesions are evident."
        },
        {
            "input": "There is a stable enhancing mass in the right parietal lobe with surrounding\nvasogenic edema measuring 13 by 12 mm. Additionally, and better seen on the\ncurrent examination, there are 3 lesions in the cerebellum with the largest 1\nin the left superior cerebellum laterally measuring 8 mm.  There is a punctate\nlesion in the left cerebellum and a 4 mm lesion in the right cerebellum.  No\nevidence of hydrocephalus or acute ischemia.",
            "output": "Unchanged right parietal metastatic lesion. Better seen on the current\nexamination, there are 3 cerebellar metastases."
        },
        {
            "input": "When compared to prior, there has been interval reduction in size of the\ndominant right occipital lobe lesion. The enhancing 8 x 3 mm focus had\npreviously measured 12 x 14 mm. FLAIR signal abnormality seen on older prior\nsurrounding the lesion has resolved. Multi focal enhancing lesions within the\ncerebellum have also significantly decreased. Faint foci of enhancement within\nthe cerebellar hemispheres (11a: 20) are seen in the region of previously\nidentified 4 mm lesion of the right, and 2 mm lesion on the left.  Other\nscattered foci of enhancement within the cerebellum on prior are no longer\nvisualized. There is no new enhancing lesion.\n\nThere is no intracranial mass effect or midline shift. Ventricles and sulci\nare age-appropriate. There is no region of restricted diffusion or abnormal\nsusceptibility artifact. Major intravascular flow voids are preserved.\n\nPost contrast images demonstrate no abnormal parenchymal or meningeal\nenhancement.\n\nVisualized paranasal sinuses and mastoid air cells are unremarkable aside\nmucous retention cyst in the right maxillary sinus.",
            "output": "Interval decreased size of dominant right occipital lobe lesion. Additional\ncerebellar lesions are either decreased in size and no longer visualized. No\nnew metastatic lesion."
        },
        {
            "input": "There is no evidence of acute intracranial hemorrhage or mass effect. The\nventricles and basal cisterns appear normal.\n\nThere is no evidence of acute ischemia based on diffusion-weighted imaging.\nThere are normal vascular flow voids. Brain parenchymal volume is within\nnormal limits.\n\nThere is increased enhancement within the region of the left superior\ncerebellar hemisphere which is concerning for recurrent metastatic disease.\nThere are no other areas of new abnormal enhancement.  The previously seen\nabnormal enhancement within the right occipital lobe has resolved.\n\nThe orbits, skull base, and paranasal sinuses are unremarkable.",
            "output": "1. Increased nodular enhancement within the region of the left superior\ncerebellar hemisphere concerning for recurrent intracranial metastatic\ndisease.\n2. Resolved enhancement within the right occipital lobe.\n\nNOTIFICATION:   Results added to the critical communication dashboard at 1500,\nand ___."
        },
        {
            "input": "There is no evidence of acute intracranial hemorrhage or mass effect. The\nventricles and basal cisterns appear normal.\n\nThere is no evidence of acute ischemia based on diffusion-weighted imaging. \nThere are normal vascular flow voids.  The brain parenchymal volume is within\nnormal limits.\n\nThere is minimal residual enhancement within the superior left cerebellar\nhemisphere in the area of the previously described metastatic lesion. There\nare no new areas of abnormal enhancement or evidence of new lesions.\n\nThe orbits, skull base, and paranasal sinuses are unremarkable.",
            "output": "1. Minimal residual enhancement within the superior left cerebellar hemisphere\nin the region of the previously described metastatic lesion.\n2. No evidence of new lesions or new areas of abnormal enhancement."
        },
        {
            "input": "Previously noted residual right occipital lobe enhancing lesion is no longer\nseen.  No clear correlate to previously 4 and 2 mm enhancing foci in the right\nand left cerebellar hemispheres are noted.  No residual FLAIR abnormality is\nclearly identified.  No new lesions are noted.\n\nThere are scattered left frontal punctate FLAIR hyperintensities noted,\nunchanged from prior exam and nonspecific.  There is no intracranial mass\neffect or midline shift. Ventricles and sulci are age-appropriate. There is no\nregion of restricted diffusion or abnormal susceptibility artifact. Major\nintravascular flow voids are preserved.  The dural venous sinuses are patent.\n\nPost contrast images demonstrate no abnormal parenchymal or meningeal\nenhancement.\n\nUnchanged right maxillary sinus mucous retention cyst, otherwise, the\nvisualized paranasal sinuses and mastoid air cells are clear.  The orbits are\nunremarkable.",
            "output": "1. Previously described enhancing lesion in the cerebellar hemispheres and\nright occipital lobes are no longer noted.\n2. No new lesions."
        },
        {
            "input": "The ventricles and extra-axial spaces are normal in size. There is no evidence\nof midline shift, mass effect or hydrocephalus. There are no acute infarcts.\nThere is no evidence of focal abnormalities.  The vascular flow voids are\nmaintained. The visualized paranasal sinuses are clear. Following gadolinium\nadministration there is no evidence of abnormal parenchymal, vascular and\nmeningeal enhancement seen.",
            "output": "No significant abnormalities are seen on MRI of the brain with and without\ngadolinium. Previously Seen enhancing lesions are no longer visible."
        },
        {
            "input": "In the left superior cerebellum laterally, there is a 7 mm ovoid enhancing\nlesion (19:37), at the location of a previously identified metastatic lesion\nwhich measured up to 10 mm in ___, which had previously intervally\ndecreased in size and disappeared, however on the most recent prior\nexamination measured 4 mm.  There is some mild surrounding edema which is new.\nNo other abnormally enhancing focus is identified.  Trace edema in the right\noccipital lobe left focus of prior metastatic lesion without enhancement. \nThere is no evidence of hemorrhage, edema, mass effect, or infarction. The\nventricles and sulci are normal in caliber and configuration.  Major\nintracranial vascular flow voids are preserved. Orbits are grossly\nunremarkable. Small mucous retention cyst in the right maxillary sinus.",
            "output": "Interval increase in size of a 7 mm enhancing lesion in the superior left\ncerebellum laterally with surrounding edema, in the location of a previously\nidentified metastatic lesion compatible with recurrent metastatic lesion."
        },
        {
            "input": "Re-identified is a 9 x 5 x 7 mm (AP, TRV, SI) enhancing lesion along the\nsuperior aspect of the left cerebellum, slightly increased in size when\ncompared the prior exam.  There is stable associated surrounding FLAIR\nhyperintense signal.  No new lesions are identified.\n\nSulci, ventricles and cisterns are within expected limits for the patient's\nage.  There is no evidence of acute infarct or hemorrhage.  The major\nintracranial flow voids are preserved.  The dural venous sinuses are patent. \nThere is a small mucous retention cyst in the right maxillary sinus.  The\nremainder the paranasal sinuses are clear.  The orbits are unremarkable.  The\nmastoid air cells are clear.",
            "output": "1. Mild interval increased size of 9 mm left cerebellar hemisphere lesion with\nstable surrounding edema pattern.\n2. No new lesions are identified."
        },
        {
            "input": "The enhancing mass in the left superior cerebellum measures 0.7 (AP) x 0.5\n(TV) x 0.7 (SI) cm compared to 0.9 x 0.5 x 0.7 cm on ___ when\nmeasured in the same planes, but sagittal postcontrast MP RAGE images suggest\nthat there is no change in the AP dimension.  Stable surrounding T2\nhyperintense signal seen.  Increased perfusion is seen within the mass on ASL\nimaging.  Evaluation on ___ perfusion imaging is limited given the small size\nof the mass.  Multi voxel spectroscopy demonstrates low metabolites in the\nvoxel containing of the lesion, but is also limited due to the small size of\nthe mass and inclusion of CSF within the voxel containing the mass.\n\nNo new enhancing lesion is seen.  There is no new edema, acute diffusion\nabnormality, or evidence for new blood products.  The ventricles and sulci are\nnormal in size.\n\nMinimal fluid is seen in the bilateral mastoid air cells.  There is a mucous\nretention cyst in the right maxillary sinus.",
            "output": "1. The superior left cerebellar mass is stable in size compared to ___.  It demonstrates increased perfusion on ASL imaging, suspicious for\nactive tumor.  MR spectroscopy demonstrates low metabolites in the voxel\ncontaining the lesion, but is not diagnostic due to the small size of the\nlesion and proximity to CSF.\n2. No evidence for new intracranial lesions."
        },
        {
            "input": "MR BRAIN:\nThere is 1.2 (AP) x 1 (TV) x 0.8 (SI) cm contrast enhancing left superior\ncerebellar mass with minimal increased surrounding FLAIR hyperintense signal. \nThere is a punctate focus of contrast enhancement, series 1300b, image 45, in\na posterior left temporal sulcus with associated FLAIR hyperintense signal\nwhich in retrospect was present on the prior MRI of ___ but not\npresent on the MRI of ___.  Multiple additional punctate foci of\ncontrast enhancement, series 1300b image 42, are seen in a medial left\ntemporal sulcus with associated FLAIR hyperintense signal, not definitively\nvisualized on the prior studies.  Multiple additional areas of periventricular\nsubcortical FLAIR hyperintensities are seen with no associated contrast\nenhancement.  In addition, subtle nodular pachymeningeal enhancement with\nassociated FLAIR hyperintense signal is noted overlying the left cerebellar\nfolia, series 1300b, image 39.\n\nThere is no evidence of hemorrhage, mass effect, midline shift or infarction. \nThe ventricles and sulci are normal in caliber and configuration.\n\nThere is mucosal thickening in the ethmoid and frontal sinuses.  A retention\ncyst is seen in the right maxillary sinus.  Minimal fluid is seen in the right\nmastoid air cells.  The orbits are normal.  The major vascular flow voids are\npreserved.  Degenerative changes are in partially visualized upper cervical\nspine.\n.\nMR ___: Limited evaluation given small size of the lesion and\nlocation..\n\nASL Perfusion: Increased perfusion is seen at the site of abnormal contrast\nenhancement of the left superior cerebellar mass.\n\nMR Spectroscopy: Limited in evaluation given the small size of the lesion and\nlocation.",
            "output": "1. Minimal interval increase in size of the left superior superior cerebellar\nmass with minimal increased surrounding abnormal signal and increased\nperfusion on ASL sequences, concerning for residual disease.\n2. Limited evaluation of spectroscopy and MR contrast perfusion given the\nsmall size and location of the lesion.\n3. Punctate foci of enhancement along left temporal subarachnoid space and\noverlying the cerebellar folia concerning for leptomeningeal carcinomatosis."
        },
        {
            "input": "Interval increased size of a left tentorial enhancing lesion measuring 1.3 x\n1.4 x 1.4 cm (TRV, AP, SI) when compared to prior examination which measured\n1.2 cm in greatest dimension.  Re-identified are multiple punctate\nleptomeningeal foci of enhancement along the medial left temporal lobe (series\n4, image 47), similar appearance to prior exam.  No definitive new lesions are\nidentified.  There is no acute infarct.",
            "output": "1. Interval increased size of a left tentorial enhancing mass measuring\napproximately 1.4 cm in greatest dimension.\n2. Multiple punctate leptomeningeal foci of enhancement along the left medial\ntemporal lobe is similar appearance to prior exam.  No definitive new\nenhancing lesions."
        },
        {
            "input": "A left tentorial enhancing lesion is not significantly changed in size or\nsignal characteristics currently approximately 1.3 x 1.1 cm in size (8:8). \nPunctate enhancing leptomeningeal foci along the mid medial left temporal lobe\nare again identified (9:35, 36).  This is not significantly change relative to\nprior study.  No new enhancing lesion is identified.\n\nVentricles and sulci are stable in size and configuration.  There is no\nextra-axial fluid collection.  Intracranial flow voids are preserved.  Major\ndural sinuses appear patent.\n\nThe orbits are unremarkable.  Imaged paranasal sinuses and mastoid air cells\nbilaterally are clear.",
            "output": "Relative to prior examination performed ___, a left tentorial\nenhancing lesion and multiple punctate leptomeningeal enhancing foci along the\nmedial left temporal lobe are essentially unchanged.  No acute intracranial\nprocess or new enhancing lesion."
        },
        {
            "input": "Interval decrease in size of enhancing left tentorial lesion measuring\napproximately 0.7 x 0.5 cm (TRV, AP; series 17, image 34) from previously\ndescribed 1.3 x 1.1 cm.  Also decreased possibly size and number of punctate\nenhancing leptomeningeal foci along the medial left temporal lobe (series 17,\nimage 40).  When compared to pre treatment examination of ___,\nthere is increased surrounding FLAIR hyperintense signal, compatible with\nposttreatment changes.  No new enhancing lesions are identified.  There are a\nfew superimposed periventricular and subcortical T2/FLAIR white matter\nhyperintensities, unchanged from prior examination, nonspecific but compatible\nwith chronic microangiopathy in a patient of this age.  Incidental note is\nmade of a stable partial empty sella.\n\nThere is no acute infarct or intracranial hemorrhage.  The major intracranial\nflow voids are preserved.  The dural venous sinuses are patent.  A small right\nmaxillary sinus mucous retention cyst is unchanged.  The orbits are\nunremarkable.  Fluid signal is noted in the bilateral mastoid air cells.",
            "output": "1. Interval decrease size and enhancement of left tentorial lesion and\nleptomeningeal enhancing foci along the medial left temporal lobe.  Associated\nincreased surrounding FLAIR hyperintense signal likely represent posttreatment\nchanges.  Continued close interval followup is recommended.\n2. No new lesions."
        },
        {
            "input": "The 7 x 6 x 5 mm, oval lesion in the left posterior temporal lobe demonstrates\nincreased, more solid enhancement centrally in comparison 2 the prior\nexamination, but is unchanged in size.  The punctate, 3 mm enhancing lesion in\nthe adjacent, more anterior temporal lobe, and punctate 2 mm enhancing lesion\nin the adjacent lateral left temporal lobe are unchanged.  The curvilinear,\nleptomeningeal enhancement in the adjacent left temporal lobe are also\nunchanged.  The irregular, enhancing lesion in the left cerebellar hemisphere\nis unchanged.  The surrounding T2/FLAIR hyperintense signal in the left\nsuperior cerebellar hemisphere and left posterior temporal lobe is unchanged. \nNo new enhancing lesions are identified.\n\nScattered foci of T2/FLAIR hyperintensities in the periventricular and\nsubcortical white matter are unchanged and nonspecific.  There is no evidence\nof hemorrhage, edema, mass effect, midline shift or infarction.   The\nventricles and sulci are normal in caliber and configuration.\n\nThe right maxillary sinus contains a small mucous retention cyst.  There is\nmild mucosal thickening in the left maxillary and bilateral ethmoid sinuses. \nThe left mastoid air cells are partially opacified.  The orbits are\nunremarkable.\n\nThe major intracranial flow voids are preserved.",
            "output": "1. Unchanged size, but apparent increased, more solid enhancement of the\nlesion in the left posterior temporal lobe, consistent with metastases.  The\nslight difference in appearance could be related to differences techniques\nContinued follow-up is recommended.\n2. Unchanged size of the 2 punctate, enhancing lesions and leptomeningeal\nenhancement in the adjacent left temporal lobe as well as in the enhancing\nlesion in the left superior cerebellar hemisphere, consistent with metastases.\n3. No new enhancing lesions."
        },
        {
            "input": "Again seen are white matter hyperintensity on FLAIR and enhancement in the\nleft posterior temporal lobe.  The FLAIR abnormality is unchanged since the\nstudy of ___.  The volume of enhancing material in the temporal lobe\nhas increased since the ___ examination.  Also again seen is enhancement in\nthe left cerebellar hemisphere adjacent to the temporal lobe enhancement.  The\ncerebellar hemispheric enhancement also has increased since ___.  The volume\nof enhancing material in the cerebellar hemisphere is markedly smaller than on\n___.  However, the temporal lobe enhancement was not identified at\nthat time.  Overall, these findings suggest treatment effect, most likely due\nto radiation.\n\nNo other lesions are identified.  There is no evidence of hemorrhage, edema,\nother masses masses, midline shift or infarction.   The ventricles and sulci\nare normal in caliber and configuration.  There is no other abnormal\nenhancement after contrast administration.",
            "output": "1. Left temporal lobe and adjacent left cerebellar hemisphere enhancement with\nwhite matter hyperintensity on FLAIR.  These findings suggest radiation\nnecrosis.  However, continued follow-up is recommended to exclude a component\nof tumor progression\n\nRECOMMENDATION(S):  Continued close follow-up of apparent radiation necrosis\nto exclude a component of tumor progression."
        },
        {
            "input": "MRI BRAIN:  There is no evidence of hemorrhage, edema, mass, mass effect, or\nacute territorial infarction. No abnormal enhancement is appreciated after\ncontrast administration. 5 mm T2/FLAIR hyperintensity is present within the\nright thalamus without associated enhancement, abnormal diffusion, or mass\neffect. A similar abnormality was described in this region on the ___ MRI report. The ventricles and sulci are normal in size and\nconfiguration. The basal cisterns are patent. The paranasal sinuses appear\nclear. Known nondisplaced left suboccipital calvarial fracture is better\nappreciated on the recent CT.\n\nMRA BRAIN:  The intracranial vertebral and internal carotid arteries and their\nmajor branches appear normal without evidence of stenosis, occlusion, or\naneurysm formation.\n\nMRA NECK: The common, internal and external carotid arteries appear normal\nwithout evidence of dissection.  There is no evidence of stenosis by NASCET\ncriteria.  There is a normal three vessel arch with conventional origins of\nthe carotid and vertebral arteries.",
            "output": "1.  No evidence for acute intracranial process. No acute hemorrhage or\ninfarction.  Normal intracranial and cervical vessels.\n\n2.  Focus of FLAIR hyperintensity in the right thalamus is in a location\nsimilar to an abnormality described on the ___ report and is most\nconsistent with a chronic lacune"
        },
        {
            "input": "There is an approximately 3 x 3 x 2.5 cm anterior-posterior by superior\ninferior by transverse dimension mass in the suprasellar region which is\npartially cystic in its superior portion and solid in the inferior portion.\nThe mass does not expand the sella turcica.  The mass extends to the foramen\n___ region with deformity and dilatation of both lateral ventricles with\nmild periventricular edema.  There is no acute infarcts seen.  No midline\nshift is identified.\n\nThe mass deform the optic chiasm from the posterior aspect.  Low signal on\nsusceptibility images indicates calcification seen on the previous CT.  No\nenhancing brain lesions are identified.",
            "output": "1. Suprasellar mass extending to foramen ___ most likely due to\ncraniopharyngioma.\n2. Obstructive hydrocephalus with mild periventricular edema seen in the\nlateral ventricles.\n3. Optic chiasm is deformed from the posterior aspect."
        },
        {
            "input": "The patient is status post resection of the sellar and suprasellar mass\npreviously demonstrated.  There are expected postoperative changes including\npneumocephalus, right hemispheric mass effect with right-to-left midline\nshift, retraction changes in the right frontal and temporal lobes, hemorrhage\nalong the surgical pathway and minimal areas of slow diffusion at the\nretraction margins.  Postoperative hemorrhage limits evaluation of possible\nresidual enhancement.  However, there is enhancement within the sella turcica,\nin regions where there is no high signal intensity on the precontrast T1\nweighted images.  Thus, this likely represents residual tumor at the depth of\nthe resection site.  This is compatible with the finding of residual\ncalcification on the postoperative CT scan.  Images of the remainder of the\nbrain appear unchanged.",
            "output": "Status post resection of the sellar and suprasellar mass with expected\npostoperative changes.\nEnhancement within the sella turcica, along with residual calcification noted\non the CT scan, suggests a small amount of residual tumor in this location."
        },
        {
            "input": "Images are limited by motion artifact, even though the MP RAGE sequence was\nrepeated.\n\nThere is susceptibility artifact from the right frontal VP shunt hardware. \nThe VP shunt catheter traverses the right frontal lobe and the corpus\ncallosum, terminating along the lateral margin of the frontal horn of the left\nlateral ventricle.  The ventricles appear stable in size compared to the ___ CT.\n\nThere is thick right hemispheric dural enhancement and thin left frontal dural\nenhancement, likely secondary to the VP shunt and the right craniotomy.  The\nright dural enhancement is thicker than on the ___ MRI, but this\nis likely secondary to interim resolution of the right extra-axial collection.\nThere is also thick contrast enhancement in the right sylvian fissure, similar\nto the ___ MRI.\n\nEvaluation of the sella and suprasellar cistern on sagittal and coronal\npostcontrast MP RAGE images is limited by motion artifact.  Enhancing tissue\nin the right sella/suprasellar cistern is difficult to measure accurately, but\nits craniocaudad extent appears decreased since ___.\n\nRight frontal, anterior parietal, and superior temporal parenchyma is obscured\nby susceptibility artifact on diffusion-weighted images.  Elsewhere in the\nbrain parenchyma, no new acute diffusion abnormality is seen.",
            "output": "1. This study is limited by motion and by susceptibility artifact from the\nright frontal VP shunt hardware.\n2. The enhancing tissue in the right sella/ suprasellar cistern is difficult\nto measure accurately, but its craniocaudad extent appears decreased since ___.\n3. Thick right hemispheric dural enhancement, thicker than on ___\nfollowing interim resolution of the prior extra-axial collection.  Persistent\nthick enhancement in the right sylvian fissure.  Persistent within left\nfrontal dural enhancement.  These findings are compatible with post treatment\nchange.\n4. Stable position of the right frontal VP shunt catheter and stable size of\nthe ventricles compared to the ___ CT."
        },
        {
            "input": "The patient is status post right pterional craniotomy and right trans frontal\nventriculostomy catheter with tip terminating along the lateral margin of the\nfrontal horn of the anterior left lateral ventricle, unchanged from prior\nexam.  Susceptibility artifact secondary to a right parietal calvarial\nexternal reservoir severely degrades evaluation of adjacent structures.  The\nexamination is mildly to moderately motion degraded.  Within these confines:\n\nPresumably postoperative right greater than left frontal dural thickening\nmeasuring up to 3-4 mm is similar in extent and configuration from prior\nexamination of ___.  Dural enhancement and thickening as well as\nperipheral enhancement along the right track along the right middle cranial\nfossa extending to the suprasellar cistern demonstrates overall decreased\nenhancement and prominence compatible with evolving postsurgical sequela. \nSuperficial hemorrhage product along the right frontal convexity, sylvian\nfissure and lateral recess of the middle cranial fossa has decreased from\nexamination of ___.  No new intracranial hemorrhage is\nidentified.  Residual 1.2 x 0.9 x 1.3 cm (TRV, AP, SI ; series 11, image 122)\nsuprasellar cystic resection cavity with mild peripheral enhancement and\npossible small nodular components is unchanged from prior exam.  Mild right\nanterior temporal lobe and encephalomalacia is re-identified.\n\nThere is no acute infarct.  The ventricles are unchanged in configuration from\nprior examination.  The major intracranial flow voids are preserved.  The\ndural venous sinuses are patent on postcontrast MP-RAGE.  No new enhancement. \nPartial opacification of the frontal sinuses and left greater than right\nethmoid air cells is noted.  There is mild mucosal thickening of the bilateral\nmaxillary sinuses.  The orbits are unremarkable.  Fluid signal is noted in the\nbilateral mastoid tips.",
            "output": "Examination is degraded by susceptibility artifact from right trans frontal\nventriculostomy catheter reservoir and patient motion.  Within these confines:\n\n1. Expected evolving sequela of right pterional craniotomy for resection and\nradiation therapy of a suprasellar mass, with decreased dural and peripheral\nenhancement and hemorrhage product along the right middle cranial fossa. \nResidual postoperative dural thickening along the right greater than left\nfrontal lobes is similar to prior exam.\n2. There remains a peripherally enhancing cystic resection cavity in the right\nsupra sellar cistern with unchanged possible small nodular components.  No\ndefinitive increasing lesion or new enhancement.\n3. Right trans frontal ventriculostomy catheter terminates along the lateral\nmargins of the anterior left lateral ventricle, unchanged.  Stable ventricular\nsize.\n4. New paranasal sinus disease as described above."
        },
        {
            "input": "There are blood products or would areas age with mild surrounding enhancement\nin the right frontal lobe and left temporal lobe with surrounding edema. \nRestricted diffusion and region likely reflects blood products.  There are\npostoperative changes in the right frontoparietal region.  A 14 mm subdural\ncollection in the right parietal region with underlying meningeal enhancement\nshows restricted diffusion which could be related to blood products.  No acute\ninfarcts are seen.  There is no hydrocephalus mild mass effect on the left\nlateral ventricle is seen.\n\nPost gadolinium images demonstrate some enhancement adjacent to the blood\nproducts and along the meninges.  No other parenchymal areas of abnormal\nenhancement seen.\n\nThe MP rage images demonstrate normal enhancement of the superior sagittal and\ntransverse sinuses and there is no evidence of dural sinus thrombosis.  There\nis no intrinsic filling defect identified.",
            "output": "1. Right frontal and left temporal hematoma is of various age with mild\nsurrounding enhancement.  No acute infarcts.\n2. Right-sided postoperative changes with parietal subdural collection which\nappears to be due to subacute blood products.  Any associated infection cannot\nbe excluded on MRI appearances alone.\n3. No evidence of dural sinus thrombosis on MP rage images."
        },
        {
            "input": "MRI Brain:\nThe patient is status post right frontoparietotemporal craniotomy with\ncontinued, interval decrease in the size of the subjacent subdural fluid\ncollection, now measuring 2 mm in thickness.  The underlying dural thickening\nand enhancement is unchanged.\n\nThe right frontal lobe hemorrhage is unchanged and size, appearance, and\nsignal characteristics with areas of T1 hyperintense, T2 hypointense signal\nwith peripheral enhancement, unchanged from ___ and decreased from\n___.  Areas of slow diffusion in the right frontal lobe are related\nto the broad products, unchanged from the prior examination.  The associated\nex vacuo dilatation of the right lateral ventricle is unchanged.  The\nencephalomalacia in the left frontal lobe is unchanged.\n\nThe curvilinear, T1 hyperintense signal in the left temporal lobe with\nsusceptibility, representing cortical laminar necrosis, is unchanged.  The\ncurvilinear enhancement in the left temporal lobe is unchanged from ___, but decreased from ___.\n\nNo new hemorrhages are identified.  There are no acute infarcts, midline\nshift, or masses.  The small herniation of the right temporal lobe through the\ngap in the right posterior craniotomy site is unchanged.\n\nThe paranasal sinuses and mastoid air cells are clear.  The orbits are\nunremarkable.\n\nMRA brain: The intracranial vertebral and internal carotid arteries and their\nmajor branches appear normal without evidence of stenosis, occlusion, or\naneurysm formation.\n\nMRA neck:  The common, internal and external carotid arteries appear normal. \nThere is no evidence of internal carotid artery stenosis by NASCET criteria. \nThe origins of the great vessels, subclavian and vertebral arteries appear\nnormal bilaterally.\n\nMRV Brain:  The superior sagittal sinus, straight sinus, right transverse\nsinus, and bilateral sigmoid sinuses are patent.  The absence of flow related\nsignal in the left transverse sinus with subsequent enhancement on the\npostcontrast MPRAGE sequences is unchanged from the prior examination.  The\njugular and internal cerebral veins are patent.",
            "output": "1. No acute infarction or dural venous sinus thrombosis.\n2. Unchanged hemorrhages in the bilateral frontal lobes, right greater than\nleft, and left temporal lobe.\n3. Status post right frontoparietotemporal craniotomy with interval decrease\nin the size of the subjacent subdural fluid collection."
        },
        {
            "input": "Study is degraded by motion.\n\nPostsurgical changes related to right frontal parietal temporal craniotomy are\nagain seen, with grossly stable underlying dural thickening.\n\nGrossly stable bifrontal encephalomalacia is again seen.  Focal right frontal\nrestricted diffusion within the right frontal lobe encephalomalacia is grossly\nunchanged (see 550, 552: 38 on current study and 5, 6:22 on prior exam).  This\nstructure does not clearly demonstrate increase susceptibility, and\ndemonstrates FLAIR hyperintensity and T2 heterogeneity, and is isointense\nsignal (see 06:18; 300:289; 07:39; 400:407; 03:29).\n\nBilateral temporal and left occipital encephalomalacia with probable chronic\nblood products is again seen.  There is nonvisualization of the anterior\nsuperior venous flow void, grossly similar to ___ prior exam (series 7 on\ncurrent study and series 4 on ___ prior exam)..\n\nGrossly stable nonspecific subdural collection overlying right posterior\nfrontal and parietal lobes with maximum diameter up to approximately 5 mm (see\n400:430) is again seen.\n\nThere is no evidence of mass effect, ormidline shift.  The ventricles and\nsulci are grossly stable in caliber and configuration.\n\nBilateral hippocampal formations and mammillary bodies are grossly preserved\nin signal and configuration. There is no disproportionate medial temporal\natrophy.",
            "output": "1. Study is degraded by motion.\n2. Grossly stable bifrontal, bitemporal and left occipital encephalomalacia.\n3. Grossly stable nonspecific subdural collection overlying right posterior\nfrontal and parietal lobes, with maximum diameter up to 5 mm.\n4. Within area of right frontal encephalomalacia, focal area of parenchymal\nsignal intensity abnormality with restricted diffusion, grossly similar\nappearance as finding on ___ prior exam as described.  While findings may\nrepresent evolving recent blood products, mass or late acute to subacute\ninfarct within residual brain tissue is not excluded on the basis of this\nexamination.  Consider contrast brain MRI for further evaluation.  Recommend\nfollow-up imaging to resolution.\n\nRECOMMENDATION(S):  Within area of right frontal encephalomalacia, focal area\nof parenchymal signal intensity abnormality with restricted diffusion, grossly\nsimilar appearance as finding on ___ prior exam as described. While findings\nmay represent evolving recent blood products, mass or subacute infarct within\nresidual brain tissue is not excluded on the basis of this examination. \nConsider contrast brain MRI for further evaluation. Recommend follow-up\nimaging to resolution.\n\nNOTIFICATION:  The impression and recommendation above was entered by Dr.\n___ on ___ at 16:56 into the Department of Radiology critical\ncommunications system for direct communication to the referring provider."
        },
        {
            "input": "Stable appearance of the right frontoparietotemporal craniotomy with unchanged\nadjacent subdural fluid collection.  Encephalomalacia with gliosis and\nsurrounding T2/FLAIR hyperintensity are again noted in the bifrontal, right\nparietal, and right temporal lobes, grossly unchanged since prior exam.  There\nis stable ex vacuo dilatation of the right ventricle.  There is unchanged\nappearance of susceptibility artifact within the area of known\nencephalomalacia.  No evidence of intracranial hemorrhage is appreciated.\n\nThere are multiple foci of diffusion restriction with associated FLAIR\nhyperintensity and peripheral enhancement.  These lesions appear decreased in\nsize compared to MRI dated ___, with the largest lesion now\nmeasuring up to 1.5 cm.\n\nThere is no large vascular distribution infarct.  The visualized vascular flow\nvoids are grossly unremarkable.  The dural venous sinuses are patent.  The\nparanasal sinuses and mastoid air cells are clear.  No abnormal marrow signal.",
            "output": "1. No acute intracranial findings.  No evidence of an acute infarction, or new\nhemorrhage.\n2. Stable postsurgical changes with unchanged encephalomalacia in the\nbifrontal, and right parietotemporal region.  Interval decrease of enhancement\nwithin the area of encephalomalacia compared to MRI dated ___.\n3. No evidence of acute dural venous sinus thrombosis."
        },
        {
            "input": "No acute infarct or intracranial hemorrhage is identified. There is no mass,\nmass effect or midline shift. The ventricles, cisterns and cerebral sulci are\nprominent reflecting a mild to moderate degree of cerebral atrophy, similar to\nthe prior CT exam. The extra-axial fluid spaces overlying the frontal and\ntemporal lobes are slightly prominentn as are the temporal horns, suggesting a\nfrontal and temporal predominance of the cerebral atrophy with atrophy of the\nhippocampi. The temporal horns appear slightly more dilated compared to the\nprior CT examination.\n\nThe patient is status post bilateral lens extractions. The visualized soft\ntissues are unremarkable.",
            "output": "1. No acute infarct, space-occupying lesion or intracranial hemorrhage.\n2. Mild to moderate cerebral atrophy with a  frontal and temporal lobe\npredominance.  The hippocampi are mildly atrophic bilaterally."
        },
        {
            "input": "Evaluation is limited due to motion, particularly on the FLAIR and T2\nsequences.\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, or infarction.\nThe ventricles and sulci are normal in caliber and configuration. There is no\nabnormal enhancement after contrast administration.\n\nMajor intravascular flow voids are preserved.  There is normal enhancement of\nthe major intracranial arteries and dural venous sinuses following contrast\nadministration.\n\nMarrow signal is within normal limits.  There is fluid in a right posterior\nethmoid air cell.  There is mild mucosal thickening of the maxillary sinuses. \nThe mastoid air cells appear clear.  The orbits are normal.  There is mild\ntonsillar ectopia noted but no other stigmata of Chiari 1 malformation.",
            "output": "1. Mildly limited study due to motion on a few sequences.  No enhancing or\nother brain lesions.\n2. Minimal paranasal sinus disease."
        },
        {
            "input": "Study is mildly degraded by motion.  There is no evidence of hemorrhage,\nedema, masses, mass effect, midline shift or infarction.   The ventricles and\nsulci are normal in caliber and configuration.  Limited imaging of the\ncervical spine demonstrates nonspecific straightening of the cervical\nlordosis.",
            "output": "1. Study is mildly degraded by motion.\n2.  No acute intracranial abnormality.\n3. No definite evidence of Chiari I or II malformation."
        },
        {
            "input": "Carotid and vertebral arteries demonstrate normal flow signal. There is no\nevidence of vascular, stenosis or dissection. The. The thoracic aorta and its\nmajor branches also demonstrate normal appearances. The vertebral artery\nartery origins are patent.",
            "output": "No significant abnormalities are seen on MRA of the neck. No evidence of\ndissection, stenosis or occlusion."
        },
        {
            "input": "MRI BRAIN:\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  Scattered foci of T2/FLAIR hyperintensities in the\nsupratentorial white matter are nonspecific, but likely represent the sequela\nof chronic small vessel ischemic disease.  The ventricles and sulci are normal\nin caliber and configuration.\n\nThere is an enhancing focus of T1 iso to hypointense, T2 hyperintense signal\nalong the inner table of the right parietal skull measuring up to 1.0 x 0.6 cm\n(series 1000B, image 97), likely corresponding to an subtly lytic lesions seen\non prior CT examination of ___.  This lesion was not seen on CT\nexamination of ___.\n\nThe paranasal sinuses and mastoid air cells are clear.  The orbits are\nunremarkable.\n\nMRA brain: The intracranial vertebral and internal carotid arteries and their\nmajor branches  are patentwithout evidence of stenosis, occlusion, or aneurysm\nformation.",
            "output": "1. No acute infarct or intracranial hemorrhage.\n2. Patent circle of ___.\n3. Incompletely characterized 1.0 cm focus of enhancement along the inner\ntable of the right parietal skull, corresponding to an lytic lesions seen on\nprior CT head of ___.  Of note, this lesion does not appear to be\npresent on CT examination of ___.  While this may represent\ninterval growth of a osseous hemangioma, recommend repeat CT examination to\ndocument interval stability since prior exam to exclude more were some lesion\ngiven its development since examination of ___.\n\nRECOMMENDATION(S):\n\n1. Incompletely characterized 1.0 cm focus of enhancement along the inner\ntable of the right parietal skull, corresponding to an lytic lesions seen on\nprior CT head of ___. Of note, this lesion does not appear to be\npresent on CT examination of ___. While this may represent\ninterval growth of a osseous hemangioma, recommend repeat CT examination to\ndocument interval stability since prior examination of ___ to\nexclude more worrisome lesion given development since examination of ___.\n\nNOTIFICATION:  The impression and recommendation above was entered by Dr.\n___ on ___ at 19:47 into the Department of Radiology critical\ncommunications system for direct communication to the referring provider."
        },
        {
            "input": "Again seen are multiple foci of white matter hyperintensity on FLAIR images\ncompatible with the diagnosis of demyelinating disease.  There is a new 3 mm\nfocus of FLAIR hyperintensity in the left posterior temporal deep white matter\ncompared to prior MRI from ___ (axial FLAIR series 5 image 14, and\nsagittal 3D FLAIR series 4 image 54). This focus does not demonstrate slowed\ndiffusion or enhancement. There is no lesion of the brainstem or cerebellum.\nBrain volume is age appropriate.\n\nThere is no evidence of hemorrhage, infarction, intracranial mass, mass\neffect, or midline shift.  Intracranial flow voids are maintained.  There is\nnormal opacification of the major intracranial arteries and dural venous\nsinuses following contrast administration.\n\nVisualized paranasal sinuses and mastoid air cells are clear.  Orbits are\nnormal.",
            "output": "1. New 3 mm focus of FLAIR hyperintensity in the left posterior temporal deep\nwhite matter compared to prior MRI from ___, consistent with an\nintervally developed demyelinating plaque. This lesion does not demonstrate\nslowed diffusion or contrast enhancement.\n2. Other foci of FLAIR hyperintensity in the white matter are unchanged from\nMRI on ___."
        },
        {
            "input": "There are at least 4 enhancing lesions, the largest measuring 2.0 x 1.6 cm in\nthe right frontoparietal lobe (10:15), 1.5 x 1.2 cm, the right cerebellum\n(10:11), 0.7 x 0.5 cm right anterior frontal lobe (10:19), and 0.4 x 0.4 cm in\nthe left anterior frontal lobe (10:18).  The cerebellar mass demonstrate\nblooming artifact on the susceptibility sensitive sequence, likely\nrepresenting hemorrhage.  The largest likely intra-axial lesion in the right\nfrontoparietal lobe demonstrated dural thickening and enhancement as well as\nextensive vasogenic edema, exerting mass effect and resulting in leftward\nshift 11 mm.  There is narrowing of the bilateral ambient cisterns, though\nbasal cisterns appears overall patent.  There is right uncal herniation.  The\nright lateral ventricle is near completely effaced with residual in the right\nfrontal horn.  There is mild prominence of the left lateral ventricle with\nmild hypodense appearance of the periventricular white matter near the antrum,\nwhich may represent transependymal flow versus nonspecific periventricular\nT2/FLAIR hyperintensity, which may be related to chronic small vessel\nischemic.\n\nThere is questionable enhancement along the right cisternal trigeminal segment\n(series 900, image 92).\n\nThere is T1 and T2 hyperintense appearance of the right petrous apex, which\nmay represent marrow signal versus fluid within the petrous apex.\n\nThere is mild bilateral anterior ethmoidal air cell mucosal thickening.  The\nremaining paranasal sinuses, middle ear and mastoid air cells are patent.  The\nglobes are unremarkable.  The major intracranial flow voids are preserved. \nThe dural venous sinuses are patent on postcontrast MP-RAGE.",
            "output": "1. At least 4 enhancing intraparenchymal lesions in both supra and\ninfratentorial distribution.  The largest lesion in the right frontoparietal\nlobe demonstrate slightly heterogeneous enhancement with dural thickening and\nextensive white matter vasogenic edema.\n2. The right frontal parietal lesion results in 1.1 cm leftward midline shift\nwith near complete effacement of the right lateral ventricle.  While narrowed,\nthe basal cisterns remain patent.  There is right uncal herniation.\n3. There is mild prominence of the left temporal horn with suggestion of\nperiventricular FLAIR white matter signal, concerning for hydrocephalus.\n4. T1 and T2 hyperintense signal of the right petrous apex, which may\nrepresent marrow versus fluid, asymmetric in appearance to the left.  This\ncould be further evaluated with dedicated CT temporal bone."
        },
        {
            "input": "Again seen are multiple enhancing brain lesions as follows:\n\nLeft frontal lobe measuring 0.3 cm TV x 0.5 cm AP x 0.4 cm SI (4:128, 401:48)\nRight frontal lobe measuring 0.6 cm TV x 0.9 cm AP x 1.0 cm SI (4:133, 401:62)\nRight frontoparietal lobe measuring 2.1 cm TV x 2.9 cm AP x 2.7 cm SI (4:112,\n401:103) with adjacent dural thickening enhancement.\nRight cerebellar hemisphere measuring 1.9 cm TV x 1.4 cm AP x 1.2 cm SI (4:89,\nfor L1: 118)\n\nThere is edema surrounding the right frontoparietal lesion causing effacement\nof the right lateral ventricle with approximately 8 mm leftward midline shift.\nThere is right-sided uncal herniation with mass effect on the right aspect of\nthe midbrain.  The dural venous sinuses appear patent on the postcontrast MP\nRAGE images.  There is slow diffusion associated with the right frontoparietal\nlesion.  There is no evidence of acute territorial infarction.  The previously\ndescribed right petrous apex lesion is better assessed on the noncontrast head\nMRI.  There is right maxillary sinus mucosal retention cyst.  The orbits\nappear unremarkable.",
            "output": "1. Redemonstration of multiple enhancing brain lesions with edema surrounding\nthe right frontal parietal lesion with resulting 8 mm leftward midline shift,\neffacement of the right lateral ventricle and presence of right-sided uncal\nherniation, as described above.\n2. Please refer to prior complete head MRI for additional details, including\nnonspecific right petrous apex lesion better seen on the prior study."
        },
        {
            "input": "The patient is status post right craniotomy and resection of the right\nposterior temporal lesion.  There are T1 hyperintense blood products in the\nsurgical bed without evidence for residual masslike enhancement.  There is\nextensive vasogenic edema in the right temporal, parietal, and frontal lobes,\nextending into the posterior external and internal capsules, not significantly\nchanged compared to ___.  Leftward shift of midline structures\nmeasures 7 mm, similar to the ___ postsurgical CT, but decreased\ncompared to the presurgical MRI exams.  Compression of the third ventricle and\nmild prominence of the posterior components of the left lateral ventricle are\nalso unchanged compared to ___ CT.  A small focus of slow diffusion\nsuperior to the surgical bed, images 6:18 and 5:18, is compatible with\nretractor injury.\n\nEnhancing lesions in the right cerebellar hemisphere (13:8), right frontal\nlobe (13:16), and left frontal lobe (100:64), are unchanged in the short\ninterim.  There is stable minimal edema associated with the right frontal\nlesion.  No additional enhancing lesions are seen.\n\nMajor vascular flow voids are grossly preserved.  Dural venous sinuses appear\npatent.\n\nThere is fluid in the right mastoid.  There are mucous retention cysts in\nright greater than left maxillary sinuses.",
            "output": "1. S/p right posterior temporal mass resection.  Allowing for T1 hyperintense\nblood products, there is no evidence for residual enhancing mass, but\nfollow-up is needed after resolution of the blood products.\n2. Residual mass effect is stable compared to the ___ postsurgical\nCT.\n3. Additional enhancing lesions in the right cerebellar hemisphere, right\nfrontal lobe, and left frontal lobe are unchanged in the short interim\ncompared to ___."
        },
        {
            "input": "Again seen are multiple enhancing supra and infratentorial parenchymal lesions\ncompatible with a history of metastatic disease.  Again seen are postoperative\nchanges after right temporal craniotomy.  There is now a small rim of\npostoperative enhancement at the surgical site.  The edema, mass effect and\nmidline shift associated with the right temporal surgical site have\ndramatically decreased since the prior study.  No new lesions are identified.",
            "output": "1. Localizing study for radiation planning.\n2. Again seen are multiple enhancing metastases.\n3. There has been a dramatic reduction in edema and mass effect associated\nwith the right temporal lobe."
        },
        {
            "input": "Postoperative changes status post right temporal craniotomy are again noted. \nMild postsurgical dural thickening and enhancement along the resection margins\nhave not changed since the prior examination.  Surrounding edema has decreased\nsignificantly since ___.  There is no evidence of local disease\nprogression/recurrence in this region.  The previously seen right frontal\nlesion (900:103) now measures 5.1 mm, previously up to 10 mm.  A left frontal\nlesion (900:98) measures 3 mm, previously 5 mm.  The previously seen right\ncerebellar (900:82) lesion measures 19 x 11 mm, previously 22 x 18 mm.  No new\nenhancing lesions are identified.  There is no acute infarct or intracranial\nhemorrhage.\n\nThe dural venous sinuses appear patent.  The major intracranial flow voids are\npreserved.  Small amount of fluid is seen within the right mastoid air cells,\nunchanged.  Mucous retention cysts are again seen in the bilateral maxillary\nsinuses.  The orbits are unremarkable.",
            "output": "1. Postsurgical changes status post right temporal craniotomy and temporal\nmass resection without evidence of disease progression/recurrence within the\nresection cavity.\n2. Overall decrease in size of multiple other metastatic lesions in the\nbilateral frontal lobes and in the right cerebellum.  No new enhancing lesions\nidentified.\n3. Additional findings described above."
        },
        {
            "input": "There is overall improvement in previously seen lesions.  At the postoperative\nsite in the right temporal region previously seen enhancement has resolved. \nSubtle FLAIR hyperintensities are seen.  Previously seen bilateral frontal and\nright cerebellar lesions have considerably decreased in size or are\nimperceptible.  There is mild FLAIR hyperintensity  at the right cerebellar\nlesion but the previously seen bilateral frontal lesions are not visible.  No\ndefinite new enhancing lesions are identified.",
            "output": "Overall considerable improvement since the previous study.  Almost complete\nresolution of enhancement previously seen lesions and subtle if any remaining\nFLAIR hyperintensities are identified.  No acute infarcts or new areas of\nenhancement."
        },
        {
            "input": "Heterogeneous enhancement and vasogenic edema is identified in the right\ncerebellar hemisphere, with no significant mass effect or narrowing of the\nfourth ventricle or cerebellar pontine angle, apparently this lesions are new\nsince the prior exam, but a focal enhancing lesion was present in this area in\nthe examination dated ___, few foci of slow diffusion are noted this\narea suggesting hypercellularity (image 9, series 502), there is no evidence\nof hemorrhagic transformation.  Supratentorially postsurgical changes are\nidentified in the right temporal region, with underlying T2/FLAIR\nhyperintensity and minimal dural enhancement, suggesting postsurgical changes,\nattention in this area in follow-up exams is advised.  FLAIR high-signal\nintensity is noted in subcortical white matter of both frontal lobes, more\nsignificant on the right, with no evidence of abnormal enhancement, the\npreviously nodular enhancing lesions noted in both frontal lobes are not\nlonger seen.  The ventricles and sulci otherwise are unremarkable.  The major\nvascular flow voids are present and demonstrate normal distribution.  The\norbits are unremarkable, the paranasal sinuses again demonstrate bilateral\nmucous retention cysts in the maxillary sinuses, no air-fluid levels are seen,\nthe mastoid air cells are clear.",
            "output": "1.  Heterogeneous enhancement and vasogenic edema is identified in the right\ncerebellar hemisphere, apparently new since the prior exam, the possibility of\nneoplastic activity is a consideration with underlying posttreatment changes.\n\n2.  Postsurgical changes identified in the right temporal region with\nunchanged T2/FLAIR hyperintense area, with minimal dural enhancement and\nlikely postsurgical.  There is no evidence of mass effect or new areas with\nabnormal enhancement.\n\n3.  FLAIR hyperintense areas are noted in both frontal lobes with no evidence\nof abnormal enhancement.\n\nNOTIFICATION:  The findings were discussed with ___, M.D. by ___\n___, M.D. on the telephone on ___ at 11:51 am, 5 minutes after\ndiscovery of the findings."
        },
        {
            "input": "Previously seen area of enhancement in the right cerebellum has become larger\nand more confluent, measuring 4 cm x 2 cm x 2.1 cm today, compared with 3.1 cm\nx 1.9 cm x 1.8 cm on ___.  Tiny foci of mineralization or\nmicrohemorrhage within the lesion centrally.  Findings are new since ___.  Enhancement pattern is ring-like, and the lesion itself is\nsituated deep and medial to the site of the originally treated metastasis. \nLesion quotient is 0.26, which is less than 0.3, and may favor radiation\nnecrosis.  Originally treated metastasis has thin linear peripheral\nenhancement today, slightly more prominent compared with prior.  Surrounding\nedema is significantly worsened since ___, involves entire right\ncerebellar hemisphere, extending to the right middle and superior cerebellar\npeduncle.  There is moderate obliteration of the fourth ventricle, no\nhydrocephalus.  Partially effaced pre pontine cistern, new since prior.  Mild\ncrowding at foramen magnum, new since prior, without tonsillar herniation. \nPartially effaced superior cerebellar cistern, new since prior.\n\nThere is re-demonstration of postsurgical changes in the right posterior\ntemporal lobe with mild dural enhancement and underlying T2 FLAIR\nhyperintensity, stable.\nNo new lesions.\nSubcortical and deep white matter T2 FLAIR hyperintensities are\nre-demonstrated in the bilateral frontal lobes, right greater than left in\nhave no associated postcontrast enhancement.\n\nThe ventricles and sulci are otherwise normal in caliber and configuration. \nThere is a right maxillary mucous retention cyst and right frontal sinus\nopacification otherwise the imaged portion of the paranasal sinuses and\nmastoid air cells are clear.  The orbits are unremarkable.",
            "output": "1. Interval increase in the size of peripheral enhancing lesion, surrounding\nedema in the right cerebellum, since ___.  Findings are essentially\nnew since ___.  Abnormality is deep to and away from the\npreviously seen treated metastasis.  Differential considerations include\nradiation necrosis and tumor progression.  Radiation necrosis is probably more\nlikely.  Consider MR perfusion and spectroscopy in further evaluation.\n2. Local mass effect in the posterior fossa, significant narrowing the fourth\nventricle, moderately effaced pre pontine, superior cerebellar cistern and\nforamen magnum, without herniation, no hydrocephalus.  Close clinical and\nimaging follow-up recommended.\n3. No new metastases.\n\nRECOMMENDATION(S):  MR perfusion, spectroscopy may be helpful in further\nevaluation"
        },
        {
            "input": "Again seen is a peripherally enhancing lesion centered in the right cerebellar\nhemisphere with associated surrounding FLAIR hyperintensity and mass effect\nwith partial effacement of the fourth ventricle.  Overall, the degree of mass\neffect and surrounding edema is grossly unchanged.  The enhancing lesion\nmeasures approximately 4.2 cm TRV x 2.4 cm AP, similar compared to prior,\npreviously 4.3 x 2.2 cm, however, the rind of peripheral enhancement\nparticularly at its lateral aspect on the MPRAGE sequences (17:45) is thicker.\n\nPatient is status post right temporal craniotomy for underlying resection. \nThere is a subtle 3 mm focus of enhancement in close proximity to though not\ndirectly abutting the postoperative bed (17:93) in the right temporoparietal\nregion, new since prior.  Associated FLAIR signal abnormality is unchanged in\nthis region.\n\nMore inferior to the surgical bed at the inferior aspect of the right\ntemporoccipital region are additional enhancing lesions which are new since\nprior.  There is more extensive associated FLAIR signal abnormalities in these\nregions as well.  Specifically, there is a new peripherally enhancing 0.9 x\n0.7 cm lesion (17:67).  There is also irregular parenchymal enhancement more\ninferiorly abutting the tentorium (17:61) measuring 1.5 cm AP x 0.7 cm TRV.\n\nThere is new enhancement in the subcortical white matter of the right frontal\nlobe which is relatively ill-defined, spanning a 1.1 x 0.9 cm area (17:95). \nThis area demonstrates associated FLAIR hyperintensity which has progressed in\nthe interim.  Of note, this had been the location of the previously seen\nenhancing metastatic lesion in ___\n\nThere is an additional subcortical white matter T2/FLAIR hyperintensity in\nleft frontal lobe (15:14) without associated underlying enhancement.  Of note,\nthis had been the location of the previously seen enhancing metastatic lesion\nin ___.\n\nThere is no acute infarct.  Mild associated susceptibility artifact seen in\nassociation with the right frontal and right cerebellar lesions.\n\nPterygoid recess of the right sphenoid sinus is opacified.",
            "output": "1. Dominant peripheral enhancing lesion in the right cerebellar hemisphere\ndemonstrates thicker rind of peripheral enhancement when compared to prior the\nsimilar degree of mass effect.\n2. Additional regions of abnormal enhancement with associated FLAIR signal\nabnormality centered at the inferior aspect of the right temporoccipital\nregion.\n3. New small area of enhancement adjacent to but not directly abutting the\npostsurgical bed of the right temporoparietal region.\n4. New enhancing focus in the right frontal lobe in the region of previously\nseen metastatic disease on remote prior exam from ___.\n5. Findings could certainly represent progression of disease though\ncorrelation regarding sites of treatment and radiation is suggested"
        },
        {
            "input": "Exam submitted for interpretation on ___.\n\nThe patient's previously noted peripherally enhancing lesion in the right\ncerebellum is again seen and has mildly worsened.  Areas of nodular,\ndiscontinuous enhancement along the undersurface of adjacent lateral right\noccipital lobe, posterior right temporal lobe are mildly more prominent, this\nis area where there was no metastases on prior imaging.  Cerebellar lesion did\nnot have increased perfusion on ASL on ___\nDistribution of findings strongly favors component of radiation necrosis.\n\n1 cm area of enhancement in the right frontal lobe is mildly more prominent\nsince prior, findings may represent posttreatment change, continued follow-up\nrecommended to exclude tumor.\n\nPostsurgical changes right lateral temporal lobe, stable minimal linear\nenhancement marginating surgical cavity.\n\nRecommend ASL.",
            "output": "1. Mild interval increase in size of previously seen lesions.\n2. Distribution of findings in the right cerebellum, and adjacent inferior\noccipital, temporal lobes strongly favors component of radiation necrosis.\n3. Recommend ASL in future follow-up.\n\nRECOMMENDATION(S):  Follow-up brain MRI without and with gadolinium, and ASL."
        },
        {
            "input": "Postoperative changes right suboccipital craniectomy, partial resection of an\nenhancing right cerebellar mass compared with ___.  Small volume\nblood products within surgical cavity is similar compared with CT head ___.  The enhancement pattern in the right cerebellum, as well as\npresence of edema and enhancement present on the adjacent undersurface of the\nright temporal, lateral occipital lobe favors component of radiation necrosis\nin the current setting.  There was no metastasis in the inferior right\ntemporal, occipital lobe on the pre SRS scan ___.  Imaging follow-up\nrecommended to exclude component of residual or new disease.  Moderately\nextensive right cerebellar edema is similar compared with ___..\nRight parietal craniotomy, posttreatment changes in the adjacent posterior\nright temporal lobe, without associated enhancement.  Posttreatment change\nright frontal lobe deep white matter at the site of previously seen\nmetastasis, surrounding edema has worsened since ___, faint focus\nenhancement associated with it measures 1 cm, similar to prior ___\nthere few punctate foci of microhemorrhage.  Findings favor post radiation\nchange.  Short-term follow-up, to include ASL, is recommended.\n\nMild paranasal sinus disease.  No acute infarcts.  No midline shift.  No new\nhemorrhage.  Intracranial vascular flow voids are preserved.  Dural venous\nsinuses are patent.  No hydrocephalus.",
            "output": "1. Postoperative changes right cerebellum, small volume blood products in the\nsurgical bed.  Residual enhancing lesion in the right cerebellum, and areas of\nenhancement across the right tentorium in adjacent right temporal and\noccipital lobe.  Overall appearance strongly favors postradiation change. \nFollow-up recommended to ensure involution.\n2. Mildly worsened edema at the right frontal lobe deep white matter treated\nmetastasis, areas of microhemorrhage.  Findings favor postradiation change. \nShort-term interval follow-up recommended, with the addition of ASL.\n\nRECOMMENDATION(S):  Short-term follow-up brain MRI without and with\ngadolinium, with ASL, at 3 tesla scanner."
        },
        {
            "input": "Postoperative suboccipital craniectomy changes as well as right parietal\ncraniotomy changes again noted.\n\nRe-demonstrated is an enhancing right cerebellar mass measuring 2.4 x 2.0 cm,\npreviously 2.8 x 1.7 cm with mild associated FLAIR signal abnormality (15:50).\nIn addition there is a 1.8 x 1.4 cm enhancing lesion in the right lateral\noccipital lobe (15:65) in the region where on the prior study there were 2\nsubcentimeter foci of enhancement.  FLAIR signal abnormality surrounding these\nthe right lateral occipital lesions has significantly increased since the\nprior study.\nIn the right inferior temporal lobe posteriorly, there is a 2.5 x 1 cm (15:35)\nenhancing lesion, previously a 5 mm focus of enhancement on the prior study. \nFLAIR signal abnormality surrounding the right posterior temporal lobe lesion\nhas significantly increased since the prior study.\nIn the right frontal lobe there is a 2.3 x 2.3 cm enhancing lesion (15:113),\nmeasuring 9 mm on the prior study.  There is extensive vasogenic edema\nsurrounding the right frontal lobe lesion, significantly increased since the\nprior study common resulting in 8 mm leftward midline shift.",
            "output": "1. Enhancing lesions in the right frontal lobe, right temporal lobe, and right\noccipital lobe increased in size and significantly increased vasogenic edema. \nFindings concerning for disease progression.\n2. Enhancing right cerebellar lesion not significantly changed in size\ncompared to the prior study with mild FLAIR signal abnormality decreased since\nthe prior study.  Findings may represent postradiation change versus\npersistent disease.\n\nNOTIFICATION:   The impression and recommendation above was entered by Dr.\n___ on ___ at 16:03 into the Department of Radiology\ncritical communications system for direct communication to the referring\nprovider."
        },
        {
            "input": "The patient's previously noted supra and infratentorial enhancing lesions are\nagain seen.  There is a mild increase in the necrotic component of the\nlesions.\n\nAllowing for differences in patient positioning, the right frontal enhancing\nlesion now measures 2.4 x 2.8 cm from 2.3 x 2.3 cm.  The right inferior\ntemporal lobe enhancing lesion now measures 2.3 x 2.4 cm from 2.5 x 1.9 cm. \nThe right lateral occipital lesion is unchanged in size measuring 1.8 x 1.4\ncm.  The right cerebellar mass now measures 2.0 x 2.2 cm from 2.0 x 2.4 cm. \nThere is mass effect with approximately 0.6 cm leftward midline shift, which\nis stable.\n\nThe dural venous sinuses are patent.  There is a mucous retention cyst in the\nright maxillary sinus.  The visualized portions of the orbit are unremarkable.",
            "output": "1. Stable to mild interval increase in size with increased necrotic appearance\nof the previously seen lesions as described above."
        },
        {
            "input": "Postsurgical changes after right parietal and right suboccipital craniotomies\nfor resection of metastatic lesions are again noted.  There is mild residual\nenhancement and FLAIR hyperintensity in the region of the previously\nidentified right temporal and right cerebellar masses which appears less\nconspicuous on today's exam.\n\nThe right frontal lobe mass has decreased in size now measuring 1.8 x 1.5 x\n2.3 cm (AP X TR X SI) from previously 2.8 x 2.4 x 2.3 cm.  There has been\nmarked interval decrease of the surrounding FLAIR hyperintensity.  Minimal\nchronic hemorrhage associated with the right frontal mass is unchanged.\n\nWaxing and waning area of FLAIR hyperintensity in the left anterior frontal\nlobe (series 7, image 14) was first identified in ___ but appears larger\nin size and more conspicuous on today's exam.  There is no contrast\nenhancement in this region.\n\nThere is no evidence of new lesions, midline shift, infarction or recent\nhemorrhage.\n\nThe ventricles and sulci are normal in caliber and configuration.\nMajor vascular flow voids are preserved.  Major dural venous sinuses are\npatent.\n\nThere is mild mucosal thickening along the ethmoid air cells.  There is a\nmucous retention cyst in the right maxillary sinus.  The mastoid air cells are\nclear.  The orbits appear unremarkable.",
            "output": "1. By postsurgical changes after resection of supra and infratentorial\nmetastases.\n2. No evidence of new lesions..\n3. Mild residual enhancement in FLAIR hyperintensity in the region of the\npreviously identified right temporal and right cerebellar masses is less\nconspicuous.\n4. Decrease in the size and enhancement of the right frontal lobe mass which\nwith marked decrease of surrounding FLAIR hyperintensity.\n5. Waxing and waning left anterior frontal lobe FLAIR hyperintensity appears\nlarger and more conspicuous on today's exam.  No associated contrast\nenhancement."
        },
        {
            "input": "Study is moderately degraded by motion.  Within these confines:\n\nPostsurgical changes seen after right parietal and right suboccipital\ncraniotomy for resection of metastatic lesions.\n\nRight frontal lesion measures 1.6 x 1.5 cm, decreased slightly in size from\nprior and is nonenhancing.  Minimal chronic hemorrhage associated with the\nright frontal mass is unchanged.\n\nRight nonenhancing temporal mass measures 1 x 1.5 cm and appears unchanged\nfrom prior.\n\nRight cerebellar lesion measures 1.7 x 2 cm and is enhancing, as on prior.\n\nPunctate left occipital enhancing lesion is unchanged (see 901:35 on current\nstudy and 100:159 on ___ prior outside exam).\n\nFLAIR hyperintensities seen in the left anterior frontal lobe (7; 13),\nunchanged from prior, and again do not demonstrate enhancement.\n\n Within limits of study, no evidence of new lesions, midline shift, infarction\nor recent hemorrhage.\n\nBilateral maxillary sinus probable mucous retention cysts are seen.  Bilateral\nethmoid air cell mucosal thickening is present.  Right frontal sinus mucosal\nthickening is noted.",
            "output": "1. Study is moderately degraded by motion.\n2. Grossly stable right frontal, right temporal, left occipital and right\ncerebellar lesions as described.\n3. Within limits of study, no definite evidence of new enhancing intracranial\nmass.\n4. Paranasal sinus disease , as described."
        },
        {
            "input": "Again seen are supra and infratentorial metastatic foci, described as follows:\n\n-Interval decrease in size of the previously noted rim enhancing left\noccipital lesion, now measuring 1.4 x 1.4 cm, previously measuring 2.0 x 1.6\ncm on ___. This lesion demonstrates moderate surrounding vasogenic\nedema (series 17, image 98; series 15, image 14) and evidence of chronic\nhemorrhage on GRE images. There is slightly decreased mass effect on the left\nlateral ventricle occipital horn.\n-Right frontal lobe rim enhancing lesion (series 17, image 104) demonstrating\nrestricted diffusion and mild adjacent edema appears grossly unchanged\ncomparison the prior study. High right frontal small craniotomy defect appears\nunchanged, likely related to prior biopsy.\n-Enhancing focus in the right temporal lobe appears unchanged in comparison to\nthe previous study, with stable postoperative changes of the overlying right\ntemporal calvarium.\n-Enhancing 1.7 x 1.7 cm focus in the right cerebellar hemisphere appears\nunchanged in size or appearance without restricted diffusion.  Stable\noverlying postsurgical changes related to prior right suboccipital craniotomy.\n-Again seen is a 7 x 7 mm focus of FLAIR signal abnormality in the left\nfrontal subcortical white matter (series 15, image 14) with questionable trace\nenhancement laterally (series 17, image 98) appears unchanged since ___\n2 mm focus of enhancement medial left IAC, not definitely seen on prior, may\nrepresent new metastases versus more prominent vessel.  Follow-up MRI IAC\nprotocol recommended.\n\nThere is no evidence of acute hemorrhage or acute infarction.  There is\napproximately 3 mm of left to right midline shift, grossly unchanged.\n\nMild right frontoethmoidal sinus mucosal thickening.  Small mucous retention\ncyst noted in the right maxillary sinus.  Otherwise, the paranasal sinuses,\nmastoid air cells and orbits appear within normal limits.",
            "output": "1. Suggestion of new 2 mm metastasis left IAC, versus more prominent vessel. \nMRI IAC recommended.\n2. Interval decrease in size of left occipital enhancing lesion, with\nposttreatment change, chronic blood products within the lesion, similar\nmoderate surrounding vasogenic edema.\n3. Additional metastatic lesions, stable as detailed above."
        },
        {
            "input": "Redemonstration of multiple intracranial metastatic foci, as described below\n\n-Interval decrease in size of a 1.4 x 1.3 cm rim enhancing lesion in the\nperiventricular white matter of the right frontal lobe, previously 1.7 x 1.5\ncm, with a minimal degree of surrounding vasogenic edema and diffusion\nrestriction (16:16).  There is a marked improvement in the adjacent there is a\nsimilar appearance of high right frontal small craniotomy defect.\n-Interval decrease in size of a 0.8 x 0.8 cm rim enhancing lesion in the left\noccipital lobe, previously 1.4 x 1.4 cm, with marked decrease in the\nsurrounding vasogenic edema (16:14), which is only minimal on current exam. \nAgain, there is evidence of chronic hemorrhage within this lesion.\n-Similar to minimally decreased size of a 1.8 x 1.2 cm enhancing right\ntemporal lobe lesion (16:11) with mild surrounding vasogenic edema.  Unchanged\nappearance of postsurgical changes of the overlying calvarium.\n-Similar size of a 1.8 x 1.7 cm enhancing focus in the right cerebellar\nhemisphere (6:8).  Again seen are postsurgical changes status post right\nsuboccipital craniotomy.\n-Within limits of slice selection, there is a similar size and appearance of a\n0.9 x 0.7 cm T2/FLAIR hyperintense and T1 hypointense focus in the subcortical\nwhite matter of the left frontal lobe without definite enhancement (5:15,\n17:98).  Given patient's history, this most likely represents an additional\nfocus of metastasis.\n-Unchanged bilateral, left greater than right, 2 mm focus of enhancement in\nthe medial IACs (17:47) when compared to the prior exam.  Additionally,\nseveral additional cranial nerves appear to be subtly enhancing, for example,\ncranial nerves 3 and 5 (17:62, 52), similar in appearance to prior exam, which\nis suggestive of possible leptomeningeal disease.\n\nThere is no evidence of new or enlarging enhancing lesions.  There is no\nevidence of acute hemorrhage or infarct.  There is no significant mass effect.\nThere is minimal, 1 mm of left-to-right midline shift.\n\nThere is mild mucosal thickening in the right frontal sinus and a mucous\nretention cyst in the right maxillary sinus.  The remainder of the paranasal\nsinuses, mastoid air cells, and orbits are normal.",
            "output": "1. Overall decreased burden of intracranial metastatic disease, as described\nabove.  There are no new or enlarging enhancing lesions.\n2. Similar size and appearance of a T2 hyperintense and T1 hypointense focus\nin the left frontal lobe subcortical white matter, which likely represents an\nadditional focus of metastasis.  Recommend attention on subsequent exams.\n3. Similar appearance of subtle enhancement of bilateral cranial nerves 3, 5,\nand ___, and especially of the left cranial nerve ___ within the medial left\nIAC, which may represent leptomeningeal spread of disease.\n4. Mild mucosal thickening in the right frontal sinus.  Mucous retention cyst\nin the right maxillary sinus."
        },
        {
            "input": "Again seen are multiple enhancing lesions in the right cerebellar hemisphere,\nright inferior temporal lobe, left occipital lobe and right frontal lobe. \nThese appear unchanged to slightly smaller than on the study of ___. \nNo new lesions are identified.  There is no evidence of hemorrhage, edema, \nmidline shift or infarction.   The ventricles and sulci are normal in caliber\nand configuration.  Postsurgical findings after right suboccipital craniotomy,\nright temporal craniotomy and right frontal burr hole are unchanged.",
            "output": "1. Multiple enhancing lesions compatible with metastases, unchanged or\nslightly decreased in size since ___"
        },
        {
            "input": "There is no evidence of acute infarction.  No intracranial hemorrhage. No\nmass, mass effect, edema or midline shift.\n\nThere is no abnormal enhancement.  The dural venous sinuses appear patent.\n\nThe ventricles and sulci are normal, without evidence of hydrocephalus. There\nis gross preservation of the principal intracranial vascular flow voids.\n\nThe visualized paranasal sinuses, middle ear cavities, and mastoid air cells\nare well aerated and clear.  The orbits are within normal limits bilaterally.",
            "output": "1. Normal brain MRI."
        },
        {
            "input": "Examination is very limited secondary to patient motion.\n\nThere is increased T2 signal and enhancement post-contrast seen within the\nretropharyngeal soft tissues, which appear thickened. There is no definite\nextension of these changes into the mediastinum. No definite enhancing fluid\ncollection is seen is to suggest presence of an abscess.\n\nNo exophytic mucosal mass. Neck vessels are patent. Normal salivary glands.\nThere are small bilateral pleural effusions. Again seen is a nodule in the\nright lobe of the thyroid gland, which measures 1.1 x 1.1 cm.",
            "output": "Induration and increased fluid signal within the retropharyngeal soft tissues,\nwhich appear thickened, consistent with infection and phlegmonous changes. No\ndefinite drainable fluid collection identified. No definite extension into the\nmediastinum."
        },
        {
            "input": "The ventricles and extra-axial spaces are normal in size. There is no evidence\nof midline shift, mass effect or hydrocephalus. There are no acute infarcts.\nThere is no evidence of focal abnormalities.  The vascular flow voids are\nmaintained. The visualized paranasal sinuses are clear. Following gadolinium\nadministration there is no evidence of abnormal parenchymal, vascular and\nmeningeal enhancement seen.",
            "output": "No significant abnormalities are seen on MRI of the brain with and without\ngadolinium."
        },
        {
            "input": "Marked motion degradation, limiting assessment. Within these confines:\n\nCompared with recent MRI from ___, there are expected postoperative\nchanges from interval right parietal craniotomy and resection of the largest\nright parietal lobe metastasis.  Evaluation is limited on this post-contrast\nonly CyberKnife planning study; within these confines, there is either\nintrinsic T1 hyperintense blood products or thin peripheral enhancement at the\nmargins of the resection cavity, improved compared to the prior exam.\n\nExtending inferiorly at the anteroinferior margin of the resection cavity\nhowever, there is hyperintense serpiginous material which, while possibly\nsimply representing blood products/postsurgical change, appearance raises\nsuspicion for residual tumor (06:17), measuring up to 18 x 15 mm axial\n___ however spanning up to 31 mm in SI dimension (500:106).\n\nThere are multiple foci of enhancing intracranial metastatic disease.  For\nexample:\n\n-Closely adjacent left cerebellar lesions, possibly along the folia, measure 5\nand 3 mm (5:122), new or newly apparent compared with prior.\n-Small foci of leptomeningeal and/or parenchymal enhancement in the left\ntemporal lobe are new or newly apparent (see series 5 images 155, 158).\n-Foci of leptomeningeal enhancement along the left insular cortex are\nsignificantly more conspicuous, not definitely present on the prior (5:192).\n-The superior left temporal lobe and left parietal lobe leptomeningeal\nenhancement is slightly increased compared with prior in terms of overall\nextent and disease burden.\n-Small foci of possible leptomeningeal and/or parenchymal disease in the right\ntemporal lobe are more conspicuous (see series 5, images 184, 196)\n-Leptomeningeal disease along the left sylvian fissure is similar to prior\n(5:73).\n-Foci of leptomeningeal disease in the frontal interhemispheric region is\nincreased/more conspicuous (5:205).\nNew from prior is a 8 mm-wide primarily right frontal subdural fluid\ncollection, indeterminate on this limited study, possibly postoperative.\n\nThere is diffuse likely postoperative supratentorial pachymeningeal thickening\nand enhancement.\n\nMild mass effect on the right subdural collection includes mild effacement of\nthe frontal horn of the right lateral ventricle without entrapment or\nherniation.  No significant midline shift.  Major dural venous sinuses are\npatent.  There is an unchanged 7 mm pineal region likely cystic focus without\nsuspicious features, incompletely evaluated however stable from prior\n(501:87).",
            "output": "1. Expected postoperative changes from right parietal craniotomy and resection\nof the largest focus of metastatic disease in the right parietal lobe.  There\nis however, suggestion of residual disease at the anteroinferior margin of the\nresection site just deep to the resection cavity, however this is incompletely\nevaluated on this CyberKnife planning MRI protocol.  Extent of T1\nhyperintensity along the postero-lateral aspect of the resection cavity has\ndecreased.\n2. New 8 mm wide right subdural extra-axial collection, incompletely\nevaluated, possibly postoperative collection.  Mild mass effect including mild\neffacement of the frontal horn of the right lateral ventricle.  No herniation.\nNo entrapment.  No midline shift.\n3. Although the current examination is performed with 3 T technique (1.5 T\ntechnique on the prior), appearance overall nonetheless suggests slight\nprogression of multifocal bilateral deposits of leptomeningeal metastatic\ndisease, worst in the left temporoparietal region.\n4. Diffuse pachymeningeal thickening enhancement, mild, likely postoperative."
        },
        {
            "input": "Patient is status post right prior craniotomy and resection of the largest\nright parietal lobe metastasis.  The previously seen right parietal cystic\ncavity has significantly decreased in size and appears to have collapsed with\nmore solid enhancement compared to prior (series 9, image 129).\n\nAlong the top of the cerebellar folia there is increased enhancement\nsuggestive of worsening leptomeningeal disease (series 9, image 63 through\n70).  There is new diffusion abnormality at the bilateral junctional pons the\nmiddle cerebellar peduncles as well as a focus at the anterior pons with\nassociated FLAIR abnormality (Series 502, image 9 and 10).\n\nMultiple foci of enhancing intracranial metastatic disease is again noted. \nThese include a faint lesion in the left cerebellum measuring up to 3 mm,\npreviously 5 mm within adjacent focus measuring 1 mm, previously 3 mm (series\n9, image 55 and 56).  Again seen are foci of either leptomeningeal or\nparenchymal enhancement in the left insular cortex, not significantly changed\ncompared to prior.  Additional foci of either leptomeningeal or parenchymal\nenhancement in the left temporal lobe have not significantly changed compared\nto prior (series 9, image 77 and 67).  Foci of possible leptomeningeal\nenhancement and/or parenchymal disease in the right temporal lobe have likely\nnot significantly changed compared to prior (series 9, image 88 and 95). \nUnchanged foci of leptomeningeal disease in the right frontal interhemispheric\nregion (Series 9, image 87).  Enhancement along the left parietal and temporal\nlobe, which is likely a combination of leptomeningeal enhancement as well as\nparenchymal enhancement has not significantly changed compared to prior\n(series 9, image 104).\n\nThe previously seen right subdural collection has decreased in size compared\nto MR from ___, measuring 5 mm, likely postoperative changes.  There\nis worsening hydrocephalus and enlargement of the lateral ventricles, aqueduct\nof sylvian, and third ventricle, with lateral ventricles measuring up to 4.4\ncm, previously measuring 3.0 cm and third ventricle measuring 1.4 cm and\npreviously measuring 0.5 cm.  There is no significant midline shift.\n\nThere is increased diffuse periventricular white matter signal compared to\nprior, which could be related to periventricular edema from developing\ncommunicating hydrocephalus versus post radiation changes.",
            "output": "1. Most multifocal areas of metastatic enhancement are unchanged, however\nalong the cerebellar folia there is new enhancement suggestive of more\nwidespread leptomeningeal disease.\n2. Right parietal fluid cavity has since collapsed and demonstrates more solid\nenhancement compared to prior.\n3. Developing communicating hydrocephalus could be secondary to worsening\nleptomeningeal carcinomatosis.\n4. New abnormal diffusion in the bilateral junctional pons and focus at the\nanterior pons may be secondary to worsening leptomeningeal disease versus\nmanifestation of paraneoplastic syndrome.\n5. Worsening FLAIR periventricular hyperintensities, which could be related to\nperiventricular edema from developing communicating hydrocephalus versus post\nradiation changes."
        },
        {
            "input": "Frontal craniotomy changes are seen.  Minimal T1 hyperintense signal is noted\nwithin the resection cavity.  There is susceptibility artifact throughout the\nresection cavity.  A small amount of layering hemorrhage is noted in the\noccipital horns and within the fourth ventricle.  Interval increased FLAIR\nhyperintense signal is noted in the bifrontal lobes.  There is stable mass\neffect and effacement of the frontal horns.  There is linear low diffusion in\nthe medial cortical right frontal lobe, series 1002, image 10.  In addition,\nthere is a low diffusion in the cortical left frontal lobe, series 1002, image\n7.  The anterior aspect of the superior sagittal sinus is not well visualized.\nThere is limited evaluation of the perfusion sequences given the degree of\nhemorrhage in the postsurgical site, however the demonstrate decreased\nperfusion in the frontal lobes.  Postcontrast sequences were not acquired.",
            "output": "1. Incomplete study demonstrates interval increased edema in the bifrontal\nlobes, out of proportion for expected post surgical changes, with stable mass\neffect and effacement of the frontal horns.  In addition, there is bifrontal\ncortical low diffusion.  These findings are concerning for venous ischemia\nsecondary to injury of the cortical veins.  Lack of visualization of the\nanterior superior sagittal sinus, likely secondary to occlusion/injury.\n2. No definite residual mass is seen in the surgical site although limited in\nevaluation given lack of postcontrast imaging."
        },
        {
            "input": "The T1 isointense, T2 hyperintense, extra-axial, well-circumscribed mass in\nthe left parasagittal frontal lobe measures 4.1 x 3.0 x 4.1 cm, unchanged in\nsize from the prior examination.  This mass demonstrates homogeneous\nenhancement and exerts local mass effect upon the adjacent sulci.  The frontal\nhorn of the left lateral ventricle is partially effaced.  The 4 mm\nleft-to-right midline shift is unchanged.  The surrounding vasogenic edema in\nthe left frontal lobe is also unchanged.  This mass does not demonstrate\nrestricted diffusion.  The mass abuts the the most anterior portion of the\nsuperior sagittal sinus, which appears patent.  Susceptibility within the\nperiphery of the mass corresponds to calcifications seen on prior CT.  No\nother masses are identified.  There are dural calcifications in the right\nparietal lobe.\n\nThere is no evidence of hemorrhage or infarction.   The ventricles are normal\nin caliber and configuration.  There is no abnormal enhancement after contrast\nadministration.\n\nThe paranasal sinuses and mastoid air cells are clear.  The patient is status\npost bilateral cataract surgery.\n\nThe major intracranial flow voids are preserved.",
            "output": "Unchanged, enhancing, 4.1 cm extra-axial mass in the left parasagittal frontal\nlobe with local mass effect, edema, and 4 mm left-to-right midline shift,\nlikely consistent with meningioma."
        },
        {
            "input": "When compared to previous exam, there has been no significant interval change.\nExtra-axial enhancing lesion abutting the anterior aspect of the falx to the\nleft of midline measures 4.4 cm AP by 3.2 cm TRV by 4.1 cm cc. As on prior,\nthe lesion abuts the superior sagittal sinus.  The degree of mass effect with\npartial effacement of the frontal horn of the left lateral ventricle and\nminimal rightward midline shift is similar compared to prior.  No other\nenhancing mass lesion identified.",
            "output": "Extra-axial left anterior parafalcine enhancing lesion as on prior, most\nlikely a meningioma."
        },
        {
            "input": "There are innumerable enhancing supra and infratentorial lesions throughout\nthe brain, corresponding to hyperdense lesions on the recent prior CT\nexamination.  Many of these are located at the gray-white junction, and there\nare areas of surrounding vasogenic edema with mild areas of localized mass\neffect, though without midline shift or herniation.  There are numerous\nlesions in the posterior fossa with prominent surrounding vasogenic edema and\nmild effacement of the fourth ventricle, though there is no associated\nhydrocephalus.  The majority of these lesions demonstrate susceptibility\nartifact, compatible with hemorrhage.  The largest supratentorial lesion is\nlocated in the left parietal lobe measuring up to 1.4 x 1.3 cm (100a:32).  The\nlargest infratentorial lesion is located in the left cerebellar hemisphere\nmeasuring approximately 1.7 x 1.1 cm (100 a:  137).  Some of these lesions\ndemonstrate peripheral slowed diffusion, which may be related to the\nhemorrhagic component.\n\nThere is no evidence of midline shift or infarction.  The ventricles and sulci\nare otherwise age appropriate in size and configuration.  The principal\nintracranial vascular flow voids are preserved.\n\nThe visualized paranasal sinuses are grossly clear.  The orbits are grossly\nunremarkable.\n\n1.1 x 0.9 cm enhancing lesion is noted in the C5 vertebral body on sagittal MP\nrage sequence (14:82).",
            "output": "1. Innumerable enhancing hemorrhagic supra and infratentorial metastatic\nlesions, as described, with surrounding vasogenic edema most notable for mass\neffect with moderate effacement of the fourth ventricle, though without\nhydrocephalus.  Largest supratentorial lesion is located in the left parietal\nlobe measure 1.4 x 1.3 cm and the largest infratentorial lesion is located in\nthe left cerebellar hemisphere measuring 1.7 x 1.1 cm.\n2. 1.1 x 0.9 cm enhancing lesion in the C5 vertebral body concerning for\nosseous metastasis.  Partially also visualized as enhancing lesion in the left\nside of C4 vertebral body.\n3. No territorial infarct."
        },
        {
            "input": "The temporal horn of the right lateral ventricle is slightly larger than the\nleft.  However, hippocampal formations appear symmetric in volume without\nevidence for signal abnormalities.  No structural abnormalities are seen\nelsewhere in the brain parenchyma.  There is no evidence for an intracranial\nmass, abnormal diffusion, blood products, or other signal abnormalities. The\nventricles are overall normal in size.  The sulci and basal cisterns also\nappear normal in size.",
            "output": "The temporal horn of the right lateral ventricle is slightly larger than the\nleft, but the hippocampal formations appear symmetric in volume without\nevidence for signal abnormalities.  The ___ EEG report stated that\nbilateral, rather than unilateral, temporal epileptogenic foci were suspected.\nTherefore, the clinical significance of the asymmetric temporal horns is\nuncertain."
        },
        {
            "input": "There is no intracranial mass, mass effect, or midline shift. Ventricles and\nsulci are age-appropriate.  Scattered periventricular and subcortical white\nmatter T2/FLAIR hyperintensities are noted, nonspecific though most commonly\ndue to chronic small vessel disease.  There is no region of restricted\ndiffusion or abnormal susceptibility artifact. Major intravascular flow voids\nare preserved.\n\nPost contrast images demonstrate no abnormal parenchymal or meningeal\nenhancement.\n\nVisualized paranasal sinuses and mastoid air cells demonstrate no abnormal\nsignal besides mucosal thickening in the left sphenoid sinus",
            "output": "No acute intracranial process.  Scattered nonenhancing T2/FLAIR\nhyperintensities which are nonspecific though likely due to chronic small\nvessel disease."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor acute infarction.  There are multiple small chronic infarcts in both\ncerebellar hemispheres, right more numerous than left.  There is also a\nprobable small chronic infarct in the left medulla.\n\nThere is extensive nodular gray matter heterotopia along the atria, temporal\nhorns, and occipital horns of both lateral ventricles.  Ventricles sulci are\nnormal in size with no evidence of hydrocephalus.\n\nThe major intracranial vascular flow voids are preserved.  Orbits are\nunremarkable.  The visualized extracranial soft tissues are unremarkable.",
            "output": "1. No evidence of acute infarction.\n2. Multiple chronic infarcts in both cerebellar hemispheres, right more\nnumerous than left, and in the ventral medulla.\n3. Extensive subependymal nodular gray matter heterotopia along the lateral\nventricles."
        },
        {
            "input": "There is diffuse, smooth pachymeningeal enhancement in pachymeningeal FLAIR\nhyperintensity overlying both cerebral hemispheres, more marked on the right\nside.  There is no other evidence for intracranial hypotension, for example no\nsagging of the brainstem, cerebellar tonsillar herniation, subdural fluid\ncollection, or engorgement of the pituitary gland.\n\nThere is no pathological leptomeningeal enhancement. There is no evidence for\nintracranial enhancing mass, acute infarction, edema, or blood products.\n\nThere are multiple T2/FLAIR hyperintensities in the periventricular, deep, and\nsubcortical white matter of the cerebral hemispheres, and in the bilateral\npons, which are nonspecific but likely sequela of chronic small vessel\nischemic disease in this age group.\n\nThere is mild age-related prominence of the ventricles and sulci.  All\ncomponents of the left lateral ventricle is slightly larger than the right,\nsuggesting congenital or developmental etiology for the asymmetry.  Basal\ncisterns are normal in size.\n\nMajor arterial flow voids are grossly preserved.  The right transverse and\nsigmoid sinuses, and the right internal jugular vein, are dominant.  The left\ntransverse and sigmoid sinuses are hypoplastic.\n\nThere is evidence of bilateral cataract surgery.  There is minimal mucosal\nthickening in the ethmoid air cells.\n\nSagittal T1 weighted images demonstrate incompletely evaluated degenerative\nchanges in the included upper cervical spine.",
            "output": "1. Diffuse, smooth pachymeningeal enhancement overlying both cerebral\nhemispheres, slightly more pronounced on the right than left.  Diagnostic\nconsiderations include idiopathic intracranial hypotension, unless there has\nbeen a recent lumbar puncture which may also cause transient smooth\npachymeningeal enhancement.  Although there are no additional imaging features\nof idiopathic intracranial hypertension, additional features are not required\nto entertain this diagnosis.  In the absence of nodularity, other diagnostic\nconsiderations are less likely, including sequela of granulomatous or other\ninfectious/inflammatory disease, pachymeningeal carcinomatosis, or\npachymeningeal lymphoma.\n2. Non dominant left transverse and sigmoid sinuses are hypoplastic.\n\nRECOMMENDATION(S):  Recommend neurology consultation.  Based on the neurology\nconsultation, MRI of the cervical, thoracic, and lumbar spine should be\nconsidered to assess for a potential source of a CSF leak.\n\nNOTIFICATION:  The impression and recommendation above were entered by Dr.\n___ on ___ at 15:50 into the Department of Radiology critical\ncommunications system for direct communication to the referring provider."
        },
        {
            "input": "Study is moderately degraded by motion.  Within these confines:\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  There is prominence of the ventricles and sulci suggestive of\ninvolutional changes, unchanged.  Periventricular and subcortical T2 and FLAIR\nhyperintensities are noted which may represent small vessel ischemic changes. \nAgain, there is no definite sagging of brainstem, cerebellar tonsillar\nherniation, subdural flow correction or enlargement of the pituitary gland. \nThe right transverse sinus is dominant and the left transverse sinus is\nhypoplastic, unchanged.\n\nGrossly stable diffuse right greater than left pachymeningeal FLAIR\nhyperintense thickening and enhancement without definite leptomeningeal\nenhancement is again seen.  Bilateral lens replacement postoperative changes\nare noted.",
            "output": "1. Study is moderately degraded by motion.\n2. No definite evidence of acute infarct or focal enhancing mass.\n3. Grossly stable right greater than left pachymeningeal thickening and\nenhancement compared to 2 weeks prior contrast brain MRI as described. \nDifferential considerations again include procedure related changes,\nintracranial hypotension, granulomatous disease, infectious, and neoplastic\netiologies.  If continued concern for CSF leak, consider radionuclide\ncisternography for further evaluation."
        },
        {
            "input": "Previously seen pachymeningeal enhancement has completely resolved. No new\nmeningeal enhancement is identified.  No abnormal parenchymal enhancement is\nseen.  There is no mass effect midline shift or hydrocephalus.  Mild brain\natrophy and early changes of small vessel disease are seen.  No acute infarcts\nare identified.  Fluid level and mucosal thickening in the left maxillary\nsinus are new since the previous MRI examination of ___.",
            "output": "1. Resolution of previously seen pachymeningeal enhancement.  No new\nenhancement is identified.\n2. No acute infarcts mass effect or hydrocephalus.\n3. New left maxillary sinusitis."
        },
        {
            "input": "There are multiple T2/FLAIR hyperintense lesions distributed within the\nbihemispheric white matter, many of which are oriented perpendicular to the\nlateral ventricles and along the callosal-septal interface. Lesions are\nscattered within the deep/periventricular and juxtacortical white matter. \nThere is a new 1.2 x 0.8 cm lesion in the right centrum semiovale which\ndemonstrates enhancement. There is also a new 0.9 cm lesion in the left medial\nleft temporal lobe which also demonstrates enhancement.  Previously enhancing\nleft temporoccipital lesion is no longer enhancing.\n\nThere is no evidence of intracranial hemorrhage or infarct. Ventricular\nmidline. Extra-axial spaces are within normal limits. Cisterns are patent.\nGray-white differentiation is otherwise maintained. Flow voids of the\nprincipal intracranial arteries are maintained. The paranasal sinuses\ndemonstrate scattered areas of mucosal thickening. The mastoid air cells are\nclear. The craniocervical junction, sella turcica, and orbits appear grossly\nunremarkable.",
            "output": "Multiple white matter lesions consistent with demyelination, with new lesions\nin the right centrum semiovale and left medial temporal lobe demonstrating\nenhancement as described above."
        },
        {
            "input": "No acute infarct, suspicious focus of intracranial hemorrhage, mass effect,\nshift of normally midline structures or hydrocephalus.\nThere are multiple small T2 FLAIR hyperintense foci in the cerebral white\nmatter in the frontal and parietal lobes and medial temporal lobes, without\nsignificant change compared to the recent study of ___. Slightly\nincreased DWI signal is noted in some of the lesions, as before.\nNo abnormal enhancement is noted in these foci except for minimal enhancement\nin the right parietal lesion, without significant change since prior.\nThe corpus callosum is mildly thinned in the body without significant change.\n\nThe ventricles, extra-axial CSF spaces, cerebral sulci and cerebellar folia\nare normal.\nThe major intracranial arterial flow voids are noted.\nVenous sinuses\nA tiny hypointense focus in the posterior aspect of the pituitary on the\nMPRAGE sequence, is stable.\n\nPineal gland, craniocervical junction regions are unremarkable.\nThe imaged paranasal sinuses and the mastoid air cells are clear.\nLimited evaluation of the optic nerves as not targeted.\nSmall cystic focus in the adenoids.",
            "output": "Multiple T2 FLAIR hyperintense lesions, felt to represent demyelianting\nlesions in the cerebral white matter as described above,, with minimal\nenhancement in the right parietal lesion, without significant change compared\nto the recent study of ___.\nNo new lesions.\n\nOther details as above.\nCorrelate for risk factors."
        },
        {
            "input": "Again noted are multiple T2/FLAIR hyperintense foci in the subcortical, deep,\nand periventricular white matter, as seen on prior MRI from ___. Some\nof the periventricular T2/FLAIR hyperintense foci are perpendicularly oriented\nto the lateral ventricles, typical of demyelinating plaques seen in multiple\nsclerosis. No new lesions are identified compared to prior MRI from ___. No lesions demonstrate slowed diffusion or contrast enhancement. There\nare no lesions of the brainstem, cerebellum, or visualized upper cervical\nspinal cord.\n\nThere is no intracranial hemorrhage. There is no acute infarct. The\nventricles, sulci, and cisterns are age-appropriate. There is no extra-axial\nfluid collection. Major intravascular flow voids are preserved. There is\nnormal enhancement of the major intracranial arterial and venous systems\nfollowing contrast administration.\n\nThe paranasal sinuses and mastoid air cells appear clear. The orbits are\nnormal.",
            "output": "Multiple T2/FLAIR hyperintense foci in the supratentorial white matter,\nconsistent with demyelinating plaques. Lesions are unchanged from MRI on ___ with no new lesions identified. No plaques demonstrate slowed\ndiffusion or contrast enhancement."
        },
        {
            "input": "Again seen are multiple foci of white matter hyperintensity on FLAIR images\nwithin the periventricular, deep and subcortical white white matter of the\ncerebral hemispheres, including the callososeptal junction, compatible with\nthe diagnosis of demyelinating disease.  Some of these lesions demonstrate T1\nhypointensity, consistent with chronic black holes.  There are no\ninfratentorial lesions.  No new lesions are seen.  There are no enhancing\nlesions or lesions with slow diffusion.\n\nThere is no evidence of an intracranial mass, acute infarction, edema, or\nblood products.  Intracranial flow voids are maintained.",
            "output": "Multiple demyelinating plaques within the supratentorial white matter are\nunchanged.  No new or active lesions are seen."
        },
        {
            "input": "Focal white matter signal abnormalities due to multiple sclerosis are again\nidentified. No new lesions are seen. No definite subcortical lesions\nidentified suspicious for progressive multifocal leukoencephalopathy. There is\nno mass effect midline shift or hydrocephalus.",
            "output": "No significant interval change since the previous MRI examination. No definite\nnew lesions are seen."
        },
        {
            "input": "Multiple scattered focal white matter signal abnormalities are overall similar\nto the prior examination.  There is no signal abnormality on\ndiffusion-weighted images.  No new lesions are identified.  There is no mass\neffect or midline shift.  The ventricles are normal in size morphology. \nPrincipal intracranial vascular flow voids are preserved.  There is mild\nmucosal thickening in the right anterior ethmoid and frontal sinuses.",
            "output": "1.  No change compared to the prior examination.\n\n2.  Multiple scattered focal white matter signal abnormalities, consistent\nwith a history of multiple sclerosis."
        },
        {
            "input": "There are moderately extensive deep white matter, and juxta cortical lesions\ninvolving bilateral cerebral hemispheres, stable since prior exam from ___..  There are no definite infratentorial lesions, or lesions in\nthe visualized upper cervical cord.  There are no new lesions.  There is no\nevidence of PML. Prominent dorsum sella, with optic chiasm mildly draping over\nit, appearance is stable since ___. Normal Ponto mammillary\ndistance, pontomesencephalic angle.\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  Paranasal sinuses, mastoid air cells are clear.  Intracranial\nvascular flow voids are preserved.",
            "output": "1. Findings consistent with chronic demyelination.  No new lesions, no\nevidence of PML."
        },
        {
            "input": "MRI BRAIN: No change in the several cerebral subcortical and periventricular\nFLAIR hyperintensities correlating with the patient's known history multiple\nsclerosis.  There is evidence a new punctate FLAIR hyperintensity in the right\nmiddle cerebellar peduncle (400:46), which may be artifactual.  There are no\nenhancing lesions.\n\nNo evidence of intracranial hemorrhage or infarction. The ventricles and sulci\nare within expected limits in caliber and configuration.  There is a 2 mm\nnonenhancing and FLAIR hyperintense focus in the right pituitary, unchanged\nsince examination of ___, potentially a pituitary microadenoma.\n\n The major intracranial vascular flow voids are maintained.  The dural venous\nsinuses are patent.  There is mild mucosal thickening of the ethmoid air\ncells, otherwise the paranasal sinuses, mastoid air cells and orbits are\nnormal.\n\nMRI CERVICAL SPINE:\nThere is straightening of the cervical spine.  The vertebral bodies are normal\nin height and signal characteristics.  Diffusely reduced T2 signal within the\nintervertebral discs represents a manifestation of degenerative change.  The\nintervertebral disc heights are relatively preserved.\n\nThere is a short-segment T2 hyperintense lesion of the right anterior cord at\nthe level of C4-C5, unchanged since ___.  There is no evidence of abnormal\nenhancement.\n\nThere is mild multilevel disc bulging most significant at C6-C7 where there is\nmild effacement of ventral thecal sac.  There is otherwise no significant\nspinal canal or neural foraminal narrowing of the cervical spine.",
            "output": "1. No change in the several cerebral white matter FLAIR hyperintensities\ncorrelating with the patient's known history of multiple sclerosis.\n2. Evidence of a new punctate FLAIR hyperintense focus within the right middle\ncerebellar peduncle, felt to be likely artifactual.  No enhancing lesions to\nsuggest active process.\n3. Short-segment T2 hyperintense lesion within the right anterior cervical\ncord at the level of C4-C5 compatible with a demyelinating plaque.  No new\ncervical lesions.\n4. No enhancing lesions to indicate active demyelinating plaques.\n5. Mild degenerative changes of the cervical spine.\n6. Unchanged appearance since ___ of a 2 mm nonenhancing and FLAIR\nhyperintense focus in the right pituitary, potentially a pituitary\nmicroadenoma.\n7. Additional findings as described above."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  The visualized vascular flow voids are grossly preserved. \nThere is minimal thickening of the ethmoid air cells, otherwise the paranasal\nsinuses and mastoid air cells are clear.  The orbits and globes are\nunremarkable.  There is no abnormal marrow signal.",
            "output": "1. Unremarkable noncontrast brain MRI.  No evidence of an acute infarct,\nintracranial mass, or hemorrhage."
        },
        {
            "input": "There is an acute infarcts seen in the left lateral thalamus (06:15).  A small\narea of hyperintensity on diffusion images in the left periventricular region\n(06:19) has high signal on ADC map and is suggestive of T2 shine through.  No\nother acute infarcts are identified.  There is no mass effect midline shift or\nhydrocephalus.  Postcontrast images demonstrate no abnormal enhancement.  No\nevidence of blood products on the GRE images.",
            "output": "1. Acute left lateral thalamic infarct.\n2. Left subacute to chronic left frontal lobe periventricular infarct.\n3. No abnormal enhancement."
        },
        {
            "input": "There is no evidence of intracranial hemorrhage,edema,masses,mass effect,\nmidline shift or infarction.   The ventricles and sulci are normal in caliber\nand configuration.  There is no abnormal enhancement after contrast\nadministration.\n\nBilateral hippocampal formations and mammillary bodies are preserved in signal\nand configuration. There is no disproportionate medial temporal atrophy. There\nis no focal lobar encephalomalacia. There are no focal cortical dysplasias or\ngray matter heterotopia noted.  A developmental venous anomaly is seen in the\nleft parietal lobe (08:16).\n\nThere is significant mucosal thickening of the right sphenoid sinus,\nsuggestive of an ongoing inflammatory process.  The mastoid air cells are\nclear.  The intraorbital contents are normal.",
            "output": "1. There is no evidence of acute intracranial process or hemorrhage\n2. High-resolution images throughout the temporal lobes are unremarkable, with\nno evidence of mesial temporal sclerosis.\n3. Significant mucosal thickening is noted on the right sphenoid sinus,\nsuggesting an ongoing inflammatory process."
        },
        {
            "input": "Axial T2 and postcontrast images are at least moderately motion degraded.\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  Periventricular and subcortical T2 and FLAIR hyperintensities\nare noted which may represent small vessel ischemic changes.  Mild prominence\nof the ventricles and sulci are suggestive of involutional changes.  There is\nno abnormal enhancement after contrast administration.",
            "output": "1. Moderately motion degraded study, particularly with respect to the axial T2\nand postcontrast images.\n2. No evidence of hemorrhage or infarction."
        },
        {
            "input": "There are multiple foci of slow diffusion in the left temporal, parietal and\noccipital region (___).  There is corresponding T2/FLAIR hyperintensity.\nThere is no intracranial hemorrhage or mass effect.  Prominent perivascular\nspaces versus chronic lacunar infarcts in the left caudate head and lentiform\nnucleus.  Predominantly periventricular and subcortical white matter T2/FLAIR\nhyperintensity also involving the pons is nonspecific, but may reflect\nsequelae of chronic small vessel ischemic disease. Prominence of the\nventricles appears disproportionate with respect to the degree of sulcal\nprominence.\n\nThere is mucosal thickening throughout the paranasal sinuses, most severe in\nthe anterior ethmoid air cells.  Partial opacification of the mastoid air\ncells is nonspecific.  Bilateral lens implants are noted.",
            "output": "1. Multiple small acute infarcts in the left temporal, parietal and occipital\nlobe.  No hemorrhage.\n2. Extensive paranasal sinus disease and partial opacification of the mastoid\nair cells, likely partially related to intubation.\n3. Prominence of the ventricular system appears disproportionate with respect\nto the degree of sulcal prominence which could reflect normal pressure\nhydrocephalus, similar to outside CT.\n4. Nonspecific white matter signal changes which may reflect chronic small\nvessel disease in this age group.\n\nNOTIFICATION:  The findings were discussed with ___, m.D. by\n___, M.D. on the telephone on ___ at 8:57 am, 5 minutes after\ndiscovery of the findings."
        },
        {
            "input": "There is a focus of increased signal in the left side of the pons near the\nsuperior cerebellar peduncle on FLAIR images which is low signal on T1\nweighted images and slightly high signal on both diffusion and ADC map. \nFollowing contrast administration peripheral enhancement is identified.  There\nare no other foci of focal signal abnormality is identified except for a small\n5 mm focus of decreased signal in the right posterior temporal region. No\nperiventricular increased signal is identified.\n\nThe ventricles and extra-axial spaces are normal in size. There is no evidence\nof midline shift mass effect or there is no evidence of other diffusion\nabnormalities.",
            "output": "Signal abnormality in the upper pons with peripheral enhancement suggestive of\nmultiple sclerosis.  No mass effect or hydrocephalus."
        },
        {
            "input": "MR head: There is no acute intracranial hemorrhage or evidence of chronic\nblood product acute deposition. There is no restricted diffusion on water\ndiffusion or ADC weighted images. There is no pathologic enhancement. There\nare foci of FLAIR hyperintensity within the left dorsal midbrain-pons junction\n(series 3, image 9) and right parietal subcortical white matter (series 3,\nimage 12), both present on prior MRI from ___. The ventricles, sulci,\nand basal cisterns are normal. The cerebellar tonsils are normal in position.\nMajor intravascular flow voids are preserved. The osseous structures are\nnormal. The paranasal sinuses and mastoid air cells are clear. The orbits are\nnormal.\n\nMR cervical spine: The vertebrae are normal in stature and alignment.\nIntervertebral discs are normal in height. The spinal cord is normal in course\nand caliber. Evaluation is limited due to motion but no cord signal\nabnormality or pathologic enhancement is identified.  At C5-6, there is a mild\ndisc bulge. The paravertebral soft tissues are normal.\n\nMR thoracic spine: The vertebrae are normal in stature and alignment.\nIntervertebral discs are normal in height. The spinal cord is normal in course\nand caliber.  There is prominent epidural fat throughout the spinal canal.\nEvaluation is limited due to motion but no cord signal abnormality or\npathologic enhancement is identified.  At T3-4, there is a right paracentral\ndisc protrusion. At T5-6, there is a disc bulge with an annular tear. The\nparavertebral soft tissues are normal.",
            "output": "1. Foci of FLAIR signal abnormality in the left dorsal midbrain-pons junction\nand right parietal subcortical white matter. These foci of can be seen due to\ndemyelinating disease. No restricted diffusion or pathologic enhancement.\n2. Limited studies due to motion but no lesions of the cervical and thoracic\nspinal cord.\n3.  Mild disc bulges and herniations at C5-6, T3-4, and T5-6 but without mass\neffect on the spinal cord."
        },
        {
            "input": "MRI BRAIN:\n\nThere are two persistent T2 hyperintense lesions in the left dorsal upper pons\n(series 22, image 8) and right posterior temporal subcortical white matter\n(series 22, image 9).  The left pons lesion has become progressively smaller\ncompared to the 2 prior MRIs, an and no longer demonstrates contrast\nenhancement. The right posterior temporal lesion is unchanged in size without\ncontrast enhancement. Neither lesion demonstrates slowed diffusion. No new\nlesions are identified. There is no evidence of intracranial masses, acute\ndiffusion abnormalities, or blood products.  Ventricles and sulci are normal\nin size. Major dural venous sinuses are patent on postcontrast MP RAGE images.\n\nMRA NECK:\n\nThere is 3 vessel aortic arch anatomy. There is a small apparent filling\ndefect in the left carotid bulb (series 107, image 9) without a stenosis by\nNASCET criteria. Right internal carotid artery, bilateral common carotid\narteries, and bilateral vertebral arteries are widely patent.\n\nMRA BRAIN:\n\nThe intracranial vertebral and internal carotid arteries and their major\nbranches appear normal without evidence of stenosis, occlusion, or aneurysm\nformation.",
            "output": "1.  The left dorsal pons T2 hyperintense lesion is progressively decreasing in\nsize compared to the 2 prior MRIs, without residual contrast enhancement.\nSmall nonenhancing right posterior temporal T2/ hyperintense lesion is stable.\nNo new lesions are identified.\n2.  Normal MRA of the head.\n3.  Small apparent filling defect in the left carotid bulb (series 107, image\n9) without an associated stenosis.  Since atherosclerotic disease would be\nunusual for a patient of this age, an artifact is not excluded, and carotid\nultrasound could be performed for further assessment."
        },
        {
            "input": "The ventricles and extra-axial spaces are normal in size. There is no evidence\nof midline shift, mass effect or hydrocephalus. There are no acute infarcts.\nThere is no evidence of focal abnormalities.  The vascular flow voids are\nmaintained. The visualized paranasal sinuses are clear. Following gadolinium\nadministration there is no evidence of abnormal parenchymal, vascular and\nmeningeal enhancement seen\n\nOccult demonstrate normal signal on inversion recovery images both optic\nnerves are normal in size.  Following gadolinium no evidence of enhancement of\nthe intraorbital or intracranial optic nerves or optic chiasm identified. \nThere is shows no evidence of intra or extraconal mass lesion seen.  The\nextraocular muscles are normal in size and appearance.  There is no evidence\nof supra or parasellar mass lesions seen.\n\nThere is no evidence of focal signal abnormality or acute infarcts within the\nbrainstem seen.",
            "output": "No significant abnormalities are seen on MRI of the brain and orbits with and\nwithout gadolinium."
        },
        {
            "input": "MR Head: On the right frontal lobe there is an extra-axial lesion measuring\napproximately 18 by 8 mm in transverse dimension apparently with a broad-based\ndural-based, probably representing a meningioma, which is not clearly\nvisualized on the prior exams due to the isodense attenuation and similar\nappearance to the adjacent brain parenchyma.  There is no evidence of\nsignificant mass effect or shifting of the adjacent structures in the right\nfrontal lobe.  There is no evidence of acute intracranial hemorrhage or mass\neffect.  Small focus of high signal intensity is noted in the subcortical\nwhite matter of the right frontal lobe, probably consistent with gliotic\nchange (image 17, series 12 and series 13.  No diffusion abnormalities are\ndetected to indicate or suggest acute or subacute ischemic changes.  There is\nno evidence of intracranial hemorrhage.  The ventricles and sulci are slightly\nprominent suggesting cortical volume loss, likely age related and involutional\nin nature.  The major vascular flow voids are present and demonstrate normal\ndistribution.  The orbits are unremarkable, the paranasal sinuses and mastoid\nair cells are clear.\n\nMRA Head: There is evidence of vascular flow in both internal carotid arteries\nas well as the vertebrobasilar system, fetal origin of the left posterior\ncommunicating artery with infundibular dilatation at its origin (Image 88,\nseries 2), the posterior circulation is patent with dominant left vertebral\nartery, the P1 segment of the left posterior cerebral artery is hypoplastic\nlikely due to fetal origin of the left posterior communicating artery.  No\nflow stenotic lesions or aneurysms larger than 3 mm in size are seen.\n\nMRA of the neck: There is evidence of vascular flow in both common carotid\narteries as well as the vertebral arteries with no evidence of flow stenotic\nlesions at the cervical carotid bifurcations, the left vertebral artery is\ndominant.  The origin of the right vertebral artery is not clearly seen and\nprobably there is mild narrowing as demonstrated on the image 12, series 105.",
            "output": "1.  Extra-axial lesion identified in the right frontal region measuring\napproximately 18 by 8 mm in transverse dimension, with no significant mass\neffect or edema in the adjacent structures, probably consistent with\nmeningioma, correlation with MRI of the head with contrast is recommended for\nfurther characterization.\n\n\n2.  Infundibular dilatation at the origin of the left posterior communicator\nartery as described above, no aneurysms larger than 3 mm in size are seen or\nflow stenotic lesions.\n\n3.  The MRA of the neck demonstrates patent carotid arteries and cervical\ncarotid bifurcations, possible narrowing at the takeoff of the right vertebral\nartery as described above\n\nRECOMMENDATION(S):  Extra-axial lesion identified in the right frontal region\nmeasuring approximately 18 by 8 mm in transverse dimension, with no\nsignificant mass effect or edema in the adjacent structures, probably\nconsistent with meningioma, correlation with MRI of the head with and with\ncontrast is recommended for further characterization.\n\nNOTIFICATION SECTION  These findings were communicated via phone call to Dr.\n___, CC5B  (extension ___ by Dr. ___ on ___ at 17:24 hours, 5\nminutes after discovery of the findings."
        },
        {
            "input": "Appearing centered within the left frontoparietal white matter and abutting\nthe left lateral ventricle is a 4.0 x 3.9 x 3.0 cm (AP x CC x TV) mildly\nheterogeneous mass which is intrinsically T1 hypointense, T2 FLAIR\nhyperintense with mild surrounding edema.  The mass appears at least partially\ncystic. Mass is suggested to abut the left lateral ventricle trigone.   Small\nfoci internal T1 hyperintensity in the inferior portion of the mass correspond\nto gradient echo susceptibility foci, compatible with subacute blood products\nfrom prior internal hemorrhage.  The mass demonstrates heterogeneous\nenhancement on post-contrast images.\n\nMultiple small foci of periventricular and deep subcortical white matter T2\nFLAIR hyperintensity are compatible with the sequelae of chronic small vessel\nischemia.  The major intracranial flow voids are preserved.  There are no\nadditional areas of abnormal enhancement.  There are no foci of abnormal\nrestricted diffusion elsewhere.  There is ethmoid air cell mucosal thickening,\nsimilar to prior head CT; otherwise the visualized paranasal sinuses and\nmastoid air cells are clear.  The globes are unremarkable.",
            "output": "1. Solitary intra-axial left frontoparietal 4.0 x 3.9 x 3.0 cm heterogeneously\nenhancing, at least partially cystic mass with possible areas of internal\nhemorrhage.   While findings are nonspecific, differential considerations\ninclude GBM, oligodendroglioma, and anaplastic astrocytoma.  Recommend\nclinical correlation.\n\nRECOMMENDATION(S):\n1. Solitary intra-axial left frontoparietal 4.0 x 3.9 x 3.0 cm heterogeneously\nenhancing, at least partially cystic mass with possible areas of internal\nhemorrhage.   While findings are nonspecific, differential considerations\ninclude GBM, oligodendroglioma, and anaplastic astrocytoma. Recommend clinical\ncorrelation."
        },
        {
            "input": "There is a 4.0 x 3.9 x 3.0 cm heterogeneous rim-enhancing mass in the left\nfrontoparietal lobe that is unchanged from ___. It closely abuts the\nleft lateral ventricle trigone (2:61), but does not result in significant mass\neffect.\n\nScattered periventricular, subcortical and deep white matter hypointensities\nare likely a sequela of chronic small vessel ischemic disease.",
            "output": "Overall similar appearance of 4.0 x 3.9 x 3.0 cm rim-enhancing lesion in the\nthe left frontoparietal lobe, which closely abuts the left lateral ventricle\nwithout significant mass effect.  Exam performed for surgical planning."
        },
        {
            "input": "A left parietal craniotomy defect is seen with a linear FLAIR hyperintense\nbiopsy tract containing blooming artifact extending to the left frontoparietal\nmass.  There is intrinsic T1 hyperintense signal and minimal blooming artifact\nin the left mass with residual nodular contrast enhancement along the\nanterior, posterior and inferior aspect of the mass.  Stable FLAIR\nhyperintense signal is seen within the mass.  There is stable sulcal\neffacement along the left frontoparietal lobe with no significant midline\nshift.  There are multiple subcortical, periventricular and deep white matter\nT2/FLAIR hyperintensities, consistent with chronic microvascular ischemic\nchanges.\n\nThere is prominence of the ventricles and sulci consistent with involutional\nchanges.  The orbits are normal.  The paranasal sinuses and mastoid air cells\nare normal.",
            "output": "1. Interval development of posttreatment changes in the left frontoparietal\nmass with residual contrast enhancement along the anterior, posterior and\ninferior aspect of the mass consistent with residual disease."
        },
        {
            "input": "There is no evidence of infarction, hemorrhage, edema, mass effect, or midline\nshift.  There are few nonspecific scattered T2/FLAIR hyperintensities within\nthe periventricular subcortical white matter.  Although of doubtful clinical\nsignificance, similar findings may be associated with chronic headaches, prior\ntrauma, infectious or inflammatory processes, or demyelinating disease.  In\ncases with a small number of small lesions, specific pathologic correlates are\nrarely identified.  The major visualized arterial vascular flow voids are\npreserved.  There is no abnormal enhancement. There is mild bilateral ethmoid\nair cell mucosal thickening.  The orbits and visualized soft tissues appear\nunremarkable.  The bilateral mastoid air cells appear clear.",
            "output": "1. No evidence of infarction, hemorrhage, mass, or abnormal enhancement.\n2. Nonspecific scattered white matter signal abnormality, of doubtful clinical\nsignificance."
        },
        {
            "input": "Post-surgical changes after right parietal craniotomy are  unchanged.\nPost-radiation  FLAIR-hyperintensity in the temporoparietal region is also u\nnchanged since ___. Ex vacuo dilatation of the adjacent right\nlateral ventricular occipital horn is also similar in degree. An 8mm round\nintrinsically slightly T1-hyperintense focus in the surgical bed (13:12)\ndemonstrates corresponding susceptibility signal loss and is unchanged over a\nseries of studies. This may represent residual mineralization or blood\nproducts or, perhaps, a secondary cavernous angioma. A cavernous angioma in\nthe left cerebellar hemisphere is unchanged since ___.\n\n There is no acute infarct, intracranial mass, mass effect, or shift of the\nnormally-midline structures. Ventricles and sulci are otherwise normal and\nunchanged in size and in shape.  There is no abnormal post-contrast\nenhancement. Principle intracranial vascular flow-voids are maintained.\nVisualized paranasal sinuses and mastoid air cells are clear. Osseous and\nextracalvarial soft tissue structures are unremarkable.",
            "output": "Stable post-surgical changes after right parietal craniotomy, with no evidence\nof local recurrence."
        },
        {
            "input": "Stable post surgical and post radiation changes in the right temporoparietal\nregion includes FLAIR hyperintensity. There has been a prior right craniotomy.\nThere is no evidence of acute hemorrhage or infarction.  There is minimal ex\nvacuo dilation of the occipital horn of the right lateral ventricle ;\notherwise, the ventricles and sulci are normal in caliber and configuration.\nThere is no abnormal enhancement after contrast administration. ___ cisterna\nmagna is incidentally noted. A left cerebellar developmental venous anomaly\nwith associated cavernoma was present on multiple prior studies.",
            "output": "Stable post treatment changes."
        },
        {
            "input": "Stable post treatment changes in the right temporoparietal region status post\nresection of previously known glioma.  Stable associated FLAIR hyperintensity\nwith volume loss and ex vacuo dilatation of the body of right lateral\nventricle.  There is no abnormal enhancement after contrast administration to\nsuggest residual or recurrent tumor.\n\nStable focus of microhemorrhage in the left cerebellar hemisphere is again\nseen.\n\nThere is no evidence of acute hemorrhage, edema, masses, mass effect, midline\nshift or infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  Incidentally seen is ___ cisterna magna.\n\nThe orbits are unremarkable.  Mucosal thickening of the right maxillary sinus\nis new compared to the prior study.  The remaining visualized paranasal\nsinuses and mastoid air cells are clear.  Intracranial flow voids are\nmaintained.  Osseous structures are unremarkable noting the prior right\nparietal craniotomy.",
            "output": "1. Stable post treatment changes related to resection of previously known\nright temporo-parietal glioma.  No  recurrent tumor is seen."
        },
        {
            "input": "Redemonstrated are post treatment changes in the right temporal parietal\nregion.  Volume loss and ex vacuo dilatation of the atrium and proximal\ntemporal and occipital horns of the right lateral ventricle and FLAIR\nhyperintense signal in this region are overall stable and there is no\nappreciable interval enhancement to suggest tumor progression.\n\nA microhemorrhage in the left cerebellum is chronic.  There is no new\nintracranial hemorrhage and no acute infarction.  The ventricles and sulci are\nage-appropriate.  Principal intracranial vascular flow voids are preserved. \nThe dural venous sinuses are patent on postcontrast MP rage sequences.\n\nThere is a small mucous retention cyst along the floor of the right maxillary\nsinus and mild diffuse mucosal thickening of the ethmoid air cells are noted. \nThe orbits are unremarkable.",
            "output": "1. Stable post treatment changes in the right temporoparietal region without\nevidence of tumor progression.\n\n2. No evidence of interval hemorrhage or acute infarction."
        },
        {
            "input": "Patient is post right temporal parietal craniectomy and mass resection.  Focal\nencephalomalacia at the surgical site and ex vacuo dilation of the right\nlateral ventricle posterior horn are similar to ___. Surrounding\nFLAIR hyperintensity is also unchanged.  There is no suspicious enhancement.\nA prominent vessel with the focus of microhemorrhage in the left cerebellum is\nunchanged. There is no evidence of midline shift or infarction.  The major\nintracranial flow voids are preserved.  Dural venous sinuses are patent.\n\nMucosal thickening is mild in the left maxillary sinus.  The orbits are\nunremarkable.  No significant fluid signal is noted in the mastoid air cells.",
            "output": "1. Stable posttreatment changes in the right temporoparietal region.  No\nfindings to suggest disease progression."
        },
        {
            "input": "There is an approximately 3.5 cm extra-axial mass in left side of the\nposterior fossa consistent with meningioma. The mass is adjacent to the\nposterior aspect of the petrous temporal bones. Normal flow related\nenhancement is identified in the left transverse sinus.  There is no midline\nshift or hydrocephalus.  Slightly prominent right temporal horn is unchanged.",
            "output": "The left posterior fossa extra-axial mass compatible with meningioma is\nidentified for surgical planning."
        },
        {
            "input": "Patient is again noted to be status post left suboccipital craniotomy for\nresection of previously demonstrated left CP angle mass. There are expected\npostoperative changes including overlying occipital region soft tissue\nswelling, a left posterior fluid collection, and postoperative blood products.\n\nThe previously noted region of slow diffusion in the lateral left cerebellar\nhemisphere has resolved.\n\nOn post-contrast images, there has been an interval increase in marginal\nenhancement surrounding the resection bed. There is also a focus of\nenhancement within the parenchyma of the left cerebellar hemisphere (series\n19, image 30) not definitively seen on prior study). It is of note that these\nchanges are in the region of previously noted slow diffusion on prior exam.\n\nThere is no shift of midline or mass effect. The ventricles and sulci are\nnormal in caliber and configuration.  The major vascular flow voids are\npreserved. The orbits are unremarkable. The paranasal sinuses are clear. There\nis fluid again identified in the left mastoid air cells.",
            "output": "Patient is status post left suboccipital craniotomy for resection of\npreviously demonstrated left CP angle mass with expected postoperative\nchanges.  Marginal enhancement surrounding the resection cavity is more\npronounced than on prior study and there is a new focus of enhancement seen\nwithin the left cerebellar hemisphere. These findings are in the region of\npreviously noted slowed diffusion on prior exam and therefore could still be\npostoperative in etiology. Continued followup is recommended to exclude\nresidual or recurrent tumor."
        },
        {
            "input": "There is left occipital craniotomy anatomy with cranioplasty hardware in\nplace.  There is subjacent foci of chronic blood products and a thin dural\nenhancement without focal nodularity.  There is left cerebellar hemisphere\nencephalomalacia.  There is no evidence of residual or recurrent meningioma. \nThe remainder of the parenchymal signal is unremarkable without acute infarct,\nhemorrhage, mass, or mass effect.  The ventricles and cortical sulci are\nnormal and caliber and configuration.  The vasculature is patent.\n\nThe orbits, calvarium, and soft tissues are unremarkable.  The paranasal\nsinuses and mastoid air cells are clear.",
            "output": "1. Left posterior fossa postsurgical changes, as described, with left\noccipital cranioplasty which demonstrates thin subjacent enhancement\nconsistent with postsurgical changes.  No evidence of residual or recurrent\nmeningioma.\n2. No acute intracranial abnormality."
        },
        {
            "input": "There are innumerable supratentorial and infratentorial enhancing lesions\nwhich appear slightly more conspicuous than on the prior study (103b:79, 75,\n21), however this could be due to technical difference.\n\nIrregularly shaped 1.2 x 0.7 x 0.9 cm lesion in the right parietal lobe\n(103b:58) features peripheral enhancement and associated susceptibility\nartifact suggesting blood products is also unchanged.  A 0.8 x 0.6 cm right\noccipital lobe enhancing lesion (103b:37) is stable in size but now enhances\nhomogeneously, previously there was a central area of nonenhancement.\n\nThere is a nonspecific 4 mm area of FLAIR hyperintensity in the left frontal\nlobe (11:15) without associated enhancement which is not definitely seen on\nthe prior study but could be due to technical differences.\n\nIn the cerebellum on the left there is an apparent new 2 mm area of\nenhancement with associated diffusion restriction and mild surrounding edema\n(103b:29 and 11:7).  Punctate areas of enhancement and associated FLAIR\nhyperintensity in the left cerebellar tonsil (103b:14) are unchanged.\n\nThere is no evidence of acute infarct.  Subarachnoid susceptibility artifact\nis extensive, similar compared to prior, potentially from prior hemorrhage. \nThe major intracranial arterial flow voids are preserved.  The dural venous\nsinuses are patent.  The basal cisterns are clear.  There is mild mucosal\nthickening in the left maxillary sinus and some fluid in the right mastoid air\ncells.",
            "output": "1. Innumerable bilateral supratentorial and infratentorial enhancing lesions\nappear slightly more conspicuous than on the prior study of ___,\nhowever this could be due to technical differences.\n2. The largest peripherally enhancing lesion in the right parietal lobe is\nunchanged, potentially a developing abscess.\n3. The only clearly new enhancing lesion is a single punctate focus in the\ncerebellum on the left.\n4. The differential for these findings as detailed on the prior study remains\nunchanged.\n5. Diffuse subarachnoid susceptibility artifact suggesting superficial\nsiderosis, potentially from prior subarachnoid hemorrhages."
        },
        {
            "input": "The majority of the supratentorial enhancing lesions with corresponding\nT2/FLAIR hyperintense signal are unchanged from the prior examination.  The\nenhancing lesion in the left cerebellar hemisphere has increased in size,\nmeasuring 6 x 4 x 3 mm, previously measuring 3 x 3 x 3 mm.  An enhancing\nlesion in the right cerebellar hemisphere has increased in size, measuring 3\nmm on 1100:66, previously measuring 2 mm.  A 3 mm enhancing lesion in the\nright posterior temporal lobe on 1100:98, has increased in size.  The 7 x 12 x\n10 mm lesion in the right occipital lobe with both a rim and curvilinear\nenhancing component is unchanged.  The enhancing lesion in the right occipital\nlobe and several of the smaller, punctate enhancing lesions in the bilateral\nfrontal and parietal lobes are associated with susceptibility.  Curvilinear\nsusceptibility in the bilateral frontal, parietal, and occipital lobes is\nunchanged.\n\nThere is no evidence of mass effect, midline shift or infarction.  The\nventricles and sulci are normal in caliber and configuration.\n\nThere is mild mucosal thickening in the left maxillary sinus.  The mastoid air\ncells are clear.\n\nThe major intracranial flow voids are preserved.",
            "output": "1. Numerous supratentorial and infratentorial enhancing lesions, the majority\nof which have remained stable with interval increase in the size of the\nenhancing lesions in the bilateral cerebellar hemispheres and right posterior\ntemporal lobe, most likely representing septic emboli and abscess formation in\nthe larger lesions.\n2. Unchanged, patchy curvilinear susceptibility in the bilateral frontal,\nparietal, and occipital lobes, which may represent siderosis from prior\nsubarachnoid hemorrhage."
        },
        {
            "input": "Overall decreased FLAIR and diffusion-weighted hyperintense signal associated\nand near complete resolution of enhancement in previously described lesions on\n___.  There remains 6 mm (series 19, image 63) and 4 mm (series\n19, image 41) enhancement of the right occipital lobe which is decreased in\nconspicuity.  Associated parenchyma gradient echo susceptibility is slightly\nmore prominent in number and conspicuity.  Superficial siderosis of the\nbilateral frontal parietal and occipital lobes is similar appearance.  No new\nenhancing lesions are identified.  The major intracranial flow voids are\npreserved.  The dural venous sinuses are patent The orbits are unremarkable. \nMild mucosal thickening of the left maxillary sinus is noted.  The remainder\nof the paranasal sinuses are essentially clear.  The mastoid air cells are\nessentially clear.  Unchanged 5 mm pineal cyst.",
            "output": "1. Near complete resolution of enhancement in multiple supra and\ninfratentorial lesions, with 2 dominant residual 6 mm and 4 mm foci of\nenhancement in the right occipital lobe.  Associated FLAIR in\ndiffusion-weighted hyperintense signal have significantly decreased in\nconspicuity.\n2. Minimal increased gradient echo susceptibility foci associated with these\nlesions, presumably posttreatment in nature.\n3. No new lesions."
        },
        {
            "input": "Again demonstrated are areas of susceptibility artifact in the left cerebellar\nhemisphere, right occipital lobe and left frontal corona radiata as well as\nextensive areas of subarachnoid susceptibility artifact appear overall\nunchanged from prior examination indicating prior areas of hemorrhage.\n\nPreviously noted enhancing FLAIR hyperintense supra and infratentorial lesions\nhave nearly completely resolved, with only a few scattered areas of\nperiventricular white matter FLAIR hyperintensity as well as a 9 x 1 mm focus\nof linear enhancement in the right occipital lobe, decreased compared to the\nprior examination with resolution of the medial nodular enhancing component. \nNo new abnormal focus of enhancement is noted.\n\nThere is no evidence of acute hemorrhage, increasing edema, new masses, mass\neffect, midline shift or infarction.   The ventricles and sulci are normal in\ncaliber and configuration.  There is no abnormal focus of slowed diffusion. \nThe dural venous sinuses are patent on MP rage images.  The principal\nintracranial vascular flow voids are preserved.  The visualized paranasal\nsinuses are grossly clear.  The orbits are grossly unremarkable.",
            "output": "1. Near complete resolution of enhancement in the right occipital lobe, with\nonly a thin linear focus of enhancement remaining.\n2. Remainder of the previously noted supra and infratentorial enhancing\nlesions demonstrated resolution of enhancement, with only trace areas of FLAIR\nhyperintensity remaining.\n3. No new focus of enhancement.\n4. Areas of scattered parenchymal and subarachnoid susceptibility artifact are\nunchanged, representing treated lesions and hemosiderin staining from chronic\nsubarachnoid hemorrhage.\n5. No acute infarct or acute hemorrhage."
        },
        {
            "input": "MR head:  There is a large region of right posterior frontal slowed diffusion\nwith associated FLAIR hyperintensity with note of occlusion of a posterior\nright M3 division of the MCA on the recent prior outside hospital CT\nexamination (2b:425 on the ___ CTA examination) leading to the area\nof infarction.  There is associated sulcal enhancement in a vascular pattern\nin the region of infarct involving a posterior M3 division and distal M4\nbranches.  There is associated susceptibility artifact in area of enhancement.\nThis likely represents enhancement of thrombus.\n\nCurvilinear focus of enhancement in the right medial occipital lobe appears\nunchanged compared to the ___ examination.\n\nThere are unchanged numerous scattered areas of punctate susceptibility\nartifact at the gray-white matter junction in the bilateral cerebral and\ncerebellar hemispheres, grossly unchanged compared the prior examination\ncorresponding to areas of microhemorrhage.  Multiple areas of scattered sulcal\nsusceptibility artifact is overall unchanged.\n\nThere is no evidence of acute hemorrhage, masses, significant mass effect, or\nmidline shift.   The ventricles and sulci are normal in caliber and\nconfiguration.  The principal intracranial vascular flow voids are preserved. \nThe dural venous sinuses are patent on MP rage images\n\nThe visualized paranasal sinuses are grossly clear.  The orbits are grossly\nunremarkable.\n\n\nMRV: Normal flow signal is demonstrated within the superior sagittal sinus,\nstraight sinus, transverse sinuses, and sigmoid sinuses. The jugular bulbs and\nproximal jugular veins are patent. Evaluation of the deep venous systems\nreveals normal flow signal in the internal cerebral veins. The vein ___\nis also unremarkable.",
            "output": "1. Acute to subacute right posterior frontal infarct as seen on recent prior\noutside hospital CT examination secondary to thrombosis of a posterior M3\ndivision of the right MCA with involvement of the distal M4 branches.  There\nis associated enhancement of thrombus.  Please note that bland thromboembolic\nand septic embolic infarcts can appear identical in the acute setting.\n2. Unchanged curvilinear focus of enhancement in the right medial occipital\nlobe in area of previously treated septic embolus.  No other enhancing lesion.\n3. Unchanged numerous scattered punctate microhemorrhage in the bilateral\ncerebral and cerebellar hemispheres corresponding to prior areas of resolved\nseptic emboli.  Unchanged scattered areas of sulcal susceptibility artifact\ndenoting prior subarachnoid hemorrhage and superficial siderosis.  No acute\nhemorrhage.\n4. No evidence of venous sinus thrombosis."
        },
        {
            "input": "There are multiple foci of hyperintense DWI/FLAIR signal predominantly\ninvolving the left superior frontal lobe with additional punctate foci noted\nin the left centrum semiovale more posteriorly.  These are dark on the ADC map\nand consistent with late acute/early subacute embolic infarcts.  Chronic right\nparietal temporal infarct and numerous scattered supra and infratentorial\nmicro hemorrhages are again noted.\n\nThere is no evidence of recent hemorrhage, masses, mass effect, or midline\nshift.   The ventricles and sulci are normal in caliber and configuration. \nThere is fluid signal in a few air cells at the right mastoid tip.  The orbits\nare unremarkable.",
            "output": "1. Multifocal late acute/early subacute infarcts in the left ACA and MCA\ndistributions are likely embolic in etiology.  There is no evidence of an\nabscess.  Bland versus septic emboli cannot be distinguished.\n2. Chronic right parietotemporal infarct.\n3. Numerous scattered supra and infratentorial punctate micro hemorrhages\nlikely corresponding to prior septic emboli."
        },
        {
            "input": "In comparison to the recent examination of ___, there is no\nsubstantial change.  Redemonstrated are evolving subacute infarcts in the left\nsuperior frontal lobe and left centrum semiovale, chronic right\nparietotemporal infarct, and multiple scattered supra and infratentorial micro\nhemorrhages.\n\nThere is mild postcontrast enhancement in the region of the old right\nparietotemporal infarct containing hemorrhagic products.  There is mild\nleptomeningeal enhancement in the region of the more recent left superior\nfrontal infarcts, best appreciated on postcontrast MP-RAGE sequences (series\n700, image 121).  There is no recent hemorrhage or interval acute infarction. \nPrincipal intracranial vascular flow voids are preserved and dural venous\nsinuses enhance appropriately on postcontrast MP rage sequences.\n\nThe ventricles and sulci are age appropriate.  Fluid signal in a few air cells\nat the right mastoid tip is unchanged.  The orbits are unremarkable.",
            "output": "1. No change compared to the prior examination of ___.  No new\ninfarction or recent hemorrhage.\n2. Evolving multifocal subacute infarcts in the left ACA and MCA distribution,\nconsistent with an embolic etiology.  Septic emboli versus bland emboli cannot\nbe distinguished as bland subacute infarcts can show enhancement.  There is no\nevidence of an abscess.\n3. Chronic right parietal temporal infarct.\n4. Numerous is scattered supra and infratentorial punctate micro hemorrhages,\ncorresponding to prior septic emboli."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.\n\nThere are few scattered foci and more confluent areas of FLAIR hyperintensity\nsignal in the subcortical and periventricular white matter, which are\nnonspecific, likely secondary to chronic small vessel ischemic disease.\n\nThe orbits are unremarkable.  There is mild mucosal thickening in bilateral\nmaxillary sinuses.  The remaining visualized paranasal sinuses and mastoid air\ncells are clear.  Intracranial flow voids are maintained.",
            "output": "1. There is no evidence of acute or subacute intracranial process, there is no\nevidence of abnormal enhancement."
        },
        {
            "input": "There is extensive confluent periventricular and subcortical white matter\nFLAIR hyperintensity, left greater than right, in addition to central and\ndorsal pontine and deep white matter FLAIR hyperintensity, likely representing\nsequela of advanced chronic microangiopathy.  There is encephalomalacia at the\nleft frontal operculum consistent with remote infarct, which is new in\ncomparison to prior study.  There is mineralization of the bilateral globus\npallidi.  There is no evidence of acute infarct, hemorrhage, mass, or mass\neffect.  There is significant ventricular dilatation which is mildly out of\nproportion to the degree of cortical sulcation.  The extra-axial spaces are\nunremarkable.  The vascular flow voids are preserved.\n\nThe orbits, calvarium, and soft tissues are unremarkable.  There is no fluid\nsignal within the paranasal sinuses.  There are bilateral mastoid air cell\neffusions.  There is a right middle ear fusion.",
            "output": "1. Extensive white matter FLAIR hyperintensity, left greater than right, as\ndescribed, likely representing sequela of chronic advanced microangiopathy,\nwhich is increased in comparison to prior study.\n2. Encephalomalacia at the left frontal operculum consistent with sequela of\nchronic infarction, which is new in comparison to prior study.\n3. Significant ventricular dilatation which is mildly out of proportion to the\ndegree of cortical sulcation.  This likely reflects disproportionate central\nvolume loss, however differential includes communicating hydrocephalus.\n4. Moderate degree of volume loss without lobar predominance, which has\nincreased.\n5. Bilateral mastoid air cell effusions, and a right middle ear effusion. \nRecommend correlation with otitis."
        },
        {
            "input": "There is acute to early subacute left PCA distribution infarction involving\nmedial and posterior left temporal lobe and left occipital lobe with\nassociated FLAIR hyperintensity.  There is no evidence of hemorrhage.\nThere is a right middle cranial fossa, measuring 4.2 x 2.9 cm extending along\nthe right frontal convexity.  The ventricles are normal in size without\nmidline shift.  There is mild paranasal sinus disease.",
            "output": "1. Acute to early subacute infarction involving the left PCA distribution,\nwithout hemorrhage.\n2. Right middle cranial fossa arachnoid cyst extending along the right\nconvexity.\n3. Mild paranasal sinus disease.\n\nNOTIFICATION:  The findings were discussed with ___, M.D. by\n___, M.D. on the telephone on ___ at 4:54 pm, 2\nminutes after discovery of the findings."
        },
        {
            "input": "There is no evidence of intracranial hemorrhage, mass, mass effect or shifting\nof the normally midline structures.  The ventricles and sulci are prominent\nfor the patient's age, suggesting cortical volume loss.  Punctate and\nconfluent areas of high-signal intensity are demonstrated in the subcortical,\nperiventricular white matter, midbrain and pons on T2 and FLAIR sequences,\nwhich are nonspecific and may reflect changes due to small vessel disease.  No\ndiffusion abnormalities are detected to indicate acute or subacute ischemic\nchanges.  The major vascular flow voids are present and demonstrate normal\ndistribution.  The orbits are unremarkable, the paranasal sinuses are notable\nfor mild mucosal thickening in the maxillary sinuses with no evidence of\nair-fluid levels, the mastoid air cells are clear.  Note is made of a possible\nsebaceous cyst in the soft tissues of the right parietal region (image 14,\nseries 5, and image 8, series 4, measuring approximately 5 x 10 mm in\ntransverse dimension.",
            "output": "1. There is no evidence of acute or subacute intracranial process, or evidence\nof intracranial hemorrhage.\n\n2.  Scatter foci and confluent areas of T2/FLAIR high-signal intensity\ndistributed in the subcortical white matter, midbrain and pons, which are\nnonspecific and may reflect changes due to chronic microvascular ischemic\ndisease.\n\n3.  The ventricles and sulci are prominent for the patient's age suggesting\ncortical volume loss."
        },
        {
            "input": "3.3 x 1.8 cm (TRV, AP) T2 slightly hyperintense, heterogeneously enhancing\nlesion anterior to the right auricle, extending posterior to the mandibular\ncondyle and ramus along the retromandibular space (along the expected course\nof the right auriculotemporal nerve), abutting the masticator space (series 6,\nimage 14).  There is soft tissue extension into the external auditory canal. \nThis appears to have slightly increased in size when compared to the prior CT\nexamination of ___.  Given its persistence and continued interval\nenlargement, the findings are compatible recurrent tumor.  There is enhancing\nwater sensitive hyperintense signal of the subjacent parotid gland and and of\nthe inferior aspects of the right lateral pterygoid muscle at its attachment\n(series 6, image 15, series 7, image 15), which may represent inflammatory\nstranding although underlying tumoral extension is not excluded.  The water\nand sensitive hyperintense signal appears to involve the left inferior\nalveolar nerve just proximal to the ostium of the inferior alveolar nerve\ncanal (series 6, image 15).\n\nThere is preservation of the right trigeminal fat pad.  There is no definitive\nabnormal enhancement or nodular lesion tracking along the visualized branches\nof the right V3 segment.  There is no evidence of intracranial extension.\n\nThere is no abnormal cortical or marrow signal of the left mandibular condyle\nand ramus.\n\nThe visualized submandibular glands are unremarkable.  The left parotid gland\nand masticator space are unremarkable.\n\nThe contents of the bilateral cerebellopontine angles are unremarkable\nincluding cranial nerves V, VI, VII/VIII complexes as well as the cranial\nnerves IX through XII.  No masses are noted within the internal auditory\ncanals.  The visualized course of the facial nerve is unremarkable.  There is\nno inner ear dysplasia.  The bilateral Meckel's cave is unremarkable without\nevidence of abnormal mass lesion or enhancement.\n\nThe aerodigestive track is unremarkable.\n\nAgain noted is trace opacification of the right mastoid tip.  Mucous retention\ncyst is noted in the right maxillary sinus.  The rear paranasal sinuses are\nclear.  The visualized orbits are unremarkable.  Visualized brain is\nunremarkable.",
            "output": "1. Re-identified is a 3.3 cm enhancing lesion anterior to the right ear with\nextension into the external auditory canal and along the retromandibular space\nand expected course of the right auriculotemporal nerve, abutting the right\nmasticator space.  The lesion may be slightly increased in size when compared\nto prior CT examination of ___.  Given its persistence and interval\ngrowth, this is highly suspicious for recurrent tumor.\n2. There is enhancing water sensitive hyperintense signal at the inferior\naspect of the right masticator space at the level of the opening of the\ninferior alveolar canal and lateral pterygoid muscle attachment, which\nsurrounds the left inferior alveolar nerve.  This may represent inflammatory\nchanges however, tumoral extension is not excluded.\n3. However, there is no nodular enhancement along the expected course of the\nright trigmenial nerve branches and the trigeminal fat pad is preserved.\n4. Enhancing water sensitive hyperintense signal of the right parotid gland is\nnoted, which may represent inflammatory changes versus tumoral extension.\n5. There is no evidence of intracranial extension\n6. Fluid signal is seen in the right mastoid tip, similar appearance to prior\nCT examination of ___."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.  Arterial flow voids are patent.  The dural venous sinuses\nappear patent on MP-RAGE images.\n\nThe paranasal sinuses, middle ear cavities, and mastoid air cells are\nunremarkable.",
            "output": "1. Unremarkable brain MRI without evidence of intracranial metastases at this\ntime."
        },
        {
            "input": "There is no evidence for an intracranial mass, and no pathologic\nleptomeningeal or pachymeningeal contrast enhancement, to suggest intracranial\nmetastatic disease. There is no edema, mass effect, abnormal diffusion, or\nevidence for blood products in the brain parenchyma.  Ventricles and sulci are\nnormal in size for age.  Major arterial flow voids are grossly preserved. \nMajor dural venous sinuses are patent.",
            "output": "No evidence for intracranial metastatic disease."
        },
        {
            "input": "There has been no significant interval change in the extent of cerebellar\ntonsillar herniation approximately 8 mm below the foramen magnum consistent\nwith patient's known Chiari 1 malformation.  No acute intracranial hemorrhage\nor infarction is identified.  Ventricles and sulci are age appropriate.  Left\nparietal deep subcortical FLAIR signal abnormality is seen measuring\napproximately 5 mm, series 14, image 13.  A left temporal lobe 9 mm FLAIR\nhyperintense lesion is also seen, series 14, image 8.\n\nMild mucosal sinus thickening is seen involving the ethmoid air cells.  The\nremainder the visualized paranasal sinuses are clear.  Principal vascular flow\nvoids appear to be well preserved.  The mastoid air cells and middle ear\ncavities are clear.",
            "output": "1. Unchanged appearance cerebellar tonsillar herniation approximately 8 mm\nbelow the foramen magnum, consistent with patient's known Chiari 1\nmalformation compared to the cervical spine MRI from ___.\n2. No acute intracranial abnormalities identified.  No evidence of mass\neffect.\n3. Nonspecific FLAIR hyperintense lesions are seen within the left temporal\nlobe and left parietal lobe measuring up to 9 mm.  Recommend correlation with\nprior outside hospital imaging if available."
        },
        {
            "input": "Postcontrast MP RAGE images are limited by motion artifact despite 2\nacquisition attempts.  Postcontrast axial T1 weighted images provided good\ndiagnostic quality.\n\nAt the sites of the previously demonstrated small FLAIR hyperintense white\nmatter lesions, largest in the left temporal subcortical white matter and left\nparietal peritrigonal white matter, there is no evidence of abnormal T1\nweighted signal or abnormal enhancement (see series 10, images 10 and 15).\n\nNo evidence for other pathologic contrast enhancement.  The ventricles and\nsulci are normal in size and configuration. 7 mm cerebellar tonsillar descent\nis re-demonstrated, consistent with patient's known Chiari 1 malformation.\nMajor dural venous sinuses are patent.",
            "output": "Previously seen scattered small foci of high FLAIR signal in the\nsupratentorial white matter, largest in the left temporal and left parietal\nwhite matter, demonstrate no contrast enhancement.  These are nonspecific in\nthis age group.  Diagnostic considerations include migraine related lesions,\nsequela of prior inflammation or demyelination, sequela of vasculitis, or\nsequela of chronic small vessel ischemia if the patient has cardiovascular\nrisk factors."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.\n\nThere is prominence and heterogeneous enhancement of the lingual tonsils with\nadjacent prominent partially visualized of the cervical lymph nodes.\n\nThe major intracranial vascular flow voids are preserved.  The ventricles and\nsulci are normal in caliber and configuration.  There is moderate mucosal\nthickening of the right ethmoid air cells.  The mastoid air cells and orbits\nare normal.",
            "output": "1. No acute intracranial abnormality.  Specifically, no evidence for venous\nsinus thrombosis.\n2. Prominent and heterogeneously enhancing lingual tonsils with associated\nprominent partially visualized bilateral cervical lymph nodes raises suspicion\nfor an infectious/inflammatory process.  Consider direct visualization for\nfurther characterization.\n3. Moderate inflammatory changes of the right ethmoid air cells.\n\nRECOMMENDATION(S):  Prominent and heterogeneously enhancing lingual tonsils\nwith associated prominent partially visualized bilateral cervical lymph nodes\nraises suspicion for an infectious/inflammatory process. Consider direct\nvisualization for further characterization."
        },
        {
            "input": "The exam is substantially degraded by motion artifact. Allowing for these\nlimitations:\n\nThere is no evidence of hemorrhage, infarction, mass or mass effect. The\nventricles and sulci are prominent, likely reflecting cortical volume loss.\nMultiple foci of high signal intensity are identified in the subcortical and\nperiventricular white matter on T2 and FLAIR sequences, which are nonspecific\nand may represent changes due to small vessel disease. The major vascular flow\nvoids are present and demonstrate normal distribution. The orbits are normal. \nOpacification of the left maxillary sinus is redemonstrated.  There is fluid\nin the right mastoid. The remaining paranasal sinuses and the left mastoid air\ncells are clear.",
            "output": "1.  No evidence of acute intracranial process.  Specifically no right frontal\nlobe lesion is identified.\n\n2.  Scattered foci of T2 and FLAIR high signal intensity in the subcortical\nand periventricular white matter are nonspecific and may reflect changes due\nto small vessel disease."
        },
        {
            "input": "There is no evidence of acute infarction.  No intracranial hemorrhage.  No\nmass, mass effect, edema or midline shift.\n\nThe ventricles and sulci are normal, without evidence of hydrocephalus. The\nbasal cisterns are patent.  Incidentally noted is an empty sella.  There is\ngross preservation of the principal intracranial vascular flow voids.\n\nBilateral hippocampal formations and mammillary bodies are preserved in signal\nand configuration. There is no disproportionate medial temporal atrophy. There\nis no focal lobar encephalomalacia. There are no focal cortical dysplasias or\ngray matter heterotopia noted.\n\nFollowing the administration of intravenous contrast material, there is no\nabnormal enhancement.  The dural venous sinuses appear patent on MP-RAGE\nimagine sequences.\n\nA mucous retention cyst is noted in the right sphenoid sinus.  The remainder\nof the visualized paranasal sinuses, middle ear cavities, and mastoid air\ncells are well aerated and clear.  The orbits are within normal limits\nbilaterally.",
            "output": "1. Unremarkable MRI examination of the brain.  Specifically, no evidence for\nintracranial hemorrhage, ischemia, infarction, or abnormal enhancement.\n2. No evidence of mesial temporal sclerosis, gray matter heterotopia or focal\ncortical dysplasia.\n3. Empty sella."
        },
        {
            "input": "There is redemonstration posteriorly rejected outpouching centered at proximal\nright posterior communicating artery measuring 3 mm in maximum depth;\nunchanged since CTA head and neck dated ___.\n\nThe intracranial vertebral and internal carotid arteries and their major\nbranches otherwise appear normal without evidence of\nstenosis,occlusion,orother aneurysm formation.",
            "output": "1. Unchanged 3 mm aneurysm at origin of right posterior communicating artery"
        },
        {
            "input": "MRI HEAD: There is a focus of diffusion-weighted signal hyperintensity with\nassociated ADC hypo intensity along the left lenticulostriate distribution\ninvolving the posterior limb of the left internal capsule extending to the\ncorona radiata. In addition, this lesion demonstrates FLAIR hyperintensity,\nsuggestive of a more late acute to subacute infarct. There is a nonspecific\nsubtle diffusion-weighted hyperintensity in the posterior parietal white\nmatter (series 6, image 26) without evidence of associated FLAIR\nhyperintensity where ADC abnormality, which is nonspecific.\n\nThere are very few scattered white matter subcortical and periventricular\nnonspecific T2/FLAIR hyperintensities, which may be seen in setting of small\nvessel ischemic disease. There is global cerebral volume loss, greater than\nwould be expected for the patient's age. In addition, the ventricles are\nenlarged, greater than would be expected for the degree of volume loss.\nHowever, there is no evidence of obstruction at the level of the aqua duct.\n\nThere is a 2.2 x 1.6 by 1.6 cm (TRV, AP, CC) mass centered in the sella, which\nan remodels the bony sella, without definite extension into the bilateral\ncavernous sinuses. The lesion extends into the suprasellar cistern, the does\nnot appear to displace the optic chiasm on these limited sequences. The lesion\ndemonstrates intrinsic T1 hyperintense signal as well as fluid fluid level on\nthe FLAIR/ T2 with prominent T2 hyperintense signal anteriorly. There\nsuggestive of a chronic pituitary macroadenoma with hemorrhage, although the\nchronicity of the hemorrhages uncertain. The size of the pituitary lesion is\nlikely chronic given the extensive remodeling of the bony sella.\n\nParanasal sinuses are clear. The orbits are unremarkable. The mastoid air\ncells are clear.\n\nHEAD MRA: Normal flow related signal is seen in the intracranial internal\ncarotid, middle cerebral and anterior cerebral arteries without significant\nmural irregularity or stenosis. There is normal symmetric arborization of the\nMCA branches. There is no aneurysm greater than 3 mm. Normal flow related\nsignal is seen in the codominant intracranial vertebral arteries, the basilar\nartery, and the bilateral superior cerebellar and posterior cerebral arteries.\n\nNECK MRA: There is a normal 3 vessel takeoff from the aortic arch. The\ncervical common carotid, internal carotid and external carotid arteries are\nnormal in course, caliber and contour. They demonstrate normal signal without\nmural irregularity, stenosis or evidence of dissection. Incidental note is\nmade of a retropharyngeal course of the right ICA. There is no significant\nstenosis of the internal carotid arteries by NASCET criteria. The left\nvertebral artery is dominant. The vertebral arteries are normal in course,\ncaliber and contour. They demonstrate normal signal without mural\nirregularity, stenosis or evidence of dissection.",
            "output": "1. There is a late acute to subacute infarct of the left posterior limb of the\ninternal capsules to corona radiata in the lateral into late striated\ndistribution. There is an additional focus of diffusion-weighted signal\nabnormality without associated ADC hypointensity were FLAIR abnormality of the\nleft, which is nonspecific.\n2. Superimposed white matter changes described above compatible with small\nvessel ischemic disease.\n3. There is a 2.2 cm lesion centered in the sella, likely a pituitary\nmacroadenoma. The lesion demonstrates layering fluid fluid levels, with T1 and\nT2 hyperintense signal anteriorly, consistent with hemorrhage although the\nacuity is uncertain.  There is remodeling of the bony sella consistent with a\nslow growing chronic lesion."
        },
        {
            "input": "MRI Brain:\n\nThere are grossly stable several scattered T2/FLAIR hyperintensity in the\nsubcortical white matter of frontal lobes and parietal lobes.  These lesions\nare unchanged in size, for instance of the largest lesion in the left frontal\nlobe measures up to 1 cm.  There is no associated enhancement to these\nlesions.\n\nAdditional increased T2/FLAIR hyperintensity are noted in the left superior\nand middle cerebellar peduncle.  These lesions demonstrate mild peripheral\nlinear enhancement (300:380, 9:8), raising concern for active demyelinating\nlesions.\n\nThere is also stable T2/FLAIR hyperintensity in the right middle cerebellar\npeduncle, without associated enhancement.\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.\n\nMRA brain: The intracranial vertebral and internal carotid arteries and their\nmajor branches appear normal without evidence of stenosis, occlusion, or\naneurysm formation.",
            "output": "1. Stable size and number of the multiple scattered T2/FLAIR hyperintensity in\nthe subcortical white matter of the frontal and parietal lobes, the left\nsuperior and middle cerebral peduncle, and right middle cerebellar peduncle,\ncompatible with multiple sclerosis.\n2. Interval appearance of enhancement of the lesion in the left superior\nmiddle cerebral peduncle, raises suspicion for active demyelinating disease."
        },
        {
            "input": "There is a focus of slow diffusion within the left inferior cerebellar\npeduncle (series 502, image 6), which is associated with FLAIR hyperintensity\n(series 7, image 5), likely representing a subacute infarct.\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, or midline\nshift.  The subcortical, deep, and periventricular white matter T2/FLAIR\nhyperintensities are nonspecific, but likely represent the sequela of chronic\nmicrovascular ischemic disease.  The ventricles and sulci are normal in\ncaliber and configuration.  There is no abnormal enhancement after contrast\nadministration.",
            "output": "1. Left inferior cerebral peduncle subacute infarct.\n2. No abnormal enhancement after contrast administration.\n\nNOTIFICATION:  The findings were discussed with ___, M.D. by\n___, M.D. on the telephone on ___ at 4:18 ___, 5 minutes\nafter discovery of the findings."
        },
        {
            "input": "Examination is mildly degraded by motion.\n\nThere is a moderate-sized area of slow diffusion in the posterior left frontal\nlobe consistent with subacute infarction as demonstrated on the prior CT head\nwithout contrast.  There are multiple small areas of associated hemorrhage\nseen on the gradient echo images.\n\nAddition small scattered areas of slow diffusion in the right corona radiata,\nright frontal, left cerebellar hemisphere, left parietal, and left occipital\nlobes with corresponding hypointensity on the ADC map are also consistent with\nacute infarctions.\n\nNo additional areas of hemorrhage are identified.  Mild prominence of the\nventricles and sulci is suggestive of involutional changes. There is no mass\neffect or midline shift.\n\nMild leftward deviation of the nasal septum.  Small mucous retention cyst in\nthe left maxillary sinus laterally.  Mild right and trace left opacification\nof the mastoid air cells.  Unremarkable intraorbital contents.",
            "output": "1. Left posterior frontal lobe infarction with hemorrhagic component.\n2. Additional small scattered infarctions in the right corona radiata, right\nfrontal, left parietal, and left occipital lobes.\n3. Mild parenchymal volume loss."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  There is global moderate prominence of the ventricles and\nsulci suggesting involutional changes, progressed compared to the prior\nexamination.  There is progressive loss of mesial temporal lobe volume with\nincreased prominent of the parahippocampal fissures when compared to the ___ examination.  .  Scattered areas of nonspecific white matter\nT2/FLAIR hyperintensity are unchanged.  Prominent VR spaces are again noted. \nThere is no abnormal focus of slow diffusion.  The principal vascular flow\nvoids are preserved.  The orbits are unremarkable.  The visualized paranasal\nsinuses are grossly clear.",
            "output": "1. Progressive moderate generalized cerebral atrophy with progressive loss of\nmesial temporal lobe volume .\n2. No acute intracranial abnormality.\n3. Stable nonspecific areas of white matter T2/FLAIR hyperintensity with a\nbroad differential including chronic small vessel ischemic disease and\nmigraines."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.\n\nThere is 6 mm herniation of the posterior cervical tonsils, right greater than\nleft through the foramen magnum, minimally decreased from the prior\nexamination in ___.  No signal abnormality is detected at the\ncervicomedullary junction.\n\nThere is minimal mucosal thickening involving the left maxillary sinus.  There\nis diffuse calvarial low signal, which may be due to marrow hyperplasia, which\nis unchanged.",
            "output": "1. Normal brain MRI.  No abnormality detected along the optic tracts.  No\nevidence of metastatic disease.\n2. Low lying cerebellar tonsils, minimally improved from the prior\nexamination."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.",
            "output": "Normal brain MRI."
        },
        {
            "input": "There is no evidence of intracranial hemorrhage, edema, masses, mass effect,\nmidline shift or infarction.   The ventricles and sulci are normal in caliber\nand configuration.  There is no abnormal enhancement after contrast\nadministration.  Incidental note of a partially empty sella. The major\nintracranial vascular flow voids are preserved. Patent dural venous sinuses.\n\nThe orbits are unremarkable.  Mild mucosal thickening of the maxillary\nsinuses, left greater than right.  Otherwise, the paranasal sinuses are clear.\nThe mastoid air cells and middle ear cavities are well aerated.",
            "output": "1. There is no evidence of acute intracranial process or hemorrhage.\n2. There is no evidence of abnormal enhancement after contrast administration."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, mass, mass effect, or infarction.\nThe ventricles and sulci are normal in caliber and configuration.\nThere is a tiny single nonspecific focus of T2 hyperintensity seen in the\nsubcortical white matter in the left frontal vertex (series 11, image 20) of\nunknown clinical etiology and uncertain clinical significance.  There is no\nabnormal enhancement after contrast administration.\nA small enhancing focus posterior to the right side of the clivus series 100,\nimage 19, likely relates to slightly tortuous venous tributary, based on\nscrolling through the images.\n\nMajor vascular flow voids are preserved.  The orbits are unremarkable.  There\nis minimal mucosal thickening within the ethmoid air cells.  The remaining\nparanasal sinuses and mastoid air cells are clear.  Slightly hypointense\nmarrow signal diffusely can relate to cellular marrow; however, can also be\nseen with anemia, systemic disease, marrow disorder, etc and can be correlated\nwith hematology labs.",
            "output": "No evidence of acute infarction, hemorrhage, or enhancing mass lesion.\nA tiny single nonspecific focus of T2 hyperintensity seen in the subcortical\nwhite matter in the left frontal vertex without enhancement.  A followup study\ncan be considered to assess for interval change in a few months or as needed."
        },
        {
            "input": "No acute infarct or acute intracranial hemorrhage is identified. There is no\nmass, mass effect or midline shift.  The patient is status post right frontal\ncraniotomy with.  Multiple foci of susceptibility are present within the right\noccipital and posterior right temporal lobe compatible with chronic blood\nproducts, and there is a focus of encephalomalacia within the anterior right\ntemporal lobe. All There is diffuse cerebral atrophy with prominence of the\nextra-axial fluid spaces. A few scattered foci of FLAIR prolongation are\npresent within the periventricular white matter.\n\nThe right maxillary mucosal thickening is noted.",
            "output": "1. No acute infarct, acute intracranial hemorrhage or space-occupying lesion.\n2. Chronic blood products within the right occipital and temporal lobes may be\nthe sequela of remote trauma."
        },
        {
            "input": "There is leptomeningeal contrast enhancement and FLAIR hyperintensity along\nthe superior aspect of the cerebellum, more marked on the left side, along the\nanterior aspect of both cerebellar hemispheres and possibly subtle enhancement\nalong the the upper aspect of the ventral pons.  There is also leptomeningeal\nFLAIR hyperintensity along the medial aspects of both anterior frontal lobes,\ninferiorly (images 7: ___. Given the patient's history, this is concerning\nfor leptomeningeal metastases. However, infectious and inflammatory causes may\nhave a similar imaging appearance (e.g. sarcoidosis, Lyme disease).\n\nThere is no evidence of a circumscribed enhancing mass, acute infarction, or\nblood products.  Numerous T2/FLAIR hyperintensities within the supratentorial\nwhite matter, which are nonspecific but likely represent mild chronic small\nvessel ischemic disease in this age group.  Several small T2 hyperintense,\nnonenhancing foci in the bilateral cerebellar hemispheres are suggestive of\nchronic infarcts (images 8: ___.  Global parenchymal volume loss is again\nseen with prominent ventricles and sulci.  Major vascular flow voids are\ngrossly preserved.  Dural venous sinuses appear patent on postcontrast MP RAGE\nimages.\n\nSeveral low T1 signal lesions are noted within the imaged upper cervical\nspine, in keeping with the known osseous metastases.  These sclerotic on the\nrecent ___ CT.\n\nThere is mild mucosal thickening in the ethmoid air cells.  The paranasal\nsinuses and mastoid air cells are otherwise clear.  Normal appearance of the\norbits.",
            "output": "1. Leptomeningeal enhancement along the superior and anterior aspects of the\ncerebellum, and leptomeningeal FLAIR hyperintensity along the medial aspect of\nthe frontal lobes inferiorly.  Given the patient's history, this is concerning\nfor leptomeningeal metastases.  However, infectious and inflammatory causes\nmay have a similar imaging appearance (e.g.  sarcoidosis, Lyme disease).\n2. Multiple small chronic infarcts in the bilateral cerebellar hemispheres.\n3. Extensive supratentorial white matter T2/FLAIR hyperintensities are\nnonspecific but likely sequela of chronic small vessel ischemic disease in\nthis age group.\n4. Known metastases in the upper cervical spine are again partially imaged.\n\nNOTIFICATION:  Oncology progress note dated ___ indicates that\nintracranial leptomeningeal contrast enhancement is already known to the\ntreating team."
        },
        {
            "input": "Encephalomalacia, FLAIR signal hyperintensity, hemosiderin deposition, and\ncurvilinear enhancement in the right occipital lobe adjacent to the craniotomy\ndefect is consistent with postsurgical changes in this region.  No prior MR\nimaging is available comparison.  A millimetric focus of T2 hyperintense\nsignal in the right basal ganglia following the signal intensity of CSF all\nsequences likely represents a prominent perivascular space.  A 3 mm rounded\nfocus of susceptibility artifact in the left centrum semiovale on gradient\necho images is consistent with a chronic microhemorrhage.  A few scattered\npunctate periventricular and subcortical white matter FLAIR hyperintensities\nare nonspecific probably sequelae of chronic microangiopathy in a patient of\nthis age.\n\nThere is no evidence of acute intracranial hemorrhage or infarction.  The\nventricles and sulci are age-appropriate.  There is no new enhancing mass. \nPrincipal intracranial vascular flow voids are preserved and arteries and\narteries of the circle of ___ and dural venous sinuses enhance\nappropriately after contrast administration.  A partially empty sella is\nnoted.",
            "output": "1. Postsurgical changes in the right occipital lobe as described above.  No\nprior brain MRI is available for comparison.\n2. No new enhancing lesions are identified.\n3. There is no evidence of acute intracranial hemorrhage or infarction."
        },
        {
            "input": "MRI Brain:\n  There is no evidence of hemorrhage, edema, mass effect, midline shift or\ninfarction.  There is prominence of the ventricles and sulci suggestive\ninvolutional changes.  Periventricular and subcortical white matter T2 and\nFLAIR hyperintense foci are noted in the frontal and the parietal lobes,\nnonspecific in appearance.  Dural ossification and hyperostosis of the bone in\nthe frontal and parietal regions noted.\n\nThe marrow signal is hypointense on the sagittal T1 weighted sequence.\n\nA left lens cataract extraction is seen.\nDegenerative changes are seen in the upper cervical spine.\n\nMRA brain:  There is a 3 mm x 3 mm posterior posteriorly pointing outpouching\nat the right internal carotid artery termination adjacent to the origin of the\nright posterior communicating artery series 6, image 76.  Fetal PCA pattern\nnoted on the right side, with absent P1 segment and prominent posterior\ncommunicating artery.\nThe intracranial vertebral and internal carotid arteries and their major\nbranches appear normal without evidence of stenosis, occlusion.\nRight vertebral artery is dominant and the left is diminutive.\n\nMRA neck:  There is suboptimal visualization of the carotid and vertebral\nvasculature secondary to  delayed vascular timing with venous contamination. \nHowever, there is no evidence of internal carotid artery stenosis by NASCET\ncriteria.  Very limited evaluation the vertebral arteries due to venous\ncontamination.\nMultilevel, multifactorial degenerative changes are noted in the cervical\nspine, not adequately assessed as not targeted.",
            "output": "1. No acute infarct.  Nonspecific cerebral white matter changes\n2. A 3 mm posteriorly pointing outpouching of the right internal carotid\nartery at the termination, close to the origin of the right posterior\ncommunicating artery consistent with a small aneurysm.\nConsider neurosurgery/interventional neuroradiology consult and further workup\nwith CT angiogram for better assessment as needed.  Further management and\nfollowup as needed if no intervention is contemplated.\n\n3. Suboptimal MRA of the carotid and vertebral vasculature due to delayed\ntiming with venous contamination.  No significant internal carotid artery\nstenosis by NASCET criteria.  Correlate with carotid Doppler ultrasound for\nbetter assessment.\n\n4. Multilevel, multifactorial degenerative changes in the cervical spine\n\nRECOMMENDATION(S):\nConsider neurosurgery/interventional neuroradiology consult and further workup\nwith CT angiogram for better assessment as needed.  Further management and\nfollowup as needed if no intervention is contemplated.\n\nNOTIFICATION:  Findings and recommendations D/w D. R. Champagne by Dr. ___\n___ phone on ___ at 3.30pm"
        },
        {
            "input": "There are numerous scattered areas of infarction involving the bilateral\ncerebellar hemispheres, bilateral frontal, parietal, and occipital lobes, in\naddition to the left splenium of the corpus callosum in the bilateral basal\nganglia.  Many of these demonstrate correlating FLAIR signal abnormality,\nlikely representing late acute to early subacute infarcts.\n\nGradient echo imaging demonstrates multiple areas of intraparenchymal\nhemorrhage, including the left cerebellar hemisphere, right occipital lobe,\nand right frontoparietal lobes.  Overall these appears similar to the recent\nCT examination.  No definite new sites for intracranial hemorrhage are seen.\n\nThere is no significant mass, mass effect, edema, or midline shift.  The dural\nvenous sinuses remain patent.\n\nThe ventricles and sulci are diffusely prominent compatible global parenchymal\nvolume loss.  Periventricular and subcortical white matter FLAIR\nhyperintensities are noted, a nonspecific finding that most likely represents\nthe sequelae of chronic small vessel ischemic disease.\n\nMucosal thickening is seen throughout scattered ethmoid air cells bilaterally.\nThere is trace bilateral mastoid fluid.  The remainder of the paranasal\nsinuses are grossly clear.  Patient is status post right lens replacement. \nThe remainder of the visualized paranasal sinuses, middle ear cavities, and\nmastoid air cells are well aerated and clear.  The orbits are within normal\nlimits bilaterally.",
            "output": "1. Diffuse areas of punctate and small late acute to early subacute infarcts,\nas above.  Many of these correspond to a bilateral watershed pattern, whereas\nothers may be explained due to a central embolic source.\n2. Areas of intraparenchymal hemorrhage predominately seen within the right\nfrontoparietal lobes, but also involving the left cerebral hemisphere and\nright occipital lobe.  Overall no significant change from the most recent CT\nexamination.\n3. Background global parenchymal volume loss, evidence of chronic small vessel\nischemic disease, and additional findings as above."
        },
        {
            "input": "There is a normal 3 vessel aortic arch.  The vertebrobasilar system is\nright-sided dominant, a normal variant.  The bilateral vertebral arteries\nremain grossly patent throughout their course.\n\nThe bilateral common carotid arteries are patent.  There is mild irregular\nnarrowing of the carotid bulbs bilaterally, likely secondary to\natherosclerosis. On the left, there is no significant stenosis by NASCET\ncriteria.\n\nHowever, the right proximal internal carotid artery demonstrates approximately\n50% stenosis by NASCET criteria.  The more distal right cervical ICA\ndemonstrates areas of mild narrowing and mild luminal irregularity, but\nremains patent.",
            "output": "1. Multifocal atherosclerosis most predominantly affecting the proximal right\ninternal carotid artery, resulting in approximately 50% stenosis by NASCET\ncriteria.\n2. Otherwise grossly patent cervical vasculature.."
        },
        {
            "input": "1.5 cm enhancing lesion in the right cerebellar hemisphere (11:6) is unchanged\ncompared to ___.\n1-mm enhancing focus is identified in the posterior left temporal region\n(1000:87).  At 2 mm focus of enhancement is seen in the right posterior\nfrontal lobe medially (11:17).  These foci where not seen on prior exam,\npossibly due to its small size and difference in study techniques.\n\nThere is no evidence of hemorrhage, edema, midline shift or infarction. \nProminence of ventricles and sulci likely reflect involutional changes. \nPeriventricular white matter high FLAIR hyperintensities are consistent with\nsequela of chronic small vessel disease.\n1 cm nonenhancing nodule is noted in the scalp overlying the left parietal\nvertex.  Prosthetic left eye is noted.",
            "output": "1. 1-2mm enhancing foci in left temporal lobe and right frontal suspicious for\nmetastatic disease were not seen on prior exam from ___, possibly\ndue to  small size and difference in study techniques or are new since the\nprevious study.\n2. Known 1.5 cm right cerebellar lesion is unchanged.\n3. No acute infarct is identified."
        },
        {
            "input": "Right cerebellar hemisphere enhancing mass measures 15 x 13 x 10 mm (AP,\ntransverse, craniocaudad, images 10:45 and 1000:102, and previously 11 x 11 x\n8 mm when measured in the same fashion.  There is no significant associated\nedema.\n\nThere are multiple new small foci of nodular contrast enhancement in the\nsuperficial left temporal lobe (10:80, 10:92), left insula (10:88), right\ntemporal lobe (10:68, 10:71, 10:78), right insula (10:85), right greater than\nleft medial frontal and parietal lobes (10:103, 10:110-119, ___,\nindicating progression of metastatic disease which may be at least in part\nleptomeningeal.\n\nThere is no significant mass effect.  There is no evidence for new blood\nproducts.  Extensive supratentorial white matter T2/FLAIR hyperintensities are\nagain seen, nonspecific but likely sequela of chronic small vessel ischemic\ndisease in this age group.  Age-related global parenchymal volume loss is\nagain seen with prominent ventricles and sulci.  Major vascular flow voids\nappear grossly preserved.\n\nSmall left parietal scalp nodule is again seen at the vertex, image 7:22,\nlikely a sebaceous cyst.",
            "output": "1. Slight interval enlargement of the right cerebellar mass without\nsignificant edema.\n2. Multiple new foci of nodular contrast enhancement in the superficial\nbilateral temporal lobes, bilateral insula, and bilateral medial frontal and\nparietal lobes, indicating progression of metastatic disease which may be at\nleast in part leptomeningeal.  No significant mass effect."
        },
        {
            "input": "The study is moderately motion degraded, especially on postcontrast imaging. \nWithin these confines:\n\nPreviously noted large left parietal scalp lesion is no longer present,\npresumably excised, and there is no abnormal enhancement in this region.\n\nA round 7 mm enhancing T1 isointense, T2 hyperintense nodule in the right\ncerebellar hemisphere is new (14:6).\n\n Periventricular and subcortical T2 and FLAIR hyperintensities are noted,\nwhich may represent small vessel ischemic changes.\n\nThere is no definite evidence of hemorrhage, midline shift or acute\ninfarction.  Prominence of the ventricles and sulci is unchanged and\nconsistent with age related atrophy.  Mildly expansile partially empty sella\nis unchanged.  Enucleation of the left globe is chronic.",
            "output": "1.  Study is moderately degraded by motion.\n2. The study and particularly the post-contrast images are moderately motion\ndegraded, lowering the sensitivity of detecting small lesions.\n3. 7 mm enhancing mass in the right cerebellar hemisphere is new compared to\nthe prior examination and suspicious for malignancy.\n4.  Within limits of study, no  evidence of intracranial hemorrhage or acute\ninfarction.\n\nNOTIFICATION:  The impression and recommendation above was entered by Dr.\n___ on ___ at 22:59 into the Department of Radiology critical\ncommunications system for direct communication to the referring provider."
        },
        {
            "input": "Postcontrast MP RAGE images are degraded by motion artifact.  Other sequences\nare mildly limited by motion artifact.\n\nA subtle, 7 mm enhancing lesion in the right cerebellar hemisphere is stable\nin size on postcontrast axial T1 weighted images compared the prior\nexamination.  Mild surrounding edema has resolved.  (11:8, 13:8).\n\nThere is no evidence of new enhancing lesions, edema, or blood products. \nThere is no acute infarction.  There is moderate prominence of the ventricles\nand sulci suggestive of involutional changes.  Moderate periventricular and\nsubcortical white matter T2/FLAIR hyperintensity is unchanged, ___ suggestive\nof chronic small vessel ischemic disease.  The principal intracranial vascular\nflow voids are preserved.\n\nPatient is status post left-sided enucleation with a left globe prosthesis.  8\nmm subcutaneous nodule with mild rim enhancement in the vertex (___) is\nunchanged since ___ and likely represents an epidermal inclusion\ncyst.",
            "output": "1. Motion limited exam.\n2. Stable 7 mm enhancing lesion in the right cerebellar hemisphere with\nresolution of surrounding edema.\n3. No evidence for new enhancing mass."
        },
        {
            "input": "Subtle 7 x 4 mm enhancing lesion in the right cerebellar hemisphere is\nunchanged in size, though decreased in conspicuity as compared to the ___ examination, definitively decreased in size compared to the ___\nexamination where it measured approximately 8 x 7 mm (13:7).  There is minimal\nFLAIR signal abnormality in this area, and there is no significant surrounding\nvasogenic edema.\n\nThere is no evidence of hemorrhage, significant edema, new masses, significant\nmass effect, midline shift or infarction.  There is moderate prominence of the\nventricles and sulci suggestive of involutional change.  Scattered areas of\nperiventricular, subcortical and deep white matter T2/FLAIR hyperintensities\nare in a configuration most suggestive of chronic small vessel ischemic\ndisease.  There is no abnormal focus of slowed diffusion.  The principal\nintracranial vascular flow voids are preserved.\n\n The visualized paranasal sinuses are grossly clear.  There are changes from\nleft-sided enucleation with prosthetic globe in place.  The right orbit is\ngrossly unremarkable.  The mastoid air cells are clear.\n\n8 mm subcutaneous nodule in the left vertex is unchanged since ___,\nlikely representing an epidermal inclusion cyst (101a:97).",
            "output": "1. Continued decrease in conspicuity of a 7 x 4 mm subtly enhancing metastatic\nright cerebellar lesion, definitively decreased in size and enhancement as\ncompared to ___.\n2. No new enhancing mass."
        },
        {
            "input": "Again noted is a faint, ill-defined enhancing lesion with minimal T2/FLAIR\nhyperintensity in the right cerebellar hemisphere measuring approximately 8 mm\nx 4 mm (16:8), without change compared to ___.  There is no associated\nedema or evidence for blood products.  No new enhancing lesion is seen.\n\nAs before, there is moderate prominence of the ventricles and sulci suggestive\nof age-related involutional change.  Numerous periventricular, deep, and\nsubcortical white matter T2/FLAIR hyperintensities are grossly unchanged,\nnonspecific but likely sequela of chronic ischemic microvascular disease.  A\nsmall T2 hyperintensity in the left cerebellar hemisphere is unchanged, image\n13:8, consistent with a small chronic infarct. Major vascular flow voids are\npreserved.  The dural venous sinuses are patent.\n\nThere is mild mucosal thickening of the ethmoid air cells.  Left globe\nprosthesis is again noted.\n\nAn 10 mm subcutaneous nodule at the left vertex is unchanged, likely a\nsebaceous cyst.\n\nSagittal images again demonstrate mild anterolisthesis of C4 on C5 and mild\nloss of height of the C5 vertebral body, with heterogeneous marrow signal\nalong the endplates of the included upper cervical spine which is likely\nsecondary to discogenic bone marrow changes.",
            "output": "Stable ill-defined small enhancing lesion in the right cerebellar hemisphere\nwithout edema.  No evidence for new enhancing lesions."
        },
        {
            "input": "There is no evidence of acute infarction.  A punctate, chronic infarct is\nagain noted in the left cerebellar hemisphere.  No intracranial hemorrhage.\n\nRedemonstrated is an area of ill-defined, subtle enhancement within the mid\nright cerebellar hemisphere with associated mild T2/FLAIR hyperintensity. \nAlthough difficult to measure, the overall size morphology of this lesion\nappears unchanged from the prior examination.  There is no associated\nsurrounding edema.\n\nNo new areas of enhancement are identified.  The dural venous sinuses appear\npatent.\n\nThe ventricles and sulci are prominent, compatible with age related atrophic\nchanges.  Periventricular and subcortical white matter FLAIR hyperintensities\nare noted, a nonspecific finding that most likely represents the sequelae of\nchronic small vessel ischemic disease.   There is gross preservation of the\nprincipal intracranial vascular flow voids.\n\nA subcutaneous FLAIR hyperintense nodule at the left parietal vertex is\nunchanged, likely representing a sebaceous cyst.  The remainder of the\nvisualized paranasal sinuses, middle ear cavities, and mastoid air cells are\nwell aerated and clear.  Postoperative changes involving the left orbit are\nagain noted.",
            "output": "1. No evidence for acute intracranial hemorrhage or infarction.\n2. Essentially unchanged appearance of an ill-defined faintly enhancing and T2\nhyperintense lesion in the right cerebellar hemisphere without associated\nedema.  This has not significantly changed since ___ and was not seen\non the earlier examination of ___.  The nature of enhancement and relative\nstability suggests possible subacute infarct as the cause of enhancement. \nAlthough metastatic disease is not completely excluded, it appears much less\nlikely given the appearance.\n3. Otherwise, no additional areas of abnormal enhancement.  No mass effect or\nedema.\n4. Chronic findings of global parenchymal volume loss and the sequelae of\nsmall vessel ischemic disease."
        },
        {
            "input": "The examination is moderately motion degraded, particularly affecting the\npostcontrast MP RAGE sequences.  Within this confine:\n\nThere is a small punctate focus of elevated signal on DWI with equivocal\nfindings on ADC seen at the left parietal lobe vertex (___), with mild\nincreased associated FLAIR hyperintensity (13:19).  No associated enhancement\nor susceptibility artifact.  Findings may represent a small subacute\ninfarction.\n\nAllowing for this, there is no other evidence of infarction.  There is no\nevidence of hemorrhage.\n\nAn ill-defined area of FLAIR hyperintensity with associated enhancement within\nthe right cerebellar hemisphere measures 1.5 x 1.0 cm (11:7, 13:6), unchanged\nfrom prior examination in ___.  No appreciable surrounding vasogenic\nedema is identified.\n\nOtherwise, there is no evidence of additional sites of abnormal intracranial\nenhancement.  No mass effect or midline shift.\n\nBackground global parenchymal volume loss is moderate.  Periventricular and\nsubcortical white matter FLAIR hyperintensities are noted, a nonspecific\nfinding that most likely represents the sequelae of chronic small vessel\nischemic disease. There is gross preservation of the principal intracranial\nvascular flow voids.\n\nThe visualized paranasal sinuses, middle ear cavities, and mastoid air cells\nare well aerated and clear.  The patient is status post left globe resection\nwith prosthetic placement.  A probable sebaceous cyst overlies the left\nvertex, unchanged from the previous examination.",
            "output": "1. Moderately motion grade examination, particularly affecting the MP RAGE\npost-contrast sequences.\n2. Small punctate focus of elevated DWI signal with associated FLAIR\nhyperintensity and equivocal ADC findings seen within the left parietal lobe\nvertex.  Findings may represent a small subacute infarction.\n3. No other evidence of infarction and no evidence of hemorrhage.\n4. Stable appearance of a 1.5 x 1.0 cm enhancing T2 FLAIR hyperintense right\ncerebellar hemispheric lesion, unchanged from ___.  No additional\nareas of abnormal enhancement are identified intracranially.\n5. Moderate global parenchymal volume loss and evidence of chronic small\nvessel ischemic disease."
        },
        {
            "input": "MRI Brain:  There are areas of confluent T2/FLAIR hyperintensity in the\nsubcortical white matter extending to the cortex in the bilateral parietal\nlobes as well as the left occipital lobe with associated volume loss\ncompatible with chronic infarcts. There is a punctate area in the right\nfrontal lobe which demonstrate slow diffusion (402:27), without definite ADC\ncorrelate, but too small to characterize and may represent a subacute infarct.\nA old right cerebellar infarct is also noted. Scattered punctate T2/FLAIR\nhyperintensities in the subcortical white matter are nonspecific, but likely\nreflect sequelae of chronic small vessel ischemic disease of the mild degree.\n\nMRA brain: The intracranial vertebral and internal carotid arteries and their\nmajor branches appear normal without evidence of stenosis, occlusion, or\naneurysm formation.\n\nMRA neck:  The common, internal and external carotid and vertebral arteries\nappear normal.  The V4 segment of the right vertebral artery is hypoplastic,\nlikely a normal variant. The left vertebral artery is tortuous and dominant\nand slightly indents the pons near the origin of the trigeminal nerve. There\nis no evidence of internal carotid artery stenosis by NASCET criteria.  The\norigins of the great vessels, subclavian and vertebral arteries appear normal\nbilaterally.",
            "output": "1. Patent vasculature in the head and neck.\n\n2.  Chronic infarcts with associated volume loss in the bilateral parietal\nlobes as well as the left occipital lobe.\n\n3.  Punctate focus of slow diffusion in the right frontal lobe, too small to\nfully characterize but likely represents a subacute infarct."
        },
        {
            "input": "MRI BRAIN:\nMultiple chronic infarcts are again demonstrated right frontal lobe, left\noccipital lobe, and bilateral parietal lobes, as seen previously.  Small\nchronic infarcts are also seen in the right cerebellar hemisphere.  There are\nscattered nonspecific T2/FLAIR hyperintensities in the subcortical and\nperiventricular white matter likely reflecting chronic small vessel disease in\nthis age group.  There are again foci of susceptibility in superficial\ndistribution suggesting amyloid angiopathy, unchanged from the previous exam. \nThere is no evidence of recent hemorrhage, and there is no acute or subacute\ninfarction.\n\nProminence of the ventricles and sulci reflecting volume loss again noted.  No\nextra-axial collection, mass effect, masses, shift of the midline structures,\nor basal cistern effacement.\n\nThe major vascular flow voids are preserved.  Orbits and extracranial soft\ntissues are unremarkable.  There is mild scattered mucosal thickening in the\nparanasal sinuses as well as a left maxillary sinus mucous retention cyst.\n\nMRA BRAIN:\nDominant and tortuous left vertebral artery.  The intracranial left vertebral\nartery as well as the visible distal V4 segment of the right vertebral artery\nare patent.  The basilar artery is patent.  Posterior cerebral arteries are\npatent.  The intracranial segments of the internal carotid arteries are\npatent.  The proximal anterior middle cerebral arteries are patent although\nsomewhat suboptimally assessed due to mild motion artifact.  No aneurysm is\ndemonstrated.  The intracranial vertebral and internal carotid arteries and\ntheir major branches appear normal without evidence of stenosis,occlusion,or\naneurysm formation.\n\nMRA NECK:\nThe origins of the vertebral and carotid arteries are not included on this\ntime-of-flight technique examination.  The proximal right vertebral artery is\nnot seen well although the vessel is diminutive.  Otherwise, the included\nportions of the right vertebral artery are patent without high-grade stenosis\ndemonstrated.  The dominant left vertebral artery is patent in its included\nsegments, with a linear defect again seen in the distal V2 segment, now\nextending into the V3 segment.  The bilateral included portions of the common\ncarotid arteries, as well as the internal and external carotid arteries appear\nnormal.  There is no evidence of internal carotid artery stenosis by NASCET\ncriteria.",
            "output": "1. No acute intracranial abnormality.\n2. Multiple chronic infarcts appear similar to the previous examination.\n3. Similar pattern of punctate foci of susceptibility likely reflecting\namyloid angiopathy.\n4. Nonspecific white matter signal changes which most likely reflect chronic\nsmall vessel disease in this age group.\n5. Generalized atrophy again demonstrated.\n6. The origins of the vertebral arteries are not included on this examination.\nTherefore, the segment of severe stenosis at the origin of the right vertebral\nartery is not assessed.  Furthermore, the distal right vertebral artery is not\nseen well, which could be due to diminutive caliber of the vessel versus\natherosclerotic disease.\n7. The imaged segments of the dominant left vertebral artery are patent, but\nthere is again a linear defect in the distal left V2 segment which now appears\nto extend into the proximal V3 segment.  The apparent change could be\ntechnical or potentially reflect increasing extent of an underlying previous\nchronic dissection.\n8. Otherwise, patent circle of ___ without evidence of\nstenosis,occlusion,or aneurysm.\n9. Patent bilateral cervical carotid arteries without evidence of stenosis,\nocclusion, or dissection.\n10. Given the very small caliber of the diminutive right vertebral artery and\nmotion on the current MRA of the head, the vasculature may be better assessed\nby CT angiography than MR angiography.\n\nNOTIFICATION:  The impression and recommendation above was entered by Dr. ___\n___ on ___ at 14:46 into the Department of Radiology critical\ncommunications system for direct communication to the referring provider."
        },
        {
            "input": "Artifact related to the patient's TB mask projects over the rectal gyri on\ndiffusion-weighted images and more broadly over the inferior frontal lobes,\nleft greater than right, on gradient echo images.  On postcontrast MP RAGE\nimages, this artifact projects over the medulla lower cerebellum, as well as\nthe included upper cervical spine.  Postcontrast MP RAGE images are also\nmoderately limited by motion artifact, and other sequences are mildly limited\nby motion artifact.\n\nThere is no evidence for abnormal diffusion, edema, mass effect, or abnormal\ncontrast enhancement in the brain parenchyma.  No evidence for blood products\nis seen on limited evaluation.  Ventricles, sulci, and basal cisterns are\nnormal in size.\n\nThis exam is not technically optimized for evaluation of the internal auditory\ncanals.  Motion limited postcontrast MP RAGE images suggest asymmetric linear\nenhancement along the margins of the right internal auditory canal.  Given the\nmarginal distribution, it is not clear whether this corresponds to the course\nof the seventh and eighth cranial nerves.   There is a vascular loop in the\nleft cerebellopontine angle cistern extending into the left porus acusticus. \nElsewhere in the intracranial compartment, no leptomeningeal abnormality is\nidentified on FLAIR or postcontrast T1 weighted images.  No abnormal\npachymeningeal contrast enhancement is seen.\n\nThis exam is not technically optimized for evaluation of the sella.  The\npituitary infundibulum is midline without evidence for thickening.  The right\npituitary lobe measures 4 mm in height and the left pituitary lobe measures 5\nmm in height, but both lobes are normal in size with normal morphology,\nincluding concave upper margins; the height asymmetry is likely related to\nanatomic variation.\n\nMajor arterial flow voids are grossly preserved.  Major dural venous sinuses\nare patent on postcontrast MP RAGE images.",
            "output": "1. Technically limited exam, as detailed above.\n2. This exam is not technically optimized for evaluation of the internal\nauditory canals.  Asymmetric linear enhancement is suggested along the margins\nof the right internal auditory canal.  Given the marginal distribution, it is\nnot clear whether this corresponds to the course of the seventh and eighth\ncranial nerves.\n3. Otherwise, no evidence for pachymeningeal, leptomeningeal, or parenchymal\nsignal abnormalities to suggest either neurosarcoidosis or TB involvement.\n\nRECOMMENDATION(S):  If clinically warranted, dedicated MRI of the internal\nauditory canals could be obtained for further evaluation."
        },
        {
            "input": "There are a few scattered periventricular and subcortical white matter\n(frontal and parietal lobes) FLAIR signal hyperintense foci.  There is no\nacute infarct, hemorrhage, mass, or mass effect.  The ventricles and\nextra-axial spaces are unremarkable ; mildly prominent bifrontal extra-axial\nCSF spaces, can be variant or related to mild volume loss.\nThe major intracranial arterial flow voids are noted.\nThe cavernous carotid segments are slightly tortuous in course.\nThe orbits, calvarium, and soft tissues are unremarkable.\nThe paranasal sinuses and mastoid air cells are clear.",
            "output": "1. Nonspecific scattered bilateral periventricular and subcortical white\nmatter FLAIR signal hyperintense foci, nonspecific in appearance, often of \nuncertain clinical significance, and may be seen in the setting of history of\nmigraines, microangiopathic changes, prior trauma, prior inflammatory sequela,\nless likely demyelinating etiology based on the appearance, etc.  Recommend\nclinical correlation for risk factors.  Further workup/followup as needed.\n2. Other details as above."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  Mild mucosal thickening paranasal sinuses.  Preserved vascular\nflow voids.  Enlarged bilateral palatine tonsils, also seen on CT cervical\nspine ___, likely reactive.  No extra-axial or parenchymal\nhemorrhage or microhemorrhage.",
            "output": "1. Normal intracranial contents.\n2. Mild mucosal thickening paranasal sinuses.\n3. Enlarged bilateral palatine tonsils, partially seen,, statistically likely\nreactive."
        },
        {
            "input": "There are multiple central bilateral enhancing masses predominantly involving\nthe basal ganglia that show slow diffusion and some contain hemorrhagic\nproducts.  The mass in the right basal ganglia measures 19 x 18 x 19 mm,\npreviously 26 x 32 x 31 mm (1000:96, 1001:77).  A conglomerate of masses are\npresent in the left basal ganglia anteriorly, that appear slightly different\nshape compared to the prior examination, but collectively measure 21 x 30 x 27\nmm, previously 26 x 29 x 27 mm (1000:91, 1001:76).  A similar mass in the tail\nof the left caudate adjacent to the atrium of the left lateral ventricle is\nalso decreased in size.  Previously seen extensive white matter high T2/FLAIR\nsignal surrounding the lesions and mass effect on the third ventricle have\nsubstantially improved.  A curvilinear focus of subependymal enhancement along\nthe anterior horn of the right lateral ventricle (series 1000, image 104\nthrough 106) likely represents a vascular structure, however close attention\non followup is recommended.  Otherwise, there is no new enhancing mass. \nIntracranial vascular flow voids are preserved.  Arteries of the circle ___\nand ___ venous sinuses enhance appropriately and postcontrast sequences. \nThe orbits are unremarkable.  The orbits are unremarkable.",
            "output": "1. Multiple central bilateral enhancing masses predominantly in the basal\nganglia demonstrating slow diffusion and petechial hemorrhages have decreased\nin size compared to the prior examination.  Subjacent areas of increased\nT2/FLAIR signal and mass effect on the third ventricle have also substantially\nimproved.\n2.  Curvilinear focus of subependymal enhancement along the anterior horn of\nthe right lateral ventricle (series 1000, image 104 through 106) likely\nrepresents a vascular structure, however close attention on followup is\nrecommended.\n3. No evidence of acute intracranial hemorrhage or infarction."
        },
        {
            "input": "There are postsurgical changes from right frontal burr hole.  Again identified\nare several heterogeneously enhancing supratentorial lesions, with slowed\ndiffusion and areas of susceptibility artifact suggestive of hemorrhage. \nThere has been extensive increase in surrounding vasogenic edema of all the\nmasses.  There has been significant increase of associated mass effect, with\nincreasing effacement of the lateral ventricles.  Increased mass effect\nproduces focal obliteration of the third ventricle, and there is interval\nincrease in size of the lateral ventricles.\n\nLesions centered in the right basal ganglia measures 40 x 30 mm, previously 19\nx 18 mm (900:100).\n\nMultilobulated enhancing mass centered in the left basal ganglia measures 51 x\n34 mm, previously 30 x 20 mm (900:94).\n\nLobulated left periatrial lesion measures 27 x 15 mm, previously 17 x 8 mm\n(900:101).\n\nNo new enhancing lesion is identified.\n\nThe principal intracranial vascular flow voids are preserved.\n\nThere is mild mucosal thickening in the right maxillary sinus and bilateral\nethmoid air cells.  The remainder of the paranasal sinuses are clear.  The\norbits are grossly unremarkable.",
            "output": "1. Substantial increase in size of previously noted enhancing masses with\nareas of hemorrhage and slowed diffusion centered in the bilateral basal\nganglia and left periatrial white matter with increase, extensive surrounding\nvasogenic edema, and resultant increased mass effect.\n2. Increased mass effect focally obliterates the third ventricle, and mild\nventriculomegaly has increased compared to the prior examination, suggesting a\ncomponent of obstructive hydrocephalus.\n3. No new enhancing mass."
        },
        {
            "input": "Decrease size of bilateral basal ganglia and left periventricular enhancing\nlesions, demonstrating gradient echo susceptibility artifact compatible with\nhemorrhage product.  The right basal ganglia enhancing lesion measures 0.9 x\n0.8 cm, the left sided lobulated enhancing lesion measures approximately 1.5 x\n0.9 cm, previously measuring 3.8 x 3.4 and or 4.6 x 2.8 cm respectively. \nThere is only trace 5 mm enhancement (series 900, image 90) in the region of\nthe left ventricular antrum, which previously measured approximately 2.3 x 1.2\ncm.  There is dramatically decreased associated white matter FLAIR edema\npattern and resolution of third ventricular effacement and ventriculomegaly.\n\nNo new enhancing lesions are identified.  No new hemorrhage.  No acute\ninfarct.  The major intracranial flow voids are preserved.  The dural venous\nsinuses are patent on postcontrast MP-RAGE.  There is mild mucosal thickening\nof the ethmoid air cells as well as a mucous retention cyst in the right\nmaxillary sinus.  The orbits are unremarkable.  Fluid signal is noted in the\nbilateral mastoid air cells.",
            "output": "1. Dramatic decrease size of bilateral basal ganglia and left periventricular\nhemorrhagic enhancing lesions with residual enhancement as described above. \nInterval resolution of third ventricular effacement and associated\nhydrocephalus.\n2. No new enhancing lesions."
        },
        {
            "input": "Overall, there has been decrease in the extent of enhancement and size of the\nbilateral basal ganglia and left periventricular enhancing lesions,\ndemonstrating low signal on the gradient echo susceptibility images compatible\nwith hemorrhagic products.  The right basal ganglia lesion centered within the\ncaudate head measures approximately 1.1 cm x 1 cm, improved in size compared\nto the prior exam at which time this measured up to 1.4 cm x 1.2 cm.  The\nextent of enhancement of this lesion has also improved compared to the prior\nexam.  The left-sided lobulated enhancing lesion measures approximately 1.5 cm\nby 1.5 cm, improved compared to the prior exam at which time this measured up\nto 2.1 cm.  The previously seen confluent enhancement of this lesion, now\ndemonstrates multifocal areas of punctate and nodular enhancement, series 900,\nimage 98.  Punctate residual enhancement is seen within the left ventricular\natrium, now measuring up to 3-4 mm.  The extent of surrounding white matter\nedema, is unchanged compared to the prior exam.  There is no evidence of mass\neffect or ventriculomegaly.  Periventricular and deep subcortical FLAIR white\nmatter hyperintensities are nonspecific however could be secondary to\nmicroangiopathy.  Mild prominence of ventricles and sulci is likely related to\nage related involutional changes.\n\nMild mucosal sinus thickening is seen involving the ethmoid air cells.  The\nremainder the visualized paranasal sinuses are clear.  Mild fluid\nopacification is seen involving the mastoid air cells bilaterally.  The globes\nare unremarkable.  The principal vascular flow voids appear to be well\npreserved.",
            "output": "1. Interval improvement in the size and extent of enhancement of the bilateral\nbasal ganglia and left periventricular hemorrhagic enhancing lesions with\nresidual enhancement as described above.  No new enhancing lesion seen.\n2. No evidence acute intracranial hemorrhage or infarction."
        },
        {
            "input": "When compared to prior, there has been continued interval decrease in degree\nof enhancement within the lesions centered at the bilateral basal ganglia. \nWhen comparing the pre contrast to the post-contrast axial T1 weighted images\nthere is no appreciable enhancement although there is somewhat nodular\nhyperintensity on the postcontrast MP RAGE inferiorly (1000:91) on the left\nsuggesting possible residual enhancement although decreased.  Susceptibility\nartifact seen in the region of the prior larger enhancing lesions centered at\nthe basal ganglia, periventricular white matter on the left and right cerebral\npeduncle.   No new enhancing lesion is seen.\n\nThere is no acute infarct, hemorrhage, mass effect, or edema.  The ventricles\nand sulci are unchanged in size and configuration.  Periventricular and\nsubcortical white matter hypodensities are nonspecific, but likely reflect\nsequelae of chronic small vessel ischemic disease.  The major intracranial\nflow voids are preserved.  The dural venous sinuses are patent.\n\nThe globes are grossly unremarkable.  There is mucosal thickening with\nair-fluid level in the right maxillary sinus and the left sphenoid sinus. \nThere is mucosal thickening in the remaining paranasal sinuses.  Mild partial\nopacification of the bilateral mastoid air cells is unchanged.  Right frontal\nburr hole is also noted.",
            "output": "Continued decrease in the size and enhancement of bilateral basal ganglia\nlesions.  Sequela of prior treated lesions including susceptibility artifact\nalso noted in the periventricular white matter on the left and within the\nright cerebral peduncle compatible with treatment response.  No new enhancing\nlesions identified."
        },
        {
            "input": "As compared to the previous examination, there has been no significant\ninterval change in the overall appearance of heterogeneous and mildly\nenhancing lesions centered within the bilateral basal ganglia (800: 89, 90),\nand within the posterior limb of the left internal capsule adjacent to the\nposterior horn of the left lateral ventricle (800:100).\n\nPersistent susceptibility artifact on gradient echo imaging is again noted\ninvolving the bilateral basal ganglia, the left periventricular white matter,\nand the right cerebral peduncle.  These findings are also unchanged from the\nprior examination, and likely represent treated disease.  No new, enhancing\nlesions are visualized.\n\nThere is no evidence of acute infarction or acute intracranial hemorrhage.  No\nmass, mass effect, edema or midline shift.  Remains minimal diffusion-weighted\nhyperintense signal along the lateral edge of the left lateral ventricle,\nunchanged from prior exam and likely corresponding to hemorrhage product.\n\nThe ventricles and sulci are unchanged in size and configuration.  Nonspecific\nperiventricular and subcortical white matter T2/FLAIR hyperintensities are\nlikely secondary to chronic microangiopathy.  The basal cisterns are patent. \nThere is no evidence of impending, downward herniation.  The dural venous\nsinuses appear patent on MP-RAGE imagine sequences.\n\nThere is mild mucosal thickening of the paranasal sinuses and mastoid air\ncells.  The orbits are unremarkable.",
            "output": "1. No new, enhancing intracranial lesions.\n2. Unchanged interval appearance of heterogeneous and mildly enhancing lesions\nwithin the bilateral lateral basal ganglia and left posterior internal\ncapsule.\n3. Stable appearance of susceptibility artifact within the bilateral basal\nganglia, left periventricular white matter, and right cerebral peduncle. \nThese findings are compatible with previously treated sites of disease."
        },
        {
            "input": "Study is mildly degraded by motion.  Again is noted minimal interval decrease\nin the small enhancing lesions centered within the bilateral basal ganglia and\nposterior limb of the left internal capsule, adjacent to the posterior horn of\nthe left lateral ventricle.  No new enhancing lesions are identified.\n\nRedemonstrated is blooming artifact on gradient echo imaging in the bilateral\nbasal ganglia, white matter adjacent to the left lateral ventricle trigone is\nwell as within the right cerebral peduncle.\n\nNo evidence of new hemorrhage, midline shift or infarction.  There are mild\nnonspecific confluent predominantly periventricular T2/FLAIR white matter\nhyperintensities.  The major intracranial vascular flow voids are maintained. \nProminence of the ventricular system and cerebral sulci are compatible with\nage related involutional changes.  There is a small retention cyst within the\nright maxillary sinus.  Bilateral, maxillary sinus, right sphenoid sinus, and\nethmoid air cell mucosal thickening is present.  The orbits and mastoid air\ncells are normal.",
            "output": "1.  Study is mildly degraded by motion.\n2. Interval decrease in enhancing lesion centered within the bilateral basal\nganglia and posterior limb of the left internal capsule.\n3.  Within limits of study, no new enhancing lesions are present.\n4. Grossly stable bilateral basal ganglia, left lateral ventricle periatrial\nand right cerebral peduncle probable regions of treated disease, as described.\n5. Paranasal sinus disease , as described."
        },
        {
            "input": "There are multiple enhancing masses which demonstrate hyperattenuation on\nprior CT and T2 hypointensity and slow diffusion, as follows:\nThere is a 2.6 cm AP x 2.8 cm TV x 2.9 cm SI homogeneously enhancing mass with\ncentral nonenhancement and long evolving the right caudate, globus pallidus\nand putamen with significant adjacent FLAIR hyperintense vasogenic edema\n(900:95).\n\nThere is a 3.0 cm AP x 2.6 cm TV s 2.6 cm SI (900:18; 901:67), homogeneously\nenhancing mass left caudate head, globus pallidus and putamen  with a small\nareas central nonenhancement which extends inferiorly to the hypothalamus and\nthe posterior orbitofrontal gyrus.  There is significant adjacent FLAIR\nhyperintense vasogenic edema.\n\nThere is a 6 mm enhancing nodule at the left mamillary body (900:82).\n\nThere is a 1.3 cm AP x 0.4 cm TV x 0.4 cm SI enhancing mass at the right\ncerebral peduncle (900:83).\n\nThere is a 1.6 cm AP x 3.2 cm TV x 2.4 cm SI enhancing mass at the left\nperiatrial white matter which extends to the ependymal surface with more\npunctate irregular enhancement at its anterior medial margin and punctate foci\nof gradient echo hypointensity, consistent blood products(900:89).\n\nThere is mass effect secondary to the aforementioned masses then the\nsignificant adjacent vasogenic edema causing effacement of the third\nventricle.  There is mild unchanged prominence of the ventricles without\ntransependymal fluid signal.  The cortical sulci are preserved.  The\nextra-axial spaces are unremarkable.  The vascular flow voids are preserved. \nThere is no acute infarct.\n\nThe orbits, calvarium, and soft tissues are unremarkable.  There is no fluid\nsignal within the paranasal sinuses, mastoid air cells, or middle ears.",
            "output": "Multiple central enhancing masses with significant adjacent vasogenic edema\ncausing effacement of the third ventricle and mild dilatation of the\nventricles, which may represent a degree of hydrocephalus.  The masses\ndemonstrate attenuation and signal characteristics of hypercellular lesions\nand given their location within the deep structures extending the ependymal\nsurface, multifocal CNS lymphoma is highly suspected, however there there are\nsmall areas of central necrosis and petechial hemorrhage in some of the\nlesions, which would be atypical lymphoma unless the patient is\nimmunocompromised.  Differential considerations include primitive\nneuroectodermal tumor, sarcoidosis or tuberculosis, multifocal glioblastoma\nmultiforme and metastatic disease."
        },
        {
            "input": "Patient is s/p sub acceptable craniectomy and infratentorial hematoma\nevacuation.  Blood products adjacent to/within the lateral right cerebellar\nhemisphere are no larger than the recent noncontrast head CT.  Right\ncerebellar hemisphere vasogenic edema is unchanged.  Mild effacement of the\nfourth ventricle and quadrigeminal plate cistern is unchanged.  Bilateral\nparietal lobe intraparenchymal hemorrhages are unchanged.  Both parietal lobe\nhemorrhages demonstrate peripheral susceptibility artifact compatible with\nhemosiderin deposition.  The left parietal lobe hemorrhage is more\nintrinsically T1 hyperintense in the right parietal lobe hemorrhage.  No\nevidence of new intracranial hemorrhage.  Trace parasagittal right parietal\nlobe subarachnoid hemorrhage is unchanged (series 502, image 23).\n\nNo evidence of new infarction.  Susceptibility artifact corresponds to\npneumocephalus and subcutaneous emphysema seen on same-day CT. Periventricular\nand subcortical white matter T2/FLAIR hyperintensities are nonspecific but\nlikely sequelae of chronic small vessel ischemic disease.  Of note, these\nwhite matter lesions do not demonstrate enhancement.\n\nThe major intracranial flow voids are preserved. Incidental note is made of a\nfetal type right posterior cerebral artery.  The dural venous sinuses are\npatent, noting a prominent arachnoid granulation in the left transverse sinus.\nPatient is status-post endoscopic sinus surgery with polypoid mucosal\nthickening of the nasal septum and left maxillary sinus.",
            "output": "1. Unchanged postoperative appearance of the right cerebellar hemisphere with\nmild effacement of the fourth ventricle and quadrigeminal plate cistern. \nBilateral parietal lobe parenchymal hemorrhages and trace right parietal lobe\nsubarachnoid hemorrhage are unchanged..  No evidence of new hemorrhage. The\nmost likely etiologies are either amyloid angiopathy or  cavernous\nmalformations.\n2. Patient is status-post endoscopic sinus surgery with polypoid mucosal\nthickening of the nasal septum and left maxillary sinus."
        },
        {
            "input": "There is a 8 mm pineal cyst with minimal mass effect on the underlying tectum.\nNo hydrocephalus.  Otherwise, there is no evidence of intracranial metastatic\ndisease at this time.  There is no acute infarct or intracranial hemorrhage. \nNo suspicious parenchymal FLAIR signal abnormality.  A small right cerebellar\ndevelopmental venous anomaly incidentally noted.  The sulci, ventricles and\ncisterns are within expected limits for the patient's age.\n\nThe major intracranial flow voids are preserved.  The dural venous sinuses are\npatent.  There is mild mucosal thickening of the paranasal sinuses.  The\norbits are unremarkable.  No significant fluid signal seen in the mastoid air\ncells.  No suspicious marrow signal.",
            "output": "1. No acute intracranial abnormality on contrast enhanced MRI brain. \nSpecifically, no acute infarct or intracranial hemorrhage.  No suspicious\nparenchymal FLAIR signal abnormality or enhancement.\n2. No evidence for intracranial metastatic disease at this time.\n3. A 8 mm pineal cyst is identified with minimal mass effect on the underlying\ntectum.  No evidence for hydrocephalus.\n4. Additional findings as described above."
        },
        {
            "input": "Please note the study is mildly degraded by motion.\n\nThere is no evidence of acute infarction, edema, mass effect, or blood\nproducts.  Small focus of T2 hyperintensity in the medial right cerebellar\nhemisphere and the lateral margin of the right cerebellar vermis, images 9:5\nand 12:5, is most consistent with a small chronic infarction.  There are small\nfoci of high T2 signal in the subcortical, deep, and periventricular white\nmatter of the cerebral hemispheres, and in the pons , nonspecific but likely\nsequela of chronic small vessel ischemic disease in this age group.  The major\nvascular flow voids are preserved.\n\nThe ventricles and sulci are age-appropriate.\n\nThere is 5.5 mm outpouching extending from the anterior sellar floor into the\nsphenoid sinus, image 8:12, which appears to covered by bone on the preceding\nCT.  It contains CSF signal intensity on T2 weighted images, image 9:8.  It\nappears to contain intermediate signal intensity on T1 weighted images, image\n8:12, but this could represent volume averaging of the contents with the\nwalls.  Appearances are most suggestive of a meningocele.  An ectopic\npituitary adenomyoma could also be considered.\n\nThere is mild partial opacification of right lateral mastoid air cells.  The\norbits and visualized soft tissues are normal.  Mucosal thickening is seen in\nthe ethmoid sinus.",
            "output": "1. No acute infarct or evidence for other acute intracranial abnormalities.\n2. Small focus of T2 hyperintensity in the medial right cerebellar hemisphere\nin the lateral margin of the right cerebellar vermis is most consistent with a\nsmall chronic infarction.  Foci of T2 hyperintensity in the supratentorial\nwhite matter and pons are nonspecific but likely sequela of chronic small\nvessel ischemic disease in this age group.\n3. 5.5 mm outpouching extending from the anterior sellar flow into the\nsphenoid sinus, with apparent bony covering on the preceding CT, most likely a\nmeningocele, although an ectopic pituitary adenoma may also be considered.\n\nRECOMMENDATION(S):  Recommend dedicated pituitary MRI with and without\ncontrast for further evaluation.  Recommend including sagittal T2 weighted\nimages through the sella, in addition to the routine pituitary MRI sequences."
        },
        {
            "input": "After contrast administration there is a focus of abnormal enhancement in the\nanterior aspect of the corpus callosum on the right, measuring approximately 4\nx 5 mm in transverse dimension (image 15, series 13, and image 64, series\n100), this lesion is partially visible on T2 and FLAIR images (for exam image\n15 series 11).  There is no evidence of mass effect or shifting of the\nnormally structures.  There is a equivocal area of abnormal enhancement noted\nin the left cerebellum, (image 100 series 32), which is not visible in other\nsequences and probably represent a pulsation artifact after contrast\nadministration, attention in follow-up exams in this area is advised. There is\nno evidence of intracranial hemorrhage, the ventricles and sulci are slightly\nprominent, likely age related and involutional in nature.  No diffusion\nabnormalities are detected to indicate acute or subacute ischemic changes.  No\nbone lesions are identified throughout the calvarium.  The orbits are\nunremarkable, the major vascular flow voids are present and demonstrate normal\ndistribution.  The paranasal sinuses and the mastoid air cells are clear.\n\nPartial evaluation of the upper cervical spine demonstrates possible abnormal\nepidural enhancement at the level of C3-C4 level anteriorly and posteriorly,\ncausing anterior thecal sac deformity apparently contacting the ventral aspect\nof the spinal cord (image 105, series 14), probably consistent with disc\ndegenerative changes, however given the clinical history, correlation with\ndedicated MRI of the cervical spine with and without contrast is recommended\nfor further characterization.",
            "output": "1.  Focus of abnormal enhancement in the anterior aspect of the corpus\ncallosum on the right, measuring approximately 4 x 5 mm in transverse\ndimension (image 15, series 13, and image 64, series 100, given the clinical\nhistory this lesion is highly suspicious for metastatic disease.\n\n2.  Questionable focus of enhancement in the left cerebellar hemisphere which\nis not visible in other sequences, probably represent a flow related artifact\nafter contrast administration, close attention in follow-up exams in this area\nis advised (image 32, series 100).\n\n2.  Limited evaluation of the cervical spine demonstrates possible abnormal\nepidural enhancement versus prominent disc bulge at the level of C3-C4 (image\n105, series 14), correlation with dedicated MRI of the cervical spine with and\nwithout contrast is recommended for further characterization.\n\nNOTIFICATION:  The findings were discussed with ___, M.D. by ___\n___, M.D. on the telephone on ___ at 3:41 pm, 5 minutes after discovery\nof the findings.\n\nRECOMMENDATION(S):  Partial evaluation of the cervical spine demonstrates\npossible abnormal epidural enhancement at the level of C3-C4 level (image 105,\nseries 14), apparently causing anterior and posterior thecal sac deformity,\ncorrelation with dedicated MRI of the cervical spine with and without contrast\nis recommended for further characterization."
        },
        {
            "input": "Please note the study is mildly degraded by motion.  Within these confines:\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.  The major vascular flow voids are preserved.  The dural\nvenous sinuses are patent.\n\nMild opacification of the mastoid air cells is seen.  There is mucosal\nthickening and air-fluid level in the right maxillary sinus.  Mucosal\nthickening is also seen in the sphenoid sinus the orbits are normal.  The\nvisualized soft tissues are normal.  A partially visualized orogastric tube is\nnoted.  Minimal fluid is noted in the posterior nasopharynx, likely secondary\nto the orogastric tube.",
            "output": "1. No evidence for intracranial metastatic disease or other acute intracranial\nabnormality.\n2. Paranasal sinus disease."
        },
        {
            "input": "There is moderate prominence of ventricles with mild-to-moderate prominence of\nsulci.  The temporal horns are also prominent.  There is no periventricular\nedema.  Early changes of small vessel disease are seen.  There is no midline\nshift.  No acute infarcts are identified.  There is no definite asymmetry seen\nor asymmetric fluid collection identified medial to the cerebellar hemispheres\nas suspected on previous cervical spine MRI.  The appearance is likely due to\npartial volume averaging.  The vascular flow voids are maintained.  The\nvisualize paranasal sinuses are clear.  L",
            "output": "1. Moderate ventriculomegaly with mild prominence of sulci suggesting\nventricular enlargement to be out of proportion for sulcal size which can be\nseen in predominantly central brain atrophy or normal pressure hydrocephalus\nin proper clinical setting.\n2. No acute infarcts mass effect seen.\n3. The abnormality suspected on cervical spine MRI is not confirmed and was\nlikely due to partial volume averaging of the adjacent CSF spaces."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  Diffuse subcortical and periventricular white matter\nhyperintensity is a nonspecific finding.  The ventricles and sulci are\nabnormally prominent reflecting involutional changes and suggesting cortical\nvolume loss.  No diffusion abnormalities are detected.  There is no abnormal\nenhancement after contrast administration, though post-contrast MP rage\nsequences are markedly limited by motion artifact.",
            "output": "Diffuse subcortical white matter hyperintensity is a nonspecific finding\npossibly reflecting chronic microangiopathy or, in this patient with\ncirrhosis, chronic changes of alcohol toxicity.  No abnormal cortical signal\nabnormality, cortical edema, or abnormal enhancement."
        },
        {
            "input": "MR BRAIN:\nRedemonstrated is a large area T2/FLAIR hyperintensity centered within the\nright frontoparietal temporal lobes, with associated cortical thickening and\nsignal abnormality.  The T2/FLAIR signal extends to the posterior right\nlateral ventricle.  Additionally, a second area of T2/FLAIR hyperintensity is\nnoted involving the posterior and lateral aspects of the right thalamus, with\ninvolvement of the posterosuperior right cerebral peduncle.\n\nThere is associated right-sided mass effect with effacement of the adjacent\nsulci and partial effacement of the right lateral ventricle, unchanged. \nSimilarly, there is a 5 mm of leftward midline shift, also unchanged from\nprevious examination.\n\nThere is no associated enhancing mass or leptomeningeal enhancement.  The\ndural venous sinuses remain patent.\n\nThere is no evidence for acute intracranial hemorrhage or territorial\ninfarction. The background ventricles and sulci are mildly prominent\ncompatible with mild global parenchymal volume loss.  The major intracranial\nvascular flow voids appear preserved.\n\nThe visualized paranasal sinuses and mastoid air cells are clear bilaterally. \nThe globes are unremarkable.\n\n\nMR CONTRAST PERFUSION:\nQualitative color maps fail to demonstrate any convincingly focal increased\narea of cerebral perfusion.\n\n\nASL PERFUSION:\nThere is increased perfusion seen along the posterior and superior aspects of\nthe right insula with extension into the adjacent frontotemporal operculum\n(most notably, 04:14).\n\nA less conspicuous area of mild, equivocally increased perfusion is seen\nwithin the right thalamus correlating with FLAIR signal abnormality in the\nregion (04:12).\n\n\nMR SPECTROSCOPY:\nSingle and multi voxel MRI spectroscopy centered over the large right\nfrontotemporal operculum lesion demonstrate increased choline, increased\ncreatinine, and decreased NAA.  On single voxel spectroscopy, the\ncreatinine/NAA ratio is greater than 1.0",
            "output": "1. Areas of FLAIR signal abnormality, cortical thickening, vasogenic edema and\nlocal mass effect most prominently involving the right frontal\nparieto-temporal lobes and adjacent structures, with a second dominant focus\ncentered in the right superior posterior thalamus.  No associated enhancement.\n2. These areas demonstrate associated edema, mass effect, resulting in\nleftward midline shift measuring 5 mm and partial effacement of the right\nlateral ventricle.\n3. ASL demonstrates a large area of increased perfusion centered at the right\nfrontotemporal operculum, with an equivocal secondary area of increased\nperfusion within the right thalamus.\n4. MR spectroscopy reveals associated increased creatinine, increased choline,\nand decreased NAA in the region of the right frontotemporal operculum lesion.\n5. Taken together, these findings are most compatible with a low-grade\nneoplasm such is glioma.  Given the involvement of the multiple right sided\nlobes, this may represent gliomatosis cerebri.\n6. No acute intracranial infarction or hemorrhage.\n7. Additional findings as above."
        },
        {
            "input": "The patient's previously noted extensive infiltrative right hemispheric mass\ninvolving cortex, subcortical and deep white matter.  Involvement of nearly\nentire right parietal lobe, with extension into posterior temporal lobe, right\nthalamus, posterior right insula.  Areas of increased signal on diffusion\nimages without corresponding decreased ADC values.  Findings suggestive of\nglioma.  Few subtle patchy areas of enhancement are seen.  Stable 5 mm right\nto left midline shift.  Stable uncal herniation.  Patent pre pontine cistern,\nforamen magnum.\nDural venous sinuses are patent.",
            "output": "1. Stable right hemispheric mass, with areas of subtle enhancement, likely\nglioma.  Stable midline shift, uncal herniation."
        },
        {
            "input": "Postcontrast MP RAGE images are limited by motion artifact.  When available,\nsome of the other sequences were repeated with motion reducing techniques.\n\nAgain seen is a large infiltrative T2/FLAIR hyperintense mass involving the\nright parietal and temporal lobes, the right posterior frontal lobe, and the\nright thalamus.  3 mm round enhancing focus along the superior margin of the\nmass in the right posterior frontal lobe, images 10:134 and 12:20, was not\nseen on prior MRIs from ___ or ___. There is mild\nleptomeningeal hyperemia along other aspects of the mass without clear\nevidence for contrast enhancement, slightly less pronounced than on the prior\nMRIs.\n\nThe posterior components of the right lateral ventricle and the third\nventricle are partially effaced.  The ventricles are overall stable in size\nand configuration compared to prior studies.  Mild leftward shift of midline\nstructures is unchanged.  There is minimal right uncal herniation without\ncomplete effacement of the perimesencephalic cistern or compression of the\nmidbrain, unchanged.\n\nThere is no evidence for acute infarction or unexplained blood products. \nSmall T2/FLAIR hyperintense focus in the left superior frontal subcortical\nwhite matter on image 11:19 is unchanged and nonspecific, though possibly\nsecondary to chronic small vessel ischemic change given patient's age.  Major\nvascular flow voids are grossly preserved.  Dural venous sinuses appear patent\non postcontrast MP RAGE images.\n\nRight parietal craniotomy is again seen.",
            "output": "1. Large infiltrative T2/FLAIR hyperintense mass is again seen involving the\nright parietal and temporal lobes, the right posterior temporal lobe, and the\nright thalamus, unchanged in extent.\n2. 3 mm round enhancing focus along the superior margin of the mass in the\nright posterior frontal lobe is new.\n3. No change in mass effect.\n4. No acute infarction and no evidence for other acute abnormalities."
        },
        {
            "input": "T2 and FLAIR signal abnormality centered in the right parietal lobe is again\nseen.  The overall extent of the signal abnormality which is seen to also\ninvolve the posterior temporal lobe a small region of the frontal lobe is\nunchanged.  Signal abnormality within the right thalamus and right cerebral\npeduncle is unchanged.  Of note, the degree of cortical thickening centered in\nthe right parietal lobe (currently series 9, image 16, previously series 9,\nimage 19 on exam from ___ has decreased.  Also, the subtle effacement\nof the right lateral ventricle particularly at the atrium has decreased.\n\nThere is is a new 4 mm enhancing nodule in the posterior temporal lobe in the\nregion of the lesion (11:15).  There is some artifact in the region of\npreviously seen enhancing nodule (11:19) which is likely present. \nPostcontrast MPRAGE sequences are significantly motion degraded.\n\nNo new parenchymal signal abnormality.  No acute infarct.  Right parietal burr\nhole is again noted.  Major intravascular flow voids are preserved.",
            "output": "1. Similar degree and extent of signal abnormality centered in the right\nparietal lobe and right thalamus as seen previously compatible with\ninfiltrative mass.  Of note the degree of cortical thickening in the right\nparietal lobe has decreased since ___.\n2. New 4 mm enhancing nodule in the region of signal abnormality in the right\ntemporal lobe.  Artifact near the vertex degrades detailed evaluation in the\nregion of previously seen enhancing nodule which is likely still present."
        },
        {
            "input": "Postsurgical changes after right parietal biopsy are again noted with mild\nthickening and enhancement of the meninges subjacent to the access site and a\nsmall amount of blood products.\n\nAgain seen is the diffusely infiltrating mass centered in the right parietal\nlobe with FLAIR hyperintensity extending anteriorly into the right frontal\nlobe, medially into the thalamus and cerebral peduncle, unchanged from ___ and\n___.  There is no definite abnormal enhancement.  Previously identified\n3 mm enhancing nodule in the high right parietal lobe in ___ as well as a\npunctate focus of enhancement in the right temporal lobe in ___ are no\nlonger visualized, although this may be secondary to motion artifact.\n\nThere is no acute intracranial hemorrhage, midline shift or acute territorial\ninfarction.\nSize and configuration of the ventricles is age-appropriate.  Major vascular\nflow voids are preserved.  Major dural venous sinuses are patent.\n\nThe paranasal sinuses and mastoid air cells are essentially clear.  The orbits\nappear unremarkable.",
            "output": "1. Stable nonenhancing and diffusely infiltrating mass centered in the right\nparietal lobe with unchanged surrounding FLAIR hyperintensity.\n2. Previously identified areas of enhancement are not appreciated on today's\nexam, although this may be secondary to motion artifact.\n3. No new intracranial abnormality identified."
        },
        {
            "input": "Study is moderately degraded by motion.  Within these confines:\n\nPostsurgical changes are seen following right parietal biopsy with mild\nthickening and enhancement of the subjacent meninges.  There is\nredemonstration of a diffusely infiltrating mass in the right parietal lobe\nwith associated FLAIR hyperintensity which extends into the right frontal lobe\nanteriorly and medially into the right thalamus and cerebral peduncle,\nunchanged since multiple prior studies dating back to ___.\n\nA 3 mm focus of enhancement in the right parietal lobe is similar to prior\nexam in ___ (9:209).  No new abnormal enhancement is identified.  There\nis no large infarct.  No evidence of midline shift.\n\nThe ventricles and sulci are grossly stable in caliber and configuration.  The\nmajor intracranial flow voids are preserved.\n\nNo mucosal thickening is seen in both ethmoid air cells.  Otherwise, the\nremaining visualized paranasal sinuses, mastoid air cells, and middle ear\ncavities appear clear.  The orbits are unremarkable.",
            "output": "1.  Study is moderately degraded by motion.\n2. Postsurgical changes from right parietal biopsy with unchanged mild\nthickening and enhancement of right adjacent meninges.\n3. Diffusely infiltrating right parietal mass is grossly stable in extent and\nappearance since ___.\n4. A 3 mm focus of enhancement in the right parietal lobe remains unchanged\nsince ___.\n5.  Within limits of study, no definite areas of new abnormal enhancement."
        },
        {
            "input": "There has been little change since ___ or ___.  Again seen\nis a right posterior temporal and parietal region of extensive white matter\ninfiltration with far less prominent cortical involvement.  The deep extension\nof this involves the right thalamus.  There has been a gradual decrease in the\nvolume of the right thalamus over several prior studies.  The cortical and\nwhite matter involvement appears overall similar.  There are no findings to\nsuggest tumor progression.\nThere is no evidence of hemorrhage, edema, or infarction.  There is no\nabnormal enhancement after contrast administration.",
            "output": "1. Right posterior temporal and parietal tumor with involvement of the right\nthalamus.\n2. No evidence of progression since the 2 most recent studies.  Over the\nlonger term, there has been a decrease in the volume of the white matter and\ncortical involvement as well as in the volume of the right thalamus."
        },
        {
            "input": "Study is moderately degraded by motion.  Within these confines:\n\nPostsurgical changes related to patient's right parietal mass biopsy are again\nseen.\n\nRight posterior temporal and parietal extensive white matter infiltration with\ngrossly stable cortical and right thalamic involvement is again seen.\n\nThere is no evidence of hemorrhage, midline shift or infarction.   The\nventricles and sulci are grossly stable in caliber and configuration.\n\nThere is no definite new enhancement after contrast administration.",
            "output": "1.  Study is moderately degraded by motion.\n2. Grossly stable right posterior temporal, parietal and right thalamic tumor\ncompared to ___ prior exam."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  No evidence of diffuse anoxic injury.  There are no areas of\nrestricted diffusion.  The ventricles and sulci are normal in caliber and\nconfiguration.  There is a small amount of fluid, mucosal thickening in the\nparanasal sinuses, likely secondary to intubation.  Preserved vascular flow\nvoids.  Trace opacification mastoids.",
            "output": "No acute findings, no infarct."
        },
        {
            "input": "Study is degraded by motion.  Within these confines:\n\nImages through the internal auditory canal demonstrates symmetric appearance\nof the seventh eighth nerve complexes.  There is no evidence of abnormal\nenhancement or mass lesion within the internal auditory canals,\ncerebellopontine angles or membranous labyrinth. No other mass lesions are\nseen within the posterior fossa.\n\nThe visualized portion of the bilateral maxillary and frontal sinuses, and\nbilateral ethmoid air cells demonstrate mucosal thickening.",
            "output": "1. Study is degraded by motion.\n2. Within limits of study, no evidence of IAC or cerebellopontine angle mass.\n3. Paranasal sinus disease , as described."
        },
        {
            "input": "There is slow diffusion within the right postcentral gyrus and right insula\nwith associated FLAIR hyperintensity, without associated hemorrhage in this\narea.  There is susceptibility artifact within the left medial frontal lobe\nwithout hyperdensity on prior CT, likely representing chronic blood products.\n\nThere is prominence of the ventricles and sulci secondary to age-related\ninvolutional changes.  There are nonspecific periventricular and subcortical\nwhite matter FLAIR hyperintensities, likely sequela of chronic small vessel\nischemic disease.  Again seen is a calcified 1.1 cm right frontal convexity\nextra-axial mass with associated susceptibility artifact (11:21) likely\nrepresenting calcified meningioma as seen on prior CT.\n\nThe major visualized arterial vascular flow voids are preserved.  There is\nmild mucosal thickening of the bilateral ethmoid air cells.  The remaining\nparanasal sinuses appear clear.  Patient is status post bilateral cataract\nsurgery.  The bilateral mastoid air cells and the visualized soft tissues\nappear unremarkable.  Susceptibility artifact associated with the surgical\nhardware within the cervical spine and the occiput partially obscures\nvisualization of the adjacent structures.",
            "output": "1. Late acute to early subacute infarctions within the right postcentral gyrus\nand right insula, without associated hemorrhage.\n2. Chronic blood products within the medial left frontal lobe.\n3. Age-related involutional changes with nonspecific white matter signal\nabnormality, likely a sequela of chronic small vessel ischemic disease.\n4. Again seen is a 1.1 cm right frontal calcified meningioma.\n5. Mild paranasal sinus disease.\n\nNOTIFICATION:  The findings were discussed with ___, M.D. by ___\n___, M.D. on the telephone on ___ at 1:35 am, 2 minutes after discovery\nof the findings."
        },
        {
            "input": "There is no evidence of acute ischemia based on diffusion-weighted imaging. \nThere is no edema, mass effect or evidence for blood products. There are\nnormal vascular flow voids. There is a single subcentimeter focus of T2/FLAIR\nsignal hyperintensity within the right corona radiata which may represents a\nchronic infarct or sequela of prior inflammation/demyelination. There is a\nsuboccipital craniectomy.  There is a large area of encephalomalacia involving\nthe right cerebellar hemisphere which may be secondary to a chronic infarct or\nsurgical resection.\n\nThere is a small air-fluid level within the right maxillary sinus and\naerosolized secretions involving the left frontal sinus, as well as mucosal\nthickening in other paranasal sinuses, similar to 1 day earlier.",
            "output": "1. No acute ischemia.\n2. Prior suboccipital craniectomy with a large area of encephalomalacia within\nthe right cerebellar hemisphere, which may represent prior infarct or sequela\nof prior surgical resection.\n3. Single subcentemeter focus of high T2 signal in the right corona radiata\nmay represent a chronic infarct or sequela of prior\ninflammation/demyelination.\n4. Fluid within the right maxillary sinus and aerosolized secretions in the\nleft frontal sinus, which may represent acute sinusitis in an appropriate\nclinical setting. Please correlate with symptoms."
        },
        {
            "input": "Right frontal craniotomy is again seen. Thin linear dural enhancement along\nthe right anterior falx and right frontal pole is stable.  There is no\nevidence of a recurrent enhancing mass at the surgical site, nor is there are\na new enhancing mass elsewhere in the intracranial compartment.  Right medial\nfrontal surgical cavity is stable. Mild surrounding high T2 signal extending\nto the right lateral ventricle is also stable.\n\nThere is no evidence for edema, abnormal diffusion, or new blood products.\nMild confluent high T2 signal along the lateral ventricles could be\nage-related or related to chronic small vessel ischemic disease. The\nventricles are normal in size for age. Prominence of multiple frontal and\nparietal sulci at the vertex is unchanged, probably secondary to age-related\nparenchymal volume loss. Major arterial flow voids are grossly preserved.\nMajor dural venous sinuses are patent.\n\nThere is a small mucous retention cyst in the left sphenoid sinus, new\ncompared to ___. However, aeration of the left sphenoid sinus is\nmarkedly improved compared to ___, when it was almost completely\nopacified.",
            "output": "Stable post treatment changes in the right frontal lobe without evidence for\nlocal tumor recurrence.  No evidence for a new intracranial mass."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor acute infarction.\n\nThere are mild scattered foci of T2/FLAIR hyperintensities within the\nperiventricular and subcortical white matter which appear progressed since\nprior examination from ___.  None of these are present in the corpus\ncallosum.\n\nThere are new T2 hyperintense, FLAIR hypointense, nonenhancing foci in the\nleft caudate nucleus and left putamen, which given their location and\nmorphology are felt to correspond to prior old lacunar infarcts (series 8,\nimage 14 and 16 ; series 10, image 14 and 16).  The ventricles and sulci are\nnormal in caliber and configuration.  There is no abnormal enhancement after\ncontrast administration.",
            "output": "1. New T2 hyperintense/FLAIR hypointense foci in the left caudate nucleus and\nleft putamen   likely secondary to old lacunar infarcts.\n2. Scattered foci of T2/FLAIR hyperintensities within the periventricular and\nsubcortical white matter appear progressed since prior examination from ___. \nAlthough these findings are nonspecific, in the presence of the above\ndescribed lacunar infarcts, findings favor changes related to chronic small\nvessel ischemic disease.  However, given patient's age and if the lacunar\ninfarcts were not present, diagnostic considerations would include\ndemyelinating disease.  Evaluation for vascular risk factors in this patient\nis therefore recommended.\n\nRECOMMENDATION(S):  Recommend evaluation for vascular risk factors in this\npatient given the present findings."
        },
        {
            "input": "Postsurgical changes in the left parietal bone related to the craniotomy and\nexcision of an intraosseous meningioma appear stable. Persistent intraosseous\nthe calvarial and dural enhancement at the resection bed these appears\nunchanged since ___. However, the subjacent dural-based extra-axial\nenhan\nCing lesion has slightly increased in size, currently measuring 11 mm AP x 10\nmm transverse (9:124, 900:105), and previously measuring 10 x 8 mm on ___, and ___.\n\nThere is no new enhancing lesion, edema, mass effect, diffusion abnormality,\nblood products. Prominent perivascular spaces or cysts in the left posterior\nparietal lobe are again noted.\nScattered subcortical, deep, and periventricular white matter foci of FLAIR/T2\nhyperintensity are non-specific but unchanged and most likely sequela of the\nmild chronic small vessel ischemic disease.\n The ventricles and sulci are normal in size for age.  The major intracranial\nvascular flow voids are preserved.  Major dural venous sinuses are patent.\n\nThere is a mucous the retention cyst in the left maxillary sinus.",
            "output": "1. Stable calvarial and dural contrast enhancement at the site of prior\nresection. The small subjacent dural-based extra-axial enhancing lesion has\nslightly increased in size compared to prior exams, suggesting a small\nresidual meningioma.\n2. No evidence for new intracranial lesions."
        },
        {
            "input": "A multiple small acute infarcts are seen in the left frontal lobe (___). \nThere is no evidence of blood product or midline shift.  A chronic left wall\nsided white matter infarct is seen (13:19).  Otherwise no significant small\nvessel disease and brain atrophy seen.\n\nMRA of the head shows normal appearance of the arteries of the anterior\ncirculation as well as the basilar artery, posterior cerebral and right\nvertebral arteries.  The origin of the posterior division of left middle\ncerebral artery is not well seen but likely all is patent.  This could be\nbetter visualized on the CT angiography with reformats are The intracranial\nleft vertebral artery is not seen although it is visualized on the neck MRA.\n\nMRA of the neck shows irregular and diminished contrast visualization of the\nleft vertebral artery from its origin to the intracranial region.  A segment\nof left vertebral artery is not visualized in the mid cervical region. \nFat-suppressed images this demonstrate tiny area increased signal along the\nleft foramen (20:11) but the appearance on MRA and with irregularity of the\ncontour and segmental visualization of the vertebral artery, atherosclerotic\ndisease appears small likely patent dissection.  Mild atherosclerotic disease\nis also seen in the distal right vertebral artery.  .",
            "output": "1. Several small acute infarcts are seen in the left middle cerebral artery\ndistribution in the left frontal lobe.  No evidence of hemorrhage mass effect\nor hydrocephalus.\n2. MRA of the neck and fat-suppressed images diffuse atherosclerotic disease\ninvolving the left vertebral artery throughout its course.  Mild\natherosclerotic disease distal right vertebral artery.\n3. No evidence of vascular occlusion or high-grade stenosis in the anterior\ncirculation.  The origin of the the posterior division of the left middle\ncerebral artery is not well seen on the MRA but could be better evaluated on\nthe reformatted images of the CT angiography when available."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.\n There are scattered T2/FLAIR hyperintensities in the cerebral hemispheres\nbilaterally, a nonspecific finding and likely related to chronic small vessel\nischemic changes.\n\nThere is mild generalized parenchymal volume loss, unchanged from prior and\nmost likely age related.  Prominence of the ventricular system and extra-axial\nCSF spaces is similar to prior and most likely age related.  Again noted are\nthe prominent bilateral extra-axial CSF spaces along the right frontal and\nleft frontoparietal convexities, unchanged from prior.  There is questionable\nmild mass effect on the left frontal parietal gyri and sulci which could\nsuggest an underlying subdural hygroma.\nMajor vascular flow voids appear preserved.\n\nThere is severe mucosal thickening in the right maxillary sinus.  The\nremainder of the paranasal sinuses appears clear.  The mastoid air cells\nappear grossly clear.  The orbits appear unremarkable.",
            "output": "1. No evidence of infarction, hemorrhage or mass.\n2. Scattered nonspecific white matter changes in the cerebral hemispheres\nbilaterally, likely sequela of chronic microangiopathy.\n3. Unchanged prominence of the bilateral extra-axial CSF spaces, partially age\nrelated but possibly also within underlying subdural hygroma along the left\ncerebral convexity.\n4. Right maxillary sinus mucosal thickening."
        },
        {
            "input": "Study is mildly degraded by motion.\n\nNonenhancing periventricular and subcortical T2 and FLAIR hyperintensities are\nnoted.  No lesions demonstrate associated restricted diffusion or increase\nsusceptibility.\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.",
            "output": "1. Study is mildly degraded by motion.\n2. Nonspecific supratentorial nonenhancing white matter lesions as described. \nDifferential considerations include history of migraine headaches,\nmicroangiopathic changes, sequela of prior infection or trauma, or\ninflammatory or demyelinating process.\n3.  Within limits of study, no evidence of intracranial mass or acute infarct"
        },
        {
            "input": "Again seen are areas of restricted diffusion involving the left caudate body,\nleft putamen and scattered areas of cortical restricted diffusion within the\nleft frontal and parietal lobes with progression towards normalization on the\nADC map and associated FLAIR hyperintensity. No new regions of restricted\ndiffusion are identified.  There is no intracranial hemorrhage. No mass,\nsubstantial mass effect or shifting of the midline structures is present. The\nventricles, cerebral sulci and cisterns are age appropriate. Flow voids for\nthe major intracranial vessels are preserved.\n\nThe visualized orbits and soft tissues are unremarkable.  Sagittal T1 images\nshow high signal in venous structures which appears artifactual related to\ntechnique.",
            "output": "Expected evolution of left basal ganglia and left cortical infarcts. No new\ninfarct or intracranial hemorrhage is identified."
        },
        {
            "input": "Study is mildly degraded by motion.  Within these confines:\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There are scattered T2/FLAIR hyperintensity in the\nperiventricular and subcortical white matter.  When there are a small number\nof small lesions such as this, often there is no known clinical correlate. \nThere is no abnormal enhancement after contrast administration.  There is mild\nmucosal thickening of the ethmoid air cells, with several mucocele in the\nright maxillary sinus.",
            "output": "1. Normal study.  No evidence of mass, hemorrhage or infarction."
        },
        {
            "input": "The ventricles and extra-axial spaces are normal in size. There is no evidence\nof midline shift, mass effect or hydrocephalus. There are no acute infarcts.\nThere is no evidence of focal abnormalities.  The vascular flow voids are\nmaintained. The visualized paranasal sinuses are clear. Following gadolinium\nadministration there is no evidence of abnormal parenchymal, vascular and\nmeningeal enhancement seen.",
            "output": "No significant abnormalities are seen on MRI of the brain with and without\ngadolinium."
        },
        {
            "input": "There are findings in the right temporal lobe that appear typical of an occult\nvascular malformation. The area of high density on the CT scan is shown to\ncontain multiple foci of hyperintensity surrounded by hypointense rings. The\nlesion blooms on the gradient echo images. There is no abnormal enhancement\nafter contrast administration.\n\nThe gradient echo images demonstrate a tiny hypodensity in the medial left\ncerebellar hemisphere suggesting a second focus of chronic hemorrhage. This is\ntoo small to further characterize, but it may represent a second occult\nvascular malformation. There is no evidence of  edema, masses, mass effect, or\ninfarction. The ventricles and sulci are normal in caliber and configuration.",
            "output": "The right temporal lesion typical of a cold vascular malformation.\n\nSmall focus of hemorrhage in the medial left cerebellar hemisphere. This is\ntoo small to characterize, but may represent a second occult malformation."
        },
        {
            "input": "Stable 1.1 x 1.3 cm (10:11) nonenhancing, heterogeneously T1 bright,\nheterogeneously T2 dark lesion within the right temporal lobe without\nrestricted diffusion. This lesion demonstrate susceptibility on GRE imaging.\nAn additional 0.4 cm (13:7) lesion within the medial left cerebellar\nhemisphere demonstrating GRE susceptibility is most likely a second cavernous\nmalformation and is stable since the previous examination.\n\nThere is no evidence of edema, mass effect, or acute infarction. The\nventricles and sulci are normal in caliber and configuration. There is no\nabnormal enhancement after contrast administration.\n\nOn T2 weighted imaging vascular flow voids are preserved. The globes are\nunremarkable. Mild mucosal thickening of the right maxillary sinus is present.\nAdditional paranasal sinuses are clear.",
            "output": "1.  Stable 1.3 cm lesion within the right temporal lobe most consistent with a\ncavernous  malformation.\n2.  Stable second focus of hemorrhage in medial left cerebellar hemisphere is\ntoo small to definitively characterize however likely represents a second\ncavernous malformation."
        },
        {
            "input": "In comparison with the prior CT examinations, there is a new left intraparotid\nmass lesion, demonstrating a thick, and avidly enhancing capsule, with some\ninternal septations and high-signal intensity on T2 weighted sequence\nsuggesting a intraparotid  metastatic lesion, from local regional spread of\nsquamous cell carcinoma, with possible cystic and necrotic changes, this\nlesion measures approximately 25 x 24 mm in transverse dimension (series 10,\nimage 4) and approximately 28 x 20 mm in coronal projection, series 1101,\nimage 76, series 11, image 139).  This lesion apparently is involving the\nsuperficial lobe of the left parotid gland with no frank evidence of invasion\ntowards the deep lobe.\nNo other areas with abnormal enhancement are seen in the parotid regions.\n\nAgain postsurgical changes are visualized towards the scalp on the left\nfrontal region (series 9, image 23) with interval improvement in the skin\nthickening in the left frontal region, and no evidence of intracranial\ninvolvement, there is persistent soft tissue swelling and thickening towards\nthe parietal convexity (series 1100, image 82).  Focal area of hyperintensity\nin the right parietal bone is unchanged, probably consistent with a non\nexpansile hemangioma (series 11, image 132).\n\nIntracranially, the ventricles and sulci are normal in size and configuration.\nThere is no evidence of intracranial hemorrhage, mass, mass effect or shifting\nof the normally midline structures.  Few scattered foci of FLAIR high signal\nintensity distributed the subcortical white matter are nonspecific and may\nreflect changes due to small vessel disease.  The orbits are unremarkable, the\nparanasal sinuses are notable for mucosal thickening in the ethmoidal air\ncells and frontoethmoidal recesses, no air-fluid levels are seen, the middle\near cavities and mastoid air cells are clear.",
            "output": "1.  In comparison with the prior examination, there is a new left intraparotid\nmass lesion, measuring approximately 25 x 24 mm in transverse dimension,\ndemonstrating a thick capsule with avid enhancement, some internal septations,\nand possible necrotic/cystic changes as described detail above, suggestive of\nintraparotid  local regional spread from squamous cell carcinoma.\n\n2.  Interval improvement in the surgical changes towards the left frontal\nconvexity soft tissues with no evidence of intracranial involvement,\npersistent soft tissue swelling towards the parietal convexity as described\nabove.\n\n3.  Unchanged focal area of T2/FLAIR hyperintensity in the right parietal bone\nsuggestive of hemangioma.\n\n4.  No other areas of abnormal enhancement are seen.\n\n5.  There is no evidence of acute intracranial process or hemorrhage.\n\nNOTIFICATION:  The impression and recommendation above was entered by Dr.\n___ on ___ at 09:52 into the Department of Radiology critical\ncommunications system for direct communication to the referring provider."
        },
        {
            "input": "Thyroid, salivary glands:\nThere is a 3.3 x 2.4 cm (AP by TV) peripherally enhancing, centrally necrotic\nmass within the left parotid, primarily involving the superficial lobe, with\nsubdermal extension.  Findings most likely represent necrotic metastasis. \nFindings are new since ___.  Lack of surrounding edema and stranding\nargues against abscess.  Left stylomastoid foramen fat pad is intact, no\nabnormal cranial nerve 7 enhancement, normal foramina ovale.  Findings have\nsignificantly worsened since prior.  No extension into mandible.  Loss of fat\nplane between the mass and masseter, without bulky tumor extension into the\nmuscle.\n\nThere is additional, similar-appearing but smaller 1.9 x 1.9 cm peripherally\nenhancing, centrally necrotic mass in the parotid tail (4:24, 5:20), increased\nin size.\n\nAdditional solid 9 mm enhancing nodule posterior left aspect of the parotid\ngland, increased in size.\n\nThere is a probable lymph node in the right parotid tail measuring 0.8 cm,\nsimilar.  Right parotid is otherwise unremarkable. Submandibular glands are\nnormal. The thyroid is unremarkable.\n\nAero digestive tract:\nThere is no aerodigestive tract mass.\n\nNeck lymph nodes:\nThere is a cluster of subcentimeter left level 2A lymph nodes, more numerous\nand increased in size since ___, largest measures 0.7 cm; some\nthese may be pathologic.\nBilateral 2A lymph nodes are morphologically normal and similar compared\nprior.\nFew tiny subcentimeter right neck lymph nodes, probably normal.\nThere is no retropharyngeal adenopathy.\n\nExtra nodal tumor spread:\n___ left parotid masses likely have extra nodal extension.\n\nDeep neck muscles, masticator space:\nThere is no muscle invasion.\n\nBones, skull base:\nThere is no bone involvement.\nNo aggressive focal osseous lesions.\nThere are no findings suggestive of perineural tumor extension. Jugular\nforamen, carotid canal, pterygopalatine fossa, infraorbital foramen, other\nskull base foramina are not involved.\n\nVessels:\nThere is no vascular invasion.\nMajor neck vessels are patent bilaterally.\n\nBrachial Plexus:\nThere is no brachial plexus contact or invasion.\n\nOther findings:\nThere are no lung nodules.\nImaged base of the brain is unremarkable.",
            "output": "1. Left parotid gland masses, largest 3.3 cm, worsened, most likely\nmetastases.\n2. Indeterminate right parotid tail nodule, similar.\n3. Cluster of subcentimeter left level 2A lymph nodes, asymmetric and\nincreased in size and number since ___, some of these nodes may be\nmetastatic.\n4. No evidence of perineural spread."
        },
        {
            "input": "There is a 25 x 20 x 21 mm avidly enhancing mass within the anterior nasal\ncavity centered within the olfactory recesses, with extent to the level of\ncribriform plate, without definite intracranial extension or dural\nenhancement..\n\nThere is an enhancing mass within the body of C2 that measures 18 x 22 x 18\nmm, with mild invasion of the anterior epidural space and C2 intervertebral\ndisc.\n\nThere is a 10 mm enhancing lesion within the right frontal calvarium (series\n9, image 151) and multiple other smaller areas of calvarial intramedullary\nenhancement throughout the calvarium.  Additionally there is a 6 mm enhancing\nlesion within the greater wing of the right sphenoid near the orbital apex\n(series 900 image 65).\n\nEcho of caudal subtle focus of enhancement along the undersurface of right\ncerebellar hemisphere, may be an artifact or represent leptomeningeal disease.\nPunctate focus of enhancement within the medial nuclei of the right thalamus\n(series 900, image 81) is indeterminate.\n\nThere is mild parenchymal volume loss.  No acute infarct, intracranial\nhemorrhage, or mass effect.  Small areas of hyperintense signal on T2/FLAIR\nwithin the subcortical and periventricular white matter nonspecific, but may\nreflect the sequela of mild chronic small vessel disease.  Incidental note is\nmade of choroid plexuses xanthogranulomatous and a partially empty sella.  The\nmajor arterial flow voids are preserved at and dural venous sinuses are\npatent.",
            "output": "1. Bone metastases.  Involvement of C2 vertebral body with mild invasion into\nthe anterior epidural space, no significant central canal narrowing.\n2. 25 x 20 x 21 mm avidly enhancing mass within the anterior bilateral nasal\ncavity, with extension to the cribriform plate is worrisome for neoplasm. \nFindings may represent sinonasal polyposis, also consider primary sinonasal\nmalignancy.  Metastasis is less likely.  ENT consult recommended\n3. Equivocal leptomeningeal enhancement along the undersurface of right\ncerebellar folia.\n4. Indeterminate punctate focus of enhancement in the right thalamus, may\nrepresent a vessel, subacute infarct or early metastasis, though atypical\nwithout adjacent edema..\n\nRECOMMENDATION(S):  ENT consult"
        },
        {
            "input": "Again seen are multiple bilateral parenchymal hematomas in the temporal and\nfrontal lobes as well as edema surrounding the hematomas.  There is a large\nextra-axial fluid collection, new since the study of ___.  This\ndemonstrates markedly slow diffusion and is hyperintense on the T1 weighted\nimages.  The collection is only mildly hypo intense on the gradient echo\nimages.  Although this may represent an infected collection, the\nhyperintensity on the T1 weighted images suggests hemorrhage.  There is no\nevidence of new parenchymal hemorrhage and no evidence of infarction.\nAgain seen is a large craniectomy defect.  .",
            "output": "1. Limited study due to motion artifact and the patient's inability to\ncomplete the examination.\n2. New large extra-axial fluid collection that appears to be most likely\nhemorrhage.  The possibility of infection cannot be excluded, but the signal\nintensity characteristics appear more typical of a hematoma"
        },
        {
            "input": "Study is  degraded by motion, especially and MPRAGE imaging.  Again is noted\nevolving postoperative changes related to the patient's left hemicraniectomy. \nIntrinsically T1 hyperintense collections are noted and the right middle\ncranial fossa, and left temporal lobe extending into the left middle cranial\nfossa.  There is an additional area of an intrinsic T1 hyperintensity within\nthe medial orbital gyrus.  No definite abnormal enhancement seen on\npostcontrast imaging.",
            "output": "1. Study is degraded by motion.\n2. Evolving postoperative changes related to left hemicraniectomy.\n3. Redemonstration of known large left hemispheric extra-axial fluid\ncollection with no definite abnormal enhancement, again suggestive of\nhematoma.\n4. Within limits of study, no definite abscess identified.\n5. Grossly stable multiple bilateral parenchymal hematomas and temporal and\nfrontal lobes."
        },
        {
            "input": "Study is mildly degraded by motion.  There are T2/FLAIR hyperintense foci in\nthe periventricular and subcortical white matter (07:15, 16) without\nassociated enhancement, definite mass effect or diffusion abnormality.  There\nis no evidence of hemorrhage, edema, masses, mass effect, midline shift or\ninfarction.  There is mild prominence of the ventricles and sulci suggestive\ninvolutional changes.  There is no abnormal enhancement after contrast\nadministration.  Right anterior middle cranial fossa nonenhancing T2\nhyperintense approximately 3.7 x 1.2 cm mass with no associated restricted\ndiffusion or increase susceptibility is noted, likely representing arachnoid\ncyst probable arachnoid cyst is noted (see 8:8).\n\nThere is a mucous retention cyst in the left maxillary sinus.  There is mild\nmucosal thickening in the bilateral ethmoid air cells.  Bilateral mastoid\nfluid is noted.  ___ termination of the left vertebral artery is noted, which\nis a normal variant.  Otherwise,  intracranial flow voids are preserved.",
            "output": "1. Study is mildly degraded by motion.\n2. No evidence of acute infarct or enhancing intracranial mass.\n3. Paranasal sinus disease and nonspecific bilateral mastoid fluid, as\ndescribed.\n4. Probable microangiopathic changes as described, without definite evidence\nof encephalitis or abscess.\n5. Right anterior middle cranial fossa arachnoid cyst."
        },
        {
            "input": "There is mild right greater than left hemispheric pachymeningeal thickening\nand enhancement (7:15, 9:15), without adjacent parenchymal signal abnormality.\nThere is mild asymmetric prominence of the right anterior temporal extra-axial\nCSF space, unchanged, which may represent an arachnoid cyst.\n\nThere is no evidence of hemorrhage, edema, parenchymal masses, mass effect,\nmidline shift or infarction.  There is mild prominence of the ventricles and\nsulci suggestive of involutional change.  Few scattered areas of\nperiventricular and subcortical white matter T2/FLAIR hyperintensities are in\na configuration most suggestive of chronic small vessel ischemic disease. \nThere is no abnormal focus of slowed diffusion.  The principal intracranial\nvascular flow voids are preserved.  The dural venous sinuses are patent on\nMP-RAGE images.\n\nThere are small mucous retention cysts in the left maxillary sinus and trace\nmucosal wall thickening of the bilateral anterior ethmoid air cells.  The\nremainder of the visualized paranasal sinuses are otherwise clear.  There is\nmild left-greater-than-right partial opacification of the mastoid air cells. \nThe orbits are grossly unremarkable.",
            "output": "1. Nonspecific right greater than left hemispheric pachymeningeal thickening\nand enhancement, suggestive of a nonspecific meningitis.  No adjacent\ncerebritis or abscess formation.\n2. No hemorrhage or infarct.\n3. Probable right anterior temporal arachnoid cyst.\n\nNOTIFICATION:  The updated findings were discussed with ___,\nM.D. by ___, M.D. on the telephone on ___ at 9:04 am, 10\nminutes after discovery of the findings."
        },
        {
            "input": "Previously demonstrated right and left hemispheric pachymeningeal enhancement\nhas resolved.\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  A few scattered nonspecific T2/FLAIR hyperintense lesions are\nnoted in the periventricular and subcortical white matter, which may be\nrelated to small vessel ischemic change.  Prominence of the ventricles and\nsulci is nonspecific but suggestive of cortical volume loss, more than would\nbe expected for a patient of this age.  There is no abnormal enhancement after\ncontrast administration.\n\nStable right anterior temporal arachnoid cyst.\n\nMucosal retention cyst is noted in the left maxillary sinus.  Mild mucosal\nthickening in the anterior ethmoid air cells bilaterally.  The remainder of\nthe paranasal sinuses are clear.  Stable opacification within the mastoid air\ncells bilaterally.",
            "output": "1. Previously demonstrated pachymeningeal enhancement has resolved.\n2. Stable right anterior temporal arachnoid cyst."
        },
        {
            "input": "Small acute infarcts are identified in the distribution of posterior limb of\nleft internal capsule.  The infarcts are seen on diffusion images as well as\non FLAIR images.  No other acute infarcts are identified in the supra or\ninfratentorial region.  No evidence of acute or chronic blood products seen. \nThere is no mass effect midline shift or hydrocephalus.",
            "output": "Acute/subacute infarcts in the distribution of the posterior limb of left\ninternal capsule."
        },
        {
            "input": "Study is moderately degraded by motion.  Within these confines:\n\nMRI BRAIN:\nThere are multiple areas of slow diffusion with low ADC values in the left\ncorona radiata consistent with acute to subacute infarct (series 6, image 22).\nIn the left parieto-occipital area in the posterior MCA distribution, there is\nredemonstration of chronic infarct with an additional area of adjacent acute\nsubacute infarct in the posterior temporal lobe (series 6, image 20).\n\nThere is a small amount of blood products within the left parietal/posterior\ntemporal infarct, grossly similar in configuration and agree compared to MRI\nfrom ___, (see 16: ___ on current study and 7: ___ on ___ prior outside brain MRI).  Precontrast T1 images in the area of this\ninfarct suggest minimal linear peripheral T1 hyperintensity (see 12: ___.  No\ndefinite corresponding T2 hypointensity or hyperintensity is seen.\n\nAn area of low GRE signal along the falx (series 16, image 21) is unchanged\nfrom prior MRI, again suggestive of dural calcification.\n\nProminence of ventricles and sulci suggestive of involutional changes.  There\nis no evidence of mass effect or midline shift.  The right maxillary sinus is\nnear completely opacified with mucous there is mild moderate mucosal\nthickening of the left maxillary sinus.  There is moderate to severe mucosal\nthickening of the ethmoidal air cells.\n\nMRA BRAIN:\nNote is made of a fetal left posterior cerebral artery configuration, a normal\nvariant. The previously seen free-floating thrombus in the left internal\ncarotid siphon on CT from ___ is not appreciated on the current\nstudy.  Nonocclusive narrowing of bilateral internal carotid artery cavernous\nsegments is noted.\n\nOtherwise, the intracranial vertebral and internal carotid arteries and their\nmajor branches appear preserved without evidence of stenosis,occlusion,or\naneurysm formation greater than 3 mm.\n\nMRA NECK:\nArtifact limits evaluation of right vertebral artery origin.  Otherwise, the\nleft vertebral artery and bilateral common carotid artery origins are patent.\n\nThere is less than 30% stenosis of the left internal carotid artery distal to\nthe carotid bifurcation.\n\nIn proximal right internal carotid artery is focal outpouching measuring at\nleast 4 mm compatible with patient's previously known ulcerative plaque (see\nseries 32).  Allowing for difference in technique, finding was at least\npartially present on ___ prior outside exam (see ___ on prior\noutside exam).\n\nOtherwise, bilateral cervical carotid and vertebral artery are grossly patent.",
            "output": "1. Study is moderately degraded by motion.\n2. Multiple small areas of acute to subacute infarct in the left corona\nradiata as well as the left parietooccipital area, including adjacent to the\narea of chronic parietooccipital infarct.\n3. Blood products within the left parietooccipital infarct are grossly similar\nin configuration and degree compared to prior MRI from ___, allowing\nfor differences in technique, most consistent with chronic hemorrhage. \nMinimal areas of T1 hyperintensity along left parietal chronic infarct margins\nare suggestive of laminar necrosis as described.\n4. Within limits of study, no definite evidence of new acute / subacute\nintracranial hemorrhage.\n5. Proximal right internal carotid artery findings compatible with provided\nhistory of ulcerated plaque, with differential consideration of focal proximal\nand distal internal carotid artery stenosis, pseudoaneurysm and FMD.\n6. Approximately 30% left internal carotid artery origin narrowing by NASCET\ncriteria.\n7. Artifact limits evaluation of right vertebral artery origin.\n8. Otherwise, grossly patent bilateral cervical carotid or vertebral arteries.\n9. Nonocclusive probable atherosclerotic narrowing of circle of ___ as\ndescribed.\n10. Otherwise, grossly patent circle of ___ without definite evidence of\nstenosis,occlusion,or aneurysm greater than 3 mm.\n11.  Paranasal sinus disease , as described.\n\nNOTIFICATION:  The findings were discussed with ___ from the Neurology team\nby ___, M.D. on the telephone on ___ at 10:32 am, 5 minutes\nafter discovery of the findings."
        },
        {
            "input": "There is no evidence of acute intracranial hemorrhage, edema, masses, mass\neffect, midline shift or infarction.  The ventricles and sulci are normal in\ncaliber and configuration.\n\nThere is encephalomalacia in the left parieto-occipital lobe, related to prior\ninfarct.  There is multiple scattered lacunar infarcts in the left corona\nradiata with scattered foci of T2/FLAIR hyperintensity in the periventricular\nwhite matter compatible with chronic microangiopathy.\n\nThe visualized vascular flow voids are grossly unremarkable.  There is mucosal\nthickening of the bilateral maxillary sinuses and ethmoid air cells.  The\nmastoid air cells are are clear.  The globes and orbits are unremarkable.  No\nabnormal marrow signal.",
            "output": "1. No acute intracranial abnormality.  No evidence of an acute stroke,\nhemorrhage, or intracranial mass.\n2. Encephalomalacia in the left parieto-occipital lobe, related to prior\ninfarct.\n3. White matter changes of chronic microangiopathy."
        },
        {
            "input": "There is a right parietal craniotomy and a right parietal surgical cavity. \nGyriform high signal on precontrast T1 weighted images along the superior\naspect of the surgical bed suggests mineralization.  There is linear contrast\nenhancement along the posterior/inferior/lateral aspect of the surgical bed,\nwhich does not lend itself to by dimensional measurements due to complex\ngeometry. Susceptibility artifact in this region relates to postsurgical blood\nproducts. Right dural contrast enhancement is likely postsurgical.\n\nAlong the superficial left parietal lobe, there is an enhancing lesion\nmeasuring 11 mm craniocaudad, 12 mm transverse, 7 mm AP (images 13:63,\n100:71). It is not clear whether this lesion is parenchymal or leptomeningeal.\n\nThere is confluent high T2 signal in the subcortical, deep, and\nperiventricular white matter of the cerebral hemispheres, nonspecific but\ncompatible with sequela of radiation therapy, if clinically applicable. There\nis asymmetric enlargement of the atrium and occipital horn of the right\nlateral ventricle, which may be secondary to adjacent parenchymal volume loss,\nbut the right temporal horn is also asymmetrically prominent, suggesting the\npossibility of congenital/developmental ventricular asymmetry. Other\nventricular system components are normal in size for age.\n\nThere is no acute diffusion abnormality. Major arterial flow voids are grossly\npreserved. Major dural venous sinuses are patent on postcontrast MP RAGE\nimages.\n\nThere is mild mucosal thickening in the ethmoid air cells.",
            "output": "1. Linear contrast enhancement along the posterior/inferior/ lateral margin of\nthe right parietal surgical cavity is of uncertain clinical significance in\nthe absence of prior studies for comparison.\n2. 11 x 12 x 7 mm enhancing lesion along the superficial left parietal lobe,\nwhich may be either parenchymal or leptomeningeal, suggesting a metastasis. \nComparison with prior studies would be helpful to assess stability.\n3. Confluent high T2 signal throughout the supratentorial white matter is\nnonspecific, but could be related to sequela of radiation therapy, if\nclinically applicable."
        },
        {
            "input": "The right parietal craniotomy is again seen.  Curvilinear enhancement within\nthe right parietal operative site is unchanged from prior MRI on ___,\nas well as prior MRIs dating back to ___.  Postsurgical blood\nproducts within the operative bed are unchanged.  The superficial left\nparietal peripherally enhancing lesion is not significantly changed from MRI\non ___, as well as older prior MRIs dating back to ___,\nmeasuring approximately 7 x 13 x 11 mm (AP x TV x SI).  Right dural\nenhancement is unchanged and is likely postsurgical.  No new enhancing lesions\nare identified.\n\nThere is no acute diffusion abnormality.  Confluent FLAIR hyperintensity in\nthe subcortical, deep, and periventricular white matter is unchanged from the\nprior study and ___ and may be due to post radiation change.\n\nMajor intravascular flow voids are preserved.  There is normal patency of the\nmajor intracranial arteries and dural venous sinuses following contrast\nadministration.",
            "output": "1. Stable right and left parietal enhancing lesions dating back to ___.  No new enhancing lesion.\n2. No acute infarction and no evidence for other acute intracranial\nabnormalities."
        },
        {
            "input": "The study is degraded by motion.\n\nThere is no evidence of hemorrhage, edema, mass, mass effect, midline shift or\nacute infarction.   The ventricles and sulci are age appropriate. \nPostcontrast sequences are limited, but do not show gross abnormalities. \nPrincipal intracranial vascular flow voids are preserved.  There is mucosal\nthickening along the floor of the right maxillary sinus.",
            "output": "No evidence of hemorrhage, edema, mass, mass effect, or acute infarction\nwithin limitations of motion artifact."
        },
        {
            "input": "MRI BRAIN and ORBITS:\n\nIn comparison with the prior CT of the paranasal sinuses, again there is\nexpansion of the sella turcica, causing erosion of the sellar floor, related\nwith a T1 hyperintense signal lesion, which apparently is consistent with\nproteinaceous material and underlying calcification, this lesion measures\napproximately 2.8 x 3.4 x 3.2 cm (AP X TR X SI), and demonstrates supra sellar\nextension resulting in compression and posterior displacement of the pituitary\ninfundibulum (series 16, image 10, and 11), contacting and displacing\nsuperiorly the optic chiasm, causing mild upward bowing of the optic chiasm\n(series 100, image 23). The right aspect of the mucocele contacts and\ndisplaced superiorly the right optic nerve (series 11, image 20), without\nevidence of significant compression at this level.\nThis lesion also protrudes into the middle cranial fossa, just posteriorly to\nthe left pterygopalatine fossa (series 22, image 67).\n\nThe left cavernous sinus is unremarkable as well as the vascular flow void for\nthe left internal carotid artery.\n\nThere is mild extension of the mucocele into the right cavernous sinus (series\n22, image 76).  There may be mild compression of the right cavernous ICA\n(series 15, image 7).\n\nThere is no evidence of acute intracranial hemorrhage, midline shift\norinfarction. There are scattered T2/FLAIR hyperintensities in the cerebral\nhemispheres bilaterally, a nonspecific finding and likely related to chronic\nsmall vessel ischemic changes.  No diffusion abnormalities are detected.\n\nThere is mild generalized parenchymal volume loss, most likely age related. \nMild prominence of the ventricular system and extra-axial CSF spaces is\nconsistent with the previously mentioned parenchymal volume loss.\nAllowing for mild narrowing of the cavernous segment of the right internal\ncarotid artery, the major vascular flow voids are preserved.  Major dural\nvenous sinuses are patent.\n\nThere is mucosal thickening along the ethmoid air cells.  The mastoid air\ncells appear essentially clear.\n\nAside from the findings above, the bony orbits and preseptal soft tissues are\nnormal. The globes are intact and normal in appearance. The extraocular\nmuscles are unremarkable.  The lacrimal apparatus is normal.",
            "output": "1. Expansion of the sella turcica, causing erosion of the sellar floor,\nrelated with a T1 hyperintense signal lesion, which apparently is consistent\nwith proteinaceous material, and underlying calcification which demonstrates\nsuprasellar extension, invasion and protrusion towards the anterior middle\ncranial fossa and right posterior ethmoid air cells.\n2. This lesion is contacting and displacing the optic chiasm, producing mild\nupward bowing of the optic chiasm, and is in close contact to the right optic\nnerve, but without evidence of frank compression, probable mild mass effect on\nthe right cavernous ICA with preserved flow void.\nThe differential diagnosis includes a possible sphenoid sinus mucocele, with\nunderlying chronic calcifications, rising the possibility of underlying fungal\ncolonization, however, and intra and suprasellar pituitary mass lesion cannot\nbe completely excluded.\n3. No evidence of acute intracranial hemorrhage or infarction.\n4. Nonspecific white matter lesions in the cerebral hemispheres bilaterally,\nlikely sequela of chronic small vessel ischemic changes."
        },
        {
            "input": "A homogeneously enhancing extra-axial right cerebellar pontine angle lesion\nmeasures 2.8 x 2.0 x 2.6 cm, grossly unchanged from the previous examination.\nThe lesion extends into the right internal auditory canal without widening the\nporous acousticus.  There is mass effect on the underlying cerebellar\nhemisphere.  No other mass or abnormal enhancement is identified. There is no\nacute infarct. Chronic left basal ganglia infarcts are noted with associated\nex vacuo dilatation of the anterior horn of the left lateral ventricle.",
            "output": "Right CPA mass consistent with the patient's given history of meningioma."
        },
        {
            "input": "Again seen within the right cerebellar pontine angle, there is a homogeneously\nenhancing extra-axial 2.0 x 3.1 x 2.7 cm lesion, previously 2.8 x 2.0 x 2.6\ncm, grossly unchanged from prior examination dated ___. This lesion\nappears to involve the adjacent internal auditory canal. This demonstrates\nmild restricted diffusion. There is T2/ FLAIR confluent surrounding\nhyperintensity within the right cerebellar hemisphere consistent with\nsurrounding edema, stable in appearance.\n\nVentricles and sulci are prominent compatible with age related involutional\nchanges. Periventricular and subcortical white matter T2 hyperintensities\nreflect chronic small vessel ischemic disease. No acute infarction is\nidentified.  Redemonstration of chronic left basal ganglia infarcts are noted\nwith associated ex vacuo dilatation of the anterior horn of the left lateral\nventricle. The principal intracranial flow voids are maintained. There is no\nadditional abnormally enhancing lesion identified. Orbits paranasal sinuses\nand mastoid air cells are unremarkable.",
            "output": "Stable right cerebellar pontine angle mass with right internal auditory canal\nextension and surrounding edema, consistent with patient's given history of\nmeningioma."
        },
        {
            "input": "Allowing for the slice selection and technique, no significant changes are\ndemonstrated in the previously demonstrated homogeneously enhancing\nextra-axial right ponto-cerebellar mass lesion, measuring approximately 19 by\n34 mm in transverse dimension, again this lesion is extending into the right\ninternal auditory canal with no significant widening of the porous acusticus.\n\nOn the FLAIR sequence, there is mild decrease vasogenic edema, previously seen\nalong the right vermis region. There is an new small area of gyriform\nhigh-signal and magnetic susceptibility on the precontrast T1 weighted and\nFLAIR images (image 5, series 12, image 6, series 15, image 89, series 18 and\nimage 6, series 14), with mild enhancement in the ventral aspect of the right\ncerebellar hemisphere, suggestive small hemorrhagic change and reperfusion,\nwith no evidence of slow diffusion to indicate acute ischemia (image 4, series\n7).\n\nSupratentorially, chronic left basal ganglia ischemic changes are again seen,\ncausing ex vacuo dilatation of the left lateral ventricle and frontal\nventricular horn.  There are few unchanged scattered foci of high signal\nintensity in the subcortical white matter, which are nonspecific and may\nreflect changes due to small vessel disease.  The major vascular structures\nare patent. The orbits are unremarkable, the paranasal sinuses and mastoid air\ncells are clear.",
            "output": "1. In comparison with prior examinations, no significant changes are\nidentified in the right cerebellar pontine angle mass lesion, likely\nconsistent with meningioma.\n\n2. New area of high signal intensity on T1 and FLAIR sequence, with gyriform\nenhancement identified in the ventral aspect of the right cerebellar\nhemisphere, suggestive of micro hemorrhage with reperfusion from prior\nischemic change, with no evidence of acute ischemic changes on the\ndiffusion-weighted images.\n\n3. Unchanged chronic left basal ganglia infarcts, associated with ex vacuo\ndilatation of the anterior horn of the left lateral ventricle as described\nabove.\n\nNOTIFICATION:  The findings were discussed by Dr. ___ with Dr. ___\non the telephone on ___ at 2:11 ___, 5 minutes after discovery of the\nfindings."
        },
        {
            "input": "In comparison with the most recent examination, again there is an extra-axial\nslightly heterogeneous enhancing lesion in the right cerebellar pontine angle,\nwith extension into the right porous acusticus, measuring approximately 14 x\n34 mm in transverse dimension and approximately 26 x 17 mm in coronal\nprojection, which is relatively stable since the prior study, however slightly\nsmaller in comparison with the study dated ___.  Also the pattern of\nenhancement appears slightly more heterogeneous with possible areas of\nnecrosis or calcifications as demonstrated in the image 107, series 901.  No\nnew lesions are identified.  The ventricles and sulci are prominent,\nsuggesting cortical volume loss, probably age related and involutional in\nnature.  Unchanged sequela of prior ischemic event is noted on the left basal\nganglia, producing ex vacuo dilatation of the lateral ventricle, magnetic\nsusceptibility changes are visualized in this region, suggesting residual\nblood products.  The major vascular flow voids are present and demonstrate\nnormal distribution.  The orbits are unremarkable, the paranasal sinuses and\nthe mastoid air cells are clear.",
            "output": "1.  In comparison with the most recent exam, there is a relatively stable\nextra-axial mass lesion in the right cerebellar pontine angle, extending into\nthe left porous acoustic, with no evidence of enlargement in this area, likely\nconsistent with meningioma.  No new lesions are identified.  This lesion\napparently is slightly smaller in comparison with the MRI dated ___.\n\n2.  Supratentorially sequela of prior ischemic hemorrhagic event is noted in\nthe left basal ganglia, causing ex vacuo dilatation of the lateral ventricle\nas described above."
        },
        {
            "input": "MRI HEAD: 5 mm focus of gradient echo susceptibility artifact in the left pons\n(series 6, image 9), is unchanged from prior exam, without demonstration of\nabnormal postcontrast enhancement, compatible with a cavernous malformation.\nOtherwise, no intra or extra-axial mass, acute hemorrhage or infarct. Sulci,\nventricles and cisterns are within expected limits. The major flow voids are\npreserved. The paranasal sinuses are clear. The orbits are unremarkable. The\nmastoid air cells are clear.\n\nNeck MRA: Again noted is a dissection flap of the extracranial internal\ncarotid artery just prior to the petrous portion (series 11, image 11),\nsimilar in appearance to prior exam, allowing for technical differences.  Mild\nbeaded appearance of the right cervical ICA (series 1501C, image 67) is again\nnoted, as well as subtle beaded appearance of the bilateral vertebral arteries\nare noted, compatible with mild fibromuscular dysplasia. There is a normal 3\nvessel arch. The left extracranial an intra vertebral artery is dominant.\nThere is no significant extracranial internal artery stenosis by NASCET\ncriteria. No evidence of aneurysm larger than 3 mm.",
            "output": "1.  Unchanged appearance of gradient echo susceptibility artifact in the left\npons, compatible with a cavernous malformation.\n\n2.  Beaded appearance of the right cervical ICA is noted, unchanged form prior\nexam, as well as subtle beaded appearance of the bilateral vertebral arteries\nare noted, which may represent fibromuscular dysplasia. Previously described\ndissection flap of the right cervical ICA is again seen, not significantly\nchanged from prior exam. No new dissections. No significant steno-occlusive\ndisease."
        },
        {
            "input": "MRI Brain:  The patient's known left pontine cavernous malformation is\nredemonstrated, measures 7 mm, appears unchanged, without evidence of recent\nhemorrhage.  No additional signs of acute or chronic hemorrhage are\ndemonstrated.\n\nOtherwise, the brain parenchyma is normal in signal intensity and morphology. \nThere is no evidence of acute infarction.  There is no extra-axial collection.\nProbable 12 mm arachnoid cyst in the left pontomedullary cistern.  The\nventricles, sulci, and cisterns appear proportional.\n\nThe globes and orbits are intact.  Mild paranasal sinus mucosal thickening. \nThe major vascular flow voids are preserved.\n\nMRA neck:  Again noted is a dissection flap of the extracranial internal\ncarotid artery, just prior to the petrous portion, with a small, stable\npseudoaneurysm.  Minimal irregularity of bilateral vertebral arteries is\nbetter appreciated on the prior exam.  Bilateral common, internal, and\nexternal carotid arteries otherwise enhance normally.  The cervical segments\nof both vertebral arteries enhance normally.\n\nThere is a normal three-vessel arch configuration.  The aortic arch, great\nvessel origins, this of and subclavian arteries enhance normally.",
            "output": "1. Stable 7 mm left superior pontine cavernous malformation without signs of\nrecent bleeding.\n2. Re- demonstration of a distal right internal carotid artery dissection flap\nand small pseudoaneurysm, unchanged from prior.  Suggestion of underlying\nfibromuscular dysplasia."
        },
        {
            "input": "MRI BRAIN:\nA 6 mm nonenhancing lesion in the left pons extensive susceptibility artifact\ndemonstrating central areas of elevated T2 signal and complete through\nperipheral rim of low signal, most consistent with a cavernous malformation is\ngrossly stable in size compared to prior examination.  There is no evidence of\nrecent hemorrhage.\n\nThere is no parenchymal signal abnormality otherwise.  There is no abnormal\nfocus of slow diffusion.  There is no mass or mass effect.  The ventricles and\nsulci are age-appropriate.  Principal intracranial vascular flow voids are\npreserved.  The dural venous sinuses are patent on postcontrast MP-RAGE\nsequences.  There is no abnormal enhancement.\n\nMRA BRAIN:\nThe intracranial vertebral and internal carotid arteries and their major\nbranches appear normal without evidence of stenosis, occlusion, or aneurysm\nformation.\n\nMRA NECK:\nRight distal cervical internal carotid artery focal dissection flap and small\npseudoaneurysm is grossly unchanged compared to prior examination (series 11\n705, image 3).  The common, internal and external carotid arteries otherwise\nappear normal.  There is no evidence of internal carotid artery stenosis by\nNASCET criteria.  The origins of the great vessels, subclavian and vertebral\narteries appear normal bilaterally.  The vertebral arteries are patent.",
            "output": "1. Grossly stable size of left pontine cavernoma.  No evidence of recent\nhemorrhage.  No acute intracranial abnormality.\n2. Stable appearance of right distal cervical internal carotid artery focal\ndissection flap and pseudoaneurysm.\n3. Unremarkable head MRA."
        },
        {
            "input": "Postcontrast MP RAGE images are severely degraded by motion artifact.  Other\nimages are mildly limited by motion artifact.\n\nThere is a peripherally enhancing intra-axial mass in the right frontal\noperculum (2.8 cm AP x 3.0 cm TV x 3.3 cm SI).  The mass demonstrates mild\nhyperdensity on the preceding CT, with corresponding T2 hyperintensity of its\nnonenhancing central portion, but no clear evidence for blooming on gradient\necho images to definitively indicate blood products.  The rim of the mass\ndemonstrates high signal on diffusion tracer images and low signal on the ADC\nmap, suggesting hypercellularity.  There is extensive vasogenic edema with\npartial effacement of the right lateral and third ventricles, but no evidence\nfor left lateral ventricle dilatation.  There is 7 mm leftward shift of\nmidline structures, as seen on the prior CT.  Basal cisterns are not\ncompressed.\n\nNo additional mass is seen allowing for motion artifact.  No acute infarction.\nThe major intracranial vascular flow voids are maintained.\n\nA right anterior ethmoid air cell is opacified.  There is mild mucosal\nthickening in other bilateral ethmoid air cells, left frontal sinus, and left\nsphenoid sinus.  There is mild mucosal thickening and at least 1 small mucous\nretention cyst in the right maxillary sinus.  There is partial right and trace\nleft mastoid air cell opacification.",
            "output": "1. Motion limited exam.\n2. 3.3 cm intra-axial mass is again seen in the right frontal operculum with\nextensive vasogenic edema and approximately 7 mm leftward shift of midline\nstructures, as seen on the same-day ___ CT.  The mass appears\nhypercellular without clear evidence for blood products.  Primary CNS neoplasm\n(e.g., glioblastoma) is most likely, though metastatic disease may also be\nconsidered.\n3. No evidence for additional intracranial masses, allowing for significant\nmotion artifact."
        },
        {
            "input": "No significant change in the peripherally enhancing intra-axial mass in the\nright frontal operculum measuring approximately 2.8 cm AP x 3.0 cm TV x 3.3 cm\nSI.  Stable extensive surrounding vasogenic edema and partial effacement of\nthe right lateral and third ventricles without evidence of ventricular\ndilatation.  No change in the associated 7 mm midline shift to the left.  No\nadditional enhancing focus is identified.  No definite evidence of hemorrhage\nor acute infarction.",
            "output": "1. Unchanged peripherally enhancing intra-axial mass centered in the right\nfrontal operculum measuring up to 3.3 cm\n2. Stable extensive surrounding vasogenic edema.\n3. No additional enhancing focus is identified.\n4. No evidence of hemorrhage or acute infarction."
        },
        {
            "input": "The patient is status post right frontoparietal craniotomy and mass resection,\nwith expected postoperative changes including postoperative blood products and\nmild associated pneumocephalus.  A postoperative seroma with air-fluid level\nis seen external to the craniotomy flap.\n\nMinimal residual peripheral enhancement is seen along the posteromedial\naspects of the resection cavity, and may reflect postoperative change versus\nresidual disease.\n\nThere is a peripheral area of restricted diffusion surrounding the resection\ncavity with extension into the adjacent anterior right frontal white matter,\npresumed postoperative.  Allowing for this, no additional areas of restricted\ndiffusion are identified.  No vascular territorial infarction.\n\nThe extent of surrounding T2/FLAIR hyperintensity is similar when compared to\nthe preoperative examination.  This FLAIR hyperintense signal extends into the\nright external capsule and posterior limb of the right internal capsule.\n\nThere is persistent local mass effect with partial effacement of the right\nlateral ventricle and 2-3 mm of leftward midline shift, slightly improved from\nthe previous examination.\n\nAllowing for this, the background ventricles and sulci are mildly prominent. \nThe basal cisterns remain patent.  There is preservation of the major\nintracranial vascular flow voids.\n\nThe visualized paranasal sinuses, middle ear cavities, and mastoid air cells\nare well aerated and clear.  The orbits are within normal limits bilaterally.",
            "output": "1. Status post right frontoparietal craniotomy and mass resection with\nextensive postoperative change, as detailed above.  Overall, local mass\neffect, partial effacement of the right lateral ventricle, and 2-3 mm of\nleftward midline shift have modestly improved from the previous examination.\n2. Blood products, pneumocephalus, and peripheral areas of restricted\ndiffusion surrounding the resection margin are all presumed postsurgical.  No\nevidence for vascular territorial infarction.\n3. Areas of residual enhancement along the posteromedial aspect of the\nresection cavity may reflect component of postoperative change though residual\ndisease would be of concern.  Recommend continued attention at follow-up.\n4. Modest interval decreased extent of surrounding T2/FLAIR hyperintensity\nwith extension into the right external and posterior limb of the internal\ncapsules.\n5. Additional findings, as above."
        },
        {
            "input": "Patient is status post right parietal craniotomy for resection of an\nunderlying mass.  Degree of surrounding vasogenic edema and mass effect have\nsignificantly decreased in the interval.  Ventricles and sulci are now\nsymmetric and unremarkable.  There is hyperintensity on the postcontrast\nsequences lining the resection cavity.  The degree of enhancement at the\nposteromedial margin has not increased though relatively thin enhancement is\nseen along the resection cavity more anterolaterally is new.  This area of new\nenhancement along the anterior resection cavity had demonstrated restricted\ndiffusion on immediate postoperative exam.  This could be post treatment\nrelated.\n\nThere is a new 1.0 x 0.9 cm area of hyperintensity on the T1 and MPRAGE\npostcontrast sequences (11:17).  This area is at the anterior aspect of the\npostoperative bed.  On prior postoperative brain MRI, this area had\ndemonstrated restricted diffusion.  As the current exam was only performed as\na postcontrast exam, degree of enhancement versus intrinsic T1 hyperintensity\ncannot be established.  However, given prior restricted diffusion, this\nfinding could represent enhancement within a late subacute infarct.\n\nThere is or overlying dural thickening and enhancement compatible with\npostoperative state.\n\nElsewhere, no evidence of new enhancing mass lesion.  No acute infarct.",
            "output": "Postoperative changes of right frontal mass resection.  New areas of presumed\nenhancement (within limitation of only post-contrast images being obtained on\ntoday's exam) are seen in areas of restricted diffusion on postoperative exam\nand could be due to post treatment/ischemic changes as opposed to progression\nof disease though suggest continued interval follow-up."
        },
        {
            "input": "The patient is status post right pterional craniotomy and resection of a right\nfrontal lobe lesion.  A 5 mm rounded enhancing focus in the right frontal\ncorona radiata is smaller when compared to prior exam which measured\napproximately 7 mm.  Linear and slightly nodular enhancement along the\nresection cavity (series 16, image 14) is slightly more confluent when\ncompared to prior examination, likely secondary to evolving and involutional\nchanges, although residual lesion cannot be entirely excluded. No new\nenhancing foci.  Expected dural thickening and enhancement underlying the\ncraniotomy is identified.\n\nThere is no acute infarct.  Residual hemosiderin staining within the resection\ncavity is identified.  Mild residual FLAIR hyperintense edema signal along the\nresection cavity is identified, significantly improved from prior\nexaminations.  The sulci, ventricles and cisterns are within expected limits\nfor the patient's age.  The major intracranial flow voids are preserved.  The\ndural venous sinuses are patent.  Mild mucosal thickening of the right\nmaxillary sinus and of the ethmoid air cells is identified.  Opacification of\nthe right mastoid air cells is noted.  No suspicious osseous lesions.",
            "output": "1. The patient is status post right pterional craniotomy and resection of a\nright frontal lobe lesion with expected dural thickening and enhancement\nunderlying the craniotomy.\n2. A 5 mm rounded enhancing focus in the right frontal cranial ___ is\nsmaller when compared to prior examination.\n3. Linear and slightly nodular enhancement along the resection cavity is more\nconfluent and prominent when compared to prior examination, likely secondary\nto posttreatment and involutional changes.  However, residual lesion is not\nexcluded and close attention on follow-up is recommended.\n4. No new regions of abnormal enhancement.\n5. Additional findings described above."
        },
        {
            "input": "Postoperative change right frontoparietal craniotomy, tumor resection right\nfrontal operculum.  Peripheral enhancement marginating surgical cavity is\nimproved.  Previously seen nodular enhancement along the deep margin of the\nsurgical bed at right centrum semiovale has resolved.  Linear dural\nenhancement at the craniotomy site, postsurgical.\n\nThere is no evidence of new mass, infarct or hemorrhage.  Mild brain\nparenchymal atrophy.  Vascular flow voids are preserved.  Mild paranasal sinus\ndisease.  Mild opacification right mastoids.  Clear left mastoids.",
            "output": "Posttreatment change.  No evidence of residual or new tumor."
        },
        {
            "input": "The patient is post right pterional craniotomy for resection of a right\nfrontal lobe lesion.  Stable postsurgical changes are seen with stable linear\nenhancement along the resection cavity, likely representing posttreatment\nchange.  No increasing nodular abnormal enhancement is seen.  No increasing\nparenchymal FLAIR signal abnormality.\n\nThere is no evidence of infarction or new intracranial hemorrhage.  Allowing\nfor postsurgical findings, the ventricles and sulci are prominent, consistent\nwith global cerebral volume loss.\n\nThe major intracranial flow voids are preserved.  The dural venous sinuses are\npatent.  The paranasal sinuses, mastoid air cells and middle ear cavities are\nclear.  The intraorbital contents are normal.",
            "output": "1. Stable postoperative changes secondary to resection of a right frontal lobe\nlesion, including stable linear enhancement along the resection cavity, likely\nrepresenting posttreatment change.  Degree of surrounding white matter edema\npattern is unchanged.  No new increasing nodular enhancement to suggest\ndisease recurrence.\n2. No acute intracranial abnormality.  No acute infarct, new enhancement or\nnew intracranial hemorrhage.\n3. Additional findings described above."
        },
        {
            "input": "There is no evidence of intracranial hemorrhage, edema, masses, mass effect,\nmidline shift or infarction.\nThere is an area of hyperdensity in the left thalamus on the postcontrast\nMPRAGE images (series 10, image 157) which is not identified on the\npostcontrast T1 imaging also does not demonstrate any other signal abnormality\nin the remaining sequences.  Therefore, the signal abnormality is considered\nto be most likely artifactual.  Otherwise, there is no abnormal enhancement\nafter contrast administration.\nThere are scattered T2/FLAIR hyperintensities in the cerebral hemispheres\nbilaterally and in the pons, a nonspecific finding and likely related to\nchronic small vessel ischemic changes.\nNote is made of a lacunar infarct in the left thalamus (08:14).\n\nThere is mild generalized parenchymal volume loss, most likely age related. \nMild prominence of the ventricular system extra-axial CSF spaces is consistent\nwith the previously mentioned parenchymal volume loss.\nMajor vascular flow voids are preserved.  Major dural venous sinuses are\npatent.\n\nThere is mild mucosal thickening along the ethmoid air cells.  The remainder\nof the paranasal sinuses and mastoid air cells appears clear.  The orbits\nappear unremarkable.",
            "output": "1. No evidence of intracranial metastatic disease.  No acute infarction,\nhemorrhage or intracranial mass.\n2. Signal abnormality in the left thalamus on the postcontrast MPRAGE images\nis not reproduced on the postcontrast T1 images and there is also no other\nsignal abnormality in the remaining sequences.  Therefore this signal\nabnormality is considered to be most likely artifactual.\n3. Nonspecific white matter changes in cerebral hemispheres bilaterally and in\nthe pons, likely sequela of chronic small vessel ischemic changes.  Small old\nlacunar infarct in the left thalamus."
        },
        {
            "input": "Examination of the distal cervical vasculature is somewhat limited secondary\nto patient motion.\n\nAllowing for this, there is a dominant appearing right-sided vertebral basilar\nsystem.  The left vertebral artery is hypoplastic, and there is loss of flow\nrelated signal within the proximal V3 segment (02:45), and within the distal\nleft V3 segment (2: 67).  There is no flow related signal identified within\nthe expected location of the left V4 segment.\n\nThe right vertebral artery appears widely patent through its visualized\ncourse.  Intracranially, there is a fetal origin of the right posterior\ncerebellar artery.  The left posterior communicating artery is dominant, with\na hypoplastic left P1 segment.\n\nThe remainder of the central intracranial vasculature is grossly unremarkable\nwithout high-grade stenosis or occlusion.  However, on review of the 3D MIP\nimages, there is apparent diffuse luminal irregularity and narrowing of the\ndistal intracranial vessels, bilaterally.",
            "output": "1. Hypoplastic left vertebral artery, with several areas of superimposed loss\nof flow related signal seen within the left V3 segment.\n2. No flow related signal is identified within the left V4 segment, a finding\nof uncertain chronicity.\n3. Moderate, irregular narrowing of the distal intracranial vasculature, seen\nbilaterally.  These findings can be seen in the setting of Vasa spasm,\nvasculitis, or septic emboli.  Recommend MRI brain examination.\n\nNOTIFICATION:  Findings were conveyed by Dr. ___ to Dr. ___ text\n___ at 15:04 on ___, 2 min after interpretation."
        },
        {
            "input": "Small focus of mildly restricted diffusion right centrum semiovale, consistent\nwith early subacute infarct.  Tiny focus of restricted diffusion posterior\nleft cingulate gyrus, consistent with early subacute infarct.  Few additional\npunctate foci of early subacute infarcts in the inferior left parietal, left\noccipital lobes.  Late subacute to chronic infarct right medial parietal lobe.\nFindings consistent with embolic etiology.\n\nChronic lacunar infarct right basal ganglia.  Mild chronic small vessel\nischemic changes. There is no evidence of hemorrhage, edema, masses, mass\neffect, midline shift.  Generalized brain parenchymal atrophy.  No\nhydrocephalus.  Severe degenerative changes cervical spine, partially seen. \nIntracranial flow voids are preserved.  Mild paranasal sinus disease.  Mild\nopacification of left and trace right mastoid air cells.",
            "output": "1. Punctate early to late subacute infarcts bilateral cerebral hemispheres,,\nsuggestive of embolic etiology.  No hemorrhage.\n2. Chronic lacunar infarct right basal ganglia"
        },
        {
            "input": "There are multiple areas of bilateral restricted diffusion, left greater than\nright, concerning for hypoxic ischemic injury. The extent of injury involves\nthe cortices in the left posterior frontal, parietal, occipital, as well as\ntemporal lobes and the right parietal and posterior frontal lobes. There is\nalso a restricted diffusion within the bilateral basal ganglia. The ventricles\nare unchanged in size and configuration.\n\nThere is no acute hemorrhage or mass effect. The major intracranial vascular\nflow voids are preserved. Air-fluid level is noted within the bilateral\nmaxillary sinuses and nasopharynx likely related to intubation. The mastoid\nair cells are partially opacified. The globes are unremarkable.  Hardware\nartifact limits evaluation left occipital lobe on GRE sequence (series 11,\nimage 14).",
            "output": "1. Multiple areas of restricted diffusion, more pronounced on the left,\ninvolving the bilateral cerebral cortices as well as the bilateral basal\nganglia compatible with hypoxic ischemic injury."
        },
        {
            "input": "There is an unchanged large right extra-axial, frontotemporal dural-based\nenhancing mass lesion, associated with midline shifting towards the left and\nuncal herniation, with approximately 16.3 mm of shifting towards the left\n(image 12, series 12), the left lateral ventricle appears slightly enlarged,\nthe FLAIR sequence is notable for mild transependymal migration of CSF,\nsuggesting of mild hydrocephalus, the right temporal ventricular horn appears\ncollapsed, no diffusion abnormalities are detected to indicate acute or\nsubacute ischemic changes.  There is significant mass effect in the right MCA\nand deviation of the midbrain towards the left as previously described on the\nCTA examination.  After the administration of gadolinium contrast, there is\nincreased enhancement in the anterior and lateral aspect of this mass, with\nslightly prominent vessels in the ___ the neoplasm.  The orbits are\nunremarkable, the paranasal sinuses and mastoid air cells are clear.",
            "output": "1.  Essentially unchanged large right extra-axial frontal temporal dural-based\nenhancing mass, causing midline shifting towards the left as described in\ndetail above, as well as uncal herniation an deviation of the midbrain, likely\nconsistent with meningioma.\n\n2.  On the FLAIR sequence, there is evidence of mild transependymal migration\nof CSF in the left lateral ventricle, suggesting mild hydrocephalus."
        },
        {
            "input": "There is a large 6.1 x 4.9 x 7.3 cm (AP x TV x SI, measured on series 2 image\n59 and series 5006b, image 84) right frontotemporal extra-axial mass lesion. \nWhen compared with MRI from ___, which was performed without and with\nintravenous contrast, this mass demonstrates homogeneous enhancement.  There\nis a CSF cleft surrounding the mass.  There is compression of the right\nlateral ventricle with 13 mm leftward midline shift and mild dilatation of the\nleft lateral ventricle, not significantly changed from prior MRI on ___.  There is T1 hypointensity surrounding the atrium of the left lateral\nventricle, suggestive of transependymal flow of CSF, unchanged.  There is\nright uncal herniation, also unchanged.  There are no additional mass lesions.\nThe right middle cerebral artery is displaced by the large extra-axial mass. \nThe major intracranial arteries and dural venous sinuses are patent.",
            "output": "1. Large right frontotemporal 7.3 cm extra-axial mass lesion causing 13 mm\nleftward midline shift, mild left lateral ventricle entrapment, and right\nuncal herniation.  This is unchanged from MRI on ___.  The appearance\nof this mass is most consistent with a meningioma."
        },
        {
            "input": "The patient is status post right craniotomy for sphenoid meningioma resection.\nThere is a small amount of subdural blood along the right convexity, right\nfalx, and within the posterior fossa bilaterally, similar to the postsurgical\nCT, without mass effect on the brain.  A small amount of globular T1\nhyperintense blood products is present along the right temporal lobe resection\nmargin, corresponding hyperdense blood on the postoperative CT. No definite\nresidual enhancing mass is seen on postcontrast images.\n\nThere is leftward shift of midline structures by approximately 8 mm, similar\nto the post-operative CT.  Mild effacement of the right lateral ventricle and\nthird ventricle, and dilatation of the left lateral ventricle, are similar to\nthe postoperative CT but have improved compared to the preoperative MRIs. \nDiffusely elevated T2 signal in the white matter along the lateral ventricles,\nmore extensive on the left than right, is unchanged, likely reflecting\ntransependymal CSF flow.\n\nThere is questionable minimal T2 hyperintensity in the anterior aspect of the\nright temporal lobe without mass effect.  No other parenchymal edema is seen. \nThere is no acute infarction. The ventricles are stable in size and\nconfiguration.  The principal intracranial vascular flow voids are patent. \nMajor dural venous sinuses are patent on postcontrast MP RAGE images.",
            "output": "1. No evidence for residual enhancing mass, allowing for T1 hyperintense blood\nproducts along the right temporal resection bed margin.\n2. Possible minimal edema in the anterior right temporal lobe without mass\neffect or evidence for acute infarction.  No parenchymal edema elsewhere.\n3. Mass effect and entrapment of the left lateral ventricle are similar to the\npostoperative CT from ___, but decreased compared to the preoperative\nMRI from ___.\n4. Small subdural hematoma along the right convexity, right falx, and within\nthe posterior fossa bilaterally, without mass effect on the brain, similar to\nthe postsurgical CT."
        },
        {
            "input": "Patient is status post right craniotomy for sphenoid meningioma resection. \nPreviously present subdural blood along the right convexity, right falx, and\nwithin the posterior fossa bilaterally has resolved.  The right temporal lobe\nsurgical bed appears cystic with associated T2 and FLAIR hyperintensity is\nconsistent with tissue loss and encephalomalacia.  Previously present residual\nblood products along the right temporal lobe are no longer present.  There is\nno abnormal enhancement associated with the resection site.  Pachymeningeal\nthickening and enhancement along the right frontal convexity subjacent to the\ncraniotomy site is likely postsurgical in etiology.  T2 and FLAIR\nhyperintensity within the osseous craniotomy sites is associated with\nenhancement (16:21, 19), potentially enhancing granulation tissue.  There is\nmild residual enhancement of the right temporalis muscle.\n\nVentricles and sulci are age appropriate in size and configuration. \nPreviously elevated T2 signal involving the periventricular white matter along\nthe lateral ventricles has resolved.  There is no shift of normally midline\nstructures. The basal cisterns are not effaced.  There is no abnormal\ndiffusion to suggest acute infarction.  Intracranial flow voids are preserved.\nIncidental note is made of a partially empty sella.\n\nMajor dural sinuses are patent on postcontrast MP rage images.  The orbits are\nunremarkable.  Mastoid air cells and paranasal sinuses are clear.",
            "output": "1.  Postsurgical changes involve the right frontotemporal craniotomy and right\ntemporal lobe.  Resection bed within the right temporal lobe appears cystic\nwith associated encephalomalacia. There is no new enhancement to suggest\nrecurrent tumor.  Pachymeningeal thickening and enhancement subjacent to the\ncraniotomy sites is felt likely postsurgical in etiology.\n2. Resolution of prior mass effect and entrapment of the left lateral\nventricle with no shift of midline structures and resolution of elevated\nperiventricular white matter signal."
        },
        {
            "input": "There been no significant changes since the prior study.  Again seen are\npostoperative changes after resection of a right middle cranial fossa\nmeningioma.  There is mild dural thickening and enhancement at the surgical\nsite.  There are no findings to suggest residual or recurrent tumor.  No other\nlesions are identified.  There is no evidence of hemorrhage or infarction.",
            "output": "1. Status post right middle cranial fossa meningioma resection with no\nevidence of residual or recurrent tumor."
        },
        {
            "input": "Examination is moderately degraded by motion.  Specifically, MPRAGE images are\nmarkedly degraded by motion artifact.\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  Mild prominence of the ventricles and sulci is suggestive of\ninvolutional changes.  Multiple scattered T2 and FLAIR hyperintense foci in\nthe periventricular and subcortical white matter are nonspecific, but may\nreflect chronic small vessel ischemic changes.\n\nPostcontrast images are markedly degraded by motion artifact.  There is no\ndefinite area of abnormal enhancement.\n\nThere is mild mucosal thickening of the ethmoid sinuses.  The mastoid air\ncells are clear.  The intraorbital contents are unremarkable.",
            "output": "1. No evidence of infarction or hemorrhage.\n2. Markedly degraded postcontrast images.  Within these limitations, no\ndefinite focal area of abnormal enhancement.\n3. Multiple scattered nonspecific white matter signal abnormalities, which\ncould represent findings of chronic small vessel ischemic disease."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  Periventricular and pontine T2 and FLAIR hyperintense changes\nare nonspecific, but most likely sequela of microangiopathy.  There are\nchronic infarctions in the basis pontis bilaterally.  The ventricles and sulci\nare normal in caliber and configuration.  The pituitary appears normal.  The\ncraniocervical junction appears normal.  The intracranial arteries demonstrate\nnormal T2 flow void.  The orbits appear normal.  The paranasal sinuses are\nclear.\nThere is no evidence of metastatic disease.  Sensitivity for detecting\nmetastases is limited without intravenous contrast.",
            "output": "Chronic pontine infarction.\nNo evidence of mass, hemorrhage, or recent infarction.\n\nNo evidence of metastatic disease.\n\nModerate periventricular and pontine white matter changes are most likely\nsequela of microangiopathy."
        },
        {
            "input": "Seen again is the large right-sided intraparenchymal hemorrhage involving\nright paramedian superior posterior frontal lobe in the area of the right\ncingulate gyrus.\n\nTrace subarachnoid hemorrhage at the vertex, stable.  Trace posterior\nparafalcine, then ___ ule, right hemispheric subdural hemorrhage, probably\nsimilar, better seen.\n\nMild enhancement of the right tentorial component of subdural hemorrhage, mild\nlinear right hemispheric pachymeningeal enhancement, can be seen in the\nsetting of early subacute hemorrhage.  No enlarged arteries, parenchymal\nenhancement, abnormal vasculature to suggest AVM or aneurysm on MRI.  Patent\ndural venous sinuses.\n\nThere is increased FLAIR signal around the bleed without contrast\nenhancement..  No evidence of superficial or deep chronic microhemorrhage. \nParanasal sinuses, mastoids are clear.",
            "output": "Large right paramedian frontal lobe hemorrhage.  No MRI evidence of mass, AVM\nor distal ACA aneurysm.  Aneurysm should be excluded on MRA or CTA.\nSmall volume subarachnoid, subdural hemorrhage.\n\nRECOMMENDATION(S):  Follow-up MRI once hematoma resolves."
        },
        {
            "input": "Patient status post left cranial frontoparietal hemicraniectomy. \nRe-identified evolving intraparenchymal hemorrhage extending from the right\nfrontal, parietal and temporal lobes and measuring 4.3 x 3.7 cm in largest\ndimension (11:16), previously 4.7 x 3 cm.  Scattered left subarachnoid\nhemorrhage.  Small amounts of dependent intraventricular blood products noted\nbilaterally (11:10).  There is stable surrounding vasogenic edema with local\nmass effect, including sulcal and left lateral ventricle effacement.  There is\nsome subtly decreased diffusion with T2 hyperintensity along the cortex of the\nadjacent temporal lobe, although diffusion sequence to be interpreted with\ncaution in the context of adjacent blood products and skin staples.  No\nappreciable midline shift.  Evolving hemorrhagic infarction is not excluded as\nan underline etiology.  The ventricles and sulci are stable in caliber and\nconfiguration.\n\nUnchanged mediastinal magnum versus retrocerebellar arachnoid cyst.  Unchanged\nminimal mucosal thickening in the ethmoid air cells.  Partially visualized\nendotracheal and orogastric tubes.  Visualized portion of the orbits are\nunremarkable.",
            "output": "1. Patient status post left frontoparietal craniectomy with relatively stable\nintraparenchymal and scattered subarachnoid hemorrhages with stable\nsurrounding vasogenic edema.  No appreciable midline shift or worsening\nhydrocephalus.  There are some potential diffusion changes in the adjacent\ntemporal lobe, possibly reflecting infarction which is a possible underlying\netiology."
        },
        {
            "input": "No exophytic mucosal mass.  No pathologic adenopathy by imaging criteria. \nNeck vessels demonstrate appropriate flow voids.  Normal salivary glands.\nNormal thyroid\n\nUnderlying the right skin marker, a soft tissue fatty lesion is seen measuring\napproximately 4.7 cm x 2 cm by 5 cm, likely secondary to a large soft tissue\nlipoma.",
            "output": "1. Underlying the right skin marker in the region of patient's palpable\nabnormality is a 5 cm lipoma.  No other abnormalities identified."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration for age.  There is no significant atrophy.  There is no\ndisproportionate mesial temporal lobe atrophy.  Scattered foci of\nperiventricular, subcortical and deep white matter T2/FLAIR hyperintensities\nare in a configuration most suggestive of chronic small vessel ischemic\ndisease.  There is no abnormal focus of slowed diffusion.  The principal\nintracranial vascular flow voids are preserved.\n\nThe visualized paranasal sinuses are grossly clear.  The orbits are grossly\nunremarkable.  The mastoid air cells are clear.",
            "output": "1. No acute intracranial abnormality including hemorrhage, infarct, or\nsuggestion of mass.\n2. No significant atrophy or disproportionate mesial temporal lobe atrophy.\n3. Scattered areas of white matter signal abnormality in a configuration most\nsuggestive of chronic small vessel ischemic disease."
        },
        {
            "input": "Areas of restricted diffusion in the left parietal lobe with ADC and FLAIR\ncorrelates, consistent with acute-subacute infarcts.  There is no evidence of\nhemorrhagic transformation.\n\nIn addition, there is a confluent area of T2/FLAIR hyperintense signal in the\nmedial right occipital lobe which demonstrates patchy areas of mild DWI\nhyperintensity and ADC correlates which most likely represents a subacute\ninfarct.  There are patchy areas of GRE susceptibility artifact in this area,\nconsistent with petechial hemorrhage.\n\nThe ventricles and sulci are normal in caliber and configuration.  There is no\nmidline shift.\n\nThe paranasal sinuses and mastoid air cells appear grossly clear.  The orbits\nappear unremarkable.",
            "output": "1. Subacute infarction involving the right occipital lobe with evidence of\npetechial blood products, unchanged.\n2. Acute-subacute infarctions in the left parietal lobe without evidence of\nhemorrhagic transformation."
        },
        {
            "input": "Scattered foci of DWI hyperintensity are seen throughout the bilateral\ncerebellar hemispheres corresponding to the SCA, AICA and ___ territories,\nwithin the pons corresponding to basilar perforator branch territories and in\nthe bilateral occipital lobes and bilateral posterior mesial temporal lobes\ncorresponding to the PCA territories.  There are accompanying hypointense foci\non ADC which confirms the DWI lesions to represent infarcts.\n\nSmall focus of susceptibility in the peripheral aspect of the right inferior\ncerebellar hemisphere (series 10, image 4) likely represents a chronic\nmicrohemorrhage.  There is no hemorrhagic transformation in the area of the\nrecent infarct.\n\nThere are scattered T2/FLAIR hyperintensities in the cerebral hemispheres\nbilaterally, a nonspecific finding and likely related to chronic small vessel\nischemic changes.  Old lacunar infarct in the left periventricular white\nmatter.\n\nThe ventricles and sulci are normal in caliber and configuration.\nMajor vascular flow voids are preserved.\n\nMild mucosal thickening in the ethmoid air cells and sphenoid sinuses.  The\nremainder of the visualized paranasal sinuses and mastoid air cells is clear. \nNote is made of leftward deviation of the nasal septum.  The orbits are\nnormal.",
            "output": "1. Recent infarcts related to the patient's a basilar occlusion are seen in\nthe bilateral cerebellar hemispheres, pons, bilateral occipital lobes and\nbilateral posterior mesial temporal lobes.  No hemorrhagic transformation.\n2. Chronic tiny focus of susceptibility in the peripheral right inferior\ncerebellar hemisphere likely represents a chronic microhemorrhage.\n3. White matter lesions in the cerebral hemispheres bilaterally are\nnonspecific but likely sequela of chronic small vessel ischemic changes.  Old\nlacunar infarct in the left periventricular white matter.\n4. Mild paranasal sinus disease.\n\nNOTIFICATION:  The Neurology clinical team was aware of these findings at time\nof this interpretation."
        },
        {
            "input": "There is an infarct involving the right inferior frontal lobe with extension\ninto the right insula and temporal lobes, corresponding to FLAIR hyperintense\nsignal.  No new additional areas of infarction are seen.  The ventricles and\nsulci are normal in caliber and configuration.  Intracranial flow voids are\npreserved.  There is no evidence of infarction.  No masses are seen.\n\nThere is extensive periventricular and subcortical FLAIR/ T2 hyperintensities,\nnonspecific, but likely related to chronic microangiopathy.\n\nThere has been a right lens replacement.  The paranasal sinuses are clear.",
            "output": "Subacute infarct involving the right MCA territory.  No evidence of\nhemorrhage."
        },
        {
            "input": "There are multiple enhancing lesions scattered throughout the diploic space of\nthe calvarium with the largest measuring up to 4.2 x 1.1 cm along the vertex\nof the right parietal bone and approximately 2.6 x 1.2 cm along the vertex of\nthe left parietal bone with destruction of the outer table and into the\noverlying scalp.  There is disruption of the inner table of the left parietal\nlesion with a soft tissue component extending and contacting the underlying\ndura (101:48 and 14:160).  There is associated underlying dural nodularity and\nthickening with a possible filling defect in the adjacent sagittal sinus (101:\n56).  This filling defect demonstrates increased T1 signal hyperintensity on\nthe precontrast images (02:12).\nThere are multiple enhancing intraparenchymal predominately T1 hypointense\nlesions throughout bilateral parietal lobes and bilateral cerebellar\nhemispheres with the largest measuring up to 1.1 x 1.2 cm along the vertex of\nthe right parietal lobe (14:143).  This lesion is T1 hyperintense on the\nprecontrast images with mild surrounding edema and associated hemorrhage . \nThere additional smaller T1 hyperintense lesions in the right cerebellar\nhemisphere with small foci of hemorrhage.  The largest enhancing lesion\nmeasures approximately 5 mm in the left parietal lobe (14:98).  There is no\nevidence of infarction or midline shift.  The ventricles and sulci are normal\nin caliber and configuration.",
            "output": "1. Multiple enhancing metastatic calvarial and intraparenchymal lesions\npredominantly in the bilateral parietal lobes and cerebellar hemispheres.\n2. Focal filling defect in the sagittal sinus with corresponding intrinsic T1\nsignal hyperintensity adjacent underlying the enhancing left parietal\ncalvarial lesion at the vertex is suspicious for nonocclusive sagittal sinus\nthrombus.\n3. Prominent enhancing left parietal skull lesion extending to the underlying\ndural margin with associated dural nodularity and thickening may represent\npachymeningeal involvement/invasion.\n4. No evidence of infarction, mass effect or midline shift.\n\nNOTIFICATION:  The findings including but not limited to the focus of\nhemorrhage were discussed with Dr.  ___. by ___, M.D. on\nthe telephone on ___ at 11:38 am, 10 minutes after discovery of the\nfindings."
        },
        {
            "input": "Multiple enhancing lesions within the left frontal, bilateral parietal, and\noccipital lobes, along with the right cerebellar hemisphere, some\ndemonstrating susceptibility artifact (for example, 14: 4, 21), appear\ndecreased in size from the prior study.  For example, a lesion within the\nright postcentral gyrus measures approximately 0.4 cm (16:138), previously 1.2\ncm.  A lesion within the right cerebellar hemisphere measures 0.5 cm,\npreviously 0.7 cm (16:26).  No new enhancing lesions are identified.\n\nMultiple enhancing lesions within the diploic space of the calvarium have\ndecreased in size, while others have increased in conspicuity or remained\nstable.  For example, a lesion within the right parietal bone, at the vertex,\nmeasures approximately 4.2 x 1.0 cm (17:40), similar in size.  A lesion within\nthe left parietal bone, at the vertex (___), appears decreased in size,\nmeasuring 1.6 x 0.7 cm, previously 2.6 x 1.2 cm.  Extension of this lesion to\nthe inner table of the calvarium appears less conspicuous.  A lesion within\nthe left parietal bone measures 0.6 cm (18:149), increased in conspicuity from\nprior.  A lesion within the left occipital bone measures 1.1 cm (16:43), also\nincreased in conspicuity.  Multiple other lesions appear grossly stable.\n\nNo evidence of acute intracranial hemorrhage or infarction.  The ventricles\nand sulci are mildly prominent, suggestive of age-related involutional change.\n\nMild mucosal thickening of the ethmoid air cells.  Otherwise, the paranasal\nsinuses, mastoid air cells, and middle ear cavities are grossly clear.  The\nmajor intracranial vessels are patent.  A nonocclusive filling defect within\nthe superior sagittal sinus appears slightly more conspicuous although the\noverall extent appears similar (16:144).  An additional focal, nonocclusive\nfilling defect is seen more superiorly within the superior sagittal sinus, at\nthe vertex (___).",
            "output": "1. Interval decrease in size of multiple enhancing lesions within the left\nfrontal, bilateral parietal, and occipital lobes, along with the right\ncerebellar hemisphere, measuring up to 0.5 cm, previously 1.2 cm.  No new\nenhancing intraparenchymal lesions identified.\n2. Mixed response of multiple enhancing lesions within the calvarium, some\nincreased in conspicuity, while others stable or decreased in size, as\ndescribed above.\n3. Interval increase in conspicuity of focal, nonocclusive filling defects\nwithin the superior sagittal sinus, which remain concerning for intraluminal\nthrombus."
        },
        {
            "input": "Again seen are multiple calvarial enhancing lesions compatible with\nmetastases.  These appear similar to or perhaps slightly increased in size\nsince ___.  Multiple enhancing brain lesions are no longer detected. \nFoci of high intensity on FLAIR are noted in the left frontal and right\nparietal lobes, best seen on image 20 of series 7 appear smaller than on the\nstudy of ___.  A left posterior temporal cortical focus also\nappears unchanged (series 7, image 13).\nThere is no evidence of hemorrhage or infarction.  No new lesions are\nidentified.",
            "output": "Enhancing brain parenchymal metastases are no longer detected.\nMultiple calvarial lesions, likely metastases, appear similar or perhaps\nslightly enlarged.\nNo new lesions identified."
        },
        {
            "input": "Punctate left precentral gyrus lesion (series 9, image 251) is unchanged.\n\n2 mm left parietooccipital lobe peripheral lesion (series 9, image 173)\ncorresponding to a subtle focus of gradient echo susceptibility artifact is\nre-identified, slightly more conspicuous when compared to prior exam, although\nthis may be secondary to differences in technique.\n\nThere are 2 punctate foci of enhancement in the left middle cerebellar\nhemisphere (series 9, image 78 and 82), not seen on prior examinations and is\nwithout associated FLAIR signal abnormality.\n\nAdditional supra and infra tentorial enhancing lesions described on\nexamination of ___ are no longer visualized.\n\nThere are multiple scattered punctate and gyriform foci of diffusion-weighted\nand FLAIR hyperintense signal involving the bilateral frontal and parietal\nlobes as well as left occipital lobe and right inferior cerebellar hemisphere.\nThe left occipital lobe lesions demonstrates mixed slow diffusion and T2 shine\nthrough.  The majority of the frontal and parietal lobe lesions demonstrates\nT2 shine through.  The findings are compatible infarcts, ranging from acute to\nsubacute.  These lesions do not demonstrate enhancement.\n\nScattered gradient echo susceptibility artifact compatible with hemorrhage\nproduct in regions of previously treated lesions are unchanged.  No new\nhemorrhage product.\n\nThe major intracranial flow voids are preserved.  The dural venous sinuses\nappear patent.\n\nMultiple calvarial lesions and of the left C2 vertebral body are\nre-identified.  The extracranial soft tissue component of the dominant vertex\ncalvarial lesions appears more conspicuous when compared to prior exam, now\nmeasuring approximately 4-5 mm in greatest thickness (series 900, image 25),\npreviously measuring approximately 2-3 mm.  The C2 lesion appears slightly\nmore conspicuous when compared to the prior examination, although this may be\nsecondary to differences in technique.\n\nMucosal thickening of the ethmoid air cells and frontal sinuses is mild.  The\norbits are unremarkable.  No significant fluid signal is seen in the mastoid\nair cells.",
            "output": "1. Punctate left precentral gyrus enhancing lesion is unchanged from prior\nexam.  Left parietooccipital lobe lesion appears slightly more conspicuous,\nhowever this may be secondary to differences in technique.\n2. 2 punctate foci of enhancement in the left middle cerebellar hemisphere is\nnot seen on prior examinations, however is without associated FLAIR signal\nabnormality.  While this could represent vasculature, recommend close\nattention to exclude new lesions.\n3. Additional enhancing lesions described on examination of ___\nare not visualized.\n4. Multiple calvarial lesions.  The extracranial soft tissue component of the\ndominant vertex calvarial lesions is larger when compared to prior exam now\nmeasuring approximately 4-5 mm in greatest thickness.\n5. A C2 left vertebral body lesion appears slightly more prominent, however\nthis may be secondary to differences in technique.  This could be further\nevaluated with dedicated examination.\n6. Findings compatible with a mix of acute to subacute infarcts involving the\nbilateral frontal and parietal lobes as well as left occipital lobe and right\ninferior cerebellar hemisphere.  No evidence of associated enhancement. \nRecommend continued follow-up to document resolution and clinical correlation\nis recommended.\n7. Additional findings described above.\n\nNOTIFICATION:  The findings were discussed with Dr.  ___, m.D. by\n___, M.D. on the telephone on ___ at 8:26 am, 5 minutes after\ndiscovery of the findings."
        },
        {
            "input": "When compared to MRI dated ___, there is continued evolution of\nseveral punctate foci of subacute infarcts in the bilateral corona radiata,\nleft parietal lobe and left cerebral hemisphere.  No new large vascular\ndistribution infarct is demonstrated.\n\nThe previously noted punctate left precentral gyrus lesion (9:251, on prior\nimage) and left parietooccipital lobe (9:173, on prior image) are not\nvisualized.  Similarly, the previously noted 2 punctate foci of enhancement in\nthe left middle cerebellar hemisphere (9:78 and 82, on prior image) are not\nvisualized.\n\nStable scattered susceptibility in the bilateral cerebral hemisphere, likely\nrepresent posttreatment changes.\n\nThere is no evidence of midline shift. The ventricles and sulci are stable in\ncaliber and configuration.\n\nNumerous calvarial osseous metastatic lesions, and left C2 vertebral body\nlesion appear unchanged.  There is also stable calvarial lesion involving the\nvertex.\n\nThere is mild mucosal of ethmoid air cells, otherwise the paranasal sinuses\nand mastoid air cells are clear.  The globes and orbits are unremarkable.",
            "output": "1. The previously noted punctate enhancing lesion in the left precentral\ngyrus, left parietooccipital lobe, and left middle cerebral hemisphere are no\nlonger visualized.  No new lesions are identified.\n2. Continued evolution of the previously noted several punctate foci of\nsubacute infarct.  No evidence of new infarct.\n3. Stable calvarial, and left C2 vertebral body osseous metastatic lesions.\n4. Additional findings as described above."
        },
        {
            "input": "There is no intra or extra-axial mass, acute hemorrhage or infarct. The\npituitary gland is prominent measuring 7 x 9 mm (CC, AP), but likely within\nexpected limits for a female patient.   Sulci, ventricles and cisterns are\nwithin expected limits for the patient's age. The major intracranial flow\nvoids are preserved. The paranasal sinuses are clear. The orbits are\nunremarkable. The mastoids are clear. No abnormal enhancement. The dural\nvenous sinuses are patent.",
            "output": "1. No evidence of intra or extra-axial mass.\n2. The pituitary gland is prominent, however within normal limits for a female\npatient.  Clinical correlation with endocrine laboratory values is\nrecommended."
        },
        {
            "input": "Study is mildly degraded by motion.  There is no evidence of hemorrhage,\nedema, masses, mass effect, midline shift or infarction.  There is prominence\nof the ventricles and sulci suggestive involutional changes.  Nonspecific\nbilateral mastoid air cell fluid is noted.  Bilateral maxillary sinus mucosal\nthickening with aerosolized mucus within the right maxillary sinus is noted. \nA of right posterior ethmoid air cell mucous retention cyst versus polypis\nseen.",
            "output": "1. Study is mildly degraded by motion.\n2.  No acute intracranial abnormality.\n3. No evidence of acute or subacute infarct.\n4.  Paranasal sinus disease as described, concerning for acute sinusitis.\n5. Nonspecific bilateral mastoid fluid."
        },
        {
            "input": "There is no evidence of acute hemorrhage, edema, masses, mass effect, midline\nshift or infarction.  An anterior falcine focus of susceptibility artifact\n(10:12) correlates with a focal calcification, as seen on prior head CT.  The\nventricles and sulci are within expected limits in caliber and configuration. \nScattered periventricular and subcortical FLAIR hyperintensities are\nnonspecific, possibly reflecting chronic ischemic small vessel disease,\nslightly advanced for age versus sequela of chronic headache such as migraine\nor prior infectious/inflammatory etiology.\nMild mucosal thickening of the ethmoid air cells.  Otherwise, the imaged\nparanasal sinuses are unremarkable.  The imaged orbits are unremarkable.  The\nmajor intracranial vasculature is patent.",
            "output": "1. No evidence of acute intracranial abnormality.  Specifically no acute\ninfarct or intracranial hemorrhage.  No intracranial mass or abnormal\nenhancement.\n2. Mild periventricular and subcortical T2/FLAIR scattered white matter\nhyperintensities are nonspecific, but can be seen with sequela of chronic\nheadache such as migraine, prior infectious/inflammatory etiology or\npotentially age advance chronic small vessel ischemic disease.  These are not\nin a pattern typical for demyelinating process.\n3. Other findings, as described above."
        },
        {
            "input": "FLAIR hyperintensities are seen in the both frontal lobes in the genu of\ncorpus callosum as on the previous MRI examination of ___.  However,\nthere are now 2 new areas of enhancement measuring 2.5 and 1.5 cm in the left\nfrontal lobe at the margin of previously biopsy site.  There is no restricted\ndiffusion visualized.  There is no evidence of enhancement within the corpus\ncallosum or right cerebral hemisphere.  Punctate area of hyperintensity seen\nin the left side of the midbrain on series 10, image 9 and 10 appears to be\nartifactual.",
            "output": "Markedly increased enhancement at the margin of biopsy site in the left\nfrontal lobe suggestive of tumor recurrence.  There is no significant change\nin mass effect seen.  No signs of acute or chronic hemorrhage.\n\nNOTIFICATION:  Findings discussed with Dr. ___ at 12:40 ___ on ___\nimmediately after the study."
        },
        {
            "input": "There are postoperative changes related to recent left frontal craniotomy and\nresection of the previously seen left frontal intraparenchymal lesion.  There\nare associated postoperative changes including intracranial pneumocephalus\nwith foci of susceptibility and blood within the resection cavity.  Evaluation\nfor enhancement on postcontrast T1 weighted images is markedly limited given\nthe motion artifact but no gross enhancing lesions are seen.  There is grossly\nstable surrounding FLAIR signal abnormality with midline shift towards the\nright by approximately 3 mm, unchanged compared to the prior study.\n\nNo new lesions are seen.\n\nThere is a 1.1 cm focus of slow diffusion along the inferior aspect of the\nresection cavity, likely reflecting surgical effect.\n\nThe orbits are unremarkable.  Intracranial flow voids are maintained. \nVisualized paranasal sinuses and mastoid air cells are clear.",
            "output": "1. Limited study given the motion artifact and limited sequence acquisition.\n2. Status post left frontal craniotomy and lesion resection with expected\npostoperative changes."
        },
        {
            "input": "Please note the study is mildly degraded by motion.\n\nMRI HEAD:  There is a large area of vasogenic edema within the left frontal\nlobe.  There is a small focus of restricted diffusion within the ___ the\nvasogenic edema.  There is mild, ill-defined enhancement scattered throughout\nthe area vasogenic edema.  There is mass effect on the involved sulci but no\ncompression of the ventricular system.  There is confluent T2/FLAIR\nhyperintensity in the right centrum semiovale, likely contralateral extension\nof vasogenic edema.  No definite blood products or mineralization are noted to\nbe associated with this process.\n\nMarrow signal is normal.  There is scattered mucosal thickening of the ethmoid\nsinuses.  The paranasal sinuses otherwise appear clear.  The mastoid air cells\nappear clear.  The orbits are normal.\n\nMRA HEAD: The major intracranial arteries appear normal with no evidence of\nstenosis, occlusion, or aneurysm formation.\n\nMRV HEAD:  The major dural venous sinuses are patent.  There is no stenosis or\nocclusion.",
            "output": "1.  Study is mildly degraded by motion.\n2. Left frontal, intra-axial, infiltrative process, with edema, mild\nenhancement with suggested extension from the left frontal lobe across corpus\ncallosum into right frontal lobe as described.  Differential considerations\ninclude astrocytoma, GBM, and cerebritis, with oligodendroglioma less likely. \nIf clinically indicated, consider repeat imaging with MR spectroscopy and\nperfusion image for further evaluation.  Recommend clinical correlation and\nattention on followup imaging.\n3. Normal MRA and MRV of the head.\n\nRECOMMENDATION(S):\n1. Left frontal, intra-axial, infiltrative process, with edema, mild\nenhancement with suggested extension from the left frontal lobe across corpus\ncallosum into right frontal lobe as described. Differential considerations\ninclude astrocytoma, GBM, and cerebritis, with oligodendroglioma less likely.\nIf clinically indicated, consider repeat imaging with MR spectroscopy and\nperfusion image for further evaluation. Recommend clinical correlation and\nattention on followup imaging."
        },
        {
            "input": "There is no evidence of acute intracranial hemorrhage.  The ventricles and\nbasal cisterns appear normal.\n\nThere are areas of slow diffusion throughout the left cerebellar hemisphere,\npredominantly within the left superior cerebellar artery distribution, though\nalso likely involving portions anterior and posterior inferior cerebellar\nartery distribution, compatible with subacute infarcts.  .  There is\nassociated edema and mild mass effect on the fourth ventricle.  There are no\nadditional areas of slow diffusion.  There is mild diffuse brain parenchymal\nvolume loss.\n\nThe orbits, mastoid air cells, and paranasal sinuses are unremarkable.",
            "output": "1. Subacute infarcts within the left cerebellar hemisphere, predominantly\ninvolving the left superior cerebellar artery territory, without evidence of\nhemorrhagic conversion although there is mild edema and mass effect on the\nfourth ventricle.\n2. Mild diffuse brain parenchymal volume loss.\n3.  Reviewed with Dr. ___."
        },
        {
            "input": "The aortic arch demonstrates conventional three-vessel branch configuration.\n\nThe left vertebral artery is occluded at its origin with minimal\nreconstitution within the V2 segment.  No flow seen within the V3 segment. \nThere is patulous flow within the V4 segment which is likely via retrograde\nfilling.  Given the minimal atherosclerotic vascular disease throughout the\nrest of the vessels, dissection is a more likely etiology although\natheromatous disease cannot be excluded.  There are the few areas of T1\nhyperintensity within the expected region of the left vertebral artery flow\nvoid on the fat saturated axial T1 images supporting dissection as an\netiology.\n\nThere is mild narrowing of the origin of the right vertebral artery.  The\nright vertebral artery otherwise appears patent throughout its course\nthroughout the neck.  The origins of the common carotid arteries and\nsubclavian arteries are patent.  The internal carotid arteries appear normal\nbilaterally.  There is no evidence stenosis by NASCET criteria.\n\nThere is an incompletely imaged left cerebellar infarct, better depicted on\nprior exams.\n\nThere are multiple bilateral thyroid nodules.",
            "output": "1. Occlusion of the left vertebral artery, beginning at its origin, with\nsegmental areas of reconstitution within the V2 and V4 segments.  Given the\nminimal atherosclerotic vascular disease throughout the rest of the vessels,\ndissection is a more likely etiology although atheromatous disease cannot be\nexcluded."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  Significant brain parenchymal atrophy, most prominent at the\nsylvian fissures, temporal, frontal lobes..  Significant atrophy of the\nmidbrain.  Prominent flow void in the cerebral aqueduct.  There is no abnormal\nenhancement after contrast administration.\n\nThere is moderate subcortical, deep and periventricular white matter T2/FLAIR\nhyperintensities are nonspecific but compatible with chronic small vessel\nischemic disease.  Linear FLAIR hyperintensity about posterior bodies, atria\nof the lateral ventricles may represent altered water content or chronic small\nvessel ischemic changes.\n\nThe major intracranial vascular flow voids are maintained.  There is mild\nmucosal thickening of the maxillary sinuses (right greater than left).  The\nmastoid air cells are normal.  There are bilateral lens replacements.",
            "output": "1. No acute intracranial abnormality.\n2. Moderate brain parenchymal atrophy\n3. Prominence of the ventricles may be in the basis of atrophy, consider\ncommunicating hydrocephalus.\n4. Moderate White matter chronic small vessel ischemic disease."
        },
        {
            "input": "Patent A-comm, bilateral PCOM.  The intracranial vertebral and internal\ncarotid arteries and their major branches appear normal without evidence of\nstenosis, occlusion, or aneurysm formation.",
            "output": "1. Normal brain MRA.  No aneurysm"
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are within expected limits in\ncaliber and configuration.  There is no abnormal enhancement after contrast\nadministration.\nNonenhancing, non restricting periventricular and subcortical white matter\nT2/FLAIR hyperintensities are overall similar to ___, nonspecific.\n\nThe major intracranial flow voids are preserved.\n\nThe dural venous sinuses appear patent without clot formation.\n\nThe paranasal sinuses demonstrate mild mucosal thickening of the ethmoid air\ncells.  The orbits are unremarkable.  Trace fluid opacification of the\nleft-greater-than-right mastoid air cells.  No suspicious marrow signal.",
            "output": "1. No dural venous sinus thrombosis identified.\n2. No acute intracranial abnormality on contrast enhanced MRI brain. \nSpecifically no intracranial hemorrhage or infarct.  No abnormal enhancement.\n3. Nonenhancing, non restricting periventricular and subcortical white matter\nT2/FLAIR hyperintensities are overall similar to ___.  In a patient\nof this age, these are nonspecific and may represent sequela of chronic\nheadache such as migraine, prior trauma/inflammatory etiology or small vessel\nischemic disease.  These are not in a distribution typical for demyelinating\nprocess."
        },
        {
            "input": "Previously noted sellar/ suprasellar mass has been resected.  There is\nenhancing material in the sella and suprasellar cistern, compatible with\npostsurgical changes, though residual tumor is not excluded. Within this\nmaterial, there is low signal on gradient echo images corresponding to\nhyperdense blood products seen on the postsurgical CT.  On the presurgical\nimaging, the mass had a left-sided component extending superiorly anterior to\nthe left thalamus and abutting the inferior surface of the left lateral\nventricle. Presently, there is fluid in this location. The frontal horn of the\nleft lateral ventricle and the anterior left aspect of the third ventricle\nremain distorted. Overall, the ventricles are stable in size without\nhydrocephalus. There is small amount of blood layering in the occipital horns\nof the lateral ventricles.\n\nThere is no evidence for an acute infarction, edema, mass effect, or\npathologic contrast enhancement in the brain parenchyma. The dura along the\nanterior aspects of the posterior fossa demonstrates high signal on FLAIR\nimages and contrast enhancement, without thickening, likely postsurgical.\nMajor arterial flow voids are grossly preserved. Major dural venous sinuses\nappear patent, allowing for hypoplasia of the left transverse and sigmoid\nsinuses, similar to the presurgical CTA.\n\nThere is fat packing in the sphenoid sinuses surrounded by fluid and mucosal\nthickening. There is mild mucosal thickening in bilateral maxillary sinuses\nwith a small amount of fluid in the right maxillary sinus. There is mild\nmucosal thickening in the right frontal sinus, and mild to moderate mucosal\nthickening in bilateral ethmoid air cells. There is minimal mucosal thickening\nin the right mastoid tip air cells.",
            "output": "1. S/p sellar/suprasellar mass resection with enhancing hemorrhagic material\nin the sella and suprasellar cistern, compatible with postsurgical change.\nfollow up Imaging is needed to exclude residual tumor. Please note that follow\nup would be best performed with a combination of complete brain MRI and\ndedicated pituitary MRI sequences.\n2. Small amount of blood in the occipital horns of the lateral ventricles.\nStable configuration of the ventricles with slight distortion of the left\nfrontal horn and left anterior third ventricle. No hydrocephalus."
        },
        {
            "input": "Right frontal lobe craniotomy is identified.  Small amount of blood products\nare seen in the region.  Compared to the prior study the FLAIR\nhyperintensities have decreased.  Again seen are areas of high signal\nintensity on diffusion images at the margin of the surgical cavity which is\ndecreased in size.  There remains some postcontrast enhancement in the region\n(09:20) which appears somewhat altered secondary to decrease in size of the\nsurgical cavity.  Change in the enhancement can be further evaluated on\nfollow-up study.  Mild pachymeningeal enhancement in the right frontal\nconvexity and in the interhemispheric region is unchanged.",
            "output": "Since the previous MRI study, FLAIR hyperintensities in the right frontal\npostoperative region have decreased.  Some areas of enhancement are again\nidentified.  Change in pattern of enhancement is difficult to assess given\nevolution of postsurgical changes.  This can be further assessed on the\nfollow-up examination."
        },
        {
            "input": "Right frontal postoperative changes are identified.  The margin of the\nsurgical cavity, enhancement is identified which appears to have slightly\ndecreased or is unchanged compared to the prior study.  The surrounding FLAIR\nhyperintensities are unchanged.  Diffuse hyperintensities in the white matter\ncould be due to combination of small vessel disease and post therapy changes. \nChronic blood products adjacent to the surgical site are also unchanged. \nThere is no midline shift or hydrocephalus.  No other areas of abnormal\nenhancement are seen.",
            "output": "Postsurgical changes are seen in the right frontal region.  Enhancement at the\nmargin of surgical cavity has minimally decreased to remain stable.  No new\nareas of abnormal enhancement seen.  FLAIR hyperintensities in the right\nfrontal region are unchanged."
        },
        {
            "input": "Right frontal postoperative changes are identified.  No significant interval\nchange of the linear and nodular enhancement at margin of the surgical cavity,\nwith the largest nodule area measuring approximately 3 x 4 mm in transverse\ndimension (series 16, image 17), close attention in this area is recommended. \nThe surrounding FLAIR hyperintensities are unchanged.  Diffuse\nhyperintensities in the white matter could be due to combination of small\nvessel disease and post therapy changes; unchanged.  Chronic blood products\nadjacent to the surgical site are also unchanged.  There is no midline shift\nor hydrocephalus.  Redemonstration of anterior right frontal and anterior\nsuperior falx pachymeningeal thickening and enhancement; likely postoperative.\nNo other areas of abnormal new enhancement are seen.\n\nNo acute intracranial abnormality.  There is no evolving acute hydrocephalus. \nThere is no mass effect or midline shift",
            "output": "1. Status post right frontal craniotomy with unchanged surgical margin nodular\nand linear postcontrast enhancement and surrounding FLAIR hyperintensity.\n2. No acute intracranial abnormality or new abnormal enhancement."
        },
        {
            "input": "Motion degraded examination.\n\nIn the right superior frontal gyrus, there is a 4.7 x 2.7 x 4.1 cm\nheterogeneous lesion with predominantly peripheral irregular and nodular\nenhancement, slowed diffusion, and susceptibility artifact reflecting small\namounts of hemorrhage (series 20, image 92).  In the slightly more anterior\nright superior/medial frontal gyrus, there is a 1.3 x 1.2 x 1.0 cm enhancing\nlesion with slow diffusion (series 20, image 95).  In the slightly more\nanterior and inferior right medial frontal gyrus, there is a 4 mm enhancing\nlesion.  There is a substantial amount of vasogenic edema throughout the right\nfrontal lobe with effacement of the right frontal lobe sulci and minimal\neffacement of the adjacent right lateral ventricle.  No midline shift.  The\nbasal cisterns are patent.\n\nNo evidence of acute infarction.  Periventricular and subcortical white matter\nT2/FLAIR hyperintensities are nonspecific but likely sequelae of chronic small\nvessel ischemic disease.  The dural venous sinuses are grossly patent. \nIntracranial flow voids are grossly preserved.  Mucosal thickening of all\nparanasal sinuses is noted.",
            "output": "1. Motion degraded examination.\n2. Right frontal lobe with findings concerning for blood products versus\nmineralization 4.7 cm and two adjacent enhancing lesions measuring up to 1.3\ncm and 0.4 cm, concerning for primary or metastatic neoplasm.\n3. Right frontal vasogenic edema as described, with effacement of right\nfrontal sulci and minimal effacement of the right lateral ventricle and no\ndefinite midline shift."
        },
        {
            "input": "Postsurgical changes after right frontal craniotomy for resection of a right\nparasagittal frontal lobe mass are noted.  Surrounding the resection cavity\nand slightly extending into the posterior frontal lobe, there is devitalized\ntissue as well as some blood products.  There is no significant change in\nextent of the previously seen FLAIR hyperintensity involving the right frontal\nlobe.  ___ patchy and confluent areas of periventricular FLAIR hyperintensity\nare unchanged and most likely reflect sequela of chronic small vessel ischemic\nchanges.\nThere is a small amount of nodular enhancement just superior and anterior to\nthe right frontal horn (series 13, image 113) and two small foci of nodular\nenhancement in the right parasagittal frontal lobe (series 13, image 128 and\n126) which could represent residual tumor and attention on follow-up is\nrecommended.\nMild enhancement about the resection cavity is most likely postsurgical.\n\nThe ventricles are notable for small amount of postsurgical blood products\nlayering in the ventricular occipital horns (series 10, image 12).\nMajor vascular flow voids are preserved.  Major dural venous sinuses are\npatent.\n\nThere is mild mucosal thickening along the ethmoid air cells and in the\nbilateral maxillary sinuses.  There is also partial opacification of the\nbilateral mastoid air cells.  The orbits appear unremarkable.",
            "output": "1. Expected postsurgical changes after right frontal craniotomy for resection\nof a right parasagittal frontal lobe mass with residual areas of nodular\nenhancement, as detailed above, which could represent residual tumor and\nattention on follow-up is recommended.\n2. Mild paranasal sinus disease and bilateral partial opacification of the\nmastoid air cells."
        },
        {
            "input": "There is motion artifact which degrades spatial resolution which is most\nsignificant on the sagittal T1 sequence.\n\nThere is extensive confluent periventricular with white matter FLAIR\nhyperintensity consistent with sequela of chronic microangiopathy.  There are\nfoci of FLAIR hyperintensity within the basal ganglia bilaterally consistent\nwith prior ischemic change.\n\nThere are small focus of diffusion weighted hyperintensity at the right\nfrontal mid corona radiata (05:53) and more superiorly (series 5, image 54)\nwith subtle associated ADC hypointensity compatible with punctate infarcts in\nthe late acute to subacute range.  There is prominence of the ventricles and\ncortical sulci consistent with volume loss.  The vasculature is patent.  There\nis no abnormal postcontrast enhancement.\n\nThe bilateral lenses are absent.  The calvarium and soft tissues are\nunremarkable.  There is an endotracheal tube in place.  There is mild mucosal\nthickening within the paranasal sinuses with dependent fluid in the sphenoid\nsinus.  There is fluid layering within the pharynx.  There are bilateral\nmastoid air cell effusions.",
            "output": "1. Punctate foci of slow diffusion in the right frontal corona radiata,\ncompatible with infarcts, presumably late acute to subacute.\n2. Sequela chronic microangiopathy with volume loss.\n\nNOTIFICATION:  The findings were discussed by Dr. ___ with Dr.\n___ on the ___ ___ at 3:25 ___, 20 minutes after discovery of\nthe findings."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, or infarction.\nThe ventricles and sulci are dilated compatible with age-related parenchymal\nvolume loss. There are scattered foci of T2/FLAIR signal hyperintensity in the\nperiventricular, subcortical, and deep white matter which is nonspecific but\nlikely on the basis of chronic small vessel ischemic disease. Similar\nhypointensity is noted within the pons and also likely reflective of chronic\nsmall vessel ischemic disease.  An empty sella is incidentally noted. There is\nno abnormal enhancement after contrast administration.\n\nMajor vascular flow voids are preserved. Patient is status post bilateral lens\nreplacement. There is minimal mucosal thickening within the ethmoid air cells.\nThe remaining paranasal sinuses and mastoid air cells are clear.\n\nThere is a 7 mm well-defined lesion in the clivus which is noted to have a\nsclerotic border on head CT. This is stable when compared to head CT dated\n___. This is felt most likely to represent a benign lesion.",
            "output": "1. No evidence of acute infarction, acute hemorrhage, or enhancing mass\nlesion.\n2. T2/FLAIR signal hyperintensity in the periventricular, subcortical, and\ndeep white matter which is nonspecific but most likely secondary to chronic\nsmall vessel ischemic disease."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  Mild chronic small vessel ischemic change.  Prominent\nprevascular spaces..  Trace mucosal thickening paranasal sinuses.  Clear\nmastoids.  Preserved vascular flow voids",
            "output": "1. Mild chronic small vessel ischemic change"
        },
        {
            "input": "There is no evidence of intracranial hemorrhage, mass, mass effect or shifting\nof the normally midline structures. The ventricles and sulci are normal in\nsize and configuration for the patient's age. There is minimal asymmetry in\nthe position of the cerebellar tonsils, previously detected by head CT, in the\nsagittal views the left cerebellar tonsil appears slightly more inferior\nthroughout the foramen magnum at 3.8 mm, which is considered within normal\nlimits, and in the superior aspect of the cervical spinal cord there is no\nevidence of syrinx. No diffusion abnormalities are detected, there is no\nevidence of abnormal enhancement. The major vascular flow voids are present\nand demonstrate normal distribution. The orbits are unremarkable, the\nparanasal sinuses demonstrate mild mucosal thickening in the ethmoidal air\ncells bilaterally with no evidence of air-fluid levels, the mastoid air cells\nare clear.",
            "output": "There is no evidence of acute intracranial process, there is no evidence of\nabnormal enhancement. Minimal asymmetry in the position of the cerebellar\ntonsils, previously demonstrated by head CT, however, there is no frank\nevidence of Chiari malformation."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.\n\nMild mucosal sinus thickening is seen involving the ethmoid air cells.  The\nremainder the visualized paranasal sinuses, mastoid air cells, and middle ear\ncavities are clear.  The orbits are unremarkable.  The principal vascular flow\nvoids appear to be well preserved.  The dural venous sinuses are patent on\npostcontrast MP-RAGE.",
            "output": "1. No acute intracranial abnormalities identified.  No concerning enhancing\nlesions seen.\n2. No definitive osseous lesions identified."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.  There is no abnormal focus of slowed diffusion.  The\nprincipal intracranial vascular flow voids are preserved.  The dural venous\nsinuses are patent on MP-RAGE images.\n\nThe paranasal sinuses are grossly clear.  The orbits are grossly unremarkable.\nThe mastoid air cells are clear.",
            "output": "1. No evidence of intracranial metastatic disease at this time.\n2. No acute intracranial abnormality including acute infarct or hemorrhage."
        },
        {
            "input": "Centered in the right temporoparietal lobe is a heterogeneously enhancing and\nlobulated hemorrhagic 5.5 x 5.7 x 4.6 cm (AP, TRV, CC) mass with significant\nsurrounding vasogenic edema pattern involving the right temporal, frontal,\nparietal lobes as well as the lateral aspects of the right basal ganglia.\nThere are smaller foci of nodular enhancement medial to the dominant mass\nmeasuring up to 8 mm. There is right hemispheric sulcal effacement as well as\napproximately 1 cm leftward midline shift. Severe effacement of the right\nlateral and third ventricles as well as mass effect on the left lateral\nventricle is noted. Effacement of perimesencephalic cisterns with mild right\nuncal herniation with mass effect on the brainstem (series 11, and 11) is\nnoted. The degree of mass effect and uncal herniation is not significantly\nchanged from outside hospital CT examination allowing for technical\ndifferences.\n\nThere is no evidence of acute infarct. The major intracranial flow voids are\npreserved.  The dural venous sinuses are patent. There is a small mucous\nretention cyst in the right maxillary sinus otherwise the paranasal sinuses\nare essentially clear. The orbits are unremarkable. The mastoid air cells are\nclear.",
            "output": "1. There is a hemorrhagic and enhancing 5.7 cm right temporoparietal lobe\nmass.  Differential considerations include primary CNS malignancy such as GBM.\n2. The mass results and significant surrounding vasogenic edema pattern with\ndiffuse right hemispheric sulcal effacement, 1 cm left fourth midline shift,\neffacement of the perimesencephalic cisterns and right lateral ventricle with\nmass effect on the brainstem. Mild left uncal herniation is noted.\n3. The degree of midline shift and uncal herniation is similar in appearance\nto CT examination of 1 day prior allowing for technical differences."
        },
        {
            "input": "External fiducial markers are noted.\n\nCentered in the right temporoparietal lobe is a heterogeneously enhancing and\nlobulated mass measuring approximately 5.5 x 5.7 x 4.6 cm (AP, TRV, CC) and 2\nsmall satellite lesions medially measuring up to 9 mm with significant\nsurrounding edema pattern involving the right temporal, frontal and parietal\nlobes as well as the right basal ganglia. There is diffuse right hemispheric\nsulcal effacement with approximately 1 cm leftward midline shift. Severe\neffacement of the right lateral and third ventricles are noted. Effacement of\nthe perimesencephalic cisterns with mass effect on the brainstem (series 2,\nimage 48) is similar in appearance to prior CTA and MR by of ___.\nThere is mild right uncal herniation, also unchanged from prior exam.\n\nThe dural venous sinuses are patent. A mucous retention cyst is seen in the\nright maxillary sinus. The orbits are unremarkable. The mastoid air cells are\ngrossly clear.\n.",
            "output": "1. Heterogeneously enhancing 5.7 cm right temporoparietal lobe mass with\nadjacent small satellite lesions are unchanged in appearance from exams 1 day\nprior.\n2. Unchanged appearance of right hemispheric sulcal effacement, 1 cm leftward\nmidline shift and effacement of the perimesencephalic cisterns with mass\neffect on the brainstem. Mild right uncal herniation is also unchanged."
        },
        {
            "input": "There is been interval right frontotemporal craniotomy with resection of the\npatient's previously known right temporoparietal lobe mass.  Postoperative\nchanges in the scalp a and calvarium are reidentified. Blood products are\nnoted within the surgical bed not significantly changed compared with\npostoperative CT allowing for technical differences. Enhancement at the\nsurgical site cannot be properly assessed due to pre-contrast increased T1\nsignal at the surgical bed.  However, there is no enhancement outside of the\nregion with high pre-contrast T1 signal to suggest residual mass. Surrounding\nFLAIR hyperintensity is also not significantly changed from pre operative\nexamination. A thin layer of T1/FLAIR bright material along the dura of the\nright hemisphere likely represents hemorrhagic products.\n\nOtherwise there is no significant interval change in the degree of leftward\nshift of midline structures compare with postoperative CT, measuring\napproximately 5 mm at the foramen of ___.  There is no hemorrhage,\ninfarction, or enhancing masses elsewhere in the brain.  The brainstem,\nposterior fossa and cervico-medullary junction are preserved. The orbits are\nwithin normal limits.  A mucous retention cyst is seen in the right maxillary\nsinus. The remaining paranasal sinuses are clear.",
            "output": "1.  Expected postoperative changes related to right frontotemporal craniotomy\nfor resection of temporoparietal lobe mass. Blood products within the surgical\nbed are not significantly changed compared with the postoperative CT allowing\nfor technical differences.\n\n2.  Enhancement at the surgical site cannot be properly assessed due to T1\nbright blood products at the surgical bed.  However, there is no enhancement\noutside of the region with high pre-contrast T1 signal to suggest residual\nmass.\n\n3.  Thin layer of T1/FLAIR bright material along the dura of the right\nhemisphere is compatible with minimal subdural blood products redistributed\nfrom the surgical site.\n\n4.  Stable leftward shift of midline structures."
        },
        {
            "input": "Again seen are postoperative changes in the right temporal lobe. There is\nhemorrhage at the surgical site with no evidence of new hemorrhage since the\nprior examination. However, there has been an increase in edema since the\nstudy of ___. There is a dramatic increase in the volume of\nenhancing tissue in a ring-like pattern in some ways reminiscent of the\npreoperative appearance. The extent of infiltration in the right temporal lobe\nappears to have increased since the prior study. There is now a focus of white\nmatter hyperintensity in the left posterior parietal region, new since the\nprior examination. Together, these findings imply rapid tumor progression.\nImages of the remainder of the brain appear unchanged. No other lesions are\ndetected.  There is no evidence of infarction or other masses.",
            "output": "Rapid increase of right temporal lobe enhancement and edema has suggesting\ntumor progression. New focus of white matter hyperintensity in the left\nposterior parietal region."
        },
        {
            "input": "The enhancing mass in the right posterior temporal lobe has markedly decreased\nin size from the prior exam on ___.  The approximate size of the\nmass is 4.0 x 2.1 x 1.0 cm (AP x TV x SI) compared to 4.0 x 4.9 x 2.4 cm on ___.  Surrounding FLAIR signal abnormality has also mildly decreased. \nThere is no increased perfusion on ASL imaging.  There is no increased\ncerebral blood volume or cerebral blood flow on contrast enhanced perfusion\nimaging.  However, within an area of FLAIR signal abnormality, there is\ndecreased NAA and increased choline consistent with tumor on single voxel\nspectroscopy.  Within this area on multi voxel spectroscopy There is also\nmildly elevated choline (voxel 9 and 10).\n\nMajor intravascular flow voids are preserved.  There is normal enhancement of\nthe major intracranial arteries and dural venous sinuses following contrast\nadministration.\n\nMarrow signal is normal.  There is a retention cyst in the right maxillary\nsinus that contains T1 hyperintense and T2 hypointense material, consistent\nwith proteinaceous material or fungal colonization.  This is unchanged from\nthe prior MRI and multiple prior studies dating back to ___.",
            "output": "Decreased size of the right temporal lobe mass compared to prior MRI from ___.  Although the mass does not demonstrate increased perfusion on ASL\nimaging or increased cerebral blood volume, there is increased choline\nconsistent with tumor on MR spectroscopy.  So although the size of the mass\nhas decreased, tumor still remains present."
        },
        {
            "input": "There is no evidence of restricted diffusion.  Enhancement of the inferior\nposterior aspect of the right temporal horn is slightly less apparent when\ncompared to prior MR examination which can be attributed to differences in\ntechnique and can be assessed on follow-up examination.  There is no evidence\nof increased brain perfusion or focal abnormality on MR perfusion an ASR\ntechniques.  Spectral analysis of the right posterior temporal lobe indicates\nincreased choline peaks in the area of enhancement which are unchanged from\nprevious examination.  T2 and inversion recovery hyperintensity within the\nright periventricular white matter is most consistent with post radiation\nchanges.  Ex vacuo dilation of the occipital horn of the right ventricle is\nunchanged.  There is no evidence of mass effect or midline shift. Normal flow\nvoids are present.  There is a right maxillary sinus mucous retention cyst.",
            "output": "1. No evidence of recurrence or significant change from prior examination.\n2. Stable post surgical and post radiation changes."
        },
        {
            "input": "MR BRAIN:  The patient is status post right parietotemporal craniotomy and\nresection of a mass with increasing, heterogeneous enhancement within the\npostoperative bed, measuring 4.1 x 2.9 x 0 1.2 cm, previously measuring 3.4 x\n1.8 x 1.1 cm.  The chronic blood products within the resection cavity are\nunchanged.  The surrounding T2/FLAIR hyperintense signal on the right\noccipital, temporal, parietal, and frontal lobes has slightly increased in\nextent, particularly in the right frontal lobe.  The mild dural thickening\nenhancement underlying the craniotomy site is unchanged.  The ex vacuo\ndilatation of the atrium and temporal horn of the right lateral ventricle is\nunchanged.  The periventricular and subcortical T2/FLAIR hyperintensities in\nthe left frontal and parietal lobes are unchanged from the prior examinations.\nNo new enhancing lesions are identified.\n\nThere is no evidence of acute intracranial hemorrhage, midline shift or\ninfarction.\n\nThere is mild mucosal thickening in the bilateral ethmoid sinuses.  The right\nmaxillary sinus contains a small mucous retention cyst.  The orbits are\nunremarkable.\n\nThe major intracranial flow voids are preserved.\n.\nMR ___: There is no increased cerebral blood flow or blood\nvolume.\n\nASL Perfusion: There is increased perfusion in the right medial temporal lobe\non 04:11.\n\n\nMR Spectroscopy: Multi voxel spectroscopy demonstrates decreased metabolites\nin the right posterior parietal and temporal lobes, likely artifactual due to\nthe proximity of the voxels to the petrous bone.  Single voxel spectroscopy in\nthe area of enhancement in the right temporal lobe is nondiagnostic.",
            "output": "1. Postsurgical changes with increasing, heterogeneous enhancement within the\npostoperative bed in the right temporal and parietal lobes with increasing,\nsurrounding T2/FLAIR hyperintense signal as well as increased perfusion on\nASL, likely representing tumor progression.\n2. No new enhancing lesions.\n\nNOTIFICATION:  The impression and recommendation above was entered by Dr.\n___ on ___ at 11:04 into the Department of Radiology critical\ncommunications system for direct communication to the referring provider."
        },
        {
            "input": "MR BRAIN:  Again seen is a large enhancing mass in the right temporal lobe. \nThis has enlarged since the study of ___.  This is associated\nwith an increase in edema spreading widely throughout the right hemisphere. \nThe diffusion coefficient in this region is similar to normal brain.  There is\nno evidence of new hemorrhage, .\n.\nMR ___: There is elevation of blood flow and blood volume in\nthe right temporal lobe tumor..\n\nASL Perfusion: There is marked increase in blood flow in the right temporal\nlobe tumor has compared to the study of ___..\n\n\nMR Spectroscopy: There is a marked increase in choline in and several voxel is\na overlying the enhancing portion of the tumor.\n\nOverall, these findings indicate tumor progression.",
            "output": "1. Progressive increase in the volume of enhancing tumor, edema, blood flow\nand blood volume in the right temporal mass.  Elevated choline in multiple\nspectroscopic voxel is a in this area.  Overall, the findings indicate tumor\nprogression."
        },
        {
            "input": "MR BRAIN:  Right parietal craniotomy is re-identified.  Underlying\nheterogeneously enhancing right temporal lobe mass measuring approximately 6.3\nx 4.8 x 3.4 cm (series 1200b, image 58; series 1201b, image 77; AP, TRV, SI)\nhas significantly increased in size from prior exam where it measured 4.9 x\n4.3 x 2.3 cm.  The lesion extends to the ependymoma surface of the occipital\nand temporal horn of the right lateral ventricle.  Interval development of\nmultiple foci of gradient echo susceptibility within the lesion, compatible\nwith interval micro hemorrhage.  No definite new enhancing lesions are\nidentified.  There is no acute infarct.  The major intracranial flow voids are\npreserved.  The dural venous sinuses are patent.  Mild mucosal thickening of\nthe ethmoid air cells is identified.  The orbits are unremarkable.  The\nmastoid air cells are clear.\n\nMR ___: As on prior examination, the right temporal lobe mass\ndemonstrates elevated blood flow and volume.\n\nASL Perfusion: As on prior examination, the right temporal lobe mass\ndemonstrates increased perfusion on ASL.\n\nMR Spectroscopy: Single voxel spectroscopy centered over the anterior aspect\nof the enhancing lesion is technically limited secondary to incomplete\ndepression of water.  Multi voxel spectroscopy centered over the medial aspect\nof the enhancing mass and the midbrain demonstrates elevated choline to NAA\nratio in voxel 1 (7.1), voxel 2 (2.2), voxel 6 (6.1), voxel 7 (4.6), and voxel\n11 (3.2), with overall paucity of metabolites compatible with residual tumor\nstatus posttreatment.",
            "output": "1. Progressive interval increased in size of right temporal lobe enhancing\nmass now measuring approximately 6.3 cm in greatest dimension compared to\npreviously measured 5.0 cm.  The lesion demonstrates increased perfusion on\ndynamic contrast susceptibility and ASL perfusion as well as increased choline\nto NAA ratio on multiple voxel centered over the lesion.\n2. The findings are highly concerning for tumor progression.  No new lesions\nare identified."
        },
        {
            "input": "Right parietal craniotomy is re-identified.  Underlying heterogeneously\nenhancing right temporal lobe mass measuring approximately 6.2 x 4.4 x 3.1 cm\n(AP, TRV, SI) is similar in appearance to examination of ___ but\nincreased in size from examination ___.  As before, the lesion\nextends to the hip abnormal surface of the occipital and temporal horn of the\nright lateral ventricle.\n\nA new punctate focus of right putamen slow diffusion (series 302, image 15;\nseries 300, image 15) is identified with suggestion of subtle linear\nenhancement on MP RAGE (series 4, image 43).  It is uncertain whether this\nrepresents a region of infarct or potentially new lesion as the linear\nenhancement appears to be vascular nature.  Close attention on followup is\nrecommended.\n\nThere is scattered regions of slow diffusion within the inferior posterior\naspects of enhancing lesion (series 302, image 12), not seen on prior\nexamination, potentially representing sequela of previously seen hemorrhages\nwithin the lesion.\n\nThe visualized paranasal sinuses are clear.  The orbits are unremarkable.  The\nmastoid air cells appear clear.  The dural venous sinuses remain patent.",
            "output": "1. Right temporal lobe heterogeneously enhancing mass measuring approximately\n6.2 cm in greatest dimension is similar appearance to prior examination of ___ but increased in size since ___.\n2. There is slow diffusion within the inferior posterior aspects of the mass,\nnot seen on prior examination, potentially representing sequela of previously\ndescribed new hemorrhages.\n3. A new punctate focus of right putamen slow diffusion.  It is uncertain\nwhether this represents a small infarct versus new lesion (aggressive disease\nprogression could present with slow diffusion), as there is no clear\nassociated enhancement.  There is linear enhancement within the region of slow\ndiffusion however this may simply represent a prominent vessel.  Close\nattention on followup is recommended.\n\nRECOMMENDATION(S):  The impression and recommendation above was entered by Dr.\n___ on ___ at 18:16 into the Department of Radiology critical\ncommunications system for direct communication to the referring provider."
        },
        {
            "input": "MR BRAIN:  Right parietal craniotomy is re-identified.  5.9 x 5.0 x 3.0 cm\n(AP, TRV, SI; series 1200b, image 58; series 1201b, image 76) heterogeneously\nenhancing right temporal lobe mass with extension along the ependyma surface\nof the temporal and occipital horn of the right lateral ventricle is minimally\ndecreased to stable in size from pre CyberKnife examination of ___. \nThe degree of enhancement appears less confluent when compared to prior exam. \nThe degree of surrounding diffuse FLAIR hyperintense white matter signal is\nessentially unchanged in configuration from examination of ___. \nPreviously described punctate focus of diffusion-weighted hyperintensity of\nthe right putaminal has resolved.  Scattered foci diffusion-weighted\nhyperintense signal along the inferior aspects of the lesion is associated\nwith gradient echo susceptibility blooming, presumably representing hemorrhage\nproduct.  Interval increased number of punctate micro hemorrhages within the\nlesion itself when compared to prior examination.  No new lesions.  No acute\ninfarct.\n\nIncrease confluence and conspicuity of superimposed periventricular\nsubcortical T2/FLAIR white matter hyperintensities, particularly in the left\nfrontal lobe, compatible with post radiation and chemotherapy changes.\n\nThe sulci, ventricles and cisterns are otherwise within expected limits. \nIntracranial flow voids are preserved.  The dural venous sinuses are patent. \nMild mucosal thickening of the maxillary sinuses and ethmoid air cells is\nidentified.  The orbits are unremarkable.  The mastoid air cells are clear.\n\nMR ___: Allowing for technical differences, apparent decreased\nperfusion in the right temporal lobe when compared to prior exam.\n\nASL Perfusion: Re-identified is increased perfusion on ASL in the right\ntemporal lobe, which also appears to be slightly decreased from prior exam.\n\nMR Spectroscopy: MRI of spectroscopy is essentially nondiagnostic secondary to\ntechnical failure, although there does appear to be increased lactate peak on\nsingle voxel spectroscopy.",
            "output": "1. Right temporal lobe heterogeneously enhancing mass with extension along the\nependymal surface of the temporal and occipital horn of the right lateral\nventricle is similar to slightly decreased in size from pre CyberKnife\nexamination.  The degree of enhancement does appear slightly less confluent.\n2. Interval increased number of micro hemorrhages within the lesion. \nScattered diffusion-weighted hyperintense signal along the inferior aspect of\nthe lesion is associated with the hemorrhages.  However aggressive disease can\ndemonstrate restricted diffusion and close attention on followup is\nrecommended.\n3. There remains elevated perfusion on ASL, slightly decreased from prior exam\ncompatible with residual tumor.\n4. MRI spectroscopy is essentially nondiagnostic secondary to technical\nfailure.\n5. Interval resolution of previously described slow diffusion of the right\nputaminal."
        },
        {
            "input": "MR BRAIN:  Again seen is a large inhomogeneous mass in the posterior right\ntemporal lobe along with stable postoperative changes.  Again seen is\nextensive hyperintensity of the white matter surrounding this area on FLAIR\nand T2 weighted images.  Given the diagnosis, this likely represents a\ncombination of edema and tumor infiltration.  There is also extensive\nperiventricular white matter hyperintensity bilaterally, likely due to\ntreatment effect.  The right posterior temporal neoplasm enhances in\nhomogeneously in a pattern that is similar to that on the most recent prior\nbrain MR of ___, but is less homogeneous than on older studies.\nThere is predominantly fast diffusion in the region of the tumor and in the\nmore extensive white matter abnormality present bilaterally.  Overall, these\nfindings suggest no evidence of tumor progression and perhaps treatment effect\naccounting for much of the white matter abnormality and a component of the\nright posterior temporal lobe enhancing abnormality.\n.\nDynamic susceptibility contrast Perfusion: There is no elevated blood volume\nin the region of the tumor..\n\nASL Perfusion: There is unchanged broad elevation in blood flow in the right\nposterior temporal lesion..\n\n\nMR Spectroscopy: Spectroscopy through the region of the tumor demonstrates no\ndetectable metabolites, suggesting extensive necrosis..",
            "output": "1. No evidence of tumor progression.  There is persistent elevated blood flow\nto suggested tumor as well as extensive enhancement that may be a combination\nof tumor and treatment effect."
        },
        {
            "input": "MR BRAIN:  In the posterior right temporal lobe, again seen is a large\nheterogeneous mass with irregular peripheral enhancement in central T1 hypo\nintensity and punctate susceptibility artifacts likely due to hemorrhage,\nsurrounded by extensive T2/FLAIR hyperintensity and postsurgical changes.  The\nmass is difficult to measure.  Extensive bilateral periventricular white\nmatter T2/ FLAIR hyperintensity may reflect posttreatment changes.   However,\nthere is increase in edema and enhancement in the inferior right basal\nganglia, internal capsule, and white matter surrounding the right antrum and\noccipital horn (13:14, 12:14, 1400b:54, 67 versus 10:15, 11:15, 1200b:63, 72 )\nsince ___.  The overall peripheral enhancement in other areas appear\nsomewhat decreased, which may be secondary to contrast bolus timing.  Mild\nmass effect on the right occipital horn is unchanged.  The tumoral region\ncontinues to demonstrate predominantly fast diffusion.  There is no evidence\nof midline shift or infarction.  There is prominence of the ventricles and\nsulci suggestive involutional changes.\n\nMR ___: In the area of new increased enhancement in right basal\nganglia, and periventricular white matter, there is relative increased blood\nflow (1000:9, 10, 11).\n\nASL Perfusion and DSC contrast perfusion: There is i mild increased profusion\nin the region of right basal ganglia (05:11) and in the right temporal region.\n\nMR Spectroscopy: Spectroscopy through the region of tumor again demonstrates\nno detectable metabolites in the regions of interest number 12 and 20, and and\nincreased lactate in the region of interest 21 suggestive of necrosis.",
            "output": "1. New mild pattern of enhancement in the inferior right basal ganglia, and\naround the right occipital horn, with mild increased ASL and blood flow to the\narea, concerning for tumor progression."
        },
        {
            "input": "Study is mildly degraded by motion.\n\nCompared to ___, mild interval increase in multiple periventricular\nand subcortical deep white matter T2/FLAIR hyperintensities.  No evidence of\nenhancement to suggest acute demyelination.  There are a few T1 hypointense\nfoci, consistent with burned-out lesions.\n\nNo evidence of leptomeningeal or parenchymal infection.  There is no evidence\nof hemorrhage, edema, masses, mass effect, midline shift or infarction.   The\nventricles and sulci are normal in caliber and configuration.  There is no\nabnormal enhancement after contrast administration.  There are few prominent,\nthough nonenlarged, right intraparotid lymph nodes (___).  There is\nbilateral, left greater than right, mucosal thickening of the maxillary\nsinuses.  There is moderate mucosal thickening of the bilateral, right greater\nthan left sphenoid sinuses.  There is minimal mucosal thickening in the\nbilateral anterior ethmoidal air cells.  Mastoid air cells are clear.",
            "output": "1. Study is mildly degraded by motion.\n2. No evidence of leptomeningeal or parenchymal infection, as clinically\nquestioned.  No hemorrhage, edema, mass, mass effect, midline shift or\ninfarction.\n3. Compared to ___, mild interval increase in multiple\nperiventricular and subcortical deep white matter T2/FLAIR hyperintensities\nwithout enhancement to suggest acute demyelination."
        },
        {
            "input": "Images through the internal auditory canal demonstrates symmetric appearance\nof the seventh eighth nerve complexes.  No evidence of abnormal enhancement or\nmass lesion within the internal auditory canals, cerebellopontine angles or\nmembranous labyrinth. No other mass lesions are seen within the posterior\nfossa.  The internal auditory canals are not expanded.\n\nLimited included imaging of the remainder of the brain demonstrates no\nevidence of hemorrhage, edema, masses, mass effect, midline shift or  acute\ninfarction.  Bilateral white matter foci of T2/FLAIR signal prolongation are\nnonspecific but can be seen as sequelae of chronic small vessel ischemic\ndisease, vasculitis, or demyelinating disease in the appropriate clinical\nsetting.  The ventricles and sulci are normal in caliber and configuration. No\nabnormal enhancement after contrast administration.\n\nMajor intracranial vascular flow voids appear preserved.\n\nNo osseous abnormalities are seen. The anterior nasal septum is deviated to\nthe left.  There is concha bullosa of the right middle turbinate.  Mucosal\nthickening of the bilateral maxillary sinuses is mild.  Some of the ethmoidal\nair cells are partially opacified.  The remaining imaged paranasal sinuses are\nclear.  The mastoid air cells and middle ear cavities are clear.  The orbits\nare unremarkable.",
            "output": "1. No evidence of IAC or cerebellopontine angle mass.\n2. Nonspecific bilateral white matter T2/FLAIR signal prolongation.  The\ndifferential includes sequelae of chronic small vessel ischemic disease,\ndemyelinating disease, or vasculitis in the appropriate clinical setting. \nCorrelate with clinical assessment.\n3. Left nasal septal deviation.\n4. Mild paranasal sinus disease."
        },
        {
            "input": "Please note the study is mildly degraded by motion.\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  The ventricles and sulci are prominent.  There is mild hazy T1\nhyperintense signal in the bilateral globus pallidi.  There is no abnormal\nenhancement after contrast administration.  The major vascular flow voids are\npreserved.  No definite seizure focus identified, although limited in\nevaluation by motion artifact.\n\nThe mastoid, paranasal sinuses and orbits are normal.  The visualized soft\ntissues are normal.",
            "output": "1. Cerebral atrophy, out of proportion for age, which may be secondary to\nalcohol abuse, given clinical history.\n2. Hazy abnormal signal in the bilateral globus pallidi which is likely\nsecondary liver disease, given history.\n3. No definite seizure focus identified, although limited in evaluation by\nmotion artifact.\n4. No acute infarct, hemorrhage or intracranial mass."
        },
        {
            "input": "A 7 mm rounded rim enhancing lesion in the white-grey matter junction of the\nright occipital lobe with minimal surrounding FLAIR hyperintensity raises\nconcern for metastatic disease. Other tiny scattered foci of high FLAIR signal\nin the periventricular and subcortical white matter do not enhance and likely\nrepresent small vessel disease. There is no evidence of hemorrhage,\ninfarction, or mass effect. Principal intracranial vascular flow voids are\npreserved. No extra-axial blood or fluid collection is present. The ventricles\nand sulci are significantly dilated, suggestive of moderate to severe brain\natrophy, likely age related. The brainstem, posterior fossa and\ncervico-medullary junction are preserved. The orbits are within normal limits.\nThe paranasal sinuses are clear.  No abnormality of the skull base or calvaria\nis identified.",
            "output": "1.  7 mm rounded rim enhancing lesion in the white-gray matter junction of the\nright occipital lobe is compatible with metastatic disease. No other abnormal\nfocus of enhancement was identified.\n\n2.  Moderate to severe brain atrophy may be age related."
        },
        {
            "input": "The ventricles and extra-axial spaces are normal in size. There is no evidence\nof midline shift, mass effect or hydrocephalus. There are no acute infarcts.\nThere is no evidence of focal abnormalities.  The vascular flow voids are\nmaintained. The visualized paranasal sinuses are clear. Following gadolinium\nadministration there is no evidence of abnormal parenchymal, vascular and\nmeningeal enhancement seen.  Both parotid glands demonstrate heterogenous\nsignal intensities which is consistent with patient's history of Sjogren\nsyndrome.",
            "output": "No significant abnormalities are seen on MRI of the brain with and without\ngadolinium.  Specifically, there is no evidence of meningeal enhancement seen."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  Prominence of the left frontal vertex extra-axial space,\nmeasures up to 1.6 cm in craniocaudal dimension (03:12), and is not\nappreciably changed compared to ___.  The ventricles and sulci are\nnormal in caliber and configuration.  Trace periventricular FLAIR\nhyperintensities are nonspecific and may reflect the sequelae of chronic\nmicrovascular ischemic disease.\n\nMinimal mucosal sinus disease involving the right maxillary sinus. The orbits\nare unremarkable. There is decrease T1 signal involving the C2 vertebra\nconcerning for osseous metastatic diease",
            "output": "1. No evidence of intracranial metastatic disease.\n2. Decreased T1 signal in the C2 vertebra is concerning for metastasis. Please\nrefer to same day MR spine for further characterization of osseous metastatic\ndisease involving the spine.\n3. Stable prominence of the left frontal vertex extra-axial space measuring up\nto 1.6 cm compared to ___, compatible with an arachnoid cyst."
        },
        {
            "input": "There is no evidence of acute infarction.  No intracranial hemorrhage. No\nmass, mass effect, edema or midline shift. There is no abnormal enhancement. \nThe dural venous sinuses appear patent.\n\nThe ventricles and sulci are diffusely prominent.  Periventricular and\nsubcortical white matter FLAIR hyperintensities are noted, a nonspecific\nfinding that most likely represents the sequelae of chronic small vessel\nischemic disease.   There is gross preservation of the principal intracranial\nvascular flow voids.\n\nTrace mucosal thickening is seen within the left maxillary sinus.  The\nremainder of the visualized paranasal sinuses, middle ear cavities, and\nmastoid air cells are well aerated and clear.  The patient is status post\nbilateral lens replacement.",
            "output": "1. No evidence for intracranial metastatic disease.\n2. No acute intracranial hemorrhage or infarction.\n3. Background global parenchymal volume loss and evidence of chronic small\nvessel ischemic disease."
        },
        {
            "input": "Numerous scattered punctate and confluent supratentorial periventricular and\nsubcortical white matter FLAIR hyperintensities, some oriented perpendicular\nto the lateral ventricles, are grossly unchanged compared to the prior\nexamination and do not demonstrate slow diffusion or enhancement.  No new\nlesions are identified.  There is a possible nonenhancing FLAIR hyperintense\nsignal of the C2-C3 cord not seen on prior examination of ___.\n\nThere is no evidence of hemorrhage, edema, mass, mass effect, midline shift or\nacute infarction.   The ventricles and sulci are age-appropriate. Principal\nintracranial vascular flow voids are preserved and arteries of the circle of\n___ and the dural venous sinuses enhance appropriately after contrast\nadministration.  There is no abnormal enhancement.",
            "output": "1. Numerous scattered supratentorial white matter lesions are grossly\nunchanged and consistent with reported history of multiple sclerosis.  No new\nenhancing lesions.\n2. A possible nonenhancing FLAIR hyperintense focus of the C2-C3 cord not seen\non prior examination."
        },
        {
            "input": "Diffusion images are limited by motion.  There is an area of slow diffusion in\nthe left thalamus indicating of an acute infarct.  Moderate changes of atrophy\nseen.  There is a chronic left occipital infarct identified.  Flow void in the\nbasilar artery as well as in the anterior circulation are maintained.  No\nevidence of micro hemorrhages.",
            "output": "Acute left thalamic infarct."
        },
        {
            "input": "MRI HEAD:  There is no evidence of acute infarction or hemorrhage.  Compared\nto ___ and ___, FLAIR signal hyperintensity and\nvolume loss in the right temporal lobe with ex vacuo dilation of the right\nlateral ventricle temporal horn are similar. Stable FLAIR hyperintensity in\nthe right parietal lobe with overlying calvarial defect and calvarial defects\nelsewhere, are likely due to prior electrode placements with right parietal\ngliosis.  Scattered foci of T2/FLAIR signal hyperintensity in the subcortical\nwhite matter, right more than left, are nonspecific but stable. Enhancement\nadjacent to the right Meckel's cave is also unchanged. No new signal\nabnormality or abnormal enhancement is identified.\n\nThere is no mass effect, edema, or hydrocephalus. Ventricles and sulci are\nunchanged. Principal vascular flow voids are preserved.  Globes and soft\ntissues are unremarkable. Visualized paranasal sinuses and mastoid air cells\nare well aerated.",
            "output": "No change from ___ and ___.  Stable post treatment\nchanges in the right temporal and parietal lobes. No new abnormal signal or\nenhancement."
        },
        {
            "input": "Right pterional craniotomy changes are seen.  Stable postsurgical changes to\nthe anterior right temporal lobe is seen with stable underlying FLAIR\nhyperintense signal.  There is ex vacuo dilatation of the right occipital and\ntemporal horns.  There is a linear band of FLAIR hyperintense signal in the\nright parietal lobe, likely from prior shunt placement.  Multiple stable\nsubcortical and periventricular FLAIR hyperintensities are seen.  The right\nhippocampus is surgically absent.\n\nThe left hippocampal formation and bilateral mammillary bodies are preserved\nin signal and configuration.  There is no focal lobar encephalomalacia. There\nare no focal cortical dysplasias or gray matter heterotopia noted.\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  There is no abnormal enhancement after contrast\nadministration.\n\nThere is mild prominence of the posterior nasopharyngeal soft tissues.  There\nis abnormal T1 hypo intense signal within the upper cervical spinal cord.",
            "output": "1. Postsurgical changes to the right temporal lobe with stable underlying\nhigh-signal.\n2. Multiple white matter signal abnormalities, which is a nonspecific finding\nand may be secondary to prior treatment, demyelination, vasculitis or\ninfectious/inflammatory etiologies.  Clinical correlation is recommended.\n3. Signal abnormality in the visualized upper cervical spinal cord.  Recommend\na dedicated contrast enhanced MRI of the cervical spine for further\nevaluation.\n4. Prominence of the posterior nasopharyngeal soft tissues, likely\nrepresenting adenoids.  Recommend correlation with direct visualization."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift,\nor infarction.  FLAIR hyperintensity and volume loss centered within the right\ntemporal lobe with associated ex vacuo dilatation of the right lateral\nventricle temporal horn appears similar to ___.  A linear band of\nFLAIR hyperintense signal within the right parietal lobe is unchanged, likely\nrelated to prior shunt placement.  Scattered subcortical and periventricular\nFLAIR hyperintensities are unchanged.  Right pterional craniotomy changes are\nstable.  Major vascular flow voids appear preserved.\n\nThere is extensive paranasal inflammatory sinus disease involving the\nbilateral maxillary sinuses, bilateral sphenoid sinuses, and anterior ethmoid\nair cells.  There is trace fluid within the left-sided mastoid air cells.",
            "output": "1. No evidence infarction or hemorrhage.\n2. Right temporal lobe tissue loss, unchanged\n3. Stable scattered white matter FLAIR hyperintensities as compared to ___.\n4. Extensive paranasal inflammatory sinus disease, as described above."
        },
        {
            "input": "There is an unchanged extra-axial hyperintense subdural collection along the\nparietal convexities, slightly larger on the right with lobulated pattern,\nmeasuring approximately 12 mm in thickness. There is a punctate focus off slow\ndiffusion in the right parietal lobe (20:7), which is too small to\ncharacterize on the ADC map. There is no evidence of abnormal enhancement to\nindicate leptomeningeal disease. On T2 or FLAIR sequences, areas of\nencephalomalacia and small vessel disease are demonstrated in the subcortical\nand periventricular white matter as well as an old infarct in the left frontal\nlobe. The ventricles and sulci are slightly prominent, suggesting cortical\nvolume loss, likely involutional in nature. The major arterial vascular flow\nvoids are present and demonstrate normal distribution, the orbits are\nunremarkable, the paranasal sinuses and mastoid air cells are clear",
            "output": "1. Unchanged extra-axial subdural hematoma with lobulated pattern along the\ncerebral convexities as described above. There is no evidence of significant\nmass effect or shifting of the normally midline structures. Small punctate\nfocus of slow diffusion is noted on the right parietal lobe, measuring\napproximately 2 x 2 mm in size and may represent an area of subacute ischemia\n(20:7)\n\n2. Chronic infarct is noted on the left frontal lobe, multiple foci of high\nsignal intensity are normal FLAIR and T2 weighted images, which are\nnonspecific and may reflect microvascular ischemic disease"
        },
        {
            "input": "There is no evidence of acute infarction.  No intracranial hemorrhage. No\nmass, mass effect, edema or midline shift. There is no abnormal enhancement. \nThe dural venous sinuses appear patent.\n\nThe ventricles and sulci are mildly prominent compatible with global\nparenchymal volume loss.  Periventricular and subcortical white matter FLAIR\nhyperintensities are noted, a nonspecific finding that most likely represents\nthe sequelae of chronic small vessel ischemic disease.   There is gross\npreservation of the principal intracranial vascular flow voids.\n\nMild mucosal thickening is seen in scattered ethmoid air cells.  The remainder\nof the visualized paranasal sinuses, middle ear cavities, and mastoid air\ncells are well aerated and clear.  The orbits are within normal limits\nbilaterally.",
            "output": "1. No evidence for acute intracranial hemorrhage or infarction.\n2. No abnormal enhancement or intra cranial mass.\n3. Mild global parenchymal volume loss and evidence of chronic small vessel\nischemic disease."
        },
        {
            "input": "MRI BRAIN:\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  Mild periventricular and deep white matter T2 and FLAIR\nhyperintense changes are nonspecific, but most likely sequela of\nmicroangiopathy.  There is no abnormal enhancement after contrast\nadministration. No epileptogenic focus identified. The hippocampi appear\nnormal bilateral.  2 mm hypoenhancement at the junction of the anterior and\nposterior pituitary seen on sagittal MP-RAGE imaging is nonspecific and may\nrepresent artifact or if this is a real finding it most likely represents a\nRathke's cleft cyst. The craniocervical junction appears normal.\n\nCentered in the left parapharyngeal space is a FLAIR and T2 hyperintense\nsmoothly marginated 3.2 x 0.8 x 2.1 cm (TRV, AP, SI) cystic focus\ndemonstrating a T1 hyperintense to CSF nonenhancing focus, potentially\nrepresenting a lymphatic malformation.\n\nMRA BRAIN:\nThe intracranial vertebral and internal carotid arteries and their major\nbranches are patent without marked stenosis, occlusion, or aneurysm formation.\nFetal type origin of the PCAs bilateral.  Diminutive V4 segment of the left\nvertebral artery.\n\nMRA NECK:\nThe carotid arteries are patent bilateral.  No proximal ICA stenosis by NASCET\ncriteria.  Dominant and patent right vertebral artery.  Diminutive left\nvertebral artery.",
            "output": "1. No acute intracranial infarct, mass or hemorrhage.\n2.   No epileptogenic focus identified.  The hippocampi appear normal\nbilateral.\n3. No intracranial arterial aneurysm, marked stenosis or occlusion.\n4.   The carotid arteries are patent bilateral.  No proximal ICA stenosis by\nNASCET criteria.\n5. Dominant and patent right vertebral artery.  Diminutive left vertebral\nartery.\n6. 2 mm hypoenhancement at the junction of the anterior and posterior\npituitary seen on sagittal MPRAGE imaging is nonspecific and may represent\nartifact or if this is a real finding it most likely represents a Rathke's\ncleft cyst.  Dedicated pituitary imaging may be performed if clinically\nindicated.\n7. Centered in the left parapharyngeal space is a partially visualized\nenhancing T2 hyperintense mostly marginated 3.2 cm cystic focus demonstrating\nT1 hyperintense to CSF focus, potentially representing a lymphatic\nmalformation.  Further evaluation with MRI neck is recommended.\n\nRECOMMENDATION(S):  Further evaluation with contrast enhanced MRI neck for\nimpression 7."
        },
        {
            "input": "There are mild scattered punctate subcortical predominant T2/FLAIR white\nmatter hyperintensities, which are nonspecific.  There is no evidence of acute\nhemorrhage, edema, masses, mass effect, midline shift or acute infarction.\n\nThe major intracranial vascular flow voids are maintained.  The ventricles and\nsulci are normal in caliber and configuration.  There is a 1.3 cm retention\ncyst within the left maxillary sinus.  The orbits are unremarkable.  The\nmastoid air cells appear clear.",
            "output": "1. No acute intracranial abnormality.\n2. Mild scattered subcortical predominant T2/FLAIR white matter\nhyperintensities are nonspecific with the differential to include a history of\nmigraines or prior trauma.  Chronic small vessel disease is an additional\nconsideration, particularly if there is a history of hypertension.  These are\nnot in a distribution typical for demyelinating process.\n3. Left maxillary sinus 1.3 cm retention cyst."
        },
        {
            "input": "There is no acute infarction, edema, evidence for blood products, or\nintracranial mass. There is no pathologic leptomeningeal or pachymeningeal\ncontrast enhancement. There is a small ovoid focus of fluid signal intensity\nin the left thalamus, compatible with a chronic infarct or a perivascular\nspace.  Sulci, ventricles cisterns are normal in size for the patient's age.\nThe major intracranial flow voids are preserved.  The pager dural venous\nsinuses are patent.",
            "output": "1. No acute infarct. No evidence for other acute intracranial abnormalities or\nintracranial mass.\n2. Small ovoid focus of fluid signal intensity in the left thalamus is\ncompatible with a chronic infarct or a perivascular space."
        },
        {
            "input": "Normal, flow related enhancement is seen in the intracranial internal carotid,\nmiddle cerebral and anterior cerebral arteries without significant mural\nirregularity or stenosis. There is normal and symmetric arborization of the\nMCA branches. There is no aneurysm greater than 3 mm. Normal flow related\nenhancement is seen in the codominant intracranial vertebral arteries, the\nbasilar artery, and the bilateral superior cerebellar and posterior cerebral\narteries.\n\nNeck MRA shows normal flow in the carotid and vertebral arteries without\nstenosis or occlusion.",
            "output": "Normal MRA of the head and neck."
        },
        {
            "input": "MR BRAIN:\nThere is a 5 mm nonenhancing focus of slow diffusion and subtle hyperintense\nFLAIR signal in the left pons, consistent with a late acute infarct (series 4,\nimage 10).  A punctate focus of DWI and FLAIR hyperintense signal in the right\nposterior parietal lobe, probably too small to have a reliable correlate on\nthe ADC map, may also represent a punctate late acute or early subacute\ninfarct (series 4, image 25).  There is no intracranial hemorrhage, edema,\nmass, for mass effect.  There is no parenchymal signal abnormality otherwise. \nVentricles and sulci are age-appropriate.  Principal intracranial vascular\nflow voids are preserved.  The dural venous sinuses enhance appropriately on\npostcontrast MP-RAGE sequences.  There is no abnormal enhancement.\n\nThere is partial polypoid opacification of the ethmoid air cells and moderate\nmucosal thickening of the sphenoid sinus.  Mild to moderate right greater than\nleft mucosal thickening of the maxillary sinuses with fluid levels are also\nnoted.\n\nMRA brain: The intracranial vertebral and internal carotid arteries and their\nmajor branches appear normal without evidence of stenosis, occlusion, or\naneurysm formation.\n\nMRV brain: The dural venous sinuses are patent.",
            "output": "1.  5 mm left pontine and punctate right posterior parietal late acute or\nearly subacute infarcts.\n\n2.  Under brain MRA.\n\n3.  The dural venous sinuses are patent.\n\n4.  Extensive paranasal sinus disease with mucosal thickening and air-fluid\nlevels as described.\n\nNOTIFICATION:  Neurology is aware of the findings at the time of reporting."
        },
        {
            "input": "ORBITS: Orbital images are moderately degraded by motion.\n\nSubtle asymmetric STIR hyperintensity of the right optic nerve sheath with\nsubtle associated patchy signal within the adjacent intraconal fat was better\nassessed on the prior examination, less apparent on today's examination given\nmotion artifact, though likely still present.  Subtle areas of STIR\nhyperintensity of the medial, inferior and lateral rectus musculature appears\ngrossly unchanged compared to the prior exam.  The extraocular muscles are\notherwise symmetric in size.  The globes are unremarkable.  The left\nretrobulbar soft tissues are unremarkable.  The lacrimal apparatus appears\npreserved bilaterally.  The right superior ophthalmic vein remains\nasymmetrically distended, unchanged compared to the prior examination. \nEvaluation for thrombus is limited given lack of postcontrast series.\n\nBRAIN: Re-identified is a subcentimeter focus of slow diffusion with\nassociated FLAIR hyperintensity in the pons to the left of midline (04:10). \nAnother similar-appearing lesion has intervally developed in the pons\nposteriorly to the right of midline (4:9).  Another punctate focus of slowed\ndiffusion is noted in the right parietal cortex ___, 10:21).  These likely\nreflect subacute infarcts.  There is no evidence of hemorrhage, mass effect or\nmidline shift.  The cavernous sinuses are unremarkable, without definite\nsecondary signs for thrombosis, though evaluation is limited given lack of\ncontrast.  The principal intracranial vascular flow voids are preserved.\n\nRe-identified is extensive paranasal sinus disease with mild mucosal\nthickening in the bilateral maxillary sinuses with layering fluid component,\nand moderate to severe mucosal wall thickening of the bilateral sphenoid and\nethmoid sinuses, appearing grossly similar to the prior examination.  The\nfrontal sinuses are clear.  There is opacification of a few right mastoid air\ncells.  The left mastoid air cells are clear.\n\nMRV: Normal flow signal is demonstrated within the superior sagittal sinus,\nstraight sinus, transverse sinuses, and sigmoid sinuses. The jugular bulbs and\nproximal jugular veins are patent. Evaluation of the deep venous systems\nreveals normal flow signal in the internal cerebral veins. The vein ___\nis also unremarkable.",
            "output": "1. Abnormal STIR signal of the right optic nerve sheath and adjacent right\nintraconal fat with involvement of the extra-ocular musculature is less well\ndefined compared to prior examination given motion artifact, though remains\npresent, consistent with cellulitis/optic perineuritis.  Evaluation is limited\ngiven lack of postcontrast series, and no definite correlate to the previously\nidentified areas of dural enhancement is noted.\n2. New punctate focus of slow diffusion in the right pons, appearing similar\nto the existing left pontine focus of slowed diffusion, compatible with\nsubacute infarcts.  Additional new punctate subacute infarct in the right\nparietal cortex.\n3. Unchanged asymmetric dilatation of the right superior ophthalmic vein, with\nprior findings suspicious of nonocclusive thrombus, incompletely assessed\ngiven lack of contrast.  No secondary findings to suggest cavernous sinus\nthrombosis estimate is limited given lack of postcontrast sequences.\n4. Severe pansinus disease, grossly unchanged.  Given history, the orbital\nfindings are again presumed infectious, with sinus disease as a likely source.\n5. No evidence of cerebral venous thrombosis.\n\nNOTIFICATION:  The updated findings were discussed with ___, M.D. by\n___, M.D. on the telephone on ___ at 8:33 am, 5 minutes after\ndiscovery of the findings."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal focus of slowed diffusion.  The principal\nintracranial vascular flow voids are preserved.\n\nThe visualized paranasal sinuses are grossly clear.  The orbits are grossly\nunremarkable.",
            "output": "Normal study."
        },
        {
            "input": "MRI BRAIN:\nThere is dysgenesis of the corpus callosum, absence of the septum pellucidum,\nstenogyria and Chiari 2 malformation, the appearance of which is unchanged\nfrom prior examination.  There is cerebral white matter volume loss as well as\ngeneral cerebral this morphology.  Periventricular subependymal white matter\ngliosis is also unchanged.  There is apparent fusion of the tectum, without\naqueductal stenosis (series 4, image 10).  A 2.4 x 1.6 cm (TRV, AP) right\ntrigonal arachnoid cyst (series 9, image 13) is unchanged.\n\nThere is no acute infarct or new intracranial hemorrhage.  Left caudate\nchronic infarct is re-identified.  Linear gradient echo susceptibility\nhypointensity of the left frontal lobe is felt to be vascular in nature or\nsequela of prior hemorrhage.\n\nThe patient is status post placement of 2 bifrontal ventriculostomy catheters,\nunchanged in position from prior exam.\n\nThe size of the ventricles are stable without ventriculomegaly.\n\nThe major intracranial flow voids are preserved.  Gyral FLAIR hyperintense\nsignal likely represents slow flow through pial collaterals (climbing ___\nsign).  The dural venous sinuses are patent.  There is mild mucosal thickening\nof the paranasal sinuses.  The orbits are unremarkable.  No fluid signal is\nseen in the mastoid air cells.  No suspicious marrow signal.\n\nMRA BRAIN: Examination is mildly motion degraded.  Within this confines:\n\nThe left internal carotid artery is highly attenuated with decreased caliber\nand flow signal, similar slightly worsened from prior examination.  No flow\nrelated signal is seen along the left M1 and proximal M2 segments, which is\nsimilar to prior.\n\nThe bilateral A1 segments as well as dominant left proximal A2 segment are\nhighly attenuated and barely visible, which can be seen on prior examination,\nbut however appears to be slightly progressed on the current examination,\nalthough this may be secondary to motion artifact.\n\nThe right ICA and and MCA demonstrate unremarkable caliber and flow related\nsignal.  There is right greater than left lateral ventricular striate moyamoya\nvessels.  This appears overall similar to prior exam.\n\nThe patient is status post bilateral superficial temporal artery indirect\nbypasses, overall similar in appearance to prior examination.  The superficial\ntemporal arteries are patent and what can be seen of the pial  collaterals\nappears similar to prior exam.\n\nThe right vertebral artery is dominant, unchanged from prior exam.  The\nposterior circulation appears unchanged from prior exam and is patent,\nalthough the right PCA does appear slightly smaller compared to the left.",
            "output": "1. Decreased caliber and flow signal of the left internal carotid artery, near\ncomplete occlusion of the left MCA M1 and M2 segments, a near complete\nocclusion of the bilateral A1 and dominant left proximal A2 segments as well\nas prominent lenticulostriate moyamoya vessels, right greater than left. \nThese findings are overall unchanged since examination of ___ to slightly\nprogressed.  The patient is status post bilateral superficial temporal artery\nindirect bypasses, which appears patent.\n2. Dysgenesis of the corpus callosum, absence of the septum pellucidum,\nstenogyria, Chiari 2 malformation, periventricular subependymal white matter\ngliosis, and aqueductal stenosis.\n3. The patient is status post bifrontal ventriculostomy catheters, unchanged\nin position.  There is no hydrocephalus.\n4. Additional findings as described above."
        },
        {
            "input": "There is no intra or extra-axial mass, acute hemorrhage or infarct. The sulci,\nventricles and cisterns are within expected limits for the patient's age.  The\nmajor intracranial flow voids are preserved.  There is mild mucosal thickening\nof the ethmoid air cells, otherwise the paranasal sinuses are essentially\nclear.  The orbits are unremarkable.  Trace fluid signal is noted in the right\ngreater than left mastoid tips.  The dural venous sinuses are patent on\npostcontrast MP-RAGE.",
            "output": "1. Unremarkable contrast-enhanced MRI of the brain.  No evidence of infarct,\nintracranial hemorrhage or mass."
        },
        {
            "input": "There is no acute infarction, intracranial hemorrhage, extracerebral fluid\ncollection, midline shift or mass effect.  Ventricles and extra-axial spaces\nare normal in size.  Flow voids are maintained. Suprasellar and craniocervical\nregions are unremarkable.",
            "output": "No significant abnormalities are seen on MRI of the brain without gadolinium."
        },
        {
            "input": "There is stable mild dilation of the right temporal horn. Otherwise, there is\nno mass, mass effect or midline shift. There is no hydrocephalus or acute\nischemia. There is mild fluid in bilateral mastoid air cells.\n\nThere is no acute infarction, intracranial hemorrhage, extracerebral fluid\ncollection, midline shift or mass effect.  The cerebral volume is appropriate\nfor the patient's stated age.  Flow voids are maintained.",
            "output": "No significant abnormality. Stable minimal prominence of the right temporal\nhorn"
        },
        {
            "input": "Study is mildly degraded by motion.\n\nThere is grossly stable focal parafalcine leptomeningeal enhancement (11:49)\nwith associated slowed diffusion, predominantly between the frontal lobes. \nFLAIR hyperintense signal correlates with the regions of enhancement, although\nthere is no definite FLAIR signal abnormality within the adjacent brain\nparenchyma.  Corresponding areas of gray matter isointense material within\ncorresponding subarachnoid spaces on T1 precontrast imaging is noted (see 9:\n___.  No definite corresponding T2 hypointense material is seen within the\ncorresponding subarachnoid spaces (see 9, 11, 12, 13: ___.  T2\nhypointensity within the anterior falx corresponding to calcification seen on\nprior head CTA is noted (see 12: ___ on current study and 201: 34-50 on\nprior outside CTA).\n\nNonenhancing bifrontal periventricular and subcortical T2 and FLAIR\nhyperintensities are noted.  These lesions or not clearly contiguous with any\nareas of leptomeningeal enhancement.  These lesions are not clearly associated\nwith increased susceptibility or restricted diffusion.\n\nThere is no evidence of acute infarction, intracranial hemorrhage, mass\neffect, or midline shift.  The ventricles and sulci are preserved in\nconfiguration.\n\nNonspecific low-lying cerebellar tonsils extending approximately 3 mm inferior\nto the foramen magnum is noted (see 02:14).  Scattered subcentimeter\nnonspecific lymph nodes are noted throughout the neck bilaterally, without\ndefinite enlargement by size criteria.  Minimal bilateral maxillary sinus and\nethmoid air cell mucosal thickening is present.  Minimal nonspecific right\nmastoid fluid is seen.",
            "output": "1. Study is mildly degraded by motion.\n2. Nonspecific focal parafalcine leptomeningeal enhancement and FLAIR\nhyperintense signal with scattered areas of slow diffusion grossly similar\ncompared to ___ outside contrast brain MRI.  Findings suggestive of\nneurosarcoid, with differential considerations of leptomeningeal tumor, and\nmeningitis not excluded.\n3. Nonspecific low-lying cerebellar tonsils extending approximately 3 mm\ninferior to the foramen magnum.\n4. Minimal paranasal sinus disease and minimal nonspecific right mastoid fluid\nas described.\n5. Nonenhancing bifrontal white matter lesions as described.  Differential\nconsiderations include sequela of prior trauma or infection, history of\nmigraine headaches, inflammatory or demyelinating process, and\nmicroangiopathic changes."
        },
        {
            "input": "Please note the study is mildly degraded by motion.  There is an area of\nrestricted diffusion involving majority of the left cerebellar hemisphere as\nwell as the left vermis with associated FLAIR hyperintensity.  There are small\npunctate foci of susceptibility within the infarct suggestive of foci of micro\nhemorrhages.\n\nThere are scattered foci of T2/FLAIR hyperintensity in the periventricular,\nsubcortical and deep white matter, nonspecific, likely secondary to small\nvessel ischemic changes.\n\nThe ventricles and sulci are normal in caliber and configuration.\n\nNo osseous abnormalities are seen. There is a small mucous retention cyst in\nthe left maxillary sinus.  The remaining paranasal sinuses, mastoid air cells,\nand middle ear cavities are clear. The visualized portion of the orbits are\nunremarkable. The visualized portion of the vascular flow voids are preserved.",
            "output": "1.  Study is mildly degraded by motion.\n2. Acute/subacute left cerebellar hemisphere and left vermis infarct in\nposterior inferior cerebellar artery distribution as described above.\n3. Small areas of susceptibility within areas of infarct concerning for\nhemorrhagic conversion.  Recommend clinical correlation and attention on\nfollowup imaging.\n\nRECOMMENDATION(S):\n1. Small areas of susceptibility within areas of infarct concerning for\nhemorrhagic conversion.  Recommend clinical correlation and attention on\nfollowup imaging."
        },
        {
            "input": "There is a 25 x 20 mm left anterior temporal extra-axial mass identified which\ndemonstrates low signal on T2 weighted images compared to the brain parenchyma\nand shows homogeneous enhancement on postcontrast images.  There is edema in\nthe left temporal lobe which extends to the left temporal operculum and\nsubinsular region but no evidence of uncal herniation or midline shift is\nseen.  There is no hydrocephalus.  No other areas of abnormal parenchymal or\nextra-axial enhancement seen.  No acute infarcts are identified.",
            "output": "25 x 20 mm left anterior temporal meningioma with associated edema in left\nanterior temporal lobe.  No acute infarcts, mass effect or hydrocephalus."
        },
        {
            "input": "Fiducial markers are in place.  21 x 26 mm in transverse dimension avid\nenhancing extra-axial mass lesion is again identified in the anterior aspect\nof the right temporal fossa, which remains grossly unchanged compared to\nprevious imaging from ___ with moderate vasogenic edema towards the\nleft temporal lobe and left sub insular region, without significant mass\neffect.  There is no evidence of acute hemorrhage or infarction. The\nventricles and sulci are normal in caliber and configuration.  The orbits are\nunremarkable, the paranasal sinuses and mastoid air cells are clear.",
            "output": "1. Unchanged avid enhancing extra-axial mass lesion identified in the anterior\naspect of the left temporal fossa, likely consistent with meningioma, with\nunchanged moderate vasogenic edema along the left temporal lobe and left\nsubinsular region\n2. No new lesions or new areas with abnormal enhancement are seen."
        },
        {
            "input": "Postsurgical changes after left temporal craniotomy for left anterior temporal\nlobe meningioma resection are noted with edema in the left temporal lobe and\nblood products about the resection site.  Cortical DWI hyperintensities with\nADC hypointense correlates around the margin of the surgical resection site.\n\nThere is mild thickening of the meninges with evidence of\ncontrast-enhancement, most likely postsurgical.\n\nAlong the anterior margin of the left temporal lobe, there is residual\nenhancement which could be postsurgical, however, residual meningioma cannot\nbe fully excluded, but difficult to assess given the degree of blood products.\n\nThere is pneumocephalus, an expected postsurgical finding, which is better\nevaluated on the most recent CT.\n\nThe ventricles and sulci are within expected limits in caliber and\nconfiguration.\nMajor vascular flow voids are preserved.  The intracranial vasculature is\npatent.  Major dural venous sinuses are patent.\n\nThe paranasal sinuses and mastoid air cells are clear.  The orbits are\nunremarkable.",
            "output": "1. Postsurgical changes after left temporal craniotomy for resection of a left\nanterior temporal meningioma as detailed above.\n2. Residual enhancement about the anterior left temporal lobe is most likely\npostsurgical, however, residual meningioma cannot be fully excluded and\nattention on follow-up is recommended.\n3. Additional findings as described above."
        },
        {
            "input": "Numerous, confluent periventricular, subcortical, deep, callosal and pontine\nwhite matter lesions are unchanged compared to the prior examination.  No\ndefinite new lesion is identified.  There is no associated post gadolinium\nenhancement.  Many of these areas demonstrate T1 \"dark hole\" appearance. \nDiffuse thinning of the corpus callosum is unchanged.\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  There is prominence of the ventricles and sulci suggesting\ninvolutional changes.  There is no abnormal enhancement after contrast\nadministration.  The principal intracranial vascular flow voids are preserved.\nThere is no abnormal focus of slowed diffusion.\n\nThere is a small mucous retention cyst in the inferior aspect of the left\nmaxillary sinus.  The remainder of the paranasal sinuses are grossly clear. \nThe orbits are grossly unremarkable.",
            "output": "Stable diffuse white matter lesions, volume loss, and thinning of the corpus\ncallosum consistent with history of multiple sclerosis.  No definite new\nlesion or associated enhancement."
        },
        {
            "input": "Numerous white matter lesions are again seen within the periventricular and\nsubcortical/deep white matter, including the pericallosal region and the pons,\ncompatible with known demyelinating process.  These lesions demonstrate\nsimilar hyperintense T2/FLAIR signal intensity without corresponding\nenhancement or slow diffusion.  Some of these lesions are again noted to\ndemonstrate hypointense T1 (\"dark hole\") signal characteristics suggesting\nchronic demyelinating process.  There is diffuse thinning of the corpus\ncallosum, which is unchanged.\n\nThere is no new lesions or abnormal enhancement after contrast administration.\nThere is no evidence of acute infarction, intracranial hemorrhage, edema, or\nmass effect.  The principal intracranial vascular flow voids are preserved.\n\nSmall mucosal retention cysts are seen within bilateral maxillary sinuses. \nThe remaining paranasal sinuses appear clear.  The orbits and soft tissues\nappear unremarkable.",
            "output": "1. Stable diffuse white matter lesions with volume loss and thinning of the\ncorpus callosum, compatible with history of multiple sclerosis.  No definite\nevidence of new lesion or associated enhancement.\n2. No acute infarction or intracranial hemorrhage.  No evidence of abscess."
        },
        {
            "input": "MRI BRAIN:\nThere is redemonstration of numerous periventricular, subcortical and deep\nwhite matter lesions, as well as pericallosal and pontine lesions, compatible\nwith known demyelinating disease.  These lesion appear grossly unchanged since\n___.  Some of these lesions displays T1 hypointensity (dark holes), without\nassociated enhancement, diffusion restriction, or susceptibility artifact. \nThere is thinning of the corpus callosum, unchanged compared to prior. \nOverall, no new lesions are identified.\n\nThere is prominence of the ventricles and sulci, reflecting brain parenchymal\nvolume loss, likely secondary to underlying demyelinating process.  There is\nmild mucosal thickening of the ethmoid air cells, otherwise the paranasal\nsinuses and mastoid air cells are clear.  There is no bone marrow signal.\n\nMRI CERVICAL SPINE:\nThe cervical spine is visualized from the clivus to T2 level.  Alignment is\nnormal.  Vertebral body heights are normal. There is no marrow signal\nabnormality or abnormal enhancement.  There is multilevel disc desiccation,\nwithout significant loss of intervertebral disc height.  There is no\nprevertebral soft tissue swelling.\n\nThere is multiple intramedullary foci demonstrating T2 hyperintensity spanning\nfrom C3-C6, grossly unchanged compared to prior exam, likely representing\ndemyelinating lesion, in keeping with the patient's history.\n\nIntervertebral disc heights and signal are preserved.\n\nAt C2-3 and C3-C4, there is no vertebral canal or neural foraminal narrowing.\n\nAt C4-5 there is mild central disc protrusion, effacing the ventral CSF space\nresulting in mild spinal canal stenosis.  There is no significant bilateral\nneural foraminal narrowing.\n\nAt C5-6 there is disc bulge with endplate osteophytes resulting in moderate\nspinal canal narrowing, stable compared to prior.  There is bilateral\nuncovertebral joint osteophyte resulting in moderate left neural foraminal\nnarrowing.  There is no significant right neural foraminal narrowing.\n\nAt C6-7 there is disc bulge resulting in mild spinal canal narrowing.  There\nis no significant bilateral neural foraminal narrowing.\n\nAt C7-T1 there is no significant disc disease, spinal canal stenosis, neural\nforaminal narrowing.",
            "output": "1. Stable numerous white matter lesion with associated diffuse brain\nparenchymal volume loss, and thinning of the corpus callosum, compatible with\nthe history of multiple sclerosis.  No evidence of new lesion or associated\nenhancement.\n2. No evidence of an acute infarct, intracranial hemorrhage.\n3. Stable multiple demyelinating lesions in the cervical spine since MRI of\n___.\n4. Cervical spondylosis as described above, unchanged compared to prior MRI,\nmore pronounced at C5-C6."
        },
        {
            "input": "The examination is moderate limited secondary to patient motion.  Gradient\necho sequences were not obtained as the examination was prematurely\nterminated..\n\nA left cerebral convexity subdural hematoma overlying left frontal, parietal,\noccipital, temporal lobes, demonstrates areas of predominantly T2\nhyperintensity and isointensity, and mixed T1 hyperintensity and isointensity,\ncompatible with an evolving subacute hematoma.  This measures up to 0.6 cm,\nand appears similar in size compared to the prior CT examination.\n\nAn extra-axial fluid collection overlying the right cerebral convexity\ndemonstrates primarily CSF signal intensity, and appears similar to the prior\nhead CT examination.\n\nAdditionally, there are areas of intraventricular hemorrhage layering in the\nbilateral occipital horns, in addition to diffuse subarachnoid hemorrhage seen\nthroughout the left cerebral convexity and predominantly affecting the right\noccipital and parietal convexity sulci.  Trace parafalcine subdural bleed.\n\nFocal T2 hyperintensity within the anterior left temporal lobe demonstrates\nscattered areas of restricted diffusion, correlating with hypodensity on prior\nCT and likely reflecting a parenchymal contusion.\n\nT2/FLAIR hyperintensity within the posterior left temporal, lateral occipital\nlobe demonstrates areas of restricted diffusion, and correlates with\nhypodensity on prior CT examination.  This likely represents an additional\nsite of partially hemorrhagic contusion.\n\nPunctate focal T2/FLAIR hyperintensity in the anterior right temporal lobe\ncorrelates with an area of hyperdensity on CT, likely reflecting a small\nhemorrhagic contusion.\n\nThe ventricles and sulci are prominent, compatible with global parenchymal\nvolume loss.  Mild chronic small vessel ischemic changes.  There is gross\npreservation of the principal intracranial vascular flow voids.\n\nKnown diastasis of the left lambdoid suture and a longitudinal left temporal\nbone fracture are better seen on prior CT.  Fluid signal throughout the\nmastoid air cells is seen on the left, correlating with areas of opacification\non CT examination.  There is mild mucosal thickening seen in scattered ethmoid\nair cells and within the sphenoid sinuses bilaterally.  Patient is status post\nright lens replacement.",
            "output": "1. Motion degraded exam, early termination and exclusion of gradient echo\nimaging, which limits evaluation for diffuse axonal injury.\n2. Stable early subacute left convexity subdural hematoma, 0.6 cm in\nthickness.\n3. Stable subarachnoid, intraventricular hemorrhage.  No hydrocephalus.\n4. Partially hemorrhagic contusions involving the anterior left temporal and\nposterior left temporal/lateral occipital lobes, with areas of restricted\ndiffusion.\n5. Punctate hemorrhagic contusion in the anterior right temporal lobe is\nsimilar.\n6. Opacified left mastoids.  Fractures were better seen on prior CT\nexamination."
        },
        {
            "input": "There is no abnormality on diffusion-weighted images.  There is no hemorrhage,\nedema, mass, mass effect, or acute infarction.  Ventricles are normal in size\nand configuration for age.  Principal intracranial vascular flow voids are\npreserved and circle of ___ and dural venous sinuses demonstrate\nappropriate enhancement after contrast administration.  There is no abnormal\nmeningeal or parenchymal enhancement.  There is minimal partial fluid\nopacification of the right mastoids, and mild mucosal thickening in the right\nmaxillary sinus.  The orbits are unremarkable.  Partially empty sella is\nnoted.",
            "output": "No evidence of hemorrhage, edema, mass, mass effect, or acute infarction. \nThere is no evidence of abnormal enhancement"
        },
        {
            "input": "There is no acute infarction, intracranial hemorrhage, extracerebral fluid\ncollection, midline shift or mass effect.  Ventricles and extra-axial spaces\nare normal in size.  Flow voids are maintained. Suprasellar and craniocervical\nregions are unremarkable.  Small amount of fluid in the sphenoid sinus.",
            "output": "No significant abnormalities are seen on MRI of the brain without gadolinium.\nMild soft tissue changes in the sphenoid sinus."
        },
        {
            "input": "There is no evidence for an acute infarction, edema, mass effect, or blood\nproducts.  No evidence of hippocampal atrophy, as clinically questioned. \nThere is confluent periventricular high T2 signal, confluent and discrete\nareas of high T2 signal in the periventricular white matter, and scattered\nsubcortical discrete foci of high T2 signal, which are nonspecific, but likely\nrepresent chronic microvascular ischemic changes.  There is global parenchymal\nvolume loss with associated prominence of the ventricles and sulci, which\nappears asymmetric on the left, with greater enlargement of the left sylvian\nfissure and left lateral ventricle compared to the right.  Volume loss in the\nmedial temporal lobes is slightly more prominent than in the remainder of the\ncortex.  Mild cerebellar volume loss is also noted.\n\nMajor intravascular flow voids appear grossly preserved.\n\nThere is mild mucosal thickening in the ethmoid air cells, maxillary sinuses,\nand left sphenoid sinus.",
            "output": "1. Extensive supratentorial white matter signal abnormalities are nonspecific\nbut likely sequela of chronic small vessel ischemic disease in this age group.\n2. Global parenchymal volume loss is slightly asymmetric, with\ndisproportionate enlargement of the left sylvian fissure and left lateral\nventricle compared to the right.  Volume loss in medial temporal lobes is\nslightly more prominent than in the remainder of the cortex."
        },
        {
            "input": "Left larger than right cerebellar hemisphere and vermian parenchymal\nhemorrhage with extension into the fourth ventricle, quadrigeminal cistern as\nwell as subdural tentorial extension and interdigitating within the bilateral\ncerebellar folia is overall unchanged from prior CT examination of ___ allowing for technical differences tears dependent hemorrhage within the\noccipital horns of the lateral ventricles as well as right frontal\npneumocephalus is also overall unchanged.  A right trans frontal\nventriculostomy catheter, terminating in the frontal horn of right lateral\nventricle is unchanged.  No evidence for acute infarct.  No abnormal\nenhancement.  Known the vermian and left cerebellar AVM are better evaluated\non prior CTA and angiogram.  There is unchanged ventriculomegaly, with\nappearance of transependymal CSF flow.  Superimposed periventricular and\nsubcortical T2/FLAIR white matter hyperintensities are nonspecific, but\ncompatible with chronic microangiopathy in a patient this age.  Severe\ncrowding of the foramen magnum is identified, without frank tonsillar\nherniation.  Severe effacement of the fourth ventricle and mass-effect on the\nmedulla and effacement of the prepontine cistern is similar.  The major\nintracranial flow voids are preserved.  The dural venous sinuses remain\npatent.  There is mild mucosal thickening of the ethmoid air cells.  The\norbits are unremarkable.  Trace signal is seen in the mastoid air cells.",
            "output": "1. Left cerebellar hemisphere, vermian and smaller right subependymal sphere\nintraparenchymal hemorrhage with extension into the fourth ventricle,\ntentorial subdural region and cerebral folia is overall similar to prior\nexamination allowing for technical differences.  Dependent hemorrhage within\nthe occipital horns of the lateral ventricles also unchanged.\n2. Severe edema and effacement of the fourth ventricle, prepontine cistern\nwith unchanged ventriculomegaly.  Crowding of the foramen magnum without frank\ntonsillar herniation is unchanged.\n3. Right trans frontal ventriculostomy catheter is stable, with postoperative\npneumocephalus re-identified.\n4. No acute infarct or abnormal enhancement.  Known left cerebellar and\nvermian AVMs are much better evaluated on prior angiographic studies.\n5. Additional findings as described above."
        },
        {
            "input": "There is no evidence of intracranial hemorrhage, mass, mass effect or shifting\nof the normally midline structures.  The ventricles and sulci are normal in\nsize and configuration for patient's age, no diffusion abnormalities are\ndetected to indicate acute or subacute ischemic changes.  The major vascular\nflow voids are present and demonstrate normal distribution.  The a few\nscattered foci of high signal intensity on FLAIR in the subcortical white\nmatter, which are nonspecific and may reflect changes due to small vessel\ndisease.  An 8 mm right frontal calvarial based enhancing focus is favored to\nrepresent a venous Lake (image 93, series 100, image 45, series 101).  There\nis otherwise no evidence abnormal enhancement.\n\nThere is minimal tonsillar ectopia.  Mild mucosal thickening of the ethmoid\nair cells.  The frontal sinuses are hypoplastic.  The remaining paranasal\nsinuses, orbits and mastoid air cells are normal.",
            "output": "1. No acute intracranial abnormality.  Specifically, no evidence for HSV\nencephalitis.\n2. A few punctate periventricular T2/FLAIR hyperintensities are nonspecific\nbut can be seen in the setting of chronic small vessel disease.\n3. Mild inflammatory changes of the ethmoid air cells."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.",
            "output": "Normal brain MRI."
        },
        {
            "input": "There is a late subacute to chronic infarcts seen in the left frontal lobe in\nthe distribution of the left anterior cerebral artery with chronic blood\nproducts.  Mild-to-moderate changes of small vessel disease seen in the white\nmatter.  There is no acute infarct identified. There is no mass effect midline\nshift or hydrocephalus. Mild mucosal thickening and fluid level seen in the\nright maxillary sinus.",
            "output": "No acute infarcts identified. Chronic left anterior cerebral artery infarct."
        },
        {
            "input": "MRI BRAIN:\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is a single nonspecific punctate focus of subcortical\nwhite matter T2/FLAIR hyperintensity in the right frontal lobe, likely of no\nclinical significance.  There is no definitive abnormal focus of slowed\ndiffusion.  Apparent increased subtle diffusion-weighted hyperintense signal\nalong the right posterior temporal lobe is without definitive FLAIR\nhyperintense signal or ADC hypointensity and is felt to be almost certainly\nartifactual.  The principal intracranial vascular flow voids are preserved. \nThe dural venous sinuses are patent on MP-RAGE images.\n\nThere is abnormal enhancing FLAIR hyperintense signal of the left parotid deep\nlobe and tail (series 30, image 3; series 114 a, image 69).  No definitive\nunderlying mass lesion is identified.  There is also associated enhancement of\nthe left facial nerve mastoid segment (series 114 a, image 75).  There is\npartial opacification of the left mastoid tip.  Although there is no\ndefinitive evidence for marrow edema abnormality.  No focal rim enhancing\ncollection to suggest abscess.\n\nThe paranasal sinuses are grossly clear.  The orbits are grossly unremarkable.\n\nMRA BRAIN:\nThere is variant fetal type origin of the bilateral posterior cerebral\narteries.  The intracranial vertebral and internal carotid arteries and their\nmajor branches appear patent without evidence of stenosis, occlusion, or\naneurysm formation.\n\nMRV BRAIN: Normal flow signal is demonstrated within the superior sagittal\nsinus, straight sinus, transverse sinuses, and sigmoid sinuses. The jugular\nbulbs and proximal jugular veins are patent. Evaluation of the deep venous\nsystems reveals normal flow signal in the internal cerebral veins. The vein of\n___ is also unremarkable.\n\nMRA NECK:\nThe common, internal and external carotid arteries appear patent.  There is no\nevidence of internal carotid artery stenosis by NASCET criteria.  The origins\nof the great vessels, subclavian and vertebral arteries appear patent\nbilaterally.",
            "output": "1. No acute intracranial abnormality including hemorrhage, infarct, or\nintracranial enhancing mass. Apparent increased subtle diffusion-weighted\nhyperintense signal along the right posterior temporal lobe is without\ndefinitive FLAIR hyperintense signal or ADC hypointensity and is felt to be\nalmost certainly artifactual.  However, repeat examination is recommended if\nthere remains clinical concern.\n2. Abnormal enhancement and FLAIR hyperintense signal of the left parotid deep\nlobe and tail without definitive underlying lesion.  There is also associated\nenhancement of the left facial nerve mastoid segment.  Associated partial\nopacification of the left mastoid tip is identified.  This is of uncertain\netiology and may be inflammatory in nature.  Clinical correlation is\nrecommended.  Further evaluation with MRI skullbase or IAC protocol may yield\nadditional information as clinically indicated.\n3. Patent intracranial vasculature without significant stenosis, occlusion, or\naneurysm.\n4. Patent cervical vasculature without significant stenosis or occlusion.\n5. No evidence of venous sinus thrombosis.\n\nNOTIFICATION:  The additional findings detailed in impression 2 was discussed\nwith ___, M.D. by ___, M.D. on the telephone on ___ at\n11:11 AM, 30 minutes after discovery of the findings."
        },
        {
            "input": "MR BRAIN:\nThere is no evidence of acute infarction, intracranial mass, edema, or blood\nproducts.  There are multiple small foci of high T2 signal in the subcortical,\ndeep, and periventricular white matter of the cerebral hemispheres,\nnonspecific but likely sequela of chronic small vessel ischemic disease in\nthis age group.  There is minimal age-appropriate prominence of the frontal\nand parietal sulci.  The ventricles are age-appropriate.  Major arterial flow\nvoids are preserved.  Dural venous sinuses appear patent on postcontrast MP\nRAGE images.\n\nThere is mild mucosal thickening in the maxillary sinuses and ethmoid air\ncells.  There is moderate mucosal thickening with partial opacification in the\nright mastoid air cells, and trace opacification of scattered left mastoid tip\nair cells.  There is evidence of left cataract surgery.\n\nMRA BRAIN:\nThere is asymmetric irregularity of the right carotid siphon with a possible\nbroad-based 3 mm aneurysm of the supraclinoid right internal carotid artery\n(images 502:8, 5:123).  No additional aneurysm is seen.  There is no evidence\nfor flow-limiting stenosis.  A1 segment of the left anterior cerebral artery\nis hypoplastic, a normal variant.  The left ophthalmic artery is larger than\nthe right, which may also represent an anatomic variant.",
            "output": "1. No evidence for an acute infarction or intracranial mass.\n2. Supratentorial white matter signal abnormalities are nonspecific but likely\nsequela of chronic small vessel ischemic disease in this age group.\n3. Possible 3 mm broad-based aneurysm of the supraclinoid right internal\ncarotid artery, versus irregularity related to asymmetric atherosclerosis.\n\nRECOMMENDATION(S):  Consider head CTA for further evaluation.\n\nNOTIFICATION:  The impression and recommendation above were entered by Dr.\n___ on ___ at 16:53 into the Department of Radiology critical\ncommunications system for direct communication to the referring provider."
        },
        {
            "input": "There is an infarction in the distribution of the superior division of the\nright middle cerebral artery with hyperintensity on FLAIR images indicating\nthat it is subacute.  There is no evidence of hemorrhage, edema, masses, mass\neffect, midline shift.  The ventricles and sulci are slightly prominent\nsuggesting age-related involutional changes.  There are mild FLAIR\nhyperintensities within the periventricular and subcortical white matter that\nare nonspecific but likely sequela of microvascular ischemic disease.\n\nThere is mild mucosal thickening of the bilateral maxillary sinuses, ethmoid\nair cells and right sphenoid sinus which may represent sinus disease.  The\nbilateral mastoid air cells are partially fluid filled which may represent of\nprior infection.  The orbits are unremarkable.",
            "output": "There is a large subacute infarction in the distribution of the superior\ndivision of the right middle cerebral artery.  No evidence of new infarction\nor hemorrhage."
        },
        {
            "input": "The common, internal and external carotid arteries appear normal.  There is no\nevidence of stenosis by NASCET criteria. The origins of the great vessels,\nsubclavian, and vertebral arteries appear normal bilaterally.  The right\nvertebral artery is dominant, a normal variant.\n\nPlease refer to the CT and MR cervical spine exams regarding known severe\ntraumatic C6-7 subluxation injury C2 fracture.",
            "output": "No arterial occlusion or findings to suggest carotid or vertebral artery\ndissection."
        },
        {
            "input": "There is a 3 vessel aortic arch.  Common carotid, cervical internal carotid,\nand vertebral arteries appear widely patent without evidence for flow-limiting\nstenosis.  Right vertebral artery is dominant.  There is ___ termination of\nthe non dominant left vertebral artery.  Fat-suppressed axial T1 weighted\nimages demonstrate no evidence for dissection or intramural hematoma.\n\nRight mandibular fracture was better assessed on the preceding CTA.",
            "output": "Normal MRA neck without evidence for dissection."
        },
        {
            "input": "The sulci, ventricles and cisterns are within expected limits with the degree\nof mild senescent related global cerebral.  There is moderate irregular\nbilateral periventricular and deep white matter hyperintense signal on T2 and\nFLAIR imaging which may reflect chronic small vessel ischemic disease.  There\nis focal T2 and FLAIR hyperintense signal within the subcortical and deep\nwhite matter of the left middle frontal gyrus superiorly which may reflect\nsmall vessel ischemic changes or small remote infarct.  Small foci of\nsusceptibility within the lentiform nucleus bilaterally likely reflect small\ncalcifications.  There is no evidence of hemorrhage, edema, masses, mass\neffect, midline shift or infarction.  There is no abnormal enhancement after\ncontrast administration.  The major intracranial flow voids are preserved. \nThe dural sinuses are patent.  The orbits are unremarkable.  There is mild\nbilateral ethmoid and right posterior sphenoid sinus mucosal thickening.  The\nmastoid air cells appear clear bilaterally.  The osseous structures\ndemonstrate no acute findings.",
            "output": "1. No acute intracranial abnormality on contrast enhanced MRI brain. \nSpecifically no acute infarct or intracranial hemorrhage.  No suspicious\nenhancement or FLAIR signal abnormality.\n2. Generalized cerebral atrophy with chronic bilateral small vessel ischemic\ndisease.  Possible small remote infarct within the left superior frontal lobe.\n3. Additional findings described above."
        },
        {
            "input": "There is no evidence of intracranial hemorrhage, edema, masses, mass effect,\nmidline shift or acute infarction.  Nonspecific multifocal subcortical, deep\nwhite matter and periventricular T2/FLAIR hyperintensities; unchanged compared\nto ___ examination, possible small remote infarct within the left\nsuperior frontal lobe remains unchanged.  The ventricles and sulci are\nslightly prominent suggesting mild cortical volume loss, likely involutional\nand unchanged.  There is no abnormal enhancement after contrast\nadministration.  The major vascular flow voids are preserved, the dural venous\nsinuses enhance normally.\n\nThe orbits are unremarkable, the paranasal sinuses, middle ear cavities and\nmastoid air cells are essentially clear.",
            "output": "1. There is no evidence of acute intracranial process or hemorrhage..\n2. Unchanged subcortical and periventricular areas of T2/high-signal\nintensity, which are nonspecific and may reflect changes due to chronic small\nvessel disease.\n3. There is no evidence of abnormal enhancement after contrast administration.\n4. No definite imaging signs to suggest typical Amyotrophic lateral sclerosis."
        },
        {
            "input": "There is no hemorrhage, edema, mass, mass effect, or evidence of infarction.\nimpression. Principal intracranial vascular flow voids are preserved. No\nextra-axial blood or fluid collection is present. The ventricles and sulci are\nnormal in size and configuration.  Numerous foci of T2/ FLAIR hyperintensity\nin the periventricular and subcortical white matter, predominantly in both\nparietal lobes, are not significantly changed from ___, and as previously\ncharacterized these are nonspecific but most consistent with small vessel\nischemic changes. No diffusion abnormality is detected.  There is no\npathologic parenchymal, leptomeningeal, or dural focus of enhancement after\ncontrast administration.\n\nThe brainstem, posterior fossa and cervical medullary junction are preserved.\nThe orbits are normal.  There is a mucous retention cyst in the left.  The\nremaining paranasal sinuses are clear.  No abnormality of the skull base or\ncalvaria is identified.",
            "output": "1.  No acute intracranial process.\n\n2.  Stable foci of signal abnormality predominantly in the subcortical white\nmatter of both parietal lobes, which are non-specific and suggests changes due\nto chronic small vessel disease."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.",
            "output": "1. Normal brain MRI."
        },
        {
            "input": "MRI BRAIN:\nThere is no evidence of intracranial hemorrhage, mass, mass effect or shifting\nof the normally midline structures.  The ventricles and sulci are normal in\nsize and configuration for patient's age, no diffusion abnormalities are\ndetected, there is no evidence of abnormal enhancement after contrast\nadministration.  The orbits are unremarkable, the paranasal sinuses are\nnotable for minimal mucosal thickening in the ethmoidal air cells, no\nair-fluid levels are seen.  The middle ear cavities and mastoid air cells are\nclear.\n\nMRA brain: The intracranial vertebral and internal carotid arteries and their\nmajor branches appear normal without evidence of stenosis, occlusion, or\naneurysm formation.",
            "output": "1.  Unremarkable MRI of the brain, there is no evidence of acute or subacute\nintracranial process, there is no evidence of abnormal enhancement after\ncontrast administration.\n\n2.  Essentially normal MRA of the head with no evidence of flow stenotic\nlesions or aneurysms.\n\n3.  Mild mucosal thickening identified in the ethmoidal air cells bilaterally,\nno air-fluid levels are seen."
        },
        {
            "input": "Scattered foci of slow diffusion throughout the left frontal, temporal and\nparietal lobes correspond with the left MCA territory.  These areas show\ncorresponding T2/FLAIR hyperintensity and drop in signal on ADC map images. \nThis is in the context of a recently diagnosed left MCA M2 segment thrombosis\nstatus post attempted thrombectomy. There is also a few scattered foci of slow\ndiffusion within the left occipital lobe corresponding to the left PCA\nterritory.\n\nThere is no evidence of acute hemorrhage, mass, mass effect or midline shift.\nThere are mild scattered nonspecific white matter T2/FLAIR hyperintensities\nthat can be seen in the setting of chronic small vessel disease.  Diffuse\nprominence of the ventricle since sulci likely related to age related\ninvolutional changes. There is extensive mucosal thickening of the right\ngreater than left maxillary sinuses.  Moderate mucosal thickening involves the\nright ethmoid air cells.",
            "output": "1. Scattered acute to subacute infarctions predominantly involving the left\nMCA territory into a lesser extent the left PCA territory in a thromboembolic\npattern.\n2. Mild nonspecific scattered white matter T2/FLAIR hyperintensities can be\nseen in the setting of chronic small vessel disease.\n3. Mild parenchymal volume loss is likely age related.\n4. Extensive inflammatory changes involving the right maxillary sinus greater\nthan the left maxillary sinus and right ethmoid air cells.\n\nNOTIFICATION:  Critical result was reported to Dr. ___ by Dr. ___\nby telephone at 13:40 on ___ approximately 30 minutes after the\nfinding was discovered."
        },
        {
            "input": "In the left frontal, and insular regions are hypointensities on FLAIR with\ncorresponding areas of hyperintensity on T2 that likely represent there is\nencephalomalacia which is likely sequela of chronic infarction.  The area of\ninterest in the left parietal region on CT demonstrates no restricted\ndiffusion which is consistent with no evidence of acute/subacute infarction.\n\n\nThere is no evidence of acute infarction, hemorrhage, edema, masses, mass\neffect, midline shift.  Prominence of the ventricles and sulci is suggestive\nof involutional changes that are likely age related.  There are multiple foci\nof T2/FLAIR hyperintensity within the subcortical, deep and periventricular\nwhite matter there may be nonspecific but likely sequela of microvascular\nischemic disease.\n\nNo acute fracture.  There is a mucous retention cyst in the posterior ethmoid\nair cells.  There is moderate mucosal thickening of the left maxillary sinus. \nThe bilateral sphenoid sinuses demonstrate mild mucosal thickening.  The\nbilateral mastoid air cells are pneumatized.  The patient is status post left\nlens replacement surgery.",
            "output": "1. No evidence of acute infarction, hemorrhage, edema mass or mass effect.\n2. Supratentorial white matter changes are non specific but likely sequela of\nchronic microvascular ischemic disease."
        },
        {
            "input": "There is slow diffusion within the left thalamus with a correlate on FLAIR\nimaging suggesting a subacute infarction.  There is a small central focus of\nhemorrhage within the infarction.  There is no evidence of masses, mass\neffect, midline shift.\nThe ventricles and sulci are prominent suggesting involutional changes. \nModerate T2/FLAIR hyperintensities within the subcortical and periventricular\nwhite matter are nonspecific but may represent sequela chronic microvascular\nischemic disease.\n\nThe medial temporal lobe atrophy score is approximately 3.\n\nThere is moderate mucosal thickening of the bilateral ethmoid air cells.  The\nother paranasal sinuses, and mastoid air cells are well pneumatized.  The flow\nvoids are preserved.",
            "output": "1. Left thalamic subacute infarction with a central focus of hemorrhage.\n2. Findings suggesting chronic small vessel ischemia.\n\nNOTIFICATION:  The findings were discussed with ___ , M.D. by\n___, M.D. on the telephone on ___ at 11:24 am, 5 minutes\nafter discovery of the findings."
        },
        {
            "input": "MRV: Normal flow signal is demonstrated within the superior sagittal sinus,\nstraight sinus, transverse sinuses, and sigmoid sinuses. The jugular bulbs and\nproximal jugular veins are patent. Evaluation of the deep venous systems\nreveals normal flow signal in the thalamostriate veins and internal cerebral\nveins. The vein ___ is also unremarkable.\n\nPRE AND POSTCONTRAST T1 BRAIN IMAGING: There is no abnormal enhancement on\npostcontrast imaging. There is no midline shift, abnormal extra-axial fluid\ncollection, or mass identified. The ventricles and sulci are preserved.  A\nsingle, left, white-matter based T2 hyperintensity is noted, of uncertain\nsignificance.  The sella is noted to be partially empty.  The orbits,\nparanasal sinuses, and mastoid air cells are preserved.  Mildly prominent CSF\nspaces are noted surrounding the bilateral optic nerves.",
            "output": "1. Findings of a partially empty sella and mildly prominent bilateral optic\nnerve sheaths can be seen in the setting of benign intracranial hypertension. \nOtherwise, unremarkable MRI of the brain.\n2. Normal MRV of the brain."
        },
        {
            "input": "Please note the examination is moderately degraded by patient motion. \nAllowing for this limitation:\n\n There is a small focus of elevated signal on diffusion-weighted sequences\nseen at the high left paramedian frontal lobe (04:27) without definite\ncorrelate on ADC map.  However, there is correlating FLAIR hyperintensity at\nthis site, suggesting a subacute infarct.  Question punctate left frontal\nmiddle gyrus punctate chronic blood products versus mineralization (see\n11:19).\n\nAllowing for this, no evidence for additional sites of infarct.  No acute\nintracranial hemorrhage is identified.  No mass, mass effect, edema or midline\nshift.  A prominent right paramedian retro cerebellar CSF space most likely\nrepresents an arachnoid cyst.\n\nThe ventricles and sulci are mildly prominent compatible with global\nparenchymal volume loss.  There is gross preservation of the principal\nintracranial vascular flow voids.\n\nMucosal thickening is seen in the bilateral sphenoid sinuses and scattered\nethmoid air cells.  Mastoid fluid is noted bilaterally.  The orbits are within\nnormal limits bilaterally.",
            "output": "1.  Study is moderately degraded by motion.\n2. Small focus of probable subacute infarction involving the left frontal\nsuperior gyrus.\n3. No acute intracranial hemorrhage.\n4. Question punctate left frontal middle gyrus chronic blood products versus\nmineralization.\n5. Mild global parenchymal volume loss, paranasal sinus disease, and bilateral\nmastoid fluid, as described."
        },
        {
            "input": "There are stable postoperative changes from right frontoparietal craniotomy\nand right frontal lobe mass resection. There is unchanged FLAIR hyperintense\nsignal within the right frontal lobe.  There is also stable right temporal\nlobe sulcal enhancement (series 102a, image 85) dating back to ___. There is\nno new FLAIR signal abnormality or abnormal enhancement. There is no infarct,\nor acute hemorrhage. Principal intracranial flow voids are present.",
            "output": "Unchanged post treatment changes in the right frontal lobe. There is no new\nenhancement or FLAIR signal abnormality to indicate disease progression."
        },
        {
            "input": "The patient is status post right frontal craniotomy with stable post treatment\nchanges of the right frontal lobe. The extent and configuration of confluent\nFLAIR white matter hyperintensity extending from the right frontal convexity\nto the level of the lateral ventricles is unchanged in configuration from\nprior exam.  Enhancing FLAIR hyperintensity in the right temporal lobe is also\nunchanged (series 10, series 9). This region FLAIR hyperintense and\ndemonstrates mild postcontrast enhancement, also essentially unchanged in\nconfiguration from prior exam. No new abnormal enhancement. No evidence of\nacute infarct. Sulci, ventricles and cisterns are within expected limits. The\nintracranial flow voids are preserved. Mild mucosal thickening of the\nmaxillary sinuses. Otherwise, the remainder of the paranasal sinuses are\nessentially clear. The orbits are unremarkable. The mastoid air cells are\nclear.",
            "output": "Unchanged posttreatment findings in the right frontal lobe.  Stable enhancing\nFLAIR hyperintense focus in the right temporal lobe.  Long term followup is\nadvised."
        },
        {
            "input": "Impression no significant interval change postsurgical changes and FLAIR\nhyperintensities identified with hypointensity on T1 weighted images.\nFollowing gadolinium there is no abnormal parenchymal vascular or meningeal\nenhancement seen. There are no acute infarcts. There are no new areas of blood\nproducts.",
            "output": "Stable appearance of the bifrontal hyperintensity without enhancement compared\nto the previous MRI examinations. No new signal abnormalities or abnormal\nenhancement seen."
        },
        {
            "input": "Please note the study is mildly degraded by motion.\n\nThe patient is again noted to be status post right frontal craniotomy with\nstable post treatment changes in the right frontal lobe. T2/FLAIR white matter\nhyperintensity extending from the right frontal convexity to the level of the\nlateral ventricles is unchanged in configuration from prior exam.  Enhancing\nFLAIR hyperintensity in the right temporal lobe is also unchanged (series 6,\nseries 11 on the current study and series 15, images 9 on the ___\nprior exam).  There are no new regions of abnormal enhancement.\n\nThere is no evidence of acute infarct. Sulci, ventricles and cisterns are\nwithin expected limits. The intracranial flow voids are preserved.  There is\nmild mucosal thickening of the maxillary sinuses. Otherwise, the remainder of\nthe paranasal sinuses are essentially clear. The orbits are unremarkable. The\nmastoid air cells are clear.",
            "output": "1. No significant interval change in post treatment findings in the right\nfrontal lobe.\n2. Stable nonspecific enhancing right temporal lobe parenchymal signal\nintensity abnormality as described, unchanged compared to ___ prior\nexam.\n3. No new enhancing lesions identified."
        },
        {
            "input": "The examination is motion degraded.  Within these confines:\n\nThe patient is status post right frontal craniotomy and resection of a right\nfrontal lobe mass.  T2/FLAIR white matter hyperintensity of the right frontal\nconvexity to the level of the lateral ventricles is unchanged in configuration\nfrom prior exam.\n\nRe-identified is enhancing FLAIR hyperintense signal of the right temporal\nlobe along its outer convexity (series 1201b, image 40) also unchanged from\nprior exam.\n\nNo new enhancement.  No new lesions.  There is no evidence of acute infarct or\nintracranial hemorrhage.  The sulci, ventricles and cisterns are within\nexpected limits for the patient's age.  The intracranial flow voids are\npreserved.  The dural venous sinuses are patent.  Re-identified are mild\nmucosal thickening of the paranasal sinuses and small mucous retention cysts\nof the maxillary sinuses.  The mastoid air cells are clear.  The orbits are\nunremarkable.",
            "output": "1. Unchanged postsurgical appearance of right frontal craniotomy and resection\nof a right frontal lobe mass.  Right frontal white matter FLAIR hyperintense\nsignal is unchanged configuration.\n2. Stable enhancing FLAIR hyperintense focus of the right temporal lobe.\n3. No new lesions.  No acute infarct or acute intracranial hemorrhage."
        },
        {
            "input": "There is a right frontal craniotomy with thin subjacent dural enhancement. \nThere is a right frontal lobe resection cavity with thin linear central\nenhancement which is unchanged comparison to multiple prior studies, likely\nrepresenting postsurgical change.  There is extensive adjacent FLAIR\nhyperintensity throughout the right frontal subcortical white matter, centrum\nsemiovale, and corona radiata, which is relatively unchanged and may represent\npost treatment change versus nonenhancing disease.  There is left\nperiventricular and right periatrial white matter FLAIR hyperintensity, likely\nrepresenting post treatment change.\n\nThere is no acute infarct or hemorrhage.  The ventricles and cortical sulci\nare normal in caliber and configuration.  The extra-axial spaces are\nunremarkable.  The vascular flow voids are preserved.\n\nThe orbits and soft tissues are unremarkable.  There is mild mucosal\nthickening within the bilateral maxillary sinuses.",
            "output": "1. Right frontal resection cavity with unchanged central linear enhancement,\nlikely representing postsurgical change.  Extensive FLAIR hyperintensity\nmarginating the resection cavity throughout the right frontal lobe white\nmatter, which is unchanged in comparison to multiple prior studies consistent\nwith posttreatment change versus nonenhancing disease.  No evidence of\nprogressive or new sites of disease.\n2. No acute intracranial abnormality."
        },
        {
            "input": "Examination is limited by motion artifact, particularly on the MP rage images.\n\nThere are postsurgical changes from right frontal craniotomy and mass\nresection including underlying dural thickening and enhancement.  Minimal\nareas of serpentine enhancement within the superior aspect of the resection\nbed are unchanged over numerous prior examinations, likely reflecting\npostsurgical change.  Areas of surrounding right frontal white matter T2/FLAIR\nhyperintensity is unchanged.  Areas of left periventricular white matter\nT2/FLAIR hyperintensity likely reflect posttreatment change.\n\nThere is no evidence of acute hemorrhage, worsening edema, new masses, mass\neffect, midline shift or infarction.   The ventricles and sulci are normal in\ncaliber and configuration.  There is no abnormal focus of slowed diffusion. \nThe principal intracranial vascular flow voids are preserved.\n\nThere is mild polypoid mucosal wall thickening in the inferior aspects of the\nmaxillary sinuses.  The remainder the visualized paranasal sinuses are grossly\nclear.  The orbits are grossly unremarkable.",
            "output": "1. Stable postsurgical changes from right frontal craniotomy and mass\nresection with unchanged areas of serpentine enhancement within the superior\naspect of the resection bed likely reflecting posttreatment change. \nSurrounding white matter FLAIR hyperintensity is unchanged, reflecting either\nposttreatment change or infiltrative disease.  No evidence of local disease\nprogression or new enhancing mass.\n2. No hemorrhage, infarct, or new enhancing mass."
        },
        {
            "input": "Again postsurgical changes are re-demonstrated in the right frontal region\nconsistent with craniotomy, the patient is status post mass resection, minimal\nunderlying vascular and dural thickening remains unchanged.  On the FLAIR\nimages, there are unchanged high-signal intensity areas in the left centrum\nsemiovale, subcortical white matter and surrounding the surgical cavity,\nconsistent with posttreatment changes.  No new enhancing lesions are seen.  No\ndiffusion abnormalities are detected.  The ventricles and sulci remain\nunchanged and are unremarkable, there is no evidence of acute intracranial\nhemorrhage, mass effect or shifting of the normally midline structures.  The\nvascular flow voids are present and demonstrate normal distribution.  The\norbits are unremarkable, the paranasal sinuses are notable for bilateral\nmucosal thickening in the maxillary sinuses bilaterally, grossly unchanged\nsince the prior exam, the mastoid air cells are clear.",
            "output": "1.  Allowing for the slice selection and technique, no significant changes are\ndemonstrated in the right frontal craniotomy site, the patient is status post\nmass resection, there is no evidence of abnormal enhancement to indicate\ntumoral recurrence or new mass lesion.\n\n2.  Subcortical and periventricular white matter hyperintensities detected on\nFLAIR and T2 weighted images remain unchanged, likely consistent with\nposttreatment changes, the possibility of infiltration cannot be completely\nrule out, and long-term followup is advised."
        },
        {
            "input": "The patient is status post right frontal craniotomy and resection of a right\nfrontal mass lesion, in comparison with the most recent exam, again there is\nminimal and stable pattern of enhancement in the surgical bed with no evidence\nof tumoral recurrence or residual mass lesion, the pattern of enhancement in\nthe surgical area apparently is dural and vascular in nature, however\nlong-term follow is recommended to demonstrate stability or any further\nchanges.  Similar pattern of T2/FLAIR hyperintensities noted in both centrum\nsemiovale with similar extension towards the right cingulate gyrus and corpus\ncallosum, likely consistent with posttreatment changes, no diffusion\nabnormalities are detected to indicate acute or subacute ischemic changes. \nThere is no evidence of acute intracranial hemorrhage.  No new lesions or new\nareas of abnormal enhancement are identified after contrast administration. \nThe major vascular flow voids are present and demonstrate normal distribution.\nThe orbits are unremarkable, the paranasal sinuses are notable for unchanged\nbilateral mucous retention cysts in both maxillary sinuses, no air-fluid\nlevels are seen, the mastoid air cells are clear.",
            "output": "1.  Status post right frontal craniotomy and right frontal mass resection with\nminimal pattern of dural and vascular enhancement in the surgical bed, likely\npostsurgical in nature there is no evidence of tumor recurrence or new mass\nlesion.\n\n2.  Unchanged T2/FLAIR high-signal intensity identified in the centrum\nsemiovale bilaterally, more extensive on the right, likely consistent with\nposttreatment changes."
        },
        {
            "input": "Brain MR ___, and ___.\n\nFINDINGS: \n\nNew since the prior studies is a 5 mm enhancing focus in the right posterior\nfrontal lobe, likely involving motor cortex. This is best seen on image 16 of\nseries 10. This is also demonstrated on image 94 of series 901. The area\ndemonstrates slightly slow diffusion, a new finding since the prior studies.\nThe etiology of this is uncertain. Given the history of a neoplasm, there is a\nconcern of a possible recurrence or disease progression. However, the\nelongated configuration of the lesion on the coronal images suggest that it\nmay be a subacute infarction instead. The lesion is far too small for\nspectroscopy to be helpful. It is likely too small to be resolved with\nperfusion imaging, although a larger area of hyperperfusion might be detected.\nEven ascent lesion such is these may be seen in regions of prior radiation. At\na minimum, careful follow-up is recommended.\n\nImages of the remainder of the brain appear unchanged. Again seen are\npostoperative findings after right frontal craniotomy for tumor resection.\nThere are broad areas of white matter hyperintensity on the FLAIR images, some\nof which wide in the overlying gyri. There is no sulcal enlargement. These\nfindings suggest that at least a component of the white-matter change reflects\nedema rather than tissue loss. However, there is no abnormal enhancement\ncenter or around the margins of the resection cavity.\n\nThere is no other abnormal enhancement. There are no other findings worrisome\nfor infarction. Mucosal thickening in the maxillary sinuses bilaterally\nappears somewhat more prominent than on the study of ___.\nThe ventricles and sulci are normal in caliber and configuration.  There is no\nabnormal enhancement after contrast administration.",
            "output": "1. 5 mm enhancing focus in the right posterior frontal lobe, perhaps involving\nthe motor cortex.  This is new since the prior study and may represent tumor\nprogression, subacute infarction, or radiation change.\n2. This new lesion is too small for spectroscopy and likely too small for\nperfusion imaging to be helpful.\n3. At a minimum, close follow-up is recommended.\n4. There have been no other significant changes.  There are no other findings\nworrisome for tumor progression or other pathology.\n\nRECOMMENDATION(S):  Close follow-up of right posterior frontal enhancing\nlesion."
        },
        {
            "input": "In comparison with the most recent examination dated ___, the focus\nof enhancement identified in the posterior aspect of the right frontal lobe\nappears slightly larger and measures approximately 7 x 6 mm in transverse\ndimension (image 18, series 10), previously 4 x 4 mm in transverse dimension,\nadditionally these lesion is extending towards the right central gyrus as\ndemonstrated on the image 20, series 10, and image 92, series 901).  Similar\npattern of high-signal intensity is identified on FLAIR and T2 weighted images\nsurrounding the surgical cavity and left centrum semiovale consistent with\nposttreatment changes, and in lesser degree in the left centrum semiovale. \nThere is minimal pattern of enhancement in the surgical bed the patient is\nstatus post bifrontal craniotomy, no other new areas with abnormal enhancement\nare seen.  No diffusion abnormalities are detected to indicate acute or\nsubacute ischemic changes.  The major vascular flow voids are present and\ndemonstrate normal distribution.  The orbits are unremarkable, the paranasal\nsinuses demonstrate bilateral mucous retention cysts in the maxillary sinuses,\nmild mucosal thickening is noted in the left mastoid air cells, apparently new\nsince the prior exam.",
            "output": "1.  In comparison with the most recent examination, the previously noted focus\nof enhancement identified in the posterior aspect of the right frontal lobe\nappears slightly larger measuring approximately 7 x 6 mm and previously 4 x 4\nmm, this finding is concerning for tumoral activity, however posttreatment\nchanges cannot be completely rule out and close attention this area is advised\nas well as follow-up with perfusion and MRI spectroscopy.  No other areas with\nabnormal enhancement are seen.\n\n2.  Similar pattern of T2/FLAIR high-signal intensity is noted in the centrum\nsemiovale bilaterally, more significant on the right consistent with\nposttreatment changes.\n\nRECOMMENDATION(S):  In comparison with the most recent examination, the\npreviously noted focus of enhancement identified in the posterior aspect of\nthe right frontal lobe appears slightly larger measuring approximately 7 x 6\nmm and previously 4 x 4 mm, this finding is concerning for tumoral activity,\nhowever posttreatment changes cannot be completely rule out and close\nattention this area is advised as well as follow-up with perfusion and MRI\nspectroscopy."
        },
        {
            "input": "MR BRAIN: The patient is status post right frontal parietal craniotomy and\nunderlying resection.  Mild postsurgical dural thickening and enhancement\nunderlying the craniotomy is overall similar to prior examination.\n\nA hazy region of enhancement along the posterior margins of the resection\ncavity at the right frontal vertex appears much less conspicuous on the\ncurrent examination, measuring approximately 2 mm (series 12, image 241;\nseries 11, image 18).  Geographic right frontal T2/FLAIR white matter\nhyperintense edema pattern are unchanged in configuration from prior exam. \nSuperimposed periventricular and subcortical T2/FLAIR white matter\nhyperintensities are unchanged from prior examination, nonspecific.  No\ndefinitive new regions of abnormal nodular enhancement.  No new FLAIR\nparenchymal signal abnormality.  The major intracranial flow voids are\npreserved.  The dural venous sinuses are patent.  Mild mucosal thickening of\nthe ethmoid air cells and maxillary sinuses with superimposed small maxillary\nsinus mucous retention cysts.  The orbits are unremarkable.  Fluid signal is\nseen in the left mastoid air cells.  No suspicious marrow signal.\n\nMR ___: No evidence of increased perfusion on dynamic\nsusceptibility contrast.\n\nASL Perfusion: No definite increased perfusion corresponding to regions of\nenhancement.\n\nMR Spectroscopy: Single voxel spectroscopy centered over the enhancing right\nfrontal lesion as well as multi voxel spectroscopy centered over the enhancing\nlesion and the contralateral normal appearing left frontal lobe.  No evidence\nof increased choline to NAA ratio.",
            "output": "1. Previously described increasing enhancement along the posterior margins of\nthe right frontal resection cavity has decreased in conspicuity since the\nprior examination.  Given overall improvement, this may represent evolving\nsequela of posttreatment change rather than tumor progression.  However,\ncontinued close interval followup is recommended to document stability or\nresolution to exclude progression.\n2. No evidence of increased perfusion on dynamic susceptibility contrast or\nASL.  Single voxel and multi voxel spectroscopy does not demonstrate increased\ncholine to NAA ratio to suggest recurrence/progression.\n3. Unchanged T2/FLAIR white matter hyperintensity of the right frontal lobe\nassociated with posttreatment sequela.\n4. Additional findings as described above."
        },
        {
            "input": "Postoperative changes in the right frontal region are demonstrated, including\nfocal dural thickening and blood products.  New heterogeneous enhancement is\nseen surrounding the resection cavity extending towards the right centrum\nsemiovale, along with new areas of slow diffusion.  The degree of surrounding\nT2 signal abnormality is unchanged.\n\nAdditionally, new foci of enhancement are seen in the right frontal lobe\n(9:110, 103) and right corona radiata (9:92).  An unchanged focus of\nenhancement is also seen in the right temporal lobe (09:43).\n\nThe ventricles and sulci are within normal limits.  There is mild mucosal\nthickening of the maxillary sinuses.  The mastoid air cells and middle ear\ncavities are clear.  The intraorbital contents are normal.",
            "output": "1. Findings concerning for tumor recurrence extending in the right frontal\nsurgical cavity,  right centrum semiovale, with new heterogeneous enhancement,\nand slow diffusion.  MRI spectroscopy and MRI perfusion analysis are\nrecommended.\n2. New foci of enhancement are seen in the right frontal lobe are corona\nradiata, concerning for additional tumor foci.\n\nRECOMMENDATION(S):  Findings concerning for tumor recurrence, with new\nheterogeneous surrounding the resection cavity, with new areas of slow\ndiffusivity.  MRI spectroscopy and MRI perfusion analysis are recommended."
        },
        {
            "input": "Study is mildly degraded by motion.\n\nThe patient's previously noted right frontal 6.7 x 3.3 x 4.5 cm\nheterogeneously enhancing mass is again seen.  There is no midline shift and\nmild regional mass effect, primarily consisting of downward mass-effect on the\nbody of the right lateral ventricle.  No herniation or ventricular entrapment.\nAgain seen are small foci of enhancement within the right corona radiata at a\nslight distance from the primary mass, most distant measuring up to 1.6 cm\nfrom the inferior margin of the mass (series 100, image 60).  Ventricles and\nsulci are grossly stable in size and configuration.\n\nThere is no evidence of infarction or extra-axial collection.  Major dural\nvenous sinuses are grossly patent.",
            "output": "1. Study is mildly degraded by motion.\n2. Limited pre-surgical planning MRI again demonstrating the heterogeneously\nenhancing 6.7 cm high right frontal lobe mass, again with small foci of\nenhancement seen lateral and inferior to the mass in the right corona radiata."
        },
        {
            "input": "Study is moderately degraded by motion.\n\nPatient is status post right frontal craniotomy for of oligoastrocytoma\nresection, with expected postsurgical changes including hemorrhage products in\nthe resection cavity and small volume pneumocephalus, which is decreased. \nThin enhancement around the periphery of the resection cavity may reflect\npostsurgical change.  Close attention on follow-up imaging is recommended. \nSmall foci of enhancement lateral and inferior to the surgical cavity, in the\nright corona radiata, remain (14: 118, 128).  There is persistent confluent\nedema in the right frontal lobe white matter.  Diffusion-weighted\nhyperintensity along the resection margins identified compatible with\npostsurgical ischemic change.\n\nThere is no acute infarction or midline shift.  No significant extra-axial\ncollection is identified.  There is decreased mass effect on the right lateral\nventricle.\n\nThe major cerebrovascular flow patterns are unremarkable.  The dural venous\nsinuses are patent.\n\nThe orbits are unremarkable.  Small mucous retention cysts are seen in the\nbilateral maxillary sinuses.",
            "output": "1. Study is moderately degraded by motion.\n2. Status post right frontal craniotomy for tumor resection with evolving\npostsurgical changes, including hemorrhage product within the resection\ncavity.\n3. Thin enhancement around the periphery of the resection cavity may reflect\npostsurgical change.  However, mall foci of enhancement lateral and inferior\nto the surgical cavity, in the right corona radiata, remain and may represent\nresidual tumor.  Close attention on follow-up is recommended.\n4. No expected intracranial hemorrhage or infarct.  Additional findings\ndescribed above."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.",
            "output": "1. Normal brain MRI."
        },
        {
            "input": "Image quality is mild to moderately degraded by patient motion, within this\nlimitation:\n\nThere are again postoperative changes from right superior frontal craniotomy\nand tumor resection.  There is stable appearance of dural thickening and\nenhancement subjacent to the craniotomy site which is probably postoperative. \nChronic blood products associated with the surgical cavity.  Enhancement in\nthe superior frontal lobe resection cavity margins has overall diminished,\nalthough there is still thickened irregular enhancement at the medial aspect\nof the cavity margin on image 135  series 8.  The extent of T2 prolongation\nsurrounding the resection cavity extending into the corona radiata is similar\nto previous exam there are a few areas of slowed diffusion in the confluent\nwhite matter changes adjacent to the cavity margin for instance on image 25 of\nseries 402, but there were similar findings previously.  No new slowed\ndiffusion.  No new signal abnormality.  No evidence of hemorrhage or infarct.\n\nElsewhere, there are scattered areas of nonspecific T2/FLAIR hyperintensity\nwhich are stable.  There is stable ventricular size with no evidence of\nhydrocephalus.  Ex vacuo dilatation of the superior body of the right lateral\nventricle adjacent to the surgical cavity is noted.\n\nThe major intracranial vascular flow voids are preserved.  Orbits are\nunremarkable.  There is scattered mucosal thickening throughout the paranasal\nsinuses and there are mucous retention cysts in the maxillary sinuses.",
            "output": "1.  Postsurgical changes following right frontal craniotomy and tumor\nresection.  Enhancement surrounding the cavity has decreased compared to the\nprevious examination.  The remaining area of somewhat irregular enhancement at\nthe medial margin probably reflects postoperative change, but attention to\nthis region on follow-up is recommended.\n\n2.  There are a few areas of persistent slow diffusion in the confluent T2\nsignal changes surrounding the resection cavity, not corresponding to the\nabove described irregular enhancing abnormality.  These regions could reflect\nresidual tumor.  Close attention to these regions on follow-up recommended.\n\n3.  No new areas of signal abnormality or abnormal enhancement."
        },
        {
            "input": "Postoperative changes from right superior frontal craniotomy with tumor\nresection are redemonstrated.  These changes are overall stable in appearance\nwhen compared to the most recent ___ MR head as well as the ___ MR head.  Right frontal dural thickening and enhancement subjacent to the\ncraniotomy site is unchanged.  Peripheral enhancement around the resection\ncavity as well as persistent irregular thickening and enhancement along the\nmedial aspect of the resection cavity are similar to ___ MR\n(___) but have improved when compared to ___ MR. ___ of\nparenchymal T2/FLAIR hyperintensity surrounding the resection cavity involving\nthe corona radiata remains unchanged (10:22, 9:22) from ___.  Areas of\nslow diffusion within the confluent white matter changes adjacent to the\ncavity margins are also unchanged, for example in series 750, image 26.  There\nare no new areas of slow diffusion.  No new areas of abnormal enhancement. \nEnhancement overlying the right temporal lobe is stable compared to numerous\nprevious exams going back to at least ___.\n\nRemainder of the brain parenchyma demonstrates scattered areas of nonspecific\nT2 and FLAIR hyperintensities which are stable.  Focal ex vacuo dilatation of\nthe superior body of the right lateral ventricle adjacent to the frontal lobe\nthe resection cavity is expected and remains unchanged.  The remainder of the\nventricles are normal in caliber.\n\n The imaged paranasal sinuses are clear. The orbits and extracranial soft\ntissues are unremarkable. The major intracranial flow voids are preserved.",
            "output": "1. Overall the postsurgical changes following right frontal craniotomy with\ntumor resection are unchanged from ___ MR head.  The degree of\nperipheral enhancement around the resection cavity particularly along the\nmedial aspect of the cavity is also unchanged from ___ MR head,\nalthough overall improved since ___ MR head; recommend attention on\nfollow-up.\n2. Areas of prominent persistent slow diffusion within the confluence T2\nsignal changes around the resection cavity remain unchanged since ___\nMR head.  These areas remain indeterminate and could represent residual tumor\nversus postoperative changes.  Continued attention on follow-up is\nrecommended.\n3. No new areas of disease identified."
        },
        {
            "input": "Postsurgical changes are again demonstrated from right superior frontal\ncraniotomy and tumor resection.  These findings are stable compared to\nprevious examinations, with areas of irregular enhancement again demonstrated,\ndecreased from ___ and stable since ___.  The extent of T2\nprolongation surrounding the cavity involving the corona radiata is similar to\nthe previous examination with no definite new signal abnormality, and no new\ndiffusion abnormality.  Diffusion changes at the posterior margin of the\ncavity appear decreased since the previous exam.  The diffusion abnormality\npersists along the rim of the surgical cavity.  No new areas of abnormal\nenhancement, diffusion abnormality, or hemorrhage.  Scattered areas of\nsusceptibility are again seen indicating old blood products.\n\nElsewhere, there are again scattered nonspecific T2/FLAIR hyperintensities in\nthe white matter which are stable.  Stable ventricular size and configuration\nwith ex vacuo dilatation of the frontal horn of the right lateral ventricle\nagain noted.\n\nThe major intracranial vascular flow voids are preserved.  Orbits and soft\ntissues are unremarkable.  There is mild scattered mucosal thickening in the\nparanasal sinuses with small mucous retention cysts in the maxillary sinuses.",
            "output": "1. Post treatment changes again demonstrated following right frontal\ncraniotomy and tumor resection.  Stable degree of peripheral enhancement\nsurrounding the resection cavity, with improved areas of slow diffusion\ncompared to the previous exam.\n2. No new area of disease is demonstrated."
        },
        {
            "input": "No evidence of mass or adenopathy.  Symmetric prominence bilateral lingual\ntonsils, likely reactive.  No MRI evidence of palatine tonsillar mass. Normal\nnasopharynx.  Anterior oral cavity suboptimally seen secondary to metal\nartifact from dental work.  Remainder of the aerodigestive tract is normal.\n\nAtrophy of bilateral superficial and deep parotid lobes with prominent\naccessory parotid gland tissue.  Atrophic submandibular glands bilaterally. \nMild paranasal sinus disease..  Degenerative changes cervical spine.  Probably\nmoderate central canal narrowing C6-C7 level.  Preserved vascular flow voids. \nPartially visualized intracranial structures are normal.",
            "output": "1. No mass or adenopathy."
        },
        {
            "input": "The right transfrontal ventriculostomy catheter tip is located within the\nfrontal horn left lateral ventricle, unchanged since the ___ CT. \nDiffuse ventriculomegaly, without enlargement of the sulci, is unchanged\ncompared to the ___ CT but slightly increased compared to ___ MRI.\n\nInterrupted foci of contrast enhancement along the margins of the right\nparietal surgical cavity are again seen, with decreased enhancement medially,\nimage 100:62.  Surrounding T2 hyperintensity is stable.\n\nThe following unchanged small supratentorial metastases are seen on series\n100:\nLeft medial parietal cortical lesion without edema, image 76.\nRight caudate lesions with interim resolution of previously seen mild edema,\nimages 69 and 63.\n\nThere is a new 3 mm enhancing focus in a medial left frontal sulcus, image\n100:69, without edema.\n\nThere is new leptomeningeal contrast enhancement along the medial temporal\nlobes, image 100:45, in the right sylvian fissure, image 100:50 and probably\nalso along the anterior temporal lobes, images 100:45 and 100:48.\n\nExtensive leptomeningeal contrast enhancement along the cerebellar folia,\ngreatest along the superior vermis, appear slightly progressed. \nLeptomeningeal contrast enhancement along the ventral brainstem may have\nslightly progressed, particularly in the interpeduncular cistern on image\n100:45.  Leptomeningeal contrast enhancement along the seventh and eighth\ncranial nerves, and, to a lesser extent, along the fifth cranial nerves, is\nagain seen.  Leptomeningeal contrast enhancement extends along the visualized\ncervical spinal cord, as seen previously.\n\nDiffusion-weighted images were obtained with incorrect coverage, including the\ncervical spine and the lower posterior fossa only.  No acute infarction is\nseen in the visualized posterior fossa or cervical cord.\n\nThere is no evidence for new blood products.  Confluent T2 hyperintensity in\nthe periventricular and deep white matter of the cerebral hemispheres, as well\nas discrete foci of T2 hyperintensity in the subcortical white matter of the\ncerebral hemispheres, are not significantly changed, likely related to sequela\nof whole brain radiation therapy as well as chronic small vessel ischemic\nchanges.  Major vascular flow voids appear grossly preserved.  Dural venous\nsinuses appear patent on postcontrast MP RAGE images.\n\nNumerous osseous metastases in the calvarium and visualized upper cervical\nspine do not appear significantly changed.  A small lipoma is again\nincidentally noted overlying the left frontal bone fall with confirmed fat\ndensity on the ___ CT, image 22:17.\n\nThere is mild mucosal thickening in the ethmoid air cells.",
            "output": "1. Progression of leptomeningeal metastatic disease, with a new 3 mm enhancing\nfocus in a medial left frontal sulcus, new leptomeningeal contrast enhancement\nalong the temporal lobes and right sylvian fissure, and slightly increased\nleptomeningeal contrast enhancement along the cerebellum.  Leptomeningeal\ncontrast enhancement is again seen along the brainstem possibly increased)\nalong the seventh, eighth, and fifth cranial nerves, and extending along the\nincluded upper cervical spinal cord.\n2. Interrupted contrast enhancement along the right parietal surgical cavity\nmargins has slightly decreased.\n3. Stable small left medial parietal cortical enhancing lesion.  Stable small\nenhancing lesions in the right caudate with interim resolution of prior mild\nedema.\n4. No significant change is seen in numerous osseous metastases.\n5. Diffusion-weighted images were obtained with incorrect coverage, including\nthe cervical spine and the lower posterior fossa only. No acute infarction is\nseen in the visualized posterior fossa or cervical cord.  If clinically\nwarranted, these may be repeated with correct coverage at no additional charge\nto the patient.\n\nNOTIFICATION:  The impression above was entered by Dr. ___ on\n___ at 14:38 into the Department of Radiology critical communications\nsystem for direct communication to the referring provider."
        },
        {
            "input": "MRI BRAIN:\n\nMultiple enhancing intracranial masses are seen, the largest of which is\nlocated in the right parietal-occipital region, measuring 3 x 2.2 cm, with\nextensive surrounding edema, which causes effacement of the occipital horn of\nthe right lateral ventricle and 3 mm of leftward shift of the normally midline\nstructures.  There is associated asymmetrical dural enhancement adjacent to\nthis lesion (12:15), which may be reactive, however tumor infiltration is not\nexcluded.  Additional enhancing lesions, some with associated edema, are seen\nwithin the right cerebellar hemisphere,  anterior cerebellar lobe, right\nfrontal lobe, right caudate head, left temporal lobe, and left parietal lobe. \nNumerous calvarial metastases are also seen.  No evidence of acute infarct or\nlarge intracranial hemorrhage.\n\nMRA brain: The intracranial vertebral and internal carotid arteries and their\nmajor branches appear normal without evidence of stenosis, occlusion, or\naneurysm formation.",
            "output": "1. Multiple enhancing intracranial masses concerning for metastatic disease. \nThe largest of these is located in the right parietal occipital region,\nmeasuring up to 3 cm.  This lesion is associated with surrounding edema, which\ncauses effacement of the occipital horn of the right lateral ventricle and\nleftward shift of the midline structures, described above.\n2. Numerous calvarial metastases.\n3. No intracranial aneurysm.\n\nNOTIFICATION:  The findings were discussed with Dr. ___,  by ___\n___, M.D. on the telephone on ___ at 10:01 AM, 5 minutes after\ndiscovery of the findings."
        },
        {
            "input": "Re-identified are several supratentorial and infratentorial enhancing\nmetastatic lesions, with several of the lesions demonstrating susceptibility\nartifact, consistent with hemorrhage.  The largest lesion, located in the\nright parietal lobe, measures 20 x 15 mm, previously 26 x 17 mm (1000b:72). \nSurrounding vasogenic edema appears decreased compared to the prior study.\n\nLeft parasagittal parietal lesion measures 3 mm, previously 5 mm (1000b:82).\n\n7 mm right caudate head lesion previously measured 9 mm (1000b:70).\n\nLeft temporoparietal lesion measures 6 mm, previously 10 mm (1000b:66).\n\n2 mm enhancing lesion at the level of the right caudate head is unchanged\n(1000b:64).\n\n5 mm right frontal operculum lesion previously measured 8 mm (1000b:58).\n\n3 mm lesion centered in the right putamen previously measured 4 mm (1000b:58).\n\n2 mm focus of left frontal paramedian leptomeningeal enhancement previously\nmeasured 3 mm (11:24).\n\nPunctate 1 mm focus of right parietal leptomeningeal enhancement is smaller\n(1000b:96).\n\nA faint punctate focus of enhancement in the left genu of the corpus callosum\nis far less apparent than on prior exam (11:17).\n\n4 mm cerebellar lesion just to the left of midline is unchanged (1000b:45).\n\n4 and 5 mm enhancing lesions in the right cerebellar hemisphere have decreased\nin size, both previously measuring 7 mm (1000 B: 26, 28).\n\nNo new enhancing lesion is identified.  Edema surrounding the metastatic\nlesions appears overall decreased.\n\nThere is no evidence of acute hemorrhage, edema, midline shift or infarction. \nThere is moderate prominence of the ventricles and sulci suggestive of\ninvolutional change.  The dural venous sinuses are patent on MP-RAGE images. \nThe principal intracranial vascular flow voids are preserved.\n\nThere is trace mucosal wall thickening in the bilateral maxillary and ethmoid\nsinuses.  The remainder the visualized paranasal sinuses are grossly clear. \nThe orbits are grossly unremarkable.  There is opacification of a few inferior\nmastoid tip air cells.\n\nRe-identified are numerous nonenhancing and enhancing calvarial lesions with\nmost prominent enhancing lesion in the left parietal calvarium measuring up to\n14 x 9 mm, and of the upper cervical spine unchanged compared to the prior\nexamination.  Numerous other calvarial lesions appear grossly unchanged.  No\ndefinite new calvarial lesion is identified.",
            "output": "1. Numerous enhancing supratentorial and infratentorial metastatic lesions,\nsome hemorrhagic, are re-identified, the majority of which demonstrate\ninterval decrease in size and decrease of surrounding vasogenic edema, though\na few small lesions are similar.  A few lesions appear to be leptomeningeal\nbased.  No new enhancing lesion.\n2. Overall unchanged numerous enhancing and nonenhancing (sclerotic) calvarial\nmetastatic lesions."
        },
        {
            "input": "When compared to prior examination of ___, previously described\nenhancing lesions have decreased in size:\n\n2 mm left occipital lesion (series 8, image 17) and surrounding FLAIR.\n\n5 mm right frontal subependymal lesion of the anterior left lateral ventricle\nand associated FLAIR  (series 8, image 14).\n\nPunctate right caudate head lesion (series 8, image 14).\n\nRight parietal occipital lobe hemorrhagic enhancing 1.7 cm lesion and\nsurrounding FLAIR (series 8, image 15).\n\nLeft temporal lobe 3 mm lesion and surrounding FLAIR (series 8, image 13).\n\nRight putamen punctate lesion (series 8, image 13).\n\n2 mm left superior cerebellar lesion (series 8, image 9) is improved.\n\nRight cerebellar lesions measuring up to 3 mm have improved (series 8, image\n5)\n\nNo new lesions are identified.\n\nMultiple calvarial lesions demonstrating mild postcontrast enhancement is\nsimilar.  No definitive new osseous lesions.\n\nThere is no acute infarct or intracranial hemorrhage.  The sulci, ventricles\nand cisterns are within expected limits for the patient's age.   The major\nintracranial flow voids are preserved.  The dural venous sinuses are patent on\npostcontrast MP-RAGE.  There is mild mucosal thickening of the ethmoid air\ncells.  The orbits are unremarkable.  Fluid signal is seen in the mastoid air\ncells, new from prior examination.",
            "output": "1. Multiple bilateral supra and infratentorial enhancing lesions have\ndecreased in size when compared to prior examination.  No new enhancing\nlesions identified.\n2. Multiple calvarial lesions are similar.  No definitive new osseous lesion."
        },
        {
            "input": "In comparison to the recent MRI performed on ___, there is new\nbilateral leptomeningeal enhancement interdigitating along the cerebellar\nfolia, as well as bilateral enhancement of the seventh eighth cranial nerve\ncomplexes and of the trigeminal nerves, compatible with leptomeningeal spread\nof tumor (series 1100; images 74 and 81).  On sagittal MPRAGE, there is\nsuggestion of leptomeningeal enhancement along the visualized cervical cord\n(series 11, image 107).\n\nIn addition, other known supratentorial and infratentorial metastases are as\nfollows (as seen on series 1100):\n- 3 mm left occipital lesion, unchanged (image 119)\n- 17 mm hemorrhagic right parieto-occipital lesion is re-demonstrated, but\nassociated with significantly less internal nodular enhancement (image 108)\n- 4 mm right caudate lesion, previously measuring 7 mm (image 106)\n- 2 mm right caudate lesion, unchanged (image 100)\n- Previously noted 3 mm left temporal lesion has resolved (series 8, image 13\non the prior study)\n\nThere is no evidence of infarction or midline shift. Ventricles and sulci are\nwithin normal limits for patient's age.  Major intracranial vascular flow\nvoids are preserved.  Dural venous sinuses are patent on post-contrast MPRAGE.\n\nThe orbits are within normal limits.  No definite abnormal enhancement within\nthe orbit, although the examination is not optimized for such evaluation. \nThere is mild mucosal thickening in the ethmoid air cells bilaterally.  Mild\nfluid signal in the mastoid air cells bilaterally is similar to the prior\nstudy.\n\nMultiple bilateral calvarial lesions are grossly unchanged from the prior\nstudy, the largest measuring up to 1.6 x 1.5 cm along the left vertex (series\n1100, image 144).",
            "output": "1. New infratentorial leptomeningeal metastases involving the cerebellar\nhemispheres, seventh eighth cranial nerve complexes and trigeminal nerves.\n2. There is also suggestion of leptomeningeal thin enhancement of the\nvisualized upper cervical cord.  Further evaluation with MRI cervical and\nthoracic spine with without contrast is recommended.\n3. Multiple additional supratentorial and infratentorial enhancing lesions\nhave either remained stable or decreased in size, but none have grown.\n4. Multiple bilateral calvarial lesions are not significantly changed from\nprior.\n\nRECOMMENDATION(S):  Further evaluation with MRI cervical, thoracic spine with\nwithout contrast for impression 2 is recommended."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are unremarkable in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.\n\nBilateral hippocampal formations and mammillary bodies are preserved in signal\nand configuration. There is no disproportionate medial temporal atrophy. There\nis no focal lobar encephalomalacia. There are no focal cortical dysplasias or\ngray matter heterotopia noted.\n\nRe-demonstrated is a partially empty sella.\n\nVisualized paranasal sinuses are clear.  Orbits are unremarkable.",
            "output": "1. No acute intracranial abnormality on contrast enhanced MRI brain.  No\nevidence of focal cortical dysplasia, gray matter heterotopia, acute infarct\nor intracranial hemorrhage.  No evidence for mesial temporal sclerosis.\n2. Partially empty sella."
        },
        {
            "input": "There is no evidence of intracranial hemorrhage, edema, masses, mass effect,\nmidline shift or territorial infarction.  Disproportionate volume loss in the\nfrontal and temporal lobes.  There is no hydrocephalus.  No diffusion\nabnormalities are detected.\n\nPeriventricular, subcortical and deep white matter T2/FLAIR hyperintensities\nfor likely sequela of chronic small vessel disease.\n\nPatient is status post bilateral lens replacement.  Maxillary sinus mucosal\nthickening, right worse than left, with heterogeneous content on the right,\ncould be secondary to inspissated secretions, however the possibility of\nfungal colonization is also consideration.  There are punctate opacifications\nin the mastoid air cells bilaterally.",
            "output": "1. No evidence of acute territorial infarct, intracranial hemorrhage or\nmasses.\n2. Prominent ventricles sulci suggesting cortical volume loss as described\nabove.  Subcortical and periventricular areas of T2/FLAIR high-signal\nintensity, are nonspecific and may represent changes due to chronic small\nvessel disease.\n3. Paranasal sinus disease as described above."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  Intracranial flow voids are preserved.",
            "output": "Normal brain MRI.  Specifically, no evidence of infarction."
        },
        {
            "input": "Images through the internal auditory canal demonstrates symmetric appearance\nof the seventh eighth nerve complexes.  There is no evidence of abnormal\nenhancement or mass lesion within the internal auditory canals,\ncerebellopontine angles or membranous labyrinth. No other mass lesions are\nseen within the posterior fossa.\n\nLimited included imaging of the remainder of the brain demonstrates no\nevidence of hemorrhage, edema, masses, mass effect, midline shift\norinfarction.  There are mild nonspecific white matter T2/FLAIR\nhyperintensities most likely reflecting chronic small vessel disease in this\nage group, with linear T2/FLAIR hyperintensity in the pons likely also\nreflecting chronic small vessel disease.  The ventricles and sulci are mildly\nprominent suggesting involutional changes..  There is no abnormal enhancement\nafter contrast administration.\n\nNo osseous abnormalities are seen.  There is fluid in the right maxillary\nsinus along with scattered mild mucosal thickening in the ethmoid air cells\nand bilateral maxillary sinuses.  The orbits are unremarkable. The visualized\nportion of the principle vascular flow voids are preserved.",
            "output": "1. No evidence of IAC or cerebellopontine angle mass.\n2. Fluid in the right maxillary sinus can be correlated for evidence of active\nsinus disease.\n3. Mild nonspecific white matter signal changes most likely reflecting chronic\nsmall vessel disease in this age group."
        },
        {
            "input": "There is no evidence of masses,mass effect,midline shift ornew infarction. \nThe ventricles and sulci are prominent, consistent with global cerebral volume\nloss.  There is no abnormal enhancement after contrast administration. \nMicrohemorrhagic foci are re-demonstrated in the right cerebellum, unchanged.\n\nT2/FLAIR hyperintense foci are re-demonstrated in the right frontal lobe\n(400:458) and left temporal lobe (400:404), unchanged.  These are likely\nsequela of prior infarcts.\n\nBilateral hippocampal formations and mammillary bodies are preserved in signal\nand configuration. There is no disproportionate medial temporal atrophy. There\nis no focal lobar encephalomalacia. There are no focal cortical dysplasias or\ngray matter heterotopia noted.",
            "output": "1. No acute infarct or intracranial hemorrhage.\n2. No abnormality suggestive of a seizure focus.\n3. Small old infarcts in the right frontal and left temporal lobes."
        },
        {
            "input": "There is a large acute infarction involving the left middle cerebral artery\nterritory, including the scratch caudate head and body, putamen, insula,\ntemporal lobe largely with medial sparing, inferior parietal lobe, occipital\nlobe, and posterior frontal lobe.  Moderate-sized acute infarction is present\nin the posterior left thalamus.  Small focus of acute infarction is present in\nthe right medial parietal cortex (___).  Areas of serpentine susceptibility\nartifact are noted within the left frontal and parietal lobes in the area of\ninfarction, and may reflect thrombosed blood vessels versus hemorrhagic\ntransformation.  Mild effacement of the left lateral ventricle is new compared\nto ___.  This is superimposed upon underlying prominence of the\nventricles and sulci due to age-related parenchymal volume loss.  There is no\nshift of midline structures.\n\nA chronic right parietal lobe infarction is again noted. Periventricular,\ndeep, and subcortical white matter T2 hyperintensities are noted, likely the\nsequelae of chronic small vessel ischemic disease in this age.\n\nBilateral proximal MCA flow voids appear symmetric in signal intensity, but\npatency of the intracranial arterial branches is well not assessed on this\nexam.\n\nThere is mild mucosal thickening in the ethmoid air cells.",
            "output": "1. Large acute infarction in the left MCA territory with some extension into\nthe left PCA territory, and a punctate acute infarction in the right medial\nparietal cortex.\n2. Multiple serpentine areas of susceptibility artifact within the infarcted\nportions of the left frontal and parietal lobes, which may reflect thrombosed\nblood vessels versus hemorrhagic transformation.  This may be reassessed by\nnoncontrast CT.\n3. Chronic right parietal infarct is again seen."
        },
        {
            "input": "There are multiple acute or early subacute infarctions.  The largest of these\ninvolves the left MCA territory, primarily involving the left precentral gyrus\nin the left superior frontal gyrus.  There are punctate bilateral cerebellar\ninfarcts, as well as bilateral occipital and left parietal infarcts (for\nexample see series 4 images 27, 24, 22, 21, 7, 8, 5).  There may be a punctate\nfocus of right frontal cortical infarction (series 4 and 3, image 25).\n\nThere is no hemorrhage.  There is no extra-axial collection or intracranial\nmass effect.\n\n The ventricles and sulci are prominent, compatible with global parenchymal\nvolume loss.\n\n Bilateral periventricular and deep white matter foci of T2/FLAIR signal\nhyperintensity are nonspecific but compatible with mild-to-moderate changes of\nchronic white matter microangiopathy.\n\n Major intracranial vascular flow voids are preserved.\n\n Aside from bilateral lens extraction, the globes and orbits are within normal\nlimits.\n\n The visualized paranasal sinuses and mastoids appear clear.",
            "output": "1. Multiple foci of acute or early subacute infarction, largest in left MCA\nterritory involving the left superior frontal and left precentral gyri, with\nmultiple punctate infarcts in the cerebellum, occipital lobes, left parietal\nlobe, possibly right frontal lobe.  Appearance raises suspicion for emboli\nfrom a central source.\n2. No hemorrhage or extra-axial collection.\n3. Age-congruent global parenchymal volume loss.\n4. Mild-to-moderate changes of chronic white matter microangiopathy.\n\nNOTIFICATION:  Per review of the online electronic medical record, the\nfindings above are known to the patient's care team at the time of this\ndictation."
        },
        {
            "input": "There are multiple foci of high signal intensity within white matter on FLAIR\nsequences suggestive of chronic small vessel ischemic disease. There are\nmultiple small areas that appear bright on diffusion-weighted sequences but\nare also bright on the ADC map, indicating that they are chronic.  There is no\nevidence of mass, edema, or hemorrhage.  There are no abnormally enhancing\nlesions.  Ventricles and sulci are normal in caliber and configuration for the\npatient's age.",
            "output": "1. No evidence of mass, edema or hemorrhage.\n2. Findings suggestive of chronic small vessel ischemic disease with several\nlikely chronic areas of white matter infarction."
        },
        {
            "input": "Multiple peripherally distributed foci of slow diffusion with FLAIR\nhyperintense signal involving the cerebral hemispheres, with dominant 1.9 x\n0.9 cm focus in the right occipital lobe, bilateral cerebellum and in the left\npons is identified, compatible with embolic late acute infarcts.  Gradient\necho susceptibility artifact in the bilateral basal ganglia and cerebellum\ncorresponds to calcifications on prior CT.  A punctate focus of gradient echo\nsusceptibility in the right frontal vertex may represent sequela of micro\nhemorrhage.\n\nRe-identified is a left frontal 4.3 x 3.8 x 3.2 cm (TRV, AP, SI) complex\ncystic mass with an extra-axial 2.3 x 1.5 cm (AP, TRV) homogeneously enhancing\ncomponent demonstrating dural tail, likely representing a cystic meningioma. \nThe cystic component demonstrates peripheral gradient echo susceptibility\nhypointensity, which may represent calcifications versus small component\nhemorrhage.  The lesion exerts mass effect on the adjacent brain parenchyma\nresulting in surrounding right frontal white matter edema pattern.\n\nThere is a 9 mm extra-axial left parietal lobe homogeneously enhancing lesion\ncompatible with a meningioma (series 15, image 17).  A single punctate subtle\n3 mm focus of enhancement in the left medial frontal lobe vertex is associated\nwith FLAIR hyperintense signal and diffusion-weighted signal abnormality,\nwhich may represent mild enhancement of a subacute infarct.\n\nSuperimposed confluent periventricular subcortical T2/FLAIR white matter\nhyperintensities are nonspecific, but compatible with chronic microangiopathy\nin a patient of this age.  The major intracranial flow voids are preserved. \nThere is opacification of the right sphenoid sinus.  The orbits are\nunremarkable, noting bilateral lens replacements.  Fluid signal opacifies the\nright mastoid tip.",
            "output": "1. Multiple foci of slow diffusion with associated FLAIR hyperintense signal\ninvolving the bilateral cerebellar hemispheres, bilateral cerebellum and left\npons are compatible with late acute infarcts.  The dominant lesions involve\nthe right occipital lobe measuring approximately 2 cm and the left pons.\n2. Re-identified is a left frontal 4.3 cm complex cystic mass within\nextra-axial 2.3 cm enhancing component which demonstrates a dural tail, likely\nrepresenting a cystic meningioma.  The cystic portion is likely also\nextra-axial, although type 4 cystic meningiomas demonstrate cysts in the\nadjacent brain parenchyma.\n3. A second 9 mm left parietal presumed meningioma is also identified.\n4. A single punctate subtle 3 mm enhancing focus of the left medial frontal\nvertex seen only on turbo spin echo sequences is associated with\ndiffusion-weighted hyperintense signal, and may represent sequela of late\nacute to subacute infarct.  Close attention on followup is recommended.\n5. Re-identified is gradient echo susceptibility of the bilateral basal\nganglia and cerebellum, which may represent senescent related calcifications,\nFahr disease or hyperparathyroidism.\n\nNOTIFICATION:  The findings were discussed with ___, M.D. by\n___, M.D. on the telephone on ___ at 2:29 ___, 2 minutes after\ndiscovery of the findings."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.\nThere is no abnormal parenchymal enhancement after contrast administration.\n\nScattered punctate T2/FLAIR hyperintensities in the periventricular white\nmatter are nonspecific but suggestive of chronic small vessel ischemic changes\nin this age group.\n\nThere is generalized parenchymal volume loss, most likely age related.  Mild\nprominence of the ventricular system is compatible with the previously\nmentioned parenchymal volume loss.\n\nMajor vascular flow voids are preserved.  Intracranial vasculature is patent. \nBulbous configuration of the basilar tip, normal anatomic variant.  Major\ndural venous sinuses are patent.\n\nMild mucosal thickening of the ethmoid air cells.  The remainder of the\nparanasal sinuses and mastoid air cells are clear.  The orbits are normal.\n\nThe diffusion images demonstrate a subtle area of increased diffusion in the\nright mastoid bone (550:10).  There is postcontrast enhancement in this region\nwith subtle adjacent dural enhancement (900:114).  This is suspicious for bony\nmetastasis given patient's history of bony metastasis.",
            "output": "1. No evidence of brain metastasis.\n2. Question of bony metastasis to the right mastoid bone.  If clinically\nindicated further evaluation can be obtained with bone scan or PET scan.\n3. Nonspecific nonenhancing, scattered and punctate periventricular white\nmatter lesions likely a sequela of chronic small vessel ischemic changes in\nthis age group.\n4. Mild paranasal sinus disease as described above\n\nNOTIFICATION:  The impression and recommendation above was entered by Dr.\n___ on ___ at 14:38 into the Department of Radiology\ncritical communications system for direct communication to the referring\nprovider."
        },
        {
            "input": "The enhancing, heterogeneously T2 hyperintense mass with slow diffusion\ncentered at the septum pellucidum, corpus callosum and atrium of the right\nlateral ventricle has increased in size now measuring 5.9 x 4.2 cm versus 5.3\nby 3.7 cm. The subependymal seeding along the right lateral ventricle, and\nfourth ventricle with extension along the left foramina Luschka is unchanged.\nThere is stable enlargement of the lateral ventricles. This mass invades the\ncorpus callosum posteriorly. There are postoperative changes in the right\nparietal region from prior biopsy. There is intrinsic T1 hyperintensity within\nthe mass (series 4, image 13) which may represent hemorrhage from the biopsy.\n\nThere is mild bilateral maxillary sinus mucosal thickening with retention\ncysts.",
            "output": "Interval increase in enhancing mass centered in the right lateral ventricle\nwith involvement of the corpus callosum now measuring 5.9 x 4.2 cm. The\nsubependymal seeding in the right lateral ventricle and fourth ventricle with\nextension through the left foramina Luschka is unchanged.\n\nStable enlargement of the lateral ventricles.\n\nPostoperative changes in the right parietal region from recent biopsy."
        },
        {
            "input": "The right A1 anterior cerebral artery is hypoplastic or absent.  There is\nfetal origin of the right posterior cerebral artery.  There is narrowing of\nthe left V4 vertebral artery distal to the origin of the left ___, a normal\nvariant.  The intracranial vertebral and internal carotid arteries and their\nmajor branches appear normal without evidence of stenosis, occlusion, or\naneurysm formation.",
            "output": "1. Unremarkable brain MRA.  No aneurysm identified."
        },
        {
            "input": "Postoperative changes are identified in the left parieto-occipital region.\nSurrounding the surgical cavity in encephalomalacia there is enhancement\nidentified which may have slightly decreased in the inner aspect but there is\nno new enhancement seen in the left occipital lobe. There is also enhancement\nseen around the tip of the occipital horn which is more prominent compared\nwith the prior study. There is no midline shift or hydrocephalus. No other new\ndistant areas of abnormal enhancement seen.",
            "output": "New areas of enhancement are seen in the left occipital lobe.  Adjacent to the\npreviously seen surgical cavity and enhancement.  There is no hydrocephalus or\nmidline shift. The examination performed for CyberKnife radiosurgery planning.\nil"
        },
        {
            "input": "Small foci of high T2 signal in the subcortical, deep, and periventricular\nwhite matter of the cerebral hemispheres, including callosal lesions, appear\nstable compared to ___.  No posterior fossa lesions, new lesions,\nor contrast enhancing lesions are identified.  Ventricles and sulci are age\nappropriate and unchanged in size.\n\nThere is no intracranial mass and no pathologic meningeal contrast\nenhancement.  There is no edema, acute diffusion abnormality, or evidence for\nblood products.  Major arterial flow voids are grossly preserved.  Major dural\nvenous sinuses appear patent on postcontrast MP RAGE images.\n\nThere is a T2 hyperintense lesion in the dorsal cord from C1-C2 through C3-C4\nlevels, with contrast enhancement in the central portion of the lesion, as\nseen on the cervical spine MRI from 1 day earlier.",
            "output": "Stable appearance of signal abnormalities in the supratentorial white matter,\nwhich compatible with demyelinating disease.  No new or contrast enhancing\nlesions."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are patent and prominent in keeping\nwith volume loss.  Also seen are areas of encephalomalacia in bilateral\ncerebellar hemispheres, likely secondary to prior insults.\n\nThere are areas of T2/FLAIR hyperintensity in the subcortical, periventricular\nand deep white matter, nonspecific, likely secondary to small vessel ischemic\nchanges.\n\nThere is a small focus of susceptibility in the right superior frontal lobe,\nlikely a small focus of chronic micro hemorrhage (image 19, series 11).\n\nThere has been prior right-sided cataract surgery.  Mucosal thickening in the\nleft maxillary sinus, bilateral ethmoid air cells, with nonspecific partial\nfluid opacification of the left mastoid air cells.  The remaining visualized\nparanasal sinuses are clear.  The intracranial flow voids are maintained. \nVisualized osseous structures are unremarkable.",
            "output": "1. No acute intracranial abnormality.\n2. Chronic infarcts in bilateral cerebellar hemispheres and areas of small\nvessel ischemic changes."
        },
        {
            "input": "There is no evidence of acute infarction intracranial blood, edema or mass few\nscattered small T2/FLAIR hyperintense foci in the periventricular and\nsubcortical white matter the cerebral hemispheres are nonspecific and may be\nseen in asymptomatic patients, with other diagnostic considerations including\nsequelae mild chronic small vessel ischemic changes versus sequela of prior\ninflammation.  The ventricles, sulci, and basal cisterns are normal in size. \nThe visualized vascular flow voids are grossly preserved.\n\nThere is a small mucous retention cyst in the right maxillary sinus, as well\nas minimal mucosal thickening in the maxillary, ethmoid, and frontal sinuses. \nFocal T1 hyperintensity in the anterior arch of C1 image ___ represent a\nfocal fat deposit or hemangioma.",
            "output": "Unremarkable noncontrast brain MRI.  No evidence of an acute infarct or other\nacute abnormalities."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  Both orbits are unremarkable.  Paranasal sinuses and mastoid\nair cells are essentially clear.\n\nBilateral hippocampal formations and mammillary bodies are normal in signal\nand configuration. There is no disproportionate medial temporal atrophy. There\nare no focal cortical dysplasias or gray matter heterotopia noted.",
            "output": "1. Unremarkable nonenhanced brain MRI utilizing seizure protocol."
        },
        {
            "input": "There is no evidence for intra-axial or extra-axial mass, abnormal\npachymeningeal or leptomeningeal contrast enhancement, edema, abnormal\ndiffusion, or evidence of blood products in the brain parenchyma.  The\nventricles, cerebral sulci, and basal cisterns are normal in size for age. \nThere are small foci of high T2 signal in the subcortical, deep, and\nperiventricular white matter of the cerebral hemispheres, which are\nnonspecific but may be related to sequela of chronic small vessel ischemic\ndisease in a patient of this age.  Major arterial flow voids are grossly\npreserved.  Visualized portions of the paranasal sinuses and mastoid air cells\nclear.  The orbits are unremarkable.",
            "output": "No intracranial metastatic disease identified."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  Suboptimally evaluated 2.0 cm x 1.0 cm bright T2 mass\nposterior left parotid gland involving superficial and deep lobe, probably\nsimilar since ___, likely benign mixed tumor.  Left stylomastoid\nforamen fat pad is preserved.  Moderate brain parenchymal atrophy.  Minimal\nopacification bilateral mastoids.  Mild mucosal thickening bilateral maxillary\nsinuses, small volume fluid right maxillary sinus..  Mild right maxillary\nsinus atelectasis.  Moderately prominent perivascular spaces preserved\nvascular flow voids.  Dural venous sinuses are patent.",
            "output": "1. No metastases.\n2. Left parotid mass, similar compared with ___, likely benign mixed tumor.\n3. Paranasal sinus disease."
        },
        {
            "input": "MR BRAIN:\nThe obtained sequences are limited by moderate motion artifact.\n\nThere are numerous small bilateral supratentorial and infratentorial foci of\nslow diffusion, likely acute/early subacute infarcts.  Many of these are are\ncompatible with the MCA/PCA watershed distribution.  Some are compatible with\nthe the MCA/ACA watershed distribution versus embolic etiology.  Others are\ncortical in the bifrontal MCA and possibly ACA territory, suggesting embolic\netiology.  Multiple small bilateral infarcts are also seen in the cerebellar\nhemispheres, compatible with embolic etiology.  No associated mass effect.\n\nNo evidence for blood products on motion limited gradient echo images.\n\nMild global parenchymal volume loss is again seen with mildly prominent\nventricles and sulci.\nSagittal images demonstrate several hypointense foci in the visualized upper\ncervical vertebral bodies, with diffuse osseous metastases demonstrated on the\nconcurrent ___ cervical spine MRI, as well as on the earlier ___ thoracic spine MRI and ___ lumbar spine MRI.  No\nexpansile calvarial metastases are seen.  Relative ___ hypointensity\nin the left occipital bone on sagittal T1 weighted image ___ be secondary\nto metastatic disease.\n\nMRA CIRCLE OF ___:\nMotion artifact moderately limits evaluation.  Intracranial vasculature is\nbetter assessed on the ___ CTA.\n\nNo flow signal is seen in the proximal V4 segment left vertebral artery, which\ndemonstrates a short-segment stenosis on the recent CTA.  Flow is seen in the\ndistal left V4 segment.  Stenosis of the mid left V4 segment is better seen on\nthe preceding CTA.  Right V4 segment and basilar artery are patent.  There is\nfetal type configuration of bilateral posterior cerebral arteries with small\nP1 segments.  Overall, no evidence for flow-limiting stenosis or large\naneurysm in the major intracranial arteries.",
            "output": "1. Incomplete brain MRI, with the available sequences limited by motion\nartifact.\n2. Numerous small bilateral acute/early subacute infarcts in the cerebral\nhemispheres, including the deep white matter and predominantly bifrontal\ncortex, as well as bilateral cerebellar hemispheres.  Embolic etiology is\nfavored, though superimposed watershed infarcts are also possible.  No mass\neffect or evidence for blood products.\n3. In the absence of intravenous contrast, evaluation for superimposed\nintracranial metastatic disease is limited.\n4. ___ T1 hypointensity in the left occipital bone may represent a\ncalvarial metastasis, given the known diffuse osseous metastatic disease in\nthe cervical, thoracic, and lumbar spine.\n5. Motion limited MRA of the circle of ___ demonstrates absence of flow in\nthe proximal V4 segment of the left vertebral artery, which demonstrates a\nshort-segment stenosis on the preceding ___ CTA.  Overall, the\nintracranial vasculature is better assessed on the preceding CTA.\n\nRECOMMENDATION(S):  When the patient is able to tolerate additional imaging,\ncontrast enhanced brain MRI should be considered to better assess for\nintracranial metastatic disease."
        },
        {
            "input": "The examination is slightly motion degraded, particularly the postcontrast MP\nRAGE sequences.  Within these confines:\n\nThere is no intra or extra-axial mass, acute hemorrhage or infarct.  Sulci,\nventricles and cisterns are within expected limits for the patient's mild age\nrelated global cerebral volume loss.  There is a single nonspecific\nnonenhancing left periventricular white matter FLAIR hyperintense focus with\nassociated T1 hypo density, likely sequela of chronic microangiopathy.  No\nabnormal enhancement.  The major intracranial flow voids are preserved.  The\ndural venous sinuses are patent.  Partial opacification of the ethmoid air\ncells is noted.  The remainder the visualized paranasal sinuses are\nessentially clear.  The orbits are unremarkable, allowing for bilateral lens\nreplacements.  The mastoid air cells are clear.  No definitive marrow signal\nabnormality.",
            "output": "1. Motion limited exam, in particular the MP-RAGE postcontrast sequences. \nSmall and subtle lesions may not be seen.  Within these confines:  No evidence\nfor metastatic intracranial disease.\n2. No definitive suspicious calvarial lesion."
        },
        {
            "input": "Study is mildly degraded by motion.\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are slightly prominent in keeping\nwith age-related volume loss.\n\nThere is no foci of abnormal enhancement to suggest intracranial metastasis.\n\nThere are scattered foci of T2/FLAIR hyperintensity in the subcortical and\nperiventricular white matter, nonspecific, likely secondary to small vessel\nischemic disease.\n\nThere is partial opacification of some anterior ethmoid air cells.  Also seen\nis a small mucous retention cyst in the right maxillary sinus.  The remaining\nvisualized paranasal sinuses and mastoid air cells are clear.  Intracranial\nflow voids are maintained.  The orbits are unremarkable noting prior bilateral\ncataract surgeries.",
            "output": "1.  Study is mildly degraded by motion.\n2. Within limits of study, no focus of abnormal enhancement to suggest\nintracranial metastasis.\n3. Findings of small vessel ischemic disease and age-related involutional\nchanges.\n4.  Paranasal sinus disease as described."
        },
        {
            "input": "The study is degraded by patient motion, particularly the postcontrast MP RAGE\nimages.\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are mildly prominent, suggesting\nage-related involutional change.  Few scattered foci of T2/FLAIR\nhyperintensity in the subcortical and periventricular white matter nonspecific\nand unchanged, likely secondary to small vessel ischemic disease. There is no\nabnormal enhancement after contrast administration to suggest the presence of\nintracranial metastases.  The major intracranial flow voids are preserved. \nDural venous sinuses appear patent on post contrast MP RAGE images.\n\nThere is partial opacification of several anterior ethmoidal air cells.  The\nremaining paranasal sinuses are clear.  The mastoid air cells are clear. \nOrbits are unremarkable, noting bilateral lens replacements.",
            "output": "The study, particularly the postcontrast MP RAGE images, is degraded by\npatient motion.  Within this limitation, no focus of abnormal enhancement\nconcerning for intracranial metastases."
        },
        {
            "input": "There is a large heterogeneously enhancing mass centered at the\ninfero-anterior left frontal lobe and extending across the midline with\nsignificant mass effect and surrounding T2/FLAIR hyperintensity. The mass\ndemonstrates regions of subtle the intrinsic T1 hyperintensity, as well as\nsusceptibility on GRE, concerning for blood products. It measures\napproximately 6.5 cm AP x 5.1 cm TR x 4.2 cm SI. There is significant midline\nshift of 11 mm to the right. There is complete obliteration of the left\nfrontal horn, as well as near complete effacement of the entire left lateral\nventricle. The right frontal horn of the lateral ventricle is also nearly\ncompletely effaced. There is a thin rim of T2/FLAIR hyperintensity surrounding\nthe right lateral ventricle, most likely representing adjacent edema although\ntransependymal flow of CSF from a degree of obstructive hydrocephalus is also\na consideration.  There is also mild effacement of the left-sided basal\ncisterns but no definite evidence to suggest uncal herniation or tonsillar\nherniation.\n\nNo other lesions or abnormal enhancement is identified.\n\nThere are no extra-axial fluid collections. There is no slow diffusion to\nsuggest acute infarct.\n\nThere is posterior displacement of the left A1 and proximal middle cerebral\nartery flow void secondary to mass effect from this described lesion.\nRight-sided flow voids appear maintained all well left-sided flow voids are\ndifficult to assess in the setting. Flow voids of the bilateral internal\ncarotid arteries are well seen.\n\nThere is mild mucosal thickening of the paranasal sinuses. There is a small\namount of fluid in the bilateral ethmoid air cells and sphenoid sinuses.\nMastoid air cells are clear.  The orbits and soft tissues are grossly\nunremarkable.",
            "output": "Large intra-axial, heterogeneously, enhancing lesion with scattered blood\nproducts, centered at the ___ left frontal lobe, and resulting in\nsignificant mass effect with 11 mm rightward midline shift.  There is\neffacement of the lateral ventricles, left greater than right, as described\nabove . Differential diagnosis  includes a primary brain neoplasm, with a\nhigh-grade glioma (GBM) as a main consideration. Metastasis is a less likely\nconsideration."
        },
        {
            "input": "Compared to recent prior examination of ___, there is no significant\nchange in the size, configuration or signal characteristics of the large\nintra-axial centered at the ___ left frontal lobe and resulting in\nsignificant mass effect with 11 mm rightward midline shift.  Mass effect on\nthe lateral ventricles, left greater than right, is unchanged. The mass\nextends inferiorly to the level of the olfactory bulb and to the border with\nthe cribriform plate, planum sphenoidale and superior orbital rim.\n\nNo new lesion is identified.",
            "output": "Unchanged large heterogeneously enhancing intra-axial lesion centered at the\n___ left frontal lobe with 11 mm rightward midline shift.  No new\nlesion identified."
        },
        {
            "input": "Since the previous MRI examination the patient has undergone resection of the\nleft frontal lobe rim enhancing mass. Postsurgical changes and blood products\nare seen in this region. There is no evidence of restricted diffusion\nsurrounding the surgical cavity or in the other parts of the brain. There\nremains a T2 and FLAIR hyperintensity with some mass effect on left lateral\nventricle which appears somewhat decreased. Blood products are seen in the\nsurgical cavity with some surrounding enhancement both anteriorly and\nposteriorly at the surgical site within the deep portions of the brain.  No\nother areas of abnormal enhancement seen within the brain. There is no\nhydrocephalus.",
            "output": "Resection of left frontal lobe lesion with expected postsurgical changes and\nresidual enhancement within the deep portions of the surgical cavity as\ndescribed above. No acute infarcts or hydrocephalus."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.\n\nThere are no osseous abnormalities.  The are orbits are unremarkable.  The\nvisualized extracranial soft tissues are unremarkable.  There is minimal\npatchy fluid signal in the mastoid air cells, left greater than right.",
            "output": "No evidence of acute infarction or intracranial hemorrhage."
        },
        {
            "input": "Study is mildly degraded by motion.  There is no evidence of hemorrhage,\nedema, masses, mass effect, midline shift or infarction.   The ventricles and\nsulci are normal in caliber and configuration.  There is no abnormal\nenhancement after contrast administration.",
            "output": "1.  Study is mildly degraded by motion.\n2. No acute intracranial abnormality, with no definite evidence of\nintracranial mass or lesion."
        },
        {
            "input": "There is no acute infarction, intracranial hemorrhage, extracerebral fluid\ncollection, midline shift or mass effect.  Ventricles and extra-axial spaces\nare normal in size.  Flow voids are maintained. Suprasellar and craniocervical\nregions are unremarkable. Mild low signal within the visualized marrow\nstructures appear to be within normal limits for a patient of this age",
            "output": "No significant abnormalities are seen on MRI of the brain without gadolinium."
        },
        {
            "input": "Minimal T2/FLAIR hyperintensities are seen in the right insula and\nperiventricular regions, suggestive of microvascular ischemic change.  There\nis no evidence of hemorrhage, edema, masses, mass effect, midline shift or\ninfarction.  Ventricles, sulci and cisterns demonstrate mild, age-appropriate\ninvolutional changes with parenchymal volume loss involving the medial\ntemporal lobes appearing proportionate to the remainder of the brain and\nsulcal cisternal enlargement appearing proportionate to ventricular size.\n\nMinimal mucosal thickening is noted in the ethmoid air cells.",
            "output": "1. Minimal probable microvascular ischemic change and mild age-appropriate\ninvolutional changes.\n2. No acute intracranial abnormality or mass."
        },
        {
            "input": "The study is normal. There is no evidence of metastatic disease. There is no\nevidence of hemorrhage, edema, masses, mass effect, or infarction. The\nventricles and sulci are normal in caliber and configuration. There is no\nabnormal enhancement after contrast administration.",
            "output": "Normal study."
        },
        {
            "input": "Study is moderately degraded by motion, especially on postcontrast imaging. \nThere are widespread, multifocal intrinsically T1 hyperintense, enhancing\nsupra- and infratentorial 2-4 mm foci with surrounding T2/FLAIR signal\nhyperintensity, the majority of which are centered on the cerebral hemispheric\ngray-white matter junction, common some of which is suggested to be\nleptomeningeal.\n\nThere is no evidence of hemorrhage, or infarction.  The ventricles are normal\nin caliber and configuration.  The major intracranial vascular flow voids are\npreserved.  The major dural venous sinuses are patent.  Note, there is\nsignificant motion degradation on the MPRAGE sequences.  The globes are\nunremarkable.  The paranasal sinuses and mastoid air cells are clear.",
            "output": "1. Study is moderately degraded by motion, especially on postcontrast imaging.\n2. Widespread, innumerable supra and infratentorial intracranial metastases as\ndescribed.\n3. No evidence of intracranial hemorrhage.\n\nNOTIFICATION:  The findings were discussed by Dr. ___ with Dr. ___ on the\ntelephone on ___ at 9:49 AM, 5 minutes after discovery of the findings."
        },
        {
            "input": "The following ring-enhancing lesions are noted, the majority of which are seen\non prior exam.\n\n5 mm left superior frontal gyrus lesion (series 12, image 175)\n\n6 mm left medial frontal lobe lesion (series 12, image 151)\n\n7 mm left pre frontal gyrus lesion (series 12, image 164), with associated\ndiffusion-weighted hyperintense signal.\n\nPunctate left frontal para falcine lesion (series 12, image 165) not seen on\nprior exam\n\n2 mm left middle frontal gyrus lesion (series 12, image 151)\n\nPunctate focus of enhancement in the right anterior temporal lobe (series 12,\nimage 84), not seen on prior exam.\n\n2 mm right prefrontal gyrus lesion (series 12, image 159).\n\nUnchanged appearance right frontal lobe encephalomalacia.  Edema pattern\nassociated with the largest lesions are also unchanged.  No acute infarct.\n\nIncidental note is made of retropharyngeal course of the left internal carotid\nartery.",
            "output": "1. Re-identified are multiple left hemispheric predominant lesions measuring\nup to 7 mm, the majority of which are unchanged in appearance from prior\nexamination.  Punctate lesions in the left anterior temporal lobe and left\nparafalcine frontal lobe are not seen on prior examination, likely secondary\nto technical differences.\n2. Additional findings described above."
        },
        {
            "input": "There are diffuse foci of restricted diffusion in white matter throughout both\ncerebral hemispheres, the left thalamus, midbrain, pons, middle cerebellar\npeduncles, and cerebellar cortices (for example 4: 8, 15, 21).  There are\ncorresponding T2 and FLAIR hyperintensities.  A punctate focus of\nsusceptibility in the left cerebellar hemisphere could reflect a chronic\nmicrohemorrhage (11:6), is not associated with diffusion-weighted signal\nabnormality.  There is no evidence of acute hemorrhage or mass.  No midline\nshift.  Prominence of the ventricles and sulci is suggestive of involutional\nchanges.  Superimposed confluent periventricular and subcortical white matter\nhypodensities are nonspecific, but compatible with chronic microangiopathy in\na patient this age.  The principal intracranial vascular flow voids are\npreserved.\n\nThe imaged paranasal sinuses are clear with the exception of mild anterior\nethmoid air cell mucosal thickening.  There is partial opacification of the\nright greater than left mastoid air cells.  The imaged orbits are grossly\nunremarkable.",
            "output": "Diffuse late acute infarcts primarily in watershed regions throughout the\ncerebral cortex, deep white matter and cerebellum.  Given the patient's\nhistory of sepsis and hypotension, this is most likely related to global\nhypoperfusion.  There is no evidence of acute intracranial hemorrhage or mass\neffect.\n\nNOTIFICATION:  The findings were discussed with ___, M.D. by ___,\nM.D. on the telephone on ___ at 12:22 pm, 5 minutes after discovery of\nthe findings."
        },
        {
            "input": "There are extensive punctate and confluent areas restricted diffusion\ninvolving subcortical and deep white matter of bilateral cerebral hemispheres,\ninvolving frontal, parietal greater old ion temporal and occipital lobes,\nextending into the centrum semiovale, corona radiata, internal capsule,\nperiatrial white matter, corpus callosum.  Involvement of the left thalamus. \nThere is infratentorial involvement centered about bilateral middle cerebellar\npeduncles, with few punctate foci at the brainstem and cerebellum.  ADC values\nhave increased in some areas compared with ___.  Findings may\nrepresent evolving subacute infarcts secondary to predominantly diffuse white\nmatter injury secondary to hypotension.  Sparing of the cortex is somewhat\natypical, though.  Differential considerations include fulminant acute\ndemyelinating process, acute toxic leukoencephalopathy, which can be seen with\ncertain medications, including antibiotics and anticancer medications, or drug\nuse, or metabolic causes.  Punctate focus of gradient abnormality left\nthalamus may be from microhemorrhage.  Punctate focus of microhemorrhage in\nleft cerebellum.  No definite new lesions.  Given symmetric appearance and\nextent of disease, prevascular infiltrative processes is very unlikely.\n\nGiven history of recent infection, post gadolinium images may be helpful in\nfurther evaluation, to exclude any ring-enhancing lesions which may be\nsuggestive of component of infection, if this is clinically suspected.\n\nConfluent deep white matter T2 signal abnormalities are likely related to\nprocess above, component may be related to prior radiation therapy if this has\nbeen performed.  No definite cortical abnormalities on diffusion or T2\nweighted images.  There is diffuse, severe brain parenchymal atrophy.  At\nleast moderate bilateral hippocampus atrophy.\nIntracranial vascular flow voids are preserved.  Severe right and mild left\nmastoid opacification, worsened since prior.  Mild opacification ethmoid air\ncells.  Paranasal sinuses are otherwise clear.",
            "output": "1. Extensive focal and confluent symmetric zones of restricted diffusion\npredominantly involving deep white matter in bilateral cerebral hemispheres\nand infratentorially, similar distribution since prior, some involution since\nprior.  Differential considerations include predominantly white matter\nischemia from hypotension, metabolic causes including toxic\nleukoencephalopathy, adem.   Consider post gadolinium images in further\nevaluation.  No definite new abnormalities.\n2. Moderate severe opacification mastoid, worse on the right, consider\notomastoiditis if clinically appropriate."
        },
        {
            "input": "There are innumerable supratentorial juxta cortical, deep white matter,\nperiventricular lesions, similar compared with ___.  Few lesions\nhave dark T1 signal, feature associated more aggressive disease.  There\nprobably few cortical lesions, similar.  There is 1 new lesion in the right\nmiddle cerebellar peduncle series 8, image 13.  Remaining infratentorial\nbrainstem, cerebellar, middle cerebellar peduncle and visualized cervical cord\nlesions are stable.  No restricted diffusion.  Mild stable brain parenchymal\natrophy.\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  There is no abnormal enhancement after contrast\nadministration.  Intracranial vascular flow voids are preserved.  Essentially\nclear paranasal sinuses, mastoid air cells",
            "output": "1. Findings consistent with multiple sclerosis.  1 new lesion since prior.\n2. No enhancement to suggest active demyelination."
        },
        {
            "input": "There is subtle susceptibility artifact corresponding to pipeline embolization\nstent device within the distal right internal carotid artery.  Flow within the\nstent appears grossly preserved.  No residual flow related signal is seen\nwithin the previously noted right supraclinoid internal carotid artery\naneurysm.\n\nA 1 mm infundibulum is seen along the left A2 segment of the ACA, appearing to\nconnect to a tiny vessel.\n\nThe intracranial vertebral and internal carotid arteries and their major\nbranches otherwise appear patent without evidence of stenosis,occlusion,ornew\naneurysm formation.\n\nThe visualized ventricles and sulci appear mildly prominent, suggestive of\nage-related involutional change.",
            "output": "1. Pipeline embolization of a right supraclinoid internal carotid artery\naneurysm, without evidence of recannulization.\n2. Patent intracranial arterial vasculature without significant stenosis,\nocclusion, or new aneurysm formation."
        },
        {
            "input": "Diffuse cortical slow diffusion involving the posterior frontal, parietal\noccipital and temporal lobes as well as caudate and putamen is identified,\ncompatible with diffuse hypoxic injury.  Subtle diffusion-weighted\nhyperintense signal involving the right middle cerebellar peduncle and pons\nmay represent wallerian degeneration.  Superimposed confluent periventricular\nand subcortical T2/FLAIR white matter hyperintensities are nonspecific, and\nsimilar in appearance to prior examination, compatible with chronic\nmicroangiopathy in a patient this age.  No acute intracranial hemorrhage.\n\nThe sulci, ventricles and cisterns are prominent, but within expected limits\nfor the degree of moderate to severe senescent related global cerebral volume\nloss, similar in appearance to prior examination.  The major intracranial flow\nvoids are preserved.  New complete opacification of the sphenoid sinuses, mild\nmucosal thickening of the maxillary sinuses and ethmoid air cells is noted. \nThe orbits are unremarkable.  Fluid signal opacifies the mastoid air cells. \nThe superior ophthalmic veins are symmetrically enlarged bilaterally, likely\nsecondary to increased intracranial pressure or Valsalva.  No secondary signs\nto suggest cavernous sinus thrombosis on this nondedicated examination.\n\nThe marrow signal is diffusely T1 slightly hypointense, which may be seen in\nsetting of reconversion with chronic anemia.  Clinical correlation is\nrecommended.",
            "output": "1. Diffuse cortical slow diffusion involving the posterior frontal, bilateral\nparietal occipital and temporal lobes as well as caudate and putamen,\ncompatible with diffuse hypoxic injury.  Subtle signs of right sided wallerian\ndegeneration also noted.\n2. Global cerebral volume loss.\n3. Paranasal sinus disease as described above.\n4. The bilateral superior ophthalmic veins are prominent, without secondary\nsigns to suggest cavernous sinus thrombosis.  This is likely secondary to\nmildly increased intracranial pressure or Valsalva.\n5. Please note, contrast extravasation occurred and no intracranial contrast\nis seen.\n\nNOTIFICATION:  The findings were discussed with Dr. ___. by ___\n___, M.D. on the telephone on ___ at 3:18 pm, 30 minutes after\ndiscovery of the findings."
        },
        {
            "input": "The examination is motion degraded.  Within these confines:\n\nThere is no acute ischemia or hemorrhage.  Confluent diffuse subcortical,\nperiventricular and pontine white matter T2/FLAIR hyperintensities have\nworsened, as compared to MR head dated ___, involving the posterior\nperiventricular region.  The ventricles are diffusely dilated, indicating\nvolume loss, slightly worse than prior.  Flow voids are preserved.  There is\nno evidence of masses, mass effect, or midline shift.  The orbits are\nunremarkable.  The mastoid air cells demonstrate fluid signal at the tips\ngreater on the left.  The paranasal sinuses demonstrate mild mucosal\nthickening.",
            "output": "1. No acute infarction.\n\n2. More diffuse subcortical white matter disease, while nonspecific likely\nrepresent sequelae of chronic small vessel disease."
        },
        {
            "input": "There is no acute infarction, intracranial hemorrhage, extracerebral fluid\ncollection, midline shift or mass effect.  There is mild brain atrophy seen.\nMild changes of small vessel disease as at the periventricular white matter\nand brainstem. There are no territorial infarcts seen. A small area of Chronic\nmicro hemorrhages seen in the right temporal region. Flow voids are\nmaintained. Suprasellar and craniocervical regions are unremarkable.",
            "output": "Mild brain atrophy and small vessel disease.  A small area of right temporal\nchronic micro hemorrhage.  Otherwise,no significant abnormalities are seen on\nMRI of the brain without gadolinium."
        },
        {
            "input": "There are multiple regions of slow diffusion involving the left frontal lobe,\nleft parietal lobe, and left insula. There is corresponding T2/FLAIR signal\nabnormalities in these regions. Findings are compatible with acute/ subacute\ninfarction in the left MCA territory.\n\nAs seen on prior CT scan, there is a left frontal developmental venous\nanomaly. On gradient susceptibility images, at the termination of this DVA\njust above the left lateral ventricle, there is a focus of hypointense\nblooming which could reflect blood products from an associated cavernoma\n(series 6, image 6).\n\nThere is no extra-axial collection, mass effect, or midline shift. The\nventricles and sulci are normal in caliber and configuration.  There are few\nadditional scattered foci of T2/FLAIR signal hyperintensity in the subcortical\nwhite matter which are nonspecific. There is no abnormal enhancement after\ncontrast administration.  The orbits are unremarkable. There is opacification\nof the left maxillary sinus and mucosal thickening in the ethmoid air cells\nunchanged. There is trace fluid in the right mastoid air cells also unchanged.",
            "output": "1.  Acute/subacute infarctions in the left frontal lobe, left parietal lobe,\nand left insula in the distribution of the left MCA.\n\n2.  Left frontal lobe DVA with associated cavernoma."
        },
        {
            "input": "There is a 6-mm left-sided subdural hematoma which appears to be isointense on\nT1 weighted imaging and predominantly hyperintense on T2 weighted imaging with\nsome T2 hypointensity and blooming.  There is midline shift to the right of\napproximately 2 mm.\n\nThere is no evidence of a large territorial infarction.  The ventricles sulci\nare normal in caliber and configuration.  There is a dominant left vertebral\nartery, otherwise the intravascular flow voids appear to be well preserved.\n\nThe visualized paranasal sinuses are clear.  Minimal opacification is seen\ninvolving the mastoid air cells bilaterally.  The middle ear cavities are\nclear.  No marrow signal abnormalities are identified.",
            "output": "1. 6-mm left-sided subdural hematoma.  There is evidence of midline shift to\nthe right, of approximately 2 mm.\n2. The globes are unremarkable.\n\nNOTIFICATION:  ___ were d/w Dr. ___ at 10AM on ___ by phone\n2-minutes after discovery by Dr. ___."
        },
        {
            "input": "Re demonstrated is the left-sided subdural hemorrhage, slightly decreased in\nsize compared to the prior exam performed on the ___, now measuring up\nto 4 mm, previously measuring up to 6 mm.  Re demonstrated is mild midline\nshift to the right of approximately 2 mm.  No concerning enhancing lesions are\nidentified.\n\nThere is no evidence of acute infarction.  Re demonstrated is a dominant left\nvertebral artery, otherwise the intravascular flow voids appear to be well\npreserved.  Aside from mild sinus disease involving the ethmoid air cells. \nThe visualized paranasal sinuses are unremarkable.  The globes are\nunremarkable.",
            "output": "1. Overall, interval improvement in the left subdural hemorrhage, decreased in\nsize compared to the prior exam, now measuring up to 4 mm.\n\n2. No enhancing lesions identified."
        },
        {
            "input": "MRV:  There is nonvisualization of the left sigmoid sinus, left internal\njugular vein, left transverse sinus for left internal cerebral vein or vein of\n___.   T1 weighted images do not demonstrate corresponding high signal\nwithin expected course of these veins (see ___.  There is suggestion of\nright transverse sinus filling defect near its junction with the sigmoid sinus\n(see 100:9), with no definite corresponding T1 hyperintensity (see ___.\n\nThe superior sagittal sinus, straight sinus, jugular bulbs and proximal\njugular veins are patent. Evaluation of the deep venous systems reveals normal\nflow signal in the internal cerebral veins. The vein ___ is also\nunremarkable.\n\nMRI brain:  Limited evaluation of the brain on sagittal T1 weighted images\ndemonstrates of mucous retention cyst in the right maxillary sinus.  The brain\nparenchyma is grossly unremarkable.",
            "output": "1. Nonvisualization of left transverse sinus, sigmoid sinus left internal\ncerebral vein, or left internal jugular vein as described.  Differential\nconsiderations include slow flow, congenital hypoplastic veins, and occlusive\nthrombus.  Recommend clinical correlation and comparison with prior\nexaminations, if available.  If clinically indicated, further evaluation with\ncontrast-enhanced MPRAGE images or CT venogram can be performed.\n2. Question focal nonocclusive thrombus in the right transverse sinus versus\nslow flow.\n3.  Paranasal sinus disease as described.\n\nRECOMMENDATION(S):  Recommend clinical correlation and comparison with prior\nexaminations, if available. If clinically indicated, further evaluation with\ncontrast-enhanced MPRAGE images or CT venogram can be performed."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.\n\nThere is congenitally hypoplastic left transverse sinus, sigmoid sinus and\nleft internal jugular vein which accounts for nonvisualization of the sinus on\nthe priors MRV.  Also seen is focal area of narrowing of the right transverse\nsinus just proximal to the sigmoid sinus as seen on image 100b:41 without any\ndefinite intraluminal filling defect, likely secondary to focal stenosis.  No\ndeep venous sinus thrombosis is seen on today's study.\n\nThe orbits are unremarkable.  There is partial opacification of bilateral\nethmoid air cells with air-fluid level in the right maxillary sinus.  Also\nseen is a mucous retention cyst in the right maxillary sinus and mucosal\nthickening in the left maxillary sinus.  The remaining visualized paranasal\nsinuses and mastoid air cells are clear.  Intracranial flow voids are\nmaintained.  The osseous structures are unremarkable.",
            "output": "1. Congenitally hypoplastic left transverse sinus, sigmoid sinus and left\ninternal jugular vein accounting for non visualization of the sinuses on prior\nMRV.\n2. Focal area of narrowing in the right transverse sinus just proximal to\nsigmoid sinus indicating stenosis of the right transverse sinus.  This may be\ncongenital in nature or secondary to remote thrombosis and recanalization.\n3. No acute intracranial abnormality.\n4. Partial empty sella is identified which is an nonspecific finding which\ncould be associated with pseudotumor cerebral ."
        },
        {
            "input": "Study is mildly degraded by motion.\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.\n\nThere is a well-defined small left nasopharyngeal cystic structure likely\nrepresenting small retention cyst.  Mild mucosal thickening involving both\nethmoid air cells and sphenoid sinuses.  Bilateral mastoid air cells mild\nfluid signal intensity.  Both orbits and globes are normal.",
            "output": "1. No acute intracranial abnormality.  No significant change."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.\n\nThere is mild mucosal thickening involving bilateral ethmoid air cells\nconsistent with mild paranasal sinuses disease.  There are scattered\nopacification of bilateral mastoid air cells.\n\nThe superior sagittal sinus is patent.  The straight sinus is patent.  The\ntransverse sinuses are patent.  The sigmoid sinuses are patent.  The internal\njugular veins bilaterally are unremarkable.",
            "output": "1. No acute intracranial pathology.\n2. Mild paranasal sinuses disease.\n3. Mild bilateral mastoid air cells opacification.\n4. No evidence of dural venous sinus thrombosis."
        },
        {
            "input": "The intracranial vertebral and internal carotid arteries and their major\nbranches appear normal without evidence of stenosis, occlusion, or aneurysm\nformation.",
            "output": "1. Normal brain MRA."
        },
        {
            "input": "There is unchanged appearance of a T2 hyperintense and T1 hypointense, cystic\nlesion demonstrating a single thin enhancing septation centered in the left\njugular foramen measuring approximately 7 x 4 x 15mm (TRV, AP, CC) since prior\nexams.\n\nNo other masses are noted. No evidence of acute hemorrhage or infarct. Sulci,\nventricles cisterns are within expected limits. The major intracranial flow\nvoids are preserved. Small mucous retention cysts in the bilateral maxillary\nsinuses are noted. Otherwise the remainder the paranasal sinuses are clear.\nThe orbits are unremarkable. The mastoid air cells are clear.",
            "output": "Unchanged appearance of a cystic lesion is centered in the left jugular\nforamen measuring up to 15 mm in craniocaudal dimension, likely representing a\nperineural cyst given the stability in size since ___, although a cystic\nschwannoma is a differential consideration but appears less likely."
        },
        {
            "input": "There is no evidence of acute infarction, edema, mass effect, or blood\nproducts.  There are discrete foci and more confluent areas of T2/FLAIR\nhyperintensity in the subcortical, deep, and periventricular white matter, and\nin the pons, nonspecific but likely secondary to small vessel ischemic disease\nin this age group.  The ventricles and sulci mildly to moderately prominent\ndue to age-related parenchymal volume loss.  Extra-axial space in the right\nposterior fossa is larger than on the left, similar to the preceding CTA, even\nthough the patient's head is no longer tilted to the left.  This may reflect\nasymmetric parenchymal volume loss.\n\nThere is evidence of bilateral cataract surgeries.  There is mucosal\nthickening and small mucous retention cysts in bilateral maxillary sinuses. \nAlso seen is mucosal thickening in bilateral ethmoid air cells and inferior\nleft frontal sinus.  There is mucosal thickening and possibly also fluid\nwithin the left mastoid air cells.",
            "output": "No acute infarction.  Supratentorial white matter and pontine signal\nabnormalities are nonspecific but likely secondary to chronic small vessel\nischemic disease in this age group."
        },
        {
            "input": "Patient is status post resection of right temporal glioblastoma.  Compared to\nprior brain MR dated ___, there is increased enhancement along the\ninferior, medial, and superior margins of the resection cavity, with the\nthickest portion measuring 7 mm x 13 mm along the medial margin (series 9,\nimage 143).  There is unchanged T2/FLAIR hyperintensity in the right\ntemporoparietal white matter and decreasing quantities of blood products.\n\nThere is decreased leftward midline shift, now measuring approximately 5 mm,\npreviously 12 mm.  There is also a decreased mass effect on the right lateral\nventricle.\n\nWithin the right transverse sinus, just inferior to the resection cavity,\nthere is redemonstration of a flow defect stop (series 9, image 116). \nHowever, compared to prior this finding is less conspicuous.\n\nNo territorial infarction or new intracranial hemorrhage",
            "output": "1. Interval increased enhancement around the right temporal resection cavity,\nmost prominent along the medial margin, which may represent postsurgical\nchanges versus underlying malignancy.  Given the interval increase, there is\nconcern for residual/progressive malignancy.\n2. Improving postoperative changes following resection of a right craniotomy\nand resection.  Decreased leftward midline shift and mass effect.\n3. Improved but persistent nonocclusive right lateral transverse sinus filling\ndefect.  This finding may again represent an intraluminal thrombus versus\npostsurgical blood products external to the sinus, compressing its lumen."
        },
        {
            "input": "The patient is status post prior right temporoparietal craniotomy and\nresection of a right temporal lobe mass.  There is been interval continued\ninvolution of the resection cavity, now measuring approximately 2.5 x 1.4 cm\n(AP, TRV), decreased in size from prior exam.  Nodular peripheral enhancement\nmeasuring up to 5 mm along the medial aspect of the resection margin is\nslightly improved from prior exam.  There remains mild surrounding FLAIR edema\npattern, significantly improved from prior exam, with improved leftward\nmidline shift.\n\nThere is no acute infarct or intracranial hemorrhage.  A single punctate focus\npostcontrast enhancement in the right medial frontal lobe (series 9, image\n107) is likely artifactual or secondary to vasculature as this is not seen on\nprior examination and is without corresponding signal abnormality on other\nsequences.  Allowing for postsurgical changes, the sulci, ventricles cisterns\nare within expected limits for the patient's age.  The major intracranial flow\nvoids are preserved.  The dural venous sinuses are grossly patent.  Previously\nseen filling defect of the distal right transverse sinus is not clearly seen.\n\nThere is mild mucosal thickening of the ethmoid air cells.  The orbits are\nunremarkable.  Trace fluid signal is seen in the right mastoid air cells,\nsimilar to prior exam.",
            "output": "1. Status post right temporoparietal craniotomy and resection of right\ntemporal lobe mass.  There is continued involution of the resection cavity and\nmild improvement in degree of nodular peripheral enhancement along the\nresection margin.  Significant improvement in degree of right temporal lobe\nedema pattern.  No findings to suggest disease progression.  Residual lesion\nwithin the enhancing nodular periphery is not excluded and continued follow-up\nper clinical protocol is recommended.\n2. A punctate focus of enhancement in the right medial frontal lobe without\nevidence of corresponding signal abnormality on other sequences.  This was not\nseen on prior exam and is felt to be most likely artifactual or vascular in\nnature.  However close attention on follow-up is recommended.\n3. Additional findings as described above."
        },
        {
            "input": "The patient is status post right temporoparietal craniotomy and underlying\nresection of a right temporal lobe lesion.  5 mm nodular enhancement in the\nresection cavity is overall unchanged from examination of ___. \nSurrounding right temporal lobe white matter edema pattern and\nencephalomalacia is also unchanged.  No new enhancing lesions.  No new\nsuspicious parenchymal FLAIR signal abnormality.  Previously seen punctate\nenhancement of the medial right frontal lobe is not visualized on current\nexam.\n\nThere is no acute infarct or intracranial hemorrhage.  The sulci, ventricles\nand cisterns are within expected limits for the patient's age.  The major\nintracranial flow voids are preserved.  Dural venous sinuses are patent.\n\nThe paranasal sinuses are essentially clear.  The orbits are unremarkable. \nThe mastoid air cells and middle ears demonstrate no significant effusion.  No\nsuspicious marrow signal.",
            "output": "1. Unchanged 5 mm nodular enhancement of the right temporal lobe resection\ncavity.  No new enhancement.  No findings to suggest disease progression.\n2. Unchanged right temporal lobe FLAIR edema pattern and encephalomalacia.\n3. Previously described punctate right medial frontal enhancement is not seen\non the current examination.\n4. Additional findings as described above."
        },
        {
            "input": "The patient is status post right temporoparietal craniotomy and underlying\nresection of a right temporal lobe lesion.  There is redemonstration of\nunchanged small extra-axial less than 3 mm collection.  Also there is\nredemonstration of postsurgical change changes on surgical bed cranial vault\nand mastoid bone.\n\nThere is mild interval further decrease in size of abnormal nodular\nenhancement in the vicinity of the surgical cavity at right posterior temporal\nregion measuring now 6 mm and previously was 8 mm on ___ examination\nand 9 mm on ___ examination.  There is no new abnormal suspicious\nenhancement along the surgical cavity or intracranial.\n\nThe surrounding T2 FLAIR abnormal hyperintensity extension is unchanged. \nThere is adjacent expansion of proximal right temporal horn suggesting\nlocoregional volume loss. No new suspicious parenchymal FLAIR signal\nabnormality.\n\nThere is no acute infarct or intracranial hemorrhage.  The sulci, ventricles\nand cisterns are within expected limits for the patient's age.  The major\nintracranial flow voids are otherwise preserved.  Dural venous sinuses are\npatent.\n\nThe paranasal sinuses are essentially clear.  The orbits are unremarkable. The\nmastoid air cells and middle ears demonstrate no significant effusion.  No\nsuspicious marrow signal.",
            "output": "1. Status post right temporoparietal craniotomy for underlying right temporal\nlesion resection with postoperative changes.\n2. There is mild interval further decrease in size of abnormal nodular\nenhancement in the vicinity of the surgical cavity with no newly developed\nsurgical margin or intracranial enhancement.\n3. Stable surrounding T2 FLAIR abnormal signal intensity.\n4. No acute intracranial abnormality."
        },
        {
            "input": "Postoperative changes are again identified in the right temporal region. \nEncephalomalacia and FLAIR hyperintensities are seen in the region.  No\ndefinite areas of abnormal enhancement identified.  No other areas of abnormal\nenhancement seen.  No mass effect midline shift or hydrocephalus.",
            "output": "Stable appearance of postoperative change in the right temporal region.  No\ndefinite new areas of abnormal enhancement are seen.  No acute infarcts mass\neffect or hydrocephalus."
        },
        {
            "input": "In the right temporal lobe there is a 5.3 x 3.4 x 3.9 cm heterogeneously\nenhancing, cystic/necrotic mass with foci of internal hemorrhage.  The more\nlateral solid, enhancing portion of the mass demonstrates restricted\ndiffusion.\n\nThere is marked perilesional FLAIR hyperintensity within the right temporal,\nparietal, and frontal white matter extending to the level of the centrum\nsemiovale.\n\nThere is extensive brain swelling and mass-effect, including effacement of the\nright lateral ventricle, 15 mm leftward shift of midline structures,\nsubfalcine and right uncal herniation.  The right PCA and anterior cerebral\narteries nonetheless appear patent on post-contrast MP RAGE images.\n\nThere is no evidence of acute infarction or extra-axial collection.  No\nadditional mass or other focus of abnormal enhancement is identified.\n\nParanasal sinuses, mastoids clear.  Globes and orbits unremarkable.  Major\ndural venous sinuses are patent.  Major intracranial vascular flow voids\nappear preserved.",
            "output": "1. 5.3 cm heterogeneously enhancing cystic/necrotic mass most consistent with\nhigh-grade glioma (glioblastoma).  Differential includes metastasis; CNS\nlymphoma considered significantly less likely given this appearance,\nparticularly if the patient is immunocompetent.\n2. Marked mass effect including 15 mm leftward shift of midline and right\nuncal and subfalcine herniation.  No ventricular entrapment.\n3. No evidence of acute infarct or extra-axial collection.\n4. Extensive right cerebral perilesional FLAIR hyperintensity."
        },
        {
            "input": "The patient's previously noted right temporal lobe heterogeneously enhancing\nmixed necrotic and solid 5.1 x 3.5 x 3.9 cm (AP by TV by SI) (09:11, 101:86)\nmass is again seen, unchanged.  Areas of slow diffusion correspond to the\nsolid enhancing components of the mass, suggestive of a highly cellular tumor.\n\nNotably, the inferior margin of the mass is inseparable from the superior\nmargin of the very lateral aspect of the right transverse sinus, without\nevidence of macroscopic invasion.  The transverse sinus remains patent.\n\nThere is unchanged 1.5 cm leftward midline shift and stable but marked mass\neffect including diffuse right-sided sulcal effacement, effacement of the\nright lateral ventricle, right uncal and subfalcine herniation, all unchanged.\n\nThere is no evidence of slow.  Major dural venous sinuses appear patent.",
            "output": "1. 5.1 cm right temporal lobe mass compatible with high-grade glioma (e.g.\nglioblastoma), differential includes metastasis.  Note, the inferior margin of\nthe mass is inseparable from the superior margin of the lateral aspect of the\nright transverse sinus; no visible macroscopic invasion, and the sinus remains\npatent.\n2. Marked mass effect is unchanged including right uncal and subfalcine\nherniation, 1.5 cm leftward shift of midline structures."
        },
        {
            "input": "Study is mildly degraded by motion.\n\nThere are new, expected interval postoperative changes from right sided\ncraniotomy and resection of the right temporal lobe mass, including scattered\nfoci of postsurgical blood products, pneumocephalus, trace extra-axial fluid,\nand skin and subgaleal fluid and air, and minimal slow diffusion along\nresection margin (see 7, 08:14).  Trace minimal nonspecific enhancement along\nthe right anterior margin of the resection cavity is noted (see 5, 15:9).\n\n FLAIR hyperintensity within the right temporoparietal white matter is\nunchanged.\n\nMass-effect is mildly improved, but still significant, with 12 mm leftward\nshift of midline structures (previously 15 mm), effacement of the right\nlateral ventricle and right cerebral sulci, persistent right uncal herniation\nand subfalcine herniation.  The cerebral aqueduct is again not definitely well\nvisualized on current study (see 101: 52-59 on current study and 100: 54-59 on\n___ prior contrast brain MRI).  Within limits of study, there is no\ndefinite ventricular entrapment is noted.\n\nThere is no evidence of acute infarct.  Major dural venous sinuses are patent.\n\nT1 isointense to brain parenchyma mildly FLAIR hyperintense lobulated focus\nalong the lateral aspect of the right transverse sinus just inferior to the\nresection site either represents an intraluminal, nonocclusive thrombus in the\ntransverse sinus, or possibly postsurgical blood products external to the\nsinus and compressing its lumen.  The remaining major dural venous sinuses\nappear patent.\n\n There is trace ethmoid air cell mucosal thickening.  There is a trace right\nmastoid effusion.",
            "output": "1. Study is mildly degraded by motion.\n2. Question new nonocclusive dural venous sinus thrombosis within the right\nlateral transverse sinus just inferior to the resection site, with\ndifferential considerations of postsurgical blood products external to the\nsinus and compressing its lumen.\n3. Expected postoperative changes status post interval right craniotomy and\nresection.\n4. Minimal nonspecific enhancement along surgical margin as described.  While\nfindings are suggestive of postoperative change, recurrent residual tumor is\nnot excluded on the basis of this examination.  Recommend attention on\nfollow-up imaging.\n5. Right temporoparietal white matter FLAIR hyperintensity is unchanged.\n6. Mild improvement in mass effect, with continued right uncal and subfalcine\nherniation and 12 mm leftward shift of midline structures (previously 15 mm),\nas described.\n\nRECOMMENDATION(S):  Minimal nonspecific enhancement along surgical margin as\ndescribed. While findings are suggestive of postoperative change, recurrent\nresidual tumor is not excluded on the basis of this examination. Recommend\nattention on follow-up imaging.\n\nNOTIFICATION:  The findings regarding impression point 1 were discussed with\n___, MD. By ___, M.D. on the telephone on\n___ at 12:47 pm, 5 minutes after discovery of the findings."
        },
        {
            "input": "There is slowed diffusion with corresponding ADC weighted hypointensity\nconsistent with an acute infarct within the left centrum semiovale and left\ncorona radiata. The extent of the infarct is not significantly changed from CT\non ___. There is no new vascular territory infarct. There is no\nintracranial hemorrhage. There is no mass effect. There are multiple foci of\nFLAIR hyperintensity in the subcortical and deep white matter and left basal\nganglia that do not demonstrate slowed diffusion, consistent with chronic\nsmall vessel ischemic disease and chronic infarcts. Ventricles, sulci, and\ncisterns are age-appropriate.\n\nFlow voids for the M1 segment of the left middle cerebral artery are partially\nvisualized (see series 5 images ___. There is a paucity of flow voids in\nthe sylvian region of the left middle cerebral artery. Major intravascular\nflow voids are otherwise preserved.\n\nThere is mild mucosal thickening of the ethmoid and sphenoid sinuses. The\nparanasal sinuses and mastoid air cells otherwise appear clear. The orbits are\nnormal.",
            "output": "1. Acute infarcts of the left centrum semiovale and left coronal radiata in\nthe distribution of a branch of the left middle cerebral artery. The extent of\nthe acute infarcts does not appear significantly changed from CT on ___. No new infarcts identified.\n2. No acute intracranial hemorrhage.\n3. Paucity of flow voids in the sylvian region of the left middle cerebral\nartery,  corresponding to diminished vascularity of M2 branches of the left\nmiddle cerebral artery seen on CTA from ___.\n4. Underlying scattered chronic infarcts of the left basal ganglia and\nscattered chronic small vessel ischemic disease."
        },
        {
            "input": "MRI BRAIN:\nRedemonstration of known bilateral intraparenchymal hemorrhages in the\ncingulate gyri, left greater than right. Scattered GRE hypodensities is also\nnoted along the left falx near the vertex, septum pellucidum, and occipital\nhorns of the lateral ventricles.  Small foci of susceptibility artifact is\nnoted in the left occipital lobe.  Overall, the extent of the hemorrhage and\nassociated mass effect is similar to prior CT dated ___,\nallowing for differences in modality.\n\nAdditionally seen small subdural hematoma is also present in the posterior\ninterhemispheric fissure and extending into the left tentorium.\n\nThe hematoma demonstrates areas of intrinsic T1 hyperintensity suggestive of\nsubacute nature.  There is no evidence to suggest acute infarct.  There is no\nmidline shift.  There is stable prominence of the ventricles, cortical sulci,\nand basal cistern, likely representing age-related involutional changes.  Few\nscattered foci of FLAIR hyperintensities in the subcortical white matter,\nlikely suggestive of chronic microangiopathy.  There is mucosal thickening\ninvolving ethmoid air cells, and bilateral maxillary sinuses.  The mastoid air\ncells are unremarkable.  Changes of right lens replacement is noted.  No\nabnormal marrow signal.\n\nThere is no evidence of dural venous sinus thrombosis.\n\nMRA BRAIN:\nThe intracranial vertebraland internal carotid arteries and their major\nbranches appear normal without evidence of stenosis,occlusion,or aneurysm\nformation.",
            "output": "1. Allowing for differences in modality, unchanged bilateral intraparenchymal\nhemorrhage in the cingulate gyrus, left greater than right, with small\nlayering hemorrhage in the bilateral occipital horn.  No midline shift or\ncerebral herniation. Small parafalcine subdural hematoma extending into the\nleft tentorium.  The etiology of the hemorrhage may be secondary to the\nreported trauma with superimposed patient being on blood thinner.  No evidence\nof dural venous sinus thrombosis\n2. No evidence of an acute stroke.\n\n3. Additional findings as described above"
        },
        {
            "input": "Study is mildly degraded by motion.\n\nMRI BRAIN:\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal focus of slow diffusion.  There are\nsubtle, nonspecific areas of mainly periventricular and deep white matter\nT2/FLAIR hyperintensity, which appears slightly more prominent adjacent to the\noccipital horn of the left lateral ventricle, however likely represent the\nsequela of chronic microvascular disease.  The principal intracranial vascular\nflow voids are preserved.\n\nThere is a moderate mucous retention cyst in the right maxillary sinus as well\nas minimal anterior ethmoid air cell mucosal thickening.  The remainder of the\nvisualized paranasal sinuses are grossly clear.  The orbits are grossly\nunremarkable.\n\nMRA BRAIN:\nThere is a left dominant vertebrobasilar system.  There is mild irregularity\nof the ophthalmic and supra clinoid internal carotid arteries, likely\nsecondary to atherosclerotic disease.  The intracranial vertebral and internal\ncarotid arteries and their major branches otherwise appear patent without\nevidence of significant stenosis, occlusion, or aneurysm formation.\n\nMRA NECK:\nThere is suggestion of mild narrowing at the origin of the right vertebral\nartery.  The distal right vertebral artery is patent.  The common, internal\nand external carotid arteries appear patent.  There is no evidence of internal\ncarotid artery stenosis by NASCET criteria.  The origins of the great vessels,\nsubclavian and vertebral arteries appear grossly patent bilaterally.",
            "output": "1.  Study is mildly degraded by motion.\n2. No acute intracranial abnormality, with no evidence acute infarct.\n3.  Probable small vessel ischemic changes as described.\n4. Patent intracranial vasculature without significant stenosis, occlusion or\naneurysm.\n5. Narrowing right vertebral artery origin.  Otherwise patent cervical\nvasculature without significant stenosis or occlusion.\n6. Paranasal sinus disease as described."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.\n\nThe orbits are unremarkable.  Intracranial flow voids are maintained.  The\nvisualized paranasal sinuses and mastoid air cells are clear.",
            "output": "1. Unremarkable brain MRI.  Specifically, no abnormal enhancement, acute\ninfarct, white matter lesions or intracranial mass."
        },
        {
            "input": "Image quality is degraded by motion artifact.\n\nThere is slow diffusion in the bilateral thalami and rostral midbrain with\ncorresponding T2/FLAIR signal hyperintensity. Findings are  felt most\nconsistent with a late acute/early subacute artery of percheron territory\ninfarct.\n\nThere is no evidence of hemorrhage, edema, masses, or mass effect. The\nventricles and sulci are enlarged most likely secondary to age related\nparenchymal volume loss. Cavum septum pellucidum et vergae is again noted. \nThere is T2/FLAIR signal hyperintensity in the periventricular white matter\nwhich is nonspecific but likely on the basis of chronic small vessel ischemic\ndisease. Vascular flow voids are preserved. This patient status post bilateral\nlens replacement. There is mild mucosal thickening within the ethmoid air\ncells. The remaining paranasal sinuses and mastoid air cells are clear.",
            "output": "1 slow diffusion in the bilateral thalami and midbrain with corresponding\nT2/FLAIR signal most consistent with late acute or early subacute infarction\nin the artery of percheron territory.  Given the location and midbrain and\nappearance, Wernicke's encephalopathy appears less likely\n\n2. T2/FLAIR signal hyperintensity in the periventricular white matter which is\nnonspecific but likely on the basis of chronic small vessel ischemic disease."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.\nThere is a right maxillary sinus mucous retention cyst.  There is partial\nopacification of the mastoid air cells bilaterally.",
            "output": "Paranasal sinus and mastoid air cell inflammatory changes.  Otherwise normal\nstudy"
        },
        {
            "input": "There is a 6 mm enhancing lesion in the right posterior parasagittal parietal\nlobe (16:114) with a small amount of regional FLAIR hyperintense edema.  There\nis a 4 mm possibly enhancing focus in the right parietal calvarium (16:136)\nand left frontal calvarium (16:121), similar to the prior exam.  There are\nperiventricular and subcortical white matter foci of T2/FLAIR signal\nhyperintensity, nonspecific but likely sequelae of chronic small vessel\ndisease.  There is no evidence of hemorrhage, mass effect, midline shift or\ninfarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  A partially empty sella is incidentally noted.\n\nThere is mild mucosal thickening within the frontal sinus and multiple ethmoid\nair cells.  No significant fluid signal is seen in the mastoid air cells. \nPostsurgical changes related to right ocular lens replacement are noted.",
            "output": "1. New 6 mm enhancing lesion in the right posterior parasagittal parietal lobe\nwith a small amount of regional edema concerning for metastatic disease.\n2. Similar possibly enhancing 4 mm foci in the left frontal and right parietal\ncalvarium may represent small vessels/venous lakes.  Osseous metastasis are\nnot excluded.\n3. Periventricular and subcortical white matter signal changes, nonspecific\nbut likely sequelae of chronic small vessel disease.\n4. Partially empty sella.\n\nNOTIFICATION:  The impression and recommendation above was entered by Dr. ___\n___ on ___ at 09:34 into the Department of Radiology critical\ncommunications system for direct communication to the referring provider."
        },
        {
            "input": "The patient's previously noted right posterior parietal lobe 6 mm metastatic\nlesion is again seen.  There is no midline shift and no mass effect.  The\nlesion is similar to the previous examination.  Nonspecific enhancing foci are\nagain seen in the right parietal and left frontal calvarium without change. \nNo new enhancing lesions are demonstrated.  Partially empty sella is again\nnoted.",
            "output": "1. No change in the right parietal lobe metastatic lesion.\n2. Redemonstration of possibly enhancing foci in the left frontal and right\nparietal calvarium, nonspecific."
        },
        {
            "input": "The enhancing metastatic lesion in the right posterior parietal lobe is\nredemonstrated, and measures approximately 4 mm.  This is slightly decreased\nin size in comparison with the prior study when it measured 6 mm (17:119).  No\nnew enhancing lesions are seen.  Redemonstration of encephalomalacia in the\nleft centrum semiovale and left cerebellar hemisphere, consistent with chronic\ninfarcts.  Periventricular and subcortical T2 and FLAIR hyperintensities are\nnoted which are nonspecific but may represent chronic small vessel ischemic\nchanges. There is no evidence of hemorrhage, edema, masses, mass effect,\nmidline shift or acute infarction.  The ventricles and sulci are normal in\ncaliber and configuration.\n\nNon-specific small enhancing foci in the right parietal (17:153, 128), and\nleft frontal calvarium (17:101) are unchanged.  Redemonstration of mild\nmucosal thickening of the anterior ethmoid air cells.  The orbits are\nunremarkable.",
            "output": "1. Interval decrease in the size of a right posterior parietal lobe metastatic\nlesion.  No new intracranial lesions are identified.\n2. Unchanged nonspecific enhancing foci in the right parietal and left frontal\ncalvarium."
        },
        {
            "input": "Again seen is 4 mm hyperenhancing metastatic lesion in the right posterior\nparietal lobe (see 9:106) .  The degree of enhancement has decreased from\nprior.  The nonspecific small enhancing foci in the right parietal calvarium\n(see 9:122; 9; 134; 9:145) are unchanged as is the nonspecific enhancing focus\nin the left frontal calvarium (see 9:100).  No new enhancing lesions are\nidentified.\n\nThere is no evidence of hemorrhage, edema, mass effect, midline shift or\ninfarction.   The ventricles and sulci are normal in caliber and\nconfiguration. There are a few periventricular, subcortical, and deep white\nmatter T2/FLAIR hyperintensities which are nonspecific, but may represent\nsmall vessel ischemic changes.\n\nThe patient has undergone right cataract surgery.  The left orbit is\nunremarkable.",
            "output": "1. Redemonstrated 4 mm hyperenhancing metastatic lesion in the right posterior\nparietal lobe.  The degree of enhancement has decreased from prior.  No new\nenhancing lesions are identified.\n2. No evidence of intracranial hemorrhage or infarction."
        },
        {
            "input": "Study is degraded by motion.  Within these confines:\n\nRight parietal cortical approximately 3 mm enhancing nodule is again seen,\nminimally decreased in size compared to ___ prior exam (see 16:15\non current study and 9:106 on prior exam).\n\nThere is no evidence of hemorrhage, mass effect, midline shift or infarction. \nThere is prominence of the ventricles and sulci suggestive of involutional\nchanges.  Periventricular and subcortical T2 and FLAIR hyperintensities are\nnoted which may represent small vessel ischemic changes.  Left cerebellar\nprobable chronic infarct is again seen.\n\n\nBilateral lens replacement postoperative changes are noted.  Minimal bilateral\nethmoid air cell, maxillary and frontal sinus mucosal thickening is present.",
            "output": "1. Study is degraded by motion.\n2. No acute intracranial abnormality, no definite evidence of acute infarct.\n3. Minimal interval decrease in size of previously noted right parietal\nenhancing lesion, now measuring approximately 3 mm.\n4. Within limits of study, no definite evidence of new enhancing intracranial\nmass.\n5. Paranasal sinus disease , as described."
        },
        {
            "input": "Overall stable to slight interval decrease in size of the previously seen 4 mm\nright parietal gray-white matter junction enhancing focus thought to represent\na focus of metastasis, now measuring 3 mm (14:18, 15:31). No new sites of\nabnormal enhancement or edema to suggest new metastasis.  There is no evidence\nof hemorrhage, mass effect, midline shift or infarction.  There are deep\nsubcortical and periventricular FLAIR hyperintensities which are nonspecific\nbut likely represent mild sequela of chronic small vessel disease.  The\nventricles and sulci are normal in caliber and configuration.\n\nPreviously seen nonspecific small foci of enhancement within the right\nparietal and left frontal calvarium are redemonstrated and remain unchanged.\n\nOrbits and paranasal sinuses are unremarkable.",
            "output": "1. Overall stable to minimally decreased size of the previously seen right\nparietal 4 mm enhancing lesion now measuring 3 mm, thought to represent a\nsmall focus of metastatic disease.  No new site of metastasis."
        },
        {
            "input": "There is an unchanged approximately 2 mm cortical enhancing focus in the left\nparietal lobe, best seen on image 86 of series 901.  This has not changed\nsince the prior study.  No other areas of abnormal enhancement are detected. \nThere is no evidence of hemorrhage, edema, other masses, mass effect, midline\nshift or infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no other abnormal enhancement after contrast\nadministration.",
            "output": "1. Unchanged left parietal enhancing focus, likely representing a metastasis.\n2. Otherwise normal study."
        },
        {
            "input": "Study is degraded by motion.\n\nGrossly stable punctate right parietal cortical enhancing structure is again\nseen (see 10:240; 1000:117; 1001:83 on current study and 9:236; 900:121;\n901:85 on ___ prior exam).\n\nThere is no evidence of hemorrhage, edema, mass effect, midline shift or\ninfarction.   The ventricles and sulci are grossly stable in caliber and\nconfiguration.  Periventricular and subcortical T2 and FLAIR hyperintensities\nare noted which may represent small vessel ischemic and/or treatment related\nchanges.\n\nLimited imaging of the parotid glands demonstrate bilateral subcentimeter\nnonspecific probable lymph nodes.  Bilateral lens replacement postoperative\nchanges are noted.",
            "output": "1. No acute intracranial abnormality, without definite evidence of acute\ninfarct.\n2. Grossly stable punctate right parietal cortical enhancing mass, again\nconcerning for metastatic lesion.\n3. Within limits of study, no definite evidence of new abnormal intracranial\nenhancement."
        },
        {
            "input": "Study is mildly degraded by motion.  There is no evidence of hemorrhage,\nedema, masses, mass effect, midline shift or infarction.  There is mild\nprominence of the ventricles and sulci suggestive involutional changes. \nPeriventricular and subcortical T2 and FLAIR hyperintensities are noted which\nmay represent small vessel ischemic changes.  Left anterior frontal corona\nradiata punctate probable chronic infarct is noted (see 07, 8:17).  There is\nno abnormal enhancement after contrast administration.  Bilateral frontal and\nsphenoid sinus and ethmoid air cell mucosal thickening is present.",
            "output": "1. Study is mildly degraded by motion.\n2. Mild global volume loss, punctate chronic left frontal infarct and probable\nmicroangiopathic changes.\n3. Within limits of study, no definite evidence of intracranial metastatic\ndisease.\n4. No acute intracranial abnormality, with no definite evidence of acute\ninfarct."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.  There are scattered periventricular white matter\nhyperintensities on the FLAIR images.  These are often attributed to chronic\nsmall vessel ischemia.",
            "output": "1. No evidence of metastatic disease.\n2. White matter hyperintensities on FLAIR likely due to chronic small vessel\nischemia, unchanged.\n3. Otherwise normal study."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are within expected limits in\ncaliber and configuration for the patient's mild senescent related global\ncerebral volume loss.  There is no abnormal enhancement after contrast\nadministration.  Minimal periventricular and subcortical T2/FLAIR white matter\nhyperintensities are nonspecific, but compatible with chronic microangiopathy\nin a patient of this age, unchanged from prior examination.  There is a\npartial empty sella.\n\nThere is mild mucosal thickening of the ethmoid air cells.  Otherwise, the\nremainder the paranasal sinuses are essentially clear.  The orbits are\nunremarkable.  No significant fluid signal is seen in the mastoid air cells. \nNo suspicious marrow signal.",
            "output": "1. Unremarkable contrast enhanced MRI brain.  Specifically no evidence of\nintracranial metastatic disease at this time.\n2. Additional findings as described above, unchanged from prior exam."
        },
        {
            "input": "There is no evidence of restricted diffusion to suggest acute infarction.  No\nevidence of acute intracranial hemorrhage.  Mild prominence of the ventricles\nand sulci is suggestive of minimal involutional changes. There is no mass\neffect or midline shift.\n\nThere is no evidence of abnormal contrast enhancement to suggest metastatic\ndisease.\n\nSeveral scattered T2 and FLAIR hyperintense foci in the periventricular and\nsubcortical white matter are nonspecific, but likely reflect chronic small\nvessel ischemic changes.\n\nPartially empty sella.  Minimal mucosal thickening of the paranasal sinuses. \nUnremarkable intraorbital contents.  The major intracranial arterial and\nvenous flow voids are preserved.",
            "output": "1. No evidence of primary or secondary malignancy in the brain.\n2. No evidence of acute infarction or intracranial hemorrhage.\n3. Mild FLAIR hyperintensities due to early changes of small vessel disease\nare unchanged from MRI of ___."
        },
        {
            "input": "There is no acute infarction, intracranial hemorrhage, extracerebral fluid\ncollection, midline shift or mass effect.  Ventricles and extra-axial spaces\nare normal in size.  Flow voids are maintained. Suprasellar and craniocervical\nregions are unremarkable.  Mild mucosal thickening is seen in the ethmoid air\ncells.",
            "output": "No significant abnormalities are seen on MRI of the brain without gadolinium. \nMild mucosal thickening in ethmoid air cells."
        },
        {
            "input": "MRI BRAIN:\nThere is no evidence of infarction or hemorrhage.  The ventricles are normal\nin size without mass effect or midline shift. There is no enhancing mass or\nabnormal enhancement.  There is mild mucosal thickening of the bilateral\nethmoid air cells.  The orbits appear unremarkable.  The bilateral mastoid air\ncells appear clear.  The visualized soft tissues appear unremarkable.   Dural\nvenous sinuses appear patent on the postcontrast MP rage images.\n\nMRA BRAIN:\nThe intracranial internal carotid arteries and the bilateral vertebral\narteries appear patent without evidence of stenosis, occlusion, or aneurysm.\n\nMRA NECK:\nThere is mild narrowing of the distal cervical right internal carotid artery\n(121:62, ___.  Otherwise, the bilateral internal carotid arteries appear\npatent without internal carotid artery stenosis by NASCET criteria.  The\nbilateral vertebral arteries appear patent.  The visualized aortic arch and\nthe bilateral subclavian arteries appear patent.\n\nADDITIONAL INFORMATION: After receiving MultiHance intravenous contrast, the\npatient reported feeling nauseated and lightheaded. It was noted at that time\nthat there was a mild rash on the patient's anterior neck which she did not\nreport symptoms from. The patient was evaluated by myself Dr.  ___\nimmediately. She was in no acute distress, alert and oriented x3, speaking in\nfull sentences without respiratory distress. By the time I had arrived, the\npatient reported that the feeling of nausea had passed. She did report feeling\na little lightheaded upon standing up from the MRI table.\n\nThe patient was then monitored in the Radiology department for 40 minutes with\nroutine Q ___ minute vitals obtained. Lungs were clear to auscultation\nbilaterally. Heart rate was noted to be 53-70 while the systolic blood\npressure was slightly elevated in the 130s/140s, which is slightly higher than\nthe patient's baseline which is 120 or less. Over this time, the rash on her\nneck resolved as did the lightheadedness. I discussed with the patient that\nshe would need to be premedicated prior to receiving gadolinium based contrast\nin the future and that this does not have a cross reactivity with iodine based\nCT contrast. She was discharged from the department in stable condition.",
            "output": "1. No evidence of infarction, hemorrhage, enhancing mass or abnormal\nenhancement.\n2. MRA head demonstrates patency of the major intracranial vasculature without\nstenosis, occlusion, or aneurysm.\n3. MRA neck demonstrates mild narrowing of the distal cervical right internal\ncarotid artery.  Otherwise, no evidence of internal carotid artery stenosis by\nNASCET criteria."
        },
        {
            "input": "There is no acute intracranial hemorrhage or evidence of chronic blood product\ndeposition. There is no acute infarct. There is no mass lesion. There is no\npathologic enhancement. There is no mass effect or midline shift.\nPneumocephalus present on CT head from ___ has resolved. There are\nnumerous foci of T2/FLAIR hyperintensity in the subcortical, deep, and\nperiventricular white matter. Some foci demonstrate CSF signal centrally,\nconsistent with tissue loss. There are T2/FLAIR hyperintensities in the pons.\nThere are no lesions of the corpus callosum. There is mild generalized volume\nloss with prominence of the ventricles, sulci, and cisterns. There is no\nextra-axial fluid collection.\nMajor intravascular flow voids are preserved. There is normal enhancement of\nthe major intracranial arteries and veins following contrast administration.\n\nMarrow signal is normal. The paranasal sinuses and mastoid air cells appear\nclear. The orbits are normal.",
            "output": "Multiple foci of T2/FLAIR hyperintensity in the subcortical, and deep, and\nperiventricular white matter of the supratentorial brain and pons. Some foci\ndemonstrate central tissue loss (\"black holes\"). None demonstrate slowed\ndiffusion or enhancement. The appearance is most suggesting of chronic small\nvessel ischemic disease. Demyelinating disease is considered less likely due\nto the as the distribution of lesions is more scattered periventricular rather\nthan callosalseptal."
        },
        {
            "input": "MRI Brain:  There is slow diffusion in the region of the right precentral\ngyrus in the region of the hand motor cortex extending to the right centrum\nsemiovale with corresponding T2/FLAIR signal hyperintensity consistent with\nacute/subacute infarction. There is no evidence of hemorrhage, edema or  mass.\nVentricles and sulci are mildly enlarged consistent with mild generalized\nparenchymal volume loss. There is T2/FLAIR signal hyperintensity in the\nperiventricular, subcortical, and deep white matter which is nonspecific but\nlikely on the basis of chronic small vessel ischemic disease.  Chronic right\ncerebellar infarct is noted. A partially empty sella is identified. Major\nvascular flow voids are patent. The orbits are unremarkable. There is fluid\nsignal opacification left maxillary sinus and in the left greater than right\nethmoid air cells.\n\nMRA brain: Image quality is severely degraded by motion. There is poor\nvisualization of the basilar artery on time-of-flight MRA. However, a flow\nvoid is seen on T2 weighted images suggesting this is secondary to its small\nsize or could be a function of the poor quality. The intracranial internal\ncarotid arteries and their major branches appear normal without evidence of\nstenosis, occlusion, or aneurysm formation.  Prominent posterior communicating\narteries are identified bilaterally.\n\nMRA neck: Exam is also somewhat limited by motion. Based on images acquired,\nthere is normal 3 vessel takeoff from the aortic arch. The common, internal\nand external carotid arteries appear normal.  There is no evidence of stenosis\nby NASCET criteria.  The origins of the great vessels, subclavian, and\nvertebral arteries appear normal bilaterally.  The vertebral arteries are\nrelatively small.\n\nScout images demonstrate T2 hyperintensity in the region of the left shoulder.",
            "output": "1.  Small region of acute/subacute infarction in the right precentral gyrus\nextending the right centrum semiovale.\n\n2.  MRA brain is severely limited by motion. Within this confine, no evidence\nof aneurysm, vascular malformation, or stenosis.\n\n3. MRA of the neck is moderately limited by motion. No evidence of stenosis by\nNASCET criteria.\n\n4.  T2 hyperintensity in the region of the left shoulder, incompletely\nvisualized but suggestive of a large joint effusion."
        },
        {
            "input": "There is a right parietal arm enhancing lesion with surrounding T2/FLAIR\nsignal hyperintensity and interval post-biopsy changes. The overall size of\nthe lesion, as well as the thickness of rim enhancement, have slightly\nincreased when compared to prior exam. The enhancing lesion now measures 2.4\ncm AP x 3.1 cm transverse. Within the central nonenhancing portion of the\nlesion, there is new slow diffusion, likely secondary to radiation therapy.\nThere are also new linear areas of T1 hyperintensity and small foci of\nsusceptibility artifact within the lesion indicating blood products, with\npossible superimposed mineralization, both of which are likely sequela of\nradiation therapy. There is decreased T2 hyperintensity and mass effect\nsurrounding the lesion, indicating decreased edema, which is likely secondary\nto treatment with dexamethasone.\n\nThere are no new enhancing lesions. The major arterial flow voids are\npreserved. There is no evidence of acute infarction. There is diffuse brain\nparenchymal volume loss which is unchanged. There is mild nonspecific T2/FLAIR\nsignal hyperintensity within the periventricular white matter which is most\noften related to chronic small vessel ischemic disease.\n\nThere is a stable 4 mm extra-axial focus of low signal on T2 weighted and\ngradient echo images overlying the right occipital lobe, corresponding to a\ncalcified lesion on prior CTs, compatible with a calcified dural plaque or\ncompletely calcified meningioma.\n\nThere is partial opacification of the left mastoid air cells.",
            "output": "1. The right parietal enhancing lesion has slightly increased in size compared\nto ___ with increased thickness of rim enhancement. This may\nrelate to radiation therapy, but tumor progression is not excluded, and close\nfollow up is recommended.\n2. Decreased edema surrounding the right parietal lesion is likely secondary\nto dexamethasone therapy.\n3. No evidence for new enhancing lesions.\n4. No evidence of acute infarction or other acute abnormalities.\n5. Stable 4 mm calcified extra-axial lesion overlying the right occipital\nlobe, compatible with a calcified dural plaque or completely calcified\nmeningioma."
        },
        {
            "input": "There is a 2.7 x 2.1 x 1.8 cm rim enhancing mass in a right parietal lobe with\nassociated vasogenic edema which extends into the right frontal lobe. This\nlesion shows no central slowed diffusion and most likely represents a primary\nmalignancy or a focus of metastasis. Additionally, there is a smaller\nsatellite nodule located medial to this lesion.  Small foci of negative\nsusceptibility within the lesion may represent blood products or\nmineralization.  Of note, increased signal in the left cerebral pontine angle\nis seen only on the axial spin echo postcontrast sequence and is likely\nartifactual as it is not seen on the other sequences; attention on followup.\n\nThe cerebral volume is appropriate for the patient's stated age. The major\nvascular flow voids are maintained, there is no evidence of abnormal\nenhancement.\n\nThe paranasal sinuses and mastoid air cells are clear. There is likely\nenucleation of the right eye ball or phthisis. Increased signal intensity on\nFLAIR seq.   Within the left eye is likely artifactual due to negative\nsusceptibility artifacts from dental hardware",
            "output": "A 2.7 x 2.1 x 1.8 cm rim enhancing mass in the right parietal lobe with\nassociated vasogenic edema that extends into the right frontal lobe most\nlikely represents a primary malignancy or focus of metastasis. Small focus of\nenhancement medial to the large lesion is likely a satellite lesion.  Rec. \nNeuroSurgery consult.\nFurther workup and followup as needed\n\nIncreased signal intensity onFLAIR seq.  In the left eye globe is likely\nartifactual due to dental amalgam. Correlate clinically."
        },
        {
            "input": "There is a peripherally FLAIR hyperintense, centrally FLAIR hypointense/T2\nhyperintense mass with central cystic components in the left temporal lobe\nwith a peripheral rim of high signal on diffusion with isointense signal on\nADC.  Mild associated mass effect is seen with no significant midline shift.\n\nThere is no evidence of hemorrhage or infarction.  A few scattered\nperiventricular and subcortical white matter T2/FLAIR hyperintensities are\nnonspecific but likely due to chronic small vessel disease.  Minimal mass\neffect and effacement of the left lateral ventricle is seen.  The major\nvascular flow voids are preserved.\n\nBilateral cataract extractions are seen.  A retention cyst is seen in the left\nmaxillary sinus.  The mastoid air cells are clear.\n\nDegenerative changes noted in the upper cervical spine.",
            "output": "Mass in the left temporal lobe with significant surrounding edema and no\nsignificant midline shift, likely representing an underlying malignancy.  The\npatient was not able to tolerate contrast enhanced imaging.  A contrast\nenhanced MRI is recommended for further evaluation.\n\nNOTIFICATION:  The results of this study were discussed with Dr. ___ at\n2:26 pm by phone by Dr. ___."
        },
        {
            "input": "The previously described left temporal lobe mass with peripheral FLAIR\nhyperintensity, central FLAIR/T2 hypointensity and a peripheral ram of\ndiffusion restriction is noted to avidly enhance peripherally, with central\nareas of hypo enhancement.  The mass itself is 4.2 (AP) x 3.1 (TV) x 3.1 (SI)\ncm, and there is re- demonstration of significant surrounding vasogenic edema,\nwith local mass effect upon the adjacent sulci and the temporal horn of the\nleft lateral ventricle.  There is no shift of normally midline structures.  No\nintracranial hemorrhage is identified.  No other areas of abnormal enhancement\nare identified intracranially.  Scattered periventricular and subcortical\nT2/FLAIR hyperintensities are unchanged, likely related to the sequelae of\nchronic small vessel ischemic disease.  The major intracranial vessels and the\ndural venous sinuses are patent.  The ventricles and sulci are unchanged in\nsize and configuration compared to the recent prior examination.  Medial left\nmaxillary mucous retention cyst is again noted.  The remaining paranasal\nsinuses and mastoid air cells are grossly clear.\n\nProminent degenerative changes of the visualize C3-C4 level is noted, which\nresults in at least moderate spinal canal narrowing, remodeling the ventral\naspect of the cord (series 2, image 13).",
            "output": "1. Peripherally enhancing mass with evidence of central necrosis and\nsignificant surrounding vasogenic edema is compatible with primary CNS\nmalignancy, most likely glioblastoma.  Other CNS primary malignancies such as\nlymphoma or metastatic disease are also possible, but less likely in the\nabsence of malignancy identified elsewhere on recent screening oncology torso\nCT.\n2. Prominent degenerative changes of the visualize C3-C4 level is noted\nresulting in at least moderate spinal canal narrowing with remodeling the\nventral aspect of the cord.  Recommend dedicated MRI of the cervical spine if\nthe patient is symptomatic.\n\nRECOMMENDATION(S):  Recommend dedicated MRI of the cervical spine if the\npatient is symptomatic from prominent partially visualized C3-C4 level\ndegenerative changes, remodeling the ventral aspect of the cord."
        },
        {
            "input": "The ventricles and extra-axial spaces are normal in size. There is no evidence\nof midline shift, mass effect or hydrocephalus. There are no acute infarcts.\nThere is no evidence of focal abnormalities.  The vascular flow voids are\nmaintained.  Mild mucosal thickening is seen within the sinuses.  Following\ngadolinium administration there is no evidence of abnormal parenchymal,\nvascular and meningeal enhancement seen.\n\nNote is made of slightly prominent right palatine tonsil, clinical correlation\nrecommended.",
            "output": "1. No significant abnormalities are seen on MRI of the brain with and without\ngadolinium.\n2. Slightly prominent right tonsil partially visualized.  Correlation with\ndirect examination recommended."
        },
        {
            "input": "The inferior portion of the left parotid gland is slightly smaller than the\nright side but this could be within normal variation.  A 4 mm signal\nabnormality within the left parotid gland in superficial portion (5:7 and 8:7)\nis likely due to a small intra parotid lymph node.  This is likely the area\nvisualized on the ultrasound.  No discrete mass lesion is seen within the\nparotid gland.  Note is made of prominent bilateral main parotid ducts with\nthe left side measuring approximately 4.5 mm and the right side measuring 2.5\nmm.  The intra parotid ducts are not enlarged but the parotid hilar ducts are\nslightly prominent.\n\nWithin the neck there is no or soft tissue asymmetry or lymphadenopathy by\nimaging criteria.  No focal abnormalities are seen within the thyroid gland. \nThe airways are maintained in the region of nasopharynx hypopharynx and\noropharynx.  Both supraclavicular regions are symmetric without\nlymphadenopathy.",
            "output": "1. The tiny abnormality seen on ultrasound within the left parotid gland could\nbe due to a small lymph node and is barely perceptible on the current study.\n2. Prominent parotid ducts could be a normal variation or could be sequela of\ninflammatory changes or prior obstruction.  Clinically correlate.\n3. Minimal asymmetry of the parotid gland could be a normal variation or could\nbe due to prior inflammation.  At this time no signs of active inflammation,\nabscess or mass is seen."
        },
        {
            "input": "There is no acute infarction.  There is encephalomalacia involving the lateral\nleft putamen, external capsule, subcortical white matter of the left insula,\nand the anterior left temporal lobe, with gliotic changes extending into the\nleft corona radiata and into the left periatrial white matter.  There is\nevidence of associated hemosiderin deposition from prior hemorrhage.  There is\nmild ex vacuo enlargement of the posterior body, atrium, occipital and\ntemporal horns of the left lateral ventricle.  Linear high T2 signal extending\nfrom the left cerebral peduncle of the midbrain into the ventral pons may\nrepresent Wallerian degeneration.  There is no edema or mass effect.\n\nRight lateral, third, and fourth ventricles are age-appropriate.  Cerebral\nsulci are age-appropriate.  Bilateral globus pallidus calcifications are\nincidentally noted with low signal on gradient echo images. Major arterial\nflow voids appear grossly preserved.  Dural venous sinuses appear patent on\npostcontrast MP RAGE images.\n\nThere is mild mucosal thickening in the paranasal sinuses and mastoid air\ncells, which may be secondary to prolonged supine positioning in the inpatient\nsetting.",
            "output": "1. No acute infarction, edema, or mass effect.\n2. Encephalomalacia involving the lateral left putamen, external capsule,\nsubcortical white matter of the left insula, and anterior left temporal lobe,\nwith surrounding gliotic changes as detailed above.  Associated hemosiderin\ndeposition from prior hemorrhage.  Associated mild Wallerian degeneration in\nthe left midbrain and pons."
        },
        {
            "input": "MRI brain:\nThere are multiple foci of slow diffusion located within bifrontal lobes,\nbilateral parietal lobes, left temporal lobe, medial right occipital lobe, and\nbilateral cerebellar hemispheres, with the larger foci demonstrating\ncorresponding hyperintense FLAIR signal abnormality.\n\nThere is no evidence of hemorrhage.  The ventricles are normal in size.  There\nis no mass effect or midline shift.  There is diffuse parenchymal volume loss.\nThere is partial mucosal opacification of bilateral ethmoid air cells, right\nsphenoid sinus, and partial opacification of bilateral mastoid air cells.\n\nMRA brain:\nThe major intracranial vasculature, including the circle of ___ is patent\nwithout significant stenosis, occlusion, or aneurysm formation.\n\nMRA neck:\nThere is poor visualization of the origins of the great vessels.  The\nvisualized portions demonstrate no significant stenosis or occlusion.  There\nis no evidence of internal carotid artery stenosis by NASCET criteria.",
            "output": "1. Multiple foci of acute to subacute infarction scattered within bilateral\ncerebral and cerebellar hemispheres, which is felt most likely to be embolic\nin origin.\n2. No evidence of hemorrhage.\n3. Unremarkable MRA brain and neck without stenosis, occlusion, or aneurysm\nformation.\n\nNOTIFICATION:  The findings were discussed with neurology resident ___,\nM.D. by ___, M.D. on the telephone on ___ at 12:03\n___, 2 minutes after discovery of the findings."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.\n\nThere is mucosal thickening in the frontal sinuses and mucosal thickening and\nfluid in the ethmoid, sphenoid and maxillary sinuses bilaterally.",
            "output": "1. Paranasal sinus inflammatory changes.  Otherwise normal study."
        },
        {
            "input": "Study is mildly degraded by motion.\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.  A 6 mm pineal cyst is noted.\n\nBilateral hippocampal formations and mammillary bodies are preserved in signal\nand configuration. There is no disproportionate medial temporal atrophy. There\nis no focal lobar encephalomalacia. There are no focal cortical dysplasias or\ngray matter heterotopia noted.",
            "output": "1. Study is mildly degraded by motion.\n2.  Within limits of study, no definite evidence of intracranial mass or\nlesion."
        },
        {
            "input": "Study is moderately degraded by motion, especially on postcontrast imaging.\n\nAn approximately 11 (AP) x 8 (TV) x 7 (SI) mm homogeneously enhancing\nextra-axial mass, abutting the superior sagittal sinus and exerting minimal\nmass effect on the left parietal lobe is noted (see 900:110, and 901:93,\n8:27).\nThere is an approximately 2 (AP) x 2 (TV) x 2 (SI) mm hypoenhancing pituitary\nlesion (see 901:61, 900:53, 9:83) .\n\n There is no evidence of hemorrhage, edema, effect, midline shift or\ninfarction.  There is prominence of the ventricles and sulci suggestive of\nmild involutional changes.  Periventricular and subcortical T2 and FLAIR\nhyperintensities are noted, which may represent small vessel ischemic changes.\nTrace nonspecific right mastoid fluid is noted.",
            "output": "1. Study is moderately degraded by motion, especially on postcontrast imaging.\n2. Approximately 11 x 8 x 7 left parasagittal probable meningioma abutting the\nsuperior sagittal sinus, with minimal mass effect on left parietal lobe as\ndescribed.\n3. Approximately 2 mm pituitary hypoenhancing lesion suggested on postcontrast\nimaging.  Recommend clinical correlation.  If clinically indicated, consider\ndedicated pituitary MRI for further evaluation.\n4. Within limits of study, no evidence of acute infarct.\n\nRECOMMENDATION(S):  Approximately 2 mm pituitary hypoenhancing lesion\nsuggested on postcontrast imaging.  Recommend clinical correlation.  If\nclinically indicated, consider dedicated pituitary MRI for further evaluation."
        },
        {
            "input": "There are minimal scattered periventricular and subcortical white matter FLAIR\nhyperintense foci, which are relatively unchanged comparison to prior study,\nlikely secondary to sequela chronic microangiopathy.  There is no acute\ninfarct, hemorrhage, mass, or mass effect.  There is unchanged mild prominence\nof the ventricles and cortical sulci consistent with mild volume loss.  There\nis a 1.0 cm TV x 1.0 cm AP x 0.7 cm SI homogeneously enhancing lesion\nmarginating the left aspect of the mid superior sagittal sinus (13:98;\n101b:96), which is relatively unchanged.  There is normal dural venous sinus\nenhancement.  There is a 2 mm nonenhancing focus at the anterior left\npituitary gland, which is relatively unchanged (13:10 6).  The vascular flow\nvoids are preserved.\n\nThe orbits, soft tissues, and calvarium are unremarkable.  There is no\nabnormal fluid signal within paranasal sinuses, mastoid air cells, or middle\nears.",
            "output": "1. No acute intracranial abnormality without infarct, hemorrhage, mass, or\nmass effect.\n2. Unchanged diffuse mild volume loss, without lobar predominance.\n3. Unchanged probable meningioma marginating the left aspect mid superior\nsagittal sinus.\n4. Unchanged 2 mm nonenhancing focus at the anterior left pituitary gland\nwhich could represent a cyst or a small microadenoma.  Recommend clinical\ncorrelation and consider dedicated pituitary MRI clinically warranted."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is a partially empty sella turcica.\n\nThere is no abnormal enhancement after contrast administration.  The\nvisualized major vascular flow voids are grossly preserved.  There is no\nevidence of dural venous sinus thrombosis.\n\nThe paranasal sinuses and the mastoid air cells are clear.  The globes and\norbits are unremarkable.  There is no abnormal marrow signal.",
            "output": "1. Normal brain MRI.  No evidence of infarction, mass, or hemorrhage.\n2. No evidence of dural venous sinus thrombosis."
        },
        {
            "input": "There few punctate deep white matter T2 signal abnormalities in the bilateral\nparietal lobes, greater on the left.  There is single periventricular focus of\nT2 signal abnormality abutting atrium right lateral ventricle.  There are no\njuxta cortical or infratentorial lesions.  No abnormalities at the level of\nthe corpus callosum or pericallosal white matter.  Visualized upper cervical\ncord appears normal.\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.",
            "output": "Few deep white matter T2 signal abnormalities, nonspecific, may represent\nearly chronic small vessel ischemic changes, sequela of chronic headaches. \nFindings do not satisfy criteria for chronic demyelination.  No abnormal\nenhancement."
        },
        {
            "input": "The 3 cm x 3 cm T2/FLAIR hyperintensity in the right frontal lobe and the\nsmaller focus in the left parieto-occipital lobe are consistent with acute\ninfarcts.  There is no evidence of mass effect or midline shift.  The\nmultifocal periventricular deep white matter hyperintensities are nonspecific\nand likely represent sequelae of chronic microvascular ischemic disease. \nThere is diffuse cerebral atrophy with prominence of the ventricles and sulci.\n\nThe paranasal sinuses are normal.  The mastoid air cells and middle ear\ncavities are patent.  The vascular flow voids are preserved.  The globes are\nsymmetric and unremarkable.",
            "output": "1. Acute infarct in the right frontal lobe and left parietal-occipital lobe.\n2. Diffuse cortical atrophy likely sequela of chronic microvascular ischemic\nchanges."
        },
        {
            "input": "Study is mildly degraded by motion.\n\nMR BRAIN:\nThe parenchymal signal is unremarkable without acute infarct, hemorrhage,\nmass, or mass effect.  The ventricles and cortical sulci are normal in caliber\nconfiguration.  The extra-axial spaces are unremarkable.  The vascular flow\nvoids are preserved.\n\nThe orbits, calvarium, and soft tissues are unremarkable.  There is mild\nprominence of the adenoid, palatine, and sublingual tonsils.\n\nMRV:\nThere is normal enhancement of the cortical veins and dural venous sinuses. \nThere is a dominant left transverse and sigmoid sinus with a diminutive right\ntransverse and sigmoid sinus.  There is no evidence of occlusion or stenosis.",
            "output": "1.  Study is mildly degraded by motion.\n2.  No acute intracranial abnormality, with no evidence of infarct.\n3. Patent cortical veins and dural venous sinuses, without evidence of\nthrombosis."
        },
        {
            "input": "There is no evidence of acute intracranial hemorrhage or mass effect.  The\nventricles and basal cisterns appear normal.\n\nThere are normal vascular flow voids.  There is a new punctate focus of\ngradient signal hypointensity in association with linear T2 hyperintensity\nwithin the left cerebellar hemisphere which may represent a tiny infarct with\nassociated microhemorrhage. Apparent increased signal on diffusion-weighted\nimaging in the corresponding location may be related to susceptibility if\nthere is adjacent microhemorrhage although overall it is too small further\ncharacterize on ADC map.\n\nThere is otherwise no evidence of acute infarct based on diffusion-weighted\nimaging.  There is unchanged T2/ FLAIR signal abnormality within the pons\nwhich could represent sequelae of chronic hypertension, chronic small vessel\nischemic disease, sequelae of myelinolysis, or vasculitis.\n\nThere is no abnormal brain parenchymal or leptomeningeal enhancement.\n\nThe orbits, skull base, and paranasal sinuses appear unremarkable.",
            "output": "1. Unchanged signal abnormality within the pons which could represent sequelae\nof chronic hypertension, chronic small vessel ischemic disease, sequelae of\nmyelinolysis, or vasculitis.\n2. Probable interval tiny infarct with associated microhemorrhage within the\nleft cerebellar hemisphere, as described above."
        },
        {
            "input": "There is no evidence of acute intracranial hemorrhage, mass, mass effect or\nshifting of the normally midline structures. The ventricles and sulci are\nslightly prominent, suggestive of mild parenchymal volume loss. No diffusion\nabnormalities are detected to indicate acute or subacute ischemic changes.\nScattered foci of high signal intensity are identified on T2 and FLAIR\nsequences, distributed in the periventricular white matter, which are\nnonspecific and may reflect changes due to small vessel disease, a slightly\nprominent perivascular space is identified on the left basal ganglia. The\norbits are unremarkable, the paranasal sinuses and mastoid air cells are clear",
            "output": "There is no evidence of acute intracranial process, scattered foci of high\nsignal intensity in the periventricular white matter demonstrated on T2 and\nFLAIR sequences are nonspecific, and may reflect changes due to small vessel\ndisease."
        },
        {
            "input": "There is no evidence of mass, hemorrhage or infarction. Sulci, ventricles and\ncisterns are within expected limits for the patient's age. No abnormal\nenhancement. The hippocampal formations are symmetric and unremarkable\nbilaterally. Evaluation of MPRAGE sequences is limited secondary to patient\nmotion. However, no clear evidence of gray matter heterotopia.  No vascular\nmalformations are noted.  The dural venous sinuses are patent.",
            "output": "1. Normal study"
        },
        {
            "input": "In comparison with the prior examinations, there is evidence of diffuse\npachymeningeal enhancement with no evidence of narrowing of the foramen magnum\nor low lying of the cerebellar tonsil, the splenium of the corpus callosum\nappears in adequate position. No diffusion abnormalities are detected. The\nventricles are normal in size and configuration for the patient's age and\nunchanged since the prior studies. The images with high-resolution through the\nposterior fossa demonstrates patency of the internal auditory canals and\nnormal appearance in the cerebellar pontine cisterns, the distribution of the\nmajor vascular structures is normal. Note is made of mild to moderate pattern\nof enhancement along the seventh cranial nerves, more significant on the left\n(image number 37, series 3301b) including the mastoid segment (image 72,\nseries 3300 b, and sagittal image number ___ series 33), this finding is\nnonspecific and more obvious in the MP-RAGE sequences. The orbits are\nunremarkable, the paranasal sinuses and mastoid air cells are clear.",
            "output": "1. Diffuse pachymeningeal enhancement, which is new since the prior\nexamination dated ___, this finding is nonspecific and probably is\nrelated with the recent lumbar puncture.\n\n2. Mild to moderate pattern of enhancement along the seventh cranial nerves,\nmore significant on the left as described in detail above, suggesting\ninflammatory changes.\n\nNOTIFICATION:  These findings were discovered and communicated via phone call\nto Dr.  ___ by Dr. ___ on ___ at 17:50 hrs."
        },
        {
            "input": "There are multiple periventricular, deep white matter and juxtacortical T2 and\nFLAIR hyperintense supratentorial lesions. Some of these lesions do have a\nperivenular distribution. There is a single T2 and FLAIR hyperintense\ninfratentorial lesion in the left cerebellar white matter (series 100, image\n46).\n\nNo signal abnormality involving the optic nerves.  No intracranial infarct or\nmass.  No hemorrhage.  The ventricles and sulci are normal in caliber and\nconfiguration.  The pituitary appears normal.  The craniocervical junction\nappears normal.  The intracranial arteries demonstrate normal T2 flow voids. \nThe orbits appear normal.  Minimal mucosal thickening involving the paranasal\nsinuses.",
            "output": "Multiple supra and infratentorial white matter T2 and hyperintense\nlesions/plaques as described above.  These lesions are highly suggestive of\ndemyelinating disease.  These lesions would fulfill the dissemination in space\ncriterion ___ criteria) for multiple sclerosis however comments cannot\nbe made about dissemination in time.\n\nReference is made to prior MRI spine done ___ for a description of\nspine findings which included 2 suspected cervical cord demyelinating lesions.\n\nClinical and laboratory correlation advised."
        },
        {
            "input": "MR BRAIN:\nThere is no acute infarction, edema, mass effect, or evidence for blood\nproducts.  Ventricles, sulci, and basal cisterns are normal in size.  Major\nintravascular flow voids are grossly preserved.\n\nThere is a small mucous retention cyst in the left maxillary sinus.\n\nMRA BRAIN:\nImages are mildly limited by motion artifact.  The intracranial internal\ncarotid and vertebral arteries, and their major branches, appear patent\nwithout evidence for flow-limiting stenosis, beading, or aneurysm formation. \nThere is a fenestration of the proximal basilar artery and possibly also a\nfenestration of the anterior communicating artery, which are normal variants.\n\nMRV BRAIN:\nNormal flow signal is demonstrated within the superior sagittal sinus,\nstraight sinus, transverse sinuses, and sigmoid sinuses. The jugular bulbs and\nproximal jugular veins are patent. Evaluation of the deep venous systems\nreveals normal flow signal in the internal cerebral veins. The vein ___\nis also unremarkable.",
            "output": "1. Normal noncontrast brain MRI.\n2. Brain MRA demonstrates no evidence for flow-limiting stenosis or aneurysm. \nNormal variant fenestration of the proximal basilar artery and possibly also\nof the anterior communicating artery is noted.\n3. Normal brain MRV."
        },
        {
            "input": "A 3.8 x 2.9 x 3.8 cm heterogenously enhancing, hemorrhagic, dural based lesion\nis seen along the posterior falx with associated white matter FLAIR signal\nabnormality in bilateral posterior parietal lobes, with greater FLAIR signal\nabnormality in the left parietal lobe compared to the right (13:128).  There\nis associated local sulcal effacement as well as mass effect on the superior\nsagittal sinus which remains patent.  A 1.6 x 1.4 cm rim enhancing,\nhemorrhagic lesion is seen in the right frontal lobe with surrounding FLAIR\nsignal abnormality and mild local sulcal effacement (13:140).  A 7 mm rim\nenhancing, hemorrhagic lesion with mild adjacent FLAIR signal abnormality is\nseen in the left temporal lobe (13:85).\nA few additional punctate foci of enhancement are seen in the right frontal\nlobe, measuring up to 4 mm along the cortex ___: 97, 114, 135).  There is no\nevidence of infarction.  There is no midline shift. The basal cisterns are\npatent. The ventricles are normal in caliber and configuration.  The principal\nintracranial vessels are patent.\n\nThere is mild mucosal thickening of the right anterior ethmoid air cells.  A\nsmall submucosal retention cyst is seen in the right maxillary sinus.  There\nremaining paranasal sinuses are clear.  The orbits are unremarkable.",
            "output": "1. Multiple intracranial lesions measuring up to 3.8 cm along the posterior\nfalx with additional lesions involving the right frontal and left temporal\nlobes concerning for metastatic disease.\n2. No evidence of infarct."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, or infarction.\nThe ventricles and sulci are normal in caliber and configuration. There is no\nabnormal parenchymal vascular or meningeal enhancement seen following\nadministration of gadolinium.  No acute infarcts are identified.",
            "output": "No significant abnormalities are seen on MRI of the brain with and without\ngadolinium."
        },
        {
            "input": "Exam is somewhat motion degraded, particularly on the T2, FLAIR and\npostcontrast T1 sequences.\n\nThere is no intracranial mass, mass effect, or midline shift. Ventricles and\nsulci are age-appropriate.  There are scattered subcortical and\nperiventricular white matter T2/FLAIR hyperintensities which are nonspecific\nwithout definite new signal abnormality.  There is no definite new focal\nparenchymal signal abnormality. There is no region of restricted diffusion or\nabnormal susceptibility artifact. Major intravascular flow voids are\npreserved.\n\nPost contrast images demonstrate no abnormal parenchymal or meningeal\nenhancement.\n\nMild mucosal thickening noted in the right maxillary sinus.  Visualized\nparanasal sinuses and mastoid air cells otherwise demonstrate no abnormal\nsignal.",
            "output": "No evidence of intracranial metastases based on a somewhat motion degraded\nexam."
        },
        {
            "input": "There is no intra or extra-axial mass, acute hemorrhage or infarct. The sulci,\nventricles and cisterns are within expected limits for the patient's age. \nMild periventricular and subcortical nonenhancing rounded T2/FLAIR white\nmatter hyperintensities are nonspecific, but compatible with chronic\nmicroangiopathy in a patient of this age, similar in configuration in\nappearance from prior examination.  The major intracranial flow voids are\npreserved.  Dural venous sinuses are patent.  There is no suspicious marrow\nsignal.  There is mild mucosal thickening of the ethmoid air cells.  The\norbits are unremarkable.  No significant fluid signal is seen the mastoid air\ncells.",
            "output": "1. No evidence of intracranial metastatic disease at this time.  No suspicious\nintracranial enhancement or FLAIR parenchymal signal abnormality.\n2. There is no acute infarct or intracranial hemorrhage.\n3. Mild periventricular and subcortical T2/FLAIR white matter hyperintensities\nare nonspecific, but compatible with chronic microangiopathy in a patient of\nthis age, similar in appearance to prior exam."
        },
        {
            "input": "There is an acute infarct in the left MCA territory, involving the left middle\nand inferior frontal gyri and anterior left insular cortex, territories M1, M\n2, insula, M4, M 5..  Linear susceptibility artifact in the small area of\ncortex upper infarcted territory infarcted territory, without significant\nassociated mass effects, is most consistent with cortical petechial\nhemorrhagic transformation.  No parenchymal hematoma.\n\nAn evolving large subacute infarct in the right MCA territory is again seen,\nwithout evidence of hemorrhagic transformation.\n\nThere is no midline shift or evidence of masses.  The ventricles and sulci are\nunchanged and age-appropriate.\n\nThe orbits are grossly unremarkable.\n\nMultiple scalp lesions, which likely represents epidermal inclusion cysts.",
            "output": "1. Acute infarct left MCA territory with cortical microhemorrhage.  No\nparenchymal hematoma.\n2. Evolving large subacute infarct in the right MCA territory, similar.\n\nNOTIFICATION:  The findings were discussed with the ___ NP by\n___, M.D. on the telephone on ___ at 12:16 pm, 5 minutes after\ndiscovery of the findings."
        },
        {
            "input": "Study is mildly degraded by motion.\n\nEvolving right MCA distribution acute to subacute infarct is again seen with\nareas of edema, without definite evidence of hemorrhagic transformation.  Area\nof restricted diffusion is suggested to extend superior to imaged portion of\nbrain on CTP.\n\nPunctate focus of trace hyperintensity within the left temporal lobe is noted\nwithout definite corresponding ADC abnormality (see 3, 04:10).  No definite\ncorresponding abnormality is seen on other sequences of the study, suggesting\nthis finding is artifactual.\n\nThere is no evidence of hemorrhage, masses or midline shift.  The ventricles\nand sulci are grossly stable in caliber and configuration.\n\nMultiple calvarial scalp probable sebaceous cysts are noted.",
            "output": "1. Study is mildly degraded by motion.\n2. Redemonstration of known right MCA distribution acute to subacute infarct,\nwithout definite evidence of hemorrhagic transformation, as described.\n3. Left temporal punctate probable artifact as described, with differential\nconsideration of small subacute infarct less likely."
        },
        {
            "input": "There is no intracranial hemorrhage, extra-axial collection, recent infarct,\nmass, edema or mass effect.  Scattered T2 FLAIR hyperintense foci in the\nsubcortical, deep and periventricular white matter of the cerebral hemispheres\nwithout associated enhancement or diffusion restriction are favored to\nrepresent chronic microangiopathic ischemic changes.  There is no abnormal\nintracranial enhancement.  Global atrophy is age-appropriate.\n\nThe major intracranial arterial flow voids are preserved.  The dural venous\nsinuses appear patent.\n\nStatus post bilateral lens replacements.  There is no abnormal enhancement\nwithin the orbits.  There is mild mucosal thickening of the maxillary and\nethmoid sinuses with a nonspecific right mastoid effusion.  There is no\nsuspicious signal alteration or enhancement in the calvaria and skull base. \nThere is benign hyperostosis frontalis interna.",
            "output": "1. No acute intracranial abnormality to account for the patient's altered\nmental status.\n2. No intracranial mass or abnormal enhancement to suggest CNS involvement of\nlymphoma.\n3. Scattered T2 FLAIR hyperintense foci in the supratentorial white matter\nwithout enhancement or diffusion restriction most likely represent chronic\nmicroangiopathic ischemic changes in this age group.\n4. Nonspecific right mastoid effusion."
        },
        {
            "input": "There is no evidence of intracranial hemorrhage, mass, mass effect or shifting\nof the normally midline structures, the ventricles and sulci are slightly\nprominent, likely involutional and appear unchanged.  In comparison with the\nprior examination, again multiple scattered foci of T2/FLAIR high-signal\nintensity distributed in the subcortical and periventricular white matter are\nseen, which are nonspecific and may reflect changes due to chronic small\nvessel disease.  No diffusion abnormalities are detected to indicate acute or\nsubacute ischemic changes.  There is no evidence of abnormal enhancement after\ncontrast administration.\n\nThe principal vascular flow voids are present and are unremarkable.  The major\ndural sinuses enhance normally.\n\nThe orbits are notable for bilateral lens replacement, otherwise are\nunremarkable.  There is mild persistent mucosal thickening in the maxillary\nsinuses and ethmoidal air cells, no air-fluid levels are seen, unchanged\npatchy mucosal thickening in the right mastoid air cells.  The bone structures\nare notable for hyperostosis frontalis interna.",
            "output": "1.  There is no evidence of acute intracranial process or hemorrhage or\nsignificant changes since the prior MRI of the brain dated ___.\n\n2.  Unchanged subcortical and periventricular foci of T2 FLAIR high-signal\nintensity, which are nonspecific and may reflect changes due to chronic small\nvessel disease.\n\n3.  There is no evidence of intracranial mass lesion or abnormal enhancement\nto indicate CNS involvement of lymphoma.\n\n4.  Unchanged right mastoid effusions."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor acute infarction.  A chronic infarct is seen in the right cerebellar\nhemisphere.  Subcortical and periventricular white matter T2/FLAIR\nhyperintensities are nonspecific, likely the sequelae of chronic small vessel\nischemic disease.  The ventricles and sulci are prominent suggestive of\ninvolutional changes.  There is no abnormal enhancement after contrast\nadministration.  The principal intracranial vessels and dural venous sinuses\nare patent.\n\nThere is mild mucosal thickening the right maxillary sinus and ethmoid air\ncells.  There is a small right mastoid effusion.  The remaining paranasal\nsinuses and left mastoid air cells are clear.  The patient is status post\nbilateral lens implants.",
            "output": "1. No acute intracranial abnormality.\n2. Mild global atrophy and chronic microangiopathy.."
        },
        {
            "input": "T1 intermediate T2 hyperintense mass with slowed diffusion in the nasal aspect\nof the right orbit associated with the conjunctiva has mildly increased in\nsize compared to ___, now measuring 25 x 10 x 13 mm, previously 23 x\n6 x 12 mm (8:9, 5:15).  There is no definite extension to the anterior chamber\non this nondedicated study.\n\nThere are multiple T1 and T2 intermediate rounded lesions within the right\nparotid gland demonstrating slowed diffusion measuring up to 1.6 x 1.3 cm,\nlikely representing enlarged parotid lymph nodes (9:3, 402:4).\n\nThere is a chronic lacunar infarct in the left thalamus.\n\nA focus of chronic susceptibility artifact in the right cerebellar hemisphere\nis unchanged, compatible with chronic microhemorrhage\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  There is moderate prominence of the ventricles and sulci\nsuggestive of involutional changes.  Areas of periventricular, subcortical and\ndeep white matter T2/FLAIR hyperintensity are in a configuration most\nsuggestive of chronic small vessel ischemic disease.  The principal\nintracranial vascular flow voids are preserved.\n\nThe paranasal sinuses are grossly clear.  The left orbit is grossly\nunremarkable.",
            "output": "1. Please note that postcontrast images were not obtained due to inability of\npatient to tolerate the examination.\n2. No infarct, acute hemorrhage, or suggestion of intracranial mass.\n3. Mild interval increase in size of a diffusion restricting 25 x 10 x 13 mm\nlesion in the right medial orbit in association with the conjunctiva,\ncompatible with lymphoma.\n4. Several diffusion restricting lesions in the right parotid gland measuring\nup to 1.6 x 1.3 cm, likely representing lymphadenopathy in the setting of\nlymphoma.\n5. Moderate atrophy and sequela of chronic small vessel ischemic change.\n6. Chronic left thalamic lacunar infarct.\n7. Chronic focus of microhemorrhage in the right cerebellar hemisphere."
        },
        {
            "input": "MRI BRAIN:\n\nIn comparison to the prior MRI of ___, there is interval development\nof multiple small foci of slow diffusion involving the right cortical and\nsubcortical frontoparietal region and right basal ganglia in the right MCA\ndistribution.  There is associated FLAIR hyperintense signal in this region. \nAdditional small areas of FLAIR hyperintense signal in in the anterior frontal\nand posterior parietal lobes of the right hemisphere likely related to prior\ninfarcts are unchanged.  Background of scattered punctate periventricular and\nsubcortical white matter FLAIR hyperintensities is likely related to chronic\nmicroangiopathy.\n\nSuperficial siderosis along the right cerebral hemisphere and sylvian fissure\nis unchanged a susceptibility artifact related to prior aneurysm coils are\nagain noted.  There is no evidence of recent hemorrhage.  There is no mass\nmass effect.  Ventricles and sulci are age-appropriate.\n\nThe orbits are grossly unremarkable.\n\nMRA BRAIN:\nEvaluation is limited by motion artifac and susceptibility artifact associated\nfrom the right MCA stent and coil packs.  In stent stenosis cannot be\nassessed, but the distal right MCA vessels are appropriately opacified. \nHowever, there is flow related signal identified throughout the right middle\ncerebral artery stent.  The right A1 segment and distal right V4 segments are\ndiminutive, similar to prior examination. The intracranial vertebral and\ninternal carotid arteries and their major branches otherwise unremarkable.\n\nMRA NECK:\nThe common, internal and external carotid arteries appear normal.  There is no\nevidence of internal carotid artery stenosis by NASCET criteria.  The origins\nof the great vessels, subclavian and vertebral arteries appear normal\nbilaterally.",
            "output": "1.  New small multifocal areas of slow diffusion and FLAIR hyperintense signal\nin the right MCA distribution, including the perirolandic region, are\nconsistent with late acute infarcts due to embolic showers.\n\n2.  Chronic small right MCA infarcts and changes of small vessel ischemic\ndisease.\n\n3.  Chronic superficial siderosis without evidence of recent hemorrhage.\n\n4.  Patency of stent in the right middle cerebral artery.\n\n5.  Unremarkable head and neck MRA otherwise."
        },
        {
            "input": "MRI BRAIN:\nThere is expected interval evolution of the intraparenchymal hemorrhage with\nmild associated vasogenic edema within the right superior parietal lobule. \nThere is no solid enhancement to suggest an underlying lesion.  There is local\nmass effect, however no midline shift.\n\nThe ventricles, sulci, and cisterns appear normal.  There is no evidence of\nacute infarction.  Small areas of hyperintense signal on T2/FLAIR within the\nsubcortical and periventricular white matter nonspecific, but likely reflect\nthe sequela of mild chronic small vessel disease.  The major vascular flow\nvoids are preserved.\n\nThere is mild mucosal thickening within the left frontal and bilateral\nanterior ethmoid air cells.  The orbits are unremarkable.\n\nMRA brain: The nonocclusive filling defect within the left lacerum segment of\nthe left internal carotid artery and mild irregularity of the intracranial\ninternal carotid arteries is better appreciated on recent CTA and likely\nsecondary to atherosclerotic vascular disease.  The vessels of the circle\n___ and ___ branches are patent without stenosis.  There is\natherosclerotic plaque within the intracranial vertebral arteries without\nstenosis.  The basilar artery is patent without stenosis.\n\nNo aneurysm or vascular malformation is identified.",
            "output": "1. Expected interval evolution of the acute intraparenchymal hemorrhage within\nright superior parietal lobule.  No underlying mass or vascular malformation\nis identified.  Recommend follow-up ___ months to ensure resolution.\n2. Probable mild chronic small vessel disease.\n3. Mild intracranial atherosclerosis, without stenosis or occlusion."
        },
        {
            "input": "There is one focus of T2/FLAIR hyperintensity in the left parietal subcortical\nwhite matter on image 500b:111, nonspecific.\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.\n\nThere is near complete opacification of right frontal sinus with mucosal\nthickening in the left frontal sinus and partial mucosal thickening in\nbilateral ethmoid air cells.  Also seen is complete opacification of right\nmaxillary sinus with mucosal thickening and mucous retention cyst in the left\nmaxillary sinus.  Bilateral mastoid air cells are clear.  The orbits are\nunremarkable.  Intracranial flow voids are maintained.",
            "output": "1. One focus of FLAIR hyperintensity in the left parietal subcortical white\nmatter, nonspecific.  Otherwise, unremarkable MRI of the brain."
        },
        {
            "input": "MR BRAIN:\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.\n\nModerate sinus disease is seen involving the sphenoid sinus, ethmoid air\ncells, left frontal ethmoidal recess and mild mucosal sinus thickening is seen\ninvolving the maxillary sinuses, suggesting an ongoing inflammatory process. \nThe mastoid air cells, and middle ear cavities are clear.  The globes are\nunremarkable.  The principal vascular flow voids appear to be well preserved.\n\nMRA brain: The intracranial vertebral and internal carotid arteries and their\nmajor branches appear normal without evidence of stenosis, occlusion, or\naneurysm formation.",
            "output": "1. No acute intracranial abnormalities identified.\n2. Unremarkable MRA of the brain without evidence of aneurysm or stenosis.\n3. Paranasal sinus disease involving the sphenoid sinus, ethmoidal air cells,\nand maxillary sinuses, suggesting an ongoing inflammatory process."
        },
        {
            "input": "There is no evidence of intracranial mass, hemorrhage or infarct. \nVentricles, cisterns and sulci are age appropriate.  There is no abnormal\nintracranial enhancement and flow voids are preserved.",
            "output": "Normal brain."
        },
        {
            "input": "Compared to the MRI from ___, the right occipital lobe component\nof the large posterior heterogeneously enhancing mass measures 3.1 cm TRV x\n4.3 cm AP by 3.8 cm CC, slightly decreased in size compared to ___\nwhen it measured up to 4.9 cm in the AP dimension.  The left occipital lobe\ncomponent of the mass has almost completely resolved, with minimal subtle\nresidual enhancement and slowed diffusion.  Adjacent edema is stable\nbilaterally.\n\nA heterogeneously enhancing mass within the right temporal lobe measures\napproximately 2.4 cm TRV by 3.1 cm AP by 1.7 cm cc, slightly increased\ncompared to the prior exam at which time this measured 2 cm TRV by 2.5 cm AP\nby 1.6 cm cc.  Small foci of central nonenhancement within this lesion have\nincreased in size.  Surrounding edema has increased.\n\nNo new enhancing lesions are identified.\n\nThere is an unchanged large area of elevated T2 signal in the right frontal\nwhite matter without contrast enhancement, with a stable small area of\ncortical volume loss in the right frontal operculum (series 10, images ___.\nIt is not clear whether this is related to a prior lesion or a prior infarct.\n\nPeriventricular high T2 signal and mild high T2 signal in the deep white\nmatter is stable in extent, compatible with sequela of whole brain radiation\nversus sequela of chronic small vessel ischemic disease.  Prominent\nperivascular spaces are again seen in the basal ganglia and surrounding white\nmatter.  Occipital horn of the right lateral ventricle remains compressed. \nThe remainder of the ventricular system is enlarged, similar to prior.  The\nsulci not involved by the above-described lesions are prominent due to\nparenchymal volume loss, unchanged.\n\n The principal vascular flow voids are grossly preserved.\n\nMild mucosal sinus thickening is seen involving the ethmoid air cells.  A\nair-fluid level seen within the right maxillary sinus.  Mild opacification is\nseen involving the right mastoid air cells.  The patient is status post\nbilateral lens replacement surgery.",
            "output": "1. Bilateral occipital mass demonstrates decreased size of the right sided\ncomponent and near complete resolution of the left-sided component, with\nstable surrounding edema.\n2. Slight interval increase in the right temporal mass with increased\nsurrounding edema.  It is not clear whether this represents tumor progression\nversus sequela of interim radiation therapy, but this can be clarified on\nfollow up imaging.\n3. Unchanged extensive white matter signal abnormality in the right frontal\nlobe with a smaller area of cortical volume loss in the right frontal\noperculum, which may be secondary to posttreatment changes of a prior lesion\nversus a prior infarct.\n4. No new enhancing lesion is identified."
        },
        {
            "input": "There is no evidence of acute intracranial hemorrhage, mass, mass effect or\nshifting of the normally midline structures. The ventricles and sulci are\nnormal in size and configuration for the patient's age. On FLAIR and T2\nweighted images, multiple scattered foci of high signal intensity are detected\nin the subcortical white matter, which are nonspecific and may reflect changes\ndue to small vessel disease. No diffusion abnormalities are seen to indicate\nacute or subacute ischemic changes. The major arterial vascular flow voids are\npresent and demonstrate normal distribution. The orbits are unremarkable, the\nparanasal sinuses are notable for mild mucosal thickening in the ethmoidal air\ncells, no air-fluid levels are identified, the mastoid air cells are clear.",
            "output": "Scattered foci of high signal intensity identified on FLAIR and T2 weighted\nimages, distributed in the subcortical and periventricular white matter, which\nare nonspecific and may reflect changes due to small vessel disease."
        },
        {
            "input": "An unchanged, 3 mm aneurysm is noted directed anteriorly and extending from\nthe junction of the P1 and P2 segments of the right posterior cerebral artery\n(image 93, series 4, and image 9, series 501).\n\nOtherwise, the remainder of the intracranial vertebral and internal carotid\narteries and their major branches appear normal without evidence of stenosis,\nocclusion, oraneurysm formation.\n\nA mucous retention cyst is noted in the left maxillary sinus.  The remainder\nof the visualized paranasal sinuses appear well aerated within the constraints\nof a noncontrast MRA examination.",
            "output": "1. Stable appearance of a 3 mm aneurysm extending from the junction of the\nP1/P2 segments of the right PCA.\n2. No additional site of aneurysm is identified within the intracranial\nvasculature."
        },
        {
            "input": "There has been interval decrease in size of a right parietal intraparenchymal\nhematoma measuring 22 x 17 mm, previously measuring 28 x 27 mm. Signal\ncharacteristics compatible with a subacute to chronic blood products. There is\nbeen interval decrease in surrounding vasogenic edema and mass effect.\nAssociated T2 \"dark through\" effect is seen on the gradient echo sequence\nrelated to artifact from blood products. There remains an irregular, nodular\nrind of post gadolinium enhancement measuring roughly 11 mm in thickness along\nthe superior aspect of the hematoma. There is associated thickening of the\nadjacent dura. This rind of enhancement demonstrates slowed diffusion.\n\nThere is no midline shift. Effacement of the right lateral ventricle has\nresolved. Mild prominence of the ventricles and sulci suggestive of age\nrelated atrophy. Scattered areas of nonspecific periventricular, subcortical\nand deep white matter T2/FLAIR hyperintensity are again demonstrated.\nIntracranial flow voids are maintained.  There is mild mucosal wall thickening\nin the left sphenoid air cell, bilateral maxillary sinuses, right ethmoid air\ncells and right frontoethmoidal recess.  The mastoid air cells are clear. The\norbits, periorbital and paracavernous spaces are unremarkable.  The brainstem,\nposterior fossa and cervicomedullary junction are preserved.",
            "output": "1. Persistent irregular, nodular enhancing rind surrounding the previously\nnoted right parietal intraparenchymal hematoma with associated slowed\ndiffusion suspicious for underlying mass lesion.\n2. Interval decrease in size of the right parietal intraparenchymal hematoma\nitself as well as decreased surrounding vasogenic edema and improvement of\nsome of the associated mass effect."
        },
        {
            "input": "Again seen is the contrast enhancement surrounding the right superior parietal\nsuperficial hematoma, with the enhancement extending to and along the adjacent\ndura. No significant change in the contrast enhancement is seen compared to ___. Signal characteristics of the hematoma have continued to evolve\nwith decreasing T1 hyperintensity. No new enhancing lesion is seen. The\nventricles and basal cisterns are normal in size. Comprehensive evaluation of\nthe brain parenchyma is otherwise not performed with this limited exam which\nis targeted for surgical planning.",
            "output": "Right superior parietal enhancing lesion is again demonstrated for surgical\nplanning."
        },
        {
            "input": "Status post right posterior parietal craniotomy with interval removal of the\npreviously noted hemorrhagic lesion in the right posterior parietal lobe.\nPostsurgical changes are noted in the bone, overlying soft tissues and\nunderlying due to a and at the surgical resection site.\nSmall amount of blood products are noted in the surgical resection bed.\nMild edema noted in the right frontal lobe.\nSmall extra-axial fluid collection with blood products noted in the right\nposterior parietal region. Mild increased signal intensity of the dura, with\nmild enhancement can be reactive to postsurgical changes.\n\nNo significant nodular enhancement noted, to suggest residual tumor however,\nassessment can be limited given the immediate postoperative condition.\nA tiny T1 hyperintense focus noted in the periphery series 13, image 20 likely\nrelates to vascular structures or dura rather than tiny component of tumor,\nbased on the MPRAGE sequences. Followup evaluation can be helpful to assess\nfor interval change.\n\nNo acute infarct, shift of normally midline structures, hydrocephalus or mass\neffect.\nNo new lesions noted.\nNon-specific cerebral white matter changes in the brain, as before.\n\nThe ventricles, extra-axial CSF spaces and sulci elsewhere are unremarkable.\nSella, pineal gland and the craniocervical junction regions are unremarkable.\nThe major intracranial arterial flow voids are noted.\n\nThe included portions of the paranasal sinuses and the mastoids are clear.",
            "output": "Right posterior parietal craniotomy with postsurgical changes as described\nabove.\nNo significant nodular enhancement noted, to suggest residual tumor however,\nassessment can be limited given the immediate postoperative condition.\nA tiny T1 hyperintense focus noted in the periphery of the surgical site\nseries 13, image 20- likely relates to vascular structures or dura rather than\ntiny component of tumor, based on the MPRAGE sequences. Followup evaluation\ncan be helpful to assess for interval change.\nOther details as above"
        },
        {
            "input": "Re- demonstration of postsurgical changes from right parietal craniotomy and\nmeningioma resection with residual susceptibility artifact from old blood\nproducts as well as trace dural thickening enhancement at the resection\nmargin.  No underlying residual or recurrent nodular enhancing focus.  No\nadjacent FLAIR signal abnormality.  No abnormal focus of slowed diffusion. \nThere is no evidence of near hemorrhage, edema, masses, mass effect, or\ninfarction. The ventricles and sulci are unchanged in caliber and\nconfiguration.  Scattered areas of periventricular, subcortical and deep white\nmatter T2/FLAIR hyperintensity are in a pattern most suggestive of chronic\nsmall vessel ischemic disease.  Orbits are unremarkable.  Major intracranial\nvascular flow voids are preserved. Trace mucosal wall thickening in the right\nethmoid air cell.",
            "output": "Stable postsurgical changes from right parietal craniotomy and meningioma\nresection without evidence of recurrence.  No acute findings."
        },
        {
            "input": "The patient is status post right parietal craniotomy and resection of the\nright parietal lobe mass with no enhancement in the postsurgical bed.  There\nare no enhancing lesions.\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  Scattered foci of T2/FLAIR hyperintensities in the\nsupratentorial white matter are nonspecific and unchanged, but may represent\nthe sequela of chronic small vessel ischemic disease.\n\nThe 1.0 cm T1 hyperintense lesion in the C4 vertebral body is unchanged from ___ and likely represents an intraosseous hemangioma.\n\nThe paranasal sinuses and mastoid air cells are clear.  The orbits are\nunremarkable.\n\nThe major intracranial flow voids are preserved.",
            "output": "1. Postsurgical changes identified at the right parietal convexity, with no\nevidence of recurrent or new neoplasm.\n2. No acute intracranial abnormality."
        },
        {
            "input": "There are a few white matter FLAIR hyperintensities that are nonspecific with\nthe differential including sequela of chronic migraine headaches, sequela of\nprior trauma, infection/inflammation or a demyelinating process given the\npatient's age.  There is no evidence of hemorrhage, edema, masses, mass\neffect, midline shift or infarction.\n\nThe major intracranial vascular flow voids are maintained.  The ventricles and\nsulci are normal in caliber and configuration.  The paranasal sinuses, mastoid\nair cells and orbits are normal.",
            "output": "1. No acute intracranial abnormality.\n2. A few scattered white matter FLAIR hyperintensities are nonspecific."
        },
        {
            "input": "Study is moderately degraded by motion, especially on postcontrast imaging.\n\nMR HEAD:  There is no evidence of hemorrhage, edema, masses, mass effect,\nmidline shift or infarction.   The ventricles and sulci are normal in caliber\nand configuration.  13 x 5 mm mildly expansile T1 and T2 hyperintense lesion\nin the right frontal calvarium with mild enhancement likely represents\nhemangioma (35:17).  Question if finding was present on ___ prior sinus CT\n(see 04:35 on ___ prior sinus CT).  There is otherwise no abnormal\nenhancement after contrast administration.  There is no abnormal focus of\nslowed diffusion.  The principal intracranial vascular flow voids are\npreserved.  The dural venous sinuses are patent on MPRAGE images.\n\nThere is trace mucosal wall thickening in the floor of the left maxillary\nsinus and left greater than right anterior ethmoid air cells.  The remainder\nthe visualized paranasal sinuses are grossly clear.  There is deformity of the\nleft globe likely representing scleral buckle surgery, also with changes from\nleft lens replacement.  The right orbit is grossly unremarkable.\n\nMRA HEAD:  There is normal variant fetal type origin of the left posterior\ncerebral artery.  The intracranial vertebral and internal carotid arteries and\ntheir major branches appear patent without evidence of significant stenosis,\nocclusion, or aneurysm formation.\n\nMRV HEAD: Normal flow signal is demonstrated within the superior sagittal\nsinus, straight sinus, transverse sinuses, and sigmoid sinuses. The jugular\nbulbs and proximal jugular veins are patent. Evaluation of the deep venous\nsystems reveals normal flow signal in the internal cerebral veins. The vein of\n___ is also unremarkable.\n\nMRA NECK:  There is a 3 vessel aortic arch.  The V3 segments of the bilateral\nvertebral arteries are not included in the imaging boundaries on postcontrast\nMRA images, though this area appears patent on the 2D and 3D time-of-flight\nimages.  The common, internal and external carotid arteries appear patent. \nThere is no evidence of stenosis by NASCET criteria. The origins of the great\nvessels, subclavian, and vertebral arteries appear patent bilaterally. The\ncommon carotid bifurcations appear patent.",
            "output": "1.  Study is moderately degraded by motion.\n2. Within limits of study, no acute intracranial abnormality including\nhemorrhage, infarct, or intracranial enhancing lesion.\n3. 13 x 5 mm mildly expansile right frontal calvarial lesion with\ncharacteristics most suggestive of hemangioma.  Allowing for difference in\ntechnique, finding may have been partially visualize on ___ prior sinus CT.\n4. Patent intracranial arterial vasculature without significant stenosis,\nocclusion, or aneurysm formation.\n5. No evidence of dural venous sinus thrombosis.\n6. Patent cervical arterial vasculature without significant stenosis, or\nocclusion, with note made that the V3 segments of the bilateral vertebral\narteries are not imaged on the postcontrast MRA images, though the V3 segments\nappear patent on the 2D and 3D time-of-flight images.\n7. Deformity of the left globe likely representing changes from scleral\nbuckle.\n8. Trace paranasal sinus disease, as described."
        },
        {
            "input": "There is no acute infarction.  There is no edema, mass effect, or evidence for\nblood products in the brain parenchyma.  Small foci of high T2 signal in the\nsubcortical, deep, and periventricular white matter of the cerebral\nhemispheres are nonspecific, but likely sequela of chronic small vessel\nischemic disease in a patient of this age.  Age-related prominence of the\nventricles and sulci is present.  Major intravascular flow voids appear\ngrossly preserved, but the intracranial vessels are better assessed on the\npreceding CTA.\n\nThere is trace right mastoid tip air cell opacification.",
            "output": "No acute infarction and no evidence for other intracranial abnormalities."
        },
        {
            "input": "There are scattered tiny foci of T2/FLAIR hyperintensities in the subcortical\nand periventricular white matter in the frontal and parietal lobes, some of\nwhich are T1 hypointense.  None of these foci enhance.  Although there is a\nlong differential diagnosis that includes demyelinating disease; inflammation\nand infection including Lyme disease, vasculitis and sarcoidosis; and white\nmatter lesions associated with chronic headaches, in many patients with a\nsimilar small number of small lesions, no pathologic correlate is identified.\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.\n\nThe left maxillary sinus contains a small mucous retention cyst.  The mastoid\nair cells are clear.  The visualized orbits are unremarkable.\n\nThe major intracranial flow voids are preserved.",
            "output": "There are several tiny supratentorial white matter lesions, of uncertain\nclinical significance.  There is a long differential diagnosis as discussed\nabove.  In many patients with a small number of small lesions, no clinical\nabnormality is identified."
        },
        {
            "input": "Please note the study is degraded by motion. MRI Brain:  There is no intra or\nextra-axial mass effect, acute hemorrhage or infarct. Sulci, ventricles and\ncisterns are within expected limits for the patient's age. The major\nintracranial flow voids are preserved. Mild mucosal thickening of the frontal\nsinuses and ethmoid air cells are noted. The remainder the paranasal sinuses\nare essentially clear. The orbits are unremarkable. The mastoid air cells are\nclear.\n\nMRA brain:  The examination is slightly suboptimal secondary to motion\ndegradation particularly at the level of the proximal ACA and MCA.\n\nA small 2 mm focal outpouching at the of the anterior communicating artery\n(series 101, image 5 and series 10, image 33 and 34), may represent a small\naneurysm versus infundibulum. There is apparent stenosis of the proximal left\nM1 segment on 3D reformats images, which is artifactual from motion as this\nsegment is unremarkable on postcontrast MRA sequences of the neck. Otherwise,\nthe remainder of the anterior circulation appears unremarkable.  There is\nfetal origin of the left posterior cerebral artery. The left vertebral artery\nis dominant. Otherwise, the posterior circulation is also unremarkable without\nevidence of stenosis, occlusion or aneurysm.\n\nMRA neck:  There is a normal 3 vessel arch. The common, internal and external\ncarotid arteries appear normal.  There is no evidence of internal carotid\nartery stenosis by NASCET criteria.  The origins of the great vessels,\nsubclavian and vertebral arteries appear normal bilaterally.",
            "output": "1.  Study is degraded by motion.\n2. There is no evidence of acute infarct or intracranial hemorrhage.\n3. 2 mm outpouching of the anterior communicating artery may represent a small\naneurysm, infundibulum or motion artifact. Recommend clinical correlation. If\nclinically indicated, consider repeat MR angiography when patient can tolerate\nexam, or Head CT angiography.\n4. No evidence of definite steno-occlusive disease or dissection.\n\nRECOMMENDATION(S):   RE 3:  Recommend clinical correlation. If clinically\nindicated, consider repeat MR angiography when patient can tolerate exam, or\nCT angiography."
        },
        {
            "input": "Motion artifact limits evaluation.  At the site of the web-like hypointensity\nin the posterior left carotid bulb on the preceding CTA, there is a 2 x 2 mm\nfocus of intermediate signal intensity (image 6:17).  No evidence for\nintramural hematoma elsewhere in the imaged portions of the carotid or\nvertebral arteries.",
            "output": "1. Motion limited exam.\n2. 2 x 2 mm focus of intermediate signal intensity in the posterior left\ncarotid bulb at the site of the abnormality on the preceding CTA, which may\nreflect nonacute intramural hematoma versus a web distorted by motion\nartifact.\n3. No evidence for acute intramural hematoma."
        },
        {
            "input": "Intraventricular blood products are seen layering within both occipital horns,\nunchanged. Small subdural hematomas are seen along the left temporoparietal\nregion, measuring 2 mm in maximal diameter, and along the tentorium,\nunchanged.  The majority of the previously seen foci of subarachnoid\nhemorrhage are resolved.  A small focus of subarachnoid hemorrhage remains at\nthe vertex (series 4, image 23).\n\nT2/FLAIR hyperintensities are seen in the cerebellar white matter, brainstem\nand in the periventricular and deep white matter.  These likely represent a\ncombination of sclerotic plaques and changes of chronic microvascular\nangiopathy.  The lesions do not demonstrate enhancement.\n\nThere is no evidence of mass effect, midline shift or infarction.  The\nventricles and sulci are prominent, consistent with global cerebral volume\nloss.  There is mild mucosal thickening of the maxillary sinuses.  The patient\nis status post bilateral cataract surgery.  There is enlargement of the\nbilateral globes in the AP diameter.  The mastoid air cells are clear.  A\nsmall right scalp laceration is re-demonstrated.",
            "output": "1. Unchanged intraventricular and subdural blood products with near complete\nresolution of the subarachnoid hemorrhages compared to previous CT.\n2. Patchy white matter lesions are most consistent with sclerotic plaques\ngiven the patient's history multiple sclerosis.  No enhancement is seen to\nsuggest an acute process.\n3. No acute infarcts are identified.  Several foci of hyperintense signal on\ndiffusion images are due to T2 shine through.\n4. Unchanged small right scalp laceration."
        },
        {
            "input": "The patient is status post coiling and stent placement right MCA bifurcation\naneurysm.  1.2 cm segment of decreased flow distal right M1 segment, most\nlikely artifact from stent which is placed in this region.  Suggestion of\ndecreased arborization of the right MCA M2, M3 branches on collapsed MIPS\nimages, however, this is likely technical, on the source images there is some\noverlap artifact laterally, and at the level of sylvian fissure there is\nfairly symmetric flow in the MCA branches.  .\nIrregular 0.5 cm x 0.4 cm bright signal within aneurysm, consistent with\nresidual flow within aneurysm, through a very narrow neck.\nOther branches of the carotid, vertebral arteries and their major intracranial\nbranches are free of aneurysm.\nMinimal atheromatous disease the left A1, left P2 segments.  Patent A-comm. \nBilateral PCOM not identified.",
            "output": "1. Residual flow within 0.5 cm right MCA bifurcation aneurysm.\n2. Appearance of right M1 segment most consistent with present stent."
        },
        {
            "input": "Poor visualization of the right MCA M1 segment most likely due to stent in\nsitu.  There is no residual filling seen of the coiled right MCA bifurcation\naneurysm.  Signal void seen in the area of the aneurysm secondary to\naneurysmal coils.  Decreased arborization of the distal right MCA vessels,\nappears grossly unchanged compared to the prior exam.\n\nNo other intracranial aneurysms, significant stenosis or occlusion.",
            "output": "Obliteration of the right MCA bifurcation aneurysm compatible with ___\ngrade 1."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are patent and prominent in keeping\nwith age-related volume loss.\n\nThe ___ index on image 4:14 is 0.35.  Also, the callosal angle (measured on\nthe coronal plane on image 801b:80) measures 110 degrees.  The threshold\nreported in literature for ___ index is greater than 0.3 and callosum angle\nof less than 90 degree normal pressure.  Hence the findings are equivocal for\nnormal pressure hydrocephalus.\n\nThere are scattered foci of T2/FLAIR hyperintensity in the subcortical and\nperiventricular white matter, nonspecific, likely secondary to small vessel\nischemic disease.\n\nThe orbits are unremarkable noting prior right-sided cataract surgery.  Mild\nmucosal thickening in bilateral ethmoid air cells.  The remaining visualized\nparanasal sinuses and mastoid air cells are clear.",
            "output": "1. Diffuse volume loss with prominence of sulci, cisterns and ventricles. \nFindings are equivocal for normal pressure hydrocephalus as described above.\n2. No acute intracranial abnormality."
        },
        {
            "input": "There are foci of slow diffusion within the bilateral thalami with\ncorresponding FLAIR signal hyperintensity, compatible with late acute to early\nsubacute infarctions (4:15, ___.  No associated mass effect.  No\nevidence for intracranial blood products.\n\nThere are mildly to moderately numerous subcortical, deep, and periventricular\nwhite matter T2/FLAIR hyperintensities, nonspecific but compatible with small\nvessel disease.  There there is mild age-related prominence of the ventricles\nand sylvian fissures.\n\nThe major intracranial vascular flow voids are grossly preserved, allowing for\nnormal-variant hypoplasia of the non dominant intracranial left vertebral\nartery distal to ___.  Small caliber of the basilar artery appears to\nbe related to bilateral fetal type configuration of the posterior cerebral\narteries.  Intracranial vasculature is overall better assessed on the\npreceding CTA.\n\nThere is minimal mucosal thickening in the ethmoid air cells.",
            "output": "Small late acute to early subacute infarcts of the bilateral thalami, without\nmass effect.  The distribution suggests embolic etiology from the posterior\ncirculation semi no artery of Percheron is clearly seen on the preceding CTA.\n\nNOTIFICATION:  The findings were discussed with ___, M.D. by ___\n___, M.D. on the telephone on ___ at 1:46 am, 5 minutes after\ndiscovery of the findings."
        },
        {
            "input": "There is no evidence of intracranial hemorrhage,edema,masses,mass effect,\nmidline shift or infarction.  The ventricles and sulci are prominent, slightly\nmore prominent in the parietal lobes, this finding is nonspecific, and\nprobably a is age related and involutional nature.  There is no abnormal\nenhancement after contrast administration.\n\nBilateral hippocampal formations and mammillary bodies are preserved in signal\nand configuration. There is no disproportionate medial temporal atrophy. There\nis no focal lobar encephalomalacia. There are no focal cortical dysplasias or\ngray matter heterotopia noted.\n\nThere is severe mucosal thickening of the right frontal sinus with\nopacification of the right frontoethmoidal recess.  There is mild mucosal\nthickening of the maxillary sinuses.  The mastoid air cells and middle ear\ncavities are clear.  The intraorbital contents are normal.",
            "output": "1. No abnormality to suggest a seizure focus.\n2. No acute intracranial abnormality.\n3. Nonspecific global cerebral volume loss, slightly more prominent in the\nparietal lobes.\n4. Severe right frontal and mild bilateral maxillary sinus disease."
        },
        {
            "input": "Study is mildly degraded by motion.\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.  A small right temporal lobe developmental venous anomaly is\nnoted.\n\nBilateral hippocampal formations and mammillary bodies are preserved in signal\nand configuration. There is no disproportionate medial temporal atrophy. There\nis no focal lobar encephalomalacia.  Within the confines of motion, there are\nno focal cortical dysplasias or gray matter heterotopia noted.\n\nThe major intracranial vascular flow voids are preserved.  Orbits and\nvisualized extracranial soft tissues are unremarkable.",
            "output": "1. Within confines of mild motion artifact, normal brain MRI."
        },
        {
            "input": "MRI: Again seen is an evolving left posterior cerebral artery distribution\ninfarction.  There are scattered areas of hemorrhage within the infarction. \nThe infarction includes the occipital cortex, posterior temporal lobe, and a\nportion of the left thalamus.\nImages of the remainder of the brain appear normal with no other evidence of\ninfarction or hemorrhage.  No masses are identified.\n\nMRA: There is questionable mild narrowing of the distal left posterior\ncerebral artery.  This may be artifactual.  The remainder of the intracranial\nvessels appear normal.",
            "output": "Evolving left posterior cerebral artery infarction with multiple areas of\nhemorrhagic transformation.\nPossible mild narrowing of the distal left posterior cerebral artery.\nNo evidence of new infarction."
        },
        {
            "input": "Aero digestive tract:\nBilobed, very bright T2 signal abnormality at the midline base of the tongue,\nextending into the root of the tongue, measuring 3.8 cm in AP diameter, and\n1.4 cm transversely.  Minimal, linear peripheral enhancement.  Intrinsically\nabnormalities not T1 bright.  Enhancement is possibly improved since ___.  No surrounding soft tissue stranding.  Lesion extends from just above\nthe hyoid bone anteriorly extends to within 8 mm from the mandible.\n\nFindings likely represent thyroglossal duct cyst possibly with resolving\nsuperinfection.  Other considerations epidermoid cyst, unilocular lymphatic\nmalformation, less likely foregut duplication cyst.\n\nNeck lymph nodes: Mildly asymmetric left level 2, 3 lymph nodes, likely\nreactive, 1 decreased, other stable since prior.  There is no adenopathy\ninvolving bilateral levels ___.  There is no retropharyngeal adenopathy.\n\nExtra nodal tumor spread: There are no findings suggestive of extra nodal\nextension.\n\nDeep neck muscles, masticator space: There is no muscle invasion.\n\nBones, skull base:\nThere is no bone involvement.\nThere are no findings suggestive of perineural tumor extension. Jugular\nforamen, carotid canal, pterygopalatine fossa, infraorbital foramen, other\nskull base foramina are not involved.\n\nVessels: There is no vascular invasion.\n\nBrachial Plexus: There is no brachial plexus contact or invasion.\n\nThyroid, salivary glands: There is no mass.\n\nOther findings: There are no lung nodules.  Mild opacification paranasal\nsinuses, mastoids.",
            "output": "1.  Suprahyoid, root of tongue cystic, minimally peripherally enhancing\nabnormality, likely thyroglossal duct cyst.  Other considerations as above."
        },
        {
            "input": "There is no acute infarct. There is no evidence for intracranial blood\nproducts, edema, or mass effect. There are a few scattered foci of high T2\nsignal in the subcortical white matter of the left frontal lobe and deep white\nmatter of the paracentral lobules.  Ventricles and sulci are age-appropriate\nin size. Basal cisterns are not compressed. There is no extra-axial\ncollection. Major intravascular flow voids are preserved.",
            "output": "Few scattered foci of high T2 signal in the supratentorial white matter are\nnonspecific but compatible with sequela of mild chronic small vessel ischemic\ndisease, or sequela of inflammation or trauma.\n\nIf clinically warranted, MRI with contrast would be more sensitive for\nexcluding any active infection/ inflammation, particularly involving the\npachymeninges leptomeninges, though no abnormal pachymeningeal or\nleptomeningeal signal is seen on FLAIR images."
        },
        {
            "input": "There is a 3 x 1.7 x 2.6 cm (AP by TV by SI) enhancing mass overlying the left\nfrontal lobe and extending along the dura with adjacent dural thickening and\nhomogeneous enhancement.  There is associated susceptibility artifact along\nthe mass, likely corresponding to calcifications seen on recent CT. There is a\nfocus of T1 hyperintensity adjacent to the anterior margin of the mass (series\n3, image 13).  There is a focus of enhancement adjacent to the medial margin\nof the mass, possibly surrounding the mass and related to hemorrhage or\nraising concern for invasion of the frontal lobe parenchyma with corresponding\nFLAIR signal hyperintensity (series 14, image 106).  There is extensive\nregional FLAIR signal hyperintensity throughout the left frontal and parietal\nlobes likely reflecting vasogenic edema with associated mass effect including\npartial effacement of the left lateral ventricle and 6 mm rightward midline\nshift at the level of the septum pellucidum.  There is no evidence of\ninfarction.  There are scattered superimposed foci of T2/FLAIR signal\nhyperintensity within the subcortical and periventricular white matter.  The\nventricles and sulci are otherwise age appropriate in caliber and\nconfiguration, allowing for mass effect from the lesion and associated white\nmatter edema pattern.\n\nThere are 2 regions of diffusion-weighted hyperintense signal; 1 in the\nposterior left insula (series 6, image 15) and 1 in the right occipital lobe\n(series 6, image 13).  They do not demonstrate associated enhancement but are\nassociated with subtle FLAIR and T2 abnormality (series 12, image ___ and 11),\nwhich may represent acute infarct.\n\nThe major intracranial flow voids are preserved.  The dural venous sinuses\nappear patent.  No suspicious osseous lesions.",
            "output": "1. 3 x 1.7 x 2.6 cm enhancing possibly dural based mass along the left frontal\nlobe with associated calcifications seen on recent CT, extensive regional\nedema and similar mass effect including partial effacement of the left lateral\nventricle and 6 mm rightward midline shift given differences in technique.\n2. Focus of T1 signal hyperintensity along the anterior margin of the mass may\nrepresent a small amount of hemorrhage or calcification and focus of\nill-defined enhancement along the medial margin of the mass may be related to\na small amount of regional hemorrhage with involvement/invasion into the\nfrontal lobe parenchyma not excluded.\n3. The most common differential considerations would include atypical\nmeningioma or hemangiopericytoma.\n4. 2 small foci of diffusion-weighted hyperintense signal in the left\nposterior insula and right occipital lobe, raising concern for acute infarct. \nThese do not demonstrate evidence of abnormal enhancement.  No associated\nabnormality in the regions on earlier CT head.\n5. Additional findings described above."
        },
        {
            "input": "Postsurgical changes of left frontal craniotomy for the resection of the left\nfrontal mass.  There is small extra-axial fluid collection along the left\nfrontal convexity, grossly unchanged compare to prior CT, taking into account\nthe difference in modality.  There is small blood product within the surgical\ncavity and pachymeningeal enhancement along the left frontal convexity,\ncompatible with expected postoperative changes.\n\nThere is small focus of enhancement along the anteromedial aspect of the\nsurgical cavity, nonspecific, which could represent postsurgical changes\nversus residual tumor.  The large vasogenic edema in the left cerebral\nhemisphere is grossly unchanged compared to prior exam.  There is associated\nmass effect on the adjacent parenchyma and effacement on the left lateral\nventricles.\n\nThere is an unchanged small focus of diffusion restriction in the left\ninferior insula (___) which could represent subacute ischemia.  No\nlarge vascular distribution infarct is identified.  The visualized vascular\nflow voids grossly preserved.  The paranasal sinuses are clear.  The globes\nand orbits are unremarkable.  No abnormal marrow signal.",
            "output": "1. Postsurgical changes of left frontal craniotomy for the resection of the\nleft frontal mass, as described above.  There is a small focus of enhancement\nalong the anteromedial aspect of the surgical cavity which could represent\npostsurgical changes versus residual tumor.\n2. Persistent vasogenic edema in the left frontal and parietal lobe with\nassociated mass effect on the adjacent parenchyma and effacement of the\nlateral ventricle.\n3. Small unchanged subacute infarct in the left inferior insula.  No large\nvascular distribution infarct is noted.\n4. Additional findings as described above."
        },
        {
            "input": "Patient is status post left pterional craniotomy for underlying tumor\nresection.  There is underlying encephalomalacia with surrounding gliosis\ncentered in the left frontal operculum.  There has been resolution of\npreviously seen mass effect.  There is mild ex vacuo dilatation of the left\nlateral ventricle.\n\nThere is mostly thin linear pachymeningeal enhancement underlying the\ncraniotomy site.  There is a thicker area of enhancement measuring up to 2.5\nmm (9:207) with linear extension into the postoperative site (901:228 and\n226).  This area could represent vessels though attention on follow-up is\nsuggested to exclude recurrence.  Elsewhere, no nodular areas of enhancement.\n\nScattered periventricular T2 and FLAIR hyperintensities are likely sequela of\nchronic small vessel disease.  There is no acute infarct.  No unexplained\nsusceptibility artifact.  Major intravascular flow voids including within the\nmajor dural venous sinuses are preserved.\n\nVisualized paranasal sinuses and mastoid air cells demonstrate no abnormal\nsignal.",
            "output": "Postoperative changes of left frontal extra-axial meningioma resection. \nAssociated encephalomalacia underlying the postoperative site with resolved\nmass effect.  Foci of enhancement along the postoperative site which are felt\nmost likely to be vascular though attention on follow-up is suggested.  No\nother findings to suggest tumor recurrence."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, or infarction.\nThe ventricles and sulci are normal in caliber and configuration.  No\ndiffusion abnormalities are detected. The major vascular flow voids appear\npatent and demonstrate normal distribution.\n\nOther than mild right maxillary sinus mucosal thickening, the paranasal\nsinuses, mastoid air cells, and middle ear cavities are clear. The orbits are\nunremarkable.",
            "output": "No evidence of intracranial hemorrhage, infarction, or mass."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.\n\nThere are minimal subcortical, deep and periventricular white matter T2/FLAIR\nhyperintensities are nonspecific but compatible with chronic small vessel\nischemic disease.\n\nThe major intracranial vascular flow voids are maintained.  The paranasal\nsinuses and mastoid air cells are normal.  Mild diffuse hyperintensity in the\nbone marrow on diffusion images could be related to marrow hyperplasia.",
            "output": "1. No acute intracranial abnormality.\n2. Minimal white matter chronic small vessel ischemic disease."
        },
        {
            "input": "There is no intracranial mass, mass effect, or midline shift. Ventricles and\nsulci are age-appropriate. There is no focal parenchymal signal abnormality.\nThere is no region of restricted diffusion or abnormal susceptibility\nartifact. Major intravascular flow voids are preserved.\n\nPost contrast images demonstrate no abnormal parenchymal or meningeal\nenhancement.\n\nVisualized paranasal sinuses and mastoid air cells are clear.",
            "output": "Normal MRI of the brain."
        },
        {
            "input": "The common, internal and external carotid arteries appear normal.  There is no\nevidence of stenosis by NASCET criteria. The origins of the great vessels,\nsubclavian, and vertebral arteries appear normal bilaterally.  The common\ncarotid bifurcations appear normal.",
            "output": "Normal MRA neck."
        },
        {
            "input": "A complete study was not performed due to marked patient motion. Available\nsequences are markedly motion degraded.\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, or infarction.\nThere are multiple foci of FLAIR hyperintensity in the deep and\nperiventricular white matter of the frontal and parietal lobes. There is mild\ngeneralized enlargement of the ventricles, sulci, and cisterns consistent with\ngeneralized parenchymal volume loss.  There is no definite predominant lobe or\nlobes affected by volume loss. White matter disease and volume loss do not\nappear significantly different from CT on ___. Major\nintravascular flow voids are grossly preserved.\n\nThere is mild mucosal thickening of the ethmoid sinuses. The paranasal sinuses\notherwise appear clear. There is fluid in the mastoid air cells, right greater\nthan left. The orbits are normal.",
            "output": "1. Incomplete study due to marked patient motion with available sequences\nmarkedly degraded by motion.\n2. Mild generalized parenchymal volume loss, not significantly changed from CT\non ___.\n3. Scattered cerebral white matter FLAIR hyperintensities consistent with\nmoderate to chronic microangiopathy, also not significantly changed from CT on\n___.\n4. Fluid in the mastoid air cells, right greater than left. This can be seen\ndue to prolonged supine positioning. Clinical correlation suggested."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  Nonspecific, nonenhancing small T2 signal abnormality\nmeasuring 0.7 cm involving medial left middle cerebellar peduncle (07:11) near\nfourth ventricle.  No other areas of supratentorial T2 signal abnormality, no\njuxta cortical, periventricular or brainstem abnormalities.  Findings in the\nleft middle cerebral peduncle in nonspecific, may be sequela of prior\ninflammatory, demyelinating or ischemic process.\n\nThere is otherwise no convincing abnormal enhancement after contrast\nadministration.  No evidence of dural venous sinus thrombosis.\n\n The major intracranial vascular flow voids are maintained.  There is a 2.1 cm\nmucous retention cyst within the right maxillary sinus.  The mastoid air cells\nand orbits are normal.",
            "output": "1. No acute intracranial abnormality..\n2. Nonspecific small FLAIR abnormality left middle cerebellar peduncle, may\nrepresent sequela of prior inflammatory, demyelinating or ischemic insult."
        },
        {
            "input": "Study is mildly degraded by motion.  There is no evidence of hemorrhage,\nedema, masses, mass effect, midline shift or infarction.   The ventricles and\nsulci are normal in caliber and configuration.  Right maxillary sinus mucous\nretention cyst versus polyp is noted.",
            "output": "1. Study is mildly degraded by motion.\n2.  No acute intracranial abnormality.\n3. No evidence of microhemorrhage."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.\n\nThe ventricles and sulci are normal in caliber and configuration.\nMajor vascular flow voids are preserved.\n\nThe paranasal sinuses and mastoid air cells appear clear.  The orbits appear\ngrossly unremarkable.",
            "output": "1. Unremarkable MRI of the brain."
        },
        {
            "input": "There is asymmetric enhancement of the tympanic and mastoid segment of the\nright seventh cranial nerve (751:36).  The left seventh nerve complex is\nunremarkable.  Images through the internal auditory canal demonstrates\nsymmetric appearance of the eighth nerve complexes.  There is normal fluid\nsignal within the cochlea and semicircular canals.  There is no evidence of\nabnormal enhancement or mass lesion within the internal auditory canals,\ncerebellopontine angles or membranous labyrinth. No other mass lesions are\nseen within the posterior fossa.\n\nLimited included imaging of the remainder of the brain demonstrates no\nevidence of hemorrhage, edema, masses, mass effect, ormidline shift.  There is\nno abnormal enhancement after contrast administration.\n\nNo osseous abnormalities are seen.  There is partial opacification of the\nright posterior ethmoid air cell.  Otherwise, the paranasal sinuses, mastoid\nair cells, and middle ear cavitiesare clear. The orbits are unremarkable. The\nvisualized portion of the principle vascular flow voids are preserved.",
            "output": "1. Asymmetric enhancement of the tympanic and mastoid segment of the right\nseventh cranial nerve, suggestive of an inflammatory or infectious process.  A\nneoplastic process is less likely given lack of nodularity of the enhancement.\n2. Normal appearance of the eighth nerve complex with normal fluid signal\nwithin the cochlea and semicircular canals.  No evidence of abnormal\nenhancement or mass in the internal auditory canal or labyrinthine structures.\n\nNOTIFICATION:  The impression and recommendation above was entered by Dr. ___\n___ on ___ at 15:44 into the Department of Radiology\ncritical communications system for direct communication to the referring\nprovider."
        },
        {
            "input": "Aero digestive tract:\n\nThere is no mass.  There is mild paranasal sinus disease, with mucosal\nthickening of the anterior ethmoid air cells and left greater than right\nmaxillary sinus.\n\nNeck lymph nodes:\nThere is no adenopathy involving bilateral levels ___.\nThere is no retropharyngeal adenopathy.\n\nDeep neck muscles, masticator space:\nUnremarkable.\n\nBones, skull base:\nThere are no worrisome osseous lesions.\nSkull base was much better evaluated on the internal auditory canal MRI dated\n___.  Specifically, nodularity and increased enhancement of the\nright facial nerve in the tympanic and mastoid segments is redemonstrated, but\nmuch better seen on the prior study.\n\nVessels:\nUnremarkable.  Flow voids in the cervical vessels are preserved.\n\nBrachial Plexus:\nUnremarkable.\n\nThyroid, salivary glands:\nThe parotid glands are symmetric, with normal signal intensity and\nenhancement.  There is no parotid mass.  Submandibular glands are normal.  The\nthyroid gland is normal.\n\nOther findings:\nThere are no lung nodules.  There are degenerative changes in the cervical\nspine with left paracentral disc protrusion at the C4-C5 level causing\nmoderate spinal canal narrowing with some flattening of the ventral spinal\ncord.  No spinal cord signal abnormality or compression is demonstrated. \nThese of the cervical spine is not evaluated in detail by this exam.",
            "output": "1. Normal right parotid gland.  No cervical lymphadenopathy.\n2. Asymmetric enlargement and enhancement of the right facial nerve mastoid\nand tympanic segments is redemonstrated, but much better seen on the internal\nauditory canal MRI of ___."
        },
        {
            "input": "Aero digestive tract:\nThere is no mass.\n\nNeck lymph nodes:\nThere is no adenopathy involving bilateral levels ___.\nThere is no retropharyngeal adenopathy.\n\nExtra nodal tumor spread:\nThere are no findings suggestive of extra nodal extension.\n\nDeep neck muscles, masticator space:\nUnremarkable.\n\nBones, skull base:\nThere is no bone involvement.\nThere are no findings suggestive of perineural tumor extension.\nJugular foramen, carotid canal,pterygopalatine fossa,infraorbital\nforamen,other skull base foramina are not involved.\n\nVessels:\nUnremarkable.\n\nBrachial Plexus:\nThere is no brachial plexus contact or invasion.\n\nThyroid, salivary glands:\nThere is no mass.\n\nOther findings:\nMild mucosal thickening involving ethmoid air cells.  Small retention cysts at\nbilateral maxillary sinuses.",
            "output": "1. Unremarkable enhanced MRI of the neck.\n2. Please refer to concurrent MRI ___ with without contrast for additional\ndetails."
        },
        {
            "input": "There is mild, asymmetric enhancement of the right seventh nerve labyrinthine,\ngenu, tympanic, and mastoid segments, but however improved when compared to\nthe prior study from ___.  No definite nodularity or enlargement\nof the right facial nerve to confirm underlying mass.\n\nThere is no evidence of abnormal enhancement or mass lesion within the\ninternal auditory canals, cerebellopontine angles or membranous labyrinth. No\nother mass lesions are seen within the posterior fossa.\n\nLimited included imaging of the remainder of the brain demonstrates no\nevidence of hemorrhage, edema, masses, mass effect, midline shift or\ninfarction. The ventricles and sulci are normal in caliber and configuration.\nThere is no abnormal enhancement after contrast administration.\n\nMild degenerative changes to the cervical spine appear similar to prior. \nThere is minimal retrolisthesis of C4 on C5.  There is mild mucosal thickening\nof the bilateral anterior ethmoid air cells and fluid within the sphenoid\nsinuses.  The mastoid air cellsand middle ear cavitiesare clear. The orbits\nare unremarkable. The visualized portion of the principle vascular flow voids\nare preserved.",
            "output": "1. There is mild, asymmetric enhancement of the right seventh nerve\nlabyrinthine, genu, tympanic, and mastoid segments, however improved from\nprior study from ___.\n2. No definite nodular enhancement or thickening of the right facial nerve to\nconfirm underlying mass.\n3. Recommend continued follow-up to document resolution of enhancement.\n4. Additional findings described above."
        },
        {
            "input": "Ventriculomegaly and colpocephaly appear unchanged as compared to the prior\nstudies. There is apparent agenesis of the posterior corpus callosum. There is\ngliosis and encephalomalacia within the white matter of the right parietal and\ntemporal lobes, which does not extend to the cortex, therefore does not meet\nspecific criteria for schizencephaly. Periventricular leukomalacia is seen\nadjacent to the lateral ventricles bilaterally (12:14).\n\nThere is no intracranial hemorrhage. Diffusion weighting imaging does not\ndemonstrate evidence of acute infarct. The major intracranial vessels exhibit\nthe expected signal void related to vascular flow. Gray white matter\ndifferentiation is preserved.\n\nThere is no abnormal parenchymal, leptomeningeal, or dural focus of\nenhancement. The sella turcica and craniocervical junction are unremarkable.\nThe paranasal sinuses and mastoid air cells demonstrate normal signal.  Again\nseen is right phthisis bulbi. The left globe is somewhat small in size, and\ndemonstrates evidence of either retinal or choroidal detachment (14:10).",
            "output": "1. Ventriculomegaly and colpocephaly is unchanged as compared to the prior\nstudies. There is gliosis and encephalomalacia within the white matter of the\nright parietal and temporal lobes, which does not extend to the cortex,\ntherefore does not meet specific criteria for schizencephaly.\n\n2. The left globe is somewhat small in size, and demonstrates evidence of\neither retinal or choroidal detachment. Again seen is right phthisis bulbi."
        },
        {
            "input": "Study is moderately degraded by motion.\n\nExamination is limited due to early termination of study from patient\ndiscomfort.\n\nMinimal T1 hyperintensity within bilateral thalami (see 05:13; 4:8,13)\ncorresponding to areas of calcific densities on prior outside noncontrast head\nCT (see 401:51 on prior exam).\n\nThe ventricle and sulci are grossly preserved in size and configuration with\nno definite mass effect or midline shift.",
            "output": "1. Study is moderately degraded by motion and limited due to lack of non T1\nimaging, due to patient inability to. patient inability to tolerate\nexamination.\n2. Bilateral thalamic T1 hyperintensities corresponding to calcifications seen\non prior outside CT suggestive of Fabry disease.\n3. Within limits of study, no definite evidence of large mass or midline\nshift."
        },
        {
            "input": "Study is mildly degraded by motion.\n\nThere is no evidence of hemorrhage, masses, acute infarct trauma mass effect\nor midline shift.  The ventricles and sulci are preserved in caliber and\nconfiguration.\n\nMinimal FLAIR hyperintensity within the cerebellum is noted.  Question\nassociated minimal slow diffusion (see 500, 502:10; 4, 8, 9, 10:10). \nFollowing the administration of contrast, there is subtle enhancement along\nthe cerebellar vermis and bilateral cerebellar hemispheres (image ___ of\nseries 10).\n\nGrossly stable minimal T1 hyperintensity within the bilateral thalami (image\n13 of series 4), which corresponds to areas of calcific densities in the prior\noutside noncontrast head CT.\n\nThere is mild mucosal thickening of the ethmoid sinuses.  Minimal bilateral\nmastoid air cell effusion is noted.  These findings may be related patient's\nintubation status.\n\nThe orbits and major intracranial arterial flow voids are preserved.  The\ndural venous sinuses are patent.  Partially empty sella is noted.",
            "output": "1. Study is mildly degraded by motion.\n2. Parenchymal signal intensity abnormality and subtle enhancement of\ncerebellar vermis and bilateral cerebellar hemispheres, concerning for\ncerebellitis.\n3. No evidence of acute intracranial hemorrhage, acute infarction, or mass\nlesion.\n4. Bilateral thalamic T1 hyperintensities corresponding to calcifications seen\non prior outside CT, again suggestive of Fabry Disease."
        },
        {
            "input": "The study is moderately degraded by motion artifact.\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.\nStable T1 hyperintensity within the bilateral thalami (series 3, image 13)\nwhich corresponds to areas of calcification seen on the prior CT head.\n\nThe broad areas of cerebellar enhancement seen on the prior examination have\ncompletely resolved.  Faint FLAIR hyperintensity in the dorsal pons appears\nreduced but persistent.\n\nThe ventricles and sulci are normal in caliber and configuration.\nMajor vascular flow voids are preserved.  Intracranial vasculature is patent. \nMajor dural venous sinuses are patent.\n\nThe paranasal sinuses and mastoid air cells are clear.  The orbits are normal.",
            "output": "1. Moderately degraded study due to motion artifact.\n2. The extensive contrast enhancement in the vermis and bilateral cerebellar\nhemispheres has resolved.\n3. Mild areas of dorsal pontine hyperintensity are reduced but persist.\n\nRECOMMENDATION(S):  If clinically indicated, a repeat MRI of the head with and\nwithout contrast is suggested."
        },
        {
            "input": "There is no evidence of infarction, hemorrhage, edema, mass, or mass effect. \nNo abnormal enhancement.  Mild brain parenchymal atrophy.  Mild chronic small\nvessel ischemic change.\n\nAside from trace ethmoid air cell mucosal thickening, the remaining visualized\nparanasal sinuses and mastoids appear clear.  Preserved vascular flow voids,\npatent dural venous sinuses.  Mildly inhomogeneous marrow signal, no\nassociated focal lesion or restricted diffusion, may be reactive.",
            "output": "1. No mass or acute change."
        },
        {
            "input": "MR BRAIN:\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  The major intracranial flow voids are preserved. Mild\nbilateral maxillary sinus and ethmoid air cell mucosal thickening.\n\nMRA brain: The intracranial vertebral and internal carotid arteries and their\nmajor branches appear normal without evidence of stenosis, occlusion, or\naneurysm formation.\n\nMRV: Normal flow signal is demonstrated within the superior sagittal sinus,\nstraight sinus, transverse sinuses, and sigmoid sinuses. The jugular bulbs and\nproximal jugular veins are patent. Evaluation of the deep venous systems\nreveals normal flow signal in the internal cerebral veins. The vein ___\nis also unremarkable.",
            "output": "1. No evidence of an acute intracranial abnormality.\n2. Mild paranasal sinus disease."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.\n\nNasal sinuses and mastoid air cells are clear.  The visualized orbits are\nunremarkable.",
            "output": "Normal brain MRI."
        },
        {
            "input": "A midline cystic mass is again identified in the suprasellar region, measuring\n7 x 6 x 6 mm (6:9 and 5:8).  Normal appearing adenohypophysis and\nneurohypophysis are seen within the sella.  The lesion demonstrates minimal\nperipheral enhancement.  A stable 3 mm enhancing nodule is seen posterior to\nthe lesion (5:9 and 6:9), which may represent a thickened infundibulum due to\nmass effect.  The lesion demonstrates stable minimal mass effect on the\nmidline aspect of the optic chiasm (4:7).  The cavernous sinuses are intact.",
            "output": "1. A stable midline cystic mass is seen in the suprasellar region\ndemonstrating minimal peripheral enhancement.  A stable 3 mm enhancing nodule\nposterior to lesion, which may represent a thickened infundibulum due to mass\neffect.  A normal appearing pituitary gland is seen within the sella. \nDifferential diagnoses include a Rathke's cleft cyst or less likely a\ncraniopharyngioma.  Stable mild mass effect on the midline optic chiasm is\nnoted."
        },
        {
            "input": "MRA brain: The intracranial vertebral and internal carotid arteries and their\nmajor branches appear normal without evidence of stenosis, occlusion, or\naneurysm formation.\n\nMRA neck: The common, internal and external carotid arteries are patent. \nThere is mild irregularity of the bilateral proximal internal carotid arteries\nat the carotid bifurcations, likely related to atherosclerotic disease, with\nno evidence of internal carotid artery stenosis by NASCET criteria.  There is\na normal 3 vessel branching pattern of the aortic arch.  Question minimal\nnarrowing without occlusion of the right common carotid artery origin (see\n___.  Otherwise, the origins of the great vessels, subclavian, and\nvertebral arteries appear normal bilaterally.",
            "output": "1. Question minimal narrowing of right common carotid artery origin without\nstenosis versus artifact.\n2. No evidence ofaneurysm, dissection or vascular malformation or significant\nluminal narrowing."
        },
        {
            "input": "MP RAGE sequences are motion degraded.  Within these confines:\n\nNumerous foci of restricted diffusion, confined to the cortex, are scattered\nthroughout the bilateral frontal, parietal, temporal, and occipital lobes and\nare associated with T2/FLAIR hyperintense signal.  There are also scattered\nfoci of T2/FLAIR hyperintense signal in the subcortical, periventricular, and\ndeep supratentorial white matter with no corresponding restricted diffusion.\n\nLinear and ill-defined enhancement in the right middle cerebellar peduncle,\nextending into the right hemi pons, has no corresponding T1, T2, or FLAIR\nhypointense or hyperintense signal.\n\nThere is no T1 or T2/FLAIR hyperintense signal in the basal ganglia to suggest\nhepatic encephalopathy or T2/FLAIR hyperintense signal in the mammillary\nbodies, hypothalamus, thalamus, periaqueductal gray, or cerebellum to suggest\nWernicke's encephalopathy.\n\nThere is no evidence of hemorrhage, edema, mass effect, midline shift or\nextra-axial fluid collection.   The ventricles and sulci are normal in caliber\nand configuration.  There is no abnormal enhancement after contrast\nadministration.\n\nThere is moderate mucosal thickening in the bilateral ethmoid sinuses, right\ngreater than left.  The orbits are unremarkable.  The mastoid air cells are\nclear.\n\nThe major intracranial flow voids are preserved.",
            "output": "1. Numerous, diffuse late acute cortical infarcts throughout the cerebral\nhemispheres.\n2. Linear and ill-defined enhancement in the right middle cerebellar peduncle,\nextending into the right hemi pons, with no associated signal abnormalities\ncould represent artifact as this finding is not correlated on any other axial\nsequence including turbo spin echo T1 postcontrast versus, if not artifact,\npotentially capillary telangiectasia associated with a developmental venous\nanomaly versus artifact.  Infectious/inflammatory etiology such as\ntuberculosis for sarcoid as mentioned in the preliminary wet read is\nconsidered much less likely.  Recommend repeat MRI head with without contrast.\n\nRECOMMENDATION(S):  Close attention on repeat MRI head with without contrast\nis recommended for impression 2."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  There is mild prominence of the ventricles and sulci\nsuggestive of involutional changes.  Confluent areas of periventricular,\nsubcortical and deep white matter T2/FLAIR hyperintensities are in a\nconfiguration most suggestive chronic small vessel ischemic disease.  There is\nno abnormal focus of slowed diffusion.  The principal intracranial vascular\nflow voids are preserved.\n\nThe paranasal sinuses are grossly clear.  The orbits are grossly unremarkable.\nThe mastoid air cells are clear.",
            "output": "1. No acute intracranial abnormality, including hemorrhage, infarct, or\nsuggestion of mass.\n2. Mild global atrophy and areas of confluent white matter signal abnormality\nin a configuration most suggestive of chronic small vessel ischemic disease."
        },
        {
            "input": "There is no acute infarct or intracranial hemorrhage. No mass, mass effect or\nmidline shift is present. The ventricles, cerebral sulci and cisterns are\nmildly prominent, reflecting a mild degree of cerebral atrophy, but unchanged\nfrom the previous examination. A chronic lacunar infarct is noted within the\nleft cerebellar hemisphere. No significant cerebellar atrophy or cerebellar\nmass identified.\n\nThe visualized soft tissues are unremarkable. The patient is status post\nbilateral lens implants.",
            "output": "No acute infarct, space-occupying lesion or intracranial hemorrhage.  No\nsignificant cerebellar atrophy is identified."
        },
        {
            "input": "There is left frontal lobe encephalomalacia.  Left frontal craniotomy changes\nare seen.  Multiples punctate foci of hemosiderin are noted in the surgical\nsite.  In addition, there is a focus of hemosiderin in the right thalamus and\nleft parietal lobe.  FLAIR hyperintense signal is noted around the left\nfrontal resection cavity.  There minimal thin contrast enhancement along the\nanterior and posterior resection margins.  There is a focus of mild restricted\ndiffusion along the lateral aspect of the resection cavity, series 402 and\n400, image 15.  There is ex vacuo dilatation of the left frontal horn.\n\nThere is questionable mild restricted diffusion in the right frontal lobe,\nseries 400, 402, image 18.\n\nThere is no evidence of acute hemorrhage, edema, masses, mass effect, midline\nshift or infarction.  Periventricular and subcortical T2 and FLAIR\nhyperintensities are noted.    The ventricles and sulci are prominent.\n\nPostsurgical changes from a right cataract extraction are seen.  The vascular\nflow voids are patent.  There is mucosal thickening in the ethmoid sinuses.\n\nDegenerative changes are noted in the cervical spine.",
            "output": "1. Postsurgical changes to the left frontal lobe with minimal thin enhancement\nalong the anterior and posterior resection margins, likely postoperative in\netiology, however recommend correlation with prior imaging to document\nstability.\n2. Focus of mild restricted diffusion along the lateral aspect of the\nresection cavity which may be artifactual in nature.  Correlation with prior\nimaging is again recommend.\n3. Questionable restricted diffusion in the right frontal lobe which is felt\nto represent artifact rather than subacute infarction.  Again correlation with\nprior imaging is recommended.\n\nRECOMMENDATION(S):  Correlation with prior imaging."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.\n\nParanasal sinuses and mastoid air cells are normal.  The orbits appear normal.",
            "output": "1. Normal enhanced brain MRI."
        },
        {
            "input": "There is no evidence of acute infarction.  There is a small, chronic appearing\ninfarct seen in the right cerebellar hemisphere.  No intracranial hemorrhage.\nNo mass, mass effect, edema or midline shift.\n\nThe ventricles and sulci are diffusely prominent.  Periventricular and\nsubcortical white matter FLAIR hyperintensities are noted, a nonspecific\nfinding that most likely represents the sequelae of chronic small vessel\nischemic disease.   There is gross preservation of the principal intracranial\nvascular flow voids.\n\nMucosal thickening is seen with chronic changes in the left maxillary sinus. \nMild mucosal thickening is also noted the left sphenoid sinus.  The remainder\nof the visualized paranasal sinuses, middle ear cavities, and mastoid air\ncells are well aerated and clear.\n\nThe patient is status post left globe replacement.  Hyperostosis frontalis is\nnoted bilaterally.",
            "output": "1. No evidence for acute intracranial hemorrhage or infarction.\n2. Chronic right cerebellar infarct.\n3. Background global parenchymal volume loss and evidence of chronic small\nvessel ischemic disease.\n4. Multifocal paranasal sinus disease and additional findings, as above."
        },
        {
            "input": "Images are substantially degraded by motion artifact.  Previously-seen signal\nabnormalities in in the paracentral and occipital cortex, cerebellum, caudate\nand lentiform nuclei, and hippocampus are less conspicuous on\ndiffusion-weighted images but remain visible on FLAIR images, likely secondary\nto expected evolution.  No large new signal abnormality is seen allowing for\nsevere motion artifact.  Ventricles and sulci are stable in size.  Cerebellar\ntonsils are normally positioned.  Basal cisterns are not compressed.",
            "output": "The study is severely degraded by motion artifact.  Previously seen signal\nabnormalities consistent with global hypoxic ischemic injury demonstrate\nexpected interim evolution.  No large new signal abnormalities seen."
        },
        {
            "input": "MRI HEAD: A single 5 mm diffusion-weighted hyperintense focus in the white\nmatter of the right parietal lobe adjacent to the posterior horn of the right\nlateral ventricle, with corresponding FLAIR and T2 hyperintensities noted,\nwhich may represent a late acute infarct. No intra or extra-axial mass or\nhemorrhage. Sulci, ventricles and cisterns are within expected limits. The\nmajor flow voids are preserved. The paranasal sinuses are essentially clear.\nThe orbits are unremarkable. The mastoid air cells are clear.\n\nHEAD MRA:  The ACA, MCA and their major branches are unremarkable without\nevidence of basal occlusive disease. There is lack of flow related signal of\nthe left V3 to mid V4 segments, which also appears slightly patulous, that\nreconstitutes at the distal V4 near its confluence with the basilar artery.\nThis may represent slow flow secondary to focal dilatation of the artery. The\nright vertebral artery is unremarkable. The remainder of the posterior\ncirculations unremarkable. No aneurysm larger than 3 mm.\n\nNECK MRA: There is a normal 3 vessel takeoff from the aortic arch. The\ncervical common carotid, internal carotid and external carotid arteries are\nnormal in course, caliber and contour.  Estimates of extracranial internal\ncarotid artery stenosis based on NASCET criteria. The right vertebral artery\nis dominant. There is lack of flow related signal of the left V3 segment,\nwhich may be secondary to slow flow.",
            "output": "1.  Single 5 mm focus of late acute infarct in the periventricular parietal\nwhite matter.\n\n2.  There is poor flow related signal of the left V3 and V4 segments, which\nmay represent slow flow. If there is clinical concern, this may be better\nevaluated with CTA.  The remainder of the MRA of the head and neck is\nunremarkable."
        },
        {
            "input": "Study is moderately degraded by motion.\n\nMRI HEAD:\n\nThere geographic areas of slow diffusion within the right occipital lobe and a\npunctate focus of slow diffusion within the left mid cerebellar hemisphere (5\n02:12; 502:4).  There is corresponding FLAIR hyperintensity without evidence\nof hemorrhagic conversion.\n\nThere are areas of encephalomalacia within the bilateral cerebellar\nhemispheres consistent with more remote infarcts.  There is background\nperiventricular and subcortical white matter FLAIR hyperintensity, likely\nreflecting sequela chronic microangiopathy.  There is prominence of the\nventricles and cortical sulci, consistent volume loss.  The vascular flow\nvoids are preserved.  The extra-axial spaces are unremarkable.  There is no\nabnormal parenchymal enhancement.  There is normal dural venous sinus\nenhancement.\n\nThe orbits, soft tissues, and calvarium are unremarkable.  There is a\nmoderately sized mucous retention cyst within the right maxillary sinus.\n\nMRA HEAD:\nThere is motion artifact which degrades spatial resolution.  Interpretation is\nbased on this limitation.\n\nThe bilateral intracranial internal carotid arteries are patent.  The anterior\nand bilateral posterior communicating arteries are visualized.  There are\nbilateral fetal origin posterior cerebral arteries the anterior and posterior\narterial circulations are patent without occlusion, stenosis, aneurysm, or\ndissection.  There is no evidence of vascular malformation.\n\nMRA NECK:\nThe dynamic postcontrast imaging depicts contrast immediately following\ninjection within the venous system than late with the preponderance of\ncontrast within the draining venous system therefore evaluation of the\narterial system is extremely limited and only distinctly visualized on the\ntime-of-flight imaging.\n\nBased on the time-of-flight imaging the right carotid artery is patent without\nstenosis by NASCET criteria.  The left carotid artery is patent with stenosis\nversus artifact at the carotid bulb which cannot be measured due to\ntime-of-flight technique.  There is absence of flow enhancement within the\nvertebral arteries along their horizontal course due to time-of-flight\ntechnique, however there is patency along their inferior to superior course.",
            "output": "1.  Study is moderately degraded by motion.\n2. Bilateral PCA distribution acute infarcts involving right occipital and\nleft cerebellar hemispheres without hemorrhagic conversion.\n3. Grossly patent intracranial vasculature without occlusion, stenosis,\ndissection, or aneurysm.\n4. Nondiagnostic MRA of the neck with early and late phase of contrast on the\ndynamic sequence which limits evaluation of the arteries.  Interpretation is\nbased off of the time-of-flight imaging which demonstrates patent bilateral\ncarotid arteries with stenosis versus artifact at the left carotid bulb.  The\nvertebral arteries are grossly patent along their inferior to superior course\nhowever there horizontal course is not visualized due to time-of-flight\ntechnique.  Consider dedicated CTA of the neck to further characterize the\nneck vasculature.\n5.  Paranasal sinus disease as described.\n\nRECOMMENDATION(S):  Consider dedicated CTA of the neck to further characterize\nthe vasculature a due to nondiagnostic postcontrast MRA neck sequences.\n\nNOTIFICATION:  The findings were discussed with ___, M.D. by\n___, M.D. on the telephone on ___ at 8:45 AM, 10 minutes after\ndiscovery of the findings."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor acute infarction.  There are multiple bilateral small chronic cerebellar\ninfarcts, without new infarcts compared to prior.  There is chronic right\noccipital lobe infarct, which was in acute phase on prior.  There is small\nchronic lacunar infarct involving posterior limb right internal capsule,\nstable.  There is small chronic cortical infarct involving left medial\npostcentral gyrus, stable since prior.  There are moderate chronic small\nvessel ischemic changes, similar.  There is generalized brain parenchymal\natrophy.  There is no hydrocephalus.  Intracranial vascular flow voids are\npreserved.  Basilar artery is diminutive in caliber, similar to prior\nbilateral PCOM is present.  Postoperative changes posterior cervical spine\nfusion is partially seen.  There is submucosal retention cyst in the right\nmaxillary sinus.  Otherwise, paranasal sinuses, mastoid air cells, middle ear\ncavities are clear.",
            "output": "1. There are chronic infarcts, without new infarcts compared to prior.\n2. There are moderate chronic small vessel ischemic changes, and generalized\nbrain parenchymal atrophy."
        },
        {
            "input": "The examination is partially limited due to patient motion, within this\nlimitation, grossly there is no evidence of intracranial hemorrhage, edema,\nmasses, mass effect, midline shift or infarction.  Periventricular and\nsubcortical T2 and FLAIR hyperintensities are noted which may represent small\nvessel ischemic changes.   Prominence of the ventricles and sulci are\nsuggestive of involutional changes.  No diffusion abnormalities are detected. \nThere is no abnormal enhancement after contrast administration.\n\nBilateral hippocampal formations and mammillary bodies are preserved in signal\nand configuration. There is no disproportionate medial temporal atrophy. There\nis no focal lobar encephalomalacia. There are no focal cortical dysplasias or\ngray matter heterotopia noted.\n\nSoft tissue swelling is redemonstrated overlying the right parietal bone. \nThere is mild mucosal thickening in the maxillary sinuses and anterior ethmoid\nair cells.  Trace fluid is seen in the left mastoid tip air cells.",
            "output": "1. There is no evidence of acute intracranial process or hemorrhage.\n2. No specific findings to explain the seizure focus."
        },
        {
            "input": "There are multiple bilateral nonspecific T2/FLAIR signal hyperintense lesions\nin the subcortical white matter.\n\nThere is no acute infarction, intracranial hemorrhage, extracerebral fluid\ncollection, midline shift or mass effect.  No diffusion abnormalities are\ndetected. The cerebral volume is appropriate for the patient's stated age. \nThe major vascular flow voids are maintained. There is no evidence of abnormal\nenhancement. The orbits are unremarkable, the paranasal sinuses and mastoid\nair cells are clear",
            "output": "1. No evidence of stroke. No abnormal enhancement.\n\n2.  Multiple nonspecific T2/FLAIR signal hyperintense lesions in the\nsubcortical white matter bilaterally. The differential diagnosis for this\nfinding includes chronic small vessel ischemic disease and demyelinating\ndisease although the distribution of the lesions on this exam is not typical\nfor these diagnoses. Other possibilities include vasculitis, Lyme disease, and\nchronic headaches. However, it is often the case with the number of lesions\nseen on this study that no pathological correlation for this finding is found."
        },
        {
            "input": "Study is mildly degraded by motion.  There is no evidence of infarction,\nhemorrhage, edema, mass effect, or midline shift.  The ventricles are normal\nin size and configuration.  The major visualized arterial vascular flow voids\nare preserved.  Few periventricular and subcortical T2 and FLAIR\nhyperintensities are noted, which may represent small vessel ischemic changes.\n\nThere is moderate mucosal thickening of the ethmoid air cells and right\nsphenoid sinus with a mucosal retention cyst in the right ethmoid sinus. \nThere is right maxillary sinus small air-fluid level.",
            "output": "1. Study is mildly degraded by motion.\n2. No evidence of infarction or hemorrhage.\n3. Moderate paranasal sinus disease as above with right maxillary sinus\nair-fluid level, which can be seen with acute sinusitis."
        },
        {
            "input": "There is no evidence of acute infarction, hemorrhage, edema, mass, or mass\neffect.\nSmall chronic infarct left vertex involving parietal lobe.  Small chronic\ninfarcts bilateral corona radiata.  Brain parenchymal atrophy.\nFindings consistent with moderate chronic small vessel ischemic changes. \nAside from bilateral lens extraction, the globes and orbits are within normal\nlimits.\n\n Major intracranial vascular flow voids are preserved.  The visualized\nparanasal sinuses and mastoids appear clear.",
            "output": "1. No acute findings.\n2. Small chronic infarcts.\n3. Parenchymal atrophy.  Moderate chronic small vessel ischemic change."
        },
        {
            "input": "Superficial hemosiderosis is noted along the frontoparietal convexities. \nThere is FLAIR hyperintense signal in the left frontal lobe, most consistent\nwith gliosis.   Postsurgical changes from clipping of the pericallosal\naneurysm is seen with minimal artifact around the clips.  There is atrophy and\nscarring of the corpus callosum with minimal enhancement along the margins of\nthe body of the corpus callosum, likely secondary to postsurgical changes\nand/or chronic blood products.  A right frontal ventriculostomy catheter tract\nis noted.\n\nBifrontal cranioplasty changes are seen, with grossly stable amount of\nsubgaleal fluid.  There is a 1.5 cm AP x 0.6 cm nonenhancing subgaleal\ncollection along the posterior lateral aspect of the left cranioplasty, series\n502, image 15 and series 8, image 12, which demonstrates mild restricted\ndiffusion.   Small bilateral frontoparietal subdural FLAIR hyperintense fluid\ncollections are noted.   In addition, grossly stable amount of epidural T2\nhyperintense signal is seen which demonstrates restricted diffusion,\nparticularly along the left lateral aspect, series 502 image ___, with\nassociated intrinsic T1 hyperintense signal (series 4, image 17).  Thick\nenhancement of the bifrontal dura is seen.\n\nThere is no evidence of acute infarction com acute hemorrhage, mass effect or\nmidline shift.  The major vascular flow voids are preserved.\n\nMinimal left periorbital soft tissue thickening is seen.  The orbits are\notherwise normal.  No retrobulbar are orbital abnormalities identified.  The\nmastoid air cells and paranasal sinuses are normal.  The visualized soft\ntissues are normal.",
            "output": "1. Prominent bifrontal epidural fluid collection demonstrating restricted\ndiffusion along the midline and left lateral aspects with underlying dural\nthickening and enhancement.  Although there is intrinsic T1 hyperintense\nsignal within this collection, compatible hemorrhage product, which in part\ncould contribute to appearance of restricted diffusion on DWI, there is\nconcern for superimposed infectious process.  Clinical correlation is\nrecommended.\n2. A 1.5 cm nonenhancing subgaleal collection along the posterior lateral\naspect of the left cranioplasty, also demonstrates restricted diffusion.  The\nrestricted diffusion raises suspicion for infectious process, although the\nlack of enhancement would not be typical.  Clinical correlation is also\nrecommended.\n3. Postsurgical changes from clipping of the pericallosal aneurysm with\ngliosis of the high left frontal lobe and corpus callosum scarring, as\ndescribed above.\n4. Minimal left periorbital soft tissue thickening, with no postseptal\nextension.\n\nNOTIFICATION:  The findings were discussed with ___, N.P. by\n___, M.D. on the telephone on ___ at 9:30 AM, 20 minutes\nafter discovery of the findings."
        },
        {
            "input": "There is mild T2/FLAIR hyperintensity in the mesial left temporal lobe without\nassociated restricted diffusion, enhancement or susceptibility artifact.\n\nThere is no acute infarction, intracranial hemorrhage or intracranial mass. \nThere is no abnormal intracranial enhancement.\n\nThere are small areas of encephalomalacia in the right post central gyrus and\nleft occipital lobe which most likely represent sequelae from remote infarcts.\nThere is a chronic lacunar infarct in the right caudate nucleus.  There are\nadditional mild T2/FLAIR hyperintensities in the periventricular and\nsubcortical white matter, which are nonspecific.\n\nThe ventricles are normal size without evidence of hydrocephalus.\n\nThe orbits are unremarkable.\n\nThere is mild scattered mucosal thickening of the paranasal sinuses.  The\nmastoid air cells are clear.\n\nThe major intracranial flow voids are preserved.\n\nThe bones and extracranial soft tissues are unremarkable.  There are overlying\nEEG electrodes.",
            "output": "1. Nonenhancing, T2/FLAIR hyperintensity in the mesial left temporal lobe,\nwhich may be related to recent seizure activity.  Differential diagnosis also\nincludes mesial temporal sclerosis, low grade neoplasm or encephalitis. \nCorrelation with CSF analysis is recommended.\n2. Encephalomalacia in the left occipital lobe and right postcentral gyrus,\nwhich likely reflect sequela from remote infarcts.  Additional chronic lacunar\ninfarct in the right caudate nucleus.\n3. Mild periventricular and subcortical T2/FLAIR white matter\nhyperintensities, which may represent chronic microangiopathic changes or\nsequelae from chronic migraines.\n\nNOTIFICATION:  The findings were discussed with ___, M.D. by ___\n___, M.D. on the telephone on ___ at 10:06 am, 5 minutes after\ndiscovery of the findings."
        },
        {
            "input": "MRI BRAIN:\nThere is no evidence of hemorrhage,edema,masses, mass effect, midline shift or\nrecent infarction.  Again seen are foci of right parietal and left occipital\ntissue loss suggesting chronic infarctions.  This appearance is unchanged\nsince the prior study.  The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.  The dural venous sinuses are patent.  There are scattered\nwhite matter hyperintensities on FLAIR imaging, similar to the prior study. \nAlthough nonspecific, these are often attributed to chronic small vessel\nischemia.\nThe region of left medial temporal lobe T2 and FLAIR hyperintensity has\nresolved since the prior examination.  This supports the spiculation that it\nmay have been due to a seizure.\n\nMRA BRAIN:\nThe intracranial vertebral and internal carotid arteries and their major\nbranches appear normal without evidence of stenosis,occlusion,or aneurysm\nformation.  There are prominent posterior communicating arteries bilaterally.\n\nMRA NECK:\nThe origins of the great vessels, subclavian and vertebral arteries appear\nnormal bilaterally.  The common, internal and external carotid arteries appear\nnormal.  There is no evidence of internal carotid artery stenosis by NASCET\ncriteria.",
            "output": "1. No evidence of mass, hemorrhage or recent infarction.\n2. Chronic infarctions in the right parietal and left occipital lobes are\nunchanged.\n3. Left medial temporal lobe FLAIR hyperintensity and swelling noted on the\nprior study has resolved.\n4. Normal appearance of the dural venous sinuses.\n5. Patent circle of ___ without evidence of stenosis,occlusion,or aneurysm.\n6. Patent bilateral cervical carotid and vertebral arteries without evidence\nof stenosis, occlusion, or dissection."
        },
        {
            "input": "MR BRAIN:\nThere is a 9 mm focus of restricted diffusion in right precentral gyrus\n(series 6, image 27), with a correlate on FLAIR (series 12, image 21),\ncompatible with late acute infarction.  No additional focus of acute or\nsubacute infarction.\n\nConfluent and severe periventricular and deep white matter T2/FLAIR\nhyperintensities, which correspond to hypodensities on CT head from ___, likely represents sequela of chronic small vessel ischemic disease.  The\nbilateral inferior olivary nuclei demonstrate T2 hyperintense signal (series\n11, image 5; series 12, image 5) and slightly enlarged, suggesting\nhypertrophic olivary degeneration.  The ventricles and sulci are mildly\nprominent, likely representing age-related change.  The major intracranial\nflow voids are preserved.  A punctate focus of gradient echo susceptibility\nartifact in the left inferior parietal lobule (series 13, image 12) likely\nrepresent sequela of prior microhemorrhage.\n\nThere is unchanged moderate left cerebellar encephalomalacia.  Note is made of\nchronic right basal ganglia and left frontal old lacunar infarcts.\n\nThe orbits are unremarkable.  The mild mucosal thickening of the ethmoid air\ncells.  No significant fluid signal is seen the mastoid air cells.\n\nMRA brain: The intracranial vertebral and internal carotid arteries and their\nmajor branches appear normal without evidence of stenosis, occlusion, or\naneurysm formation.",
            "output": "1. Small, right precentral gyrus late acute infarct.  No evidence of acute\nintracranial hemorrhage.\n2. No evidence of stenosis, thrombosis, dissection or aneurysm greater than 3\nmm on MRI.\n3. Confluent and severe periventricular subcortical T2/FLAIR white matter\nhyperintensities are nonspecific, but commonly seen in setting chronic\nmicroangiopathy in a patient this age.\n4. There is enlargement and T2 hyperintense signal of the bilateral inferior\nolivary  nuclei, suggesting hypertrophic olivary degeneration.  Clinical\ncorrelation with patient's symptoms is recommended.\n5. Additional findings as described above\n\nNOTIFICATION:  The findings detailed in impression 1 were discussed with Dr.\n___. by ___, M.D. on the telephone on ___ at 1:30\npm, 5 minutes after discovery of the findings."
        },
        {
            "input": "MRI head: There is no acute intracranial hemorrhage or evidence of chronic\nblood product deposition. No acute process is identified on the water\ndiffusion or ADC weighted images. There is no mass, edema, mass effect, or\nmidline shift. There is no pathologic enhancement. There is a small old\ninfarct of the left cerebellum. There are a few foci of T2 and FLAIR\nhyperintensity in the deep white matter, nonspecific. The ventricles and sulci\nare normal for age. Major flow voids are patent. The calvarium is intact. The\nparanasal sinuses and mastoid air cells are clear. The orbits are normal.\n\nMRA neck: There is conventional aortic arch anatomy. The common carotid,\ncervical internal carotid, and external carotid arteries are normal. The\nsubclavian and cervical vertebral arteries are normal. There is no dissection,\nhemodynamically significant stenosis, or aneurysm.\n\nMRA head: The vertebral arteries, vertebrobasilar junction, and basilar artery\nare normal. The bilateral PCAs are normal. Bilateral posterior communicating\narteries are present. The intracranial carotid arteries. The bilateral MCAs\nand ACAs are normal. The A-comm region is normal. There is no dissection,\nhemodynamically significant stenosis, or aneurysm.",
            "output": "1. No intracranial hemorrhage or acute infarct.\n2. Small chronic left cerebellar infarct.\n3. Normal MRA of the head and neck."
        },
        {
            "input": "There is no evidence for an intra-axial or extra-axial mass.  There is no\nevidence for pathologic leptomeningeal or pachymeningeal contrast enhancement.\nThere is no evidence for edema, abnormal diffusion, or blood products.  There\nare nonspecific periventricular and subcortical white matter T2\nhyperintensities, likely representing sequela of chronic microangiopathy given\nthe patient's age, which appear similar to the ___ MRI allowing for motion\nartifact on the FLAIR sequence of the prior MRI.  Ventricles, sulci, and basal\ncisterns are normal in size.  Major arterial flow voids are grossly preserved.\nMajor dural venous sinuses appear patent on postcontrast MP RAGE images.\n\nFluid in the nasopharynx is likely related to endotracheal intubation.\n\nConcurrent MRI of the cervical, thoracic, and lumbar spine is reported\nseparately.",
            "output": "No evidence for intracranial metastatic disease or acute intracranial\nabnormalities."
        },
        {
            "input": "MR BRAIN:\nThere is a moderate-sized area of restricted diffusion involving the left\npostcentral gyrus and left parietal lobe.  There are additional small foci of\nrestricted diffusion in the right frontal, right parietal, left posterior\ntemporal, and right cerebellum.  There is no evidence of intracranial\nhemorrhage.\n\n Mild prominence of the ventricles and sulci is suggestive of involutional\nchanges.  No mass effect or midline shift.  Patchy to confluent areas of T2\nand FLAIR hyperintense signal abnormalities in the periventricular and\nsubcortical white matter are nonspecific, but likely reflect chronic small\nvessel ischemic changes.  There is a chronic infarct in the left centrum\nsemiovale.\n\nThe paranasal sinuses and mastoid air cells are grossly clear.  Postsurgical\nchanges of left lens replacement.\n\nThere is a small focus of restricted diffusion within the left parietal bone\n(302:24) with high signal on FLAIR and T2 weighted images measuring\napproximately 8 mm.  This was also visualized on the recent CT.\n\nMRA BRAIN:\n Examination is moderately degraded by motion.\n\nThe intracranial vertebral and internal carotid arteries and their major\nbranches demonstrate grossly normal flow signal without convincing evidence of\nfocal stenosis or aneurysm formation.",
            "output": "1. Acute infarction in the left postcentral gyrus extending into the left\nparietal lobe.\n2. Small scattered focal infarcts in the right frontal, right parietal, left\nposterior temporal, and right cerebellum.\n3. No evidence of intracranial hemorrhage.\n4. Limited MRA of the head with no focal stenosis or evidence of aneurysm\nformation.\n5. Mild cerebral atrophy and moderate to extensive chronic small vessel\nischemic disease.\n6. Less than 1 cm left parietal bone abnormality suspicious for lymphoma\ndeposit or metastatic disease in correlation with the clinical history."
        },
        {
            "input": "There is no evidence of intracranial hemorrhage, edema, masses, mass effect,\nmidline shift or infarction.   The ventricles and sulci are normal in caliber\nand configuration.  No diffusion abnormalities are detected. There is no\nabnormal enhancement after contrast administration.  The visualized vascular\nflow voids are patent.  The major dural venous sinuses are patent, with no\nevidence of dural venous sinus thrombosis.  There is small mucous retention\ncyst in the left maxillary sinus, otherwise the paranasal sinuses mastoid air\ncells are clear.  The globes and orbits are unremarkable.  There is no\nabnormal marrow signal.",
            "output": "1. Unremarkable brain MRI.  No evidence of an acute infarct, intracranial\nmass, or hemorrhage.\n2. No evidence of dural venous sinus thrombosis."
        },
        {
            "input": "Axial FLAIR sequence is somewhat motion degraded.\n\nTiny extra-axial dural-based enhancing lesion at the vertex on the right is\nagain seen.  It measures 6 mm TRV by 6 mm cc, similar compared to prior exam\nfrom ___.  This is compatible with a meningioma.  There is no significant\nmass effect or underlying edema.\n\nSingle periventricular white matter T2/FLAIR hyperintensity in the right\nfrontal lobe is unchanged.  There is no associated enhancement nor restricted\ndiffusion.  No new parenchymal signal abnormality.\n\nNo additional abnormal enhancement identified. There is no acute infarct. No\nevidence of hemorrhage.\n\nFluid noted within the left mastoids.  There is mucosal thickening in the\nmaxillary sinuses and right ethmoid air cells.  Remaining paranasal sinuses\ndemonstrate no abnormal signal.",
            "output": "1. Unchanged subcentimeter extra-axial enhancing lesion at the vertex on the\nright compatible with a meningioma.\n2. Single nonspecific periventricular white matter T2/FLAIR hyperintensity in\nthe right frontal lobe.  No new parenchymal signal abnormality."
        },
        {
            "input": "MRA brain: The intracranial vertebral and internal carotid arteries and their\nmajor branches appear normal without evidence of stenosis, occlusion, or\naneurysm formation.\n\nMRA neck: Evaluation of the proximal neck is severely limited by motion\nartifact and the right brachiocephalic, origins of the common carotid and\nvertebral arteries are poorly evaluated.  Within this limitation, the\nvisualized common,internal and external carotid arteries appear normal.  There\nis no evidence of stenosis by NASCET criteria. The right\nbrachiocephalic,subclavian,and vertebral arteries appear grossly normal\nbilaterally.  The common carotid bifurcations appear normal.",
            "output": "1. Examination of the proximal neck vessels is severely limited by motion\nartifact.  Within this limitation, the right brachiocephalic artery, origins\nof the bilateral common carotid and vertebral arteries are grossly patent. \nThe remainder of the visualized cervical vessels are unremarkable.  There is\nno stenosis of the cervical internal carotid arteries by NASCET criteria.\n2. The cervical of ___, and their principal intracranial branches appear\nnormal without stenosis, occlusion, or aneurysm formation."
        },
        {
            "input": "There is no evidence of acute infarction or intracranial hemorrhage.  The\nventricles and sulci are age-appropriate.  There is no mass-effect or midline\nshift.\n\n Multiple scattered T2 and FLAIR hyperintense foci in the periventricular and\nsubcortical white matter are nonspecific, but likely reflect chronic small\nvessel ischemic changes.\n\nMinimal mucosal thickening of the ethmoid sinuses.  Mastoid air cells are\nclear.  Unremarkable intraorbital contents.  The major intracranial arterial\nand venous flow voids are preserved.",
            "output": "1. No acute infarction or intracranial hemorrhage.\n2. Probable findings of chronic small vessel ischemic disease."
        },
        {
            "input": "Study is mildly degraded by motion.  There is minimal irregularity of the\ndistal left common carotid artery without significant narrowing, consistent\nwith atherosclerotic disease.  There is mild irregularity at the right carotid\nbifurcation consistent with atherosclerotic disease with 30% narrowing of the\nright internal carotid artery by NASCET criteria.  There is no significant\nnarrowing of the left internal carotid artery by NASCET criteria.  The common,\ninternal and external carotid arteries otherwise appear patent without\nhigh-grade narrowing or occlusion.  The origins of the great vessels,\nsubclavian, and vertebral arteries appear normal bilaterally.  The common\ncarotid bifurcations appear normal.",
            "output": "1.  Study is mildly degraded by motion.\n2. 30% stenosis of the right internal carotid artery by NASCET criteria.\n3. Otherwise patent cervical arterial vasculature without evidence of\nhigh-grade stenosis, occlusion or dissection."
        },
        {
            "input": "Examination is limited due to susceptibility artifact in the left frontal and\nbiparietal regions.\n\nMR BRAIN:\nA large intraparenchymal hematoma in the left frontoparietal lobes is not\nsubstantially changed compared to prior CTs given differences in modalities. \nThe intraparenchymal hematoma measures 8 x 4 cm in maximal axial ___. \nThe intraparenchymal hematoma demonstrates a fluid-fluid level with a majority\nrepresenting layering blood products and a small amount of CSF.  There is\nmoderate surrounding vasogenic edema.  There is associated effacement of the\noverlying sulci and mild mass effect of the left lateral ventricle. \nApproximately 4 mm of left-to-right midline shift.\n\nCurvilinear areas of apparent restricted diffusion along the periphery of the\nhematoma may relate to compressive/ischemic affects.\n\nAdditionally there is a small amount of hemorrhage in the posterior right\nfrontal and right temporal lobes, as demonstrated on the CT head.  No new\nareas of intracranial hemorrhage are identified.\n\nSmall right subdural fluid collection along the entire right cerebral\nconvexity and a small left subdural fluid collection along the left frontal\nconvexity are unchanged compared to prior CTs.\n\nNo definite underlying mass is visualized.  There is mild diffuse dural\nthickening and enhancement.  Otherwise, there is no evidence of abnormal\nenhancement.\n\nPostsurgical changes of right lens replacement.  Mild mucosal thickening of\nthe maxillary and ethmoid sinuses.  Near complete opacification of the left\nsphenoid sinus.  The mastoid air cells are clear.\n\nMRA BRAIN:\nOn the provided images, no definite source of bleed is identified\ncorresponding to the left frontoparietal intraparenchymal hemorrhage.\n\nThere is a bulbous appearance of the basilar tip.  The intracranial vertebral\nand internal carotid arteries and their major branches appear normal without\nevidence of stenosis, occlusion, or aneurysm formation.",
            "output": "1. Overall stable left intraparenchymal hematoma in the left frontoparietal\nlobes with internal fluid fluid levels.\n2. Stable mass effect on the left lateral ventricle with approximately 4 mm of\nleft-to-right midline shift.\n3. Curvilinear areas of apparent restricted diffusion along the periphery of\nthe hematoma may relate to compressive/ischemic affects.\n4. Additional scattered areas of hemorrhage in the right frontal and right\ntemporal lobes are unchanged.  No new areas of intracranial hemorrhage.\n5. Stable subdural fluid collections are on the right cerebral convexity and\nleft frontal regions.\n6. No definite underlying mass in the region of the intraparenchymal\nhemorrhage.  Recommend follow-up to resolution to definitively assess for\nunderlying mass.\n7. No definite source of bleed identified corresponding to the left\nfrontoparietal intraparenchymal hemorrhage.  Given small subtle areas of\nhemorrhages adjacent to the main hematoma on GRE images (08:17) this could be\nrelated to amyloid angiopathy.\n8. Patent circle of ___ with no focal stenosis or evidence of aneurysm\nformation."
        },
        {
            "input": "The left lateral nasal mass that extends superiorly to the medial canthus\nappears larger than on the prior CT. This demonstrates heterogeneous low\nsignal intensity on the T1 weighted images and heterogeneous high signal\nintensity with several foci of apparent necrosis on the T2 weighted images.\nThe fluid filled areas on the T2 weighted image do not demonstrate\nenhancement. Otherwise, the lesion enhances in a heterogeneous fashion.\n\n\nIn the interval since the prior examination, the patient has undergone a left\nmodified radical neck dissection.  The large nodal mass noted on the prior CT\nhas been removed.  Imaging does not extend through the entire limits of the\nneck dissection.  Two small left level 1 nodes, measuring 8 and 3 mm in short\naxis dimension respectively, are identified.  Allowing for differences in\ntechnique, these appear somewhat larger than on the study of ___.\n\nAgain seen is mucosal thickening and loculated fluid in the left maxillary\nsinus.  This appears more prominent than on the prior study.  There is partial\nopacification of the ethmoid air cells bilaterally.",
            "output": "1. Left lateral nasal mass extending to the medial canthus appears larger than\non the study of ___.\n2. There has been an interval left modified radical neck dissection with\nremoval of the large nodal mass in ___. Two small level 1 lymph nodes just to left of midline appear somewhat\nlarger than on the prior study."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.",
            "output": "1. Normal brain MRI."
        },
        {
            "input": "The study is severely degraded by motion artifact.  This greatly limits\nsensitivity for abnormalities potentially causing seizures.  There is no\nevidence of hemorrhage, edema, masses, mass effect, midline shift or\ninfarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.\n\nWithin the limitations noted above, the bilateral hippocampal formations and\nmammillary bodies are preserved in signal and configuration. There is no\ndisproportionate medial temporal atrophy.",
            "output": "1. No abnormalities detected.  However, image quality is severely degraded by\nmotion artifact.  Sensitivity would be low for focal cortical dysplasia."
        },
        {
            "input": "3D FLAIR images are moderately motion degraded, limiting contribution from the\nseries, decreases sensitivity in detection of cortical dysplasia.  Other\nseries are diagnostic quality.\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.\n\nSuggestion of mild posterior left hippocampal atrophy, formal volumetric\nanalysis would be helpful to compared to the right side.  No hippocampal\nsignal abnormality.  Otherwise, bilateral hippocampal formations and\nmammillary bodies are preserved in signal and configuration.  Symmetric\nfrontal horns, collateral white matter remainder of the temporal lobe is not a\ntrophic.  There is no focal lobar encephalomalacia. There are no focal\ncortical dysplasias or gray matter heterotopia noted.",
            "output": "1. Suggestion of mild atrophy posterior left hippocampus.  Formal volumetric\nanalysis would be helpful to compare with right side.\n2. Motion compromised 3D FLAIR images, limiting sensitivity in detecting\nsubtle focal cortical dysplasia."
        },
        {
            "input": "There is motion artifact which limits evaluation.  Within these confines:\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are preserved in caliber and\nconfiguration.  Few bifrontal and left parietal T2 and FLAIR hyperintense\nlesions are noted.  These lesions do not have definite associated restricted\ndiffusion or increase susceptibility.\n\nLimited imaging of the parotid glands demonstrate bilateral subcentimeter\nnonspecific probable lymph nodes.",
            "output": "1.  No acute intracranial abnormality.\n2. Within limits of study, no definite evidence of intracranial mass.\n3. Nonspecific supratentorial white matter lesions as described.  Differential\nconsiderations include sequela of prior trauma or infection, history of\nmigraine headaches, inflammatory or demyelinating process, and\nmicroangiopathic changes.  If concern for active demyelinating process,\nconsider contrast enhanced brain MRI for further evaluation."
        },
        {
            "input": "There is no evidence of intracranial hemorrhage, edema, masses, mass effect,\nmidline shift or infarction.   The ventricles and sulci are normal in caliber\nand configuration.  Major intracranial vascular flow voids are preserved.  The\norbits are within normal limits.  There is mild mucosal thickening in the\nethmoid and sphenoid sinuses.",
            "output": "No evidence of infarction, mass, or hemorrhage."
        },
        {
            "input": "No acute infarct, suspicious focus of intracranial hemorrhage, mass effect,\nshift of normally midline structures or hydrocephalus.\nThere are no obvious focal lesions noted on the routine FLAIR sequence.\nOn the postcontrast images, there is no abnormal enhancement noted in the\nbrain parenchyma or meninges.\nThe CSF in the Meckel's caves, the intracranial portions of the trigeminal\nnerves and seventh and eighth nerve complexes in the internal auditory canals\non both sides appear unremarkable on the routine sequences.\nA venous tributary, is in proximity to the cisternal portion of the left\ntrigeminal nerve series 13, image 7. This can represent normal anatomy and the\nclinical significance is uncertain in particular on the routine study.\n\nThe ventricles, extra-axial CSF spaces, cerebral sulci and cerebellar folia\nare normal.\nThe major intracranial arterial flow voids are noted.\nLeft vertebral artery is dominant with a diminutive right vertebral artery.\nVenous sinuses are unremarkable\nSella and craniocervical junction regions are unremarkable.  A small 4 mm\npineal cyst noted without mass effect.\n\nThere is mild to moderate ethmoidal mucosal thickening.\nA retention cyst noted in the right maxillary sinus.\nThe mastoids are clear.\nMildly prominent palatine tonsils right more than left on the coronal\npostcontrast sequence, inadequately assessed as not targeted.\n\nThe imaged orbits are unremarkable.\nBone marrow signal is unremarkable.",
            "output": "1.  No acute infarct or mass effect or enhancing lesions in the brain\nparenchyma or meninges.  No obvious focal lesions on the routine axial FLAIR\nsequence to suggest demyelinating lesions.\n2. The CSF in the Meckel's caves, the intracranial portions of the trigeminal\nnerves and seventh and eighth nerve complexes in the internal auditory canals\non both sides appear unremarkable on the routine sequences. However, dedicated\nthin section Spine echo  imaging is not performed on the present routine\nstudy.\nCorrelate clinically and if necessary dedicated thin section MR\nimaging(MS/IAC/Trigeminal Neuralgia protocol) or followup can be considered.\n3.  Small 4 mm pineal cyst without mass effect\n4.  Mild to moderate ethmoidal mucosal thickening and right maxillary sinus\nretention cyst."
        },
        {
            "input": "MRA brain: The intracranial vertebral and internal carotid arteries and their\nmajor branches appear normal without evidence of stenosis, occlusion, or\naneurysm more than 3 mm within the resolution of the study.\nTiny outpouching like appearance seen inferiorly from the left cavernous\ncarotid segment on the MIPS reformations series 403, image 2 is not\nconvincingly identifiable on the source images. It is unclear if this relates\nto a tiny aneurysmal appearance or related to a branch vessel.\n\nThe left vertebral artery is dominant.\nRight vertebral artery is diminutive, and not well seen of to the origin of\nthe right posterior inferior cerebellar artery, representing effective plica\ntermination.\n\n\nMRA neck:\n\nThe common, internal and external carotid arteries appear normal.  There is no\nevidence of stenosis by NASCET criteria.  The origins of the great vessels,\nsubclavian and vertebral arteries appear normal bilaterally.\nOn the axial T1 fat sat sequences, slightly altered signal intensity through\nthe left common carotid, left internal carotid arteries and the left internal\njugular ___ relate to flow related phenomenon or inadequate fat\nsuppression.\n\nVallecular retention cysts are incidentally noted.",
            "output": "1.  Patent major intra and extracranial arteries as described above without\nfocal flow-limiting stenosis or occlusion.\n2. Tiny outpouching like appearance seen inferiorly from the left cavernous\ncarotid segment on the MIPS reformations is not convincingly identifiable on\nthe source images. It is unclear if this relates to a tiny aneurysmal\nappearance or related to a branch vessel.\nCorrelate clinically to decide on the need for further imaging workup or\nfollowup."
        },
        {
            "input": "There is a left suprasellar aneurysm clip and gliotic changes in left temporal\nlobe from prior surgery. There is evidence of a left frontotemporal\ncraniotomy. No large territorial infarction is seen. A few scattered presumed\nsmall vessel ischemic changes is seen in the bifrontal white matter.\nCerebellar tonsils are low-lying.\n\nThere is no acute infarction, intracranial hemorrhage, extracerebral fluid\ncollection, midline shift or mass effect.  The cerebral volume is appropriate\nfor the patient's stated age.  Flow voids are maintained.\nNo significant change from prior examination.",
            "output": "No evidence for large territorial infarction. Postsurgical changes as\ndescribed."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  Findings consistent with moderate chronic small vessel\nischemic changes.  Mild generalized brain parenchymal atrophy.  Small benign\nmucosal retention cyst posterior nasopharynx.  Intracranial vascular flow\nvoids are preserved.  Clear paranasal sinuses, mastoids.  No abnormal\nenhancement.  Dural venous sinuses are patent.",
            "output": "No acute findings.\nBrain parenchymal atrophy.\nFindings consistent with moderate chronic small vessel ischemic changes."
        },
        {
            "input": "There is no evidence of parenchymal hemorrhage, edema, mass effect, midline\nshift or infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.\nThere is linear extra-axial isointense T1, increased T2 signal abnormality\nwith mild enhancement overlying bilateral frontal, parietal lobes at the\nvertex, and lateral frontal, temporal lobe, posterior left parietal lobe, with\nlinear areas of associated enhancement.  No associated blooming on gradient\nimages.\nParanasal sinuses, mastoids are clear.  Intracranial vascular flow voids are\npreserved.\nDegenerative changes in the partially seen cervical spine, mild\nanterolisthesis C2-C3, C3-C4, likely degenerative.\nThere is inhomogeneous T1 signal throughout calvarium, with probable\npreservation of central ___ represent red marrow conversion/treatment\nrelated change or diffuse marrow infiltration.  2 foci of enhancement, 1 at\nright occipital condyle measuring 1.0 cm, second 0.7 cm focus of enhancement\nat C4 vertebral body, worrisome form osseous metastases.",
            "output": "2 foci of osseous metastases.\nNo brain parenchymal metastases.\nLinear dural thickening and enhancement overlying bilateral cerebral\nhemispheres, may represent sequela of subacute subdural hematoma, dural\nmetastatic disease cannot be excluded.  Less likely differential\nconsiderations include inflammatory process, infection.  Recommend head CT\nwithout contrast in further evaluation, or follow-up MRI to document\nresolution.  There is no leptomeningeal enhancement.\n\nRECOMMENDATION(S):  Head CT without contrast.\n\nNOTIFICATION:  The findings were discussed with ___, M.D. by\n___, M.D. on the telephone on ___ at 3:16 pm, 5 minutes\nafter discovery of the findings."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.\n\nA mucous retention cyst is seen in the left maxillary sinus.  There is\nmoderate mucosal thickening of the ethmoid sinuses.  The mastoid air cells are\nclear.  The intraorbital contents are normal.",
            "output": "1. No acute infarct or intracranial hemorrhage.\n2. Moderate sinus disease."
        },
        {
            "input": "The area of restricted diffusion in the medial aspect of the right thalamus\nseen on the prior study in ___ is no longer demonstrated on today's\nexam. There is now residual persistent T2 and FLAIR hyperintense signal in\nthis region, compatible with CSF, indicating a chronic lacune (7:13). There\nare no new areas of restricted diffusion.\n\nThere is no acute intracranial hemorrhage, cerebral edema, or new infarction.\nNo parenchymal masses are seen. Ventricles and sulci are normal in size and\nconfiguration. Basal cisterns are patent. There is mild mucosal thickening\nwithin bilateral maxillary sinuses. Remainder of the visualized paranasal\nsinuses are clear. Previously seen T2 hyperintense signal in the right petrous\napex is no longer seen, suggesting that it may have been due to fluid at the\ntime.",
            "output": "Normal evolution of old right lacunar infarct.  No new infarcts or hemorrhage."
        },
        {
            "input": "There is no intracranial mass, mass effect, or midline shift.  Prominent\nventricles and sulci are suggestive of age-related involutional change.\nScattered areas of periventricular, subcortical and deep white matter T2/FLAIR\nhyperintensities are nonspecific, mildly increased compared to the prior study\nbut are in a distribution suggestive of chronic small vessel ischemia. The\nbasal cisterns are patent. The brainstem, posterior fossa and cervicomedullary\njunction are preserved. The orbits, periorbital and paracavernous spaces are\nunremarkable. There is no abnormality of the skull base or calvarium. There is\nno abnormal focus of slowed diffusion.  There is no abnormal focus of\nsusceptibility artifact. Intracranial flow voids are maintained.  There is\ntrace mucosal wall thickening in the bilateral ethmoid air cells. Visualized\nparanasal sinuses and mastoid air cells are otherwise clear.",
            "output": "1. No acute findings to explain persistent headache.\n2. Slight interval increase in the nonspecific white matter T2/FLAIR\nhyperintensities though they remain in a distribution most consistent with\nchronic small vessel ischemia in this age group."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  Redemonstrated are chronic lacunar infarcts in the right\nthalamus, left basal ganglia, and left corona radiata.  Extensive\nperiventricular and subcortical white matter T2 and FLAIR hyperintensities are\nnonspecific, but probably reflect sequelae of chronic small vessel ischemic\ndisease.  Prominence of ventricles and sulci is suggestive of a involutional\nchanges.\n\nThere is mild mucosal thickening in the maxillary sinuses and moderate mucosal\nthickening of the anterior ethmoid air cells bilaterally.  The imaged mastoid\nair cells are clear.  The orbits are unremarkable.",
            "output": "1. No evidence of hemorrhage, edema, masses or acute infarction.\n2. Multiple chronic lacunar infarcts, and white matter signal abnormalities\nwhich are most consistent with small vessel ischemic changes."
        },
        {
            "input": "Two heterogeneously enhancing lesions are noted in the left frontal lobe.\nThe larger lesion located medially, measures approximate 2.7 x3.4 x2.8 cm on\nwith a nonenhancing central component and irregular peripheral enhancement,\nwith nodularity.\nThe central component of the lesion is slightly smaller compared to the prior\nstudy.\nThere is also mild decrease in the peripheral enhancing component in\nparticular posteriorly and anterosuperiorly.\nThe smaller lesion located inferolateral to the larger lesion, measures\napproximately 2.5 x 1.3 x1.8 cm, with decrease in the enhancing peripheral\ncomponent and increase in the central nonenhancing component, likely necrosis.\nThis can relate to treatment related changes.\nModerate surrounding FLAIR hyperintense signal, related to edema, is decreased\nsince the prior study as also the mass effect.\n\nA small lesion is noted in the left medial temporal lobe, with associated\nincreased cortical thickness and edema, measuring approximately 0.8 x 0.9 cm,\nwith small central nonenhancing component; the lesion is mildly decreased in\nsize, with interval development of small amount of central necrosis.\nThis is in close proximity to the left middle cerebral artery.\nNo obvious new lesions are noted.\nStatus post left frontal craniotomy with adjacent postsurgical/post biopsy\nrelated changes.\n\nNo acute infarct, suspicious focus of intracranial hemorrhage, mass effect,\nshift of normally midline structures or hydrocephalus.\nThere are multiple small T2 FLAIR hyperintense foci in the cerebral white\nmatter in the frontal and parietal lobes and a few in the pons, nonspecific in\nappearance.\nThe ventricles, extra-axial CSF spaces, cerebral sulci and cerebellar folia\nare dilated/prominent related to volume loss.\nThe major intracranial arterial flow voids are noted; tortuous cavernous\ncarotid and vertebral segments.\nVenous sinuses are unremarkable.\nSella, pineal gland, craniocervical junction regions are unremarkable.\n\nThe imaged paranasal sinuses and the mastoid air cells are clear.\nThe imaged orbits are unremarkable.  S/p left lens replacement.\nBone marrow signal is unremarkable",
            "output": "Redemonstration of the heterogeneously enhancing lesions, 2 in the left\nfrontal lobe and 1 in the left medial temporal lobe as described above with\ninterval changes likely related to the treatment.\nCorrelate clinically to decide on the need for further imaging workup (MRS/MR\n___ for better assessment and followup."
        },
        {
            "input": "There is re- demonstration of previously described heterogeneous lesions in\nthe left frontal lobe, with heterogeneous nonenhancing central components, and\nnodular peripheral rim enhancement.  The medial larger lesion now measures\napproximately 2.7 x 3.7 x 2.1 cm, previously 2.7 x 3.4 x 2.8 cm (19:58,\n18:35).  The degree of peripheral enhancement and overall appearance of this\nlesion is not significantly changed.  The smaller, lateral lesion has similar\nenhancement characteristics, and now measures approximately 2.0 x 1.3 x 2.0\ncm, previously 2.5 x 1.3 x 1.8 cm (19:67, 18:42), slightly decreased in size\ncompared to the prior study.  A small enhancing lesion in the medial left\ntemporal lobe with surrounding FLAIR signal abnormality has decreased in size\nsince the prior study, now approximately 5 mm in greatest dimension,\npreviously 8 x 9 mm (19:46).  No new focus of enhancement is identified.\n\nNo acute infarct, intracranial hemorrhage, midline shift, or hydrocephalus is\nidentified.  Multiple scattered T2/FLAIR signal hyperintensities in the\ncerebral white matter are nonspecific, as are previously seen basal ganglia\nenhancing foci, possibly small vessels.  Tortuousity of the cavernous portions\nof the bilateral interal carotid arteries is again noted.  Major intracranial\narterial flow voids are preserved.",
            "output": "1. Heterogeneously enhancing lesions in the left frontal and medial temporal\nlobes, as described above, with stable size of the largest lesion, and\ninterval decrease of the smaller lesions since the prior study.\n2. No new enhancing intracranial lesion is identified."
        },
        {
            "input": "Multiple, heterogeneous, enhancing lesions are again noted within the left\nfrontal and temporal lobes.  The larger, more medial lesion in the left\nfrontal lobe now measures 3.0 x 3.0 x 1.9 cm (1001b:113, 1000b: 95),\npreviously measuring 2.7 x 3.7 x 2.1 cm on the prior examination dated ___.  Gradient echo susceptibility and intrinsic T1 hyperintense signal\ncompatible with blood product associated with this lesion is unchanged.  The\nmore lateral lesion within the left temporal lobe now measures 2.4 x 1.5 x 2.0\ncm (1001b:128, 1000b:  110), previously measuring 2.0 x 1.3 x 2.0 cm.  Both of\nthese lesions again demonstrate restricted diffusion.  A small focus of\nenhancement with mild surrounding T2/FLAIR hyperintense signal is again noted\nwithin the medial left temporal lobe, now measuring 6 mm (1001b:99),\npreviously measuring 5 mm. There are no new, enhancing intracranial lesions\nidentified.\n\nThere is no evidence of acute intracranial hemorrhage, midline shift, or\ncerebral ischemia. A likely chronic infarct in the left parietal lobe is\nunchanged. The ventricles and sulci are grossly unremarkable in size and\nconfiguration.  Periventricular and subcortical white matter T2/FLAIR\nhyperintensities are noted, likely the sequelae of chronic small vessel\nischemic disease.  No overt osseous lesion is identified. The paranasal\nsinuses, middle ear cavities, and mastoid air cells are clear. The bilateral\norbits are unremarkable in appearance. The major intracranial flow voids are\npreserved.",
            "output": "1.  Heterogeneous, enhancing lesions within the left frontal and medial\ntemporal lobes, as described above, which are essentially unchanged in size\nand morphology as compared to the prior examination dated ___,\nallowing for differences in measurement technique.\n2.  No new, enhancing intracranial lesion is identified."
        },
        {
            "input": "There is increased T2 signal intensity within the bilateral substantia nigra,\nprimarily on the left.  There is prominence of the ventricles and cerebral\nsulci suggestive of global parenchymal volume loss, predominantly in the\nmedial temporal lobes bilaterally.  There are periventricular and subcortical\nwhite matter foci of T2/FLAIR hyperintensity, nonspecific but may reflect\nsequelae of chronic microangiopathy.  There is no evidence of hemorrhage,\nedema, masses, mass effect, midline shift or infarction.\n\nThere is mild mucosal thickening in multiple ethmoid air cells.  No\nsignificant fluid signal is seen in the mastoid air cells.  The major\nintracranial flow voids are preserved.  The visualized orbital structures are\nunremarkable.",
            "output": "1. Increased T2 signal intensity in the bilateral substantia nigra,\npredominately on the left.  This may be related to imaging technique or\nrelated to given history of parkinsonism.\n2. Global parenchymal volume loss, particularly involving the bilateral medial\ntemporal lobes.\n3. Periventricular and subcortical white matter signal changes may represent\nsequelae of chronic ischemic microvascular disease."
        },
        {
            "input": "Mild brain atrophy is identified. There is no evidence of midline shift, mass\neffect or hydrocephalus. FLAIR hyperintensities predominantly in the\nsubcortical and deep white matter of both cerebral hemispheres to indicate\nmoderate changes of small vessel disease. No evidence of chronic micro\nhemorrhages. No acute infarcts are seen. Following gadolinium administration\nthere is no evidence of abnormal parenchymal, vascular and meningeal\nenhancement seen.\n\nAlthough the study is not focused on the orbits or in the region of optic\nnerves, there is no obvious compression of the optic chiasm identified or\nintraorbital mass lesion seen.\n\nA small retention cyst is seen in the left maxillary sinus.",
            "output": "Moderate changes of small vessel disease. No enhancing brain lesions are\nidentified.  No obvious optic chiasm compression or intraorbital mass lesion\nidentified on this brain MRI study."
        },
        {
            "input": "There is no abnormal enhancement.  There is no diffusion abnormality.  There\nis no evidence of hemorrhage, edema, or masses.  Major intracranial flow voids\nare preserved.  The ventricles and sulci are grossly unchanged compared to CT\nhead dated ___.  Scattered area of T2/FLAIR hyperintensity along the\nbilateral centrum semiovale nonspecific but likely due to chronic small vessel\nischemic disease, similar to MR ___ from ___.  The dural venous\nsinuses are patent.\n\nThere is small amount of fluid in the bilateral mastoid air cells.  The\nremaining paranasal sinuses are clear.  The patient is status post right lens\nreplacement.  Otherwise the bilateral orbits are unremarkable.",
            "output": "1. No evidence of intracranial metastatic disease.  No change from the\nprevious MRI examination."
        },
        {
            "input": "There is no evidence of acute infarction.  No intracranial hemorrhage.  No\nmass, mass effect, edema or midline shift.\n\nThe ventricles and sulci are prominent.  Periventricular and subcortical white\nmatter T2/FLAIR hyperintensities are noted, likely the sequelae of chronic\nsmall vessel ischemic disease. The basal cisterns are patent.  There is gross\npreservation of the principal intracranial vascular flow voids.  Note is made\nof a partial empty sella, unchanged.\n\nFollowing the administration of intravenous contrast material, there is no\nabnormal enhancement.  The dural venous sinuses appear patent on MP-RAGE\nimagine sequences.\n\nTrace fluid is noted in the bilateral mastoid air cells.  The remainder of the\nvisualized paranasal sinuses and middle ear cavities are well aerated and\nclear.  The patient is status post right lens resection.",
            "output": "1. No evidence for intracranial metastatic disease at this time.\n2. Chronic findings of global cerebral atrophy and the sequelae of chronic\nsmall vessel ischemic disease.\n3. Additional findings as described above."
        },
        {
            "input": "Previously seen left tentorial leaf en-bloc meningioma extending and involving\nthe left cavernous sinus is not significantly changed in appearance and size\ncompared to the prior study.  There is no acute infarcts seen.  Mild changes\nof small vessel disease are noted.  Postoperative changes in the right\nmaxillary sinus are again seen.",
            "output": "Stable appearance of previously seen left tentorial meningioma compared with\nthe prior MRI of ___.  No significant new abnormalities."
        },
        {
            "input": "There is no intra or extra-axial mass, acute hemorrhage or infarct. Sulci,\nventricles and cisterns are within expected limits for the degree of\nage-appropriate global cerebral volume loss. There are confluent\nperiventricular and subcortical periventricular white matter FLAIR/ T2\nhyperintensities, which are nonspecific, but commonly seen in setting of small\nvessel ischemic disease. The major intracranial flow voids are preserved. The\ndural venous sinuses are patent. There is no abnormal enhancement.\n\nNear-complete opacification of the frontal sinuses and right maxillary sinus\nas well as partial opacification of the ethmoid air cells are noted. The\nmastoid air cells are essentially clear. The orbits are unremarkable.\n\nLeft parietal scalp resection defect is unchanged from prior exam. There are\nno suspicious osseous lesions.",
            "output": "1. No evidence of intracranial metastatic disease. No acute infarct or\nhemorrhage.\n2. Sinus disease as described above.\n3. Left parietal scalp resection defect is unchanged from prior CT."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, midline shift or infarction.   The\nventricles and sulci are normal in caliber and configuration.  A couple of\nsmall, punctate T2 and FLAIR periventricular and deep white matter T2 and\nFLAIR hyperintensities are nonspecific, likely mild chronic small vessel\nischemic changes.  3 subcutaneous lesions in the posterior scalp soft tissues\nbeing T1 Iso and T2 hypointense, most likely representing sebaceous cysts. \nProminent falx calcification in the frontal area.  The orbits appear normal. \nThe paranasal sinuses are essentially clear. The intracranial arteries\ndemonstrate normal T2 flow void.  Fluid present in the right mastoid air\ncells.  No nasopharyngeal mass.",
            "output": "1. No infarct, intracranial mass or hemorrhage.\n2. A couple of small, punctate parenchymal T2 hyperintensities are\nnonspecific, likely represent mild chronic small vessel ischemic changes."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  A few scattered white matter T2 and FLAIR hyperintensities are\nnonspecific, but most likely represent sequela of microangiopathy.  The\nventricles and sulci are normal in caliber and configuration.  There is no\nabnormal enhancement after contrast administration.  The pituitary appears\nnormal.  The craniocervical junction is normal.  Mild mucosal thickening\ninvolving the paranasal sinuses.  Mucous retention cyst present in the\ninferior aspect of the maxillary sinus bilateral (left more than right) nasal\nseptal deviation to the right.  The orbits appear normal.  The intracranial\narteries demonstrate normal T2 flow void.  The dural venous sinuses are\npatent. The CP angles appear normal.  Partial opacification of the mastoid air\ncells (right more than left).",
            "output": "1. No evidence of intracranial metastatic disease at this time.\n2. No intracranial mass, hemorrhage or infarct.\n3. Very few scattered white matter T2 and FLAIR hyperintensities are\nnonspecific, but most likely represent sequela of microangiopathy and is of\ndoubtful clinical significance.\n4. Paranasal sinus disease as described above.  Partial opacification of the\nmastoid air cells bilaterally."
        },
        {
            "input": "No intra or extra-axial mass, acute hemorrhage or infarct. There is global\ncerebral volume loss, unchanged from prior CT examination of ___, greater\nthan would be expected for the patient's age. There is prominence of the\nventricles and sulci, however within expected limits for the degree of volume\nloss. There are confluent periventricular, nonspecific T2/FLAIR\nhyperintensities, which may be seen in the setting of chronic small vessel\nischemic disease. Small focus of coronal radiata encephalomalacia and gliosis\nis noted. Gradient echo susceptibility artifact of the bilateral cerebral\nhemispheres as well as of the left basal ganglia is seen, likely representing\nprior small micro hemorrhages. The major flow voids are preserved. The\nparanasal sinuses are clear. Note is made of bilateral lens replacements.\nOtherwise, the orbits are unremarkable. Fluid signal within the bilateral\nmastoid air cells is also seen.",
            "output": "1.  No findings to suggest PRES or regions of acute infarct.\n\n2.  Confluent nonspecific periventricular white matter changes as described\nabove, which may be seen in setting of small vessel ischemic disease.\n\n3.  Sequela of micro hemorrhages in the bilateral cerebellar hemispheres, as\nwell as the left basal ganglia and small focus of right frontal\nencephalomalacia as described above."
        },
        {
            "input": "There is no intracranial hemorrhage. Diffusion weighting imaging does not\ndemonstrate evidence of acute infarct. Gray white matter differentiation is\nmaintained. Ventricles and extra axial spaces are within normal limits.\n\nNo enhancing mass is identified. There is no abnormal meningeal enhancement.\nThe paranasal sinuses and mastoid air cells demonstrate normal signal. The\nmajor intracranial vessels exhibit the expected signal void related to\nvascular flow. The sella turcica, craniocervical junction, and orbits are\nunremarkable.",
            "output": "Normal MRI examination of the brain."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.  There are scattered white matter hyperintensities on FLAIR. \nAlthough nonspecific, these are often attributed to chronic small vessel\nischemia.",
            "output": "1. No evidence of metastatic disease.\n2. Scattered white matter changes on FLAIR.\n3. Otherwise normal study"
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, or infarction.\nThe ventricles and sulci are normal in caliber and configuration. There is no\nabnormal enhancement after contrast administration.  A few scattered foci of\nT2 hyperintensity are seen in the subcortical white matter. The previously\nseen hyperintensity in the left parietal subcortical white matter is also\nnoted and likely due to small vessel disease. No abnormal enhancement is seen\nin this region. The there is no evidence of micro hemorrhages.  Subtle\nsusceptibility abnormality in the left posterior temporal region on series 10,\nimage ___ be artifactual.",
            "output": "A few subcortical hyperintensities in both cerebral hemispheres with\nperiventricular hyperintensities are nonspecific in nature and likely due to\nmild changes of small vessel disease. The previously seen left parietal\nabnormality also appears to be related to small vessel disease. No enhancing\nbrain lesions. No acute infarcts are seen. No mass effect or hydrocephalus."
        },
        {
            "input": "There is a hypointense focus in the left side of the clivus on the precontrast\nT1 weighted images.  This enhances after contrast administration.  Given the\nhistory of skeletal metastases, this presumably represents a metastasis.\n\nSagittal T1 weighted imaging of the head demonstrates marked hypointensity of\nthe C3 and C4 vertebral bodies on the right with extension of hypointensity\nalong the right pedicle and into the right lamina.  Given the history of\nmetastatic disease, these presumably represent osseous metastases.  This\nregion is not covered in the other images.\n\nThere is a faint area of hyperintensity on the T2 weighted images in the right\npons.  In retrospect, this was probably present on the study ___. \nThe appearance is nonspecific but perhaps a manifestation of chronic small\nvessel ischemia.\n\nImages of the remainder of the brain appear normal.  There is no evidence of\nhemorrhage, edema, masses, mass effect, midline shift or infarction.   The\nventricles and sulci are normal in caliber and configuration.  There is no\nabnormal enhancement after contrast administration.",
            "output": "1. Enhancing clival lesion, likely a metastasis.\n2. Lesions in the C3 and C4 vertebral bodies, likely due to metastases.\n3. Faint hyperintensity on T2 weighted images in the right side of the pons,\nprobably unchanged since the prior study.  This is nonspecific but may be a\nconsequence of small vessel ischemia.  It does not appear to represent a\nmetastasis."
        },
        {
            "input": "A left clival lesion measuring approximately 1 cm in diameter, with mild\ncortical remodeling and expansion is similar in size to most recent MRI\ncervical spine of ___, but increased in size from prior MRI head of\n___.  No definite soft tissue cortical breakthrough.  Additional\nosseous lesions involving the visualized upper cervical spine is also\nidentified, also similar to most recent MRI exam.  No definite new osseous\nlesions.  No evidence of intracranial metastatic disease at this time.  No\nsuspicious parenchymal FLAIR signal abnormality.  No acute infarct or\nintracranial hemorrhage.  The sulci, ventricles and cisterns are within\nexpected limits for the degree of mild senescent related global cerebral\nvolume loss.  The major intracranial flow voids are preserved.  The dural\nvenous sinuses are patent.  There is mild mucosal thickening of the paranasal\nsinuses.  The orbits are unremarkable noting bilateral lens replacements. \nThere is elongated AP dimension of the globes, compatible with axial\nmyopia/staphyloma.  No significant fluid signal is seen in the mastoid air\ncells.",
            "output": "1. A left clival lesion measuring approximately 1 cm in diameter demonstrates\nmild cortical expansion without definitive soft tissue breakthrough.  This\nlesion is similar in size to prior outside hospital MRI cervical spine of ___, but significantly increased in size since prior MRI head of ___.  No definite new osseous lesions.\n2. Additional osseous lesions of the upper cervical spine is also similar to\nrecent outside hospital exam.\n3. No evidence of intracranial metastatic disease at this time.\n4. No acute intracranial abnormality on contrast enhanced MRI brain.\n5. Additional findings as described above."
        },
        {
            "input": "Study is degraded by motion.  Within these confines:\n\nThere is no evidence of hemorrhage, edema, intracranial masses, mass effect,\nmidline shift or infarction.   The ventricles and sulci are prominent, likely\nreflecting age-related involutional changes.  There is no abnormal\nintracranial enhancement after contrast administration.  The visualized\nvascular flow voids are grossly preserved.  There is no dural sinus venous\nthrombosis.  There is mild thickening of ethmoid air cells, otherwise the\nparanasal sinuses and mastoid air cells are clear.  Status post bilateral lens\nreplacement.\n\nThere is grossly stable expansile left clival lesion, which measures\napproximately 1 cm in diameter, with associated cortical remodeling and\nexpansion. There is diffuse heterogeneous T1 hypointensity throughout the\nvisualized upper cervical spine consistent with metastatic disease, is grossly\nunchanged compared to prior cervical MRI.\n\nAn approximately 4 mm left parietal calvarial enhancing lesion that is new\ncompared to ___ and ___ prior exams is seen (see 1000:131;\n4, 9:13).  Question additional adjacent foci of marrow enhancement versus\nartifact (see 1001:54).\n\nAn approximately 4 mm pineal cyst is noted. Limited imaging of the parotid\nglands demonstrate bilateral subcentimeter nonspecific probable lymph nodes.",
            "output": "1.  Study is degraded by motion.\n2.  No acute intracranial abnormality, with no definite evidence of acute\ninfarct.\n3. New approximately 4 mm left parietal calvarial enhancing mass concerning\nfor additional metastatic lesion. Question additional adjacent foci of marrow\nenhancement versus artifact.\n4. Grossly stable approximately 1 cm expansile left clival lesion and upper\ncervical metastatic lesions compared to cervical MRI dated ___,\nbetter assessed on prior cervical MRI."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are age appropriate.  Note is made\nof an partially empty sella on the sagittal T1 weighted images.  No\nparenchymal signal abnormality. The principal vascular flow voids appear to be\nwell preserved.\n\nThe visualized paranasal sinuses, mastoid air cells, and middle ear cavities\nare clear.  The globes demonstrate AP elongation bilaterally most likely axial\nmyopia.  The patient is status post bilateral lens replacement surgery.",
            "output": "No evidence of intracranial mass or mass effect.  No acute intracranial\nabnormalities identified."
        },
        {
            "input": "There is no evidence of acute intracranial hemorrhage or mass effect.\n There is no evidence of acute infarct based on diffusion-weighted imaging.\nThere are several extensive subcortical and periventricular T2/FLAIR signal\nhyperintense foci throughout the bilateral cerebral hemispheres with\ninvolvement pericallosal regions and a small focus in the left medial\ncerebellar hemisphere series 401, image 52, the findings which are nonspecific\nthough compatible with patient's reported history of multiple sclerosis.\nThere is mild prominence of the lateral ventricles and some of the sulci at\nthe vertex, that can relate to mild brain parenchymal volume loss.  There is\nalso mild  thinning of the corpus callosum in the posterior part of the body.\n\nThere is no abnormal brain parenchymal or leptomeningeal enhancement to\nsuggest active demyelination or inflammatory disease.\nThere are normal vascular flow voids.\nThe orbits, skull base, and paranasal sinuses are unremarkable.\nRight cerebellar tonsil is slightly lower than the left, and just below the\nmargin of foramen magnum, question variant.\nLimited assessment of the optic nerves and  the upper cervical spinal cord is\nnot targeted.",
            "output": "1. No acute intracranial hemorrhage, mass effect, or acute infarct.\n2. Extensive subcortical and periventricular T2/FLAIR signal hyperintense\nlesions throughout the bilateral cerebral hemispheres and a small focus in the\nleft middle cerebellar hemisphere, the findings which are nonspecific though\ncompatible with patient's reported history of multiple sclerosis.  No priors.\n3. No abnormal brain parenchymal or leptomeningeal enhancement to suggest\nactive demyelination or inflammatory disease.\n\nRECOMMENDATION(S):  Follow-up as needed to assess for interval change."
        },
        {
            "input": "The intracranial vertebral and internal carotid arteries and their major\nbranches appear normal without evidence of stenosis, occlusion, or aneurysm\nformation.",
            "output": "1. Patent intracranial vasculature without significant stenosis, occlusion, or\naneurysm.\n2. No frank evidence of vascular malformation, though this was better assessed\non prior gadolinium-enhanced MR and CTA examinations of the head, where no\nmalformation was seen."
        },
        {
            "input": "There is no evidence of acute intracranial hemorrhage, mass, mass effect or\nlarge territorial infarction.  Ventricles and sulci are age appropriate.\n\nMild mucosal sinus thickening is seen involving the ethmoid air cells.  Mucous\nretention cysts are seen within the bilateral maxillary sinuses.  The mastoid\nair cells, and middle ear cavities are clear.  The globes are unremarkable. \nThe principal vascular flow voids appear to be well preserved.",
            "output": "1. No acute intracranial abnormalities identified."
        },
        {
            "input": "There is a 9 mm focus of enhancement just superior to the temporal horn of the\nleft lateral ventricle (series 14, image 11 and series 13, image 93.  There is\nno significant surrounding edema.  Medial to this, the posterior limb of the\nleft internal capsule, there is FLAIR and T2 hyperintense signal which\ntracking inferiorly to the pons (series 12, image 39 and series 11, image 13).\nThere is some increased diffusion-weighted signal along this tract, without\nlow ADC values.  This likely represents sequela of prior insult, and the\nappearance suggests Wallerian degeneration.  Bilateral hippocampal formations\nand mammillary bodies are preserved in signal and configuration.  There is no\nfocal lobar encephalomalacia. There is no gray matter heterotopia.\n\nAgain, there is extensive mucosal thickening involving bilateral maxillary and\nsphenoid sinuses, with incomplete opacification of the sphenoid sinuses and\nair fluid levels noted. Multiple retention cysts are noted in the bilateral\nmaxillary sinuses. Postsurgical change with injection material is again noted\nin the right orbit. Prominent T1 hyperintense signal in the posterior chamber\nwith mild postcontrast enhancement likely reflects left sided retinopathy.\n\nThere is no evidence of hemorrhage, edema, mass effect, midline shift or acute\nterritorial infarction.  No abnormal leptomeningeal enhancement.  The\nventricles and sulci appear slightly prominent suggesting mild cortical volume\nloss.  Major vascular flow voids and the dural venous sinuses are patent. \nPostsurgical changes are demonstrated in the orbits with unchanged right eye\nglobe vitreous injection, low signal is noted on the left eye globe, anterior\nto the optic disc, likely consistent with sequela of vitreous hemorrhage,\npreviously described in the clinical notes by Ophthalmology in ___.",
            "output": "1. Linear T2/FLAIR hyperintense region in the posterior limb of the left\ninternal capsule with extension into the pons likely represents sequela of\nprior insult and suggests Wallerian degeneration.\n2. 9 mm focus of enhancement just superior to the temporal horn of the left\nlateral ventricle without surrounding edema.  This appearance is nonspecific. \nRecommend follow-up MRI without and with contrast in 3 months to assess for\nstability.\n3. Severe sinus disease with evidence of ongoing inflammation on a background\nof possible nasal polyposis.\n\nRECOMMENDATION(S):   Recommend follow-up MRI brain without and with contrast\nin 3 months."
        },
        {
            "input": "There is mild enhancement along the suboccipital craniotomy site, in keeping\nwith postsurgical change.  There is no enhancing collection or slow diffusion\nto suggest an abscess.  The dural venous sinuses are patent.  There is stable\nsuperficial siderosis, on the gradient echo sequence, along the cerebellar\nfolia at the site of prior hemorrhage. There is no evidence of edema, masses,\nmass effect, midline shift or infarction.   The ventricles are stable in size\nand configuration.",
            "output": "1.  Stable postsurgical changes following suboccipital craniotomy.\n2.  No evidence of an enhancing lesion.\n3.  There is stable superficial siderosis, on the gradient echo sequence,\nalong the cerebellar folia at the site of prior hemorrhage"
        },
        {
            "input": "MRI BRAIN:\nPreviously seen T1 hyperintense cerebellar blood products have resolved. \nResidual hemosiderin deposition along the cerebellar folia at the site of\nprior hemorrhage, best seen on gradient echo images, limits evaluation for an\nunderlying cavernous malformation, but no evidence for cavernous malformation\nis seen on T2 weighted, T1 weighted, or other sequences.  There is no evidence\nfor an enhancing mass or abnormal blood vessels at the site of the prior\nhemorrhage.  There is no evidence for new blood products.  There is no acute\ninfarction or edema.  Major arterial flow voids are grossly preserved.  Dural\nvenous sinuses appear patent on postcontrast MP RAGE images.\n\nThere is mild mucosal thickening in the ethmoid air cells.\n\nMRA CIRCLE OF ___:\nThe intracranial vertebral and internal carotid arteries and their major\nbranches appear widely patent without evidence for flow-limiting stenosis or\naneurysm.  No enlarged proximal arterial branches are seen to suggest an\narteriovenous malformation.",
            "output": "1. Resolution of T1 hyperintense cerebellar blood products.  No evidence for\nan underlying mass or new blood products.\n2. Hemosiderin deposition along the cerebellar folia at the site of prior\nhemorrhage slightly limits evaluation for an underlying cavernous\nmalformation, but no evidence for a cavernous malformation is seen on other\nsequences.\n3. Unremarkable MRA of the circle of ___."
        },
        {
            "input": "There is no evidence of acute intracranial hemorrhage. The ventricles and\nbasal cisterns appear stable.\n\nThere are multiple new enhancing infratentorial lesions within the bilateral\ncerebellar hemispheres and within the cerebellar vermis.  The largest lesion\nin the left cerebellar hemisphere measures 0.8 cm transverse by 0.4 cm AP. A\npreviously seen large enhancing lesion within the cerebellar vermis no longer\ndemonstrates enhancement. Additionally, there are multiple new enhancing foci\nwithin the left cerebral hemisphere, including the left frontal lobe and left\ncentrum semiovale. A lesion within the left centrum semiovale demonstrates\nslow diffusion.  Enhancement along a sulcus in left medial parietal lobe\nsuggest leptomeningeal disease.\n\nThere are multiple new enhancing lesions within the calvarium compatible with\nskull metastases. The largest such lesion is within the frontal bone and\nmeasures 1.0 cm AP x 0.9 cm transverse.\n\nAreas of T1 hypointensity within the odontoid process and right lateral mass\nof C2 are again seen and likely compatible with osseous metastatic disease.",
            "output": "1. Multiple new infratentorial and supratentorial parenchymal metastases, as\nwell as multiple new osseous skull metastases, as described.."
        },
        {
            "input": "Compared to prior, there has been interval progression of disease. There are\nnumerous supratentorial and infratentorial lesions. While some of these\nlesions are stable for example the 4 x 5 mm left superior vermian lesion\n(19:80) and punctate left occipital enhancing lesion (19:50) and inferior\nright cerebellar 6 mm lesion (19:24). There has been interval enlargement of\nnumerous other lesions, specifically a medial left occipital lesion measuring\n8 x 13 mm (19:56) previously 5 x 8 mm, a lesion within the cerebellum on the\nleft currently 14 x 9 mm, previously 9 x 6 mm, and an inferior left frontal 8\nx 8 mm lesion (19:57) previously 5 x 6 mm. There is at least 1 new punctate\nlesion in the right frontal lobe (19:99).  Additional lesions are seen\nscattered throughout the cerebellum and bilateral cerebral hemispheres. There\nis evidence of leptomeningeal disease including within the left frontal region\n(19:87), right parietal region (19:85), left internal auditory canal and at\nthe left cerebellopontine angle (19:32). FLAIR signal hyperintensity seen in\nassociation with the lesions, some of which demonstrate T1 hyperintensity\nsuggesting blood products. There is no significant mass effect.\n\nThere is no acute infarct or midline shift. Ventricles and sulci are stable in\nconfiguration. Major intravascular flow voids including within the major dural\nvenous sinuses are preserved. Multiple calvarial metastases are again\nidentified.\n\nThe left mastoid air cells are entirely fluid filled. There is small amount of\nfluid in the right mastoids. Right frontal sinus and ethmoid air cell mucosal\nthickening is identified.",
            "output": "Interval progression of disease with multiple supra and infratentorial\nlesions. Some of them have remained stable since ___ although many\nhave enlarged and there is at least 1 new lesion."
        },
        {
            "input": "The patient's previously noted right frontal AVM is again seen.  There is no\nmidline shift and mild mass effect on the adjacent sulci.\nNo new lesions are visualized since the prior examination.",
            "output": "Stable appearance of the right frontal AVM.\nFiducial markers are in place."
        },
        {
            "input": "Incomplete exam, see technique above.\nSeverely motion degraded images.\n\nThe no midline shift, no hydrocephalus.  Diffusion-weighted images are not of\ndiagnostic quality, no large infarct.",
            "output": "1. Nondiagnostic, incomplete brain MRI exam."
        },
        {
            "input": "There are scattered periventricular and subcortical white matter FLAIR\nhyperintense foci in addition to central and dorsal pontine FLAIR\nhyperintensity, which are nonspecific but likely reflect sequela of chronic\nmicroangiopathy.  There is no acute infarct, hemorrhage, mass, or mass effect.\nThere is no abnormal parenchymal enhancement.  The ventricles and cortical\nsulci are normal in caliber and configuration.  The extra-axial spaces are\nunremarkable.  The vascular flow voids are preserved.\n\nThe left native lens is absent, otherwise the orbits are unremarkable.  The\ncalvarium and soft tissues are unremarkable.  There is mild mucosal thickening\nwithin the left maxillary sinus.  There is a left mastoid air cell effusion.",
            "output": "1. Nonspecific periventricular, subcortical, and pontine FLAIR hyperintensity,\nas described likely reflecting sequela of chronic microangiopathy.\n2. No acute intracranial abnormality without infarct, hemorrhage, or mass.  No\nevidence of metastatic disease."
        },
        {
            "input": "The previously seen 2.5 mm anterior communicating artery aneurysm directed\nanteriorly and superiorly is again seen on image 3:47, relatively unchanged\ncompared to the prior study.\n\nThe remaining intracranial vertebral and internal carotid arteries and their\nmajor branches appear normal without evidence of stenosis or occlusion. \nIncidentally seen are hypoplastic bilateral posterior communicating arteries.",
            "output": "1. Stable 2.5 mm anterior communicating artery aneurysm.\n2. Otherwise, unremarkable MRA of the brain noting the anatomic variants."
        },
        {
            "input": "Again demonstrated is an anteriorly and superiorly directed 2.6 mm anterior\ncommunicating artery aneurysm (3:68) which is increased in size compared to\nMRA brain performed ___, and grossly unchanged in caliber compared\nto at least ___. Incidental note is made of bilateral hypoplastic\nposterior communicating arteries.  Otherwise, the remaining intracranial\nvertebral and internal carotid arteries and their major branches appear normal\nwithout evidence of stenosis or occlusion.\n\nNo gross intracranial parenchymal abnormalities are identified on this limited\nexamination.\n\nThere is mild mucosal thickening of the right maxillary sinus and bilateral\nanterior ethmoid air cells.  The visualized globes are unremarkable.",
            "output": "1. 2.6 mm anterior communicating artery aneurysm is unchanged in appearance\nsince at least ___.\n2. Mild paranasal sinus disease involving the right maxillary and bilateral\nethmoid air cells."
        },
        {
            "input": "The left MCA M1/M2 calcified thrombus demonstrated on CTA from ___\nis unable to be appreciated on MRI. Major intravascular flow voids are\npreserved. No acute process is identified on water diffusion or ADC weighted\nimages. There is no acute intracranial hemorrhage or evidence of chronic blood\nproduct deposition. There is no extra-axial fluid collection. There is no mass\neffect or midline shift. Ventricles and sulci are normal in size and position.\n\nThere is no lesion of the brain stem, cerebellopontine angles, or cerebellum.\nThe calvarium is intact. The paranasal sinuses and mastoid air cells are\nclear. The orbits are normal.",
            "output": "1. No evidence of infarction.\n2. Left MCA vascular calcification and resultant stenosis demonstrated on\nrecent CTA are not appreciated by MRI."
        },
        {
            "input": "An 11 mm elongated focus of slow diffusion is seen within the right posterior\ninferior cerebellar hemisphere with associated FLAIR signal abnormality,\nimages 6:8, 17:7.\n\nPunctate foci of high signal on the diffusion tracer images in the right\nfrontal corona radiata (6;22), right occipital cortex (___) and right\nsuperior parietal cortex (___) demonstrate no definite correlate on the ADC\nmap or FLAIR sequences.\n\nA punctate focus of slow diffusion within the right precentral gyrus in the\nright frontal cortex, series 12, image 28 demonstrates associated FLAIR signal\nabnormality (17;22).  A punctate focus of slow diffusion in the left\nperiatrial white matter, series 12, image 15 demonstrates low signal on the\nADC map without a definite correlate on the FLAIR sequences.\n\nThere is no edema or mass effect.  There is no enhancing mass.  There is no\nevidence of intracranial blood products, allowing for susceptibility artifact\nfrom the parietal scalp at the vertex on gradient echo images (16:23, 18:2). \nVentricles and sulci are age appropriate.  Additional scattered punctate T2\nhyperintense foci in the periventricular and deep white matter of the cerebral\nhemispheres are nonspecific but likely sequela of mild chronic small vessel\nischemic disease in this age group.\n\nThere is mild asymmetric left medial temporal volume loss without evidence for\nassociated signal abnormality.  There is no evidence for focal lobar\nencephalomalacia, no focal cortical dysplasias, or gray matter heterotopia.\n\nPrincipal vascular flow voids are preserved.  Dural venous sinuses are patent\non postcontrast MP RAGE images.\n\nThere is minimal mucosal thickening in the ethmoid air cells.",
            "output": "1. Multiple small acute and subacute infarctions in bilateral cerebral\nhemispheres, and a small evolving acute infarction in the right posterior\ninferior cerebellar hemisphere, with the distribution suggesting embolic\netiology.\n2. Mild asymmetric left medial temporal volume loss without evidence for\nassociated signal abnormalities.  Please correlate with EEG findings given the\nhistory of seizures.\n\nNOTIFICATION:  The findings were discussed with ___ care NP\nChampagne by ___, M.D. on the telephone on ___ at 10:35 am, 2\nminutes after discovery of the findings."
        },
        {
            "input": "No evidence of hemorrhage, edema, masses, mass effect, midline shift or\ninfarction.  Ventricles and sulci are normal in caliber and configuration for\nthe patient's age.  No significant cerebral atrophy.  No abnormal enhancement\non post-contrast images.  Principal T2 flow voids are well preserved.  Dural\nvenous sinuses are patent.\n\nExtensive thickening of the anterior ethmoidal air cells.  Moderate right and\nmild left maxillary sinus mucosal thickening compatible with chronic\nsinusitis.  In addition there is an air-fluid level within the right maxillary\nsinus compatible with an acute component.  Mastoid air cells and orbits are\nunremarkable.",
            "output": "1. No acute intracranial abnormality on contrast enhanced MRI brain.  No\nsuspicious parenchymal FLAIR signal abnormality or enhancement.\n2. Acute on chronic sinusitis predominantly involving the right maxillary\nsinus as described above."
        },
        {
            "input": "There are small areas of slow diffusion in the left cerebellar peduncle and\ncerebellar hemisphere.  There is no evidence of associated hemorrhage and\nthese regions are not detectable on FLAIR imaging.  This finding suggests\nsmall areas of acute infarction.\nAgain seen is an old infarction involving the right putaminal and head of the\nright caudate nucleus, traversing the internal capsule.  There is no evidence\nof hemorrhage, edema, masses, mass effect, or midline shift.  Again seen is ex\nvacuo dilatation of the frontal horn of the right lateral ventricle.  The\nventricles and sulci otherwise are normal in caliber and configuration.",
            "output": "1. Small areas of infarction in the left cerebellar peduncle and cerebellar\nhemisphere without hemorrhage or abnormality on FLAIR.\n2. Unchanged chronic infarction involving the right putaminal, internal\ncapsule and head of the caudate nucleus."
        },
        {
            "input": "Evaluation for metastatic disease is suboptimal secondary to the lack of\nintravenous contrast. There is no obvious intracranial mass, mass effect, or\nmidline shift.  Mild cerebral atrophy with commensurate dilatation of the\nventricles and widening of the cortical sulci is present. There are linear\nareas of T2 and FLAIR prolongation within the pons which are likely the result\nof chronic small vessel ischemic disease. A chronic lacunar infarct is noted\nwithin the left thalamus. Prominent in CSF pulsation artifact is seen within\nthe third and fourth ventricles as well as within the pre pontine cistern.\nThere is no acute infarct or acute intracranial hemorrhage. A focus of\nsusceptibility within the left cerebellar hemisphere and a punctate focus of\nsusceptibility within the left parietal lobe without associated FLAIR\nhyperintensity likely represents chronic micro hemorrhages.\n\nIncidentally noted is ectasia of the left carotid terminus, and the A2\nsegments of both anterior cerebral arteries arise from a prominent right A1\nsegment.",
            "output": "1. No evidence for metastatic disease within the limitations of a non contrast\nexamination.\n2. Pontine signal abnormalities are most likely the sequela of chronic small\nvessel ischemic disease. Chronic left thalamic lacunar infarct.\n3. Two foci of susceptibility, likely representing chronic micro hemorrhages."
        },
        {
            "input": "Study is moderately degraded by motion, especially on MR angiography,\nespecially limiting evaluation of left proximal M2 vessels.  Within these\nconfines:\n\nMRI BRAIN:\nThere is no evidence of acute infarction.  A small, chronic infarct is noted\nwithin the right cerebellar hemisphere.  No mass effect, edema, or midline\nshift.\n\nSeveral punctate areas of susceptibility artifact on gradient echo sequences\nwithin the posterior right parietal (13:11, 15), and within the medial right\noccipital lobes (13:10), may represent the sequelae of prior microhemorrhage. \nThere is no evidence for acute infarction.\n\nThe ventricles and sulci are mildly prominent.  Periventricular white matter\nFLAIR hyperintensities are noted, likely the sequelae of chronic small vessel\nischemic disease.   The basal cisterns are patent.\n\nMild mucosal thickening is seen in scattered ethmoid air cells.  There is\nmucous retention cyst in the left maxillary sinus.  Trace fluid signal is seen\nin the left mastoid air cells.  The orbits are within normal limits\nbilaterally.\n\nMRA BRAIN:\nNonocclusive bilateral A1 irregularity is noted.  Nonocclusive irregularity of\nthe P1 segment is noted.  There is a fetal origin of the right posterior\ncerebral artery, and a trident configuration of the A2 vessels.  Otherwise,\nthe intracranial vertebral and internal carotid arteries and their major\nbranches appear patent without evidence of stenosis, occlusion, or aneurysm\nformation.\n\nMRA NECK:\nNoncontrast MRA examination of the neck is severely limited secondary to\npatient motion.  Allowing for this there is no high-grade stenosis or\nocclusion of the carotid or vertebral arteries.",
            "output": "1. Study is moderately degraded by motion.\n2. No evidence for acute intracranial hemorrhage or infarction.\n3. Small chronic right cerebellar hemisphere infarct.\n4. Multiple punctate likely chronic microhemorrhages, as described.\n5. Limited visualization of proximal left M2 inferior branch, which may be\nartifactual, with suggested flow within distal left MCA vessels.\n6. Nonocclusive irregularity of bilateral A1 and left P1 segment, which may\nrepresent atherosclerotic changes.  If clinically indicated, consider head CTA\nfor further evaluation.\n7. Otherwise grossly patent intracranial vasculature without high-grade\nstenosis, occlusion, or aneurysm.\n8. Severely motion degraded MRA examination of the neck especially limiting\nevaluation of bilateral carotid or vertebral artery origins.  Within limits of\nstudy, no definite evidence for vessel occlusion or severe stenosis.  If\nclinically indicated, consider neck CTA for further evaluation.\n9. Paranasal sinus disease and fluid signal within the left mastoid air cells,\nas above."
        },
        {
            "input": "Study is moderately degraded by motion.  Within these confines:\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  There is prominence of the ventricles and sulci suggestive\ninvolutional changes.  Periventricular and subcortical T2 and FLAIR\nhyperintensities are noted which may represent small vessel ischemic changes.\n\nMinimal nonspecific right greater than left mastoid fluid is present.  Minimal\nbilateral ethmoid air cell and maxillary sinus mucosal thickening is present. \nLeft globe lens replacement postsurgical changes are noted.",
            "output": "1. Study is moderately degraded by motion.\n2. No acute intracranial abnormality.\n3. Nonspecific global volume loss and probable microangiopathic changes as\ndescribed.\n4. Paranasal sinus disease and nonspecific bilateral mastoid fluid, as\ndescribed."
        },
        {
            "input": "There are at least 5 enhancing lesions which exhibit T1 iso to hypointensity\nand T2 hyperintensity scattered throughout the bilateral cerebral hemispheres\nwith the largest dominant lesions (9:109, 127) seen in the region of the\nposterior right superior frontal gyrus and posterior right inferior frontal\ngyrus.  The largest lesion at the posterior right frontal lobe measures 2.1 x\n1.8 x 1.6 cm (10:17, 3:21).  T2 FLAIR hyperintensity surrounding these lesions\nindicates perilesional vasogenic edema with resultant sulcal effacement along\nthe right convexity and right vertex.  No midline shift or ventricular\neffacement.\nThese 2 dominant lesions within the right hemisphere exhibit central\nsusceptibility artifact on gradient echo images indicating hemorrhagic masses,\nalthough the remaining enhancing lesions do not exhibit evidence of\nhemorrhage.  The other enhancing lesions are seen at the anterior right\nsuperior frontal gyrus (10:17), the right precentral gyrus (9:131), and the\nleft precentral gyrus (9:124).  Curvilinear, subcortical FLAIR hyperintensity\ndeep to the left supra marginal gyrus and superior temporal gyrus is\nnonspecific in does not exhibit enhancement.\n\nThe ventricles and sulci are normal in caliber and configuration. The\nparanasal sinuses are grossly clear.  Partial opacification of the left\nmastoid air cells is nonspecific but may be related to supine positioning.",
            "output": "1. Multiple enhancing lesions scattered throughout the bilateral cerebral\nhemispheres with 2 dominant hemorrhagic lesions with surrounding vasogenic\nedema in the right frontal lobe are consistent with metastases.\n2. Nonspecific subcortical FLAIR hyperintensity deep to the left supra\nmarginal gyrus and superior temporal gyrus does not exhibit enhancement,\nalthough given the clinical context, metastasis is difficult to exclude."
        },
        {
            "input": "The patient status post right parietal craniotomy for tumor resection.  Small\nvolume blood products at the surgical bed.  Surrounding edema is stable. \nThere is thin, linear postoperative segmental slow diffusion in the resection\nbed, with extension medially into right corona radiata and centrum semiovale. \nNo definite abnormal enhancement to suggest residual tumor in the resection\nbed.\n\nOther enhancing brain parenchymal lesions are again seen, there are consistent\nwith metastases.  There has been interval growth of few lesions.  Lesion in\nleft precentral gyrus, which measures 3.7 mm today, compared with 2 mm on ___.  Right medial precentral gyrus lesion, which measures 3.2 mm today\ncompared with 2.4 mm on recent comparison.  Lesion involving right centrum\nsemiovale is partially magic, with more prominent blood products since prior..\nAnterior right superior frontal gyrus lesion measures 4.2 mm today, compared\nwith 3.0 mm on prior\n\nThe ventricles and sulci are normal in morphology.  The dural sinuses appear\npatent.\n\nThe orbits are unremarkable.  There is mild ethmoidal mucosal thickening. \nOtherwise the paranasal sinuses are clear.  There is mild opacification of\nmastoid air cells on the right and moderate opacification the mastoid air\ncells on the left, similar to ___.",
            "output": "1. Status post right hemispheric tumor resection.  Mild volume surgical bed\nblood products.  No evidence residual tumor.  Restricted diffusion about\nsurgical cavity extends into the right centrum semiovale, corona radiata, may\nrepresent postsurgical changes or infarct.\n2. Additional enhancing lesions, few have increased in size since ___.  Increased microhemorrhage within 1 lesion.  If pathology analysis shows\nmetastatic disease, consider initiation of chemotherapy or radiation therapy\nto stabilize lesions.  Infection/inflammatory process could show interval\ngrowth as well."
        },
        {
            "input": "The study is degraded by motion artifact.\n\nThe patient is status post right parietal craniotomy for tumor resection. \nThere is interval decrease in slow diffusion in relation to the surgical bed\nwith increase in enhancement favoring devitalized tissue over disease\nrecurrence, but the latter cannot be excluded with absolute certainty and\ncontinued imaging follow-up is advised.  The blood products in the surgical\nbed demonstrates normal expected interval evolution.\nResidual right frontoparietal extra-axial collection measuring 5 mm in\ndiameter.  This collection does not demonstrate slow diffusion.  Associated\ndural enhancement is nonspecific.\nExtracranial soft tissue swelling demonstrating central nonenhancing fluid\noverlying the right parietal craniectomy has progressed compared to prior\nimaging done ___ and infection should be clinically excluded.\n\nAll the previously noted metastatic lesions demonstrate marked interval\nincrease in size as well as surrounding edema for example the hemorrhagic\nlesion in the right frontal lobe measuring 11 mm in diameter (previously 7)\nand the lesion in the left frontal lobe measuring 10 mm in diameter\n(previously measuring 4 mm).  New enhancing lesion in the left frontal lobe\n(series 14, image 147).  New FLAIR hyperintensity in the left frontal lobe\n(series 11, image 14).  New enhancing lesion in the left cerebellum (series\n13, image 6).\nNew area of nodular enhancement in the right temporal area (series 13, image\n12).\n\nThe pituitary appears normal.  The craniocervical junction appears normal. \nThe intracranial vessels demonstrate normal T2 flow void.  Opacification of\nthe left mastoid tip.  Mild mucosal thickening involving the paranasal\nsinuses.  The orbits appear normal.",
            "output": "The study is degraded by motion artifact.\n\nAll of the known enhancing intracranial metastatic lesions demonstrate\ninterval increase in size compared to prior imaging with a few new lesions. \nThere is also marked increase in surrounding edema compared to MR done ___.\n\nThe patient is status post right parietal craniotomy for tumor resection.\nNormal evolution of the devitalized tissue in the surgical bed.  Residual\ndisease cannot be excluded and continued imaging follow-up advised.\nExtracranial soft tissue swelling demonstrating central nonenhancing fluid\noverlying the right parietal craniectomy has progressed compared to prior\nimaging done ___ and infection should be clinically excluded.\n\nNo evidence of new hemorrhage or infarction."
        },
        {
            "input": "The patient is status post right parietal craniotomy for tumor resection. \nCompared to the most recent prior study, slow diffusion within the right\nfrontoparietal surgical bed with postcontrast enhancement appears similar.  An\nextra-axial collection overlying the right frontoparietal region appears\nunchanged.  Soft tissue swelling adjacent to the craniotomy site has\ndecreased.  A 0.7 cm enhancing lesion of the left cerebellum (15:6) appears\nmore conspicuous and slightly increased in size, previously 0.5 cm.  Multiple\nenhancing metastatic lesions - including a left frontal lesion (15:20), left\nparietal lesion (15:14), left frontal lobe (series 14, image 101) and right\nfrontal lesion (15:16) - measuring up to 1.3 cm (15:20) also appears slightly\nincreased in size.  ___ FLAIR hyperintense signal is similar to\nslightly increased from prior exam.  Nodular enhancement in the right temporal\nresection cavity (15:14) appears similar to prior.  Many of these lesions\ndemonstrate gradient echo susceptibility artifact compatible with tumoral\nhemorrhage.\n\nNo evidence of new metastatic lesions.  No evidence of new hemorrhage or\ninfarction.  The ventricles and sulci are within expected limits in caliber\nand configuration.\n\nMild mucosal thickening of the ethmoid air cells and frontal sinuses and\nopacification of the left-greater-than-right mastoid air cells appear\nunchanged.  Otherwise, the paranasal sinuses and remaining mastoid air cells\nare unremarkable.  The orbits are unremarkable.  No suspicious osseous\nlesions.",
            "output": "1. Overall slight increase in size of supra and infratentorial lesions\npreviously described, with similar appearance to slight increase in size of\nsurrounding ___ lesional FLAIR edema pattern.  Nodular enhancement of the\nleft frontal parietal resection cavity is overall similar.  Majority of these\nlesions demonstrates gradient echo susceptibility artifact compatible with\nhemorrhage, also unchanged.\n2. No evidence of new metastatic lesions. No evidence of new hemorrhage or\ninfarction.\n3. Unchanged extra-axial collection overlying the right frontoparietal region,\nwith overall improvement in surrounding soft tissue edema pattern.\n4. Additional findings described above."
        },
        {
            "input": "Study is moderately degraded by motion.  Within these confines:\n\nPostsurgical changes related to patient's known right craniotomy and\nmetastatic lesion resection are again noted.  Nonspecific enhancement along\nthe resection cavity bed is again noted, decreased compared to prior exam.\n\nMultiple supratentorial and left cerebellar enhancing lesions with adjacent\nedema and suggested blood products are again seen.  Compared to ___\nprior exam lesions overall demonstrate decreased enhancement and adjacent\nedema.\n\nThere is no evidence of midline shift or acute territorial infarction.  The\nventricles and sulci are grossly stable in caliber and configuration.\n\nA right frontal developmental venous anomaly is again noted.\n\nBilateral mastoid air cell fluid is present.  Bilateral maxillary sinus,\nethmoid air cell, frontal sinus mucosal thickening is present.  Patient's\nknown right maxillary periodontal apical lucency is again noted (see 04:16;\n11:13 on current study and 303:72 on prior sinus CT).",
            "output": "1. Study is moderately degraded by motion.\n2. Numerous intracranial enhancing lesions as described, again compatible with\nmetastatic disease, with interval decrease extent of enhancement and adjacent\nedema.\n3. Within limits of study, no definite new enhancing intracranial lesions\nidentified.\n4. Grossly stable periodontal disease as described, better demonstrated on\nprior sinus CT.\n5. Evolving postsurgical change related to patient's known right\nfrontoparietal craniotomy and mass resection with residual adjacent\nnonspecific enhancement, overall decreased compared to prior exam.  While for\nenhancement may represent postoperative changes, residual tumor is not\nexcluded on the basis of this examination.  Recommend attention on follow-up\nimaging.\n6. Paranasal sinus disease and nonspecific mastoid fluid, as described.\n\nRECOMMENDATION(S):  Evolving postsurgical change related to patient's known\nright frontoparietal craniotomy and mass resection with residual adjacent\nnonspecific enhancement, overall decreased compared to prior exam.  While for\nenhancement may represent postoperative changes, residual tumor is not\nexcluded on the basis of this examination. Recommend attention on follow-up\nimaging."
        },
        {
            "input": "Postoperative changes right parietal operculum, minimal linear enhancement\nsurrounding surgical cavity, improved since prior.  Surrounding edema has\nimproved.  All previously seen parenchymal metastases have decreased in size,\nlargest today at the left vertex measures 5 mm, compared with 9 mm on prior. \nNo definite new metastases.  Previous seen surrounding edema has nearly\nresolved.  Minimal leptomeningeal enhancement at the right vertex seen on\nFLAIR images, may be related to prior surgery, similar.  Punctate foci of\nparenchyma chronic blood products, likely related to treated metastases\n\nVascular flow voids are preserved.  Mild mucosal thickening paranasal sinuses.\nModerate opacification bilateral mastoid air cells, mildly worsened since\nprior, may be reactive, very little complex fluid or enhancement to suggest\notomastoiditis, correlate clinically.  Mild brain parenchymal atrophy.  Dural\nvenous sinuses are patent.",
            "output": "1. Decreased previously seen metastases.\n2. No new metastases.\n3. Moderate bilateral mastoid opacification, may be reactive or inflammatory."
        },
        {
            "input": "Again seen are postoperative changes after a right parietal craniotomy.  There\nis minimal residual enhancement at the surgical site.  There has been\ncontinued reduction in the size of the enhancing lesions since the most recent\nprior study.  The left posterior frontal enhancing focus is now barely\ndetectable.  The other enhancing lesions are no longer visible.  No new\nlesions are identified.\nMultiple areas of chronic hemorrhage in the supra and infratentorial brain are\nagain identified, unchanged.\nBilateral mastoid fluid appears somewhat more extensive than on the prior\nstudy.  Mucosal thickening and small fluid collections in the ethmoid air\ncells are slightly more prominent than previously.\nThere is no evidence of hemorrhage, edema, midline shift or infarction.   The\nventricles and sulci are normal in caliber and configuration.  There is no\nother abnormal enhancement after contrast administration.",
            "output": "1. Only a single left frontal enhancing lesion remains detectable.  This\nlesion is considerably smaller than on prior studies.\n2. Multiple chronic hemorrhages again identified, unchanged"
        },
        {
            "input": "Areas of late acute to early subacute infarction are seen within the left\nsubinsular cortex and temporal lobes, with a small focus of infarction in the\nleft periventricular white matter.  There is no evidence for hemorrhagic\nconversion or other signs of acute intracranial hemorrhage.\n\nNo mass, mass effect, or midline shift.  The ventricles and sulci are\ndiffusely prominent compatible with global parenchymal volume loss. \nPeriventricular and subcortical white matter FLAIR hyperintensities are noted,\na nonspecific finding that most likely represents the sequelae of chronic\nsmall vessel ischemic disease.  There is gross preservation of the principal\nintracranial vascular flow voids.\n\nRight-sided mastoid fluid is noted.  The remainder of the visualized paranasal\nsinuses, middle ear cavities, and mastoid air cells are well aerated and\nclear.  The orbits are within normal limits bilaterally.",
            "output": "1. Late acute to early subacute infarctions within the left frontal and\ntemporal lobes, correlating with findings seen on recent CT perfusion\nexamination.\n2. No evidence for hemorrhagic conversion or other acute intracranial\nhemorrhage.\n3. Background global parenchymal volume loss and evidence of chronic small\nvessel ischemic disease.\n4. Additional findings as above."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.  Major dural venous sinuses are patent.  Major intracranial\nvascular flow voids are preserved.  The visualized paranasal sinuses and\nmastoids appear clear.  The globes and orbits are unremarkable.",
            "output": "Normal brain MRI.  No evidence of dural venous sinus thrombosis."
        },
        {
            "input": "There is no enhancing mass, acute infarction, edema, blood products, or other\nsignal abnormalities in the brain parenchyma.  Ventricles, sulci, and basal\ncisterns are normal in size.  Cerebellar tonsils are normally positioned.\n\nMajor vascular flow voids are grossly preserved.  Multiplanar MPRAGE images\ndemonstrate patency of the superior sagittal sinus, straight sinus, transverse\nsinuses, and sigmoid sinuses. The jugular bulbs and proximal jugular veins are\npatent.  There is flow signal in the paired internal cerebral veins and vein\nof ___.\n\nThe adenoids are prominent bilaterally.  According to the neurology clinic\nvisit note in the ___ medical record dated ___, enlarged adenoids\nwere also previously seen on an outside sinus CT.",
            "output": "Normal brain MRI.  No evidence of dural venous sinus thrombosis."
        },
        {
            "input": "There is a 3 vessel aortic arch.  Cervical common carotid, internal carotid\nand vertebral arteries appear widely patent.  Specifically, there is no\ncarotid stenosis by NASCET criteria.\n\nThe delayed phase images demonstrate contrast opacification of the internal\njugular veins throughout the neck.  There are areas of apparent narrowing of\nthe upper internal jugular veins bilaterally at the level of C2 and C3 (the\nlevel of the lower parotid glands), which may be artifactual.",
            "output": "1. Normal neck MRA.\n2. Patent internal jugular veins of the neck.  Apparent areas of narrowing of\nbilateral upper internal jugular veins at the level of C2 and C3 (the level of\nthe lower parotid glands) may be artifactual, but could be further assessed by\nultrasound if clinically warranted."
        },
        {
            "input": "MRI head: Contrast was not able to be administered due to the patient's poor\nrenal function. Patchy areas of slow diffusion are present within the left\nparietal occipital lobe with corresponding FLAIR signal abnormality compatible\nwith subacute infarct. There is a subacute to chronic infarct within the right\noccipital lobe. No intracranial hemorrhage is identified. There is no mass,\nmass effect or midline shift.\n\nElsewhere within the brain parenchyma, there are patchy areas of T2 and FLAIR\nprolongation within the periventricular and subcortical white matter as well\nas within the pons which are consistent with the sequela of chronic small\nvessel ischemic disease. The ventricles, cerebral sulci and cisterns are\nprominent reflecting a moderate degree of cerebral atrophy.\n\nA small subdural collection overlies the left cerebral convexity, as seen on\nthe CT examination.\n\nMRA head: There is lack of flow related enhancement within the right posterior\ncerebral artery just after the P1 segment., which is narrowed. The left\nposterior cerebral artery is patent. Duplicated right superior cerebellar\narteries are presentl; the origin of the larger SCA is stenotic.  The right\nposterior communicating artery is narrowed or occluded just after its origin.\nThe right vertebral artery is hypoplastic.\n\nThere is narrowing of the mid M1 segment of the left middle cerebral artery,\nand narrowing at the left middle cerebral artery bifurcation. The remainder of\nthe intracranial vessels are patent. There is no other evidence of occlusion,\nstenosis or aneurysm formation.\n\nMRA neck: The bilateral common carotid, external carotid and internal carotid\narteries are patent. Both vertebral arteries are patent. The right vertebral\nartery is hypoplastic. There is no evidence of significant stenosis by NASCET\ncriteria.",
            "output": "Subacute left parietal occipital infarct.\n\nLeft subdural fluid collection. This represents either a subacute to chronic\nsubdural hematoma or subdural hygroma.\n\nSubacute to chronic right occipital infarct and stenosis or occlusion of the\nright posterior cerebral artery, and the right PCOM is occluded or severely\nnarrowed just after its origin.\n\nMulifocal stenoses of the left middle cerebral artery."
        },
        {
            "input": "Multiple enhancing calvarial lesions are identified, many of which\ndemonstrates diffusion-weighted hyperintense signal, predominantly noted in\nthe bifrontal calvaria.  The dominant lesion is a left parasagittal parietal\nskull heterogeneously enhancing 2.5 x 1.8 x 2.4 cm (TRV, SI, AP) lesion which\nerodes through the inner and outer calvaria with extension to the subcutaneous\ntissue and underlying dura.  There is trace dural enhancement underlying the\nlesion without clear evidence of extension into the adjacent superior sagittal\nsinus (series 401 B, image 80).  The remainder the osseous lesions do not\nappear to erodes through the inner table.  There is a nonenhancing 2.7 x 1.0\ncm (AP, TRV ; series 4, image 77) T1 hypointense posterior left parietal\ncalvarial focus (series 4, image 77), potentially representing sclerotic\nlesion/previously treated disease.  Correlation with outside imaging is\nrecommended.  No parenchymal lesions are identified.\n\nIncidental note is made of a 1.7 x 1.2 cm right ventricular trigone on choroid\nplexus xanthogranuloma.\n\nThere is no evidence of acute infarct.",
            "output": "1. Multiple diffuse enhancing calvarial lesions, with dominant 2.5 cm left\nparasagittal posterior parietal lesion with extension into cutaneous tissue\nand to the dura, resulting in mild pachymeningeal enhancement and thickening. \nNo evidence of extension into the adjacent superior sagittal sinus.\n2. In addition to the enhancing lesions, there is a 2.7 cm T1 hypointense\nposterior left parietal lesion, which may represent a sclerotic\nfocus/previously treated disease.  Correlation with prior imaging is\nrecommended."
        },
        {
            "input": "There are numerous T1/T2 hypointense lesions throughout the calvarium, some of\nwhich demonstrate contrast enhancement and others of which do not.  Direct\ncomparison to prior imaging is limited given that only postcontrast sequences\nwere previously performed.  However, there appear to be multiple new contrast\nenhancing lesions throughout the calvarium.  A dominant lesion measuring 2.6\ncm x 1.1 cm is seen in the left parasagittal parietal skull which appears to\nerode through the inner and outer table of the skull, with minimal associated\ndural enhancement, grossly unchanged in comparison to the prior study, seen\nbest on series 18, image 86.  In addition, there is a stable enhancing lesion\nin the greater wing of the right sphenoid at the sphenoid triangle, series 19,\nimage 28 with associated dural enhancement along the anterior right temporal\nlobe.  There is apparent lesion involving the dens (11:13)\n\nThere is no evidence of hemorrhage, edema, intracranial masses, mass effect,\nmidline shift or infarction.   The ventricles and sulci are normal in caliber\nand configuration.  Periventricular and subcortical T2 and FLAIR\nhyperintensities are noted.  The major vascular flow voids are preserved.\n\nThe orbits are normal.  Minimal mucosal thickening of the ethmoid sinuses is\nseen.  There is fluid in the bilateral mastoid air cells.",
            "output": "1. Numerous calvarial lesions, some of which demonstrate signal suggestive of\nsclerosis, possibly representing previously treated metastatic disease. \nDirect comparison to prior imaging for new lesions is limited given the fact\nthat only postcontrast sequences were previously performed, however it appears\nthat multiple of the contrast enhancing calvarial and C2 lesions are new. \nRecommend correlation with prior studies.\n2. Stable appearance of the left parasagittal parietal skull lesion which\nerodes the inner and outer table of the skull with minimal associated dural\nenhancement.\n3. Stable appearance of the lesion in the greater wing of the right sphenoid\nwith associated underlying dural enhancement.\n4. Nonspecific white matter signal abnormality, likely secondary to chronic\nmicrovascular ischemic changes."
        },
        {
            "input": "Innumerable T1 and T2 enhancing hyperintense lesions are noted throughout the\ncalvarium, dens, temporal mandibular joints are similar appearance to prior\nexamination, compatible with osseous metastatic disease.\n\nA dominant left parietal skull parasagittal lesion measuring up to 2.6 cm in\ngreatest diameter, which may extend through the inner table.  An additional\nright frontal lobe lesion measuring up to 1 cm in is greatest dimension\n(series 900b, image 38) also appears to erodes through the inner table.  There\nappears to be underlying mild enhancement.\n\nA right greater sphenoid wing osseous lesion (series 901 B, image 33) is\nre-identified with associated dural thickening.  There is possible thickening\nof the right V2 segment at the level of the foramen ovale extending into the\nright Meckel's cave (series 901b, image 33, series 900b, image 55).\n\nThere is mild convex shape of the pituitary gland measuring up to 6 mm in SI\ndimension, unchanged from prior exam.  Unchanged appearance of a 1.7 cm right\nventricular trigone choroid plexus xanthogranuloma.\n\nThere is no enhancing parenchymal lesion.  There is no acute intracranial\nhemorrhage or acute infarct.  Scattered periventricular subcortical T2/FLAIR\nwhite matter hyperintensities are nonspecific and unchanged from prior exam. \nThe major intracranial flow voids are preserved.  The dural venous sinuses are\npatent.  The paranasal sinuses are essentially clear.  The orbits are\nunremarkable.  Right much greater than left fluid signal is noted in the\nmastoid air cells.",
            "output": "1. Re-identified are innumerable enhancing calvarial lesions.  A right frontal\nand left parietal parasagittal lesion erodes through the inner table,\nresulting in mild dural thickening and enhancement, similar in appearance to\nprior exam.\n2. A right greater wing of the sphenoid lesion is again noted.  There may be\ninvolvement of the right V2 segment at the level of the foramen ovale with\nextension into the Meckel's cave.  Close attention on followup is recommended.\nClinical correlation is recommend.\n3. Enhancing lesion of the dens is re-identified\n4. No definite evidence for parenchymal metastatic disease."
        },
        {
            "input": "Again seen are innumerable calvarial lesions and a mass, presumably a\nmetastasis, in the odontoid.  These appear unchanged since the prior study. \nThere is no evidence of intraparenchymal or leptomeningeal metastatic disease.\nThere is no evidence of hemorrhage, edema,  midline shift or infarction. \nAgain seen are numerous white matter hyperintense foci on FLAIR.  Although\nnonspecific, these are often attributed to chronic small vessel ischemia.  The\nventricles and sulci are normal in caliber and configuration.  There is no\nabnormal enhancement after contrast administration.",
            "output": "1. No evidence of parenchymal metastases.\n2. Unchanged multiple skeletal lesions, likely metastases, in the odontoid and\nthroughout the calvaria."
        },
        {
            "input": "There are scattered periventricular and subcortical white matter FLAIR\nhyperintense white matter lesions, which are relatively unchanged.  There are\nno enhancing parenchymal lesions.  There is no acute infarct, hemorrhage,\nmass, or mass effect.  The ventricles and cortical sulci are normal in caliber\nconfiguration.  The extra-axial spaces are unremarkable.  The vascular flow\nvoids are preserved.\n\nThere are numerous variably enhancing and sclerotic lesions throughout the\ncalvarium, which are relatively unchanged comparison to prior study.  The\nlargest on the left measures 4.6 cm (11:11).  The largest on the right\nmeasures 4.0 cm (11:18).  There is asymmetric T1 hypointensity at the right\ngreater wing of the sphenoid with mild asymmetric associated enhancement\n(12:10; 19:44), which could represent osseous disease as described on prior\nMRI, however this is not well visualized on this study.  There is a 1.1 cm T1\nhypointense lesion at the base of the dens, which is relatively unchanged.\n\nThe orbits and soft tissues are unremarkable.  There is no abnormal fluid\nsignal within the paranasal sinuses.  There are bilateral mastoid air cell\neffusions.",
            "output": "1. Numerous variably sclerotic and enhancing lesions throughout the calvarium\nand at the base the dens, consistent with osseous metastatic disease, which is\nrelatively unchanged comparison to prior study.\n2. Osseous disease with previously described at the right greater wing of the\nsphenoid is poorly visualized on this study, but is grossly unchanged\ncomparison to prior examination.\n3. No evidence of parenchymal metastatic disease.\n4. Unchanged nonspecific periventricular and subcortical white matter FLAIR\nhyperintense lesions, likely reflecting sequela of chronic microangiopathy. \nNo acute infarction or hemorrhage."
        },
        {
            "input": "There are numerous enhancing lesions diffusely throughout the calvarium, which\nare similar in size and number compared to the MR dated ___.  The\nT1 hypointense lesion within the odontoid appears to have increased in size\ncompared to the MR dated ___, now measuring up to 1.4 cm in the\nsagittal plane.\n\nThere is no evidence of abnormal parenchymal enhancement. There is no evidence\nof hemorrhage, edema, masses, mass effect, midline shift or acute infarction. \nThe scattered subcortical and deep white matter T2/FLAIR hyperintensities, are\nstable, but are not in the typical distribution seen with either microvascular\nangiopathy or demyelination. The ventricles and sulci are normal in caliber\nand configuration.\n\nThe vessels of the circle of ___ and dural venous sinuses are grossly\npatent.  The orbits, paranasal sinuses, and mastoids are within normal limits.",
            "output": "1. Numerous enhancing lesions within the calvarium, stable in size and number\ncompared to the MR dated ___, compatible with metastatic disease.\n2. Increased size of the odontoid lesion, measuring up to 1.4 cm.\n3. No evidence of abnormal parenchymal enhancement.\n4. Scattered white matter T2/FLAIR hyperintensities of indeterminate etiology,\nwhich are stable, but not in the typical distribution seen with either\nmicrovascular angiopathy or demyelination."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, mass effect, midline shift or acute\ninfarction.  Numerous scattered periventricular, subcortical, and deep white\nmatter foci of T2/FLAIR hyperintense signal without associated slow diffusion\nor enhancement are unchanged dating back to at least ___ and\nremain nonspecific.  The ventricles and sulci are age-appropriate.  Principal\nintracranial vascular flow voids are preserved and dural venous sinuses\nenhance appropriately on postcontrast MP-RAGE sequences.  There is no abnormal\nparenchymal enhancement after contrast administration.\n\nMild diffuse mucosal thickening of the ethmoid air cells and opacification of\nthe mastoid air cells, left greater than right is unchanged.  The orbits are\nunremarkable.\n\nEnhancing lesion in the odontoid process has minimally increased in size and\nenhancement. Numerous additional T1 hypointense enhancing calvarial lesions\nare again seen, consistent with metastatic disease.",
            "output": "1. Multifocal calvarial metastatic disease, similar to prior examination. \nAdditional metastatic focus in the odontoid process demonstrates minimal\nincrease in size and enhancement.\n2. Numerous scattered periventricular, subcortical, and deep white matter\nT2/FLAIR hyperintense foci are stable dating back to at least ___\nand remain nonspecific.\n3. There is no evidence of hemorrhage, edema, mass effect, or abnormal\nparenchymal enhancement."
        },
        {
            "input": "The ventricles and sulci are normal in size and configuration.  No enhancing\nparenchymal mass is identified.  Scattered areas of white matter T1\nhypointensity correspond to the areas of FLAIR signal abnormality on prior\nexamination, consistent with chronic small vessel ischemic disease. \nIncidental choroid plexus xanthogranuloma is noted in the occipital horn of\nthe right lateral ventricle, unchanged.  Innumerable T1 hypointense calvarial\nmetastatic lesions, some enhancing are again identified, measuring up to 31 x\n27 mm in the left parietal calvarium, grossly unchanged.  A heterogeneously\nenhancing lesion in the dens measuring 15 x 6 mm is also grossly unchanged. \nThere is no abnormal focus of slowed diffusion.",
            "output": "1. Innumerable calvarial metastatic lesions are grossly unchanged compared the\nprior examination.\n2. 15 x 6 mm heterogeneously enhancing metastatic lesion within the dens is\nalso unchanged.\n3. No parenchymal enhancing lesion."
        },
        {
            "input": "Scattered periventricular and subcortical white matter/ T2 hyperintensities\nare again noted, only 1 of which is new when compared to the prior exam in the\nsubcortical white matter of the left frontal lobe (07:17).  There is no\nassociated abnormal enhancement in these foci which are likely sequela of\nchronic small vessel disease.  There is no acute infarct, intracranial mass,\nmass effect or midline shift.  Ventricles and sulci are stable in\nconfiguration.  There is no abnormal susceptibility artifact. Major\nintravascular flow voids are preserved.\n\nPost contrast images demonstrate no abnormal parenchymal or meningeal\nenhancement.\n\nNumerous calvarial T1 and T2 hypointense enhancing lesions are compatible with\nknown osseous metastases.  No definite interval change in size.  Lesion within\nthe odontoid measuring 1.4 cm cc is grossly unchanged.  Lesion again seen\nwithin the right sphenoid wing",
            "output": "Osseous metastatic disease as seen on prior.  No parenchymal metastatic\nlesions."
        },
        {
            "input": "There is no evidence of acute intracranial hemorrhage or infarction. \nVentricles and sulci are age appropriate.  Scattered periventricular and deep\nsubcortical FLAIR white matter hyperintensities are unchanged compared to the\nprior exam from ___ and likely sequelae of mild-to-moderate\nchronic small vessel ischemic disease.  There is no evidence of acute\nintracranial hemorrhage or infarction.  Choroid plexus xanthogranuloma within\nthe occipital horn of the right lateral ventricle is unchanged compared to the\nprior exam.  Innumerable T1 hypointense calvarial metastatic lesions some of\nwhich enhance are again identified, measuring up to 1.3 cm x 3.8 cm in the\nleft parietal bone are grossly unchanged compared to the prior exam.  A 1.2 cm\nx 1 cm heterogeneously enhancing lesion within the dens is also grossly\nunchanged.  Partially visualized is T1 hypointense bone marrow within the C4\nvertebral body.\n\nOn the postcontrast T1 spin echo sequence, a 0.4 cm enhancing abnormality is\nseen within the left temporal lobe, series 10, image 10, not seen on the prior\nexam.  This lesion is not seen on the postcontrast MPRAGE images, there is no\nassociated FLAIR abnormality.\n\nMild mucosal sinus disease is seen involving the ethmoid air cells.  The\nremainder of the visualized paranasal sinuses are clear.  Partial fluid\nopacification is seen involving the left mastoid air cells.  The right mastoid\nair cells are clear.  The bilateral middle ear cavities are clear.  The\nprincipal vascular flow voids appear to be well preserved.  The globes are\nunremarkable.",
            "output": "1. 0.4 cm enhancement on spin echo images in anterior left temporal lobe is\nnot seen on other sequences.  There is other areas of flow artifact in\nbilateral temporal lobes, and finding is likely an artifact.  Attention to\nthis area on subsequent follow-up is recommended.\n2. Stable osseous metastatic disease compared to the prior exam, including\ninvolvement of the cervical spine.\n3. No acute intracranial abnormalities identified.  Chronic microangiopathy.\n\nRECOMMENDATION(S):  Follow-up brain MRI with gadolinium"
        },
        {
            "input": "In comparison with the most recent exam, again multiple calvarial metastatic\nlesions are re-demonstrated some of them showing T1 hypointense signal, and\nheterogeneous bone marrow signal  on T1 and FLAIR sequences, grossly unchanged\nlesions are also visualized in the upper cervical spine, however partially\nevaluated in this exam.  Intracranially there is no evidence of hemorrhage,\nterritorial infarct or shifting of the normally midline structures.  The\npreviously 4 mm small enhancing lesion identified in the left temporal lobe is\nnot longer seen.  Again numerous scattered subcortical and periventricular\nT2/FLAIR white matter hyperintensities are seen, grossly unchanged, which are\nnonspecific and may reflect microvascular ischemic disease.  No diffusion\nabnormalities are detected.  The ventricles are unchanged and again\ndemonstrate a choroid plexus xanthogranuloma within the right occipital\nventricular horn, measuring approximately 13 x 18 mm in transverse dimension\n(image 13, series 13).  The major vascular flow voids are present and\ndemonstrate normal distribution.  The orbits are unremarkable, unchanged\nmucosal thickening is noted in the ethmoidal air cells with no evidence of\nair-fluid levels.  Partial fluid opacification involving the left mastoid air\ncells appears unchanged, the right mastoid air cells and bilateral middle ear\ncavities are clear.",
            "output": "1.  The previously described 4 mm enhancing lesion in the anterior left\ntemporal lobe is no longer seen.\n\n2.  Numerous osseous metastatic lesions remain unchanged, including lesions in\nthe upper cervical spine.\n\n3.  Chronic microangiopathic changes, with no evidence of acute intracranial\nprocess.\n\n4.  Partial opacification of the left mastoid air cells remains unchanged."
        },
        {
            "input": "Multiple bony metastatic lesions including areas of low signal indicating\nsclerosis are again identified.  Mild pachymeningeal enhancement in the\nparietal region is also again seen.  No intrinsic brain parenchymal\nenhancement is identified.  Subtle enhancement in the left temporal lobe\n(10:9) appears artifactual at it is not confirmed on the MP rage images. \nFLAIR hyperintensities are unchanged.  A right atrial dental granuloma of the\nchoroid plexus is unchanged.",
            "output": "Stable appearance compared to the previous MRI.  No abnormal parenchymal\nenhancement is seen.  Unchanged bony metastatic disease."
        },
        {
            "input": "Re-identified are diffuse metastatic osseous lesions involving the calvarium,\nand visualized upper cervical spine.  Since the prior exam, there is increased\nsoft tissue extension through the inner table involving the right occipital\nskull measuring approximately 3.3 x 0.9 cm (TRV, AP; series 1000, image 94). \nThere is associated nonenhancing FLAIR hyperintense signal of the underlying\nright parietal and occipital lobes (series 6, image 14 through 17).\n\nHyperintense parenchymal cortical extension through the left frontal vertex is\nsimilar to the prior examination.  Interval increase in right greater than\nleft pachymeningeal thickening and enhancement (series 9, image 17).\n\nNo intra-axial enhancing lesions are identified.  Unchanged right choroid\nplexus xanthogranuloma.  There is no acute infarct or intracranial hemorrhage.\nSuperimposed periventricular and subcortical T2/FLAIR white matter\nhyperintensities are nonspecific and unchanged from prior examination, likely\nrepresenting sequela of chronic microangiopathy in a patient of this age.  The\nmajor intracranial flow voids are preserved.  There is severe stenosis the\nbilateral mid V4 segments, unchanged from prior exam.  The dural venous\nsinuses are patent.  There is mild mucosal thickening of the ethmoid air\ncells.  The orbits are unremarkable.  Fluid signal is noted in the left\nmastoid air cells, similar to prior examination.",
            "output": "1. Interval increased epidural extension of right occipital osseous lesions,\nmeasuring approximately 3.3 x 0.9 cm along the inner table, resulting in FLAIR\nhyperintense signal of the underlying right parietal and occipital lobes. \nThere is increased right greater than left pachymeningeal enhancement and\nthickening.\n2. No intra-axial enhancing lesion is identified.\n3. Diffuse osseous metastatic disease and subtle epidural extension along the\nleft frontal vertex is unchanged.\n4. Additional findings as described above.\n\nNOTIFICATION:  The impression and recommendation above was entered by Dr.\n___ on ___ at 15:25 into the Department of Radiology critical\ncommunications system for direct communication to the referring provider."
        },
        {
            "input": "Diffuse sclerotic metastatic disease is seen involving the skull and upper\ncervical spine.  In the right parietal region epidural enhancement has\nincreased and now measures approximately 10 mm in thickness compared to 6 mm\non the previous study on a comparable slice.  There is increased in white\nmatter edema in the right parietal lobe but without midline shift or\nhydrocephalus.  Previously seen subtle epidural enhancement in the left\nfrontal region is unchanged.  Mild pachymeningeal enhancement along both\ncerebral convexities is also unchanged.No definite parenchymal areas of\nabnormal enhancement seen.  There is opacification of the left frontal sinus\nwhich is new since the previous study.",
            "output": "1. Increase in thickness of right parietal epidural metastasis adjacent to the\nbony metastasis compared to the previous MRI of ___.  There is\nalso slight increase in adjacent edema.\n2. Diffuse metastasis within the skull and upper cervical spine with mild\ndiffuse pachymeningeal enhancement is unchanged.\n\nNOTIFICATION:  The impression and recommendation above was entered by Dr.\n___ on ___ at 14:41 into the Department of Radiology\ncritical communications system for direct communication to the referring\nprovider."
        },
        {
            "input": "Extensive areas of low T1 and T2 signal diffusion abnormality in the skull\nconsistent with sclerotic bony metastasis are again identified.  Dural\nenhancement is seen in the right parieto-occipital and left parietal region\nwith focal thickening of the extra-axial space in the right parietal region. \nFLAIR hyperintensities are seen in the right periventricular and occipital\nregion indicating brain edema.  Compared to the prior study the D myeloma\nright occipital lobe has slightly decreased.  In addition, the focal\nextra-axial thickening now measures 7 mm (9:86) compared to 11 mm (17:100) on\nthe previous study.  No new areas of extra-axial thickening identified.  No\nnew parenchymal areas of abnormal enhancement are seen.  Scattered FLAIR\nhyperintensities due to small vessel disease are again identified.  There is\nno hydrocephalus or midline shift.  Previously seen soft tissue changes in the\nleft frontal sinus have resolved.",
            "output": "1. Extra-axial metastatic lesion in the right parieto-occipital region has\nslightly decreased in thickness compared to the prior study with slight\ndecrease in right occipital edema.\n2. Diffuse bony abnormalities suggestive of sclerotic metastasis are again\nseen seen in the skull with pachymeningeal enhancement in the temporoparietal\noccipital regions.\n3. No abnormal parenchymal area of enhancement is identified."
        },
        {
            "input": "Again seen are extensive areas of T1 hypointensity in restricted diffusion and\nheterogeneous enhancement in the calvarium compatible with metastatic disease.\nComponents in the scalp have enlarged, specifically a 1.9 by 1.3 cm lesion\noverlying the left frontoparietal region (10:139) measured 1.6 x 1.2 cm in ___\nand 1.0 by 0.8 cm in ___.  The lesion overlying the right\nparieto-occipital region in the scalp has also enlarged now measuring 3.0 x\n0.7 cm, previously 2.5 x 0.6 cm though now is centrally nonenhancing, which is\ndifferent since prior.  Additional smaller lesions centered at the outer\nperiosteum have also enlarged and the left parietal region (10:140) in the\nright parietal region posteriorly (10:124).\n\nOverall, there is thin pachymeningeal thickening and enhancement, right more\nso than left and overall more conspicuous compared to previous exams.  The\nmore focal areas of irregular dural enhancement in the right parieto-occipital\nregion is similar compared to ___, decreased since ___. \nSurrounding edema in the right occipital lobe continues to decrease. \nAdditional irregular extra-axial enhancement overlying the left frontoparietal\nregion has slightly enlarged, specifically nodular component (1001:91)\nmeasuring 0.6 x 1.0 cm, previously 0.4 x 0.9 cm in ___.  Associated\nunderlying left frontal FLAIR/T2 hyperintensity is slightly increased (08:21).\n\nThere are other areas of T2 and FLAIR hyperintensity in the periventricular\nand subcortical white matter, either due to chronic small vessel disease are\npost treatment related.  There is no acute infarct or mass effect.  No\nabnormal susceptibility artifact.  Major intravascular flow voids are\npreserved.\n\nT1 hypointense lesion within the dens is compatible with additional metastatic\nlesion.",
            "output": "1. Abnormal bone marrow signal and enhancement in the calvarium compatible\nwith metastatic disease.  Progression of disease centered at the outer\ncalvarial periosteum with enlarging scalp lesions.\n2. Diffuse mostly thin pachymeningeal thickening and enhancement now seen\nalong both cerebral convexities though more prominent on the right than on the\nleft.\n3. Stability of the more focal and irregular extra-axial enhancement in the\nright parieto-occipital region with continued decrease in degree of\nsurrounding parenchymal edema.\n4. Slight increased focal extra-axial enhancement overlying the left\nfrontoparietal region with marginally increased underlying left frontal edema."
        },
        {
            "input": "Metastases C2-C4 levels.  C2 metastasis is similar compared with ___. \nMetastases at C3, C4 were not covered on ___, C3 is mildly worsened\nsince ___.  Extensive calvarial metastases.  Enhancing extracranial\nsoft tissue component of tumor associated with calvarial metastases has mildly\nworsened at the left vertex, example 3.1 cm x 0.9 cm lesion series 19, image\n16, compared with 2.9 cm x 0.8 cm on ___.  Nonenhancing extracranial\nsoft tissue component of the tumor at the right parietal scalp is stable.\n\nExtensive pachymeningeal thickening and enhancement overlying bilateral\ncerebral hemispheres, predominantly linear, stable since prior.  Nodular\nenhancing component of dural enhancement overlying posterior left frontal lobe\nis more prominent compared to prior, measuring 0.9 cm in thickness overlying\nmedial margin of the left precentral gyrus, and 0.9 cm thickness just lateral\nto this area overlying postcentral gyrus, compared with 0.6 cm, and 0.6 cm\nrespectively on ___.  These changes exert mild local mass effect and\nthere is mild brain parenchymal edema, worsened.\n\nLinear pachymeningeal enhancement and thickening overlying posterior right\nparietal lobe measures 3.2 cm x 0.7 cm, similar to prior, with worsened\nadjacent leptomeningeal enhancement.  New small foci of adjacent parenchymal\nenhancement within right parietal lobe, with single focus of punctate focus of\nmicrohemorrhage may represent postradiation change.  Moderately extensive\nsurrounding brain parenchymal edema has worsened since prior, may represent\nposttreatment change.\n\nNo evidence of acute infarct, hydrocephalus or midline shift.  Findings\nconsistent with moderate chronic small vessel ischemic changes.  Vascular flow\nvoids are preserved, dural venous sinuses are patent.  Mild opacification\nbilateral mastoids.  Clear paranasal sinuses.",
            "output": "1. Extensive osseous metastases, C3 metastasis is more prominent since ___.\n2. Worsened nodular intracranial dural enhancement left vertex, likely\nrepresents tumor progression, adjacent worsened mild brain parenchymal edema.\n3. Stable dural thickening overlying right parietal lobe.  Worsened adjacent\nfoci of parenchymal enhancement right parietal lobe which may represent\npostradiation change, and worsened, moderate parenchymal edema.  Adjacent\nextracranial component of nonenhancing tumor is stable.\n4. Mildly worsened enhancing extracranial tumor at the left frontal scalp.\n5. Extensive linear pachymeningeal bihemispheric enhancement, stable.\n\nNOTIFICATION:  The impression and recommendation above was entered by Dr.\n___ on ___ at 16:05 into the Department of Radiology\ncritical communications system for direct communication to the referring\nprovider."
        },
        {
            "input": "Widespread enhancing calvarial lesions are not appreciably changed.\nWidespread, relatively linear pachymeningeal thickening and enhancement is not\nappreciably changed since the prior examination.\n\nNodular thickening and enhancement overlying the posterior left frontal lobe\nhas decreased since the prior examination, measuring 0.6 cm from the inner\ntable overlying the superior left prefrontal gyrus, previously 0.9 cm (series\n18, image 21); 0.5 cm overlying the slightly more lateral and inferior left\nprecentral gyrus and central sulcus, previously 0.9 cm (series 18, image 14);\nand 0.4 cm overlying the left middle frontal gyrus, previously 0.7 cm (series\n18, image 14).  Adjacent vasogenic edema is decreased since the prior\nexamination.  Extracranial extension is decreased in size, measuring 0.4 cm\nfrom the outer table, previously 0.8 cm from the inner table (series 19, image\n16).\n\nNodular thickening and enhancement overlying the right parieto-occipital\nregion, extending into the parenchyma, is not appreciably changed, allowing\nfor differences in axial slice selection, best compared on coronal and\nsagittal MPRAGE, measuring up to 1.6 cm from the inner table (series 18, image\n41).  Adjacent vasogenic edema is not appreciably changed.  Extracranial\nextension is not appreciably changed in size, measuring up to 8 mm from the\nouter table, but with new heterogeneous enhancement on postcontrast imaging\n(series 16, image 19).\n\nIn the right parietal corona radiata, there is a new approximately 7 mm focus\nof restricted diffusion without associated enhancement (series 7, image 16).\n\nOn precontrast sagittal images, T1 hypointense lesions in the vertebral bodies\nand posterior elements of C2 through C4 are not appreciably changed.\n\nThere is no evidence of significant mass effect or midline shift.  Numerous\nperiventricular, deep, and subcortical white matter T2/FLAIR hyperintensities\nare grossly unchanged, nonspecific but likely sequelae of chronic small vessel\nischemic disease in this age group.  The ventricles are normal in size.\n\nThere is increased nonspecific opacification of the right mastoid air cells. \nThe major intracranial flow voids are preserved.",
            "output": "1. A new approximately 7 mm focus of restricted diffusion without associated\nenhancement in right parietal corona radiata, compatible with an acute or\nearly subacute infarct.\n2. Extensive osseous metastases are not appreciably changed.\n3. Nodular thickening and enhancement overlying the right parieto-occipital\nregion with a small amount of intraparenchymal extension is unchanged. \nAdjacent vasogenic edema is unchanged. Adjacent extracranial disease is\nunchanged in size, but demonstrates no enhancement.\n4. Nodular thickening and enhancement overlying the posterior left frontal\nlobe is improved.  Adjacent vasogenic edema is improved.  Adjacent\nextracranial disease is improved.\n5. Diffuse pachymeningeal thickening and enhancement is otherwise unchanged.\n\nNOTIFICATION:  The acute to early subacute infarction in the right corona\nradiata was discussed with ___, M.D. by ___, M.D. on the\ntelephone on ___ at 16:16, approximately 2 hours after discovery."
        },
        {
            "input": "MR BRAIN:\nThere is subtle signal abnormality within the posterior portion of the pons\n(04:10) and within the right side of the pons (04:11).  The ventricles are\nnormal in size without midline shift.  The major visualized arterial vascular\nflow voids are preserved.  The paranasal sinuses and bilateral mastoid air\ncells appear clear.  Patient is status post right lens replacement.\n\nMRA brain: There is a hypoplastic A1 segment of the right anterior cerebral\nartery, likely a congenital variant.  Otherwise, the intracranial internal\ncarotid arteries and vertebral arteries and their major branches appear patent\nwithout stenosis, occlusion, or aneurysm.  There is a left dominant vertebral\nartery.",
            "output": "1. Acute infarcts in the posterior pons and right side of the pons..\n2. No evidence of stenosis, occlusion, or aneurysm."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  There are a few scattered foci of nonspecific T2/FLAIR\nhyperintensity in the subcortical and periventricular white matter and in the\npons most likely reflecting chronic microangiopathy in this age group.  The\nventricles and sulci are mildly prominent reflecting involutional changes.\n\nThe major intracranial vascular flow voids are preserved.  Bilateral\nintra-ocular lens replacements are noted.  There is moderate scattered\nparanasal sinus mucosal thickening predominantly affecting the left frontal\nsinus and the left ethmoid air cells.  The visualized extracranial soft\ntissues are unremarkable.",
            "output": "1. No acute intracranial abnormality.  No evidence of acute infarction.\n2. Mild nonspecific white matter signal changes which most likely reflect\nchronic microangiopathy in this age group.\n3. Paranasal sinus disease as above."
        },
        {
            "input": "There is no intracranial mass, mass effect, or midline shift. Ventricles and\nsulci are age-appropriate. There is no focal parenchymal signal abnormality.\nThere is no region of restricted diffusion or abnormal susceptibility\nartifact. Major intravascular flow voids are preserved.\n\nVisualized paranasal sinuses and mastoid air cells are clear.",
            "output": "Normal MRI of the brain."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor acute infarction.  4 mm old lacunar infarct in the left pons. T2 and FLAIR\nhyperintense changes with associated atrophy in the posterior right parietal\nlobe as well as in the left occipital lobe most likely represent old infarcts.\nGeneralized cerebral and cerebellar atrophy (cerebellar atrophy is slightly\nmore pronounced compared to cerebral).  Prominence of the ventricular system. \nProminence of the fourth ventricle and the cerebellomedullary cistern.  Flow\nvoid seen in the cerebral aqueduct.  Nonspecific periventricular and deep\nwhite matter T2 and FLAIR hyperintensities are indeterminate.  There is no\nabnormal enhancement after contrast administration.  Right-sided ocular\nstaphyloma.  Mucous retention cyst present in the left maxillary sinus being\nT1 hyperintense and T2 hypo intense most likely representing inspissated\nsecretions in a mucous retention cyst or proteinaceous content.  Presence of a\ncavum velum interpositum.",
            "output": "Generalized cerebral and cerebellar atrophy (cerebellar slightly more\npronounced).\n\nPeriventricular and deep white matter T2 and FLAIR hyperintensities are\nnonspecific, but most likely represent sequela of microangiopathy.\n\nOld lacunar pontine infarct.  The areas of T2 and FLAIR hyperintense changes\nwith associated atrophy in the right parietal and left occipital lobe most\nlikely represents old infarcts.\n\nProminence of the ventricular system with a prominent fourth ventricle,\ncisterna magna and prominent flow void in the cerebral aqueduct may represent\ncommunicating hydrocephalus or be secondary to ex vacuo dilatation of the\nventricular system."
        },
        {
            "input": "Study is moderately degraded by motion.\n\nThere are symmetric bilateral extra-axial collections with minimal FLAIR\nhyperintensity and no definite areas of increase susceptibility, with maximum\ndiameter up to 8 mm, with effacement of the ventricles and sulci.  Within\nlimits of study, no definite vessels crossing through collection are noted.\n\nThere are small chronic lacunar infarcts in the left caudate head, right\ncaudate body, and right putamen.  There is no evidence of acute intracranial\nhemorrhage, edema, masses, midline shift or acute/subacute infarction. \nPeriventricular and subcortical white matter T2/FLAIR hyperintensities are\nnonspecific but likely sequelae of chronic small vessel ischemic disease.  \nThere is nonspecific mineralization of the bilateral globus pallidus.  The\npituitary gland appears grossly preserved in size.  There is no definite\ncerebellar tonsillar ectopia.  Question mamillopontine distance of\napproximately 5 mm (see 03:11) versus volume averaging artifact.  The orbits\nare grossly preserved, without definite flattening of the posterior globes.\nThe major intracranial flow voids are preserved.\n\nBilateral ethmoid air cell and maxillary sinus mucosal thickening is present. \nLeft maxillary sinus hypoplasia is again seen.  There is leftward nasal septum\ndeviation.  Bilateral lens replacement postoperative changes are noted.",
            "output": "1. Study is moderately degraded by motion.\n2. Grossly stable symmetric bilateral subdural probable hygromas compared to ___ and ___ prior outside exams, again resulting in\ndiffuse effacement of the ventricles and sulci, and with question decreased\nnominal pontine distance as described.  While findings are nonspecific,\nsimilar findings may be seen in the setting of intracranial hypotension.\n3. No definite evidence of acute infarct.\n4. Paranasal sinus disease with probable chronic left maxillary sinusitis, as\ndescribed.\n5. Chronic infarcts and probable microangiopathic changes as described."
        },
        {
            "input": "MR BRAIN:\n There is no evidence of infarction, hemorrhage, edema, or mass.\n\nAgain seen are bilateral subdural collections, stable in size, measuring 8 mm\nwith on the left and 6 mm on the right in width.  Minimal mass effect includes\nbilateral cerebral sulcal effacement.  No herniation or midline shift.  No\nventriculomegaly.\n\nThere are findings suggestive of intracranial hypotension.  Specifically, the\n___ pontine distance is decreased, 3 mm (105:55).  There is a downwardly\ndisplaced splenium of the corpus callosum.  There is a slightly sagging\nappearance of the midbrain.  Additionally, there is diffuse pachymeningeal\nenhancement and engorgement of the dural venous sinuses, which are widely\npatent.\n\nThere are multiple small chronic lacunar infarcts in the region of the basal\nganglia and right periventricular white matter.\n\nThere is circumferential moderate left maxillary sinus mucosal thickening,\nwith internal inspissated secretions.  Mild right maxillary sinus and ethmoid\nair cell mucosal thickening.  No air-fluid levels.  Mastoids are clear.\n\n Aside from bilateral lens extraction, the globes and orbits are within normal\nlimits.\n\nMRA brain:\n Diminutive distal right vertebral artery, with decreased flow related\nenhancement along its horizontal V3 segment (05:44).  This may relate to\nmoderate luminal narrowing due to underlying atheromatous disease.  Distal to\nthis, the artery demonstrates a diminutive caliber but is patent to the\nbasilar origin.  Normal, patent distal left vertebral artery.  Widely patent\nbasilar artery.  Conventional bilateral PCA anatomy.  Widely patent posterior\ncerebral arteries with normal distal runoff.  Right posterior communicating\nartery is diminutive but patent.  Left posterior communicating artery is not\nwell seen, either diminutive or absent.\n\nLikely moderate to severe luminal narrowing, paraclinoid right ICA, presumably\ndue to underlying atheromatous disease (5:95).\n\nModerate luminal narrowing, paraclinoid left intracranial ICA, presumably due\nto underlying atheromatous plaque (5:97).  Remainder of the bilateral\nintracranial ICAs are patent.\n\nPatent bilateral middle cerebral arteries with normal distal runoff.\n\nPatent bilateral A1, A2, and more distal bilateral anterior cerebral arteries,\nwith normal distal runoff.  The anterior communicating artery is not well\nseen.\n\nNo additional stenosis.  No large vessel occlusion.  No aneurysm.",
            "output": "1. Spectrum of findings consistent with intracranial hypotension.  Correlate\nclinically with any history of postural headaches.\n2. Bifrontal subdural hygromas, 8 mm on the left and 6 mm on the right, likely\nrelating to intracranial hypotension.\n3. Moderate to severe right and moderate left paraclinoid segment intracranial\nICA luminal narrowing, presumably due to underlying atheromatous plaque. \nModerate luminal narrowing, distal horizontal V3 segment, right vertebral\nartery.  Otherwise, widely patent circle of ___ vasculature.  No additional\nstenosis.  No large vessel occlusion.  No aneurysm.\n4. Multiple bilateral small chronic lacunar infarcts, basal ganglia, right\nperiventricular white matter.\n5. Opacified left maxillary sinus with inspissated secretions and\ncircumferential mucosal thickening.\n6. Additional findings described above."
        },
        {
            "input": "Numerous infra and supratentorial enhancing lesions are visualized in both\ncerebral hemispheres and cerebellum. The largest enhancing lesion in the\ncerebellum is visualized in the left cerebellar hemisphere (07:14), with\nirregular contour and associated vasogenic edema, measuring approximately 14 x\n14 mm in transverse dimension, additionally multiple punctate enhancing\nlesions are visualized in both cerebellar hemispheres. Supratentorially, there\nis a ring-enhancing lesion in the left thalamus measuring approximately 12 x\n15 mm in transverse dimension with associated vasogenic edema and mild\nnarrowing of the third ventricle with no evidence of hydrocephalus (14:4).\nSlow diffusion is noted in this lesion suggested and abscess formation.\nMultiple enhancing lesions are visualized in the brain convexity, the largest\nlesion in the area of the primary motor cortex on the left (image 20, series\n4). The majority of these lesions may demonstrate mild vasogenic edema evident\non FLAIR and T2 weighted images, there is no evidence of acute intracranial\nhemorrhage or significant shifting of the normally midline structures. The\nmajor arterial vascular flow voids are present and demonstrate normal\ndistribution. The orbits are unremarkable, the paranasal sinuses are clear as\nwell as the mastoid air cells, there is mucosal thickening in the right Peters\napex.",
            "output": "Numerous infra and supratentorial enhancing lesions as described above, the\nlargest in the left thalamus with slow diffusion and vasogenic edema\nsuggestive of an abscess formation. Multiple foci of abnormal enhancement in\nboth cerebral hemispheres and cerebellum likely consistent with septic emboli.\n\nNOTIFICATION:  These findings were discovered and communicated via phone call\nto Dr. ___ by Dr. ___ of on ___ at 09:45 hrs."
        },
        {
            "input": "Motion artifact mildly limits evaluation.\n\nThere is no evidence for an enhancing mass, acute infarction, edema, or blood\nproducts.  No pathologic leptomeningeal or pachymeningeal contrast\nenhancement.  Minimal T2/FLAIR hyperintensity along the lateral ventricles and\nat least 1 T2/FLAIR hyperintense focus in the right frontal subcortical white\nmatter on image 7:17 are nonspecific but likely sequela of minimal chronic\nsmall vessel ischemic disease in this age group.  Ventricles, sulci, and basal\ncisterns are normal in size for the patient's age, without evidence for\nsignificant parenchymal volume loss.  Specifically, no medial temporal volume\nloss is identified.\n\nMajor vascular flow voids are grossly preserved.  There is apparent 6 mm\noutpouching at the right middle cerebral artery bifurcation, image 8:11,\nsuggestive of an aneurysm.  Dural venous sinuses are patent on postcontrast MP\nRAGE images.\n\nThere is mild mucosal thickening in the ethmoid air cells.  There is right\ngreater than left mastoid air cell opacification.",
            "output": "1. No evidence for intracranial metastatic disease or acute intracranial\nabnormalities.\n2. Apparent 6 mm outpouching at the right middle cerebral artery bifurcation,\nsuggestive of an aneurysm.\n\nRECOMMENDATION(S):  Recommend head CTA and vascular neurosurgery consultation.\n\nNOTIFICATION:  The impression and recommendation above were entered by Dr.\n___ on ___ at 10:54 into the Department of Radiology critical\ncommunications system for direct communication to the referring provider."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.\n\nThe ventricles and sulci are normal in caliber and configuration.\nMajor vascular flow voids appear preserved.\n\nThere is moderate mucosal thickening along the ethmoid air cells and mild\nmucosal thickening in the frontal and maxillary sinuses.  The mastoid air\ncells appear clear.  The orbits appear unremarkable.",
            "output": "1. Unremarkable MRI of the brain without evidence of acute infarction,\nhemorrhage or intracranial mass.\n2. Paranasal sinus disease."
        },
        {
            "input": "The apparent hyperintensity within the inferior left occipital lobe on the\ndiffusion-weighted images persists, but is artifactual in nature given a\nsimilar appearance on the contralateral side (series 4, image 2), as well as\nno abnormalities on the ADC or FLAIR images.\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor acute territorial infarction.  Punctate T2/FLAIR hyperintensity within the\nright periatrial white matter is nonspecific, but unchanged.  The ventricles\nand sulci are normal in caliber and configuration.  Orbits are normal.",
            "output": "No acute intracranial abnormalities or evidence of acute stroke.  Apparent\nhyperintensity within inferior left occipital lobe on the diffusion weighted\nimages appears artifactual."
        },
        {
            "input": "The patient was unable to remain still within the magnet and the study was\nterminated following acquisition of only localizer and sagittal T1 sequences.\nThere are T1 hypointense areas in the left temporal lobe, bilateral basal\nganglia, and bilateral cerebellar hemispheres.  These areas of signal\nabnormality correspond to hypodensities seen on recent noncontrast CT head\nfrom ___.\nHowever, these are not adequately assessed on the present incomplete study.\nInferior aspect of the fourth ventricle/obex is not well seen-?  Related to\nadjacent cerebellar edema\nHypointense marrow signal in particular in the cervical spine, occipital bones\nand in the clivus.",
            "output": "Only limited MR ___ and sagittal T1 images were obtained only as the patient\ncould not remain still within the scanner.\n\n1. Foci of abnormal signal in the left temporal lobe, bilateral basal ganglia,\nand bilateral cerebellar hemispheres. Complete MRI of the brain without and\nwith intravenous contrast is recommended for further evaluation when the\npatient is clinically suitable.\n\n2. Hypointense marrow signal in particular in the cervical spine, occipital\nbones and in the clivus.\nInadequately assessed on the present incomplete MRI study.\nCorrelate clinically and with hematology labs for anemia, systemic disease,\nmyeloproliferative or infiltrative disorders, etc."
        },
        {
            "input": "The ventricles and sulci are normal in caliber and configuration.  There are\nmultiple ring-enhancing and solid enhancing T2/FLAIR lesions in the bilateral\ncerebral hemispheres with the largest lesions noted in the corona radiata of\nthe left frontal lobe, bilateral basal ganglia and thalami, bilateral temporal\nlobes.  There are also enhancing T2/FLAIR hyperintense lesions in the\nbilateral cerebellar hemispheres and cerebellar vermis as well as within the\nmidbrain.  There is local mass effect with sulcal effacement noted within\nthese regions. Several of these lesions demonstrate slow diffusion. There is\nno definite leptomeningeal enhancement noted. Vascular flow voids are\npreserved. There is minimal mucosal thickening within the ethmoid air cells\nand left greater than right maxillary sinuses. The mastoid air cells are\ngrossly clear.\n\nInflammatory changes including post-contrast enhancement is noted adjacent to\nthe bilateral temporomandibular joints.\n\nDiffuse T1 hypointensity is again noted in the marrow of the cervical spine\nsimilar to prior study.",
            "output": "Multiple ring and solid enhancing lesions in the supratentorial and\ninfratentorial white matter and within the bilateral basal ganglia and bowel\nMRI. Differential diagnosis for these findings is broad and includes\nopportunistic infections such as toxoplasmosis, fungal disease, bacterial\nabscess, CNS lymphoma, and less likely metastatic disease."
        },
        {
            "input": "Again multiple enhancing lesions are identified in the supra and\ninfratentorial brain involving both cerebral hemispheres, brain stem and both\ncerebellar hemispheres. Compared to the prior study, the size of the enhancing\nlesions has considerably decreased with decreasing surrounding edema. Multiple\nenhancing lesions are still visualized bilaterally. Some of the previously\nseen lesions are not perceptible on the current study. The mass effect on the\nfourth ventricle has decreased. There is no hydrocephalus or midline shift.\nThere are no acute infarcts.",
            "output": "Decrease in size of the enhancing lesion seen previously in the supra and\ninfratentorial brain. Surrounding edema has also decreased.  Multiple\nenhancing lesions are still identified. Followup as clinically indicated."
        },
        {
            "input": "There has been a reduction in the volume of edema and extent of enhancement\nassociated with the multiple bilateral supra and infratentorial lesions. There\nis no evidence of hemorrhage. No new areas of edema or abnormal enhancement\nare identified. No masses are identified.",
            "output": "Continued gradual decrease in edema and enhancement associated with multiple\nbilateral lesions."
        },
        {
            "input": "Compared to prior study, there has been a significant interval increase in\nsize of a previously identified enhancing lesion centered in the left basal\nganglia with an associated increase in surrounding T2/FLAIR signal\nhyperintensity.  On today's study, T2/FLAIR signal hyperintensity likely\nrepresenting vasogenic edema is seen extending into the left posterior frontal\nlobe, left insula, and left internal and external capsule.  There is resulting\nlocal mass effect with mild effacement of adjacent sulci and of the left\nlateral ventricle.\n\nThere are multiple new punctate enhancing lesions noted with subtle\nsurrounding vasogenic edema not previously seen on prior study.  This includes\na tiny enhancing lesion in the right posterior frontal lobe (series 100 b,\nimage 90), left medial occipital lobe (series 100 b, image 69), left temporal\nlobe (series 100 b, image 48), medial left frontal lobe (series 100b, image\n83) and right cerebellar hemisphere (series 100 b, image 23).\n\nOther previously identified enhancing lesions appear unchanged.\n\nThere is no evidence of hemorrhage, acute infarction, midline shift, or\nextra-axial collection.  The ventricles and sulci are normal in caliber and\nconfiguration.  Major vascular flow voids are preserved.  The orbits are\nunremarkable.  The paranasal sinuses and mastoid air cells are clear.",
            "output": "Significant interval increase in size of enhancing lesion centered in the left\nbasal ganglia with associated increased in surrounding vasogenic edema with\nresulting mass effect.  Additionally, there has been interval development of\nmultiple punctate enhancing lesions with subtle associated T2/FLAIR signal\nhyperintensity as detailed above.  Differential diagnosis for these findings\nremains broad but includes infection such as toxoplasmosis and fungal\n(cryptococcus) disease as well as CNS lymphoma."
        },
        {
            "input": "In comparison to the most recent MRI dated ___, there has been\ninterval decrease in size of the dominant enhancing left basal ganglia lesion,\nwhich currently measures 10 x 6 mm (14:14), previously 15 x 11 mm.  There is\nstill mild surrounding edema which abuts the left lateral ventricle (12:15),\nbut there is no significant mass effect; this has also improved significantly\ncompared to the prior study.\n\nAdditional clusters of enhancing foci within the bilateral basal ganglia\n(100a: 61) has also decreased since the prior study.  Lesions within the\nbilateral cerebellar hemispheres have resolved (100b:31).  Additional tiny\nenhancing lesions noted on the prior study involving the bilateral frontal\nlobes, left medial occipital lobe, left temporal lobe and right cerebellum are\nno longer visualized on the current study.  No new enhancing lesions. No acute\nischemia or intracranial hemorrhage.  No shift of midline structures.\n\nMajor intracranial vascular flow voids are preserved.\n\nThere is minimal mucosal thickening in the bilateral maxillary sinuses. \nRemainder of the visualized paranasal sinuses are clear.  The orbits are\nunremarkable.\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.",
            "output": "Interval decrease in size of the dominant enhancing left basal ganglia lesion\nwith improvement in surrounding vasogenic edema compared ___.  Additional\nclusters of enhancing foci within the bilateral basal ganglia have decreased\nin number and severity.  Several additional enhancing lesions described above\nhave resolved.  No new enhancing masses."
        },
        {
            "input": "Left coronal radiata 9 x 6 mm FLAIR (TRV, AP) and diffusion-weighted\nhyperintense focus with central enhancement is significantly smaller when\ncompared to examination of ___.  No new regions of abnormal\nenhancement or diffusion-weighted signal abnormality.  There are superimposed\nscattered FLAIR hyperintense punctate lesions,  most prominent in the basal\nganglia, corresponding to prior enhancing lesions, unchanged from the prior\nexam.  Bilateral cerebellar encephalomalacia is also noted.  The majority\nthese lesions no longer demonstrate enhancement with trace residual foci of\nsubtle enhancement within bilateral basal ganglia.\n\nThe major intracranial flow voids are preserved.  The dural venous sinuses are\npatent.  Mild bilateral maxillary sinus mucosal thickening is noted.  The\nremainder the paranasal sinuses are essentially clear.  The orbits are\nunremarkable.  The mastoid air cells are poorly pneumatized but essentially\nclear.",
            "output": "1. Dominant left corona radiata 9 mm FLAIR hyperintense enhancing focus has\ndecreased in size from the prior exam.  Residual nonenhancing scattered\nT2/FLAIR hyperintense punctate foci as well as minimal enhancement of the\nbilateral basal ganglia is unchanged from prior exam, corresponding to\npreviously seen ring-enhancing lesions on examination of ___.\n2. No new lesions."
        },
        {
            "input": "There is a 4mm AP by 7mm TV by 10mm SI mm enhancing nodule at the left mid\ncentrum semiovale with adjacent FLAIR hyperintensity (16:16).  There are\nadditional clustered punctate foci of enhancement within the bilateral globus\npallidi with correlate FLAIR hyperintensity (16:13).  These findings have\ndecreased in size as compared to more remote study from ___, but is\nrelatively unchanged in comparison to prior study from ___. \nThere are no additional sites of abnormal postcontrast enhancement.  The\npreviously described new focus of enhancement in the right cerebellar\nhemisphere is less conspicuous on this study.\n\nThere is no acute infarct, hemorrhage, mass, or mass effect.  The ventricles\nand cortical sulci are normal and caliber and configuration.  The vasculature\nis patent.\n\nThe orbits, calvarium, and soft tissues are unremarkable.  There is mild\nmucosal thickening within the bilateral maxillary sinuses.  The mastoid air\ncells are clear.",
            "output": "1. Nodular enhancement in the left mid centrum semiovale and clustered\nbilateral punctate enhancement within the globus pallidi which are relatively\nunchanged in comparison to most recent prior study but decreased in comparison\nto more remote studies consistent sequela of toxoplasmosis as clinically\nreported.\n2. No new or enlarging sites of disease.\n3. Focus of enhancement within the right cerebellar hemisphere is less\nconspicuous."
        },
        {
            "input": "There is 4 mm linear enhancement of the left coronal radiata (series 14, image\n16), decreased in size from examination of ___.  There is\nassociated linear FLAIR hyperintense signal which is also slightly less\nconspicuous when compared to prior exam.  No other enhancing lesions are\nidentified.  Previously described punctate enhancement and FLAIR hyperintense\nsignal in the globus palladi have significantly decreased compared to prior\nexam.\n\nThere is no acute infarct or intracranial hemorrhage.  The major intracranial\nflow voids are preserved.  The dural venous sinuses are patent on MPRAGE. \nMild mucosal thickening of the ethmoid air cells is identified.  The orbits\nare unremarkable.  The mastoid air cells are essentially clear.",
            "output": "1. There is residual 4 mm linear enhancement of the left coronal radiata,\nsignificantly decreased in size when compared to prior exam.  Associated\nlinear FLAIR hyperintense signal is also decreased in conspicuity.\n2. There is residual FLAIR hyperintense signal of the bilateral globus\npallidus, with interval near-complete resolution of associated punctate\nenhancement.\n3. No new enhancing lesions are identified."
        },
        {
            "input": "Previously noted focus of linear enhancement in the left frontal corona\nradiata has resolved, with small area of residual FLAIR hyperintensity in area\nof previous enhancement (07:15).  There is unchanged residual FLAIR\nhyperintensity of the bilateral globus pallidi without associated enhancement.\nThere also unchanged areas of FLAIR hyperintensity in the left temporal lobe\nand bilateral putamina without associated enhancement in areas of prior\nenhancing disease.  Similar subtle appearing areas are noted in the bilateral\ncerebellar hemispheres and right mid brain.  There is no evidence of\nhemorrhage, edema, masses, mass effect, midline shift or infarction.   The\nventricles and sulci are normal in caliber and configuration.  There is no\nabnormal enhancement after contrast administration.  The principal\nintracranial vascular flow voids are preserved.\n\nThere is mild mucosal wall thickening in the bilateral maxillary sinuses and\nbilateral ethmoid air cells.  The remainder the visualized paranasal sinuses\nare clear.  The orbits are grossly unremarkable.  The mastoid air cells are\nclear.",
            "output": "1. Areas of unchanged residual nonenhancing FLAIR signal abnormality in the\nleft frontal lobe, left temporal lobe, bilateral putamina and globus pallidi,\nbilateral cerebellar hemispheres and right midbrain representing sequela of\ntreated toxoplasmosis.\n2. No new enhancing lesion."
        },
        {
            "input": "Previously noted areas of FLAIR hyperintensity in the left frontal lobe, left\ntemporal lobe, bilateral putamini and globus pallidi, bilateral cerebellar\nhemisphere and right midbrain appear similar compared to prior.  No\nenhancement of this lesions post contrast.  There is no evidence of\nhemorrhage, edema, masses, mass effect, midline shift or infarction.   The\nventricles and sulci are normal in caliber and configuration.  The orbits\nappear normal.  Small mucosal retention cyst present in the inferior aspect of\nthe left maxillary sinus.",
            "output": "1. No new lesions identified.  No abnormal enhancement.  No infarction.\n2. Multiple previously described lesions are unchanged."
        },
        {
            "input": "The nonenhancing FLAIR hyperintensities in the bilateral cerebellar\nhemispheres appear more conspicuous on today's exam when compared to ___.\nThe FLAIR hyperintensity in the left periventricular white matter appears a\nlittle bulkier when compared to the prior study.\n\nThe remaining nonenhancing FLAIR hyperintensities in the right midbrain, left\ntemporal lobe and in the putamen and globus pallidus bilaterally appear not\nsignificantly changed when compared to ___. FLAIR hyperintensity  extending\nfrom the left corona radiata towards the posterior limb of the left internal\ncapsule suggest the possibility of wallerian degeneration.\n\nThere are no new lesions or abnormal enhancement.\n\nThere is no evidence of acute intracranial hemorrhage, mass effect, midline\nshift or acute territorial infarction.\n\nThere is mild generalized parenchymal volume loss, more than expected for\npatient's age but likely disease related.  Mild prominence of the ventricular\nsystem and extra-axial CSF spaces is compatible with the previously mentioned\nparenchymal volume loss.\n\nThere is mucosal thickening in the inferior left maxillary sinus.  There is\nminimal mucosal thickening along the ethmoid air cells.  The mastoid air cells\nappear grossly clear.",
            "output": "1. Nonenhancing FLAIR hyperintensities in the bilateral cerebellar hemisphere\nand in the left periventricular white matter appear a little more conspicuous\nand slightly bulkier on today's exam.  The remaining nonenhancing FLAIR\nhyperintensities appear unchanged from ___.\n2. Unchanged mild parenchymal volume loss which is more than expected for\npatient's age but likely disease related."
        },
        {
            "input": "There is a mixed intensity right hemispheric subdural collection measuring up\n6 mm in greatest thickness with gradient echo susceptibility, involving the\nconvexity and anterior falx, compatible with mixed age subdural hematoma. \nThis results in mild sulcal effacement at the vertex and 4 mm leftward midline\nshift.  Dependent hemorrhage product is also noted in the right much greater\nthan left occipital horns of the lateral ventricles (series 12, image 10 and\nseries 10, image 10).\n\nGradient echo susceptibility in the left cerebellar hemisphere (series 10,\nimage 5) likely represent sequela of micro hemorrhage.  Pachymeningeal\nthickening and enhancement overlying the right cerebral hemisphere is presumed\nreactive secondary to trauma and hematoma.\n\nThere is no acute infarct or intracranial mass.  Superimposed periventricular\nand subcortical T2/FLAIR white matter hyperintensities are nonspecific, but\ncompatible with chronic microangiopathy in a patient of this age.  The major\nintracranial flow voids are preserved.  Mucosal thickening of the ethmoid air\ncells is identified.  The orbits are unremarkable, noting right lens\nreplacement.  Fluid signal is noted in the right greater than left mastoid air\ncells.\n\nIncidental note is made of right frontal and parietal burr holes.",
            "output": "1. Right cerebral hemispheric subacute hematoma measuring up to 6 mm in\ngreatest thickness.  Presumed hemorrhage product is also seen in the bilateral\nright much greater than left occipital horns of the lateral ventricles.  There\nis a right hemispheric pachymeningeal thickening and enhancement, presumably\nreactive.\n2. A punctate gradient echo susceptibility focus in the left cerebellar\nhemisphere, may represent sequela prior micro hemorrhage.\n3. No acute infarct or intra mass.\n\nNOTIFICATION:  The findings were discussed with ___, M.D. by ___\n___, M.D. on the telephone on ___ at 8:48 AM, 2 minutes after\ndiscovery of the findings."
        },
        {
            "input": "Based on images provided, there is no intracranial mass, mass effect, or\nmidline shift.  There is no focal parenchymal signal abnormality within the\nlimitation of lack of T2 and FLAIR sequences.  Ventricles and sulci are\nage-appropriate.  There is no restricted diffusion to suggest acute infarct.",
            "output": "Patient declined completion of the exam.  Based on T1 and diffusion sequences,\nunremarkable exam.  No acute infarct."
        },
        {
            "input": "There are late acute infarcts of the peripheral right pre and postcentral\ngyrus, right frontal convexity, right angular gyrus, right insula, right basal\nganglia and right anterior hippocampal formation/amygdala.  Subtle gradient\necho susceptibility artifact of the right caudate, lentiform nucleus and\nanterior insula is compatible with micro hemorrhagic transformation.  There is\na focus of diffusion-weighted hyperintensity along the posteromedial right\ntemporal lobe (series 1002, image 16).  A punctate focus of diffusion-weighted\nhyperintense signal without slow diffusion of the right parietooccipital lobe\n(series 1002, image 12).\n\nThe edema results in effacement of the frontal horn of the right lateral\nventricle.  There is no hydrocephalus.  Otherwise, the sulci, ventricles and\ncisterns are within expected limits for the patient's age.\n\nSuperimposed punctate periventricular and subcortical T2/FLAIR white matter\nhyperintensities are nonspecific, but commonly seen in setting chronic\nmicroangiopathy in a patient of this age.\n\nThe visualized intracranial flow voids are preserved.  The mild mucosal\nthickening of the paranasal sinuses.  The orbits are unremarkable noting\nbilateral lens replacements.  No significant fluid signal is seen in the\nmastoid air cells.",
            "output": "1. Diffuse right MCA distribution late acute infarcts involving the frontal\nlobe, insula, basal ganglia, angular gyrus and anterior hippocampal\nformations/amygdala.  The insula and basal ganglia demonstrates mild micro\nhemorrhagic transformation.\n2. Edema from the infarct effaces the frontal horn of the right lateral\nventricle.  No hydrocephalus.  No significant midline shift.\n3. Additional focus of late acute infarct along the posteromedial right\ntemporal lobe.  Possible subacute punctate infarct of the right\nparietooccipital lobe.\n4. Additional findings as described above.\n\nNOTIFICATION:  The findings were discussed with Dr.  ___, M.D. by\n___, M.D. on the telephone on ___ at 7:56 pm, 10 minutes\nafter discovery of the findings."
        },
        {
            "input": "Images through the internal auditory canal demonstrates symmetric appearance\nof the seventh eighth nerve complexes.  There is no evidence of abnormal\nenhancement or mass lesion within the internal auditory canals,\ncerebellopontine angles or membranous labyrinth. No other mass lesions are\nseen within the posterior fossa.  The inner ear structures appear\nunremarkable.\n\nIncompletely characterized is a T1 intrinsically hyperintense 8 x 6 mm (series\n6, image 3) potentially hypoenhancing focus of the right pituitary gland.\n\nLimited included imaging of the remainder of the brain demonstrates no\nevidence of hemorrhage, edema, other masses, mass effect, midline shift or\ninfarction. The ventricles and sulci are normal in caliber and configuration.\nThere is no abnormal enhancement after contrast administration.\n\nNo osseous abnormalities are seen. The paranasal sinuses, mastoid air cells,\nand middle ear cavitiesare clear. The orbits are unremarkable. The visualized\nportion of the principle vascular flow voids are preserved.",
            "output": "1. No evidence of IAC or cerebellopontine angle mass.\n2. Incompletely characterize is a 8 mm T1 intrinsically hyperintense focus of\nthe right pituitary gland.  The T1 intrinsic hyperintense signal would suggest\na Rathke's cleft cyst, however hemorrhagic adenoma is a consideration. \nFurther evaluation with dedicated pituitary MRI is recommended.\n\nRECOMMENDATION(S):  Further evaluation of a 8 mm T1 intrinsically hyperintense\nfocus the right pituitary gland with dedicated pituitary MRI."
        },
        {
            "input": "The T1 hyperintense, nonenhancing, heterogeneously T2 hypointense and\nhyperintense nodule in the right posterior pituitary gland is unchanged in\nsize and appearance from the prior examination, measuring 7 x 5 x 6 mm.  A\nsecond, right lateral nodular area is also T1 hyperintense and does not\nenhance,.  This nodular area measures 3 mm, unchanged from the prior\nexamination, and appears contiguous with the largest nodule.  No new nodules\nare identified.\n\nThe pituitary gland is normal in size.  The suprasellar cistern and cavernous\nsinuses appear normal.\n\nScattered foci of T2 hyperintensities in the periventricular and subcortical\nwhite matter are nonspecific, but may represent the sequela of chronic small\nvessel ischemic disease.",
            "output": "No significant change in the size and appearance of the 2 nodules within the\nright pituitary gland, which appear contiguous and likely represent a single\nlesion, most consistent with a Rathke's cleft cyst."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  Subcortical T2/ FLAIR white matter hyperintensities are\nnonspecific, however likely represent sequela of chronic small vessel ischemic\ndisease.  There is no abnormal enhancement after contrast administration.\n\nBilateral hippocampal formations and mammillary bodies are preserved in signal\nand configuration. There is no disproportionate medial temporal atrophy. There\nis no focal lobar encephalomalacia. There are no focal cortical dysplasias or\ngray matter heterotopia noted.\n\nAgain seen is a 2 mm infundibulum at the origin of the right anterior temporal\nartery at the right MCA bifurcation, and a 1 mm infundibulum along the\nsuperior aspect of the M1 branch.  The intracranial vessels are patent,\nwithout evidence of stenosis or occlusion.\n\nThere is mucosal thickening of the left maxillary sinus, similar to priors. \nMild mucosal thickening of the ethmoid air cells is also noted.  The remainder\nof the paranasal sinuses are clear.",
            "output": "1. Subcortical T2/FLAIR white matter hyperintensities are nonspecific, however\nlikely represent sequela of chronic small vessel ischemic disease.\n\n2.  No evidence acute infarct, intracranial hemorrhage or mass. The\nhippocampal formations are unremarkable.  No evidence for gray matter\nheterotopia, no cortical dysplasia or mesial temporal sclerosis.\n3. Re- demonstration of a 2 mm infundibulum at the origin of the right\nanterior shoulder artery, and a 1 mm infundibulum along the superior aspect of\nthe M1 branch."
        },
        {
            "input": "There is no acute infarction, intracranial hemorrhage, extracerebral fluid\ncollection, midline shift or mass effect.  No diffusion abnormalities are\ndetected. Subtle FLAIR FLAIR hyperintense signal in the bilateral parietal/\noccipital lobes, seen on the axial reformations of the FLAIR sequence is not\nconfirmed on the coronal and the sagittal source for 3D FLAIR sequences.\nHence, it is unclear if this is real or artifactual.\nThere is no evidence of abnormal enhancement.\n\nThere are bilateral chronic lacunar infarcts in the basal ganglia. There are\nscattered foci of T2/FLAIR signal hyperintensity in the periventricular and\nsubcortical white matter which are likely secondary to small vessel ischemic\ndisease. The cerebral volume is appropriate for the patient's stated age.  The\nmajor vascular flow voids are maintained.\nThe orbits are unremarkable. The paranasal sinuses and mastoid air cells are\nclear",
            "output": "No acute infarct or mass effect or abnormal enhancement.\nSubtle FLAIR hyperintense signal in the bilateral parietal and occipital lobes\non the reformations, not confirmed on the source FLAIR sequences. Hence, of\nquestionable significance.\n\nCorrelate clinically and with EEG and if necessary, consider followup.\nSmall vessel ischemic changes and chronic lacunar infarcts in the basal\nganglia"
        },
        {
            "input": "There is susceptibility artifact from EEG electrodes over the scalp.\n\nMultiple small foci of diffusion restriction and FLAIR hyperintense signal are\nseen bilateral frontal, parietal, temporal and occipital lobes, in a watershed\ndistribution.  No mass effect.  No evidence for blood products on gradient\necho images.\n\nModerate global parenchymal volume loss with prominent ventricles and sulci. \nMild confluent periventricular to white matter T2/FLAIR hyperintensity may be\nsecondary to either chronic small vessel ischemic disease or ventriculomegaly.\nNo evidence for signal abnormalities in the pons.  No edema or mass effect.\n\nThere is near complete opacification of an atelectatic left maxillary sinus\nwith wall thickening, as seen on the preceding CT, consistent chronic\nsinusitis.  There is small amount of fluid in the bilateral sphenoid sinuses\nand in the nasopharynx, similar to the prior CT, which may be secondary to\nendotracheal intubation and prolonged supine positioning in the inpatient\nsetting.  The mastoids are not pneumatized.",
            "output": "1. Multiple small early subacute infarcts involving the bilateral frontal,\nparietal, temporal occipital lobes, in a watershed distribution, suggesting\nsequela of hypoperfusion.  No mass effect or evidence for blood products.\n2. No evidence for pontine signal abnormalities.\n3. Chronic left maxillary sinusitis.\n4. Persistent fluid in the bilateral sphenoid sinuses compared to the head CT\nfrom 2 days prior which may be secondary to endotracheal intubation and\nprolonged supine positioning in the inpatient setting.  However, given the\nrecent sepsis, please correlate clinically regarding the possibility of\nsuperimposed infection.\n\nNOTIFICATION:  At the time of discovery of the findings, Dr. ___\nthe ___ Consult Note in the ___ Record dated ___,\nwhich indicated awareness of the MRI results."
        },
        {
            "input": "There is no intra or extra-axial mass, acute hemorrhage or infarct. The sulci,\nventricles cisterns are within expected limits for the degree of mild\nsenescent related global cerebral volume loss.  There are periventricular and\nsubcortical T2/FLAIR white matter hyperintensities, unchanged in configuration\nand from prior examination of ___, nonspecific, but commonly seen in the\nsetting of chronic microangiopathy in a patient of this age.  The major\nintracranial flow voids are preserved. There is mild mucosal thickening of the\nethmoid air cells.  The orbits are grossly unremarkable.  Fluid signal is seen\nin the right mastoid air cells.",
            "output": "1. No acute intracranial abnormality on noncontrast MRI head.  Specifically no\nintracranial hemorrhage or infarct.\n2. No interval change in subcortical and periventricular FLAIR white matter\nhyperintensities, nonspecific, but commonly seen in the setting of chronic\nmicroangiopathy."
        },
        {
            "input": "MRI BRAIN:\nThere is a focus of slow diffusion in the left parietal lobe extending to the\ncortex (series 18 images 21 through 23).  There is no associated hemorrhage. \nThis likely represents a small acute infarction.  There is no other evidence\nof infarction.  There is no evidence of edema or mass effect.  There is marked\nenlargement of the ventricles and sulci in an atrophic pattern.  This is\nparticularly striking involving the hippocampal formations bilaterally.  The\nFLAIR images demonstrate extensive periventricular and subcortical white\nmatter hyperintensity.  This is often attributed to chronic small vessel\nischemia.\n\nThere is extensive mucosal thickening in the right maxillary sinus and milder\nmucosal thickening bilaterally in the ethmoid sinuses.\n\nMRA BRAIN:\nThe intracranial vertebral and internal carotid arteries and their major\nbranches appear normal without evidence of stenosis, occlusion, or aneurysm\nformation.\n\nMRA NECK:\nThe left common, internal and external carotid arteries appear normal with no\ninternal carotid artery stenosis by NASCET criteria.  The right common and\nexternal carotid arteries appear normal.  There is atherosclerotic plaque at\nthe proximal left internal carotid artery with no stenosis by NASCET criteria.\nThe origins of the great vessels, subclavian and vertebral arteries appear\nnormal bilaterally.",
            "output": "1. Focal left parietal white matter infarction extending to the subcortical\nwhite matter.\n2. No evidence of hemorrhage or other infarction.\n3. Atherosclerotic plaque without stenosis by NASCET criteria at the right\ninternal carotid artery origin."
        },
        {
            "input": "There is no evidence of acute hemorrhage, edema, masses, mass effect, midline\nshift or infarction.  There is no abnormal enhancement after contrast\nadministration.  Vascular flow voids are preserved.  Paranasal sinuses,\nmastoids are clear.  Dural venous sinuses are patent.  Generalized brain\nparenchymal atrophy, most prominent at the temporal lobes and sylvian\nfissures, with mild-to-moderate bilateral hippocampal atrophy..  Minimal\nchronic small vessel ischemic changes.  No evidence of superficial or deep\nchronic microhemorrhage.  No significant parietal lobe atrophy.",
            "output": "1. No acute findings.\n2. Brain parenchymal atrophy."
        },
        {
            "input": "There is a solitary, punctate focus of diffusion-weighted and FLAIR\nhyperintense signal seen within the left paramedian frontal lobe (302:22),\nwithout ADC hypointensity, likely representing subacute infarct.  Numerous\nsmall chronic infarctions are noted within the right greater than left\ncerebellar hemispheres, pons, and left thalamus.\n\nNo intracranial hemorrhage. A stable, small probable choroidal fissure cyst is\nnoted.\n\nThe ventricles and sulci are prominent compatible with global parenchymal\nvolume loss.  Periventricular and subcortical white matter FLAIR\nhyperintensities are noted, a nonspecific finding that most likely represents\nthe sequelae of chronic small vessel ischemic disease.   There is gross\npreservation of the principal intracranial vascular flow voids.\n\nFluid signal is noted within the left greater than right mastoid air cells. \nThe remainder of the visualized paranasal sinuses are otherwise clear.  The\norbits are within normal limits bilaterally.",
            "output": "1. Single, punctate focus of diffusion-weighted and FLAIR hyperintense in the\nleft paramedian frontal lobe compatible with subacute infarction.\n2. No intracranial hemorrhage.\n3. Moderate global parenchymal volume loss and evidence of chronic small\nvessel ischemic disease.\n4. Left greater than right mastoid fluid."
        },
        {
            "input": "Single punctate focus of DWI hyperintensity in the anterior left frontal lobe\nsubcortical white matter (series 4, image 21) with corresponding ADC\nhypointensity is consistent with an acute infarct.  Small late subacute\ninfarct anterior right frontal lobe deep white matter.\n\nInnumerable chronic small infarcts involving right greater than left\ncerebellum, brainstem, right corona radiata, probably left corona radiata,\nright greater than left basal ganglia, left thalamus.  Findings consistent\nwith severe chronic small vessel ischemic changes.  Brain parenchymal atrophy.\nSignificant corpus callosum atrophy.  Wallerian degeneration right cerebral\npeduncle.  No acute hemorrhage, edema, masses, mass effect or midline shift.\n\nThere is mild mucosal thickening along the floors of the bilateral maxillary\nsinuses.  Mild partial opacification of the bilateral mastoid air cells, left\ngreater than right.  Preserved vascular flow voids.",
            "output": "1. Single punctate acute infarct in the anterior left frontal lobe.\n2. Late subacute punctate infarct right frontal lobe.\n3. Innumerable, small chronic infarcts cerebellum, brainstem, basal ganglia,\ncerebral hemispheres deep white matter.  Severe chronic small vessel ischemic\nchanges.  Brain parenchymal atrophy.\n\nNOTIFICATION:  Findings discussed with Dr. ___ by Dr. ___\n(neuroradiology fellow) on ___ via telephone at 09:30 am"
        },
        {
            "input": "Study is degraded by motion.\n\nThere is a right anterior parietal small focal cortical diffusion restriction\nwith corresponding T2/FLAIR hyperintensity measuring about 7 mm in keeping\nwith late acute/subacute infarct.  Another small punctate focus of diffusion\nrestriction also noted at medial left thalamus/midbrain junction.  There is no\nacute intraparenchymal hemorrhage.\n\nThere are bilateral either hemisphere chronic infarct; more on the right\nhemisphere.  Numerous punctate chronic infarcts are again seen. \nPeriventricular and subcortical T2 and FLAIR hyperintensities are noted which\nmay represent small vessel ischemic changes.   There is prominence of the\nventricles and sulci suggestive of involutional changes.\n\nIncidental finding of left choroid fissure cyst measuring 1.5 cm maximum axial\ndiameter.\n\nThere is no evidence of masses, mass effect or midline shift.\n\n Mild opacification of both mastoid air cells.  Left small retention cyst at\nthe left maxillary sinus.",
            "output": "1. Study degraded by motion.\n2. Right parietal and left medial thalamic/midbrain junction acute to subacute\ninfarct without definite evidence of hemorrhagic transformation.\n3.  Atrophy, probable small vessel ischemic changesand chronic infarcts as\ndescribed.\n4. Paranasal sinus disease , as described."
        },
        {
            "input": "No areas of slow diffusion.  No intracranial hemorrhage.  No intracranial\nmass.  The brain is normal in signal intensity and morphology.  The\nventricular profile is normal.  The intracranial arteries demonstrate normal\nT2 flow void.  The orbits appear normal.  The paranasal sinuses are clear. \nThe pituitary appears normal.  The craniocervical junction is normal.",
            "output": "1. Essentially normal MRI head."
        },
        {
            "input": "Contrast was not able to be administered due to the patient's renal function.\n\nA T1 isointense, T2 slightly heterogeneous lesion in the left aspect of the\nsella measures 1.8 x 1.2 x 1.3 cm, unchanged from the previous examination.\nThere is no mass effect on the optic chiasm.  The mass extends into the left\ncavernous sinus as seen previously, but does not encase the carotid artery.\nDisplacement of the infundibulum to the right is unchanged. No intrinsic T1\nhyperintensity is seen within the mass to suggest hemorrhage.\n\nElsewhere within the brain parenchyma, there are scattered foci of T2 and\nFLAIR prolongation compatible with chronic small vessel ischemic disease.  The\nventricles, cerebral sulci and cisterns are unchanged in size and\nconfiguration.",
            "output": "Stable left-sided sellar lesion."
        },
        {
            "input": "There is a focus of restricted diffusion in the left frontal lobe (series 502,\nimage 22) which may represent acute/subacute infarct versus a nonenhancing\nmetastatic lesion.  Please correlate clinically.  There is a focus of\nsusceptibility artifact in the right temporal lobe (series 11, image 8) which\nmay represent a chronic microhemorrhage.  There is a 0.9 x 1.3 cm enhancing\nmass (series 9, image 81) in the left occipital horn choroid plexus with no\nrestricted diffusion which may represent a choroid plexus papilloma.  There is\nno evidence of edema, mass effect, midline shift or infarction.  Moderate\nperiventricular and subcortical white matter hypodensities are nonspecific but\nlikely sequelae of chronic small vessel ischemic disease.  There is mild\nprominence of the ventricles and sulci suggestive of involutional changes.",
            "output": "1. A focus of restricted diffusion in the left frontal lobe which may\nrepresent acute/subacute infarct versus a nonenhancing metastatic lesion. \nPlease correlate clinically.\n2. A  0.9 x 1.3 cm enhancing lesion in the left occipital horn choroid plexus\nwhich may represent a choroid plexus papilloma vs less likely a\nxanthogranuloma.  Attention on follow up is recommended.\n3. Moderate periventricular and subcortical white matter disease.\n\nRECOMMENDATION(S):  MRI brain without and with contrast in 3 months is\nrecommended."
        },
        {
            "input": "There is no acute infarct or intracranial hemorrhage.  A enhancing left\nchoroid lesion in the trigone is unchanged.  No new intracranial mass or\nenhancement.  Previously described left frontal cortical diffusion-weighted\nsignal abnormality has resolved.  The sulci, ventricles and cisterns are\nwithin expected limits for the degree of mild senescent related global\ncerebral volume loss.  Severe confluent periventricular and subcortical\nT2/FLAIR white matter hyperintensities are nonspecific and unchanged.  The\nmajor intracranial flow voids are preserved.  The dural venous sinuses are\npatent.\n\nThere is mild mucosal thickening of the ethmoid air cells.  The orbits are\nunremarkable.  No significant fluid signal is seen the mastoid air cells.  No\nsuspicious marrow signal.",
            "output": "1. No new intracranial lesions.  No new abnormal enhancement.  No findings\nsuggestive of metastatic disease at this time.\n2. Enhancing lesion of the left trigonal choroid plexus is unchanged from\nprior examination, potentially representing a choroid plexus papilloma.\n3. There is no acute infarct or intracranial hemorrhage.  Severe confluent\nperiventricular and subcortical T2/FLAIR white matter hyperintensities are\nunchanged.\n4. No suspicious osseous lesions.\n5. Additional findings described above."
        },
        {
            "input": "There has been no significant interval change.  Diffuse hyperintensities in\nthe white matter as well as in the pons are unchanged compared to the prior\nstudy.  No micro hemorrhages are seen.  There is no mass effect midline shift\nor hydrocephalus.  Following gadolinium no abnormal parenchymal enhancement is\nidentified.  Enhancement within the left trigone is unchanged related to\nchoroid plexus.  No focal bony signal abnormalities are identified.  No acute\ninfarcts are seen.",
            "output": "No change from the previous MRI examination of ___.  No enhancing\nbrain lesions are seen.  No significant new abnormalities."
        },
        {
            "input": "Study is moderately degraded by motion.  Within these confines:\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  There is mild prominence of the ventricles and sulci\nsuggestive of involutional changes.  There is no abnormal enhancement after\ncontrast administration.  Nonspecific low-lying cerebellar tonsils with\napproximately 2 mm extension inferior to foramen magnum.  Mucosal thickening\nof all paranasal sinuses noted.  Left frontal calvarial probable hemangioma is\nnoted (3:6; 9:152).\n\n No definite focal white matter lesion seen.  No prepontine cisternal masses. \nBilateral probable SCA branches are suggested to contact bilateral prepontine\ncistern cranial nerve 5 segments (see (see 600:80-85).  No definite\ncompressing adjacent large vessels along course of CN5 into cavernous sinus\nare seen.  No abnormal enhancing masses on post contrast images are noted.",
            "output": "1. Study is moderately degraded by motion.\n2. No acute intracranial abnormality.\n3. Extensive paranasal sinus disease , as described.\n4. Within limits of study, no definite evidence of abnormal intracranial\nenhancement, or cerebellar pontine or IAC mass.\n5. Suggested nonspecific probable SCA branches contacts bilateral CN V\nprepontine cistern segments.\n6. Nonspecific low-lying cerebellar tonsils as described."
        },
        {
            "input": "Limited examination due to patient motion despite multiple attempts, within\nthis limitation, grossly there is no evidence of acute intra",
            "output": "Essentially normal MRI of the brain with and without contrast, there is no\nevidence of acute intracranial process, there is a grossly unchanged left\nhemispheric porencephalic cyst, apparently communicating with the left lateral\nventricle producing thinning of the adjacent structures like corpus callosum\nand cingulate gyrus.  Similar pattern of brain atrophy is redemonstrated\ninvolving the left greater than right anterior temporal lobes and left\ncerebral hemisphere.  Unchanged subcortical and periventricular areas of FLAIR\nhigh-signal intensity, which are nonspecific and may reflect changes due to\nchronic small vessel disease.  Within the limits of this exam, grossly there\nis no evidence of abnormal enhancement after contrast administration.  There\nis no evidence of acute intracranial hemorrhage.  No diffusion abnormalities\nare detected.  The major vascular structures are present and demonstrate\nnormal distribution.  The orbits are notable for scleral band on the left, the\nparanasal sinuses appear normally pneumatized.  The middle ear cavities and\nmastoid air cells are clear.  Mild degenerative changes are visualized in the\nupper cervical spine with spondylosis at C3-C4 level, partially evaluated this\nexam (series 2, image 11)..\n\nNOTIFICATION:  1.  Limited examination due to patient motion, within this\nlimitation, grossly there is an unchanged large left hemispheric porencephalic\ncyst, apparently communicated with the left lateral ventricle as described\nabove.\n\n2.  There is no evidence of acute intracranial process or hemorrhage.  There\nis no evidence of abnormal enhancement after contrast administration.\n\n3.  Similar pattern of atrophy subcortical areas of high-signal intensity on\nFLAIR and T2 weighted images, which are nonspecific and may represent changes\ndue to chronic small vessel disease."
        },
        {
            "input": "Head MRI: There is a large right occipital pole acute infarct with two small\nfoci of hemorrhagic transformation. Additional smaller acute infarcts are also\npresent in the right occipital and parietal lobes, posterior right frontal\nlobe, anterior right external capsule, and right thalamus.   A left occipital\nchronic infarct is noted. Numerous foci of high T2 signal in the subcortical,\ndeep and periventricular white matter of the cerebral hemispheres are likely\nsequela of chronic small vessel ischemic disease. Mild age-appropriate\nprominence of the ventricles and sulci is noted.\n\nNeck MRA:There is a 3 vessel aortic arch. Axial T1 weighted fat suppressed\nimages demonstrates high signal, consistent with an intramural hematoma, in\nthe right carotid system involving the distal common carotid artery, proximal\nexternal carotid artery, and proximal and mid right internal carotid artery.\nThe CTA from 4 days earlier demonstrates a filling defect in the right\ninternal carotid artery from its origin to the distal supraclinoid segment,\nand corresponding luminal narrowing is unchanged on the gadolinium enhanced\nMRA compared to the CTA. However, the distal cervical and intracranial right\ninternal carotid artery does not demonstrate T1 hyperintensity of intramural\nhematoma on fat suppressed T1 weighted images. The left cervical carotid\nsystem, and the cervical vertebral arteries, are widely patent.\n\nHead MRA: Distal supraclinoid right ICA is reconstituted. There is diminished\ncaliber of the right MCA compared with the left, which is new from the recent\nCTA. The bilateral A1 segments of the ACAs are small in caliber, new from the\nCTA, but this symmetric finding could be related to motion artifacts.  There\nis a 4 mm aneurysm of the paraclinoid left ICA projecting medially, as seen on\nthe CTA.\n\nThe right PCA demonstrates slight irregularity of the P1 segment and\nmoderately decreased caliber distally. The left PCA demonstrates an irregular\nP1 segment, a high-grade stenosis in the P2 segment, and robust distal\nreconstitution. These findings are similar to the CTA and likely related to\natherosclerosis, given the patient's age.",
            "output": "1.  Large right occipital pole acute infarct. Multiple small acute infarcts in\nthe right occipital, parietal, and posterior frontal lobes, as well as right\nanterior external capsule and right thalamus. This distribution suggests\nembolic etiology. Chronic left occipital infarct is also noted.\n\n2. Intramural hematoma of the distal right CCA extending into the proximal\nright ECA and the proximal and  mid right ICA, indicating dissection. The\ngadolinium enhanced MRA indicates that luminal narrowing related to dissection\nalso extends into the distal cervical, petrous and cavernous right ICA, as\nseen on the recent CTA from ___, though no corresponding intramural\nhematoma is seen in the false lumen at these levels.\n\n3. Right PCA demonstrates slight irregularity of the P1 segment and moderately\ndecreased caliber distally. Left PCA demonstrates an irregular P1 segment,\nhigh-grade stenosis of the P2 segment, and robust distal reconstitution. These\nfindings are similar to the recent CTA and likely related to atherosclerosis.\n\n4.  4 mm aneurysm of the paraclinoid left ICA projecting medially, as seen on\nthe recent CTA."
        },
        {
            "input": "There is no intra or extra-axial mass effect, acute hemorrhage or infarct.\nSulci, ventricles and cisterns are within expected limits for age. There are\nvery few subcortical and periventricular T2/FLAIR white matter\nhyperintensities, which are nonspecific, but commonly seen in the setting of\nchronic microangiopathy.\nSubtle increased signal intensity in the region of the mamillary bodies and in\nthe posterior midbrain are of equivocal and uncertain significance.\nThere is a enlarged 5 mm saccular hypointense focus can relate to flow void\narising from the basilar artery (series 5, image 9) suspicious for an aneurysm\nor pneumatized portion of the sphenoid or dorsum sella.\nSmall mucous retention cyst in the right maxillary sinus is noted. Otherwise\nthe paranasal sinuses are clear.\nThe orbits are unremarkable. The mastoid air cells are clear.",
            "output": "1. No evidence of acute infarct or intracranial hemorrhage.\n2. Nonspecific very few punctate T2/FLAIR white matter hyperintensities,\ncommonly seen in the setting of chronic microangiopathy. Clinical correlation\nis recommended.\n3. Subtle increased signal intensity in the region of the mamillary bodies and\nin the posterior midbrain are of equivocal and uncertain significance as can\nbe seen even otherwise; given the clinical concern as mentioned on the\nrequisition, clinical correlation and followup study can be considered to\nassess for any interval change.\n4. 5 mm T2 hypointense focus in proximity to the basilar artery, may represent\nsaccular flow void arising from the basilar artery, suspicious for an aneurysm\nor pneumatized portion of the sphenoid or dorsum sella. Further evaluation\nwith CTA of the head or MRA is recommended.\n\nNOTIFICATION:   The findings were discussed by Dr. ___ with Dr.\n___ on the telephone on ___ at 8:31 AM, at the time of\ndiscovery of the findings."
        },
        {
            "input": "There is no acute infarction in the brainstem or elsewhere in the brain\nparenchyma.  There is no evidence for edema, mass effect, or parenchymal blood\nproducts.  The ventricles, basal cisterns, and cerebral sulci are normal in\nsize for age. The cerebellar tonsils are normally positioned. Major arterial\nflow voids are grossly preserved. The intracranial vasculature was better\nassessed on the preceding CTA.",
            "output": "No acute infarction. No evidence for other intracranial abnormalities on\nnoncontrast MRI."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.",
            "output": "No acute intracranial abnormalities identified.  No concerning enhancement\nidentified.\n\nNOTIFICATION:  The impression above was entered by Dr. ___ on\n___ at 16:44 into the Department of Radiology critical communications\nsystem for direct communication to the referring provider."
        },
        {
            "input": "The 3.2 x 3.3 x 2.8 cm heterogeneously enhancing mass in the right cerebellar\nhemisphere is unchanged.  The surrounding edema and local mass effect with\neffacement of the fourth ventricle is unchanged.  Downward herniation of the\ncerebellar tonsils and upward herniation of the cerebellar vermis are\nunchanged.  The lateral and third ventricles are enlarged, unchanged from the\nprior examination.  No new enhancing lesions are identified.",
            "output": "Unchanged, heterogeneously enhancing mass in the right cerebellar hemisphere,\ncausing obstructive hydrocephalus.  Differential diagnosis includes\nmetastases, medulloblastoma, hemangioblastoma, or astrocytoma."
        },
        {
            "input": "Right occipital/ suboccipital craniectomy and cranioplasty is again seen. \nFluid collection in the scalp overlying the cranioplasty appears increased\ncompared to the ___ CT, now 10 mm in width the level of the right\noccipital lobe as well as at the level of the right parietal lobe, and\npreviously 10 mm in width at the level of the right parietal lobe and 3 mm in\nwidth at the level of the right occipital lobe.  There is no rim enhancement. \nAir within this collection has slightly decreased in extent.\n\nCompared to ___, extra-axial pneumocephalus has decreased but not\ncompletely resolved.  Small extra-axial hematoma remains present along the\nright cerebellar hemispheric convexity.  There is expected postsurgical dural\nenhancement in the posterior fossa.\n\nIn the right cerebellar surgical bed, there is a small focus of air, decreased\ncompared to ___, fluid, and blood products.  The blood products\ndemonstrate mixed hyperintensity and hypo intensity on precontrast T1 weighted\nimages and heterogeneous susceptibility artifact on gradient echo images. \nPostcontrast images demonstrate no definite masslike enhancement outside of\nthe blood products to suggest residual tumor.\n\nThere is persistent edema in the right cerebellar hemisphere and right\nsuperior vermis.  Leftward displacement and partial effacement of the fourth\nventricle, as well as severe effacement of the basal cisterns at the level of\nthe medulla and pons and moderate effacement of the basal cisterns at the\nlevel of the midbrain , are similar to the ___ pre-surgical MRI\nand the ___ postsurgical CT.  Left greater than right cerebellar\ntonsillar herniation into the foramen magnum persists, similar to ___.\n\nThe third and lateral ventricles have decreased in size compared to ___ and ___.  Occipital horns remain mildly prominent for age,\nbut the patient's baseline is not known.  Thin linear T2 hyperintensity along\nthe ependymal margins of the lateral ventricles is unchanged.\n\nMinimal signal abnormality on diffusion-weighted images along the anterior\nmargin of the right cerebellar surgical bed on images 5:5 and 6:5, as well as\nminimal signal abnormality on diffusion-weighted images along the posterior\nmargin of the right cerebellar surgical bed on images 5:6 and 6:6, is probably\nsecondary to susceptibility artifact from blood products, rather than minimal\ncontusion.",
            "output": "1. Increased fluid collection in the right scalp overlying the occipital/\nsuboccipital cranioplasty, with slightly decreased air.  No rim enhancement to\nsuggest infection.\n2. Stable small extra-axial hematoma along the right cerebellar hemispheric\nconvexity, with resolved or decreased extra-axial pneumocephalus.\n3. Fluid, blood, and decreasing air in the right cerebellar surgical bed.  No\nevidence for residual enhancing mass.\n4. Edema in the right cerebellar hemisphere and vermis has not significantly\nchanged since ___.  Partial effacement of the fourth ventricle,\nsevere mass effect on the basal cisterns, and herniation of left greater than\nright cerebellar tonsils, are similar to ___.  However,\nsupratentorial hydrocephalus has improved.\n\nRECOMMENDATION(S):  Follow up MRI with and without contrast is recommended\nafter resolution of T1 hyperintense blood products in the surgical bed."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.\n\nThere is a small retention cyst in the left maxillary sinus.  Minimal mucosal\nthickening ethmoid sinus.  The orbits are unremarkable.  The principal flow\nvoids are preserved.  The dural venous sinuses are patent.",
            "output": "1. No acute findings.  No mass."
        },
        {
            "input": "Multiple punctate foci of low diffusion are seen in the bilateral frontal\nlobes and occipital lobes.  There is no evidence of hemorrhage, edema, masses,\nmass effect, or midline shift.  There is focal encephalomalacia in the left\ncerebellum, likely secondary to prior lacunar infarction.  Periventricular and\nsubcortical T2 and FLAIR hyperintensities are noted.  There is prominence of\nthe ventricles and sulci suggestive involutional changes.  There is loss of\nthe normal left petrous ICA flow void with reconstitution at the terminal ICA.\nFLAIR hyperintense signal is noted in the terminal left ICA and MCA branches,\nlikely secondary to slow flow.\n\nA retention cyst is seen in the left maxillary sinus. Minimal mucosal\nthickening in the ethmoid sinuses is noted.  Bilateral cataract extractions\nare seen.\n\nMinimal fluid is seen in the left mastoid air cells.",
            "output": "1. Multiple acute infarctions in the bilateral cerebral hemispheres, likely\nembolic in etiology.  No mass effect, midline shift or hemorrhage.\n2. Loss of the normal flow void in the left petrous internal carotid artery\nwith reconstitution at the terminal left ICA and probable slow flow distally. \nThis can be further evaluated on a dedicated CTA or MRA."
        },
        {
            "input": "There is symmetric T2/FLAIR hyperintensity within the bilateral basal ganglia\nincluding the caudate head and putamen.  There is symmetric increased signal\nintensity in the bilateral basal ganglia, corona radiata, perirolandic cortex\nand along the cortex of the medial occipital lobes on the diffusion-weighted\nimages.  There is no evidence of hemorrhage, masses, mass effect or midline\nshift.  The ventricles and sulci are normal in caliber and configuration. \nThere is no abnormal enhancement after contrast administration.\n\nThere is mucosal thickening within the paranasal sinuses with bilateral\nmaxillary mucous retention cyst.  There is a small amount of fluid signal\nintensity noted in the bilateral mastoid air cells.  The orbital structures\nare unremarkable.",
            "output": "1. Symmetric slow diffusion within the bilateral basal ganglia, thalami,\ncorona radiata, perirolandic and medial occipital cortex with T2/FLAIR\nhyperintensity in the basal ganglia and thalami consistent with sequelae of\nglobal hypoxic ischemic injury."
        },
        {
            "input": "There is no evidence of acute infarction.  No intracranial hemorrhage.  No\nmass, mass effect, edema or midline shift.\n\nThe ventricles and sulci are prominent, compatible with global cerebral\natrophy with demonstrating frontal lobe predominance.  Numerous T2/FLAIR\nhyperintensities within the periventricular, deep, and subcortical white\nmatter are nonspecific and likely reflect the sequelae of chronic small vessel\nischemic disease.\n\nThe basal cisterns are patent.  There is no evidence of impending, downward\nherniation.  There is gross preservation of the principal intracranial\nvascular flow voids.\n\nMild mucosal thickening are noted within several scattered bilateral ethmoid\nair cells and within the frontal sinuses.  The remainder of the visualized\nparanasal sinuses, middle ear cavities, and mastoid air cells are well aerated\nand clear.  The orbits are within normal limits bilaterally.",
            "output": "1. No evidence for acute intracranial process.\n2. Global cerebral atrophy with bifrontal lobe predominance, and evidence for\nchronic microangiopathy."
        },
        {
            "input": "There is no evidence of acute infarction.  No intracranial hemorrhage.  No\nmass, mass effect, edema or midline shift.\n\nThe ventricles and sulci are normal, without evidence of hydrocephalus. The\nbasal cisterns are patent.  There is no evidence of impending, downward\nherniation.  There is gross preservation of the principal intracranial\nvascular flow voids.\n\nFollowing the administration of intravenous contrast material, there is no\nabnormal enhancement.  The dural venous sinuses appear patent on MP-RAGE\nimagine sequences.\n\nThe visualized paranasal sinuses, middle ear cavities, and mastoid air cells\nare well aerated and clear.  The orbits are within normal limits bilaterally.",
            "output": "1. Unremarkable contrast-enhanced MRI examination of the head."
        },
        {
            "input": "MRI BRAIN:\n\nThere are punctate foci of slow diffusion in bilateral para hippocampal gyri\nand the left crus of fornix (series 602, images 11, 12, 14).  There is no\ndefinite FLAIR signal abnormality although this may be due to very small size\nof these lesions.\n\nThere is no evidence of blood products, mass effect, or contrast enhancement. \nThere is no evidence for an enhancing mass.  The ventricles and sulci are\nage-appropriate.  Mild periventricular white matter T2 hyperintensity and\nscattered foci of T2 hyperintensity in the subcortical and deep white matter\nare nonspecific but likely sequela of mild chronic small vessel ischemic\ndisease in this age group.  Dural venous sinuses are patent on postcontrast MP\nRAGE images.\n\nThere is mild mucosal thickening in the left frontal, bilateral ethmoid and\nbilateral sphenoid sinuses.  There is a small mucous retention cyst in the\nright maxillary sinus.\n\nMRA NECK:\nCervical carotid and vertebral arteries appear widely patent without evidence\nfor flow-limiting stenosis.  There is no evidence of internal carotid artery\nstenosis by NASCET criteria.  There is a 3 vessel aortic arch.\n\nMRA BRAIN:\nThe intracranial vertebral and internal carotid arteries and their major\nbranches appear normal without evidence of stenosis, occlusion, or aneurysm\nformation.",
            "output": "1. Three punctate acute infarcts involving bilateral para hippocampal gyri and\nthe left crus of fornix.\n2. Unremarkable head and neck MRA.\n\nNOTIFICATION:  Findings were communicated by Dr. ___ to Dr. ___\n___, on ___ at 4:55  pm."
        },
        {
            "input": "Previously seen seen punctate foci of acute infarcts involving bilateral\nmedial temporal regions have resolved.  No new infarcts are seen.  There is no\nmass effect or midline shift.  Mild mucosal thickening is seen in the sphenoid\nand ethmoid sinuses.  Vascular flow voids are maintained.",
            "output": "Resolution of previously seen diffusion abnormalities in bilateral medial\ntemporal lobes.  No new abnormalities are seen."
        },
        {
            "input": "There is no intra or extra-axial mass effect, acute hemorrhage or infarct. \nThe sulci, ventricles and cisterns are within expected limits for the\npatient's age.  There are mild periventricular and subcortical T2/FLAIR white\nmatter hyperintensities, nonspecific, but compatible with chronic\nmicroangiopathy in a patient of this age.  The major intracranial flow voids\nare preserved.  The dural venous sinuses are patent.  No abnormal enhancement\nof the visualized cranial nerves.\n\nModerate mucosal thickening of the ethmoid air cells and mild mucosal\nthickening of the maxillary sinuses.  The orbits are unremarkable.  Trace\nfluid signal is seen in the bilateral mastoid tips.  No suspicious marrow\nsignal.",
            "output": "1. Unremarkable contrast enhanced MRI brain.  There is no acute infarct or\nintracranial hemorrhage.  No intracranial mass.  No abnormal enhancement.\n2. There is no abnormal enhancement of the visualized cranial nerves.\n3. Mild periventricular and subcortical T2/FLAIR white matter hyperintensities\nare nonspecific, but compatible with chronic microangiopathy in a patient of\nthis age.\n4. Paranasal sinus disease as described above."
        },
        {
            "input": "There are areas of tissue loss in the medial left cerebellar hemisphere\nconsistent with the history of left ___ infarction.  There is no other\nevidence of infarction.  There is no evidence of hemorrhage.\n\nPrincipal intracranial vascular flow voids are preserved. The ventricles and\nsulci are normal in size and configuration.  No intracranial mass is\nidentified.\n\nThe brainstem, posterior fossa, and cervicomedullary junction are preserved.\nThe orbits, periorbital and paracavernous spaces are normal.  No abnormality\nof the skull base or calvarium is identified.",
            "output": "1. Sequelae of left ___ infarction.\n\n2.  No evidence of hemorrhage."
        },
        {
            "input": "MRA brain: The intracranial vertebral and internal carotid arteries and their\nmajor branches appear normal without evidence of stenosis, occlusion, or\naneurysm formation.  The left vertebral artery is dominant.\n\nVisualized aspect of the brain is grossly unremarkable.  No acute hemorrhage,\nedema, mass effect or infarction is seen.",
            "output": "1. No intracranial aneurysm, stenosis or occlusion is seen.\n2. No acute intracranial abnormality."
        },
        {
            "input": "MR BRAIN:\nThere are small late acute to early subacute infarcts involving the right\noccipital pole and the posterior right cingulate gyrus, with high signal on\ndiffusion-weighted images, partial low signal on the ADC map, and high signal\non T2 weighted/FLAIR images, new compared to the ___ MRI.\n\nThere is also new 5 mm focus in the superolateral left cerebellar hemisphere,\nwhich demonstrates high signal on the diffusion-weighted images, partial high\nsignal on the ADC map, high signal on T2 weighted/FLAIR images, and contrast\nenhancement, consistent with a late subacute infarct which is older than 10\ndays.\n\nRedemonstrated is a posterior right frontal lobe late subacute infarct\ndemonstrating post-contrast serpiginous enhancement and hemorrhagic\ntransformation.  Increased associated low signal on gradient echo images\ncompared to the ___ MRI may represent a slight increase in blood\nproducts, as evidenced on the ___ CT compared to the ___ CT.\n\nThere is no shift of midline structures.  There is no effacement of the\nventricles and basal cisterns.  Mild age-related prominence of the ventricles\nand sulci is again seen. Moderately numerous subcortical, deep and\nperiventricular white matter T2/FLAIR hyperintensities are nonspecific but\ncompatible with chronic small vessel ischemic disease given the patient's age.\nAge-related parenchymal volume loss is again noted with prominent ventricles\nand sulci.\n\nPostcontrast MP RAGE images demonstrate patent dural venous sinuses.\n\nNo significant change in the lobulated left intra parotid mass measuring up to\n2.9 x 1.9 x 2.4 cm with areas of T2 hyperintense signal.\n\nThere is a left concha bullosa.  Anterior to the concha bullosa is a 0.9 cm AP\nx 1.5 cm TV nasal polyp.  There is mild mucosal thickening in the ethmoid air\ncells.\n\nSagittal images demonstrate degenerative changes in the included upper\ncervical spine.\n\nMRA BRAIN:\n\nMotion artifact limits evaluation.  Visualization of the proximal V4 segments\nof the vertebral arteries is technically limited; they are better assessed on\nthe prior head and neck CTA.  There is ___ termination of the non dominant\nright vertebral artery, as seen on the prior head and neck CTA.  The large\ndominant left vertebral artery and the basilar artery are tortuous.  The right\nPCA P3/P4 segments are relatively small in caliber compared to the left,\nunchanged since the prior CTA.  There is no evidence for a new flow-limiting\nstenosis.  No evidence for an aneurysm larger than 3 mm.",
            "output": "1. Small late acute to subacute small infarcts involving the right occipital\npole and the posterior right cingulate gyrus, new compared to ___.\n2. New 5 mm late subacute infarct in the left cerebellum, older than 10 days,\nwith associated contrast enhancement.\n3.  Posterior right frontal lobe late subacute infarct is again seen with\npossible increase in associated blood products.  No significant mass effect.\n4. No evidence of dural venous sinus thrombosis.\n5. Motion limited brain MRA.  Persistent diminished caliber of the distal\nright PCA.  No evidence for a new flow-limiting stenosis.\n6. Unchanged lobulated left intra parotid mass measuring up to 2.9 x 1.9 x 2.4\ncm possibly representing a pleomorphic adenoma (benign mixed tumor). \nDifferential considerations also include Warthin's tumor, with other salivary\ngland malignancies felt to be less likely.  Recommend comparison with any\navailable outside imaging to evaluate for stability.\n\nNOTIFICATION:  The following preliminary report was provided electronically on\n___ at 18:49 by Dr. ___: \"MRI head: Re-identified is a\nsubacute right frontal infarct with hemorrhagic transformation, with\nassociated enhancement, likely secondary to infarction itself.  Mild rim of\nedema is again demonstrated.  There is also punctate areas of slow diffusion\nin the right medial occipital lobe with associated FLAIR hyperintensity,\nlikely reflecting late acute to early subacute infarcts. An additional small\narea of additional slowed diffusion with FLAIR hyperintensity is noted in the\nright posterior occipital lobe, an additional site of late acute to early\nsubacute infarct.  Additionally, there is a small 5 mm focus of enhancement in\nthe left cerebral hemisphere which is FLAIR hyperintense, without significant\nsurrounding edema, though without slowed diffusion.  No definite correlate for\nthis area seen on prior CT, though may be heart resolve given its small size. \nThis could represent an additional area of enhancement denoting subacute\ninfarction, though an underlying mass lesion is not excluded, and follow-up is\nadvised.  No other areas of abnormal enhancement are seen.     MRA head: There\nis a left dominant vertebrobasilar system it is suspected that the right\nvertebral artery is hypoplastic, with ___ termination, with lack of flow in\nthe MRA due to small size/slow flow, though this area is suggested to be\npatent on the postcontrast MP rage series.  Otherwise, the intracranial\narterial vasculature appears patent without high-grade stenosis, occlusion, or\naneurysmal formation.\""
        },
        {
            "input": "There is slowed diffusion in the posterior right frontal lobe (05:24),\ncorresponding to the location of the known infarct.  Minimal curvilinear\nenhancement and edema are noted within this region.  There are foci of\nsusceptibility on gradient echo, compatible with blood products.\n\nNo other areas of acute infarction are noted.  There is mild local mass\neffect, without shift of normally midline structures.  Prominence of the\nventricles and sulci are compatible with age related involutional changes. \nScattered areas of periventricular/subcortical T2/FLAIR white matter\nhyperintensities are nonspecific, but likely reflect a sequela of chronic\nsmall vessel disease.  Major intracranial vascular flow voids are preserved. \nLeft vertebral artery appears dominant.  Dural venous sinuses are patent.  The\norbits are within normal limits.  Mild mucosal thickening of the ethmoid air\ncells is noted.\n\nThere is a lobulated mass in the left parotid gland that measures\napproximately 2.9 x 1.9 x 2.4 cm (11:1, 100:70).  It is heterogeneous in\nsignal intensity on T2 weighted imaging, but with areas that are moderately\nhyperintense on T2 weighted imaging (11:2).",
            "output": "1. Acute infarction of the posterior right frontal lobe with associated blood\nproducts.  No additional infarctions identified.\n2. Lobulated intraparotid mass measuring up to 2.9 x 1.9 x 2.4 cm with areas\nof T2 hyperintense signal, may represent a pleomorphic adenoma (benign mixed\ntumor).  Differential considerations would include a Warthin tumor, with other\nsalivary gland malignancies felt to be less likely.  Recommend comparison with\nprior imaging to evaluate for stability.\n\nRECOMMENDATION(S):  Recommend comparison with prior imaging to evaluate\nstability of the left parotid tumor.\n\nNOTIFICATION:   The findings were discussed with ___, M.D. by ___\n___, M.D. on the telephone on ___ at 1:24 pm, 10 minutes after\ndiscovery of the findings."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  The major intracranial flow voids are preserved. The\nventricles and sulci are prominent, similar to ___.  Bilateral\nperiventricular and subcortical white matter T2/FLAIR hyperintensities are\nnonspecific but most likely representing sequela of chronic small vessel\nischemic changes.\n\nThe paranasal sinuses are clear.  There is small amount of fluid in the right\nmastoid air cells.  Fluid is also seen in the nasopharynx.  These are\nnonspecific but likely related to intubation.  The orbits are unremarkable.",
            "output": "1. No acute intracranial abnormality on noncontrast head MRI.  Specifically no\nacute infarct or intracranial hemorrhage.\n2. There are periventricular and subcortical T2/FLAIR white matter\nhyperintensities, which are nonspecific, but compatible with chronic\nmicroangiopathy in a patient of this age.\n3. Additional findings described above."
        },
        {
            "input": "There are foci of slow diffusion with intermediate/low signal on the ADC map\nin hyperintensity within the medial left cerebellum and left cerebellar\nvermis.  Superimposed scattered subcortical and periventricular white matter\nFLAIR hyperintensities are compatible with small vessel disease given the\npatient's age.\n\nThere is a focus of susceptibility within the right cerebellar hemisphere\nlikely representing an old microhemorrhage.\n\nThe there is no evidence of recent hemorrhage, mass effect or midline shift. \nProminence of the ventricles and cerebral sulci are compatible with age\nrelated involutional changes.\n\n The major intracranial vascular flow voids are maintained.  The paranasal\nsinuses, mastoid air cells and orbits are normal.",
            "output": "1. Evidence of late acute to early subacute infarcts of the medial left\ncerebellum and left cerebellar vermis.\n2. A focus of susceptibility within the right cerebellar hemisphere likely\nrepresents an old microhemorrhage.\n3. Moderate white matter small vessel disease.\n4. Generalized parenchymal volume loss, likely age related.\n\nRECOMMENDATION(S):  The findings were discussed with ___, M.D. by\n___, M.D. on the telephone on ___ at 9:13 am, 10 minutes\nafter discovery of the findings."
        },
        {
            "input": "MRI BRAIN:\nThere are multifocal acute infarcts.  The largest infarction is of the right\nmiddle cerebral artery territory involving the right frontal lobe and anterior\nright temporal lobe.  Additional moderately sized acute infarcts involve the\nleft temporoparietal periventricular white matter (60:19) and the right\ncerebellar hemisphere (650:12).  A moderate area of slow diffusion about the\nright superior frontal gyrus near the vertex may reflect acute infarct versus\nsubarachnoid blood products (60:27, 7:21).  Numerous additional foci of slow\ndiffusion are scattered throughout both cerebral hemispheres.  Some of these\nmay reflect acute infarcts while others may be related to diffusion-weighted\nsignal changes from hemorrhage.  With respect hemorrhage, there are multifocal\nareas of blooming artifact on the gradient echo sequences, which are\npredominantly intraparenchymal but there may also be a new subarachnoid\ncomponents.  The largest focal areas of hemorrhage include the right occipital\nlobe (7:10), left temporal lobe (7:12), the and right cerebellar hemisphere\n(7:8).  Only the right occipital and left posterior temporal hemorrhage was\nclearly seen on head CT from 1 day prior.  There is trace intraventricular\nhemorrhage layering dependently.\n\nThere is mild mass effect on the right lateral ventricle from edema associated\nwith the right middle cerebral artery infarction.  This is overall similar to\nthe day prior, and ventricular size is unchanged.  There is about 2 mm of\nleftward midline shift.  Trace layering fluid is present in the sphenoid\nsinuses.  There is mild mucosal thickening of the anterior ethmoid air cells. \nThere is opacification of the bilateral mastoid air cells.  The orbits are\nunremarkable.\n\nMRA BRAIN:\n\nThe right superior division of the M2 middle cerebral artery branches\ncompletely occluded, and nonvisualized open (851:1).  The inferior division\ndemonstrates severe narrowing shortly after its origin, seen on the same\nimage.  There are no additional areas of large vessel occlusion.  No\naneurysms.\n\nMRV: There is relatively diminished signal within the left transverse and\nsigmoid sinus, with signal visualized in the right jugular vein.  This is\noverall indeterminate, and could be related to asymmetry of dural venous sinus\nis versus venous sinus thrombosis.\n\nMRA NECK:\nThe origins of the great vessels, subclavian and vertebral arteries appear\nnormal bilaterally.  The common, internal and external carotid arteries appear\nnormal.  There is no evidence of internal carotid artery stenosis by NASCET\ncriteria.",
            "output": "1. Multifocal acute infarctions, including the right middle cerebral artery\nterritory, left temporoparietal periventricular white matter, and right\ncerebellar hemisphere.  Multifocal infarcts are most consistent with an\nembolic process.\n2. Numerous additional small foci of slow diffusion and scattered throughout\nboth cerebral cortices may reflect tiny infarcts versus is diffusion-weighted\nsignal changes associated with hemorrhage.\n3. Numerous scattered intraparenchymal and subarachnoid hemorrhage throughout\nboth cerebral hemispheres and in the right cerebellar hemisphere.\n4. Mild mass effect from edema involving the right middle cerebral artery\nterritory is similar, without herniation.\n5. MRA of the brain is notable for occlusion of the superior division right M2\nmiddle cerebral artery, and severe narrowing of the inferior division.\n6. Unremarkable MRA of the neck.\n7. MRV demonstrates asymmetric diminished signal within the left transverse\nand sigmoid sinus, which could be related to asymmetric dural venous drainage\npathway versus venous sinus thrombosis.\n8. Nonspecific bilateral mastoid effusions."
        },
        {
            "input": "When compared to prior, there has been no significant interval change. Again\nseen are periventricular and subcortical white matter T2/FLAIR\nhyperintensities. Additional lesion involving the left middle cerebellar\npeduncle is again seen. Overall, the distribution, size and extent of these\nlesions has not changed. There is no associated restricted diffusion. There is\nno associated enhancement based on the somewhat limited post-contrast sequence\ndue to patient motion despite repeat acquisition.\n\nThere is no infarct or hemorrhage. Ventricles and sulci are stable in\nconfiguration. Major intravascular flow voids are preserved.\n\nNo abnormal signal seen the paranasal sinuses. There is a 6 mm T2 hyperintense\nperipherally enhancing lesion with high signal on diffusion just posterior to\nthe right auricle within the subcutaneous tissues (8:1) potentially sebaceous\ncyst.",
            "output": "No significant interval change. White Matter lesions centered in the\nperiventricular white matter with additional lesions involving the subcortical\nwhite matter on the left middle cerebellar peduncle compatible with patient's\nhistory of multiple sclerosis. No evidence of new lesion."
        },
        {
            "input": "S compared to the prior examination dated ___, there has been no\nsignificant interval change with regard to the morphology in extent of\nnumerous bilateral T2/STIR hyperintensities within the periventricular and\nsubcortical white matter.  A lesion within the left middle cerebellar peduncle\n(4:9) is also minimally changed.  None of the visualized lesions demonstrate\nrestricted diffusion or contrast enhancement.\n\nThere is no evidence of acute infarction.  No intracranial hemorrhage.  No\nmass, mass effect, edema or midline shift.\n\nThe ventricles and sulci are normal, without evidence of hydronephrosis.  The\nbasal cisterns are patent.  There is no evidence of impending, downward\nherniation.  The sella turcica is within normal limits.\n\nThe visualized paranasal sinuses, middle ear cavities, and mastoid air cells\nare well aerated and clear.  The orbits are within normal limits bilaterally.",
            "output": "Numerous periventricular and subcortical white matter T2 hyperintense lesions,\nalso involving the left middle cerebellar peduncle, none of which are\nsignificantly changed from prior examination.  No discrete new lesion is\nidentified.  There is no evidence of restricted diffusion or contrast\nenhancement."
        },
        {
            "input": "The examination is severely limited secondary to extensive patient motion. \nWithin these confines:\n\nA previously noted 4 mm focus of FLAIR hyperintensity within the inferior\nmedial left frontal lobe (08:12), decreased in conspicuity as compared to the\nprior examination ___.  However, there is an new moderately\nextensive area ill-defined FLAIR hyperintensity within the inferior left\ncerebellar hemisphere involving the left middle cerebellar peduncle (8:7) with\nassociated mild enhancement (12:7).  Punctate focus of mildly decreased T2\nsignal within the area of enhancement series 10, image 7, associated subtle\ngradient abnormality, new finding since ___ and ___,\nfindings which favor infection.\n\nA punctate focus of high signal on DWI seen within the area FLAIR\nhyperintensity in the left inferior cerebellar hemisphere (702:9), without\ndefinite ADC correlate.  Otherwise, no additional candidate areas restricted\ndiffusion are identified.  There is no evidence for acute intracranial\nhemorrhage.  Previously seen pachymeningeal enhancement, dural thickening has\nnearly resolved.\n\nThere is new periatrial T2 signal abnormality on both sides, right greater\nthan left, with suggestion of subtle ependyma enhancement.\n\nThe ventricles and sulci are prominent, compatible global parenchymal volume\nloss.  There is gross preservation of the principal intracranial vascular flow\nvoids.\n\nMild mucosal thickening is seen in scattered ethmoid air cells, and fluid\nsignal is present in the right mastoid air cells.  The remainder of the\nvisualized paranasal sinuses, middle ear cavities, and mastoid air cells are\nwell aerated and clear.  The orbits are within normal limits bilaterally.",
            "output": "1. Severely motion limited examination.\n2. New enhancement, edema inferior left cerebellar hemisphere, middle\ncerebellar peduncle.  Area of abnormality has punctate focus of mineralization\nor microhemorrhage, which overall favors infection, and can be seen with\ntoxoplasmosis.  Lymphoma, PML, infarct are less likely.\n3. New mild periventricular edema, mildly more dilated ventricular system. \nSuggestion of subtle periatrial enhancement along the ependymal surface, may\nrepresent ventriculitis.  Meningitis component should be considered.\n4. Known, medial inferior left frontal lobe focus of infection has near\nresolved.\n5. Paranasal sinus disease and right mastoid fluid, as above."
        },
        {
            "input": "The study is markedly limited by motion artifact.  Please note that the MP\nrage postcontrast imaging is rendered uninterpretable.\n\nThe previously noted area of T2 and FLAIR hypointense signal abnormality in\nthe inferior aspect of the left cerebellar hemisphere with extension into the\nleft inferior, middle cerebellar peduncle and left lateral medulla (series 8,\nimage 7) demonstrates enhancement postcontrast and is increased in size\ncompared to prior imaging currently measuring 32 x 19 mm in the axial plane\n(20 x 12 mm previously).  Adjacent mild mass effect on the fourth ventricle\nwhich is partially effaced, worsened since prior.  No restricted diffusion. \nModerately worsened surrounding T2 signal abnormality.  There is mild\nhydrocephalus, which has been developing since ___ and ___.\n\nVentricular periatrial FLAIR edema with associated linear ependyma surface\nenhancement involving the atria bilateral (right more than left) shows\ninterval progression compared to prior.  Associated prominent enhancement of\nthe choroid plexus bilateral in this area is worsened since prior, a new since\n___.  Mild global periventricular edema elsewhere in the lateral\nventricles may be secondary to this process or from developing hydrocephalus..\nNo herniation.\n\nT2 and FLAIR hyperintense signal change involving the pineal gland with\nassociated mild enhancement is also more prominent compared to prior,\nmeasuring 1.3 cm x 0.9 cm today, compared with 0.8 cm x 0.6 cm on ___, and is new compared with ___.  Mass effect on the upper\ntectum is more prominent, with narrowed cerebral aqueduct.  New edema in the\nupper midbrain.\n\nThere is new FLAIR signal abnormality and subtle enhancement along the\nposteromedial margin of the right thalamus.\n\nT2 and FLAIR hyperintense changes in keeping with known infection in the\ninferior aspect of the left frontal lobe (series 7, image 14) appears fairly\nsimilar compared to most recent prior, but improved compared to MR done ___.  The previously known focus of infection in the posterior aspect\nof the right temporal lobe (series 7, image 11) is also markedly decreased in\nsize compared to prior imaging done ___.\n\nNo areas of microhemorrhage.  No areas of restricted diffusion within lesions.\n\nNo acute intracranial infarct.  No hemorrhage.  Partial opacification of the\nright mastoid air cells appear similar compared to prior.  The intracranial\narteries demonstrate normal T2 flow voids.\nMild mucosal thickening involving the paranasal sinuses.  The orbits appear\nnormal.  The dural venous sinuses are patent.",
            "output": "The study is markedly limited by motion artifact.\n\nInterval worsening, with increased size of enhancing lesion in the left\ncerebellum and cerebellar peduncles, worsened surrounding edema, worsened\nchoroid plexus and dependent mole enhancement the lateral ventricles, new\nenhancement in the right thalamus, increasing pineal nodule.\n\nWorsening hydrocephalus, may be sequela of ependymoma process, or increasing\nhydrocephalus.\n\nMass effect on the upper midbrain, tectum from pineal mass, with narrowed\ncerebral aqueduct, midbrain edema.\n\nConsider lymphoproliferative disease, probably less likely infective process\ngiven pineal gland involvement.  Granulomatous process, atypical infections\nincluding tuberculosis are unlikely.\n\nThe known foci of prior infection in the inferior aspect of the left frontal\nlobe and posterior aspect of the right temporal lobe appears fairly similar.\n\nRECOMMENDATION(S):  Correlation with LP may recommended.\n\nNOTIFICATION:  The findings were discussed with ___, M.D. by ___\n___, M.D. on the telephone on ___ at 11:46 am, 10 minutes after\ndiscovery of the findings."
        },
        {
            "input": "There is no evidence of edema, mass effect, acute or chronic infarction, or\nblood products.  There is mild global prominence of the ventricles and sulci\nconsistent with parenchymal involutional changes, without disproportionate\nmedial temporal or disproportionate parietal involvement.  Minimal linear\nperiventricular white matter T2 hyperintensity is nonspecific, but likely\nsequela of chronic small vessel ischemic disease in this age group. Principal\nintracranial flow voids are preserved.\n\nSmall mucosal retention cyst is identified in the right sphenoid sinus.",
            "output": "1. Mild global parenchymal volume loss without this portion and medial\ntemporal lobe parietal lobe involvement\n2. Minimal linear periventricular T2 hyperintensity is nonspecific but may be\nsecondary to minimal chronic small vessel ischemic disease in this age group.\n3. No evidence for acute or chronic infarction, mass effect, or blood\nproducts."
        },
        {
            "input": "There is no intra or extra-axial mass, acute hemorrhage or acute infarct.  No\nsignificant parenchymal signal abnormality is identified.  The sulci,\nventricles and cisterns are within expected limits for the degree of mild to\nmoderate senescent related global cerebral volume loss.  The major\nintracranial flow voids are preserved.  There is mild mucosal thickening of\nthe ethmoid air cells.  The remainder the paranasal sinuses are essentially\nclear.  The orbits are unremarkable.  There is new fluid opacification of the\nright mastoid air cells.",
            "output": "1. No acute intracranial abnormality on noncontrast MRI head.  Specifically no\nintracranial hemorrhage, acute infarct or mass.  No new parenchymal signal\nabnormality.\n2. There is new fluid opacification of the right mastoid air cells since\nexamination of ___."
        },
        {
            "input": "Motion artifact degrades the diagnostic quality of the imaging.  The T2\nimaging is rendered uninterpretable.  The T1 MP rage imaging is moderately\ncompromised.\n\nSmall solid nodular, and rim enhancing lesions with associated FLAIR\nabnormality are seen in the bilateral cerebral hemispheres.  1 lesion is in\nthe posterior aspect of left medial orbital gyri (series 7, image 11),\nenhancement is measuring 7 mm in diameter demonstrating rim enhancement\npostcontrast.  Additional lesion abutting lateral aspect of the probable left\npostcentral gyrus focus of enhancement measures 0.3 cm, adjacent or coursing\nartery.\nAdditional small enhancing lesion involving posteromedial right temporal lobe,\nsuperior left frontal gyrus, on the upper margin of the left insula.\nTwo 3 mm foci of high signal on diffusion weighted imaging present in the\nright middle frontal gyrus, right occipital lobe, without definite enhancement\nAbove lesions are new since MRI brain ___.\nGeneralized cerebral atrophy with ex vacuo dilatation of the ventricular\nsystem.  The craniocervical junction is normal.  The pituitary is normal.  The\ndural venous sinuses are patent.  Mild chronic small vessel ischemic changes.\nFairly diffuse and heterogenous decrease in bone marrow signal intensity in\nkeeping with history of AML.",
            "output": "1. Multiple small foci of enhancement involving bilateral cerebral\nhemispheres, 1 has rim enhancement, largest lesion measures 0.7 cm.  These\nlesions have developed since ___, and appearance favors\ninfectious process, possibly from systemic disseminated infection, with\npossible component of septic emboli. Some of the tiny lesions may represent\nsubacute infarcts.  Metastatic disease, lymphoproliferative disorder is less\nlikely.  No abscess.\n2. 1 small nodular enhancement at left inferior parietal lobe is adjacent to a\ncoursing artery, mycotic aneurysm cannot be excluded, MRA brain recommended\nfurther evaluation.\n\nRECOMMENDATION(S):  MRA brain without contrast to cover entire convexity.\n\nNOTIFICATION:   The findings were discussed with ___, M.D. by ___\n___, M.D. on the telephone on ___ at 9:38 am, 10 minutes after\ndiscovery of the findings.\n\nThe findings were discussed with ___, M.D. by ___\n___, M.D. on the telephone on ___ at 10:02 pm, 10 minutes after\ndiscovery of the findings."
        },
        {
            "input": "Assessment is moderate to severely limited by motion.  Within these limits,\nthe previously identified rim enhancing lesions are less evident on today's\nstudy.  A single 7 mm left medial frontal cortical lesion involving the medial\norbital gyrus demonstrates faint rim enhancement and appears diminished from\nprior MRI when it measured 10 mm (series 9, image 12; series 10, image 12). \nThe other previously described lesions are not appreciated on today's exam,\nsuggesting resolution.\n\nAs described on prior head CT, bilateral subdural fluid collections measure up\nto 13 mm on the right and 10 mm on the left are most prominent overlying the\nfrontal and temporal lobes, cause mass effect on the bilateral cerebral\ncortices, and appear overall stable in size from prior examination.  Several\nfoci of blooming on gradient echo sequences overlying the right posterior\nfrontal cortex suggest trace blood products within this collection (series 7:\nimage 7).  There is no significant midline shift.  The basal cisterns are\npatent.  Ventricles are stable in size and configuration from prior head CT\ngiven differences in technique. There is no evidence of infarction.",
            "output": "1. Moderate to severely motion degraded examination.\n2. Interval improvement of multifocal rim enhancing lesions, the majority of\nwhich are not appreciated on today's examination with isolated persistent left\nmedial frontal lesion measuring 7 mm.\n3. Overall stable bilateral subdural hygromas since ___ likely\ncontaining a small amount of blood products on the right."
        },
        {
            "input": "There is no evidence of edema, mass, mass effect, or acute infarction.  Two\npunctate foci of low signal on gradient echo images in the right inferior\nfrontal and right posterior paramedian parietal lobe, likely represent micro\nhemorrhages (series 6, images 17 and 19).  The scattered periventricular and\nsubcortical white matter foci of FLAIR hyperintense signal are nonspecific but\nlikely sequelae of chronic microangiopathy in this age group.  Prominence of\nthe ventricles and sulci is in keeping with age related global involutional\nchanges.  Principal intracranial vascular flow voids are preserved.\n\nThere is mucosal thickening in the right maxillary, bilateral ethmoid, and to\na lesser extent bilateral frontal and left maxillary sinuses.  There is near\ncomplete opacification of the right anterior ethmoid air cells.  Deviation of\nthe nasal septum, mucosal thickening, and secretions results in asymmetric\nnarrowing of the right nasal passage.  Aside from right cataract extraction,\nthe orbits are unremarkable.",
            "output": "1.  No evidence of mass, mass effect, or acute infarction.\n\n2.  Punctate foci of microhemorrhage in the right frontal and parietal lobes\nmay represent sequelae of prior injury or amyloid angiopathy.\n\n3.  Moderate white matter changes suggestive of chronic small vessel ischemic\ndisease and age related global atrophy.\n\n4.  Paranasal sinus disease as described, most severe in the right anterior\nethmoids."
        },
        {
            "input": "There is no evidence of enhancing mass, abnormal enhancement, or\nleptomeningeal disease.  There is no acute infarction.  There are stable foci\nof microhemorrhage within the right frontal and right parietal lobes.\n\nThere is diffuse parenchymal volume loss with prominence of the ventricles and\nsulci.  There are nonspecific periventricular and subcortical FLAIR\nhyperintensities, likely a sequela of chronic small vessel ischemic disease in\na patient of this age.  The major visualized arterial vascular flow voids are\npreserved.  The dural venous sinuses appear patent on post-contrast MPRAGE\nimages.\n\nThere is mucosal thickening of bilateral ethmoid air cells and a small left\nmaxillary sinus mucosal retention cyst.  There is stable partial fluid\nopacification of the right mastoid air cells.  Patient is status post right\nlens replacement.  Unchanged T1 intrinsically hyperintense focus along the\ninferior aspect of the clivus with questionable enhancement (10:118) likely\nrepresenting a hemangioma or fatty deposit.  Additional rounded lesions seen\non the prior skeletal survey within the calvarium are difficult to assess on\nthis study.",
            "output": "1. No evidence of enhancing mass or leptomeningeal disease.\n2. Stable right frontal and right parietal micro hemorrhages.  No acute\ninfarction.\n3. Diffuse parenchymal volume loss with probable chronic small vessel ischemic\ndisease.\n4. Additional findings as described above.\n5. MRI orbits, if there remains clinical concern, may yield additional\ninformation."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  Mild opacification right mastoids, more prominent since prior.\nClear paranasal sinuses, left mastoids.  Findings consistent with moderate\nchronic small vessel ischemic changes, with areas of confluence.  Mild brain\nparenchymal atrophy, similar to prior.  Preserved vascular flow voids.  2 foci\nof superficial microhemorrhage, stable since prior, suggestive of amyloid\nangiopathy.  No subarachnoid signal abnormality.  No brain parenchymal edema.",
            "output": "1. No acute infarcts.\n2. Moderate chronic small vessel ischemic changes.\n3. Brain parenchymal atrophy.\n4. Suggestion of amyloid angiopathy."
        },
        {
            "input": "MRI BRAIN:\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are within expected limits in\ncaliber and configuration.  No suspicious parenchymal FLAIR signal\nabnormality.\n\nThere is mild mucosal thickening of the right maxillary sinus.  The mastoid\nair cells are clear. The intraorbital contents are unremarkable.\n\nMRA BRAIN:\nThe right A1 segment is hypoplastic.  There is normal flow signal in the left\nA1 segment and both A2 segments.  1-2 mm infundibular origin of the left\nposterior communicating artery (series 9, image 100) is identified. \nOtherwise, the remainder of the intracranial vertebral and internal carotid\narteries and their major branches appear normal without evidence of stenosis,\nocclusion, or aneurysm formation.\n\nMRA NECK:\nThe common, internal and external carotid arteries appear normal.  There is no\nevidence of internal carotid artery stenosis by NASCET criteria.  The origins\nof the great vessels, subclavian and vertebral arteries appear normal\nbilaterally.",
            "output": "1. No evidence of acute intracranial hemorrhage, infarction, or mass lesion.\n2. Patent circle of ___ with no evidence of focal stenosis or aneurysm\nformation.\n3. Patent neck vasculature without evidence of focal stenosis or aneurysm\nformation.\n4. Additional findings described above."
        },
        {
            "input": "Multiple images are limited by motion artifact.  Axial gradient echo images\nare severely degraded.  Postcontrast T1 weighted and MP RAGE images are\nmoderately degraded.\n\nThere are a focus of susceptibility artifact and high signal on T2 weighted\nimages corresponding to the parenchymal calcification in the right cerebellar\nvermis seen on the preceding CT (13:8).  There are foci of high signal on T2\nweighted images corresponding to other bilateral cerebellar calcifications, as\nwell as scattered supratentorial calcifications at the gray/white matter\njunction of the left occipital and right posterior temporal lobes (15:14,\n15:12), and in the right frontal periventricular white matter (15:16).  There\nis no evidence for associated contrast enhancement.\n\nOverall, there is no evidence for an enhancing mass or abnormal meningeal\ncontrast enhancement.\n\nThere is no evidence for an acute infarction.  Confluent periventricular high\nsignal on T2 weighted and FLAIR images, and a focus of high T2 signal in the\ndeep white matter of the left insula (16:16), are nonspecific but likely\nsecondary to chronic small vessel ischemic disease in this age group. \nVentricles and sulci are age-appropriate.\n\nMajor vascular flow voids are grossly preserved.  Major dural venous sinuses\nappear patent on postcontrast MP RAGE images.\n\nThe bone marrow is diffusely heterogenous.  Small lytic lesions in the\ncalvarium seen on the preceding CT demonstrate no discrete correlates on the\npresent MRI.\n\nThere is a moderate mucous retention cyst in the floor of the right maxillary\nsinus with area of central intrinsic T1 hyperintensity likely representing\ninspissated mucus, as well as mild mucosal thickening in the right maxillary\nsinus.",
            "output": "1. Motion exam.\n2. No evidence for an intracranial enhancing mass or acute intracranial\nabnormalities.\n3. Multiple parenchymal calcifications with cerebellar predominance are again\ndemonstrated, nonspecific but compatible with sequela of prior infection or\nradiation if clinically applicable.  Diffusely heterogenous bone marrow\nsignal.\n4. Small lytic lesions in the calvarium seen on the preceding CT, which are\nprobably related to the patient's multiple myeloma, demonstrate no discrete\ncorrelates on the present MRI."
        },
        {
            "input": "The left vertebral artery is tiny. And poorly demonstrated. This corresponds\nto the appearance on the neck CTA. The axial T1 weighted images demonstrate no\nevidence of a flow void. However, there is no hyperintensity to indicate\ndissection. The noncontrast neck MRA is quite limited in its dysplasia of the\nthe vertebral arteries. The right vertebral artery is dominant and widely\npatent. Its origin is not displayed on this study.\n\nThere is atheromatous disease in the proximal right internal carotid artery.\nThe caliber of the vessel is very poorly displayed on these images that are\ndegraded by artifact. However, there is an approximately ___ percent\nstenosis by NASCET criteria.\n\nThere is mild atheromatous disease in the proximal left internal carotid\nartery with no stenosis by NASCET criteria.",
            "output": "Narrowed left vertebral artery without.  Evidence of recent thrombus.  This\nmay represent a dissection of indeterminate age.\n\nPoorly characterized right internal carotid artery atheromatous disease with\nan estimated ___ percent stenosis. However, this is far better characterized\non the CTA."
        },
        {
            "input": "There is a 2.5 x 3.0 x 3.2 cm (AP x TV x SI) enhancing mass in the right base\nof the tongue (series 9, image 21). The mass appears to cross the midline and\nextends into the pre epiglottic fat. There is an enlarged right level IIa\nlymph node that measures 3.6 cm in long axis (series 14, image 15). This lymph\nnode correspond to the palpable lesion site marked by the patient with a\nmarker. This lymph node is not significantly changed in size from CT on ___. There is a prominent right level Va lymph node that measures 1.2\ncm long axis (series 13, image 22).\n\nThe parotid, submandibular, and thyroid glands are normal.\n\nThere is mucosal thickening and fluid in the left frontal sinus, bilateral\nethmoid sinuses, and left greater than right maxillary sinuses. The sphenoid\nsinuses appear clear.\n\nThe included brain is normal.",
            "output": "1. Right base of tongue 3.2 cm enhancing mass that appears to cross the\nmidline and extends into the pre epiglottic fat. This lesion is highly\nsuspicious for a malignant neoplasm.\n2. Enlarged right level IIa lymph node measuring up to 3.6 cm (this enlarged\nlymph node corresponds a marker placed by the patient at their site of\npalpable concern) and a prominent right level Va lymph node measuring up to\n1.2 cm. These lymph nodes are suspicious for metastatic lymphadenopathy."
        },
        {
            "input": "There is a 30 x 40 mm area of vasogenic edema, with low signal on T1,\nhyperintense signal on T2, FLAIR, and DWI images, causing effacement of the\nsulci on the left frontal lobe (image 18, series 11), with no evidence of\nabnormal enhancement or restricted diffusion, there is no evidence of\nhemorrhage or shifting of the normally midline structures.  Additionally\nmultiple smaller but with similar signal lesions are visualized in both\ncerebral hemispheres, involving the right occipital lobe (image 11, series\n11), right temporal lobe image (9, series 11), left temporal lobe image (10,\nseries 11), and left centrum semiovale (images 17, 18 and 19, series 11). \nOnly one lesion identified in the left centrum semiovale demonstrates mild to\nmoderate pattern of enhancement (image 19, series 14).  There is no evidence\nof hemorrhagic transformation or magnetic susceptibility changes in these\nlesions.  The major vascular flow voids are present and demonstrate normal\ndistribution.  The orbits are unremarkable, the paranasal sinuses and mastoid\nair cells are clear.",
            "output": "1.  Multiple bilateral apparently intra-axial lesions, associated with\nvasogenic edema, identified in the subcortical white matter as described\ndetail above, the largest lesion appears on the right frontal lobe, similar\nbut smaller lesions are visualized in both cerebral hemispheres involving the\ntemporal lobes, right occipital lobe and left frontal parietal lobes, with no\nevidence of hemorrhage, significant mass effect or shifting of the normally\nmidline structures.\n\n2.  One lesion identified in the left centrum semiovale shows mild to moderate\npattern of enhancement (image 19, series 14), with no significant mass effect\nor hemorrhage.  Given clinical history of  CLL, intra cerebral infiltration\ndue to chronic lymphocytic leukemia is a consideration.\n\nNOTIFICATION:  The findings were discussed by Dr. ___ with Dr.\n___ on the telephone on ___ at 8:44 AM, 2 minutes after\ndiscovery of the findings."
        },
        {
            "input": "Numerous non or minimally enhancing parenchymal lesions are redemonstrated,\nsimilar in size and extent to prior exam.  The largest lesion remains in the\nright frontal lobe, and measures 3.5 x 4.0 cm, similar to prior.  Additional\nlesions are as follows:\n\nLeft centrum semiovale, 12 mm unchanged.\nRight occipital, 2 cm, unchanged.\nA previously noted 13 mm lesion within the left temporal lobe is less\nconspicuous, likely due to technical differences, but is also essentially\nstable.\nRight anterior temporal, 2.2 cm, unchanged.\n\nFaint enhancement associated with the lesion in the left centrum semiovale\nappears more conspicuous, a difference that may be technical.  Patchy\nleptomeningeal enhancement along the right frontal lesion is either new, or\nnewly visualized.  Multifocal punctate enhancement in bilateral striatum.\n\nNumerous enlarged cervical lymph nodes.  Residual scarring over right parietal\nscalp, reflecting recent trauma.",
            "output": "1. No new or enlarging parenchymal lesions.  No significant mass effect or\nmidline shift.\n2. Increased enhancement of the previously identified left centrum semiovale\nlesion may be technical.  There is, however, concern for progression of\nleptomeningeal disease.  Correlation with CSF sampling could be performed. \nClose follow-up is recommended.\n\nNOTIFICATION:   Patient experienced a contrast reaction during this exam.  It\nis recommended that this patient receive premedication prior to future studies\ncontaining this contrast material. For details please see note in the\nelectronic medical record/OMR. The patient has received instruction on how to\nmanage this event at home."
        },
        {
            "input": "MR BRAIN:  Postcontrast MPRAGE sequences are severely motion degraded.\n\nThe patient is status post right trans frontal burr hole and a biopsy of a\nright frontal lobe lesion with enhancing biopsy track noted.\n\nRe-identified are FLAIR hyperintense subcortical lesions, which includes the\nfollowing:\n\nDominant 3.8 x 3.0 cm (AP, TRV ; series 11, image 24) right frontal centrum\nsemiovale lesion, similar in size to the prior examination allowing for\ntechnical differences.\n\nRight anterior temporal lobe 1.7 cm (series 11, image 13) lesion is similar in\nsize.\n\nRight occipital lobe 2.2 x 0.8 cm (series 11, image 13) lesion has increased\nin conspicuity when compared to prior exam.\n\nLeft frontal centrum semiovale 1.1 x 0.7 cm (series 11, image 23) lesion is\nsimilar in size to prior exam.\n\nLeft coronal radiata 2.2 x 0.8 cm lesion (series 11, image 21) is more\nconspicuous when compared to the prior exams.\n\nPunctate left frontal punctate lesions measuring up to 4 mm (series 11, image\n17 and 19) are similar in size.\n\nLeft anterior temporal lobe 1.2 x 0.5 cm (series 11, image 12) lesion is\nsimilar to examination of ___.\n\nLeft lateral temporal lobe lesions measuring 1.4 x 1.4 cm (series 11, image 11\nand 12 is more conspicuous or new from prior exam.\n\nThese lesions do not demonstrate definitive enhancement on postcontrast\nsequences.  There does remain punctate striated all enhancement.  Bilateral\ntemporal lobe enhancement on MPRAGE sequences is considered artifactual.\n\nThe dominant right frontal lobe lesion demonstrates intrinsic 6 mm T1\nhyperintense focus with peripheral gradient echo susceptibility compatible\nwith recent biopsy.\n\nThere is no slow diffusion to suggest acute infarct.  The above lesions do\ndemonstrate diffusion-weighted hyperintense signal without associated ADC\nhypointensity, likely T2 shine through.  Sulci, ventricles and cisterns are\nwithin expected limits for the patient's age.\n\nThe major intracranial flow voids are preserved.  The dural venous sinuses are\npatent.  The maxillary sinuses demonstrate small mucous retention cysts.  The\norbits are unremarkable.  The right mastoid air cells demonstrates trace fluid\nsignal in the tips.\n\nMR ___: No increase perfusion of the FLAIR hyperintense lesions\nare noted.\n\nASL Perfusion: There does appear to be increased perfusion along the lateral\naspect of the left temporal lobe, approximately corresponding to the new FLAIR\nhyperintense lesions.\n\nMR Spectroscopy: Single voxel spectroscopy centered over the left frontal\ncentrum semiovale lesion does not demonstrate increased choline to NAA ratio.\n\nMulti voxel spectroscopy centered over the dominant right centrum semiovale\nlesion demonstrates increased choline to NAA ratio near 2 in voxels 3 (1.9)\nand 8 (1.8).  Voxels 11 through 12 demonstrate increased ratios of\napproximately 1.5.",
            "output": "1. There are apparent new FLAIR hyperintense lesions in the left lateral\ntemporal lobe.\n2. Many of the existing lesions appear slightly more conspicuous when compared\nto the prior exam, including lesions in the right occipital lobe and the left\ncorona radiata.\n3. The lesions do not clearly demonstrate postcontrast enhancement.  There\nremains punctate striated all enhancement.\n4. Post biopsy changes of the right frontal centrum semiovale lesion is noted.\nOf note, the blood product from the biopsy track appears centered within the\nlesion.\n5. Apparent increased ASL perfusion of the new FLAIR hyperintense foci,\nhowever this may be artifactual.  No increase perfusion on dynamic contrast\nsusceptibility.\n6. Multi voxel spectroscopy demonstrates increased choline to NAA ratio in the\ndominant right frontal centrum semiovale lesion.\n7. No acute infarct or intracranial hemorrhage."
        },
        {
            "input": "There is no evidence of acute infarction or hemorrhage.  Again noted are\nmultiple nonenhancing supratentorial subcortical FLAIR hyperintense areas. \nThese appear similar in number but slightly increased in size from ___.\n\nA dominant right frontal centrum semiovale lesion has increased from 3.8 x 3.0\ncm to 3.7 x 5.0 cm (series 7:image 17).  A right anterior temporal lobe lesion\npreviously measured 1.7 cm and now measures 2.2 cm.  A right occipital lobe\nlesion is increased from 2.2 x 0.8 cm to 2.3 x 1.1 cm (series 7:image 12).  A\nleft anterior temporal lobe lesion has increased from 1.4 x 0.5 cm to 1.8 x\n0.6 cm (series 7:image 9).  Previously noted left lateral temporal lobe lesion\nis not well seen on this exam.  A left frontal centrum cement bowel lesion\nplease measure 1.1 x 0.7 cm now measures 1.5 x 1.6 cm (series 7: Image 17). \nThere is also a dominant previously biopsied right frontal lobe lesion\nmeasuring 7 mm, which previously measured 6 mm (series 7:image 16).  There is\na subtle faint enhancement of this lesion.\n\nThe ventricles and sulci appear normal in size and configuration.  The\nprincipal intracranial vascular flow voids appear grossly patent.  Prior right\nfrontal burr hole is noted.  The orbits are unremarkable.  There is mild\nmucosal thickening of the left sphenoid sinus.  The mastoid and middle ear\ncavities are grossly clear.",
            "output": "1. Mild increase in size of multiple nonenhancing FLAIR hyperintense lesions. \nNo enhancing lesions are identified.  There differential diagnosis includes\nlymphoma and progressive multifocal leukoencephalopathy.\n2. No acute infarct or intracranial hemorrhage."
        },
        {
            "input": "In comparison with the most recent MRI examination dated ___,\nthere is new pattern of diffuse enhancement in the right frontal lobe\nsubcortical white matter (images 14 through 19, series 10).  Additionally\nthere is a focus of enhancement in the left centrum semiovale, which\napparently is new since the prior study.  The pattern of vasogenic edema\ninvolving the right frontal subcortical white matter remains similar in\ncomparison with the most recent study, and also areas of vasogenic edema\nremain unchanged in the right occipital region and adjacent to the right\noccipital ventricular horn (images 11 and 12, series 7), slightly more\nconspicuous areas of T2 shine through effect in the occipital lobes are\ndemonstrated on the diffusion-weighted images with no frank evidence of slow\ndiffusion, and are consistent with vasogenic edema.  Unchanged areas of FLAIR\nhyperintensity signal are present on the temporal lobes.  There is no\nsignificant mass effect or shifting of the midline structures.  The major\nvascular flow voids are present and demonstrate normal distribution.  The\norbits are unremarkable, the paranasal sinuses and mastoid air cells are\nclear.",
            "output": "1.  New pattern of diffuse enhancement identified in the subcortical white\nmatter of the right frontal lobe as described, additionally there is a new\nfocus of enhancement in the left centrum semiovale.  No significant mass\neffect is identified, persistent and unchanged areas of vasogenic edema in the\ntemporal lobes and occipital lobes.\n\n2.  The differential diagnosis for this lesions remains broad, and probably is\nrelated with lymphocytic encephalitis in the setting of underlying malignancy\nor viral etiology.\n\nNOTIFICATION:  The findings were discussed by Dr. ___ with Dr. ___\n___ on the telephoneon ___ at 1:57 ___, 5 minutes after discovery\nof the findings."
        },
        {
            "input": "There is some residual T2 and FLAIR hyperintensity within the previously noted\ndominant right frontal lesion although the degree and extent of the signal\nabnormality has significantly decreased.  There is also decreased mass effect\nwith less effacement of the overlying sulci on today's exam.  Associated\nenhancement within this dominant lesion seen on prior has also resolved.\n\nAdditional regions of signal abnormality in the subcortical white matter of\nthe left frontal lobe and left occipital lobe have nearly resolved, as has the\nenhancement.  There is some persistent abnormal FLAIR/T2 signal abnormality in\nthe right occipital lobe (08:14) which is decreased at its posterior aspect\nbut it appears to extend marginally more anterolaterally when compared to\nprior.  There is also possible persistent but not definitive associated\nenhancement (11:14).\n\nThere is no acute infarct or mass effect.  Major intravascular flow voids are\npreserved.  Ventricles and sulci are age appropriate.\n\nVisualized paranasal sinuses and mastoid air cells demonstrate no abnormal\nsignal.  Right parietal burr hole is again noted.",
            "output": "Overall improvement of previously noted parenchymal signal abnormality with\nassociated enhancement.  Decrease in size and resolution of enhancement of\ndominant right frontal lesion.  Additional left-sided lesions have nearly\nresolved altogether.\nRight occipital white matter T2/FLAIR hyperintensity is slightly different in\nconfiguration, smaller posteriorly with slightly more extensive signal\nabnormality extending anterolaterally with questionable persistent enhancement\nas on prior."
        },
        {
            "input": "There is no evidence of intracranial hemorrhage, mass, mass effect or shifting\nof the normally midline structures. The ventricles and sulci are normal in\nsize and configuration for the patient's age.  There are few small scattered\nfoci of high signal intensity are identified on the FLAIR sequence,\ndistributed in the subcortical white matter (images 15, 16, series 7), which\nare nonspecific and may reflect changes due to small vessel disease. No\ndiffusion abnormalities are detected. There is no evidence of abnormal\nenhancement after contrast administration.  The major vascular flow voids are\npresent and demonstrate normal distribution. The orbits are unremarkable, the\nparanasal sinuses and mastoid air cells are clear.  Note is made of mild\ndegenerative changes identified in the spine at the level of C5/C6, and\ndemonstrated on the sagittal MPRAGE (image 120, series 9), however partially\nevaluated in this exam, if clinically warranted, correlation with dedicated\nMRI of the cervical spine is advised..",
            "output": "1.  There is no evidence of acute intracranial process or hemorrhage.\n\n2.  Few scattered foci of high signal intensity detected on FLAIR images\n(images 15, 16, series 7), distributed in the subcortical white matter, which\nare nonspecific and may reflect changes due to small vessel disease.There is\nno evidence of abnormal enhancement.\n\n3.  Incidentally noted, mild cervical spine degenerative changes are\nvisualized at C5/C6 level, partially evaluated in this exam, if clinically\nwarranted, correlation with dedicated MRI of the cervical spine is\nrecommended.\n\nRECOMMENDATION(S):  Mild degenerative changes identified in the cervical spine\nat C5/C6 level, partially evaluated in this exam, if clinically warranted,\ncorrelation with dedicated MRI of the cervical spine is recommended."
        },
        {
            "input": "The study is limited by patient motion.\n\nThere is no evidence of intracranial hemorrhage, mass, mass effect or shifting\nof the normally midline structures.  The ventricles and sulci appear normal\nfor the patient's age.  There is no abnormal enhancement after contrast\nadministration.  The pituitary appears normal.  The craniocervical junction\nappears normal.  Mild mucosal thickening involving the paranasal sinuses\n\nOn the high-resolution images there is a small FLAIR hyperintense area in the\nleft temporal lobe (image 120, series 700, image 134, series 701, and image\n42, series 6), extending from the margin of the temporal horn of the left\nlateral ventricle to the left middle temporal gyrus.  Although this finding is\nnonspecific and may represent a gliotic area, the possibility of small\ncortical dysplasia cannot be completely rule out.\n\nBilateral hippocampal formations and mammillary bodies are preserved in signal\nand configuration. There is no disproportionate medial temporal atrophy. There\nis no focal lobar encephalomalacia. There is no gray matter heterotopia noted.\n\nThe major vascular flow voids are present and demonstrate normal distribution.\nThe orbits are unremarkable, the paranasal sinuses and mastoid air cells are\nclear.",
            "output": "1.  Limited examination due to patient motion, within this limitation, grossly\nthere is no evidence of acute intracranial process or hemorrhage.\n\n2.  Small FLAIR hyperintense area in the left temporal lobe left, extending\nfrom the margin of the temporal horn of the left lateral ventricle to the left\nmiddle temporal gyrus, which is nonspecific and may represent gliosis, however\na cortical migrational abnormality is a consideration (transmantle sign), with\nsuspected overlying focal cortical thickening suggesting focal cortical\ndysplasia.  No obvious signal abnormality of the cortex.\n\n3.  There is no evidence of mesial temporal sclerosis, the hippocampal\nformations are normal."
        },
        {
            "input": "There are multiple bilateral foci of slow diffusion suggestive for acute\ninfarcts.  These include a dominant irregular peripheral nodular focus of\nrestricted diffusion involving the right parietal and occipital lobes,\nassociated with small irregular foci of susceptibility consistent with a small\nhemorrhage.  Smaller foci of restricted diffusion are also identified\ninvolving the left occipital lobe, right medial and posterior frontal lobe,\nand medial and superior aspect of the precentral gyrus bilaterally, consistent\nwith small acute infarcts.  There is mild bilateral periventricular T2 and\nFLAIR hyperintense foci suggestive for chronic microangiopathy.  There is no\nsignificant mass effect or midline shift.  The ventricles and sulci are normal\nin caliber and configuration.  There are normal intracranial arterial flow\nvoids suggestive for patency.  There is diffuse thickening and increased FLAIR\nintensity involving the superior rectus and medial rectus bilaterally.  The\noptic globes appear grossly unremarkable.  The paranasal sinuses appear\npatent.  There is increased T2 signal within the mastoid air cells bilaterally\nsuggestive for effusions.  The osseous structures demonstrate no acute\nfindings.",
            "output": "1. There is a dominant focus of restricted diffusion involving the right\nposterior parietal and occipital lobes consistent with acute infarction,\nassociated with a small underlying hemorrhage.  A follow-up brain MRI with\ncontrast is recommended to assess for a possible underlying brain lesion.\n2. There are smaller scattered foci of restricted diffusion involving the left\noccipital lobe and bilateral superior frontal lobes which may reflect embolic\ninfarcts.\n3. Diffuse thickening and increased FLAIR hyperintensity involving the medial\nrectus and superior rectus muscles bilaterally with differential\nconsiderations to include thyroid ophthalmopathy or orbital pseudotumor.\nClinical correlation/ophthalmology consult and follow-up imaging recommended\nwith an orbits mri protocol could be considered.\n\n\nRECOMMENDATION(S):  Follow-up contrast enhanced MRI brain recommended.\nConsider MRI orbits with and without contrast\n\nNOTIFICATION:  These findings were discussed with Dr. ___ from the\nMedicine Service on ___ at 17:35."
        },
        {
            "input": "The patient is status post evacuation of a left frontoparietotemporal subdural\nhematoma.  The burr hole in the left parietal calvarium is unchanged.  A left\nfrontoparietotemporal postoperative subdural fluid collection, measuring 2.0\ncm in thickness, is unchanged from the prior examination.  There is stable\nlocal mass effect upon the adjacent frontal, parietal, and temporal lobes.  A\n1.0 cm left-to-right midline shift has minimally decreased from the prior\nexamination.  The left uncus is medially deviated, unchanged from prior.  The\nleft cerebral dura is thickened and enhancing.   The subdural fluid collection\ncontains locules of gas and layering T1 hyperintense subacute blood products. \nThe alternative is local infection.\n\nThere is leptomeningeal enhancement after contrast administration in the left\nhemisphere.  This may be a consequence of subarachnoid hemorrhage associated\nwith trauma.\n\nThe left lateral ventricle is partially effaced.  There is no evidence of\nacute infarction.  No masses are identified.\n\nThere is mild mucosal thickening in the right posterior ethmoid air cells.",
            "output": "1. Unchanged size and local mass effect of a large left frontoparietotemporal\nsubdural fluid after hematoma evacuation.\n2. Leptomeningeal enhancement in the left hemisphere that may be a consequence\nof prior hemorrhage.  However, the possibility of infection should be\nconsidered.\n3. No acute infarction or masses."
        },
        {
            "input": "Left parietal craniotomy is again seen.  Small epidural collection of fluid\nand air deep to the craniotomy is again noted.  The left convexity subdural\ncollection containing foci air and heterogeneous blood products is stable in\nsize compared to the CT from 1 day earlier.  There is persistent\nhyperintensity in the left-sided sulci on FLAIR images, similar to the ___ contrast enhanced MRI when it also demonstrated contrast enhancement. \nThere is stable rightward shift of midline structures and left to right\nsubfalcine herniation, as well as stable partial effacement of the left\nlateral and third ventricles compared to the most recent CT.\n\nThere is no evidence of acute infarction.  Few scattered small T2\nhyperintensities are again noted in the supratentorial white matter,\nnonspecific but likely related to mild chronic small vessel ischemic disease\nin this age group. The major vascular flow voids are preserved.\n\nMild mucosal thickening is noted in the ethmoid air cells.",
            "output": "1. Heterogeneous left subdural hematoma and associated mass effect are stable\ncompared to the most recent CT from ___.\n2. High signal on FLAIR images in the left-sided sulci is similar to the ___ contrast enhanced MRI, when associated contrast enhancement was\nalso demonstrated.  This may be secondary to prior subarachnoid hemorrhage,\nthough infection cannot be excluded on the basis of imaging, as discussed in\nthe prior MRI report.\n3. No evidence for an acute infarct."
        },
        {
            "input": "There is a focus of slowed diffusion within the right hippocampus and right\nmedial temporal lobe. No additional diffusion abnormalities are detected. On\nT1 weighted images, there is no evidence of overt architectural distortion,\nmass, midline shift, or ventriculomegaly. No extra-axial fluid collection is\nidentified.\nThe brainstem, posterior fossa, and cervicomedullary junction are preserved.\nThe orbits, periorbital and paracavernous spaces are normal.",
            "output": "Limited examination demonstrating acute infarction of the right hippocampus\nand medial temporal lobe, in the vascular territory of the right posterior\nchoroidal artery."
        },
        {
            "input": "There is persistent mild to moderate slow diffusion and edema on the right\ntemporal lobe, with no evidence of uncal herniation or significant mass effect\n(image 10, series 7), there is no evidence of acute intracranial hemorrhage.\nMild foci of high signal intensity are seen in the subcortical and\nperiventricular white matter on T2 and FLAIR sequences, which are nonspecific\nand may represent changes due to small vessel disease. The ventricles and\nsulci are normal in size and configuration for the patient's age. There is no\nevidence of abnormal enhancement. The major arterial vascular flow voids are\npresent and demonstrate normal distribution. The orbits are unremarkable, the\nparanasal sinuses are clear, mild mucosal thickening is noted on the left\nmastoid air cells.",
            "output": "1. Persistent slow diffusion and edema is identified in the right temporal\nlobe, with no evidence of uncal herniation or hemorrhagic transformation,\nthese findings suggest the possibility of herpes virus encephalitis, however a\nsubacute ischemic event may have similar appearance.\n\n2. Multiple foci of T2 and FLAIR hyperintensity identified in the subcortical\nand periventricular white matter, which are nonspecific and may reflect\nchanges due to small vessel disease. There is no evidence of abnormal\nenhancement."
        },
        {
            "input": "Previously noted elevated T2 signal in the medial right temporal lobe has\ndecreased in extent. Associated swelling has resolved. Associated slow\ndiffusion has also resolved. There is no associated blood products or\npathologic contrast enhancement. Coronal MP RAGE images demonstrate no\nsignificant volume loss in the medial right temporal lobe compared to the\nleft.\n\nThere is no evidence for an intra-axial or extra-axial mass, and no pathologic\npachymeningeal or leptomeningeal contrast enhancement.  There is no evidence\nfor edema or blood products.\n\nRetrocerebellar fluid signal intensity is again seen, with slight remodeling\nof the posterior cerebellar hemispheres, compatible with either an arachnoid\ncyst ___ cisterna magna.\n\nMajor intracranial arterial flow voids are grossly preserved. Major dural\nvenous sinuses appear patent on postcontrast MP RAGE images.",
            "output": "1. Previously noted elevated high T2 signal in the medial right temporal lobe\nhas decreased in extent, with resolution of associated edema and diffusion\nabnormality, and no evidence for significant volume loss.  This is compatible\nwith sequela of viral encephalitis, and less likely with sequela of\ninfarction.\n2. No evidence for new intracranial abnormalities."
        },
        {
            "input": "Multiple sequences are limited by motion artifact.\n\nMRI BRAIN:  There is a small focus of slowed diffusion in the left coronal\nradiata indicating an acute infarct. There is encephalomalacia in the right\nmiddle cerebral artery territory with evidence of chronic blood products,\nconsistent with a chronic infarct, and associated ex vacuo dilatation of the\nright lateral ventricle. There is underlying global mild to moderate\nenlargement of the ventricles and sulci secondary to cerebral atrophy. There\nis also confluent periventricular high T2 signal and small foci of high T2\nsignal in the subcortical and deep white matter of the cerebral hemispheres,\nlikely sequela of chronic small vessel ischemic disease in a patient of this\nage.\n\nMRA NECK:  There is a 3 vessel aortic arch. Though evaluation is limited by\nmotion artifact, there is asymmetric signal loss in the proximal left internal\ncarotid artery, suggesting some degree of stenosis. No flow-limiting stenosis\nis seen in the right internal carotid artery. Dominant left vertebral artery\nappears patent, though evaluation of its origin is technically limited.\nNondominant right vertebral artery is hypoplastic, and its origin and cervical\ncourse is poorly evaluated.\n\n\nMRA BRAIN:  Images are severely degraded by motion artifact.  Intracranial\nportion of the small nondominant right vertebral artery is not visualized on\nthe 3D time-of-flight images, but it appears patent on the gadolinium enhanced\nneck MRA. No ___ or ___ is visualized on either side. Left vertebral,\nbasilar, superior cerebellar, posterior cerebral, internal carotid, anterior\ncerebral, and middle cerebral arteries appear patent, but evaluation for\nstenoses or aneurysms is markedly limited.",
            "output": "1.  Small acute infarct in the left coronal radiata.\n2.  Large chronic infarct in the right middle cerebral artery territory with\nevidence of chronic blood products.\n3.  MRAs are significantly limited by motion artifacts. Brain MRA is barely\ndiagnostic. Neck MRA demonstrates an apparent stenosis of the proximal left\ninternal carotid artery, which could be better assessed by carotid sonography\nor CTA. Hypoplastic nondominant right vertebral artery is poorly assessed, and\ncould be better assessed by CTA, if clinically warranted."
        },
        {
            "input": "In the medial aspect of the inferior right parietal lobe, there is an\nirregularly marginated, lobulated mass with peripheral contrast enhancement,\nwhich measures 1.9 cm transverse, 2.4 cm AP, 1.9 cm craniocaudad (images\n100:65 and 14:114).  The mass demonstrates extensive low signal on gradient\necho images and mild high signal on precontrast T1 weighted images, as well as\nhyperdensity on the prior CT, consistent with blood products.  The mass\ndemonstrates peripheral high signal on diffusion tracer sequence and low\nsignal on the ADC map, likely secondary to susceptibility artifact from the\nblood products.  The nonenhancing ___ the mass does not demonstrate slow\ndiffusion.  There is mild surrounding edema without significant mass effect. \nThere is no shift of midline structures or ventricular effacement.\n\nNo additional enhancing mass is seen.\n\nThere are symmetric, non masslike areas of high T2 signal in the deep white\nmatter of the bilateral inferior parietal lobe without contrast enhancement,\nmeasuring 15 x 15 mm on the right and 12 x 11 mm on the left, image 11:15, of\nuncertain significance.  There is also punctate T2 hyperintense focus in the\nmore superior left parietal white matter on image 11:17.\n\nVentricles, sulci away from the above-described mass, and basal cisterns are\nnormal in size for age.  Major intravascular flow voids are grossly preserved,\nbut the blood vessels are better assessed on the CTA from 1 day earlier.\n\nFluid and mucosal thickening in the paranasal sinuses are new compared to the\ninitial CT from the morning of ___, suggesting sequela of\nprolonged supine positioning in the inpatient setting and endotracheal\nintubation.  There is also mild mucosal thickening in bilateral mastoid air\ncells.\n\nSagittal images demonstrate degenerative changes in the included upper\ncervical spine at C3-4 level, with a disc herniation deforming the ventral\nspinal cord.",
            "output": "Irregularly marginated, lobulated mass with peripheral contrast enhancement in\nthe medial aspect of the inferior right parietal lobe, with blood products and\nmild surrounding edema, but no significant mass effect.  Metastatic or primary\nmalignancy is the primary consideration.\n\nGiven the presence of nonenhancing areas of T2 hyperintensity in bilateral\nparietal deep white matter, acute hemorrhagic encephalomyelitis could be\nconsidered, but is less likely in the setting of diffuse rather than punctate\nblood products within the lesion, and given the complete rather than\ninterrupted rim of contrast enhancement.  Other diagnostic considerations for\nthe 2 symmetric nonenhancing white matter lesions include nonenhancing primary\nCNS malignancy, sequela of prior inflammation/infection, PRES, or drug\ntoxicity."
        },
        {
            "input": "Study is moderately degraded by motion.  Fiducial markers are noted.  Again is\nnoted an approximately 2.5 (AP) x 1.8 (TV) x 2.2 (SI) cm (see ___ right parietal mass with adjacent edema and mass effect on adjacent\nsulci.  There is no ventriculomegaly.  Basilar cisterns are patent.\n\nNonspecific opacification and mucosal thickening of the paranasal sinuses\nagain seen, similar most prior exam, and which again may be related to\nintubation status.",
            "output": "1. Study is moderately degraded by motion.\n2. 2.5 x 1.8 x 2.2 cm right parietal mass as described."
        },
        {
            "input": "The patient is status post right parietal craniotomy and resection of the\nright parietal lobe mass with intrinsic T1 hyperintense signal,\npneumocephalus, and blood products within the postsurgical bed.  There is mild\nenhancement at the anterior superior aspect of the resection cavity.  The\nT2/FLAIR hyperintense signal in the right parietal lobe, anterior to the\nresection cavity has slightly increased, likely partially related to edema. \nThe T2/FLAIR hyperintense signal within the deep white matter of the left\nparietal lobe is unchanged.  No enhancing lesions are identified.\n\nThere is a small air-fluid level in the right sphenoid sinus.  A few right\nmastoid air cells are opacified.  The orbits are unremarkable.  There is\nminimal edema within the bilateral parietal scalp, right greater than left.\n\nThe major intracranial flow voids are preserved.",
            "output": "1. Postsurgical changes status post resection of a right parietal lobe mass\nwith mild residual enhancement at the anterior superior margin of the surgical\ncavity.\n2. Unchanged T2/FLAIR hyperintense signal within the left parietal lobe.\n3. Mild marginal restricted diffusion to the surgical cavity related to\nsurgery.  No evidence of territorial infarct.\n4. No new enhancing lesions."
        },
        {
            "input": "Again seen are postoperative changes after resection of a right parietal\nenhancing lesion.  The degree of swelling and edema at the surgical site has\ndecreased dramatically since ___.  Bilateral posterior parietal\nwhite matter hyperintensity on FLAIR is unchanged.  There continues to be\nenhancement of the brain parenchyma at the surgical site, but this is minimal\nand suggests post operative change rather than residual enhancing tumor. \nThere is a small amount of residual postoperative hemorrhage at the surgical\nsite.  No new lesions are identified.  There is no evidence of infarction or\nother masses.  The ventricles and sulci are normal in caliber and\nconfiguration.   The ventricles and sulci are normal in caliber and\nconfiguration.",
            "output": "1. Reduction in enhancement and edema since the early postoperative study of\n___.  Minimal enhancement at the surgical site is likely\npostoperative.  There is no evidence of residual enhancing tumor."
        },
        {
            "input": "The patient is status post right parietal craniotomy and resection of the\nright parietal mass with chronic blood products in the postoperative bed.  The\ndural thickening and enhancement underlying the craniotomy site is unchanged. \nThe more posterior, nodular component of a lobulated, heterogeneously\nenhancing lesion is unchanged in size, measuring 0.9 x 0.9 x 1.1 cm.  The more\nanterior and inferior, nodular component of this lesion demonstrates\nincreased, heterogeneous enhancement, measuring 1.1 x 1.0 x 0.9 cm on 1000:99\nand 1001:119.  The patchy T2/FLAIR hyperintense signal in the bilateral\nparietal lobes is unchanged.\n\nAn ill-defined, new enhancing lesion in the left corona radiata measures 0.8 x\n1.1 x 0.6 cm and is associated with T2/FLAIR hyperintense signal.  This lesion\ndemonstrates a of rim of hyperintense signal on diffusion weighted sequence\nand isointense signal on the corresponding ADC map.\n\nThe scattered foci of T2/FLAIR hyperintensities in the periventricular and\nsubcortical white matter are unchanged and nonspecific.  There is no evidence\nof acute hemorrhage, mass effect, midline shift or acute infarction.   The\nventricles and sulci are normal in caliber and configuration.\n\nThere is minimal mucosal thickening in the bilateral ethmoid sinuses.  The\nmastoid air cells are clear.  The orbits are unremarkable.\n\nThe major intracranial flow voids are preserved.",
            "output": "1. New 1.1 cm enhancing lesion in the left corona radiata, potentially\nrepresenting recurrent neoplasm versus subacute infarct.  Close interval\nfollowup or further evaluation with MRI spectroscopy can be performed.\n2. Postsurgical changes with a lobulated, heterogeneously enhancing lesion in\nthe postoperative bed within the right parietal lobe, which has increased in\nenhancement anteriorly and inferiorly, which may represent posttreatment\nchanges or residual neoplasm.  Continued follow-up is recommended.\n\nRECOMMENDATION(S):  Close interval follow-up or further evaluation with MRI\nspectroscopy for impression 1.\n\nNOTIFICATION:  Finding of lesion concerning for recurrent neoplasm (without\ndifferential consideration of subacute infarct) was entered by Dr. ___\non ___ at 09:23 into the Department of Radiology critical communications\nsystem for direct communication to the referring provider.\n\nThe addition of subacute infarct as a differential consideration was discussed\nwith ___, M.D. by ___, M.D. on the telephone on ___\nat 3:37 ___, 20 minutes after discovery of the findings."
        },
        {
            "input": "The patient is status post right parietal craniotomy and resection of a right\nparietal mass with unchanged, chronic blood products in the postoperative bed.\nThe dural thickening and enhancement underlying the craniotomy site is\nunchanged.  There is a heterogeneously enhancing, lobulated lesion in the\nright parietal postoperative bed.  The more anterior and inferior nodular\ncomponent of this lesion has slightly increased in size, measuring 1.3 x 1.3 x\n1.1 cm, previously measuring 1.1 x 1.0 x 0.9 cm.  The more posterior and\nnodular component of this lesion has decreased in size, measuring 0.6 x 0.5\ncm, previously measuring 0.9 x 0.6 cm.  This lesion demonstrates increased,\nsome more solid and central enhancement.\n\nThe rim enhancing lesion in the left corona radiata is unchanged in size,\nmeasuring 1.1 x 0.5 cm.  This lesion demonstrates hyperintense signal on both\nthe diffusion and ADC map.\n\nThe T2/FLAIR hyperintense signal in the bilateral parietal lobes and left\ncorona radiata are unchanged.\n\nNo new enhancing lesions are identified.\n\nThere is no evidence of acute hemorrhage, midline shift, or acute infarction. \nThe ventricles and sulci are normal in caliber and configuration.\n\nThe paranasal sinuses and mastoid air cells are clear.  The orbits are\nunremarkable.\n\nThe major intracranial flow voids preserved.",
            "output": "1. Unchanged size of the enhancing lesion in the left corona radiata which\nlikely represents a subacute to chronic infarction rather than neoplasm but\ncontinued followup is suggested.\n2. Post treatment changes with increased, solid, central enhancement within\nthe lobulated lesion in the right parietal lobe resection cavity.  Interval\nincrease in the size of the more anterior and inferior, nodular component and\ninterval decrease in the size of the more posterior, nodular component of this\nlesion, which may reflect posttreatment changes however continued followup is\nsuggested.\n3. No new enhancing lesions."
        },
        {
            "input": "As before, the patient is status post right parietal craniotomy and resection\nof a right parietal mass with unchanged, chronic blood products in the\npostoperative bed.  Again seen is dural thickening and enhancement underlying\nthe craniotomy site.\n\nCompared to ___, there is mildly increased size of a heterogeneously\nenhancing lobulated lesion in the right parietal postoperative bed with\nassociated heterogeneous FLAIR hyperintense signal, measuring approximately 22\n(AP) x 18 (TV) x 20 (SI) mm ___, 901b/99).  A rim enhancing lesion in the\nleft corona radiata it is no longer visualized.  There is unchanged\nsurrounding T2/FLAIR hyperintensity, likely representing edema.  There is\nunchanged bilateral parietal lobe and left corona radiata T2/FLAIR\nhyperintensity.\n\nNo new enhancing lesions are identified.  No evidence of hemorrhage, mass\neffect, midline shift or infarction.  Ventricles and sulci are normal in\ncaliber and configuration.  Major intravascular flow voids are preserved.  The\ndural venous sinuses are patent and postcontrast MP rage.  Visualized\nparanasal sinuses and mastoid air cells are clear.  Orbits are normal.",
            "output": "1. Compared to ___, there is mildly increased size of a\nheterogeneously enhancing lobulated lesion in the right parietal postoperative\nbed,, measuring approximately 2.2 cm in greatest dimension.  While this may\nrepresent posttreatment changes, recurrence or residual glioblastoma cannot be\nexcluded.  Close attention on followup is recommended.\n2. No new enhancing lesions."
        },
        {
            "input": "Patient is status post right parietal craniotomy and resection of right\nparietal mass with chronic blood products and postoperative bed.  Again seen\nis dural thickening underlying the craniotomy site.\n\nIn comparison to ___ there has been dramatic interval progression of\na heterogeneously enhancing ill-defined mass within the right posterior\nparietal and occipital lobe with extension to the splenium of the corpus\ncallosum (10:14) measuring approximately 5.4 x 3 cm (previously 2.2 x 1.8 cm).\nThere has also been a dramatic increase in the volume of surrounding vasogenic\nedema causing sulcal effacement, mass effect, and near complete effacement of\nthe right lateral ventricle atria consistent with known GBM.  1 cm of leftward\nshift of normally midline structures is unchanged from ___ but\nhas progressed since ___.  Unchanged bilateral parietal lobes and left\ncorona radiata T2/FLAIR hyperintensities are again noted.  Patent basal\ncisterns.\n\nThere is no evidence of hemorrhage or infarction. There is subtle asymmetric\nprominence of the right lateral ventricle temporal horn which is similar to\nprior ___ MR without evidence of trapped ventricle.  The ventricles and\nsulci are otherwise normal in caliber and configuration.  Major intracranial\nvascular flow voids are preserved.  Orbits are unremarkable.  Visualized\nparanasal sinus and mastoid air cells are clear.",
            "output": "1. Traumatic progression of glioblastoma involving the right parietal and\noccipital lobe with extension to the splenium of the corpus callosum causing 1\ncm leftward shift of normally midline structures and near complete effacement\nof the right lateral ventricle atria which is unchanged from ___\nbut has progressed from ___.\n2. Subtle asymmetric prominence of right lateral ventricle temporal horn,\nsimilar to ___ MR without evidence of trapped ventricle.  Close\nattention on follow-up is recommended.\n\nNOTIFICATION:  The findings were discussed with ___, M.D. by ___\n___, M.D. on the telephone on ___ at 11:52 AM, 10 minutes after\ndiscovery of the findings."
        },
        {
            "input": "The patient is status post right parietal craniotomy and resection of right\nparietal mass lesion, in comparison with the prior exam, there is significant\ndecreased vasogenic edema and also decreased mass effect, in the current exam\nthere is no evidence of shifting of the normally midline structures, however\nthere is a persistent heterogeneous enhancement at the surgical bed, involving\nthe left parietal lobe, extending towards the right periventricular atrium and\nsplenium of the corpus callosum, measuring approximately 32 x 48 mm in\ntransverse dimension, note is made of persistent slow diffusion in this area\nsuggestive of pseudo response (image 19, series 302).  On the left cerebral\nhemisphere there is no evidence of abnormal enhancement, there is no evidence\nof hydrocephalus, the orbits are unremarkable, the paranasal sinuses and the\nmastoid air cells are clear.",
            "output": "1.  Postsurgical changes consistent with right parietal craniotomy remain\ngrossly unchanged since the prior exam.\n\n2.  In comparison with the most recent exam, there is significant improvement\nwith reduced vasogenic edema and mass effect, however there is a persistent\narea of heterogeneous enhancement at the surgical site, involving the right\nparietal lobe extent towards the right periventricular atrium and splenium of\nthe corpus callosum on the right, suggestive of tumoral progression.\n\n3.  Persistent areas of slow diffusion in the tumoral region are suggestive of\npseudo response in the appropriate clinical context.\n\nNOTIFICATION:  The findings were discussed with ___, M.D. by ___\n___, M.D. on the telephone on ___ at 10:40 AM, 5 minutes after\ndiscovery of the findings."
        },
        {
            "input": "MR Head: There is no intracranial hemorrhage, mass, mass effect or shifting of\nthe normally midline structures. Diffusion weighting imaging does not\ndemonstrate evidence of acute infarct.\n\nThere is no abnormal meningeal enhancement. The paranasal sinuses and mastoid\nair cells demonstrate normal signal.  The sella turcica, craniocervical\njunction, and orbits are unremarkable.\n\nGray-white matter differentiation is preserved. There is no parenchymal signal\nabnormality or intracranial mass lesion. No extra-axial collection is\nvisualized. No abnormal restricted diffusion, blooming and/or susceptibility\nartifact is demonstrated.  The lateral ventricles appear slightly asymmetric,\nlikely consistent with a developmental variation, there is no evidence of\nhydrocephalus, the sulci are within normal limits for age. Cisterns are\npatent. CSF signal is normal. Flow-voids of the major intracranial vasculature\nand major dural sinuses are preserved.  The orbits are unremarkable, the\nparanasal sinuses are notable for mucosal thickening in the ethmoidal air\ncells bilaterally, bilateral mucous retention cysts are visualized in the\nmaxillary sinuses with mild mucosal thickening, no air-fluid levels are\nidentified the mastoid air cells are unremarkable.\n\nMRA Head: Normal flow signal is noted in the petrous, cavernous, and\nsupraclinoid portions of the internal carotid arteries. The anterior and\nmiddle cerebral arteries are normal. The anterior communicating artery region\nis normal.\n\nThe posterior cerebral arteries and basilar artery are unremarkable.  The\nsuperior cerebellar arteries are normal. The intradural segments to both\nvertebral arteries are patent; the vertebral arteries are codominant. Normal\nbilateral posterior communicating arteries are identified.  No arterial\nstenosis, saccular aneurysm, or AVM is identified.\n\nMRV of the head:  The major dural venous sinuses are patent with no evidence\nof venous sinus thrombosis.",
            "output": "1. There is no evidence of acute or subacute intracranial process, essentially\nnormal MRI of the brain with no evidence of intracranial hemorrhage or\ndiffusion abnormalities to suggest acute or subacute ischemic changes.\n2. Normal MRA of the head with no evidence of flow stenotic lesions or\naneurysms.\n3. Normal MRV of the head with no evidence of venous sinus thrombosis\n4. Mucosal thickening is identified in the ethmoidal air cells bilaterally,\nthere are bilateral mucous retention cysts in the maxillary sinuses with no\nevidence of air-fluid levels.\n\nNOTIFICATION:     The findings were discussed by Dr. ___ with Dr.\n___ on the telephoneon ___ at 2:37 ___, 5 minutes after\ndiscovery of the findings."
        },
        {
            "input": "Some of the images have been degraded by movement artifact.  Allowing for\nthis;\n\nThere are foci of mild hyperintensity on the diffusion-weighted imaging in the\nleft centrum semiovale (602: ___, and in the periventricular white matter\nlateral to the trigone of the right lateral ventricle, there is mild\nassociated hypointensity on the ADC map in the two foci in the centrum\nsemiovale and isointensity on the ADC map in the right-sided focus.  Findings\nare in keeping with late acute (left side) and subacute (right-sided) focal\ninfarcts.\nThere are small old focal infarcts in the corona radiata and centrum semiovale\nbilaterally.\nOn the gradient echo sequence, there is focal low signal intensity in the\nperiventricular white matter adjacent to the midportion of the body of the\nright lateral ventricle, and punctate low signal intensity in the thalami\nbilaterally and in the right lentiform nucleus, and in the left corona\nradiata.  These are in keeping with old microhemorrhages, most likely due to\nhypertension.  There is no evidence of  edema, masses, mass effect, midline\nshift or recent infarction.  There are nonspecific bilateral supratentorial\nT2/FLAIR white matter hyperintensities, which may represent the sequelae of\nchronic microangiopathy.  The ventricles and sulci are normal in caliber and\nconfiguration.",
            "output": "1. Focal late acute infarcts in the left centrum semiovale and a focal\nsubacute infarct in the periventricular white matter lateral to the trigone of\nthe right lateral ventricle.\n2. Old focal infarcts in the corona radiata and centrum semiovale bilaterally.\n3. Old microhemorrhages suggesting hypertension.\n4. Nonspecific bilateral supratentorial T2/FLAIR white matter\nhyperintensities, which may represent the sequelae of chronic microangiopathy.\n\nNOTIFICATION:  The findings were discussed with ___, M.D. by ___\n___, M.D. on the telephone on ___ at 12:31 pm, 5 minutes after\ndiscovery of the findings."
        },
        {
            "input": "MRA NECK:\n\nThere is a 3 vessel aortic arch.  Right common carotid and cervical internal\ncarotid arteries appear widely patent without stenosis by NASCET criteria. \nThere is mild irregularity of the left carotid bulb, corresponding to mixed\nplaque on the preceding CTA, without stenosis by NASCET criteria.  Evaluation\nof bilateral vertebral artery origins and right proximal V1 segment is\ntechnically limited.  The remainder of the vertebral arteries appear patent\nwithout evidence for flow-limiting stenosis.\n\nMRA BRAIN:\n\nImages are limited by motion artifact.  Images through the proximal\nintracranial vertebral arteries are particularly degraded, but the proximal\nintracranial vertebral arteries are well seen on the gadolinium enhanced neck\nMRA.  Otherwise, the intracranial internal carotid and vertebral arteries\ndemonstrate no evidence for flow-limiting stenosis or aneurysm.\n\nPlease note that the brain parenchyma is not assessed on this exam.\n\nOTHER:\n\nEnlarged and nodular thyroid gland is noted, better seen on the preceding CTA\nof the head and neck.  It was last assessed by ultrasound on ___.",
            "output": "1. No cervical carotid stenosis by NASCET criteria.  Mild atherosclerosis of\nthe left carotid bulb is again demonstrated.\n2. Motion limited brain MRA demonstrates no evidence for flow-limiting\nstenosis or aneurysm.\n3. Please note that the brain parenchyma is not assessed on this exam.\n4. Enlarged and nodular thyroid gland is again seen.  Please refer to the ___ thyroid ultrasound report for management recommendations."
        },
        {
            "input": "On FLAIR images, there is hyperintense signal following the sulci in the left\nposterior parietotemporal and to a lesser extent right posterior parietal\nregion.  There is no susceptibility artifact or T1 hyperintense signal in this\nregion.\n There is a more prominent area of FLAIR hyperintense signal involving the\ncortex and subcortical white matter in the right posterior parietal region\n(series 5, image 15).\n\nMultiple additional small scattered periventricular and subcortical white\nmatter foci of FLAIR hyperintense signal are also present bilaterally.  These\nmay be related to chronic small vessel ischemic changes.\n\nThere is no evidence of hemorrhage, edema, mass effect, or acute infarction. \nCavum septum pellucidum et vergae anatomic variant noted.  Prominence of the\nventricles and sulci is in keeping with age related involutional change. \nPrincipal intracranial vascular flow voids, including those of the dural\nvenous sinuses are patent.  A 1 cm T1 and T2 hyperintense lesion in the left\nparietal bone may represent intraosseous hemangioma (series 7, image 6). \nLinear thickening of the anterior falx and a small focal thickening of the\nleft tentorial leaflet demonstrates susceptibility artifact on gradient echo\nimages correspond to areas of heavy calcification on CT and probably represent\ndural calcifications or hemorrhage calcified meningiomas.  Aside from\nbilateral cataract extractions, the orbits are grossly unremarkable.",
            "output": "1.  Left greater than right posterior temporoparietal sulcal FLAIR\nhyperintense signal.  Lack of susceptibility artifact on gradient echo images\nin this region makes subarachnoid hemorrhage unlikely.  This can be seen in\npatients who are intubated or receiving supplemental oxygen therapy, if such\nhistory exists.  Alternatively, an inflammatory, infectious, or neoplastic\nprocess of the leptomeninges should be considered.  Further evaluation with\ncontrast, if not contraindicated, would be helpful.\n\n2.  More focal cortical and subcortical area of FLAIR hyperintense signal in\nthe right posterior parietal region may be related to the process discussed\nabove or represent a small chronic infarct in this region.\n\n3.  1 cm left parietal bone lesion, probably represents an intraosseous\nhemangioma.\n\n4.  No intracranial hemorrhage or acute vascular territorial infarction."
        },
        {
            "input": "There is no abnormal focus of slow diffusion to suggest acute infarction. \nThere is no hemorrhage.  Focal dense calcification without associated\nenhancement at the left tentorial incisura probably represents dural\ncalcification, less likely heavily calcified meningioma.  Dural calcifications\nare also noted along the anterior falx.\n\nPreviously noted sulcal FLAIR abnormalities along the posterior cerebral\nhemispheres are no longer present.  Small scattered periventricular and\nsubcortical white matter foci of T2/FLAIR signal hyperintensity are grossly\nunchanged and although nonspecific probably sequelae chronic small vessel\nischemic disease.  Increased conspicuity and apparent presence of new such\nlesions on the current study is likely related to obscuration on the prior\nstudy as a result of moderate motion artifact.  The ventricles are stable and\nprominence is in keeping with age related involutional changes.  Cavum septum\npellucidum et vergae variant noted.\n\nThere is no mass, mass effect, or midline shift.  There is no abnormal\nenhancement.  Principal intracranial vascular flow voids are preserved.  The\ndural venous sinuses enhance appropriately on postcontrast MP-RAGE sequences.\n\nAn approximately 1 cm T1 and T2 hyperintense lesion in the left parietal\ncalvarium may represent an intraosseous hemangioma (series 4, image 19).",
            "output": "1. Interval resolution of previously noted sulcal FLAIR hyperintensity in the\nposterior cerebral hemispheres.\n2. Small scattered periventricular subcortical white matter FLAIR hyperintense\nfoci, remain nonspecific but likely sequelae of chronic small vessel ischemic\nchanges in this age group.\n3. No evidence of hemorrhage or acute infarction."
        },
        {
            "input": "MRI BRAIN:  The examination is motion degraded.  Within these confines:\nAgain seen is an intraparenchymal hemorrhage in the left globus pallidus,\nrelatively unchanged compared to the prior CT allowing for the differences in\ntechnique measuring approximately 4.5 x 2.1 cm.  The lesion does not\ndemonstrate any focal areas of enhancement though evaluation is limited given\nthe areas of intrinsic T1 hyperintensity.  Follow-up to resolution is\nrecommended.\n\nThere is associated surrounding FLAIR signal abnormality with minimal mass\neffect causing partial effacement of left lateral ventricle.  No midline shift\nis seen.\n\nThere are few other scattered punctate foci of susceptibility in left frontal\nlobe, the right occipital lobe and left cerebellar hemisphere.\n\nThere is focal area of encephalomalacia in the right temporal lobe anteriorly\nwith FLAIR signal abnormality in the right inferior frontal lobe, likely\nsecondary to prior insult.  Left cerebellar hemisphere encephalomalacia with\nsurrounding superficial siderosis is also noted.\n\nThere are scattered foci of T2/FLAIR hyperintensity in the subcortical and\nperiventricular white matter, nonspecific, likely secondary to small vessel\nischemic disease.\n\nNo intracranial mass, midline shift or acute infarct is seen.  There is\ndiffusion-weighted hyperintense signal of the right thalamus which appears to\ndemonstrate ADC, T2 and FLAIR hyperintensity, presumably T2 shine through. \nThe ventricles, sulci and cisterns are patent and prominent in keeping with\nage-related volume loss.\n\nThe orbits appear unremarkable.  There is mucosal thickening in bilateral\nethmoid air cells, bilateral sphenoid sinuses, right frontal sinus and right\nmaxillary sinus.  Also seen is minimal nonspecific fluid opacification of left\nmastoid tip air cells.  The right mastoid air cells are clear.\n\nMRA brain: The intracranial vertebral and internal carotid arteries and their\nmajor branches appear normal without evidence of stenosis, occlusion, or\naneurysm formation.",
            "output": "1. Relatively stable left globus pallidus intraparenchymal hemorrhage with\nsurrounding mass effect and FLAIR signal abnormality.  No definite areas of\nenhancement are seen.  However follow-up to resolution is recommended given\nthe focal areas of T1 intrinsic hyperintensity limiting the evaluation for\nenhancement and underlying mass.\n2. Few other punctate foci of micro hemorrhages in bilateral cerebral and\ncerebellar hemispheres.  This could be secondary to underlying amyloid\nangiopathy.\n3. Unremarkable MRA of the brain."
        },
        {
            "input": "In comparison with the most recent head CT dated ___, there is a\ngrossly unchanged right frontal lobe hemorrhagic contusion extending towards\nthe right orbital gyrus and associated with vasogenic edema measuring\napproximately 32 by 46 mm in transverse dimension (image 11, series 14), the\nhematoma is producing mild mass effect,  asymmetry of the right frontal\nventricular horn and small amount of right frontal intraventricular hemorrhage\n(Image 15, series 6).  Please note that this hemorrhagic lesion is new in\ncomparison with the study dated ___.\nThere is also diffuse bilateral subarachnoid hemorrhage, the ventricles and\nsulci are slightly prominent suggesting cortical volume loss, unchanged since\nthe prior exams.  The major vascular flow voids are present and demonstrate\nnormal distribution.  The orbits are unremarkable the paranasal sinuses\ndemonstrate mild mucosal thickening on the left maxillary sinus with air-fluid\nlevel, the mastoid air cells demonstrates mild partial opacification of the\nright mastoid air cells.",
            "output": "1.  In comparison with the prior head CT dated ___, there is an\nunchanged right frontal lobe hemorrhagic contusion, please note that this\nhemorrhagic lesion is new since the prior head CT dated ___.\n\n2.  The right frontal hemorrhagic contusion is causing effacement of the sulci\nand mass effect in the right frontal ventricular horn, there is diffuse\nunderlying subarachnoid hemorrhage and small amount of intraventricular\nhemorrhage in the right frontal ventricular horn."
        },
        {
            "input": "Geographic late acute infarct of the right basal ganglia, involving the\ncaudate, with extension into the centrum semiovale as well as smaller foci\nalong the subependymal right trigone and anterior temporal horn is overall\nsimilar in distribution when compared to prior CTA head and neck of ___ allowing for technical differences.  No evidence for new infarct. \nSuperimposed periventricular and subcortical confluent T2/FLAIR white matter\nhyperintensities are nonspecific, but commonly seen with chronic\nmicroangiopathy in a patient of this age.  Minimal effacement of the right\nlateral ventricle is unchanged from prior exam.  There is no midline shift. \nThe sulci, ventricles and cisterns are otherwise within expected limits for\nthe degree of moderate senescent related global cerebral volume loss.\n\nPunctate bifrontal gradient echo susceptibility foci are unchanged from prior\nexamination, compatible with micro hemorrhages.  No new intracranial\nhemorrhage is identified.\n\nLack of the right M1 segment flow void corresponds to occlusion demonstrated\non CTA of ___.  The remainder of the intracranial flow voids are\npreserved.  There is mild mucosal thickening of the ethmoid air cells.  The\norbits are unremarkable feared fluid signal is noted in the bilateral mastoid\nair cells.",
            "output": "1. Geographic late acute infarct of the right basal ganglia involving the\ncaudate with extension into the centrum semiovale as well as smaller foci\nalong the subependymal right trigone and anterior temporal horn are unchanged\ninto configuration it should be shin from prior CTA head and neck of ___.\n2. Lack of right M1 segment flow void corresponding to known occlusion.\n3. No new infarct.  No evidence of hemorrhagic transformation.\n4. Micro hemorrhages of the bilateral frontal lobes are unchanged from prior\nexamination.\n5. Additional findings as described above."
        },
        {
            "input": "The 2 previously demonstrated small foci of hemorrhage in the subcortical\nwhite matter of the right anterior frontal lobe are stable in extent,\ndemonstrating susceptibility artifact on gradient echo images and intrinsic\nhyperintensity on precontrast T1 weighted images, without evidence for\nsuperimposed contrast enhancement.  There is mild surrounding edema without\nsignificant mass effect.\n\nThere is no evidence for blood products or edema elsewhere in the brain\nparenchyma.  There is no acute infarction.  There is no evidence for an\nenhancing mass.  There is no pathologic pachymeningeal or leptomeningeal\ncontrast enhancement.  There are confluent areas and numerous discrete foci of\nhigh T2 signal in the subcortical, deep, and periventricular white matter of\nthe cerebral hemispheres, as well as high T2 signal in the bilateral central\npons, nonspecific but likely sequela of chronic small vessel ischemic disease\nin this age group.  Ventricles and sulci are prominent due to age-related\nparenchymal volume loss.\n\nMajor arterial flow voids appear grossly preserved.  Major dural venous\nsinuses appear patent on postcontrast MP RAGE images.",
            "output": "1. Stable small foci of blood products in the subcortical white matter of the\nright anterior frontal lobe, with mild surrounding edema, but no significant\nmass effect. No evidence for new blood products.\n2. No evidence for an intracranial mass.\n3. Extensive signal abnormalities in the supratentorial white matter and pons\nare nonspecific but likely sequela of chronic small vessel ischemic disease in\nthis age group."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  The ventricles and sulci are prominent, consistent with global\ncerebral volume loss.  Patchy periventricular T2 hyperintensities are most\nconsistent with chronic microvascular ischemic disease.\n\nMild opacification of the right, trace of the left mastoids.  The patient is\nstatus post bilateral cataract surgery.  The paranasal sinuses are clear. \nThere is moderate rightward deviation of the nasal septum.",
            "output": "1. No acute intracranial abnormality.\n2. Changes consistent with mild chronic small vessel ischemic changes."
        },
        {
            "input": "There is no evidence of intracranial hemorrhage, mass, mass effect or shifting\nof the normally midline structures, the ventricles and sulci appear slightly\nprominent suggesting mild cortical volume loss, likely involutional. \nSubcortical and periventricular areas of high-signal intensity on T2 and FLAIR\nremain grossly unchanged, which are nonspecific and may reflect changes due to\nchronic small vessel disease.  No diffusion abnormalities are detected.  There\nis no evidence of abnormal enhancement after contrast administration.  The\nmajor vascular flow voids are present and demonstrate normal distribution. \nAgain postsurgical changes are visualized in the orbits consistent with\nbilateral lens replacement.  The paranasal sinuses demonstrate mild mucosal\nthickening in the ethmoidal air cells, no air-fluid levels are seen, the\npatient is status post left turbinectomy and uncinectomy. There is persistent\nopacification at the tip of the right mastoid air cells.",
            "output": "1.  There is no evidence of acute intracranial process or hemorrhage.\n\n2.  Unchanged subcortical and periventricular areas of high-signal intensity,\nwhich are nonspecific and may reflect changes due to chronic small vessel\ndisease.\n\n3.  There is no evidence of abnormal enhancement after contrast\nadministration."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  No diffusion abnormalities are detected.\n\nThe paranasal sinuses and mastoid air cells are clear.  The orbits are\nunremarkable.\n\nThe major intracranial flow voids are preserved.",
            "output": "1. No evidence of acute infarction, masses, or intracranial hemorrhage.\n2. Unremarkable MRI of the head."
        },
        {
            "input": "There is no intra or extra-axial mass, acute hemorrhage or infarct. There is\nno abnormal postcontrast enhancement.  The sulci, ventricles and cisterns are\nwithin expected limits for the patient's mild senescent related global\ncerebral volume loss.  No abnormal parenchymal FLAIR signal.  The major\nintracranial flow voids are preserved.  The dural venous sinuses are patent. \nThere is mild mucosal thickening of the ethmoid air cells.  The orbits are\nunremarkable.  No fluid signal is seen in the mastoid air cells.  No\nsuspicious marrow signal.",
            "output": "Unremarkable contrast enhanced MRI head.  Specifically no acute infarct,\nintracranial hemorrhage or mass.  No abnormal enhancement."
        },
        {
            "input": "There is a focus of slow diffusion within the left occipital lobe likely\nrepresenting a punctate acute infarct.  There are mild scattered subcortical\nand periventricular white matter FLAIR hyperintensities compatible\nsmall-vessel disease.\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.\n\nThere is a dural-based homogeneously enhancing lesion along the right greater\nwing of the sphenoid, measuring 1.6 AP x 1.3 T x 1.7 cm SI cm.\n\nThe major intracranial vascular flow voids are maintained.  The maxillary\nsinuses are hypoplastic bilaterally.  Mild mucosal thickening of the posterior\nright ethmoid air cells.  Status post bilateral lens replacements.",
            "output": "1. Evidence of a punctate acute infarct within the left occipital lobe.\n2. Right greater wing of the sphenoid meningioma measuring up to 1.7 cm.\n3. Mild white matter small vessel disease.\n\nNOTIFICATION:  The findings were discussed with ___, M.D. by\n___, M.D. on the telephone on ___ at 10:42 am, 10 minutes\nafter discovery of the findings."
        },
        {
            "input": "Surgical calvarial markers are identified at the anterior and bilateral\nfrontal lobes. Again identified along the olfactory groove and planum\nsphenoidale within the right frontal region is a predominantly homogeneously\nenhancing mass which demonstrates mass effect upon the frontal horn of the\nright lateral ventricle. There is a persistent 9 mm leftward shift of normally\nmidline structures. When compared to prior examination, there has been little\ninterval change in appearance. No new enhancing lesion is identified.\n\nNo evidence of acute intracranial hemorrhage. Basal cisterns appear\nunremarkable. The orbits and paranasal sinuses are unremarkable. Mastoid air\ncells are clear.",
            "output": "Unchanged appearance of large right frontal extra-axial dural-based mass along\nthe olfactory groove and planum sphenoidale. Pre-surgical mapping markers\nabout the calvarium are noted."
        },
        {
            "input": "Patient is status post right-sided orbital, cranial, and skullbase approach to\nthe anterior and middle cranial fossa for resection of right planum\nsphenoidale meningioma. Within the surgical bed, there are postoperative\nchanges including air and hemorrhage           .  There is residual\nenhancement within the tuberculum sella in the region of prior mass.\nPersistent mass effect and T2 and FLAIR confluent hyperdensity within the\nright frontal lobe is compatible with edema present on prior examination and\noverall unchanged. There is a 9 mm shift of normally midline structures stable\nsince prior examination. Ventricles are similar in size and shape when\ncompared to most recent examination dated ___ prior to surgical\nintervention.\n\nPosterior to the surgical bed and lateral to the frontal horn of the right\nlateral ventricle, there is a 1.3 x 2.5 cm area of slow diffusion best seen on\nsequence 6 image 17 and sequence 5 image 18. This may reflect infarction or\nmechanical injury.\n\nScattered T2 and FLAIR subcortical white matter foci present on prior\nexamination and though nonspecific likely reflect sequela of chronic small\nvessel ischemic disease.  Postsurgical changes about the calvarium are noted\nmore prominent along the right convexity. The orbits are unremarkable.\nPrincipal intracranial flow voids appear preserved.",
            "output": "Status post resection of right planum sphenoidale meningioma with\npostoperative blood products and fluid within the surgical bed.\n\nFocal area of enhancement within the tuberculum sella in a region previously\nshowing mass invasion is compatible with residual tumor.\n\nFocal area of slow diffusion within the classical medial lenticulostriate\nright artery may refelct post surgical tissue injury versus infarction."
        },
        {
            "input": "There are multiple new acute infarcts of the high right frontal lobe in the A2\ndivision of the right ACA territory compared to prior MRI from ___\n(series 502, image 23). Only the most posterior of these was present on the\nprior MRI. There is a subacute infarct of the right caudate head that\ndemonstrates expected evolution compared to prior MRI.\n\nThe large right frontal lobe hematoma and surrounding edema are not\nsignificantly changed in size from prior CT on ___. Associated mass\neffect is unchanged with compression of the right frontal horn and lateral\ndisplacement of the left frontal horn. Leftward displacement of the septum\npellucidum by 9 mm is unchanged. The bilateral ACAs remain displaced to the\nleft. Epidural hematoma overlying the right frontal lobe and right parietal\nsubarachnoid hemorrhage are unchanged. No new hemorrhage is identified.\n\nThe large right subgaleal fluid collection is not significantly changed in\nsize compared to recent prior CT from ___ but has increased compared\nto initial postoperative CT on ___.",
            "output": "1. Multiple new acute infarcts of the right ACA territory compared to prior\nMRI from ___.\n2. Expected evolution of the right caudate infarct.\n3. Stable large right frontal lobe hematoma, surrounding edema, and associated\nmass effect compared to recent prior CTs. The bilateral ACAs remain displaced\nto the left. Additional stable multi compartment hemorrhage compared to recent\nprior CTs. No new hemorrhage.\n\nNOTIFICATION:  Finding #1 was discussed with ___ by phone at 15:50 ___."
        },
        {
            "input": "The hematoma in the right frontal lobe operative bed is not significantly\nchanged in size or appearance from MRI on ___. It again demonstrates\nrestricted diffusion and minimal enhancement, not significantly changed. No\nnew enhancement is identified. There is no enhancement within the ventricular\nsystem. Mass effect causing leftward midline shift is unchanged.\nThe right frontal extra-axial collection is slightly decreased compared to\nprior MRI from ___. Blood products along the internal margin of the\ncollection and along the anterior falx are unchanged.\nScattered infarcts within the distribution of the right ACA are unchanged.\n\nMajor intravascular flow voids are preserved, however, evaluation of the ACAs\nis somewhat limited due to mass effect from the frontal hematoma.\n\nThe large right frontal scalp collection has near completely resolved.\n\nThe paranasal sinuses are clear. There is fluid in the mastoid air cells, not\nsignificantly changed.",
            "output": "1. Right frontal lobe operative bed hematoma, not significantly changed from\nprior MRI on ___. The hematoma demonstrates restricted diffusion and\nminimal enhancement, unchanged. The signal characteristics are nonspecific and\ncan be seen with both evolving hematoma and infection if there is concern fo\ninfection; correlate clinically and close f/u.\n2.  Stable scattered right ACA territory infarcts.\n3.  Slightly decreased size of the right frontal extra-axial fluid collection.\n4.  Interval near complete resolution of the large right scalp collection."
        },
        {
            "input": "Again seen is a hematoma in the right frontal lobe operative bed, stable in\nsize from the prior MRI on ___. It shows slowed diffusion and\nminimal enhancement, similar in appearance to the prior study. There is no\nenhancement within the ventricular system. Mass effect causing leftward\nmidline shift is stable. Additionally, a right frontal extra-axial fluid\ncollection is stable in size compared to the prior study. Extensive vasogenic\nedema surrounding the frontal lobe lesion is unchanged. Scattered T2\nhyperintense foci throughout the periventricular and subcortical white matter\nare not significantly changed from the prior exam. A focus of slow diffusion\nin the left parietal subcortical white matter (402, 19) is similar appearing\nto the prior study.\nThe major intravascular flow voids are preserved. The paranasal sinuses are\nclear. Fluid in the mastoid air cells is again seen and stable.",
            "output": "1. Right frontal lobe in operative bed hematoma is stable from the prior MRI\nof ___. The hematoma shows slow diffusion with minimal enhancement,\nwhich is unchanged from the prior examination. Mass effect with leftward\nmidline shift is stable.\n2. Right frontal extra-axial subdural collection is stable in size from the\nprior exam as is extensive vasogenic edema surrounding the right frontal lobe\nlesion.\n3. Multiple small hyperintense foci throughout the periventricular and deep\nsubcortical white matter are similar in appearance and are consistent with\nareas of prior infarction."
        },
        {
            "input": "MRI HEAD:  Allowing for technical differences, unchanged appearance of a small\nsubdural hematoma overlying the right cerebral hemisphere, measuring\napproximately 3 mm in greatest thickness.  No new hemorrhages are noted. \nUnchanged appearance of mild 2 mm leftward shift.  No evidence of acute\ninfarct. Sulci, ventricles and cisterns are within expected limits for the\npatient's age. The major intracranial flow voids are preserved. There is a\nsingle punctate focus of gradient echo susceptibility along the corpus\ncallosum (series 11, image 16) which may represent a small micro hemorrhage\nfrom axonal injury. Mild mucosal thickening of the paranasal sinuses are\nnoted.  Mild fluid signal is also seen in the bilateral mastoid air cells. The\nleft orbit is unremarkable.  On the gradient echo sequences, there appears to\nbe increased right retrobulbar susceptibility relative to the left orbit,\nconsistent with blood product or potentially air.\n\nExtensive subgaleal hematoma with gradient echo susceptibility consistent with\nemphysema, debris and hemorrhage products is identified. The appearance of the\ngradient echo susceptibility is greater in extent than would be expected for\nthe amount of air noted on prior CT brain.  Extensive right periorbital\nswelling and hematoma is also noted.",
            "output": "1. A single punctate gradient echo susceptibility focus of the mid corpus\ncallosum, which may represent a small micro hemorrhage from diffuse axonal\ninjury.  No other evidence of intraparenchymal hemorrhage, infarct or diffuse\naxonal injury.\n2. Unchanged appearance of 3 mm thick subdural hematoma overlying the right\ncerebral hemisphere.  No new hemorrhages are noted.\n3. Suggestion of a right retro bulbar hematoma versus air. Clinical\ncorrelation is recommended.\n4. The degree of subcutaneous susceptibility is greater than would be expected\nfor the amount of air seen on most recent CT examination. Clinical correlation\nwith interval instrumentation or worsening injury is recommended."
        },
        {
            "input": "Stable large right frontal intraparenchymal hemorrhage measuring approximately\n4.9 x 2.5 cm (4: 24).  Surrounding vasogenic edema is present with associated\nmass effect on at the lateral ventricle and sulcal effacement. Stable 6 mm\nleftwards shift of midline structures.  In addition to the vasogenic edema\nsurrounding the hemorrhage, there is a crescent of slow diffusion along the\nposterior margin of the hemorrhage, image 3:25, compatible with contusion or\ninfarction.\n\nAn acute infarct is seen within the medial right temporal lobe (4: 14) with\nassociated faint high in signal on FLAIR images.\n\nThere is high signal on the diffusion tracer sequence and low signal on the\nADC map along the cortex of left greater than right occipital lobes, bilateral\nparietal lobes, medial frontal lobes, and right insula, which may represent\nacute cortical infarction, but could be an artifact related to the known\nextensive subarachnoid hemorrhage seen in these locations on ___,\nwhich is currently subacute. FLAIR in T2 weighted images demonstrate cortical\nswelling in the same areas with minimal elevation in signal intensity, but\nthis could be secondary to impaired venous drainage in the setting of\nextensive subarachnoid hemorrhage, versus acute infarction.\n\n0.9 x 0.6 cm (09:14) left thalamic subacute/chronic infarction is noted.\n\nMild T2 hyperintensity within the dorsal pons and midbrain is present without\ndiffusion abnormality, indicating mild edema without infarction.\n\nBasal cisterns remain crowded.\n\nThere is expected susceptibility artifact along the left frontal\nventriculostomy catheter. The catheter tip is seen within the left lateral\nventricle.  Intraventricular hemorrhage is not significantly changed. The\nventricles are small in size, similar to the CT from 1 day earlier.\n\nBlooming artifact from basilar tip aneurysm coiling is present. A 0.7 x 0.6 cm\n(09:11) right MCA aneurysm at M1/ M2 segment is again noted.\n\nMucosal thickening and fluid in the paranasal sinuses, as well as partial\nbilateral mastoid air cell opacification, are likely sequela of endotracheal\nintubation and prolonged supine positioning.",
            "output": "1.  Signal abnormality along the the cortex in left greater than right\noccipital lobes, bilateral parietal lobes, right insula, and medial temporal\nlobes, corresponding to sites of extensive subarachnoid hemorrhage, which is\nnow subacute. The signal abnormalities are probably related to this\nsubarachnoid hemorrhage, with associated cortical swelling secondary to\nimpaired venous drainage. However, acute infarctions are not excluded.\nRecommend followup MRI in 1 day to assess for any evidence for progressing\ninfarction on FLAIR/ T2 weighted images.\n2.  Small acute infarct in the medial right temporal lobe.\n3.  Large right frontal intraparenchymal hemorrhage with surrounding vasogenic\nedema and mass effect is unchanged.  Acute infarction or contusion along its\nposterior portion, superimposed upon vasogenic edema.\n4. Mild edema in the dorsal pons and midbrain without evidence for acute\ninfarction.\n5.  Stable intraventricular hemorrhage. Stable small size of the ventricles.\n6.  0.7 cm right MCA aneurysm at M1/M2 segment is again noted.\n\nNOTIFICATION:  The updated findings were discussed by Dr. ___ with\n___ NP on the telephone on ___ at 2:20 ___, 5 minutes after\ndiscovery of the findings."
        },
        {
            "input": "There is a small acute to early subacute infarction in the anterior aspect of\nthe left upper pons with slow diffusion and with high signal on T2\nweighted/FLAIR images.\n\nThere also multiple discrete and confluent foci of high T2 signal in the\nperiventricular, deep, and to a lesser extent subcortical white matter of the\ncerebral hemispheres, nonspecific but likely sequela of chronic small vessel\nischemic disease, given the patient's age and clinical history. Within this\nsignal abnormality, a linear focus of encephalomalacia in the right frontal\ncentrum semiovale is consistent with a small chronic infarct. Small chronic\ninfarcts as well as prominent perivascular spaces are also present in the\nbasal ganglia.\n\nIn the left cerebellar hemisphere, there is a focus of susceptibility artifact\nindicating chronic blood products, with corresponding 4 mm round focus of low\nsignal on T1 weighted, T2 weighted, and and FLAIR images. This is consistent\nwith a chronic microhemorrhage. An underlying cavernous malformation is less\nlikely, given absence of high signal on T1 and T2 weighted images.\n\nMinimal prominence of the ventricles is likely age-related. There is moderate\nenlargement of the sylvian fissures and mild to moderate enlargement of\nbiparietal and bilateral paracentral sulci, indicating cerebral atrophy. There\nis no disproportionate medial temporal lobe atrophy.\n\nMajor intravascular flow voids are grossly preserved.\n\nThere is minimal mucosal thickening in the frontal, ethmoid, and maxillary\nsinuses.",
            "output": "1. Small acute to early subacute infarct in the anterior left upper pons.\n2. Extensive supratentorial white matter signal abnormalities are likely\nsequela of chronic small vessel ischemic disease in a patient of this age with\nthe clinical history of vascular dementia. Small chronic small-vessel infarcts\nare present in the right frontal centrum semiovale in bilateral basal ganglia.\n3. Moderate perisylvian parenchymal atrophy and mild to moderate biparietal\nand bilateral paracentral parenchymal atrophy. No disproportionate medial\ntemporal lobe atrophy.\n\nNOTIFICATION:  The impression above was entered by Dr. ___ on\n___ at approximately 17:00 into the Department of Radiology critical\ncommunications system for direct communication to the referring provider."
        },
        {
            "input": "There is no intracranial hemorrhage. Diffusion weighting imaging does not\ndemonstrate evidence of acute infarct. There there are a few tiny T2/FLAIR\nhigh signal foci in the left parietal subcortical and left frontal deep white\nmatter, nonspecific. There is no lesion of the brainstem or cerebellum. Gray\nwhite matter differentiation is maintained. Ventricles and extra axial spaces\nare within normal limits. The major intracranial vessels exhibit the expected\nsignal void related to vascular flow.\n\nNo enhancing mass is identified. There is no abnormal meningeal enhancement.\nThe paranasal sinuses and mastoid air cells demonstrate normal signal. The\nsella turcica, craniocervical junction, and orbits are unremarkable.",
            "output": "Few tiny scattered T2/FLAIR high signal foci in the subcortical and deep white\nmatter, nonspecific. These can be seen due to chronic small vessel ischemic\ndisease, demyelinating disease, prior infectious/inflammatory disease,\nvasculitis, and chronic headaches. Frequently, no specific etiology can be\ndetermined."
        },
        {
            "input": "There is no evidence of acute infarction.  No intracranial hemorrhage.  No\nmass, mass effect, edema or midline shift.  No diffusion abnormalities are\ndetected.\n\nThe ventricles and sulci are prominent, compatible with atrophic changes.  The\nbasal cisterns are patent.  There is no evidence of impending, downward\nherniation.\n\nFollowing the administration of intravenous contrast material, there is no\nabnormal enhancement.  The dural venous sinuses appear patent on MP-RAGE\nimagine sequences.\n\nMild mucosal thickening is noted in the left greater than right frontal\nsinuses and within scattered bilateral ethmoid air cells.  Scattered partial\nopacified right mastoid air cells are noted.  The remainder of the visualized\nparanasal sinuses, middle ear cavities, and mastoid air cells are well aerated\nand clear.  The orbits are within normal limits bilaterally.",
            "output": "1. No evidence for intracranial metastatic disease.\n2. Moderate global cerebral atrophic changes."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  Prominence of the ventricles and sulci are compatible with\ninvolutional change.  There is no abnormal enhancement after contrast\nadministration.\n\nPeriventricular and deep white matter FLAIR hyperintensities are nonspecific\nbut likely represent sequela of chronic small vessel ischemic disease.\n\n\nThere is mild ethmoid mucosal thickening, otherwise the paranasal sinuses and\nmastoid air cells are clear.  The orbits are unremarkable.  No suspicious\nmarrow signal.",
            "output": "1. No evidence of intracranial metastatic disease at this time.\n2. No acute intracranial abnormality.\n3. Additional findings described above."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  Cerebellar tonsils are slightly low lying, similar to the\nprior cervical spine MRI performed in ___.  The ventricles and sulci\nare normal in caliber and configuration.  There is no abnormal enhancement\nafter contrast administration.  Major intracranial arterial vasculature is\nunremarkable.  Dural venous sinuses are patent.  The orbits are within normal\nlimits.",
            "output": "1. No acute intracranial abnormality.\n2. Stable appearance of slightly low-lying cerebellar tonsils."
        },
        {
            "input": "There is no intra or extra-axial mass, acute hemorrhage or infarct. The sulci,\nventricles and cisterns are within expected limits for the patient's age. \nThere are mild periventricular and subcortical punctate T2/FLAIR white matter\nhyperintensities, which are nonspecific, but compatible with chronic\nmicroangiopathy in a patient of this age.  The major intracranial flow voids\nare preserved.  There is mild mucosal thickening of the ethmoid air cells. \nThe orbits are unremarkable.  The mastoid air cells are clear.",
            "output": "1. No acute intracranial abnormality on noncontrast MRI head.  Specifically no\nintracranial mass, acute hemorrhage or infarct.\n2. Minimal periventricular and subcortical T2/FLAIR white matter\nhyperintensities are nonspecific, but compatible with chronic microangiopathy\nin a patient this age."
        },
        {
            "input": "The examination is mildly degraded by patient motion, allowing for this:\n\nSeen again is a large intraparenchymal hemorrhage centered in the right\ntemporal occipital region with surrounding edema and local mass effect,\noverall similar in size and appearance as compared to the prior examination. \nThere is again partial effacement involving the temporal horn of the right\nlateral ventricle.  Leftward midline shift measures 1.0 cm, also unchanged. \nThin sliver of subdural hematoma seen overlying the right temporal lobe and\noverlying the occipital lobe posteriorly as seen on prior CT.\n\nIntraventricular extension of hemorrhagic products is again noted, also\nunchanged.  There are no new areas of acute intracranial hemorrhage\nidentified.\n\nThere is high signal on diffusion in the left frontal lobe near the vertex\nwith matching hyperintensity on the ADC map, in a distribution and appearance\nsimilar compared to prior MRI and potentially subacute/chronic infarct.  The\npreviously seen foci of high signal on diffusion surrounding the parenchymal\nhemorrhage are now no longer clearly delineated by diffusion sequence but\ndemonstrate enhancement suggesting a subacute infarct.   A new punctate focus\nof restricted diffusion is noted at the left frontoparietal vertex (___) is\nnew since prior MRI.  Otherwise, no additional sites of new restricted\ndiffusion are identified.\n\nOn the postcontrast sequences, no discrete enhancing nodule or mass is\nidentified in the vicinity of the intraparenchymal hemorrhage noting moderate\ndegree of intrinsic T1 hyperintensity associated with the hematoma.  Mild\nenhancement at the high left frontal lobe correlates with area of subacute\ninfarction detailed above.  Additional areas of enhancement surround the\nparenchymal hematoma are as detailed above as well.  There is additional focus\nof enhancement in the left frontal lobe (13:17) with subtle high signal on\ndiffusion, new since prior suggesting an interval though subacute infarct\ngiven additional findings.  The dural venous sinuses are patent.\n\nThe background ventricles and sulci otherwise appear grossly age-appropriate. \nThere is gross preservation of the principal intracranial vascular flow voids.\n\nMild mucosal thickening is seen in scattered ethmoid air cells.  The remainder\nof the visualized paranasal sinuses, middle ear cavities, and mastoid air\ncells are well aerated and clear.  The orbits are within normal limits\nbilaterally.",
            "output": "1. Essentially unchanged large intraparenchymal hemorrhage centered in the\nright temporal occipital region with intraventricular extension, a stable\ndegree of local mass effect, and 1.0 cm of leftward midline shift.  Unchanged\nright-sided subdural hematoma overlying the occipital lobe with a thin sliver\nalso seen overlying the right temporal lobe.\n2. No new sites of acute intracranial hemorrhage are identified.\n3. New, punctate focus of restricted diffusion at the high left frontoparietal\nlobe is most compatible with a late acute to early subacute infarct.\n4. Additional areas of subacute infarction are seen at the high left\nparamedian frontal lobe and surrounding the parenchymal hemorrhage.\n5. No evidence for underlying abnormal enhancement or mass lesion.\n6. Additional findings, as above."
        },
        {
            "input": "There is a large acute intraparenchymal hemorrhage within the right parietal\nand occipital lobes with decompression of the ventricular system.  There is\nlocal mass effect with narrowing of the atrium of the right lateral ventricle.\nThere is minimal midline shift.  The basilar cisterns are patent.  Several\npunctate areas of restricted diffusion are seen adjacent to the hemorrhage\nwhich could be due to blood products or associated infarcts in the adjacent\nregions.  In addition, there is a focus of mildly decreased diffusion in the\nleft parietal posterior frontal region (502:24) which demonstrates subtle\nenhancement on the postcontrast images.\n\nNo underlying enhancing mass lesion is identified.  The major cortical veins\nand dural venous sinuses are patent.\n\nNo background of chronic microhemorrhage is identified.\n\nThere are areas of white matter signal abnormality within the bilateral\ncerebral hemispheres, nonspecific of the likely a sequela of moderate chronic\nsmall vessel disease.  There is likely an old infarct within the left\nparacentral lobule.  The major vascular flow voids appear intact.\n\nThe orbits are unremarkable.",
            "output": "Large acute intraparenchymal hemorrhage within the right parietal occipital\nlobes with decompression into the ventricular system.  No underlying enhancing\nmass lesion is identified.  Adjacent punctate areas of infarcts are seen.  A\nsubacute infarct is seen in the left frontal lobe.  The major cortical veins\nand dural venous sinuses are patent.  Recommend follow-up contrast enhanced\nbrain MRI following resolution of hematoma  to exclude underlying abnormality."
        },
        {
            "input": "Postoperative changes following right frontal craniotomy and duraplasty.  A 14\nmm mixed intensity extra-axial collection should be compared with prior\noutside hospital imaging to evaluate stability.  Right anterior and inferior\nfrontal encephalomalacia without nodular thickening or enhancement to suggest\nresidual or recurrent tumor.\n\nT2 FLAIR hyperintense signal and volume loss is present in both frontal lobes,\nmore prominent on the right and genu of the corpus callosum with ex vacuo\ndilatation of the frontal horns, reflecting gliosis.  More subtle T2 FLAIR\nhyperintense signal also extends into the right anterior and mesial temporal\nlobes - this is also likely related to gliosis, may be contributing to the\npatient's seizures, and should be compared with outside hospital imaging.\n\nFew scattered prominent perivascular spaces are seen in both frontal lobes. \nFew scattered foci of T2 FLAIR hyperintense signal within the periventricular\nand subcortical white matter are nonspecific, but likely related to chronic\nmicroangiopathic ischemia in a patient of this age.  There is no evidence of\nacute infarction.  There are no signs acute parenchymal hemorrhage.\n\nGlobes and orbits are intact.  The paranasal sinuses and mastoid air cells\nappear clear.  Numerous indeterminate scalp lesions are noted.",
            "output": "1. Postsurgical changes following right frontal craniotomy, duraplasty for\nresection of an underlying tumor.  No evidence of residual or recurrent tumor.\n2. Abnormal signal within the right anterior and mesial temporal lobes is\npresumed related to gliosis, which should be compared with prior outside\nhospital imaging.\n3. 14 mm mixed density right frontal extradural collection should be compared\nwith prior outside hospital imaging to document stability.\n4. No evidence of acute infarction, acute parenchymal hemorrhage, or\nhydrocephalus."
        },
        {
            "input": "There are several foci of slow diffusion, with increased DWI signal, in the\ncerebral hemispheres, in the frontal, parietal and the occipital lobes on both\nsides. The larger areas demonstrate low ADC signal;  limited assessment of the\nsmaller foci on the ADC signal. Questionable foci in cerebellar hemispheres on\nDWI seq.  not confirmed on ADC seq.\nSeveral of the lesions are predominantly cortical based extending into the\nadjacent white matter.\nThere is associated increased FLAIR signal intensity without significant\nsurrounding edema or mass effect.\nNo significant foci of negative susceptibility are noted, to suggest\nassociated hemorrhage.\n\nThe ventricles, the extra-axial CSF spaces and the sulci are unremarkable.\nA few small FLAIR hyperintense foci, nonspecific in appearance are also noted.\nThe major intracranial arterial flow voids are noted on the axial T2 weighted\nimages.\nDedicated MR angiogram not performed as not requested.  Right vertebral artery\nis dominant.\nSella, pineal gland and the craniocervical junction regions are unremarkable.\n\nFluid in the bilateral mastoid air cells, sphenoid sinus and the nasopharynx,\nlikely related to intubation.\nThe imaged orbits are unremarkable.",
            "output": "Multiple acute to subacute infarcts scattered in the cerebral hemispheres on\nboth sides as described above, without significant surrounding edema or mass\neffect. Likely embolic etiology.\nCorrelate clinically for source and consider MR angiogram as needed.\nPlease see the concurrent MR ___ study report for other important details\nand recommendations.\n\nNOTIFICATION:  D/w ___ by ___ on ___ at 8.30 am over phone\nsoon after review"
        },
        {
            "input": "Areas of increased FLAIR signal hyperintensity in the subarachnoid space along\nthe gyral surfaces in the left frontal lobe (09:21) and right parietal lobe\n(09:17) is compatible with known subarachnoid hemorrhage.  Layering blood\nproducts are also noted in the occipital horns of the lateral ventricles\nbilaterally (09:13).  A left temporal lobe contusion is present, with\nsusceptibility artifact on the gradient recalled echo sequence images (07:10).\n\nSmall foci of restricted diffusion are noted along the atrium of the left\nlateral ventricle in parieto-occipital region, as well as adjacent to the\nfrontal horn of the right lateral ventricle with associated flair\nhyperintensity (400:16, 402:16).  Another area of apparent restricted\ndiffusion in the posterior left pons, just above the cerebellar peduncle\n(42:10, 400:10) corresponds to a focus of susceptibility artifact on gradient\nrecalled echo sequence images and known subarachnoid hemorrhage on the prior\nCT (07:11).  A small subdural hematoma is noted along the left parietal\nconvexity, extending towards the falx, corresponding to the finding described\non the prior CT (3:14, 9:17).\n\nThe size and configuration of the ventricles is unchanged compared to the\nprior CT, allowing for inter modality differences.  There is no evidence of\nmass-effect or shift of the normally midline structures.  Mild mucosal\nthickening is present in the posterior bilateral maxillary sinuses is\nnonspecific and may be related to intubation status (5:6).  Susceptibility\nartifact overlying the right temporal scalp corresponds to the site of\nmetallic skin staples.  EEG leads are also noted along the scalp.",
            "output": "1. Small foci of late acute to subacute infarction in the right frontal and\nparieto-occipital regions adjacent to the right lateral ventricle.\n2. Questioned left superior cerebellar peduncle and left midbrain late acute\nto subacute infarcts vs hemorrhages.\n3. Subarachnoid hemorrhage in bilateral cerebral hemispheres with\nintraventricular extension appears grossly stable.\n4. Stable small subdural hemorrhage along the left parietal convexity in\nextending towards the falx.\n5. Left temporal lobe evolving intraparenchymal contusion.\n\nNOTIFICATION:  The findings were discussed via telephone by Dr. ___ with\n___ (neurosurgery P.A.) on ___ at 3:13 ___, 5 minutes after\ndiscovery of the findings."
        },
        {
            "input": "The ventricles and extra-axial spaces are normal in size. There is no evidence\nof midline shift, mass effect or hydrocephalus. There are no acute infarcts.\nThere is no evidence of focal abnormalities.  The vascular flow voids are\nmaintained.  A retention cyst is incidentally seen in the right maxillary\nsinus.  Following gadolinium administration there is no evidence of abnormal\nparenchymal, vascular and meningeal enhancement seen.",
            "output": "No significant abnormalities are seen on MRI of the brain with and without\ngadolinium."
        },
        {
            "input": "There are two relatively homogeneously enhancing supratentorial metastatic\nlesions within the left hemisphere.\n\nThe first measures approximately 1.5 x 1.7 x 1.7 cm within the paramedian left\nparietal lobe (series 12 image 123 and series 101 image 32).  There is\nextensive surrounding edema.\n\nThe second metastatic lesion is within the left occipital lobe measuring 2.0 x\n1.9 x 2.0 cm (series 12, image 88 and series 101, image 27).  Again, this\nlesion enhances relatively homogeneously with extensive surrounding vasogenic\nedema.\n\nIs significant vasogenic edema resulting in effacement of the sulci within the\nleft parietal and occipital lobes, as well as moderate effacement of the left\nlateral ventricle.  There is also approximately 6 mm of left to right midline\nshift as well as anterior shifting of the splenium of the corpus callosum. \nThe basal cisterns are patent.  There is no evidence of downward herniation.\n\nThere is moderate slow diffusion in the left occipital lesions suggesting\nhypercellularity there is no evidence of hemorrhage or acute territorial\ninfarction.  Multiple chronic lacunar infarcts within the left caudate head\nand caudate bodies bilaterally.  Prominent perivascular spaces within the\ninsula bilaterally.\n\nThe circle of ___ is patent.  Dural venous sinuses are also patent.  Orbits\nare unremarkable.",
            "output": "1. Two relatively homogeneously enhancing lesions within the left hemisphere\nmeasuring 2.0 cm within the left occipital lobe, and 1.7 cm within the left\nparietal lobe.  Extensive surrounding vasogenic edema.\n2. Effacement of the sulci, left lateral ventricle, and 6 mm of left to right\nmidline shift.\n3. No evidence of acute territorial infarction or intracranial hemorrhage."
        },
        {
            "input": "Postsurgical changes after left posterior parietal craniotomy for excisional\nbiopsy are again noted with residual air-fluid collection and enhancement\nabout the resection site.  There is a small amount of residual pneumocephalus.\nDiffuse pachymeningeal enhancement along the left cerebral convexity is most\nlikely postsurgical.\n\nAllowing for differences in technique, there appears to be similar to\nminimally increased rightward midline shift measuring approximately 4-5 mm\nfrom previously 3-4 mm when compared to the most recent prior CT.\nThere is unchanged effacement of the anterior and occipital horns of the left\nlateral ventricle secondary to vasogenic edema.  The ventricular system\nappears otherwise similar in size and configuration.\n\nAgain identified are two fairly homogeneously enhancing lesions in the left\nparieto-occipital region measuring 2.0 x 1.7 x 2.0 cm (AP X TR X SI).  As well\nas a left parasagittal parietal lesion measuring 1.5 x 1.5 x 1.7 cm (AP X TR X\nSI).",
            "output": "1. Postsurgical changes after left posterior parietal craniotomy for\nexcisional biopsy with residual small pneumocephalus and air fluid collection\nin the surgical bed.  Enhancement about the resection site and diffuse\npachymeningeal enhancement along the left cerebral convexity are most likely\npostsurgical.\n2. Unchanged fairly homogeneously enhancing lesions in the left\nparieto-occipital and left parasagittal parietal region with extensive\nvasogenic edema.\n3. Similar to minimally increased rightward midline shift measuring\napproximately 4-5 mm from previously 3-4 mm.\n4. Stable configuration of the ventricular system with unchanged effacement of\nthe anterior and occipital horns of the left lateral ventricle."
        },
        {
            "input": "Postsurgical changes after the left posterior parietal craniotomy for\nresection of metastatic parieto-occipital and parietal lesions with blood\nproducts throughout the resection cavities are noted.\nThere is an extra-axial collection subjacent to the craniotomy site which\nmeasures up to 11 mm in maximum thickness.  Pachymeningeal enhancement along\nthe cerebral convexity is most likely postsurgical.  There is no significant\nchange of the previously seen edema involving the left frontal, parietal and\noccipital lobes.\nA small amount of residual enhancement is seen in the regions of the prior\nmetastatic lesions at the parieto-occipital junction and parasagittal left\nparietal lobe which may be postsurgical.  However, residual tumor cannot be\nfully excluded and attention on follow-up is recommended.  No other lesions\nare identified.\n\nThere is a tiny focus of cortical enhancement in the right postcentral gyrus\n(series 13, image 19 and series 14, image 130 ___ which is new since the\nprior studies.\n\nThere is unchanged effacement of the posterior horn of the left lateral\nventricle.  Mild rightward midline shift is again noted measuring up to 4 mm,\nsimilar to prior.  The ventricular system is otherwise stable in\nconfiguration.\n\nAgain noted is generalized parenchymal volume loss, which is most likely age\nrelated.  There is mild mucosal thickening along the ethmoid air cells. \nPartial opacification of the bilateral inferior mastoid air cells is noted. \nThe orbits appear grossly unremarkable.",
            "output": "1. New tiny focus of cortical enhancement in the postcentral gyrus, new since\nthe prior studies.\n2. Expected postsurgical changes after left posterior parietal craniotomy for\nresection of metastatic left parietal and parieto-occipital lesions within\nextra-axial collection subjacent to the craniotomy site measuring up to 11 mm\nin maximum thickness.\n3. Residual enhancement in the surgical cavities of the resected metastatic\nlesions may reflect postsurgical changes, however, residual tumor cannot be\nfully excluded and attention on follow-up is recommended.\n4. Stable vasogenic edema in the left cerebral hemisphere with unchanged 4 mm\nrightward midline shift."
        },
        {
            "input": "Again seen are postoperative changes from prior left parietal craniotomy and\nresection of left parietal and parieto-occipital lesions.  Linear hyperintense\nT1 signal on postcontrast images may represent a combination of postsurgical\nenhancement at the margins of the resection sites in conjunction with evolving\npostsurgical blood products, however absence of precontrast T1 weighted images\nas part of this protocol limits this assessment.\n\nThe previously demonstrated punctate focus of cortical enhancement along the\nposterior margin of the right postcentral gyrus is no longer identified (see\nseries 4, image 131 on the current study, compared with series 14, image 137\non the prior study from ___.\n\nThere is a 9 mm wide extra-axial postoperative collection subjacent to the\nleft parietal craniotomy, similar to prior, mild mass effect on the adjacent\nbrain parenchyma.  Posterior-to-anterior mass-effect on the body and atrium of\nthe left lateral ventricle is decreased from prior likely due to decrease in\nvasogenic edema as evidence by the decreased extent of T1 hypointense signal\nwithin the left occipital and parietal white matter. No shift of the normally\nmidline structures.  No new mass effect.\n\nNo new lesions.  No new abnormal enhancement. Outside of the resection bed,\nthere is no evidence of acute infarction.\n\nThe ventricles and sulci are prominent, compatible with global parenchymal\nvolume loss.\n\nMajor dural venous sinuses are patent.",
            "output": "1. Previously demonstrated punctate focus of cortical enhancement along the\nposterior margin of the right postcentral gyrus is no longer identified.\n2. No new lesions or new abnormal enhancement.\n3. Evolving expected postoperative changes from prior left parietal craniotomy\nand resection, with improved mass effect."
        },
        {
            "input": "The patient is status post left parietal craniotomy and resection of left\nparietal and parieto-occipital metastatic lesions with stable postsurgical\nchanges.  There is redemonstration of pachymeningeal enhancement along the\ncerebral convexity, likely postsurgical and unchanged from prior study.  There\nis interval decrease in the size of the fluid collections at the resection\nsites.  Otherwise, there is no evidence of new lesions or new areas of\nabnormal enhancement.\n\nThere is a 6 mm wide extra-axial postoperative collection adjacent to the left\nparietal craniotomy, previously measuring 9 mm on prior study dated ___.  There is redemonstration of mild vasogenic edema with interval decrease\nin mild mass effect on the adjacent brain parenchyma.  There is no evidence of\nnew mass effect or midline shift.\n\nThere is no evidence of acute hemorrhage or infarction.  The ventricles and\nsulci are prominent, compatible with involutional change.",
            "output": "1. No evidence of new suspicious lesions or areas of abnormal enhancement.\n2. Status post left parietal craniotomy, and resection of left parietal and\nparieto-occipital metastatic lesions with evolving  changes."
        },
        {
            "input": "Treatment bed:\nPosttreatment changes.  Minimal, linear residual enhancement in the treatment\nbed left parietal, occipital lobes is minimal, and mildly improved since\nprior.  Surrounding nonenhancing T2 signal abnormality is similar to mildly\nworsened, likely postradiation change..  Stable left frontal lobe\nencephalomalacia, nonenhancing T2 signal abnormality, no associated\nenhancement..  Stable mild dural thickening, enhancement overlying left\nparietal lobe, postsurgical.\n\nNo new metastases\n\nOther:\nFew tiny chronic cerebellar infarcts, similar.  Brain parenchymal atrophy. \nChronic lacunar infarcts bilateral basal ganglia, similar.  No acute infarct. \nPreserved vascular flow voids.  Patent dural venous sinuses..  Clear paranasal\nsinuses, left mastoids.  Minimal opacification right mastoids.",
            "output": "1. Improving posttreatment changes.  No residual tumor.\n2. No new metastases."
        },
        {
            "input": "Again postoperative changes are identified in the left hemisphere.  FLAIR\nhyperintensities in the left frontal lobe indicating encephalomalacia and in\nthe parieto-occipital lobe indicating posttreatment changes are stable.\nPreviously noted enhancement has further decreased.  No new areas of abnormal\nenhancement are seen.  Brain atrophy seen without mass effect or midline\nshift.  There is no hydrocephalus.  There are soft tissue changes within the\nright mastoid air cells without soft tissue changes within the middle ear.  No\nacute infarcts are identified.",
            "output": "Further decrease in enhancement compared to the previous MRI examination with\nunchanged T2 and FLAIR hyperintensities.  No definite new areas of abnormal\nenhancement, mass effect or hydrocephalus."
        },
        {
            "input": "Postoperative changes are again demonstrated from left parietooccipital\ncraniotomy with dural thickening and enhancement subjacent to the craniotomy\nsite which is probably postoperative.  There are mild areas of curvilinear\nenhancement overlying the left parietal and occipital lobes which appear\nstable with no definite new areas of abnormal enhancement.  In addition, there\nis T2/FLAIR hyperintensity in the left frontal lobe which may reflect\nencephalomalacia.  Chronic blood products are noted at the operative site.\n\nSmall chronic infarcts in the cerebellar hemispheres noted.\n\nNo evidence of acute or subacute infarct or recent hemorrhage.  Scattered\nareas of nonspecific T2/FLAIR hyperintensity in the white matter are noted\nwhich are nonspecific but likely reflect chronic small vessel disease in this\nage group.\n\nProminence of the ventricles and sulci likely reflects age-related\ninvolutional change.\n\nThe major intracranial vascular flow voids are preserved.  Orbits and\nvisualized extracranial soft tissues are unremarkable.  There is minimal\nmucosal thickening in the ethmoid air cells.  Mild patchy fluid signal in the\ninferior mastoid air cells, right greater than left.",
            "output": "1. Post treatment changes are again demonstrated with no evidence of new or\nprogressive disease.\n2. Chronic bilateral cerebellar infarcts, and encephalomalacia in the left\nfrontal lobe."
        },
        {
            "input": "The patient is status post left parietooccipital craniotomy for resection of\nunderlying mass, with unchanged chronic hemorrhage product.  Mild residual\ndural thickening and enhancement is unchanged from prior exam.  No areas of\ngrowing nodular enhancement.  Associated T2/FLAIR white matter edema pattern\nof the left parieto-occipital lobe is unchanged.  Mild encephalomalacia and\nFLAIR hyperintense white matter edema of the left frontal lobe and right\noccipital lobe is unchanged.\n\nNo new enhancement.  No acute infarct or intracranial hemorrhage.  Lacunar\ninfarcts of the bilateral cerebellar hemispheres are re-identified.  The major\nintracranial flow voids are preserved.  The dural venous sinuses are patent.\n\nThere is mild mucosal thickening of the paranasal sinuses.  The orbits are\nunremarkable.  Trace fluid signal is seen in the right mastoid tip.  No\nsuspicious marrow signal.",
            "output": "1. Status post left remote parietooccipital craniotomy, with unchanged chronic\nhemorrhage product as well as underlying mild dural thickening and\nenhancement.  Associated white matter edema pattern of the left\nparietooccipital lobe is unchanged.  Additional regions of encephalomalacia\nand FLAIR white matter edema pattern of the left frontal lobe and right\noccipital lobe are unchanged.  There is no evidence of disease progression or\nnew abnormal enhancement.\n2. No acute infarct or intracranial hemorrhage.\n3. Chronic bilateral cerebellar lacunar infarcts.\n4. Additional findings as described above."
        },
        {
            "input": "There is no evidence of acute infarction or intracranial hemorrhage.  There is\nmild global cerebral volume loss.  There are nonspecific periventricular and\nsubcortical FLAIR hyperintense foci, likely a sequela of chronic small vessel\nmicroangiopathy.  The ventricles are normal in size without mass effect or\nmidline shift.\n\nThe postcontrast axial T1 and MPRAGE images are moderate to severely motion\ndegraded.  Within this limitation, there is no definite evidence of an\nenhancing mass or abnormal enhancement.  The major visualized arterial\nvascular flow voids are preserved.\n\nThere is mild mucosal thickening of the left maxillary sinus and bilateral\nethmoid air cells.  Patient is status post right cataract extraction.  There\nis moderate bilateral mastoid air cell fluid opacification, which may be\nreactive or inflammatory.  The visualized soft tissues appear unremarkable.",
            "output": "1. No evidence of acute infarction, intracranial hemorrhage, or imaging\nevidence of amyloidosis.\n2. Postcontrast images are moderate to severely motion degraded.  Within this\nlimitation, no evidence of an enhancing mass or abnormal enhancement.\n3. Global cerebral volume loss with probable chronic small vessel\nmicroangiopathy."
        },
        {
            "input": "MR BRAIN:\nThe patient is intubated.  Status post coiling of an anterior communicating\nartery aneurysm with associated susceptibility artifact.  There are multiple\nsmall foci of slow diffusion involving the bilateral frontal lobes, genu\n(series 4, image 18) and splenium (image 19) of the corpus callosum.  These\nareas have mildly increased signal intensity on the FLAIR images compatible\nwith acute to subacute infarction.\n\nNo significant change in the scattered bilateral subarachnoid hemorrhage, some\nof which demonstrate corresponding high signal on diffusion-weighted imaging. \nNo change in size of the trace subdural hematoma tracking along the right\nposterior convexity.\n\nStatus post right frontal ventriculostomy with the tip of the ventriculostomy\ncatheter terminating at the foramen of ___, unchanged.  Associated T2\nhyperintensity surrounding the catheter tract is compatible with\nedema/gliosis.  There is interval decreased size of the right lateral\nventricle.\n\nMild-to-moderate mucosal thickening of the maxillary sinuses (right greater\nthan left) likely represents sequela of intubation.\n\nMRA brain: There is narrowing of the bilateral supraclinoid ICAs as well as a\nbeaded appearance of the bilateral MCA M1 segments.  Nonvisualization of the\nbilateral ACA A1 segments likely relates to susceptibility artifact arising\nfrom the aneurysm coils.  There is a partial persistent fetal origin of the\nright PCA, better characterized on the recent CTA.  The intracranial vertebral\nandinternal carotidarteriesand their major branchesappear otherwise\nnormalwithout evidence of stenosis, occlusion, or aneurysm formation.",
            "output": "1. Scattered acute to subacute infarction involving the bilateral frontal\nlobes and corpus callosum.\n2. Narrowing of the bilateral supraclinoid ICAs as well as a beaded appearance\nof the bilateral MCA M1 segments is compatible with vasospasm.\n3. No significant change in scattered subarachnoid hemorrhage and\nintraventricular extension of blood products.\n4. No change in size of the trace subdural hematoma tracking along the right\nposterior convexity.\n5. Status post right frontal ventriculostomy with no change in position of the\ncatheter and slight interval decompression of the right lateral ventricle.\n\nNOTIFICATION:  The findings were discussed with NP ___ by ___\n___, M.D. on the telephone on ___ at 1:15 pm, 30 minutes after\ndiscovery of the findings."
        },
        {
            "input": "MR BRAIN:\nExternal ventricular drain in situ via a right frontal approach with the drain\npassing through the right ventricle with the tip present in the superior\naspect of the third ventricle.  The ventricular system is symmetrical. \nResidual blood products present surrounding the drain in the high right\nfrontal area with associated surrounding edema.\n\nSignal loss in the area of the previously coiled anterior communicating artery\naneurysm.  Due to susceptibility caused by the coils it is difficult to\ncomment on recanalization of the aneurysm.\nBlood products persists in the area of the coiled anterior communicating\nartery aneurysm measures 20 x 18 mm and in the anterior pericallosal cistern.\n5 mm subdural hemorrhage in the right occipital parietal area is unchanged. \nNo midline shift.\nSmall amount of blood products in the occipital horns of the lateral\nventricles bilateral.\nA couple of punctate foci of blood products over the cerebral hemispheres and\nadjacent to the falx.\n\nSubacute areas of slow diffusions/infarct in the centrum semiovale and\nanterior corpus callosum are again demonstrated.  The area of slow diffusion\nin the left centrum semiovale (series 4, image 24) is slightly increased in\nsize compared to prior.  This may represent interval increase in size of the\ninfarct or be technical in nature.  No new infarcts.\nMild opacification of the sphenoid sinuses bilateral.  Mild opacification of\nthe mastoid air cells.  No CP angle masses.  The orbits appear normal.\n\n\nMRA BRAIN:\nPlease note that there is technical limitations of the study secondary to\nsusceptibility artifact by the aneurysm coil, patient movement, inhomogeneous\nlocal magnetic field due to the presence of blood products as well as interval\nchange in head position compared to prior MRA.\n\nTaking all of these limitations into account there is decreased visualization\nof the supraclinoid ICAs with no flow seen on the MRA sequence in the distal\nICA/proximal MCAs bilateral (2 mm on the left and 4 mm on the right).  Beaded\nappearance of the M1 segments bilateral.  There is improved visualization of\nthe distal M2 and M3 segments bilateral (which appear similar compared to\nprior).\n\nPoor visualization of the A1 and A 2 segments which may be secondary to\ntechnical limitations as described above or be due to real\nnarrowing/vasospasm.\n\nNarrowing of the right PCA appear similar compared to prior.",
            "output": "1. Due to technical factors as described above this study is limited in\nevaluating the aneurysm and vasospasm in the area of the circle of ___. \nAlternative investigation should be considered to provide a more robust answer\nto the clinical question.\n2. Area of slow diffusion/infarct in the left semi centrum semiovale is\nslightly increased compared to prior, but this may represent real interval\nincrease in size or be artifactual in nature.  The rest of the infarcts are\nessentially unchanged.  No new infarcts.\n3. Poor visualization of the supraclinoid ICAs as well as bilateral M1\nsegments (worse compared to prior), again this most likely reflect artifact\nbut may also reflect to narrowing/spasm.\n4. The A1 and A2 segments are extremely poorly visualized, and thus difficult\nto comment on."
        },
        {
            "input": "There is a focus of restricted diffusion in the left thalamus (images 15 on\nseries 450 and 452) with associated T2 and FLAIR hyperintensity compatible\nwith a late acute to subacute infarction.  There is no evidence of hemorrhage,\nedema, mass, mass effect, or midline shift\nThe ventricles and sulci are normal in caliber and configuration.",
            "output": "Focus of restricted diffusion in the left thalamus with associated\nhyperintense signal on T2 and FLAIR sequences compatible with a late acute to\nsubacute infarction.\n\nNOTIFICATION:  The findings were discussed by Dr. ___ with Dr. ___ on\nthe telephone on ___ at 11:20 am, 5 minutes after discovery of the\nfindings."
        },
        {
            "input": "Study is mildly degraded by motion.\n\nMRA BRAIN:\nThe intracranial vertebral and internal carotid arteries and their major\nbranches appear grossly patent without evidence of stenosis, occlusion, or\naneurysm formation.  There is a patent left posterior communicating artery.\n\nT1 fat saturated sequences through the cervical vasculature are grossly\npreserved, without evidence of intramural hematoma to suggest focal\ndissection.\n\nMRA NECK:\nThe common,internal and external carotid arteries appear grossly patent. \nThere is no evidence of stenosis by NASCET criteria. The origins of the great\nvessels, subclavian, and vertebral arteries appear grossly patent bilaterally.\nThe vertebral basilar system is left-sided dominant, a normal variant.  The\ncommon carotid bifurcations appear normal.",
            "output": "1. Study is mildly degraded by motion.\n2. No evidence of bilateral carotid or vertebral artery high-grade stenosis,\nvessel occlusion, aneurysm, or dissection."
        },
        {
            "input": "There are multiple areas of slow diffusion involving the right frontal and\nparietal lobes cortical and subcortical structures with associated T2/FLAIR\nhyperintensity, in the distribution of the right ACA and MCA territories\n(___).  There is no evidence of hemorrhage, masses, mass effect, or\nmidline shift.  The ventricles and sulci are normal in caliber and\nconfiguration for age. There are prominent vessels in the right parietal\nsubarachnoid space, best seen on the gradient echoes, images 17 through 20. \nThis likely represents dilated arterial collaterals.\n\nThe FLAIR images also demonstrate hyperintensity in the left frontal and\nparietal lobes, best seen on images 13 through 21.  There is no associated\ndiffusion abnormality in these locations.  Although the normal diffusion in\nthese areas argues against infarction, the predominant cortical pattern on\nFLAIR suggests ischemia.\n\nThere are no osseous abnormalities.  The orbits are unremarkable.  The\nvisualized paranasal sinuses, mastoid air cells, and middle ear cavities are\nclear.",
            "output": "Multiple areas of slow diffusion in the right frontal and parietal lobes\ninvolving both the right ACA and MCA territories, consistent with acute\ninfarcts and suggestive of an embolic etiology.  No evidence of hemorrhage.\nAbnormalities on FLAIR in the left frontal and parietal lobes also suggest\nischemia.\nProminent vessels in the subarachnoid space on the gradient echo images may\nrepresent dilated collaterals.\n\n\nNOTIFICATION:  The findings were discussed with ___, M.D. by ___\n___, M.D. on the telephone on ___ at 8:38 am, 5\nminutes after discovery of the findings."
        },
        {
            "input": "There is persistent irregular T1 hypointensity, with surrounding T2 and FLAIR\nhyperintensity involving the right anterior and superior frontal lobe as well\nas the right posterior and superior parietal lobe, which may reflect sequelae\nof remote infarcts and parenchymal scarring.  There is cortical gyriform T1\nhyperintensity involving the right posterior and superior parietal lobe,\nassociated with restricted diffusion along the course of the right posterior\ncentral gyrus which is suggestive for acute infarction.  There is mildly\nincreased irregular susceptibility artifact and increased arterial collaterals\nwithin the right parietal lobe, which may be related to remote infarction. \nThere is mild irregular bilateral periventricular T2 and FLAIR hyperintensity\nsuggestive for chronic microangiopathic changes.  There is no significant mass\neffect or midline shift.  There is no appreciable contrast enhancement.  The\norbits are unremarkable.  There is mild peripheral T2 mucosal thickening\ninvolving the right lateral frontal sinus.  The paranasal sinuses and mastoid\nair cells otherwise appear clear.  The osseous structures demonstrate no acute\nfindings.\n\nBoth trigeminal nerves are well visualized on the MP rage images and\ndemonstrate no abnormal enhancement.  Both cavernous sinuses are symmetric. \nThe infratemporal regions are partially visualized and appear symmetric.",
            "output": "1. Restricted diffusion along the course of the right posterior central gyrus\nsuggestive for acute infarction.  There is gyriform T1 hyperintensity within\nthe right parietal lobe which may reflect subacute/chronic infarction.  Small\nresidual arterial collaterals are re-identified within the right parietal\nlobe, likely related to previous infarction\n2. Remote infarct within the right anterior frontal lobe.\n3. There is no evidence of acute intracranial hemorrhage.\n4. No abnormal enhancement or mass lesion seen in relation with the central\nand skull base portions of both trigeminal nerves.\n\nNOTIFICATION:  These findings were discussed with Dr. ___ on ___\nat 12:28 ___"
        },
        {
            "input": "Findings again seen is an enhancing left frontal mass with surrounding edema.\nThe extent of enhancement and the size of the enhancing mass appear unchanged\nsince the prior studies. However, the severity of edema has increased. Mild\nperiventricular white matter hyperintensities other than the edema surrounding\nthe lesion appears unchanged. No new lesions are identified. There is\nhemorrhage at the lesion site. There is no other evidence of hemorrhage. .",
            "output": "Increasing edema surrounding and otherwise unchanged left frontal enhancing\nmass compatible with the  history of glioblastoma."
        },
        {
            "input": "MRI HEAD: Postsurgical changes at the left frontoparietal convexity with blood\nproducts are again noted. A ring-enhancing lesion in the deep white matter of\nthe posterior left frontal lobe is larger than on ___, now measuring\n19 x 17 x 25 mm, previously 14 x 15 x 21 mm. Additionally, there is a new\nnodular focus of enhancement anterior to the dominant lesion (900b:30, 9:67)\nwith slightly increased periventricular enhancement. The degree of surrounding\nedema has minimally increased in the left centrum semiovale (8:19) but is\notherwise similar. A focus of susceptibility within the lesion suggests\nhemorrhage, unchanged.\n\nThere is no evidence of acute infarction or interval hemorrhage. No\nhydrocephalus. Principal vascular flow voids are preserved. Small fluid in the\nmastoid air cells is similar.",
            "output": "Interval increase in size of enhancing left frontal mass with increased foci\nof adjacent enhancement, compatible with glioblastoma, with minimal increased\nsurrounding edema."
        },
        {
            "input": "MRI HEAD:  Prior left parietal craniotomy with left frontoparietal convexity\nresection bed is again noted. A 2.0 x 2.1 cm left posterior frontoparietal\nperipherally enhancing lesion, demonstrates decreased enhancement and\nperipheral nodularity when compared to prior exam but is similar in size.\nGradient echo susceptibility artifact within the lesion is again noted, likely\nrepresenting hemorrhagic products and prominent surrounding white matter edema\ninvolving the left frontal, parietal lobes extending into the left basal\nganglia are also unchanged in configuration and extent. No new enhancing\nlesions are noted. Superimposed scattered nonspecific too small to completely\ncharacterize punctate subcortical and periventricular T2/FLAIR white matter\nhyperintensities are noted, also stable, commonly seen in setting of small\nvessel ischemic disease.  At the periphery and inferior aspects of the\nenhancing lesion along the posterior horn of the left lateral ventricle it is\nnew diffusion-weighted hyperintensity, not seen on prior exam, likely\nrepresenting a posttreatment changes.\n\nThe major flow voids are preserved. The paranasal sinuses are clear. The\norbits are unremarkable. The mastoid air cells are clear.",
            "output": "1. Although there is no interval decrease in size of previously described\nenhancing left frontal lesion, there is significantly decreased degree of\nenhancement and peripheral nodularity.  Surrounding left hemispheric edema is\nsimilar in size and configuration from prior exam.\n\n2. There is new diffusion-weighted hyperintense signal along the periphery of\nthe enhancing lesion, likely representing posttreatment changes."
        },
        {
            "input": "The patient is status post left parietal craniotomy with resection of left\nfrontal lesion. Left periventricular heterogeneous focus measuring\napproximately 2.1 x 1.8 cm (08:21) has shown progressive interval collapse\nwith decrease of central fluid cavity since ___. There are coarse\nareas of intrinsic T1 hyperintensity (13:16) similar to prior. Thin marginal\nenhancement appears minimally more conspicuous likely secondary to progressive\ncollapse (20:79).\n\nWallerian degeneration is again seen tracking inferiorly into the left\ncerebral peduncle. Confluent signal abnormalities in the vicinity of the left\nfrontal lesion are not appreciably changed since the prior study. Blood\nproducts are also unchanged (15:17).\n\nSize and configuration of the ventricles and sulci are grossly stable. The\nbasal cisterns are patent. The paranasal sinuses are grossly clear. The major\nintracranial flow voids are preserved.",
            "output": "1. Progressive central collapse of the left frontal lesion with decrease in\nsize of central fluid component. Thin marginal enhancement is unchanged.\n2. White matter signal abnormality in the vicinity of the lesion is also\nunchanged."
        },
        {
            "input": "The patient is status post left parietal craniotomy and resection of a left\nfrontal parietal lesion. The degree and configuration of FLAIR hyperintense\nsignal overlying the left frontoparietal lobe extending to the left cerebral\npeduncle is unchanged from prior exam. Again noted is gradient echo\nsusceptibility within the FLAIR hyperintensity and peripheral intrinsic T1\nhyperintense signal along the resection bed consistent with blood product.\nThere is near-complete resolution of previously described peripheral nodular\nenhancement within the resection bed. No new regions of abnormal enhancement.\nSuperimposed scattered subcortical nonspecific FLAIR/ T2 white matter FLAIR\nhyperintensity is noted, unchanged from prior exam. Again noted is a focus of\nslow diffusion at the periphery in the inferior aspect of the resection bed\nextending to the posterior horn of the left lateral ventricle, stable from\nprior exam.\nAllowing for posttreatment changes, sulci, ventricles and cisterns are within\nexpected limits. The paranasal sinuses are essentially clear. The orbits are\nunremarkable. The fluid signal seen within bilateral mastoid air cells.",
            "output": "1. Near-complete resolution of previously described peripheral and nodular\nenhancement of a left frontal lesion.\n2. Unchanged diffusion-weighted hyperintense signal along the periphery of the\nleft frontal lobe lesion/resection bed."
        },
        {
            "input": "There is redemonstration of previously noted postsurgical changes related to\nthe patient's prior left parietal craniotomy, left frontal GBM resection and\nradiation therapy. There is redemonstration of a grossly stable left\nfronto-parietal periventricular T1 heterogeneous, enhancing mass with areas of\nblood products versus mineralization and a stable rim of restricted diffusion.\nIt again demonstrates a residual enhancing component abutting the left lateral\nventricle, that measures approximately 2.0 x 1.7 cm (series 8, image 21),\npreviously having measured approximately 2.1 x 1.8 cm.\n\nStable wallerian degeneration extending into the left cerebral peduncle is\nagain noted. There are no new enhancing lesions or new intracranial\nhemorrhage, or acute infarction. The ventricles and sulci are stable in size\nand configuration. Intracranial flow voids, orbits are, paranasal sinuses and\nmastoid air cells are preserved.",
            "output": "1. Grossly stable left frontal lesion with heterogeneous enhancement and\nrestricted diffusion.\n2. No new mass effect or new enhancement.\n3. Stable postsurgical changes related to prior left parietal craniotomy, left\nfrontal GBM resection and radiation therapy."
        },
        {
            "input": "There is redemonstration of postsurgical changes related to patient's prior\nleft parietal craniotomy and left frontal glioblastoma resection. There is\nstable heterogeneous left frontal parietal lesion containing regions of T1\nhyperintensity abutting the left ventral ventricle. There is stable restricted\ndiffusion and susceptibility artifact in this region. T2/FLAIR signal\nhyperintensity surrounding the resection cavity and marginal enhancement\naround the resection cavity appears unchanged. There are no new enhancing\nlesions identified.\n\nThe ventricles and sulci are stable in configuration. There is no evidence of\nacute hemorrhage, extra-axial fluid collection, or acute infarction. Foci of\nperiventricular and subcortical T2/FLAIR signal hyperintensity in the right\ncerebral hemisphere are unchanged.  Mild wallerian degeneration in the left\ncerebral peduncle is unchanged.  Major vascular flow voids are preserved. The\norbits are unremarkable. The paranasal sinuses and mastoid air cells are\nclear.",
            "output": "1. Postsurgical changes related to patient's prior left parietal craniotomy\nand left frontal lobe GBM resection.\n2. Stable heterogeneous lesion again noted in the left frontal lobe as\ndescribed above.\n3. No new regions of enhancement are identified."
        },
        {
            "input": "There postoperative changes of prior left-sided craniotomy with subjacent\nresection cavity, chronic underlying blood products, and postoperative dural\nenhancement.  There is a rounded focus of gradient signal hypointensity with\nintrinsic T1 signal hyperintensity within the left centrum semiovale which\nmeasures 1.7 cm transverse by 1.9 cm AP and is unchanged when compared to\nprior exam.  There is a punctate focus of enhancement along the left\nprecentral gyrus which appears unchanged.  Prominent T2/FLAIR signal\nhyperintensity surrounding the lesion, extending superiorly into the centrum\nsemiovale and superior aspects of the left frontal and parietal lobes which\nappears unchanged.  There is slightly increased slow diffusion in the\ncorresponding regions within the left centrum semiovale, particularly along\nthe temporal horn of the left lateral ventricle.  MRI spectroscopy may be\nuseful for further evaluation.\n\nThere is no evidence of acute intracranial hemorrhage.  The ventricles and\nbasal cisterns appear stable.\n\nThere are normal vascular flow voids.  There is no evidence of acute infarct\nbased on diffusion-weighted imaging.  There is moderate diffuse brain\nparenchymal volume loss.  There is additional confluent of subcortical\nperiventricular T2/FLAIR signal hyperintensity which may be related to chronic\nmicroangiopathy and/or treatment related change.\n\nThere are no additional areas of abnormal brain parenchymal or leptomeningeal\nenhancement.\n\nThe mastoid air cells, paranasal sinuses, and orbits are unremarkable.",
            "output": "1. Postoperative changes prior left-sided craniotomy with underlying blood\nproducts and heterogenous lesion centered within the left centrum semiovale\nwith chronic blood products and minimal enhancement.  There are areas of slow\ndiffusion which are slightly progressive when compared to prior exams,\nparticularly along the temporal horn of the left lateral ventricle, this area\nshould be closely evaluated on followup examination to exclude progression.\n2.  MRI spectroscopy may be useful for further evaluation.\n\nRECOMMENDATION:  MRI spectroscopy may be useful for further evaluation."
        },
        {
            "input": "Again seen are postsurgical changes related to prior resection of the left\nparietal lobe glioblastoma with stable postoperative dural enhancement along\nthe left cerebral convexity, with chronic hemorrhage in the resection cavity. \nThere is stable residual nodular enhancement in the resection cavity along the\nsuperior aspect of the body of left lateral ventricle as seen on image 17:56\nmeasuring approximately 1.6 x 2.1 cm with slow diffusion, unchanged compared\nto the prior study.  There is residual surrounding FLAIR signal abnormality in\nkeeping with posttreatment changes.  The previously seen slow diffusion\n\nThe previously seen 1.7 cm focus of chronic hemorrhage in the left centrum\nsemiovale is again.\n\nNo acute intracranial hemorrhage or infarct is seen.  The ventricles, cisterns\nand sulci are patent and prominent in keeping with volume loss.\n\nThere are confluent areas of FLAIR hyperintensity in the periventricular white\nmatter, nonspecific, likely secondary to small vessel ischemic changes.\n\nMild mucosal thickening in bilateral ethmoid air cells.  The remaining\nvisualized paranasal sinuses and mastoid air cells are clear.  The orbits are\nunremarkable.  Intracranial flow voids are maintained.  Visualized osseous\nstructures are unremarkable.",
            "output": "1. Stable postsurgical changes related to prior resection of the left parietal\nglioblastoma with stable residual nodular enhancement and slow diffusion as\ndescribed above. ."
        },
        {
            "input": "Prior left frontoparietal craniotomy and resection of a left parietal lobe GBM\nwith stable postoperative dural enhancement and thickening along the left\nhemispheric convexity and a chronic blood product is essentially unchanged\nfrom prior exam.  There is mild residual of nodular enhancement within the\nresection cavity along the superior aspect of the left lateral ventricle with\nassociated slow diffusion is unchanged.  Slow diffusion extending along the\nsubependymal surface to ventricular trigone on is less conspicuous when\ncompared to the prior exam.  Chronic hemorrhage in the left centrum semiovale\nis unchanged.  Posttreatment FLAIR white matter hyperintensity of the left\nfrontal parietal lobe is unchanged.\n\nThere is no evidence of acute intracranial hemorrhage or infarct.  No new\nenhancing lesions are identified.  Allowing for postoperative changes,\nventricles, cisterns and sulci are within expected limits given the degree of\nage related global cerebral volume loss.  There are superimposed\nperiventricular and subcortical white matter T2/FLAIR hyperintensities, which\ncommonly seen in setting of chronic microangiopathy in a patient of this age. \nThe major intracranial flow voids are preserved.  The dural venous sinuses are\npatent.  The paranasal sinuses are clear.  The orbits are unremarkable.  The\nmastoid air cells are clear.",
            "output": "1. Unchanged postsurgical findings from prior resection of a left parietal\nlobe GBM with stable mild nodular enhancement and restricted diffusion within\nthe resection bed.  No new enhancing lesions are identified."
        },
        {
            "input": "Postsurgical changes involve a left frontoparietal craniotomy and resection of\na left parietal lobe glioblastoma.  Pachymeningeal thickening and enhancement\nsubjacent to the craniotomy site is stable.  Chronic blood product along the\nleft hemispheric convexity is essentially unchanged.\n\nIntrinsically heterogeneous T1 hyperintensity within the resection cavity\nalong the superior aspect of the left lateral ventricle is associated with\nslow diffusion, unchanged. Slow diffusion extends inferiorly along the\nsubependymal surface to the level of the trigone, unchanged.  Focus of chronic\nhemorrhage in the left centrum semiovale is unchanged.  No evidence of new\nhemorrhage. No new enhancing focus is identified.  T2 and FLAIR hyperintensity\ninvolving the periventricular deep and subcortical white matter are grossly\nstable relative to most recent examination dated in ___ though\nappear to have progressed relative to examination dated one year ago.\n\nVentricles are stable in size and configuration. There is no shift of normally\nmidline structures. There is no effacement of basal cisterns. Intracranial\nflow voids are preserved.\n\nThe orbits are unremarkable.  Fluid signal within the right mastoid air cells\nis minimal.  Mucosal thickening and opacification of the sphenoid sinus\nappears to been present on prior study.  Remaining paranasal sinuses are\nclear.",
            "output": "Postsurgical changes involving resection of left parietal lobe glioblastoma\nare associated with unchanged slow diffusion within the resection bed. No new\nenhancing lesion is identified.  FLAIR hyperintensity involving the\nperiventricular deep and subcortical white matter are stable relative to most\nrecent examination dated ___ but appears progressed relative to\nexamination dated one year prior, potentially treatment effect, although tumor\nprogression cannot entirely be excluded. Attention on follow up is warranted."
        },
        {
            "input": "There have been no significant changes since the prior study.  Again seen is\nan area of hemorrhage at the tumor site.  There is no evidence of new\nhemorrhage.  Again seen is extensive white matter hyperintensity that may be a\ncombination of treatment effect and edema associated with the neoplasm. \nPortions of the tumor bed are hyperintense before contrast on the T1 weighted\nimages.  There is no evidence of abnormal enhancement.  No new lesions are\ndetected.\n\nThere is no evidence of infarction.   The ventricles and sulci are enlarged in\nan atrophic pattern, unchanged.",
            "output": "1. Stable appearance after therapy for or a left frontal glioblastoma.  No\nevidence of tumor progression."
        },
        {
            "input": "Prior left parietal craniotomy and left parietal lobe resection is\nre-identified.   Extensive T2 hyperintensity in the white matter in the left\ncerebral hemisphere is unchanged, likely a combination of treatment effect and\nedema associated with the neoplasm.  There is an unchanged 1.9 x 2.2 cm\n(series 12 and 16, image 17) heterogeneous intrinsically lesion along the\ninferior aspects of the resection margins would extending to the subependymal\nsurface of the left lateral ventricle, without definite evidence for\npostcontrast enhancement.  There is no new enhancement.  Gradient echo\nsusceptibility compatible with hemorrhage product within this lesion is\nre-identified.  Slow diffusion is again seen extending inferiorly along the\nsubependymal surface to the level of the trigone (7:15).  There is new\ndiffusion is signal abnormality extending anteriorly from the resection cavity\n(07:21).\n\nThe ventricles are stable in size and configuration.  There is no shift of\nnormally midline structures.  Intracranial flow voids are preserved.  The\ndural venous sinuses are patent.  Mucosal thickening of the right sphenoid\nsinus is again noted.",
            "output": "1. New diffusion signal abnormality extending anterior to the resection cavity\nwithout evidence of associated FLAIR signal abnormality or enhancement.  While\nthis is nonspecific, close attention on follow-up is recommended as this can\nbe an early sign of recurrence/progression.\n2. Otherwise, no other interval change in the appearance of the left parietal\nresection or new enhancing lesion.\n\nNOTIFICATION:  The impression above was entered by Dr. ___ on\n___ at 12:42 into the Department of Radiology critical communications\nsystem for direct communication to the referring provider.\n\nPer clinic notes, Dr. ___ is aware of the findings."
        },
        {
            "input": "When compared to most recent exam from in ___, there has been no\nsignificant change.  Heterogeneous mixed signal in the periventricular white\nmatter of the left frontoparietal region in the postoperative bed is\nunchanged.  There is some internal T1 hyperintensity with additional foci of\nenhancement at as periphery (16:19, 18, and 16).  These are all unchanged\ncompared to prior exam dating back to ___.  Foci of high signal on\ndiffusion anterior to the lesion (07:21) and slightly more inferior (07:19)\nare unchanged from most recent exam.  There is no new region of restricted\ndiffusion.  There is no change in extent or configuration of the surrounding\nFLAIR hyperintensity.  There is FLAIR signal hyperintensity in the left\nfrontoparietal white matter as well as involving the splenium of the corpus\ncallosum and less extensively the right frontoparietal white matter.  There is\nno new parenchymal signal abnormality.  There is no acute infarct.\n\nMild left sided pachymeningeal thickening particularly under the craniotomy\nsite has marginally decreased in degree.",
            "output": "No significant interval change since recent exam, no evidence of disease\nprogression.  Post treatment changes noted without new enhancement or abnormal\nsignal in diffusion."
        },
        {
            "input": "The patient is status post remote left parietal craniotomy and underlying\nresection with unchanged expected postoperative left convexity dural\nthickening and enhancement.  Left posterior frontal and parietal resection\ncavity extending to the posterior body of the left lateral ventricle\ndemonstrates mild increased enhancement along the peripheral margins,\nextending along the subependymal surface.  In particular, there is increased\nnodular enhancement along the left lateral aspect of the left ventricular\nependymal surface (series 19, image 57).  Unchanged surrounding geographic\nFLAIR white matter edema pattern.  A smaller confluent white matter FLAIR\nedema pattern of the right frontal centrum semiovale is compatible with\nposttreatment changes.\n\nNo new enhancing lesions are identified.  There is no acute infarct or\nintracranial hemorrhage.  The major intracranial flow voids are preserved. \nThe dural venous sinuses are patent on postcontrast MP rage.  The paranasal\nsinuses are essentially clear.  The orbits are unremarkable.  Mastoid air\ncells are clear.",
            "output": "1. Mild interval increased nodular enhancement along the margins of the\nresection bed, particularly along the left ventricular ependymal surface.\n2. The findings raise concern for disease progression.  Close attention on\nfollowup exam is recommended.  Alternatively, this could be further evaluated\nwith MRI spectroscopy and perfusion."
        },
        {
            "input": "There are stable postoperative changes from left frontoparietal craniotomy and\nmass resection.  There has been interval increase of heterogeneously rim\nenhancing material of the prior surgical bed, with main component measuring up\nto 46 x 23 mm, previously 33 x 20 mm (19:86).  There has been increase of\nsubependymal enhancement along the surface of the left lateral ventricle\nleading anteriorly and superiorly into the left frontal lobe, as well as\nposteriorly and inferiorly along the occipital horn, with increase of areas of\nleft periatrial enhancement measuring up to 17 x 10 mm, previously 9 x 4 mm\n(19:62).  Subependymal enhancement wraps posteriorly along the occipital horn\nof the left lateral ventricle, and there is an additional focus anterior to\nthe splenium of the corpus callosum measuring 13 x 10 mm (19:69).  Adjacent\nareas of white matter T2/FLAIR hyperintensity appear roughly similar to the\nprior examination, crossing midline along the splenium of the corpus callosum\ninto the right periatrial area.  There is additional increase in nodular\nenhancing components along the body of the corpus callosum.  Some areas of the\nmass continue to demonstrate areas of slowed diffusion and susceptibility\nartifact suggestive of hemorrhage\n\nThere is no evidence of new hemorrhage, midline shift or infarction.  There is\nprominence of the ventricles and sulci suggestive of involutional changes.. \nThe principal intracranial vascular flow voids are preserved.\n\nThe paranasal sinuses are grossly clear.  The orbits are grossly unremarkable.\n.",
            "output": "Interval disease progression with increased enhancement within the resection\nbed, with increased nodular subependymal spread along the left lateral\nventricle wrapping around the occipital horn of the left lateral ventricle,\nextending medially with increased nodular component along the body of the\ncorpus callosum along with a new 13 x 10 mm enhancing focus anterior to the\nsplenium of the corpus callosum, which is suspicious for disease progression. \nSurrounding white matter FLAIR hyperintensity is unchanged."
        },
        {
            "input": "The patient is status post remote left parietal craniotomy and underlying\nresection.  Mild dural thickening overlying the resection cavity is unchanged\nfrom prior exams.\n\nRe-identified is a nodular enhancement along the left posterior lateral\nventricular ependymal surface, similar in configuration to prior examination. \nEnhancement along the splenium of the corpus callosum, new on examination of ___ has intervally increased in size.  Scattered regions of the\nenhancement is associated with slow diffusion, also similar to prior\nexamination.  Associated geographic left frontal parietal and occipital lobe\nwhite matter edema pattern is also unchanged. No new regions of enhancement.\n\nThe dural venous sinuses are patent of postcontrast MP-RAGE.",
            "output": "1. Re-identified is nodular enhancement along the left lateral ventricular\nependymal surface, similar in configuration to examination of ___,\ndemonstrating scattered regions of associated restricted diffusion.\n2. Enhancement along the splenium of the corpus callosum has increased in\nprominence, compatible with given history of disease progression.\n3. No new enhancing lesions."
        },
        {
            "input": "Re-identified is a nodular enhancement along the left lateral ventricle\nependymal surface, with extension along the splenium and body of the corpus\ncallosum, similar in configuration to prior exam, however demonstrating\nincreased nodular thickening along the superior margins of the corpus callosum\nand along the atrium of the left lateral ventricle.  There is associated new\nregion of diffusion-weighted hyperintense signal along the superior margins of\nthe corpus callosum as well as increased prominence of peripheral gradient\necho cystic affect along the enhancement, potentially secondary to radiation\ntreatment.  Right frontal and parietal hemispheric white matter FLAIR\nhyperintensity is unchanged from prior exam.  There is wallerian degeneration\ninvolving the left cerebral peduncle.\n\nThere is no acute infarct.  No new enhancing lesion is identified.  The major\nintracranial flow voids are preserved.  The orbits are unremarkable.  There is\nmild mucosal thickening of the ethmoid air cells and opacification of the\nposterior aspect of the right sphenoid sinus otherwise the remainder the\nparanasal sinuses are essentially clear.  Trace fluid signal is noted in the\nbilateral mastoid tips.  Fluid is noted in the nasopharynx.",
            "output": "1. Nodular enhancement along the left lateral ventricle with extension along\nthe splenium and body of the corpus callosum is similar in configuration to\nprior exam, however with increasing nodular thickening and enhancement along\nthe superior margins of the corpus callosum and along the atrium of the left\nlateral ventricle.  While these findings may represent posttreatment changes,\nclose interval followup is recommended to exclude progression.\n2. There is increased associated diffusion-weighted hyperintense signal at the\nsuperior aspect of the corpus callosum as well as gradient echo\nsusceptibility, which may represent posttreatment changes.\n3. No new enhancement is identified.  Additional findings as described above."
        },
        {
            "input": "In comparison to prior MRI of ___, T2/FLAIR hyperintense signal\nin the left cerebral hemisphere has increased.  The heterogeneous left\nperiventricular lesion extending to the corpus callosum appears larger on T2\nweighted images and there is increased FLAIR signal hyperintensity in the\ncorpus callosum, particularly the anterior body and rostrum, which is new\ncompared to the prior examination.  A large component of the mass demonstrates\nslow diffusion measuring approximately 4.8 x 3.6 cm as compared to 1.1 x 1.3\ncm previously (602:24).  The tumor continues to demonstrate rim enhancement\nhowever the intensity and thickness of enhancement appears to have decreased. \nThis may be in part due to the technique and severe motion degradation on the\npostcontrast MP RAGE sequences and possible necrosis and recent Avastin\ntreatment.  Additional periventricular and subcortical white matter FLAIR\nhyperintensities in the contralateral hemisphere are unchanged.\n\nA focus of susceptibility in the left frontoparietal periventricular white\nmatter is unchanged and corresponds to calcifications in this region on CT. \nThere is no evidence of interval hemorrhage.  There is no acute vascular\nterritorial infarction.  FLAIR hyperintense signal and decreased size of the\nleft cerebral peduncle is unchanged and consistent with wallerian\ndegeneration.  Prominence of ventricles and sulci reflecting global atrophy is\nunchanged.  The ventricles are grossly stable.  There is no midline shift.\n\nPrincipal intracranial vascular flow voids are preserved.  The dural venous\nsinuses are patent on postcontrast MP-RAGE allowing for motion artifact.  The\norbits are unremarkable.",
            "output": "1.  Increased size of heterogeneous left periventricular mass with increased\ninvolvement of the corpus callosum and increased edema in the left cerebral\nhemisphere and a much larger component demonstrating slow diffusion is\nconcerning for tumor progression.\n\n2.  Apparent decreased enhancement may be in part due to suboptimal motion\ndegraded images or increased intratumoral necrosis as well as recent Avastin\ntreatment.\n\n3.  No evidence of interval hemorrhage or acute vascular territorial\ninfarction.\n\n4.  No additional findings to suggest superimposed meningoencephalitis on\nimaging."
        },
        {
            "input": "Study is degraded by motion.\n\nThere is a focus of diffusion signal abnormality without definite T2/FLAIR\ncorrelate involving the left frontal cortex, likely representing an\nacute/subacute infarct.  No evidence of hemorrhage, mass or midline shift. \nChronic infarcts involving the bilateral basal ganglia are noted.\n\n There is prominence of the ventricles and sulci suggestive of involutional\nchanges.  The ventricles and sulci are enlarged, consistent with age-related\ninvolutional changes.  Bilateral lens replacements are noted.",
            "output": "1. Foci of acute/subacute infarct of the left frontal cortex without\nhemorrhagic transformation or mass effect.\n2. Global brain atrophy and chronic ischemic vessel disease."
        },
        {
            "input": "Again seen is a homogeneously enhancing extra-axial mass in the midline along\nthe planum sphenoidale, consistent with a meningioma.  It measures 8 mm\ntransverse, 10 mm AP, 5 mm craniocaudad, unchanged compared to ___\nand ___.  Mild adjacent hyperostosis is again noted.  There is no\nedema in the adjacent brain parenchyma.  Evaluation for blood products or\ncalcifications on gradient echo images is limited by extensive blooming\nartifact from the adjacent paranasal sinuses.\n\nNo new intracranial mass is seen.  There is no acute diffusion abnormality. \nNumerous small foci of high T2 signal are again seen in the subcortical, deep,\nand periventricular white matter of the cerebral hemispheres, nonspecific but\nlikely sequela of chronic small vessel ischemic disease in this age group. \nVentricles, sulci, and basal cisterns are normal in size.  Major arterial flow\nvoids are grossly preserved.  Major dural venous sinuses appear patent on\npostcontrast MP RAGE images.\n\nThere is a small mucous retention cyst in the left maxillary sinus, unchanged.\n\nDegenerative changes are again seen in the included upper cervical spine on\nsagittal images.",
            "output": "Small planum sphenoidale meningioma appears stable compared to ___ and\n___."
        },
        {
            "input": "MR BRAIN:\nRe- demonstrated is a midline homogeneously enhancing extra-axial mass along\nthe planum sphenoidale, measuring 10 x 8 x 5 mm (1000b:46, 10:85), unchanged\nsince ___, and compatible with meningioma.  Again noted is minimal\nadjacent hyperostosis.  No definite hemorrhage is identified.  In addition,\nmore conspicuous on the current examination than on priors, though likely\npresent on prior examinations as well, is another, right frontal,\nhomogeneously enhancing apparently extra-axial lesion measuring 6 x 4 x 4 mm\n(1000b:81, 10:119).  This may represent a second meningioma.  A vessel courses\nadjacent to this.\n\nAside from a tiny mucous retention cyst in the left maxillary sinus, the\nparanasal sinuses middle ear cavities, and mastoid air cells are clear.  The\nventricles and sulci are normal in caliber.  Scattered subcortical and\nperiventricular T2/FLAIR white matter hyperintensities are noted, nonspecific,\nbut commonly seen in the setting of of chronic small vessel ischemic disease. \nThe major dural venous sinuses appear patent.\n\nMRA brain:\nThe intracranial vertebral and internal carotid arteries and their major\nbranches appear normal without evidence of stenosis, occlusion, or aneurysm\nformation.",
            "output": "1. Stable planum sphenoidale meningioma in comparison to examination from\n___.\n2. Possible tiny right frontal meningioma.  Attention on follow-up\nexaminations is recommended."
        },
        {
            "input": "MRV: Normal flow signal is demonstrated within the superior sagittal sinus,\nstraight sinus, transverse sinuses, and sigmoid sinuses. The jugular bulbs and\nproximal jugular veins are patent. Evaluation of the deep venous systems\nreveals normal flow signal in the internal cerebral veins. The vein ___\nis also unremarkable.",
            "output": "1. No evidence for sinus venous thrombosis."
        },
        {
            "input": "A 4 x 6 x 6 mm focus of enhancement in the right frontal lobe (101:884,\n100:68), with perhaps a small linear focus of increased T1 signal but without\ndiffusion abnormality, is concerning for metastatic disease. No other focus of\nenhancement is identified. There is no evidence of hemorrhage, edema, mass\neffect, or infarction. The ventricles and sulci are normal in caliber and\nconfiguration for the patient's age. Periventricular and deep white matter\nT2/FLAIR hyperintensities likely represent sequela of chronic small vessel\nischemic disease. The major intracranial flow voids are preserved. Visualized\nparanasal sinuses and mastoid air cells are clear. There is opacification of\nscattered anterior ethmoid air cells.",
            "output": "1. 4 x 6 x 6 focus of enhancement in the right frontal lobe, concerning for\nmetastatic disease.\n2. Age-related involutional change and sequela of chronic small vessel\nischemic disease.\n3. Opacification of scattered anterior ethmoid air cells."
        },
        {
            "input": "There is a new 7 mm enhancing lesion with mild surrounding edema seen in the\nleft posterior temporal occipital region best visualized on series 11, image\n11.  The previously seen right frontal lobe lesion measuring 7 mm has\nminimally decreased in size. A punctate focus of enhancement in the right\nparietal lobe series 11, image 18 does not have any corresponding FLAIR\nabnormality and could be secondary to a vascular structure. However, this area\ncan be evaluated on followup studies. No other areas of abnormal enhancement\nseen. No leptomeningeal enhancement identified. There is no mass effect\nmidline shift or hydrocephalus. There are no other products.  Small vessel\ndisease seen.",
            "output": "New no 7 mm lesion is identified in the left temporal occipital region.\nPreviously noted right frontal lobe lesion appears slightly smaller in size.\n\nNOTIFICATION:  Critical communication dashboard."
        },
        {
            "input": "There is significant motion artifact on the postcontrast 3D MPRAGE sequence.\n\nThere is a 6 mm a partially peripherally enhancing lesion within the left\ninferior parietal lobule which is decreased in size and degree of enhancement\nas compared to prior when it measured 7 mm (11:13).\n\nThere is a 4 mm enhancing lesion at the right lateral precentral gyrus (11:16)\nwhich previously measured 3 mm.  There is increased surrounding FLAIR\nhyperintense signal (series 9, image 16) not seen on the prior exam.\n\nThe following nodules are new comparison prior study:\nThere is a 3 mm enhancing lesion at the mid left superior frontal gyrus\n(11:21).  There is a 7 mm enhancing lesion at the posterior left frontal\noperculum (11: 13).  There is a 4 mm enhancing nodule within the lateral left\nparietal post central gyrus (11:16).\n\nThere is associated adjacent mild FLAIR signal hyperintensity marginating\nthese sites of disease.\n\nThere are superimposed periventricular, subcortical, and pontine FLAIR signal\nhyperintense foci likely representing chronic microangiopathy.  There is no\nacute infarct or hemorrhage.  The ventricular size extra-axial spaces are\nunremarkable.  The vasculature is unremarkable.  The orbits, calvarium, and\nsoft tissues are unremarkable.  The paranasal sinuses and mastoid air cells\nare clear.",
            "output": "1. Significant motion artifact on the postcontrast 3D MPRAGE sequence which\nlimits detection of small metastases.\n2. 3 new enhancing lesions within the left frontal and left parietal lobes, as\ndescribed.  Mild increased size of a right frontal enhancing lesion.  Interval\ndecrease size of a left parietal enhancing nodule.  Overall findings are\nconsistent with disease progression.\n\nNOTIFICATION:  Results discussed by Dr. ___ with Dr. ___ at 13:00 on ___."
        },
        {
            "input": "There is mild increase in the size and surrounding edema in the right frontal\nlesion series 7, image 17 series 10, image 17.  The lesion now measures 8 mm,\ncompared to the prior of 5 mm.\nA tiny lesion is noted anterosuperiorly in the right frontal lobe series 10,\nimage 17 more conspicuous compared to the prior study.\nLeft frontal lesion series 10, image 16 is stable to minimally decreased.\nThe left parietal lesion is less conspicuous.\nAssessment on the MPRAGE sequences somewhat limited due to motion and\npulsation artifacts.\n\nMultiple nonspecific scattered FLAIR hyperintense foci are noted in the\ncerebral white matter as before.\nMildly prominent ventricles and sulci related to mild diffuse parenchymal\nvolume loss.\n\nPartially empty sella.\nThe major intracranial arterial flow voids are noted.\n\nMinimal ethmoidal mucosal thickening.\nThe mastoid air cells are clear.\nIncluded orbits are clear.",
            "output": "Mild increase in the size and surrounding edema in the right frontal lesion-\ncan relate to treatment related changes or tumor progression.\nOther details as above.  Further workup and followup as need"
        },
        {
            "input": "There is no evidence intracranial enhancing mass, nor pathologic\nleptomeningeal or pachymeningeal contrast enhancement.  No evidence for acute\ninfarction, edema, or intracranial blood products.  Moderately numerous small\nT2/FLAIR hyperintense foci in the subcortical, deep, and periventricular white\nmatter of the cerebral hemispheres are nonspecific but likely sequela of\nchronic small vessel ischemic disease in this age group.\n\nMajor arterial flow voids of the circle of ___ appear grossly preserved.  A\nprominent flow void in the anterior interhemispheric fissure on image 10:13\ncorresponds to tortuous A2 segments of bilateral anterior cerebral arteries on\npostcontrast MP RAGE images.  Dural venous sinuses appear patent on\npostcontrast MP RAGE images.",
            "output": "No evidence for intracranial metastatic disease or acute intracranial\nabnormalities."
        },
        {
            "input": "There is no evidence of infarction, enhancing mass, edema, or blood products. \nVentricles, sulci, and basal cisterns are normal in size.  Major arterial flow\nvoids are grossly preserved.  The dural venous sinuses are patent.\n\nThere is a small amount of fluid in the left sphenoid sinus.  There is mild\nmucosal thickening of the bilateral anterior ethmoidal air cells extending\ninto the right frontoethmoidal recess and into the inferior right frontal\nsinus.",
            "output": "1. No evidence for an acute infarction, other acute intracranial\nabnormalities, or intracranial mass.\n2. Small amount of fluid in the left sphenoid sinus.  Mucosal thickening in\nthe anterior ethmoid air cells with occlusion of the right frontoethmoidal\nrecess.  Please correlate with any associated symptoms."
        },
        {
            "input": "MRI Brain:\nThere is a acute infarction in the left side of the pons.  This is best seen\non the diffusion images, images 10 through 13 of series 4.  There is an old\nleft cerebellar hemispheric infarction.  There is no evidence of hemorrhage. \nThe periventricular white matter demonstrates numerous areas of white matter\nhyperintensity on FLAIR, suggesting chronic small vessel ischemia.\n\nThere is loss of flow signal in the intracranial right vertebral artery on the\nT2 weighted images.  This is worrisome for occlusion or slow flow in this\nvessel.\n\nMRA brain:  The intracranial portion of the right vertebral artery is not seen\non the MRA.  The distal cervical right vertebral artery is identified.  The\nremainder of the intracranial vertebral and internal carotid arteries and\ntheir major branches appear normal without evidence of stenosis, occlusion, or\naneurysm formation.\n\nMRA neck:  The common, internal and external carotid arteries are patent. \nNote that the noncontrast technique does not provide visualization of the\norigins of the great vessels.  There are atheromatous narrowings of the\ninternal carotid artery's bilaterally near their origins.  Due to the low\nresolution of the noncontrast technique, measurement is difficult to perform\nwith reliability.  However, there appears to be an approximately 75% stenosis\nof the right internal carotid artery by NASCET criteria.  On the left, the\ninternal carotid artery is mildly narrowed by plaque at the origin but without\nevidence of stenosis by NASCET criteria.  More reliable characterization of\nthe internal carotid artery origins would be obtained with contrast-enhanced\nMRA, CTA, or ultrasound.",
            "output": "1. Left pontine acute infarction without evidence of hemorrhage.\n2. Nonvisualization of the intracranial portion of the right vertebral artery\nsuggests severe stenosis or occlusion.\n3. Limited evaluation of the neck due to the absence of intravenous contrast. \nThere are atheromatous changes at the origins of the internal carotid arteries\nbilaterally.  Suboptimal imaging on the right suggests a 75% stenosis."
        },
        {
            "input": "There is no evidence of infarction, hemorrhage, edema, mass, or mass effect. \nNo abnormal enhancement.  There is an 8 mm pineal region cystic lesion without\nsuspicious features, likely a pineal cyst (1000:81, 10:79).\n\nThe ventricles and sulci are normal in caliber and configuration.\n\nThe visualized paranasal sinuses and mastoids appear clear.  The globes and\norbits are unremarkable.  Major intracranial vascular flow voids are\npreserved.  Major dural venous sinuses are patent.",
            "output": "1. No acute intracranial abnormality.\n2. Probable 0.8 cm pineal cyst.  No suspicious features."
        },
        {
            "input": "There is a a prominent syrinx within the upper cervical spinal cord which is\nunchanged when compared to prior exam.  The cerebellar tonsils lie\napproximately 1.1 cm below foramen magnum and demonstrate \"peg-like\"\nconfiguration, the findings of which are compatible with Chiari I\nmalformation.\n\nThe ventricles are stable in size.  There is no evidence of infarction,\nhemorrhage or mass effect.\n\nThere are normal vascular flow voids.  The brain parenchymal volume is within\nnormal limits.  There is minimal subcortical and periventricular T2/FLAIR\nsignal hyperintensity, a nonspecific finding though presumably on the basis of\nsequelae of chronic small vessel ischemic disease.\n\nThe mastoid air cells, orbits, and paranasal sinuses are unremarkable.",
            "output": "1. Chiari I malformation with upper cervical spinal cord syrinx, as described\nabove.\n2. Unable to obtain CSF flow imaging secondary to technical difficulty.\n3. No hemorrhage, mass effect, or acute infarct.\n4. Probable sequelae of chronic microangiopathy.\n\nRECOMMENDATION(S):  Recommend the patient return for CSF flow imaging only at\nno additional charge."
        },
        {
            "input": "Examination is performed as pre-surgical evaluation for Chiari 1 malformation.\nThere is cerebellar tonsillar herniation and syringohydromyelia identified in\nthe upper cervical spinal cord as before.  There is no hydrocephalus.  No\nenhancing brain lesions are seen.",
            "output": "Cerebellar tonsillar ectopia and upper cervical spinal cord syringomyelia are\nseen.  Examination performed for surgical planning."
        },
        {
            "input": "The patient is status post Chiari 1 decompression with suboccipital\ncraniectomy, C1 laminectomy and superior C2 partial laminectomy.  The downward\ndisplacement and configuration of these cerebellar tonsils are similar in\nappearance to prior exam.  Expected pneumocephalus and hemorrhage products\nwithin the surgical bed is identified.  There is slow diffusion of the\nbilateral cerebellar tonsils with associated FLAIR hyperintense signal (series\n6, image ___, likely representing postsurgical change.  There are stable\nsuperimposed very few nonspecific subcortical T2/FLAIR white matter\nhyperintensities.  The sulci, ventricles and cisterns are unchanged from prior\nexam.  The major intracranial flow voids are preserved.  The dural venous\nsinuses are patent.  Unchanged appearance of C2 through C4 syringohydromyelia.\nThe paranasal sinuses are clear.  The orbits are unremarkable.  The mastoid\nair cells are clear.",
            "output": "1. The patient is status post Chiari 1 decompression with suboccipital\ncraniectomy, C1 laminectomy and superior C2 partial laminectomy and expected\npostoperative changes.\n2. There is a slow diffusion of the bilateral cerebellar tonsils, most\ncompatible with postsurgical change.  Clinical correlation and correlation\nwith operative findings is recommended.\n3. Unchanged appearance of upper cervical syringohydromyelia.\n\nNOTIFICATION:  The findings were discussed by Dr. ___ with Dr. ___\n___ on the telephone on ___ at 2:13 ___, at the time of discovery\nof the findings."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, or infarction.\nThe ventricles and sulci are normal in caliber and configuration. There is no\nabnormal enhancement after contrast administration.  Mild changes of small\nvessel disease seen.\n\nThe images through the trigeminal nerve demonstrates no evidence of mass or\nabnormal enhancement.  With Meckel's caves are symmetric in appearance.\nEvaluation of the skullbase demonstrate no abnormal enhancement. There is a\nvascular structure adjacent to the  left trigeminal nerve without displacement\nnoted as an incidental finding.",
            "output": "Classes of small vessel disease.  No abnormal enhancement.  No evidence of\nmass lesion or abnormal enhancement in relation to the trigeminal nerves."
        },
        {
            "input": "There is extensive susceptibility artifact arising from the oral cavity\nconsistent with braces.  This causes geometric distortion and signal loss\nwhich most severely affects the gradient, FLAIR, and diffusion images, on\nwhich portions of the intracranial compartment are obscured.  It also causes\nprominent artifact on the remaining sequences.\n\nWithin the technical limitations of the examination, there is no evidence of\nhemorrhage, edema, masses, mass effect, midline shift or infarction.   The\nventricles and sulci are normal in caliber and configuration.\n\nThe visualized major intracranial vascular flow voids are preserved.  The\nvisualized soft tissues are unremarkable.  The orbits and maxillofacial region\nare mostly obscured by susceptibility artifact.",
            "output": "1. Within the confines of extensive susceptibility artifact from braces, no\nsignificant intracranial abnormality is demonstrated."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor acute infarction.  A focal FLAIR hyperintensity in the right thalamus\nlikely reflects a subacute to chronic infarct, given low level increased\nsignal on diffusion-weighted image, which appears normalized to mildly\nhyperintense on ADC map (6:15).  Periventricular and subcortical T2 and FLAIR\nhyperintensities are noted which may represent small vessel ischemic changes. \nThere is no abnormal enhancement after contrast administration.\n\nThere is asymmetric prominence of the right lateral ventricle, which may be\nseen as an anatomic variant.  Although the right temporal horn is larger\nrelative to the left the size of the hippocampal formations are similar and\nthere does not appear to be disproportionate mesial temporal volume loss with\nMTA score of 1.\n\nThere is minimal anterior ethmoid air cell mucosal thickening.  Mastoid air\ncells are clear.  Orbits are unremarkable.",
            "output": "1. No acute infarct, mass, or hemorrhage.\n2. Subacute to chronic right thalamic lacunar infarct.\n3. White matter changes, most likely related to chronic small vessel disease.\n4. Moderate parenchymal volume loss.  Although there is asymmetric prominence\nof the right lateral ventricle in general relative to the left (which can be\nseen as an anatomic variant), there is no evidence for disproportionate mesial\ntemporal volume loss, with mesial temporal atrophy score of 1."
        },
        {
            "input": "Abnormality of the distal V3 segment left vertebral artery is better seen on\noutside CTA exam ___.\nOtherwise, the common, internal and external carotid arteries appear normal. \nThere is no evidence of stenosis by NASCET criteria. The origins of the great\nvessels and subclavian arteries appear normal bilaterally.  There is a left\ndominant vertebral artery with the right vertebral artery being tiny.  The\nvisualized cervical vertebral arteries are otherwise unremarkable.  The common\ncarotid bifurcations appear normal.\nThere is no evidence of hematoma about vessels or within vessel wall.",
            "output": "Abnormality at the left V3 segment vertebral artery is better seen on the MRA\nhead.\nOtherwise no abnormality."
        },
        {
            "input": "MR BRAIN:\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is mild mucosal thickening of the paranasal sinuses. \nClear mastoid air cells.  Benign Thornwaldt cyst posterior nasopharynx.  There\nis no evidence of intramural hematoma on fat-suppressed images.\n\nMRA brain:\nThere is a dissection of the left vertebral artery V3 segment with slight\nextension into the intracranial V4 segment.  This correlates with that seen on\nthe recent CTA head and neck.  There is ectasia of the V3 segment of the level\nof dissection, measuring 6.0 mm, stable since prior, vessel proximal to the\ndissection measures 4.0 mm.  Patent left ___.\nThere is artifact through the level of the para clinoid, supraclinoid ICAs,\nthere may be mild narrowing on the left.\nOtherwise could the visualized right vertebral arteryandinternal carotid\narteries and their major branches appear normal without evidence of stenosis,\nocclusion, or aneurysm formation.",
            "output": "1. Abnormality of the left vertebral artery V3 segment with slight extension\ninto the intracranial V4 segment.  Vertebral artery dissection is more likely\nthan fenestration.  No evidence of intramural thrombus ectasia of the involved\nvessel measuring 6.0 mm, stable.  No perivascular or intramural hematoma.\n2. No evidence of acute intracranial hemorrhage or infarction.\n\nNOTIFICATION:   The findings were discussed with ___ , M.D. by ___\n___, M.D. on the telephone on ___ at 2:24 am, 2 minutes after\ndiscovery of the findings."
        },
        {
            "input": "There is no evidence of acute intracranial hemorrhage. The ventricles stable\nin size.\n\nThere is diffuse pachymeningeal enhancement with there is severe\nirregular/nodular thickening in the left frontal regions and right middle\ncranial fossa, the appearance of which is most compatible with intracranial\nmetastatic disease as opposed to subdural hematoma.\n\nThere are normal vascular flow voids. There is no evidence of acute infarct\nbased on diffusion-weighted imaging. There is mild diffuse brain parenchymal\nvolume loss. There are confluent and punctate foci of T2/FLAIR signal\nhyperintensity within the subcortical and periventricular white matter, a\nnonspecific finding though presumably on the basis of sequelae of chronic\nsmall vessel ischemic disease.\n\nThere is scattered paranasal sinus mucosal thickening. There is fluid in the\nbilateral mastoid air cells. The orbits are unremarkable. There is\nheterogenous bone marrow signal with areas of enhancement, most prominently\nwithin the calvarium, most prominently within the bilateral frontal regions,\nwhich could represent a osseous metastatic disease.\n\nThere are severe degenerative changes of the left temporomandibular joint.",
            "output": "1. Diffuse pachymeningeal enhancement/thickening with more irregular, nodular\nareas of dural thickening along the left frontal and right middle cranial\nfossa regions, the appearance of which is most compatible with intracranial\nmetastatic disease as opposed to subdural hematoma.\n2. Heterogenous bone marrow signal with areas of enhancement, most prominently\nwithin the frontal calvaria, concerning for osseous metastatic disease.\n3. No evidence of acute infarct.\n4. Brain parenchymal volume loss and presumed sequelae of chronic small vessel\nischemic disease.\n\nNOTIFICATION:  The findings were discussed by Dr. ___ with Dr. ___ by\ntelephone on ___ at 2:15 ___."
        },
        {
            "input": "Multiple ring enhancing lesions consistent with history of metastatic disease\nare again noted in the right frontal and parietal lobes. These have not\nsignificantly changed compared to prior study. No new enhancing lesions are\nseen. There is mild local mass effect associated with these lesions without\nsignificant shift of midline. The ventricles are normal in size and\nconfiguration. The orbits are unremarkable. The visualized paranasal sinuses\nand mastoid air cells are clear.",
            "output": "Post-contrast MRI performed for surgical mapping.  No significant interval\nchange in multiple enhancing lesions in the right frontal and parietal lobe. \nNo new enhancing lesions are identified.\n\n."
        },
        {
            "input": "There are postoperative changes of a prior right parietal craniotomy with\nsubjacent resection cavity, underlying chronic blood products, and dural\nenhancement.  There is intrinsic T1 hyperintensity within the more posterior\nof the 2 right cerebral hemisphere lesions, within the right parietal lobe,\ncompatible with interval resection. The right parietal lesion demonstrates\nnodular enhancement at its anterior margin (series 1200b image 96). The\nparasagittal right frontoparietal lesion is increased in size when compared to\nprior exams, demonstrates increased surrounding vasogenic edema and increased\nT2/FLAIR signal hyperintensity, and local mass effect on adjacent sulci. This\nlesion now measures 4.2 cm AP x2.6 cm transverse, previously 2.5 cm AP x 1.2\ncm transverse.  Perfusion imaging demonstrates increased perfusion around the\nmargins of the frontal parietal parasagittal mass, corresponding with the\nareas of enhancement. There is no evidence of increased perfusion within the\nright parietal resection cavity. Multivoxel spectroscopic evaluation\ndemonstrates increase choline NAA ratio within the medial portion of\nenhancement (voxel 4 and 9), the configuration of which is concerning for\nmalignancy. Several other areas demonstrate necrosis the more within the\ncentral nonenhancing portion of the mass, as evidenced by elevated lipid\nlactate peaks.  There is additional T2/FLAIR signal hyperintensity within the\nleft frontoparietal region which appears similar when compared to prior exam.\n\nThere is no evidence of acute hemorrhage or mass effect. The ventricles are\nnormal in size.\n\nThere are normal vascular flow voids.  There is no evidence of acute infarct\nbased on diffusion-weighted imaging.\n\nThe orbits, skull base, and paranasal sinuses are unremarkable.",
            "output": "1. Postoperative change of right parietal craniotomy with subjacent resection\ncavity and chronic underlying postoperative change.\n2. Nodular enhancement at the anterior margin of the resection cavity\ndemonstrates no clearly increased perfusion abnormality although continued\nfollowup is recommended.\n3. Increased size of right frontoparietal parasagittal lesion with peripheral\nenhancement, associated increased perfusion, and increased vasogenic\nedema/signal abnormality with spectroscopic findings suggesting\nresidual/recurrent tumor and necrosis, as described above."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, or infarction.\nThe ventricles and sulci are slightly prominent for the patient's age,\nsuggestive of mild cortical volume loss, however, this finding is nonspecific.\nThere is minimal nonspecific T2/FLAIR signal hyperintensity in the\nperiventricular white matter.  There is no abnormal enhancement after contrast\nadministration.  Major vascular flow voids are preserved.  The orbits are\nunremarkable.  There is mild mucosal thickening within the ethmoid air cells\nand bilateral maxillary sinuses.  There is a small amount of fluid in the\nright mastoid air cells.",
            "output": "No evidence of acute infarction, hemorrhage, or enhancing mass lesion. \nSlightly prominent ventricles and sulci for the patient's age, this finding is\nnonspecific, however suggest mild cortical volume loss."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is punctate loss of signal on gradient images in the\ncentral pons, similar to ___, may represent small capillary telangiectasia,\nthere was subtle faint enhancement on prior scan.  No associated edema on\ntoday's exam.  Intracranial vascular flow voids are preserved.  Trace mucosal\nthickening of the paranasal sinuses.  Clear mastoids, middle ear cavities.\n\nNo evidence of amyloid angiopathy or macro hemorrhage on gradient images. \nThere are mild chronic small vessel ischemic changes, without confluence,\ngrade 1 on a ___ scale.  There are no chronic lacunar or large vessel infarct.\nThere are moderately prominent perivascular cular spaces at the level of basal\nganglia greater than cerebral hemispheres.  There is grade 2 bilateral\nhippocampal atrophy, on a ___ scale..  There is diffuse moderate cortical\natrophy, most prominent at the parietal lobes, were there is grade 3 parietal\nlobe atrophy, on a ___ scale, mildly worsened since ___.  There is moderate\nfrontal and anterior temporal lobe atrophy.",
            "output": "Advanced brain parenchymal atrophy, more prominent since ___.\nMild chronic small vessel ischemic changes."
        },
        {
            "input": "Please note that metallic/air artifact obscures evaluation of the inferior\nbilateral frontal lobes.  Please correlate clinically.  Furthermore, there is\nmoderate motion degradation.  In the context of these limitations, there is no\nevidence of hemorrhage, edema, masses, mass effect, midline shift or\ninfarction.  Mild prominence of the ventricles and sulci may be secondary to\nalcohol related disease.  Additionally, atrophy of the superior cerebellum may\nalso be sequelae of alcohol use.  There is no abnormal enhancement after\ncontrast administration.\n\nModerate mucosal sinus thickening is seen involving the ethmoid air cells. \nThe visualized paranasal sinuses, mastoid air cells, and middle ear cavities\nare clear.  The globes are unremarkable.  The principal vascular flow voids\nappear to be well preserved.",
            "output": "1. Limited study secondary to metallic/air artifact obscuring evaluation of\nthe inferior bilateral frontal lobes and moderate motion degradation.\n2. No acute intracranial abnormalities identified.  No concerning enhancement\nafter contrast administration.\n3. Moderate mucosal sinus thickening is seen involving the ethmoid air cells.\n4. Global atrophy and superior cerebellar atrophy, may be sequelae of alcohol\ndisease."
        },
        {
            "input": "MRI Brain:\nLeft frontal subdural 9 mm thick extra-axial CSF intensity collection is\nunchanged in size from prior exam, likely representing a hygroma or chronic\nhematoma.  Otherwise, there is no intra or extra-axial mass, acute hemorrhage\nor infarct.  Sulci, ventricles cisterns are within expected limits for the\npatient's age related global cerebral volume loss.  The major intracranial\nflow voids are preserved.  Mucous retention cysts are noted in the right\nmaxillary sinus and there is mild mucosal thickening of the ethmoid air cells,\nfrontal and left sided sphenoid sinuses.  The orbits are unremarkable.  The\nmastoid air cells are clear.\n\nMRA brain: The intracranial vertebral and internal carotid arteries and their\nmajor branches appear normal without evidence of stenosis, occlusion, or\naneurysm formation.\n\nMRA neck:  There is a normal 3 vessel arch.  There is mild narrowing of the\nright carotid bifurcation without stenosis of the proximal right cervical\ninternal carotid artery by NASCET criteria.  There is no stenosis of the\nproximal left cervical internal carotid artery by NASCET criteria.  The common\nand external carotid arteries appear normal.  There is no evidence of internal\ncarotid artery stenosis by NASCET criteria.  The origins of the great vessels,\nsubclavian and vertebral arteries appear normal bilaterally.",
            "output": "1. No acute intracranial hemorrhage or infarct.  No mass effect.\n2. No T1 hyperintense signal abnormality of the basal ganglia, specifically\nthe globus pallidi to suggest imaging findings of hepatic encephalopathy.\n3. Essentially unremarkable MRA of the neck and head."
        },
        {
            "input": "MRI Brain:\nLeft frontal subdural 9 mm thick extra-axial CSF intensity collection is\nunchanged in size from prior exam, likely representing a hygroma or chronic\nhematoma.  Otherwise, there is no intra or extra-axial mass, acute hemorrhage\nor infarct.  Sulci, ventricles cisterns are within expected limits for the\npatient's age related global cerebral volume loss.  The major intracranial\nflow voids are preserved.  Mucous retention cysts are noted in the right\nmaxillary sinus and there is mild mucosal thickening of the ethmoid air cells,\nfrontal and left sided sphenoid sinuses.  The orbits are unremarkable.  The\nmastoid air cells are clear.\n\nMRA brain: The intracranial vertebral and internal carotid arteries and their\nmajor branches appear normal without evidence of stenosis, occlusion, or\naneurysm formation.\n\nMRA neck:  There is a normal 3 vessel arch.  There is mild narrowing of the\nright carotid bifurcation without stenosis of the proximal right cervical\ninternal carotid artery by NASCET criteria.  There is no stenosis of the\nproximal left cervical internal carotid artery by NASCET criteria.  The common\nand external carotid arteries appear normal.  There is no evidence of internal\ncarotid artery stenosis by NASCET criteria.  The origins of the great vessels,\nsubclavian and vertebral arteries appear normal bilaterally.",
            "output": "1. No acute intracranial hemorrhage or infarct.  No mass effect.\n\n2. No T1 hyperintense signal abnormality of the basal ganglia, specifically\nthe globus pallidi to suggest imaging findings of hepatic encephalopathy.\n\n3. Essentially unremarkable MRA of the neck and head."
        },
        {
            "input": "Within the right external capsule/posterior putamen, there is a 5 mm T2 and\nFLAIR hyperintense, T1 hypointense focus with bright DWI signal but without\nADC signal abnormality, which may reflect subacute/late subacute lacunar\ninfarct.\n\nAgain seen is a CSF signal extra-axial collection along the left frontal\nconvexity measuring up to 10 mm in diameter, with associated 8 mm\nleft-to-right midline shift.  In addition, there is a CSF density extra-axial\ncollection along the right anterior falx extending to the right frontal vertex\nmeasuring up to 8 mm.  These collections appear similar in comparison to\nprevious studies when measured similarly.  Findings may reflect subdural\nhygromas versus chronic subdural hematomas.\n\nIn addition, there is prominence of the ventricles and sulci compatible with\nglobal parenchymal atrophy.\n\nThere is no evidence of acute intracranial hemorrhage, edema or mass. \nPeriventricular and subcortical T2 and FLAIR hyperintensities are noted which\nare nonspecific but compatible with small vessel ischemic changes.  Small\nchronic infarct in the lateral right cerebellum.  There is no abnormal\nenhancement after contrast administration.\n\nThere is near complete opacification of the left sphenoid sinus air cell with\nperipheral enhancement.  A mucosal retention cyst is noted within the inferior\naspect of the right maxillary sinus.  There is trace nonspecific fluid within\nthe bilateral mastoid air cells.  Question mild right proptosis.  Otherwise,\nthe orbits and globes appear within normal limits.",
            "output": "1. There is a 5 mm subacute versus late subacute infarct within the right\nexternal capsule/posterior putamen.\n2. Small chronic infarct in the right cerebellum, new from ___.\n3. CSF density extra-axial collections along the left frontal convexity and\nalong the right anterior falx/right frontal vertex measure up to 10 mm and 8\nmm, respectively, not significantly changed in comparison to prior studies\nwhen measured similarly with approximately 8 mm left to right midline shift,\nalso unchanged.  Findings may reflect subdural hygromas versus chronic\nsubdural hematomas.\n4. Chronic left sphenoid sinusitis.\n5. Question mild right proptosis."
        },
        {
            "input": "The patient is status post mechanical thrombectomy for large vessel occlusion,\nstroke of the basilar artery on ___.\n\nAcute/subacute ischemic changes are visualized in the left side of the pons,\nwith a large area of slow diffusivity measuring approximately 12 x 12 mm in\ntransverse dimension (series 402, image 12), there is no evidence of\nhemorrhagic transformation.  Additional areas of slow diffusion are visualized\nin the cerebellum posterior to the cerebellar nodule on the left (series 402,\nimage 7), focus of magnetic susceptibility is identified in the left\ncerebellar hemisphere.\n\nThere is no evidence of narrowing of the cerebellar pontine and\nperimesencephalic cisterns.  The vascular flow void for the basilar artery is\nslightly heterogeneous, however grossly patent, if there is persistent concern\nfor reocclusion, correlation with MRA of the head is recommended.\n\nSupratentorially the ventricles and sulci are prominent suggesting cortical\nvolume loss, subcortical and periventricular areas of T2/FLAIR high-signal\nintensity are nonspecific and may reflect changes due to small vessel disease.\nNo diffusion abnormalities are detected supratentorially.  There is no\nevidence of acute intracranial hemorrhage.\n\nThe major vascular flow voids for the internal carotid arteries, anterior\ncerebral arteries, and middle cerebral arteries demonstrate normal\ndistribution.  The orbits are unremarkable, the paranasal sinuses demonstrate\nmild mucosal thickening in the ethmoidal air cells, the mastoid air cells\ndemonstrate mild mucosal thickening at the tip of the right mastoid air cells,\nthe middle ear cavities are clear.",
            "output": "1.  The patient is status post mechanical thrombectomy for large vessel\nocclusion, stroke of the basilar artery on  ___.\n\n2.  Acute/subacute ischemic changes are seen in the left side of the pons with\na 12 x 12 mm area of slow diffusion, with no evidence of hemorrhagic\ntransformation.\n\n3.  Additional foci of slow diffusion are visualized in the cerebellum\nposterior to the cerebellar nodule as described above.\n\n4.  Focus of magnetic susceptibility is noted in the left cerebellar\nhemisphere.\n\n5.  Supratentorially subcortical and periventricular areas of T2/FLAIR\nhigh-signal intensity are nonspecific and may reflect changes due to small\nvessel disease."
        },
        {
            "input": "MRA brain: Susceptibility artifact extending along the right A2 through left\nA1 segment as well as along the inferior aspect of the anterior communicating\nartery is compatible with stent mediated coil embolization of previously\ndescribed anterior communicating artery aneurysm.\n\nThere is a punctate focus of T1 hyperintense signal at the base of the\naneurysm coil pack (series 2, image 131), likely representing residual\nthrombus although trace flow is not entirely excluded.  A 2 mm medially\noriented outpouching along the genu of the left internal carotid artery is not\nwell visualized on current examination.  Otherwise, no evidence of new\naneurysm.  The right A1 segment is hypoplastic and unchanged in appearance\nfrom prior examination.  Bilateral fetal type origins of the posterior\ncerebral arteries is again noted.  There is apparent high-grade termination of\nthe diminutive right vertebral artery.  The remainder of the intracranial\ncirculation is unremarkable without high-grade stenosis, occlusion.\n\nIncidental note is made of a subependymal vein along the head of the caudate,\nsimilar appearance to prior CTA.",
            "output": "1. The patient is status post stent mediated coil embolization of an anterior\ncommunicating artery aneurysm with stent extending from the right A2 through\nleft A1 segment.\n2. Punctate T1 hyperintense signal at the base of the aneurysm coil pack\nlikely represents residual thrombus versus trace residual flow.  There is no\nevidence for recanalization.\n3. Additional anatomic findings as described above.  No new aneurysm."
        },
        {
            "input": "There are few scattered areas of nonspecific bifrontal subcortical, left\nparieto-occipital subcortical and left periatrial white matter T2/FLAIR\nhyperintensities (images 17 through 20, series 7 and series 8).  There is\nsuggestion of a few prominent perivascular spaces in the left periatrial white\nmatter.  There is no evidence of hemorrhage, edema, masses, mass effect,\nmidline shift or infarction.   The ventricles and sulci are normal in caliber\nand configuration.  There is no abnormal enhancement after contrast\nadministration.  There is no abnormal focus of slowed diffusion. The principal\nintracranial vascular flow voids are preserved.  The dural venous sinuses are\npatent on MP-rage images.  The cerebellar tonsils are normally positioned.\n\nThe visualized paranasal sinuses are grossly clear.  The orbits are grossly\nunremarkable.  The mastoid air cells are clear.",
            "output": "1. Scattered areas of nonspecific white matter T2/FLAIR signal abnormality, as\ndescribed.  Differential considerations include sequela of prior trauma or\ninfection, history of migraine headaches, inflammatory or demyelinating\nprocess.\n2. No hemorrhage, infarct, or enhancing mass."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  Rounded dilated third and lateral ventricles with relative\nsparing of the fourth ventricle, mild periventricular FLAIR hyperintensity\nwhich may represent slow transependymal flow (11:16), ___ index ratio\ngreater than 0.3 (ratio of 0.41, 11:15), a callosal angle less than 90 degrees\n(79 degrees, 100:100), relatively thin  corpus callosum (33:97), and relative\ndisproportionate enlargement of the sylvian fissures (100:89, 11:12).\n\nFew periventricular T2/FLAIR hyperintensities however are nonspecific and may\nrepresent sequelae of chronic microangiopathic changes.  However of note, is\nrelative lack of subcortical or deep white matter FLAIR hyperintensities\ntypically seen in conjunction with chronic microangiopathic changes.\n\nThere is no abnormal enhancement after contrast administration.\n\n The major intracranial flow voids are preserved. The dural venous sinuses are\npatent on post-contrast MPRAGE sequences.\n\nThere are small mucous retention cysts in the bilateral maxillary sinuses, as\nseen on prior CT.  Otherwise, the remaining imaged paranasal sinuses, middle\near cavities and mastoid air cells are clear. The orbits do not demonstrate\nany acute abnormalities bilaterally.",
            "output": "1.  Constellation of findings may be representative of normal pressure\nhydrocephalus in the appropriate clinical setting, as described above. \nHowever, not definitive and may represent age-related cerebral volume loss..\n\n2.  There is no evidence of acute intracranial process or hemorrhage.  No\ndiffusion abnormalities are detected."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.\n\nThe visualized paranasal sinuses are normal.  The mastoid air cells are clear.\nThe intraorbital contents are normal.",
            "output": "1. Normal brain MRI."
        },
        {
            "input": "There are multiple areas of restricted diffusion in the right temporal lobe,\nright thalamus, right basal ganglia, right parietal lobe, right postcentral\ngyrus, and posterior limb of the right internal capsule extending into the\ncorona radiata.  These areas of restricted diffusion are associated with\nT2/FLAIR hyperintense signal.  There is susceptibility within the right\ncaudate and putamen on 11:15 and 11:14.\n\nThere is no evidence of masses, mass effect, midline shift or extra-axial\nfluid collection.   The ventricles and sulci are normal in caliber and\nconfiguration.\n\nThere is mild mucosal thickening in the bilateral ethmoid, right maxillary,\nand left sphenoid sinuses.  A few mastoid air cells bilaterally are opacified.\nThe orbits are unremarkable.\n\nThe major intracranial flow voids are preserved.",
            "output": "Acute infarction in the right parietotemporal lobes, thalamus, posterior limb\nof the internal capsule, and corona radiata with hemorrhagic conversion in the\nright basal ganglia.\n\nNOTIFICATION:  The findings were discussed by Dr. ___ with Dr. ___ on\nthe ___ ___ at 9:22 AM, 10 minutes after discovery of the\nfindings."
        },
        {
            "input": "Study is moderately degraded by motion.\n\nQuestion punctate left postcentral gyrus parietal lobe restricted diffusion\nversus artifact, with no definite associated increase susceptibility (see 6,\n07:19; 12, 13, 14:18).\n\nThere is no evidence of hemorrhage, edema, masses, mass effect or midline\nshift.  There is mild prominence of the ventricles and sulci suggestive\ninvolutional changes.  Extensive periventricular and subcortical T2 and FLAIR\nhyperintensities are noted, which may represent small vessel ischemic changes.\nA partially empty sella is noted.",
            "output": "1. Study is moderately degraded by motion.\n2. Mild global volume loss and extensive probable microangiopathic changes, as\ndescribed.\n3. Question punctate left parietal lobe postcentral gyrus acute infarct versus\nartifact, with no definite evidence of hemorrhagic transformation.\n\nNOTIFICATION:  The impression and recommendation above was entered by Dr.\n___ on ___ at 10:22 into the Department of Radiology critical\ncommunications system for direct communication to the referring provider."
        },
        {
            "input": "The study is mildly degraded by motion artifact.\n\nThere is a large heterogenous T1 hypointense, T2 hyperintense mass with mild\nassociated microhemorrhage demonstrating irregular enhancement involving the\nposterior right temporal, right parietal as well as right occipital lobes. It\nmeasures approximately 76 x 26 mm in the axial plane.  It extends across the\nsplenium of the corpus callosum to the left. This lesion effaces/infiltrate\nthe trigone, occipital and proximal temporal horns of the right lateral\nventricle with ependymal enhancement suggesting involvement of the ventricular\nsystem.  There is a second more solid enhancing component immediately\nposterosuperior to the dominant lesion in the right occipital parietal area\nconnected by the T2 hyperintense signal changes.\nThere is no evidence of infarction.  The pituitary appears normal.  The\ncraniocervical junction appears normal.  The orbits appear normal.  The\nparanasal sinuses are clear.  The intracranial arteries demonstrate normal T2\nflow voids.",
            "output": "Findings suggestive of a multifocal right temporoparietaloccipital\nglioblastoma with extension across the splenium of the corpus callosum to the\nleft as described above."
        },
        {
            "input": "Fiducial markers are in place.  The patient's known multifocal right\ntemporoparietal occipital mass with extension across the splenium of the\ncorpus callosum to the left is again noted with no significant changes in this\nshort interval.  For a full description please refer to prior MR report dated\n___.",
            "output": "1. No interval change compared to prior imaging dated ___.\n2. Findings is most consistent with a multifocal glioblastoma, with extension\nacross the splenium of the corpus callosum."
        },
        {
            "input": "MRI Brain:\nThere is slow diffusion within the inferior mid right cerebellar hemisphere\nwith correlate FLAIR hyperintensity consistent with late acute infarct. \nPunctate subtle diffusion-weighted hyperintense signal of the right mid\ncerebellar peduncle (series 402, image 10) may represent a superimposed older\ninfarct.  There is faint slow diffusion within the right of midline midbrain\nwithout definite FLAIR hyperintensity, also likely representing late acute to\nsubacute infarct.  Trace gradient echo susceptibility of the right posterior\nmedial temporal lobe, likely representing prior MR micro hemorrhage.\n\nThere is background periventricular and subcortical white matter FLAIR\nhyperintensity which is confluent periventricular white matter, likely\nrepresenting sequela of chronic microangiopathy.  There is mild prominence of\nthe ventricles and cortical sulci, all consistent with volume loss.  The\nextra-axial spaces are unremarkable.  The flow voids are preserved.\n\nThe native lenses are absent, otherwise the orbits are unremarkable.  The soft\ntissues and calvarium are unremarkable.  There are bilateral mastoid air cell\neffusions.  There is no fluid signal within the paranasal sinuses.\n\nMRA head:  There is motion artifact which is severe at the skullbase, which\ndegrades spatial resolution.  Evaluation of the cervical and proximal internal\ncarotid arteries, proximal basilar arteries and intracranial vertebral\narteries is nondiagnostic due to the severity of motion artifact in the\ninferior portion of the sequence.  These portions are evaluated on the\ntime-of-flight neck MRA.\n\nThe anterior and right posterior communicating arteries are visualized.  There\nis mild short-segment stenosis versus flow artifact at the anterior right\ncavernous segment internal carotid artery.  Otherwise the visualized\nintracranial arteries are patent without occlusion, dissection, or aneurysm.\n\nMRA neck:\nThere is a 3 vessel aortic arch.  The right carotid artery is patent with 25%\nstenosis at the carotid bulb by NASCET criteria.  The left carotid artery is\npatent without significant stenosis by NASCET criteria.  Evaluation of the\nproximal vertebral arteries and their origins is limited due to time-of-flight\ntechnique, however the flow voids appear patent on the axial T1 fat sat spin\necho sequence.  The vertebral arteries are patent and demonstrate codominance.\nThere is no evidence of dissection, occlusion, or aneurysm.",
            "output": "1. Late acute infarct involving the mid inferior right cerebellar hemisphere\nand likely subacute infarct of the right cerebellar peduncle.  Additional late\nacute to subacute infarct involving the right midline midbrain.  No evidence\nof associated acute hemorrhage.\n2. Background sequela of advanced chronic microangiopathy.\n3. Bilateral mastoid air cell effusions.\n4. Motion artifact on the head MRA, degrading spatial resolution.  Within this\nlimitation, the intracranial arterial vasculature is patent, without\nocclusion, does or aneurysm.\n5. Short segment mild stenosis versus flow artifact at the anterior right\ncavernous segment internal carotid artery.\n6. Limited evaluation of the aortic arch and great vessel origins due to\ntime-of-flight technique.  Within this limitation, the neck vasculature is\npatent without occlusion, dissection, or aneurysm.\n7. 25% stenosis of the right carotid bulb by NASCET criteria.  No significant\nstenosis at the left carotid bulb."
        },
        {
            "input": "There is an area of slow diffusion in the right corona radiata (402/400:20)\nextending to the centrum semiovale.  There is no significant mass effect.  No\nadditional foci of infarction are identified.\n\nCorresponding T2 and FLAIR hyperintense signal may be present although\nextensive periventricular, subcortical, and deep white matter T2 and FLAIR\nhyperintense signal are present symmetrically and bilaterally.  Additional\nT2/FLAIR hyperintense signal is seen in the midbrain and pons.\n\nNumerous scattered foci of susceptibility on gradient echo sequences with\nperipheral and central foci seen in the bilateral cerebral hemispheres,\ncerebellum, pons, and midbrain, consistent with microhemorrhages.  The most\nprominent hemorrhagic focus is in the left caudate head measuring\napproximately 9 x 6 mm (08:13).  Focus of susceptibility in the left occipital\nlobe follows the contour of a gyrus, suggesting hemosiderin staining due to\nprior hemorrhage (08:16).\n\nThere is prominence of the ventricles and sulci for a age suggestive\ninvolutional changes.  There is no midline shift.  Mucosal thickening is\npresent in the bilateral maxillary sinuses.  Remaining visualized paranasal\nsinuses are clear.  The orbits are unremarkable.",
            "output": "1. Acute/subacute infarct in the right corona radiata extending to the centrum\novale.  No significant mass effect.\n2. Numerous scattered foci of microhemorrhage throughout the brain. \nPeripheral foci are suggestive of underlying amyloidosis and\ncentral/cerebellar foci suggest hypertensive pathology.  Both etiologies may\nbe present.\n3. Brain atrophy prominent for age.\n\nNOTIFICATION:  The findings were discussed with ___, M.D. by\n___, M.D. on the telephone on ___ at 4:40 ___, 2 minutes after\ndiscovery of the findings."
        },
        {
            "input": "Diffusion-weighted hyperintense signal of the left precentral gyrus (series\n302, image 25), left middle frontal gyrus (series 302, image 23) and left\nfrontal operculum (series 302, image 22) with subtle associated FLAIR\nhyperintensity is compatible with late acute infarcts.\n\nConfluent periventricular and subcortical T2/FLAIR white matter\nhyperintensities as well as hyperintensities of the deep gray matter, pons and\ncerebellum are nonspecific, but compatible with chronic microangiopathy in a\npatient of this age, unchanged from prior examination.  Scattered lacunar\ninfarcts are also identified, also unchanged.  The sulci, ventricles cisterns\nare prominent, but unchanged from prior exam.\n\nInnumerable peripheral punctate foci of gradient echo susceptibility artifact,\nwhich also involves the brainstem and bilateral cerebellar hemispheres likely\nrepresents amyloid angiopathy with potential component of hypertension,\nunchanged from prior examination.  Left parietal occipital lobe superficial\nsiderosis is unchanged.\n\nThe major intracranial flow voids are preserved.  The orbits are unremarkable.\nMild mucosal thickening of the ethmoid air cells and left greater than right\nmaxillary sinuses is identified.  Fluid signal is noted in the left mastoid\ntip.",
            "output": "1. Late acute infarct of the left precentral gyrus, left middle frontal gyrus\nand left frontal operculum.\n2. Unchanged findings suggestive of amyloid angiopathy and possible\nhypertensive micro hemorrhages.\n3. Additional findings as described above.\n\nNOTIFICATION:  The findings were discussed with Dr. ___. by ___\n___, M.D. on the telephone on ___ at 4:58 pm, 5 minutes after discovery\nof the findings."
        },
        {
            "input": "MRI BRAIN:\nImages are mildly motion degraded.  No evidence of acute intracranial\nhemorrhage, infarction, edema, mass, or mass effect.  Mild prominence of the\nventricles and sulci is in keeping with global involutional changes.  Minimal\nbilateral periventricular white matter T2/FLAIR signal hyperintense foci are\nnon-specific however compatible with minimal sequelae of chronic white matter\nmicroangiopathy.  Globes are intact.  Patent major dural venous sinuses.  ___\ncisterna magna is noted, a normal anatomic variant.\n\nMRA BRAIN:\nImages are mildly motion degraded. There is mild-to-moderate focal likely\natherosclerotic luminal narrowing of the distal M1 segment MCA near the\nproximal M2 segment (101:1). The distal visible M2 and M3 left MCA segments\nappear patent.  Otherwise, within limitation, the intracranial vertebral and\ninternal carotid arteries and their major branches appear normal without\nevidence of high-grade stenosis, occlusion, or aneurysm formation.  Fetal-type\nleft PCA is noted, a normal vascular anatomic variant.  Dominant left\nvertebral artery is noted.\n\nMRA NECK:\nThe common, internal and external carotid arteries appear normal.  There is no\nevidence of internal carotid artery stenosis by NASCET criteria.  The origins\nof the great vessels, subclavian and vertebral arteries appear normal\nbilaterally with dominance of the left vertebral artery.",
            "output": "1. MRA images of the brain are slightly motion degraded, somewhat limiting\nassessment.  Within limitation, there is likely mild to moderate\natherosclerotic luminal narrowing of the distal M1 MCA segment near the\nproximal M2 segment.  Remaining distal left MCA branches are patent. \nRemaining intracranial vertebral and internal carotid arteries and major\nbranches are unremarkable.\n2. Unremarkable MRA neck.\n3. No acute intracranial abnormality."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor recent infarction.  Periventricular and FLAIR signal hyperintensities are\nnonspecific, unchanged since the prior MR examination and likely sequela of\nchronic small vessel ischemic disease.  Mild prominence of the ventricles and\nsulci suggest involutional changes.\n\nLeft lens replacement is noted.",
            "output": "No acute intracranial abnormality."
        },
        {
            "input": "A right-sided vestibular schwannoma measuring 13 mm in its maximum length\nextending both within the canal and the cerebellopontine angle is again\nidentified.  The mass demonstrates intrinsic low signal.  The left internal\nauditory canal is patent without abnormal enhancement.  No other posterior\nfossa or supratentorial mass lesions are identified.  No acute infarcts are\nseen on diffusion images.",
            "output": "Right-sided vestibular schwannoma unchanged from prior study.  Examination\nperformed for the planning of radio surgery."
        },
        {
            "input": "Again seen is a well-circumscribed, lobulated enhancing mass lesion in the\nright internal auditory canal, which partially extends into the right\ncerebellopontine angle, most consistent with a vestibular schwannoma.  There\nis unchanged expansion of the right IAC.  The vestibular schwannoma measures\napproximately 1.0 x 1.4 x 0.8 cm (AP X TR X SI) which is similar to the most\nrecent prior exam from ___.\n\nImages through the left internal auditory canal demonstrate symmetric\nappearance of the seventh eighth nerve complexes.  There is no evidence of\nabnormal enhancement or mass lesion within the left internal auditory canal,\nleft cerebellopontine angle or membranous labyrinth.\n\nNo other mass lesions are seen within the posterior fossa.\n\nLimited included imaging of the remainder of the brain demonstrates no\nevidence of acute hemorrhage,edema, masses, mass effect, midline shift or\ninfarction.\nNo diffusion abnormalities are detected.  Again seen are extensive confluent\nwhite matter changes in the cerebral hemispheres bilaterally, consistent with\nsevere chronic small vessel ischemic changes.\n\nUnchanged mild generalized parenchymal volume loss, most likely age related. \nStable prominence of the ventricular system and extra-axial CSF spaces is\nconsistent with the previously mentioned parenchymal volume loss. \nXanthogranulomas appear unchanged in the bilateral occipital ventricular horns\n(series 450, image 14).\n\nThe major vascular flow voids are present and demonstrate normal distribution.\nThe orbits are unremarkable.",
            "output": "1. No significant change in size of the right internal auditory canal\nvestibular schwannoma.\n2. Unchanged severe chronic small vessel ischemic changes."
        },
        {
            "input": "Heterogeneously enhancing, internal low signal residual mass in the right\ncerebellopontine angle extending into the right internal auditory canal\nmeasures 1.4 cm TV x 1 cm AP x 0.8 cm SI (image 51 of series 7), unchanged\ndating back to ___ (image 38 of series 9).  Right IAC is\nexpanded.  No evidence of a vestibular, cochlear extension.  No mass effect on\nthe brainstem.\n\nLeft internal auditory canal demonstrates normal MRI appearance of the seventh\nand eighth cranial nerve complexes.  No evidence of abnormal enhancement or\nmass lesion within the left internal auditory canal or left cerebellopontine\nangle. No other mass lesions are seen within the posterior fossa.",
            "output": "Unchanged right vestibular schwannoma measuring 1.4 cm."
        },
        {
            "input": "There is redemonstration of a 1.0 x 1.2 x 1.5 cm enhancing lesion in the right\ncerebellopontine angle with extension to the internal auditory canal grossly\nunchanged from previous study in ___ consistent with known vestibular\nschwannoma (series 9, image 38; series 901, image 97).  The left internal\nauditory canal is unremarkable.  There is no evidence of hemorrhage, edema,\nmass effect, midline shift or infarction.   There are moderate confluent\nprominence of the ventricles and sulci suggestive of involutional changes. \nPeriventricular and subcortical white matter T2/FLAIR hyperintensities are\nnonspecific but likely sequelae of severe chronic small vessel ischemic\ndisease.\n\nVascular flow voids are maintained.",
            "output": "1. Stable right cerebellopontine angle vestibular schwannoma.\n2. Severe changes of small vessel disease in the white matter and moderate\nbrain atrophy.\n3. No acute infarcts."
        },
        {
            "input": "Please note that the intracranial vertebral arteries, including the ___\n___, are excluded from the field-of-view.  ___ termination of the non\ndominant right vertebral artery was demonstrated on the ___ MRI.  The\nvisualized ___ branches, basilar artery, right AICA, bilateral superior\ncerebellar arteries, bilateral posterior cerebral arteries, and the major\nanterior circulation arteries appear patent without evidence for flow-limiting\nstenosis.  There is 6 mm asymmetric fusiform dilatation of the supraclinoid\nleft internal carotid artery.  There is no saccular aneurysm.  In addition to\nthe ___ termination of the non dominant right vertebral artery, other normal\nvariants include hypoplastic right A1 segment of the anterior cerebral artery\nand fetal origin of the right posterior cerebral artery.",
            "output": "6 mm fusiform dilatation of the supraclinoid left internal carotid artery.  No\nsaccular aneurysm.  No follow-up needed."
        },
        {
            "input": "Redemonstrated is a heterogeneously enhancing mass centered at the right\nporous acusticus extending into the internal auditory canal measuring 9 x 12 x\n6 mm (AP x TV x SI).  The mass does not reach the cochlear nerve aperture and\nis stable in size and morphology as compared to the prior examination of ___.  The mass obliterates the proximal portion of the right internal\nauditory canal and is inseparable from the seventh and eighth cranial nerve\ncomplexes which cannot be distinctly visualized in this region.\n\nExtensive confluent and scattered focal periventricular, subcortical, and deep\nwhite matter FLAIR hyperintensities including FLAIR hyperintense foci in\nbilateral pons are grossly unchanged compared to the prior examination and\nremain nonspecific but likely sequelae of chronic small vessel ischemic\ndisease.  Prominence of the ventricles and sulci is in keeping with moderate\nglobal atrophy.\n\nThere is no evidence of new enhancing mass, edema, mass effect, or acute\ninfarction.  The dural venous sinuses are patent on postcontrast MP rage\nsequences.  The orbits are unremarkable, the paranasal sinuses are clear.",
            "output": "Stable size and morphology of right CPA/IAC mass likely representing a\nschwannoma.  The mass obliterates the proximal right IAC and is indistinct\nfrom the seventh and eighth cranial nerve complexes."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, or infarction.\nThe cerebellar tonsils are normal in position and configuration. Again noted\nis a partially empty sella, unchanged from MRI on ___. The\nventricles and sulci are normal in caliber and configuration.  Major\nintravascular flow voids are preserved.\n\nThere are round foci of gradient susceptibility in the bilateral frontal\nregion (series 20, image 18) that correspond to bony excrescences of the\nfrontal calvarium or a small calcified meningioma as, better seen on CT from\n___. The paranasal sinuses. Mastoid air cells appear clear. The\norbits are normal.",
            "output": "1. No evidence of a mass lesion.\n2. Normal appearance of the brain on noncontrast MRI.\n3. Partially empty sella, unchanged from MRI on ___. This is\nnonspecific and can be seen in asymptomatic patients, but can also be seen in\nassociation with intracranial hypertension. Clinical correlation suggested."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  The ventricles and sulci are prominent, consistent with global\ncerebral volume loss. The intraorbital contents are normal. The paranasal\nsinuses are clear.  Postcontrast images demonstrate no abnormal parenchymal\nvascular or meningeal enhancement.\n\nFLAIR images demonstrate increased signal within the left membranous labyrinth\nincluding cochlear vestibule and semicircular canal (7:7).  This region is\nalso high signal on pre gadolinium and post gadolinium T1 weighted images (4\nand 10:7).  This findings are suggestive of left inner ear hemorrhage of\nunknown chronicity.  There is no abnormal enhancement seen within the facial\nnerves or membranous labyrinth bilaterally on postcontrast MP rage images.\n\nThere is moderate fluid in the right mastoid air cells.  No abnormal\nenhancement or diffusion restriction are seen to suggest infectious process.",
            "output": "1. Findings suggestive of left membranous labyrinth hemorrhage of unknown\nchronicity but likely subacute.\n2. Moderate right mastoid effusion without evidence of an infectious process,\nintracranial extension or leptomeningeal enhancement.\n3. No abnormal intracranial enhancement.\n4. No acute infarct or intracranial hemorrhage.\n5. Patent dural venous sinuses."
        },
        {
            "input": "There is no intra or extra-axial mass, acute hemorrhage or infarct. The sulci,\nventricles and cisterns are within expected limits for the patient's minimal\nsenescent related global cerebral volume loss.  Very few scattered\nperiventricular and subcortical T2/FLAIR white matter hyperintensities are\nnonspecific, but commonly seen in the setting of chronic microangiopathy in a\npatient of this age, and also within expected limits.  The major intracranial\nflow voids are preserved.  Partial opacification of scattered right greater\nthan left ethmoid air cells and of the bilateral frontal ethmoidal recesses as\nwell as mild mucosal thickening of the remainder the paranasal sinuses.  The\norbits are unremarkable.  No fluid signal is seen in the mastoid air cells. \nNo suspicious osseous lesions.",
            "output": "1. No acute intracranial abnormality on noncontrast MRI head.  Specifically no\nintracranial hemorrhage, acute infarct or mass.  No disproportionate lobar\nvolume loss.\n2. Very minimal periventricular and subcortical T2/FLAIR white matter\nhyperintensities are nonspecific, but commonly seen in the setting of chronic\nmicroangiopathy in a patient of this age.\n3. Paranasal sinus disease as described above."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.\n\nScattered bilateral lymph nodes which demonstrate slow diffusion are not\nenlarged by size criteria.\n\nSubtly enhancing foci in the parotids, bilaterally which demonstrate slow\ndiffusion (series 9, image 2) measuring up to 1.2 x 0.8 cm, likely represent\nintraparotid lymph nodes.\n\nThere is mild-to-moderate mucosal thickening in the maxillary sinuses,\nbilaterally.  The orbits are unremarkable.",
            "output": "1. No evidence of intracranial malignancy.  No hemorrhage, edema, mass effect\nor infarction.\n2. Bilateral intraparotid lymph nodes are not enlarged by size criteria, but\nappear prominent.  Prominent upper cervical lymph nodes are partially\nvisualized."
        },
        {
            "input": "There is a cortical based lesion in the left perirolandic cortex (series 7,\nimage 25).  The lesion is hyperintense on diffusion weighted imaging, mildly\nlow on ADC (may be due to small size or pseudonormalization) as well as being\nhyperintense on T2 weighted imaging and not demonstrating any enhancement post\ncontrast.\n\nNo other areas of slow diffusion.  Multiple T2 and FLAIR hyperintense white\nmatter lesions: 2 being periventricular, and the majority of the other lesions\nbeing juxta cortical which do not demonstrate slow diffusion or enhancement\npostcontrast.  The ventricular system is symmetrical.  The intracranial\narteries demonstrate normal T2 flow void.  Minimal mucosal thickening\ninvolving the ethmoid air cells and left maxillary sinus.  The orbits appear\nnormal.",
            "output": "Nonspecific cortical based lesion in the left perirolandic cortex is most\nlikely the index lesion explaining the clinical symptoms.\nThis lesion may represent an acute demyelinating plaque (in the setting of\nmultiple other plaques).  An alternative diagnosis is subacute cortical\ninfarction, which would not explain the white matter lesions.\n\nMultiple other white matter plaques (with a juxta cortical predominance) as\ndescribed above without enhancement or restricted diffusion suggests a\ndemyelinating disease.  Although these lesions are not in the typical\nperiventricular distribution I would still consider MS at the top of my\ndifferential and MS workup is advised.\nAs the differential diagnosis includes a small cortical infarct a cardiac echo\nis also suggested if clinically indicated.\n\nPlease see separately dictated report for spine findings.\n\nNOTIFICATION:  The findings were discussed by Dr. ___ with\nDr. ___ on the ___ ___ at 9:07 am, 10 minutes after discovery\nof the findings."
        },
        {
            "input": "Previously seen focus of left precentral gyrus restricted diffusion and T2\nsignal abnormality at the vertex has nearly resolved, with trace residual\nFLAIR abnormality.  No new T2 signal abnormalities.  No restricted diffusion..\nRemaining previously seen juxta cortical, deep white matter, periventricular\nT2 signal abnormalities involving cerebral hemispheres are stable.  No\ninfratentorial abnormality.  Findings are nonspecific, may be sequela of\ndemyelinating process, systemic inflammatory process, sequela of distant\ninfectious process, early chronic small vessel ischemic changes.\nClear mastoids, paranasal sinuses.  Intracranial vascular flow voids are\npreserved.\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor acute infarction.  The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.  No abnormal meningeal enhancement.",
            "output": "1. Previously seen abnormality left precentral gyrus has nearly resolved..\n2. Stable small foci of juxta cortical, deep white matter, periventricular T2\nsignal abnormalities, nonspecific, may be sequela of prior demyelinating,\ninflammatory, infectious process or chronic small vessel ischemic changes.  No\nnew or enhancing lesions.  No infratentorial abnormalities."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.  The major intracranial flow voids are preserved.  The dural\nvenous sinuses are patent.  The pituitary appears normal.  The craniocervical\njunction appears normal.  The orbits appear unremarkable.  The paranasal\nsinuses are essentially clear.",
            "output": "1. Unremarkable contrast enhanced brain MRI.\n2. No acute infarct, intracranial hemorrhage or abnormal enhancement.  No\nparenchymal FLAIR signal abnormality.  No intracranial mass."
        },
        {
            "input": "MRI head:\n\nA 1.6 x 1.4 x 1.2 cm cm T2/FLAIR hyperintense lesion in the left superior\ntemporal subcortical white matter enhances.  The 2.0 x 1.6 by 0.9 cm T2/FLAIR\nhyperintense lesion in the right superior temporal periventricular white\nmatter does not enhance.  There is a 3 mm T2/FLAIR hyperintense lesion in the\nright posterior temporal lobe white matter on 101b:90 and a 4 mm T2/FLAIR\nhyperintense lesion in the left cerebellar hemisphere on 101b:47.  No other\nT2/FLAIR hyperintense lesions are identified.  The corpus callosum is normal.\n\nThere is no evidence of hemorrhage, edema, midline shift or infarction.   The\nventricles and sulci are normal in caliber and configuration.\n\nThe paranasal sinuses and mastoid air cells are clear.  The orbits are\nunremarkable.\n\nThe major intracranial flow voids are preserved.\n\nMRI cervical spine:\n\nThe alignment of the cervical spine is normal.  Images are somewhat degraded\nby motion artifact The bone marrow is normal in signal.  The height of the\nvertebral bodies are maintained.  The C5-C6 vertebral bodies are partially\nfused.  The spinal cord is normal in signal and caliber.  There is no abnormal\nenhancement.  A broad-based disc protrusion is noted at C4-C5.  There is no\nspinal canal or neural foraminal stenosis.  There are small bilateral\nperineural cysts at C7-T1.  The prevertebral and paraspinal soft tissues are\nnormal.",
            "output": "1. One enhancing T2/FLAIR hyperintense lesion in the white matter of the left\ntemporal lobe and 3 nonenhancing T2/FLAIR hyperintense lesions, 2 in the right\ntemporal lobe and 1 in the left cerebellar hemisphere, most likely\nrepresenting a demyelinating process.  Differential diagnosis also includes\ninflammatory or infectious processes.\n2. No T2 hyperintense or enhancing lesions in the cervical spinal cord.\n\nNOTIFICATION:  The findings of multiple T2/FLAIR hyperintense lesions in the\nbilateral temporal lobes and left cerebellar hemisphere, 1 of which enhances\nin the left temporal lobe were discussed with Dr. ___. by\n___, M.D. on the telephone on ___ at 3:47 ___, 10 minutes after\ndiscovery of the findings."
        },
        {
            "input": "MRI head:\n\nA 1.6 x 1.4 x 1.2 cm cm T2/FLAIR hyperintense lesion in the left superior\ntemporal subcortical white matter enhances.  The 2.0 x 1.6 by 0.9 cm T2/FLAIR\nhyperintense lesion in the right superior temporal periventricular white\nmatter does not enhance.  There is a 3 mm T2/FLAIR hyperintense lesion in the\nright posterior temporal lobe white matter on 101b:90 and a 4 mm T2/FLAIR\nhyperintense lesion in the left cerebellar hemisphere on 101b:47.  No other\nT2/FLAIR hyperintense lesions are identified.  The corpus callosum is normal.\n\nThere is no evidence of hemorrhage, edema, midline shift or infarction.   The\nventricles and sulci are normal in caliber and configuration.\n\nThe paranasal sinuses and mastoid air cells are clear.  The orbits are\nunremarkable.\n\nThe major intracranial flow voids are preserved.\n\nMRI cervical spine:\n\nThe alignment of the cervical spine is normal.  Images are somewhat degraded\nby motion artifact The bone marrow is normal in signal.  The height of the\nvertebral bodies are maintained.  The C5-C6 vertebral bodies are partially\nfused.  The spinal cord is normal in signal and caliber.  There is no abnormal\nenhancement.  A broad-based disc protrusion is noted at C4-C5.  There is no\nspinal canal or neural foraminal stenosis.  There are small bilateral\nperineural cysts at C7-T1.  The prevertebral and paraspinal soft tissues are\nnormal.",
            "output": "1. One enhancing T2/FLAIR hyperintense lesion in the white matter of the left\ntemporal lobe and 3 nonenhancing T2/FLAIR hyperintense lesions, 2 in the right\ntemporal lobe and 1 in the left cerebellar hemisphere, most likely\nrepresenting a demyelinating process.  Differential diagnosis also includes\ninflammatory or infectious processes.\n2. No T2 hyperintense or enhancing lesions in the cervical spinal cord.\n\nNOTIFICATION:  The findings of multiple T2/FLAIR hyperintense lesions in the\nbilateral temporal lobes and left cerebellar hemisphere, 1 of which enhances\nin the left temporal lobe were discussed with Dr. ___. by\n___, M.D. on the telephone on ___ at 3:47 ___, 10 minutes after\ndiscovery of the findings."
        },
        {
            "input": "Again seen are FLAIR lesions in the bilateral superior temporal lobes, right\nposterior temporal lobe, likely secondary to demyelinating process.  The\npreviously seen lesion in the left cerebellar hemisphere is not well\nvisualized on today's study.\n\nNo definite T2 hyperintensity is seen in the region of medial longitudinal\nfasciculus on the Fiesta sequences.  Please note that evaluation on thin slice\naxial T2 weighted images is likely more sensitive than FIESTA sequence for\ndemyelinating lesions.\n\nPlease refer to separate dictation for complete head MRI from ___\nfor detailed findings.",
            "output": "1. No definite T2 hyperintense lesion is seen in the region of medial\nlongitudinal fasciculus on the FIESTA sequence.  Please note that thin slice\naxial T2 weighted sequences are more sensitive for evaluation.\n2. Please refer to separate dictation of head MRI from ___ for\ndetailed findings."
        },
        {
            "input": "The patient's previously noted left frontal lobe, ring-enhancing mass is again\nseen.  Today, this lesion measures 2.1 cm, previously 2.2 cm. There is 6 mm of\nrightward midline shift and moderate, unchanged mass effect due to vasogenic\nedema.  Fiducial markers are in place.",
            "output": "1. Unchanged 2.1 cm left frontal, ring-enhancing mass with significant\nvasogenic edema causing 6 mm of rightward midline shift, also unchanged from\nprior.\n2. No new enhancing lesions are demonstrated in the short interval."
        },
        {
            "input": "Patient is status post resection of the known right frontal lobe mass, now\nwith intrinsic hyperintensity on precontrast T1 weighted images, small foci of\npneumocephalus in the surgical bed and along the inner table of the calvarium.\nOn postcontrast images, there is trace amount of enhancement around the focus\nof pneumocephalus (13:16), and along the periphery of the parenchyma,\ncontinuous with the dural enhancement (13:15).  However, majority of\nhyperintensity on postcontrast T1 weighted images were present on precontrast\nT1 weighted images, compatible with postsurgical blood products, limiting\nevaluation for residual tumor in the region.  The degree of surrounding\nvasogenic edema is persistently extensive, resulting in stable 5 mm rightward\nshift of midline structures, effacement of the adjacent sulci and narrowing of\nthe frontal horn of the left lateral ventricle.\n\nTrace amount of extra-axial hyperintensity on T2 weighted images along the\nleft frontal and parietal convexity may represent postsurgical blood products.\nIn addition, there is trace amount of extra-axial postsurgical fluid\ncollection at the surgical bed measuring 3 mm (13:15).  There is no acute\ninfarct.  The dural venous sinuses are patent.  The major intracranial flow\nvoids are preserved.\n\nNew enhancement of the dura overlying the left temporal, frontal and parietal\nlobes compatible with sequela of recent procedure.  There is post surgical\nsoft tissue swelling and subgaleal hematoma.\n\nThere is air-fluid level in the left mastoid air cells.",
            "output": "1. Postsurgical changes from resection of the known right frontal mass, with\nrounded area of hyperintensity on precontrast T1 weighted imaging, compatible\nwith postsurgical blood product without evidence of nodular enhancement to\nsuggest residual disease, although subtle enhancement may be obscured by the\nblood product.\n2. No significant change in vasogenic edema or midline shift.\n3. Additional findings as described above."
        },
        {
            "input": "There is minimal discontinuous, linear enhancement within the left frontal\nlobe surgical resection bed.  Low signal on T1 weighted images within the left\nfrontal lobe adjacent to the resection bed likely reflects residual vasogenic\nedema which has significantly decreased from the ___ MRI. \nPreviously seen midline shift has resolved, left frontal horn has re-expanded.\nThere is a small extra-axial fluid collection underlying the left craniotomy\nflap, with minimal mass effect on the underlying left frontal lobe.  No new\nintracranial enhancement is identified.  There is benign developmental venous\nanomaly in the left middle cerebellar peduncle, pons, adjacent cerebellum,\nstable.\n\nThere is mild global parenchymal volume loss.  There is no acute infarct,\nlarge intracranial hemorrhage, or midline shift.  The orbits are grossly\nunremarkable.",
            "output": "Interval improvement, with linear, discontinuous enhancement surrounding\nsurgical cavity, and significantly improved edema.\n\nNo new enhancing lesions."
        },
        {
            "input": "Left frontal postoperative changes are again identified with pachymeningeal\nenhancement and a small rim enhancing cystic area in the left frontal lobe. \nThe rim of enhancement is better visualized on the current study.  Adjacent\nFLAIR hyperintensities are unchanged.  Developmental venous anomaly in the\nleft cerebellum is again seen.  The adjacent postoperative changes have\nresolved.  FLAIR hyperintensities at the left frontoparietal convexity (08:21)\nare better visualized on the current study but there is no corresponding\nenhancement identified and could be related to prior infarcts.",
            "output": "Left frontal rim enhancing area demonstrates slightly better visualization of\nthe  rim compared to the prior study but no new areas of abnormal enhancement\nidentified.  Otherwise the examination is unchanged."
        },
        {
            "input": "The patient is status post left frontal craniotomy and radiation treatment of\nleft frontal tumor.\n\nThere is a thick rind of inhomogeneous enhancement surrounding the resection\ncavity, demonstrating blood products on gradient images, and area of\nperipherally restricted diffusion,.  Enhancing abnormality measures 3.8 cm x\n3.3 cm.  There is moderate surrounding T2 signal abnormality extending\nthroughout the anterior left frontal lobe.  Mild-to-moderate local\nmass-effect, 6 mm midline shift to the right at the level of the anterior\nfrontal lobes, ___ of corpus callosum.  On prior exam ___, there\nwas very thin linear peripheral enhancement and mild surrounding edema. \nDifferential considerations are tumor progression or radiation necrosis.  MR\nperfusion recommended in further evaluation.\n\nLinear area of leptomeningeal enhancement overlying right inferior parietal\nlobule, stable since ___, indeterminate, may be vascular in etiology,\nstability argues against metastatic disease.\n\nPunctate focus of subacute infarct right cerebellum.  Small chronic focus of\ncortical, subcortical encephalomalacia left vertex, stable.  Developmental\nvenous anomaly left middle cerebellar peduncle.\n\nThe ventricles and sulci are normal in caliber and configuration.  There is\nmild mucosal thickening of the right maxillary sinus.  Otherwise, The\nparanasal sinuses, mastoid air cells and middle ear cavities are clear.  The\nintraorbital contents are normal.",
            "output": "1. 3.8 cm heterogeneously peripherally enhancing mass left frontal lobe at the\ntreatment bed.  Differential considerations are tumor progression or radiation\nnecrosis.  ASL, DC perfusion recommended.\n2. Punctate subacute infarct right cerebellum.\n3. Small area of right parietal leptomeningeal enhancement overlying, stable\nsince ___, may be vascular, stability argues against metastatic disease.\n\nRECOMMENDATION(S):  MR perfusion including ASL, DSC perfusion."
        },
        {
            "input": "Postcontrast MP RAGE images are moderately degraded by motion artifact. \nPostcontrast axial T1 weighted images are mildly limited by motion artifact. \nMild to moderate motion artifact is seen on several other sequences.\n\nThere is an irregularly shaped, heterogenously enhancing superficial left\nfrontal mass involving the middle frontal gyrus, which measures 2.3 x 2.3 x\n2.2 cm on images 900:96, 9:77.  The mass demonstrates mild peripheral\nhyperintensity on precontrast T1 weighted images (which may be related to\nmineralization, blood products, plus/minus mucin) and heterogenous low signal\nintensity on T2 weighted images, with foci of low signal on gradient echo\nimages which may represent calcifications plus/minus blood products.  The mass\nwas mildly hyperdense on the prior CT, which may also be secondary to\ncalcifications plus/minus blood products.  There is an ill-defined focus of\ncontrast enhancement adjacent to the medial margin of the mass, image 10:16,\nsuggesting infiltrative nature.\n\nThere is extensive left frontal vasogenic edema, with 6 mm rightward shift of\nmidline structures, partial effacement of the frontal horn and anterior body\nof the left lateral ventricle, and partial effacement of the upper third\nventricle best seen on coronal image 901:89.  Frontal horn of the right\nlateral ventricle is also mildly effaced.  There is no evidence for right\nlateral ventricle dilatation to indicate entrapment.  There is no uncal\nherniation or compression of other basal cisterns.\n\nThere is a developmental venous anomaly involving the left cerebellar\nhemisphere, left middle cerebellar peduncle, and left pons.  There is no\nevidence for a cavernous malformation.\n\nThe M1 segment of the left middle cerebral artery may be mildly narrowed by\nthe mass effect from the left frontal lobe.  A2 segments of the anterior\ncerebral arteries are displaced to the right.  There is ___ termination of\nthe non dominant right vertebral artery.\n\nThere is a small mucous retention cyst in the right maxillary sinus.  There is\nmild mucosal thickening in the ethmoid air cells and left greater than right\nfrontoethmoidal recesses.  There is trace fluid in the dependent left mastoid\nair cells.",
            "output": "1.  2.3 x 2.3 x 2.2 cm heterogenous mass with small foci of calcifications\nplus/minus blood products, and mild intrinsic T1 hyperintensity which may be\nsecondary to mineralization, blood products, plus/minus mucin.  Faint focus of\ncontrast enhancement along the medial border of the mass suggest infiltrative\nnature.  Appearances are most consistent with a metastasis.\n2. Extensive left frontal vasogenic edema with 6 mm rightward shift of midline\nstructures, partial effacement of left greater than right lateral ventricles\nanteriorly, and mild partial effacement of the third ventricle.\n3. Developmental venous anomaly involving the left cerebellar hemisphere, left\nmiddle cerebellar peduncle, and left pons.\n4. The M1 segment of the left middle cerebral artery may be mildly narrowed by\nthe mass effect from the left frontal lobe.\n\nNOTIFICATION:  Preliminary report was transmitted electronically at 20:28 on\n___ by ___: \"There is a 2.3 x 2.3 x 2.4 cm enhancing\nsubcortical left frontal mass with significant associated edema in the left\nfrontal lobe effacing the frontal horn of the left lateral ventricle and\ncausing approximately 7 mm of rightward midline shift.  Lesion is consistent\nwith metastasis. There is no evidence of hemorrhage or infarction. No other\nmasses are appreciated.\""
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.  Mild prominence of the pituitary gland measuring\napproximately 9 mm in the craniocaudal dimension is unchanged compared to the\nprior exam.\n\nBilateral hippocampal formations and mammillary bodies are preserved in signal\nand configuration. There is no disproportionate medial temporal atrophy. There\nis no focal lobar encephalomalacia. There are no focal cortical dysplasias or\ngray matter heterotopia noted.",
            "output": "1. No acute intracranial abnormalities identified.  No concerning seizure\nfocus is seen.\n2. No abnormal enhancement identified."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  Orbits are unremarkable.  Paranasal sinuses are patent.",
            "output": "1. No acute intracranial abnormalities identified on this limited study."
        },
        {
            "input": "Postsurgical changes relating to left frontal craniotomy for electrode/strip\nplacement demonstrating associated susceptibility artifact.  Depth electrodes\nextending to the left anteromedial temporal lobe noted.  There is a small\namount of left convexity extra-axial fluid/blood and a 5 mm midline shift to\nthe right.\n\nThere is no evidence of infarction.  The sulci, ventricles and cisterns are\nwithin expected limits for postoperative findings.\n\nAllowing for postsurgical changes and artifact from the electrodes, the\nbilateral hippocampal formations and mammillary bodies are preserved in signal\nand configuration. There is no disproportionate medial temporal atrophy. There\nis no focal lobar encephalomalacia. There are no definite focal cortical\ndysplasias or gray matter heterotopia noted.",
            "output": "1. Postsurgical changes relating to left frontal craniotomy for\nelectrode/strip placement demonstrating associated susceptibility artifact.\n2. Small amount of postsurgical left convexity extra-axial fluid/blood and a 5\nmm midline shift to the right.  No evidence of acute infarct.\n3. Additional findings described above."
        },
        {
            "input": "Image quality is moderately degraded by motion artifact.\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, or infarction.\nThe ventricles and sulci are normal in caliber and configuration.  The\nhippocampal formations symmetric in size and signal intensity.  There is no\nabnormal enhancement after contrast administration.  Major vascular flow voids\nare preserved.  The orbits are unremarkable.  The paranasal sinuses and\nmastoid air cells are clear.  The pituitary gland is prominent measuring\napproximately 9 mm in cranial caudal dimension.  This is within the range of\nnormal for a woman of this age and unchanged since ___.",
            "output": "Unremarkable MRI of the head without evidence of infarction, hemorrhage, or\nmass."
        },
        {
            "input": "MRI BRAIN:\n\nThere are multiple scattered bilateral predominantly peripherally located\nenhancing parenchymal lesions, some hemorrhagic, highly suspicious for\nmetastatic disease.  The largest lesion or conglomerate of lesions is in the\nleft posterior parietal and occipital lobes demonstrating heterogeneous\nenhancement and multiple foci of hemorrhage with surrounding vasogenic edema\nwith the enhancing component measuring approximately 2.3 x 3.0 x 5.9 cm (AP x\nTV x SI).  The remaining lesions are subcentimeter and predominantly\nsupratentorial.  There is a questionable punctate focus of enhancement in the\nright cerebellar hemisphere (series 14, image 6).  The ventricles and sulci\nare age-appropriate.  There is no evidence of acute infarction.  Principal\nintracranial vascular flow voids including those of the dural venous sinuses\nare preserved.  There are a few opacified air cells at the left mastoid tip. \nThe orbits are grossly unremarkable.\n\n\nMRA brain: The intracranial vertebral and internal carotid arteries and their\nmajor branches appear normal without evidence of stenosis, occlusion, or\naneurysm formation.",
            "output": "1.  Numerous enhancing bilateral predominantly supratentorial and a possible\npunctate single right cerebellar foci of enhancement with intralesional\nhemorrhage, are highly concerning for metastases.  There is a large\nconglomerate lesion in the left parieto-occipital region measuring 2.3 x 3.0 x\n5.9 cm.\n\n2.  There is no evidence of diffuse leptomeningeal involvement."
        },
        {
            "input": "The dominant left parieto-occipital enhancing lesion seen on the previous\nstudy has considerably decreased in size with decrease in surrounding edema. \nA rim of head-hemosiderin is seen surrounding the lesion with subacute blood\nproducts which are new since the previous study.  Several punctate areas of\nhemosiderin deposition in the surrounding areas representing chronic blood\nproducts are also seen at the site of previously seen metastatic foci.  A\nsmall focus of chronic microhemorrhage in the right occipital lobe at the site\nis seen with associated enhancement  less apparent compared to the prior\nstudy.  Other and punctate enhancing lesions are also less apparent or not\nvisualized.  Leptomeningeal enhancement along the sulci of the medial aspect\nof the occipital lobe is also less apparent.  Previously seen punctate\nenhancement within the right cerebellar hemisphere is not visible.  No new\nareas of abnormal enhancement identified..",
            "output": "Decrease in size of previously seen parieto-occipital enhancing lesion with\nevidence of new blood products in the region.  Decrease in size or complete\nresolution of several other punctate enhancing lesions in the supra and\ninfratentorial regions.  No definite new abnormalities are identified.  No\nacute infarcts are seen."
        },
        {
            "input": "FLAIR hyperintensities are seen in the periventricular white matter including\nareas of low T1 signal .  FLAIR hyperintensities are also seen within the pons\nand also in the right side of the medulla (11:4).  There are several tiny\nsubcortical hyperintensities.  No abnormal post gadolinium enhancement is\nidentified.  Diffusion images demonstrate a curvilinear high signal within the\nright side of the pons (6:9) without corresponding ADC or FLAIR abnormality\nand could be artifactual.  Ventricles are normal in size and there is no\nmidline shift or hydrocephalus.",
            "output": "Although the FLAIR hyperintensities in the periventricular region are not in\nthe typical distribution of demyelinating disease, hypointense T1 lesions as\nwell as the medullary lesion are likely representative of demyelinating\ndisease.  No enhancing lesions are seen."
        },
        {
            "input": "Redemonstrated are numerous scattered bilateral foci of T2/FLAIR hyperintense\nsignal in the periventricular, subcortical, and deep white matter, as well as\nthe pons and medulla, some of which appear more confluent in the\nperiventricular region and are oriented somewhat perpendicular to the the\nlateral ventricle, consistent with history of demyelinating disease.  Even\nthough an exact comparison to prior study is difficult due to difference in\nslice selection and lack of 3D FLAIR sequences on the prior study, no definite\nnew lesion is identified.  There is no slow diffusion or enhancement\nassociated with the lesions.\n\nThere is no evidence of hemorrhage, edema, mass, mass effect, midline shift or\ninfarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  Principal intracranial vascular flow voids are preserved. \nThere is no abnormal enhancement after contrast administration. The orbits are\nunremarkable.\n\nPartially imaged upper cervical spinal cord is notable for a focal T2\nhyperintense lesion in the left side of cord (series 13, image 3).  Please\nrefer to recent cervical spine MRI dated ___ for full description\nof spinal cord lesion.",
            "output": "1. Innumerable white matter lesions in bilateral cerebral hemispheres, pons,\nand medulla are overall unchanged in number and distribution as compared to\nprior examination.  There is no associated slow diffusion or enhancement.\n2. Please refer to recent cervical spine MRI dated ___ for full\ndescription of spinal cord lesion."
        },
        {
            "input": "MRI BRAIN:\nNumerous foci of FLAIR hyperintense signal are re-demonstrated in the\nbilateral periventricular, subcortical and deep white matter, pons and medulla\nand upper cervical cord (8:1).  These are again consistent with demyelinating\nplaques.\n\nNew abnormal enhancement of the right trigeminal nerve cisternal segment\n(series 12, image 44), superimposed on pre-existing plaques seen on prior\nexam.  No other new intracranial enhancement is identified.\n\nThere is no acute infarct or intracranial hemorrhage.  The sulci, ventricles\nand cisterns are within expected limits for the patient's age.  The major\nintracranial flow voids are preserved.  The dural venous sinuses are patent. \nThere is mild mucosal thickening of the paranasal sinuses.  The orbits are\nunremarkable.  No significant fluid signal is seen in the mastoid air cells.\n\nMRI CERVICAL SPINE:\nFoci of demyelinating plaques are re-demonstrated in the left upper cervical\ncord (8:1) and at the level of C4-5 (19:14), unchanged.  The previously seen\nlesion at T2-3 is not visualized on the current exam.  No new lesions or\nenhancement are seen.\n\nThere is 2 mm anterior subluxation of C7-T1.  The bone marrow signal is within\nnormal limits.  There is multilevel loss of disc height.\n\nC2-C3: No spinal canal or foraminal narrowing.\n\nC3-C4: Posterior and bilateral facet uncovertebral osteophytes, no spinal\ncanal narrowing, unchanged moderate bilateral foraminal narrowing.\n\nC4-C5: Central disc protrusion, posterior and bilateral facet and\nuncovertebral osteophytes, no spinal canal narrowing, unchanged moderate right\nand mild left foraminal narrowing.\n\nC5-C6: Disc bulge, posterior and bilateral facet and uncovertebral\nosteophytes, thickening of ligamentum flavum, unchanged mild spinal canal\nnarrowing, moderate bilateral foraminal narrowing.\n\nC6-C7: Posterior and bilateral facet uncovertebral osteophytes, unchanged mild\nspinal canal narrowing, moderate right and mild left foraminal narrowing.\n\nC7-T1: Anterior subluxation, disc bulge, bilateral facet and uncovertebral\nosteophytes, unchanged mild spinal canal narrowing, moderate right and severe\nleft foraminal narrowing.\n\nOTHER:\nThe visualized paraspinal soft tissues are unremarkable..",
            "output": "1. New abnormal enhancement of the right trigeminal nerve cisternal segment. \nThis is superimposed on pre-existing FLAIR hyperintense lesions.\n2. No other new demyelinating plaques are identified.  Previously described\ndemyelinating plaques in the cerebral hemispheres and brainstem are unchanged\nin appearance.\n3. Unchanged foci of demyelinating plaques in the upper and mid cervical\nspine.  No enhancement.  No new lesions.\n4. Resolution of the previously seen cord lesions at T2-3.\n5. Unchanged cervical spondylosis with mild spinal canal narrowing at C5-6,\nC6-7 and C7-T1 with multilevel moderate to severe foraminal narrowing.\n6. Additional findings as described above."
        },
        {
            "input": "Redemonstrated are numerous foci FLAIR hyperintense lesion in the bilateral\nperiventricular, subcortical, and deep white matter, pons and medulla as well\nas the upper cervical spine, consistent with patient's known demyelinating\nplaques.  Enhancement of the right trigeminal nerve appears slightly\nprogressed compared to the prior exam (15; 62).  Otherwise, the remainder\ndemyelinating lesions do not appear to enhance.\n\nThere is no evidence of acute infarction.  No evidence of acute intracranial\nhemorrhage.\n\nMild mucosal sinus thickening is seen involving the ethmoid air cells.  The\nremainder of the visualized paranasal sinuses, mastoid air cells, and middle\near cavities are clear.  The globes are unremarkable.  The principal vascular\nflow voids appear to be well preserved.",
            "output": "1. Overall, no significant interval change in the burden of supra and\ninfratentorial demyelinating plaques compared to the exam from ___. \nNo evidence of enhancement to suggest active demyelination.\n2. Slight interval increase in enhancement involving the right trigeminal\nnerve compared to the prior exam.\n3. Upper cervical cord lesions, incompletely characterized on the current\nexam.  If there is further clinical concern, dedicated MRI of the cervical\nspine may be helpful for further evaluation."
        },
        {
            "input": "There is cortical slow diffusion involving the left posterior paramedian\nfrontal lobe including cingulate gyrus, extending into the parietal lobe, very\nposterior temporal and superior occipital lobe.  No hemorrhage is seen. \nPreviously suggested foci of hemorrhagic transformation are not evident on\ngradient images.  Mild hyperemia of the vasculature is seen on postcontrast\nimages.  Dural venous sinuses patent.\n\nChronic infarct left frontal lobe involving insula, triangulum, frontal\noperculum.\n\nBrain parenchymal atrophy.  There is severe bilateral temporal lobe atrophy. \nFindings consistent with moderate chronic small vessel ischemic changes. \nSmall chronic right cerebellar infarct.  2 punctate foci of superficial\ncerebral chronic microhemorrhage, suggestive of amyloid angiopathy.\n\nThere is complete opacification of the right maxillary sinus, with chronic\natelectasis..  The patient is status post bilateral cataract surgery.  The\nmastoid air cells and middle ear cavities are clear.",
            "output": "1. Findings consistent with large left posterior hemispheric subacute infarct.\n2. No evidence of hemorrhage on MRI.\n3. Chronic left frontal lobe infarct.  Small chronic right cerebellar infarct.\n4. Severe bilateral temporal lobe atrophy.  Suggestion of amyloid angiopathy.\n5. Paranasal sinus disease, maxillary sinus atelectasis.."
        },
        {
            "input": "There is expected evolution of large subacute infarct involving the left\nparieto-occipital region.  Areas of susceptibility artifact within this\ninfarcted area consistent with hemorrhagic transformation as seen on recent CT\nare more conspicuous on today's exam compared to the prior MRI.  Surrounding\nassociated FLAIR hyperintense signal is decreased compared to prior.  Chronic\ninfarcts involving the left frontal lobe and right cerebellar hemisphere again\nnoted.  Diffuse subcortical and periventricular FLAIR hyperintensities are\nsuggestive of chronic small vessel ischemic disease.  Ventricles and sulci are\nprominent suggesting age-related involutional changes, unchanged, with\ndisproportionate extensive temporal lobe atrophy.  Punctate gradient echo\nsusceptibility hypointensity of the right parietooccipital lobe likely\nrepresents sequela prior microhemorrhage.  Trace hemosiderin staining along\nthe anterior aspect of left frontal encephalomalacia is also unchanged.  The\nmajor intracranial flow voids appear preserved.\n\nRight maxillary sinus is again noted to be fluid-filled.  There is also\ncomplete opacification of an anterior ethmoidal air cells.  Paranasal sinuses\notherwise appear clear.  Orbits are unremarkable.  Bilateral lens replacements\nare noted.",
            "output": "1. Evolving large left parieto-occipital region infarct.  Areas of hemorrhagic\ntransformation within appear overall stable compared to recent CT, though more\npronounced compared to the prior MRI.\n2. Chronic large left frontal lobe and small right cerebellar hemisphere\ninfarcts.\n3. Paranasal sinus disease as described above, unchanged.\n4. Additional findings described above."
        },
        {
            "input": "There has been significant interval decrease in the size of the enhancing\nright basal ganglia lesion, now measuring 1.1 x 1.1 cm, previously measuring\n2.3 x 2.2 cm 6 days ago (12; 150).  There is also decreased edema, mass\neffect, and midline shift from 8 mm to about 3 mm. In addition, the left basal\nganglia lesion has also slightly decreased in size no residual rim\nenhancement, now measuring 6 x 6 mm, previously measuring 8 x 8 mm 6 days ago\n(12; 150).  There is no evidence of hemorrhage or infarction.  There are no\ndiffusion abnormalities identified and there is no evidence of increased\nperfusion on ASL.\n\nOn MR spectroscopy, there is a multi voxel gradient ratio of greater than 1.6\n(choline/NAA) in both basal ganglia, consistent with cellular infiltration and\nis suspicious for underlying tumor.  There is no significant lactate peak,\nindicating that the lesions are less likely to be infection.\n\nThe ventricles and sulci are normal in caliber and configuration.  The major\nflow voids are preserved.\n\nThe visualized portion of the orbits is normal.  There is no abnormal bone\nmarrow signal.  There is an incidental venous anomaly in the left parietal\nlobe (12; 201-248).",
            "output": "1. Interval decrease in size of the enhancing right basal ganglia lesion, now\nmeasuring 1.1 x 1.1 x 1.1 cm, previously measuring 2.3 x 2.2 cm.  There is\nalso decreased edema, mass effect, and midline shift from the prior study.\n2. Bilateral basal ganglia lesions are consistent with tumor, such as lymphoma\nor glioma. While infection may still remain in the differential, the\nappearance on MR is more in favor of neoplastic origin.\n3. Interval decrease in size of left basal ganglia lesion, now measuring 6 x 6\nmm, previously measuring 8 x 8 mm."
        },
        {
            "input": "There has been interval increase in the size of the heterogeneously enhancing\nright basal ganglia mass, now measuring 2.4 x 2.1 cm (TRV by AP), previously\nmeasuring 1.1 x 1.1 cm on the most recent MRI (9:76).  There is central and\nfocal areas of internal low signal on T1 weighted sequences, suggestive of\nnecrosis.  There is irregular enhancement of a thick capsule surrounding the\nlesion.  Interval worsening of the surrounding vasogenic edema throughout the\nright basal ganglia, external capsule, right thalamic nuclei and corona\nradiata extending inferiorly to involve the right cerebral peduncle and pons. \nThe mass effect results in approximately 6 mm of leftward midline shift,\npreviously 3 mm on the prior study.  The degree of edema and mass effect is\ndecreased relative to the most recent prior study, however is improved\nrelative to the initial MRI of the brain from ___.\n\nThere is a similar appearance of the left basal ganglia lesion, measuring\napproximately 0.5 x 0.4 cm (AP by TV) centered in the left global pallidus\nwithout significant surrounding edema.  There is mild peripheral rim\nenhancement, increased relative to the prior study but remains decreased\ncompared to the study from ___.\n\nThere is no evidence of hemorrhage or infarction.  The visualized orbits are\nnormal.  Paranasal sinuses, mastoid air cells and inner ears are clear.\n\nIncidental note is made of a developmental venous anomaly in the left parietal\nlobe (9:102).",
            "output": "1. Interval increase in the heterogenously enhancing right basal ganglia\nlesion, now measuring 2.4 x 2.1 cm, previously measuring 1.1 x 1.1 cm on the\nmost recent MRI.  There has been significant interval increase in the extent\nof the surrounding vasogenic edema, which now extends to the right cerebral\npeduncle and pons, with mass effect causing approximately 6 mm of leftward\nmidline shift.\n2. The extent of the lesion and surrounding edema is worse relative to the\nstudy from ___, however remains improved relative to the initial\nMRI from ___.  This lesion remains nonspecific in etiology,\nhowever as previously discussed, the differential includes primary neurologic\nmalignancy such as lymphoma or an atypical infection.\n3. Similar appearance of the left basal ganglia lesion, measuring 0.5 cm\nmaximum thickness with mild surrounding edema compared to the most recent\nstudy but improved relative to the initial study from ___."
        },
        {
            "input": "The patient's previously noted enhancing right basal ganglia lesion with\nadjacent edema is again seen.  Patient's previously noted left basal ganglia\napproximately 4 x 5 mm peripherally enhancing lesion is also again seen. \nThere is grossly stable approximately 1.2  cm right to left midline shift and\ngrossly stable mass effect.",
            "output": "Limited imaging for the purposes of pre-surgical planning demonstrating\ngrossly stable right basal ganglia enhancing mass with adjacent edema and mass\neffect and left basal ganglia of peripherally enhancing lesion, compared to 2\nday prior contrast brain MRI."
        },
        {
            "input": "There are postsurgical changes from right transfrontal approach biopsy of the\nmass centered in the right basal ganglia with a small amount of chronic blood\nproducts and enhancement along the biopsy tract.\n\nThe lobulated enhancing mass in the right basal ganglia is slightly decreased\nin size compared to most recent prior study, now measuring up to 2.0 x 2.1 cm\n(TR x AP) , previously 2.4 x 2.1 cm.  There is new susceptibility artifact\nwithin the lesion, which most likely represents microhemorrhage.  The\nsurrounding vasogenic edema has slightly increased anterior to the caudate\nhead and putamen (series 9, images ___ and posterolaterally into the right\ntemporal stem (series 9, image 14).  The vasogenic edema within the right\ncorona radiata, external capsule, thalamus, cerebral peduncle and right side\nof the pons is overall unchanged.  Mass effect resulting in partial effacement\nof right lateral ventricle and third ventricle and 6 mm of leftward midline\nshift at the level of the septum pellucidum is unchanged.\n\nThe 6 x 4 mm lesion in the left globus pallidus is not significantly changed\nin size but demonstrates decreased enhancement and T2/FLAIR hyperintense\nsignal.  There is new susceptibility artifact, which most likely represents\nmicrohemorrhage.\n\nThere is no evidence of acute infarction or acute intracranial hemorrhage.  No\nnew enhancing lesions are identified.\n\nThe orbits are unremarkable.\n\nThe paranasal sinuses and mastoid air cells are clear.\n\nThe major intracranial flow voids are preserved.  There is a developmental\nvenous anomaly in the left parietal lobe.\n\nThe marrow signal is within normal limits.  The extracranial soft tissues are\nunremarkable.",
            "output": "1.  Interval decrease in the size of the enhancing mass centered in the right\nbasal ganglia but slight increase in the surrounding vasogenic edema.\n2.  Stable size but decreased enhancement and surrounding edema of the lesion\ncentered in the left globus pallidus.\n3.  New susceptibility artifact within both lesions most likely represents\nmicrohemorrhage related to posttreatment changes.\n4.  No significant change in the local mass effect and leftward midline shift."
        },
        {
            "input": "The lobulated enhancing lesion centered in the right basal ganglia is\nunchanged in size compared with the most recent CT, however is increased in\nsize compared with the most recent MR. ___ lesion measures 2.3 cm (AP) by 2.3\ncm (TV).  There is stable surrounding vasogenic edema extending into the right\nfrontal and right temporal lobes, unchanged compared with the most recent CT\nbut increased compared with the most recent MR. ___ changes are again\nnoted in relation to the right transfrontal approach biopsy of the right basal\nganglia mass, with chronic blood products and mild enhancement noted along the\nbiopsy tract.  Chronic blood products are also noted within the right basal\nganglia lesion.  There is an increase in the degree of T2/FLAIR hyperintensity\nin the mid brain, predominantly in the right side, in the pons, predominantly\non the right side and in the right cerebellar hemisphere anteriorly.  Some of\nthis T2/FLAIR hyperintensity demonstrates mild mass-effect, and may represent\na combination of tumor and edema.  Stable appearance of the 6 mm x 4 mm\nnonenhancing mildly T2 hyperintense lesion in the left globus pallidus.  There\nis no evidence of acute hemorrhage or infarction.  The ventricles and sulci\nare stable in caliber and configuration compared with the most recent CT.",
            "output": "1. The enhancing lesion centered in the right basal ganglia is unchanged in\nsize compared with the most recent CT, however is increased in size compared\nwith the most recent MR. T2/FLAIR hyperintensity extending inferiorly to the\nmidbrain, predominantly in the right side, in the pons, predominantly on the\nright side and in the right cerebellar hemisphere anteriorly, may represent\ncombination of tumor and edema.\n2. Adjacent T2/FLAIR hyperintensity extending into the right frontal and right\ntemporal lobes is stable compared with the most recent CT but increased\ncompared with the most recent MR. ___ is stable 8 mm leftward midline shift.\n3. No acute intracranial hemorrhage or acute infarct."
        },
        {
            "input": "MRA neck:\nThere is intermittent visualization of the left vertebral artery in the\ncervical region.  The left vertebral artery is not well seen near the origin\nbut then subsequently visualized.  Distally the left vertebral artery appears\nto be reconstituting in the V4 segment.  Fat-suppressed images demonstrate no\nevidence of increased signal in the approximate position of the vertebral\nartery to indicate dissection.  The right vertebral and both carotid arteries\nare patent without stenosis or occlusion.\n\nThe intracranial MRA demonstrates reconstitution of the left V4 segment distal\nto the left posterior inferior cerebellar artery but the proximal left V4\nsegment is not visualized.  Otherwise the intracranial arteries are patent\nwithout stenosis occlusion or an aneurysm greater than 3 mm in size.",
            "output": "1. Decrease in partial visualization throughout the left vertebral artery\nreason new finding since the previous MRI of ___ and is likely a chronic\nfinding from atherosclerotic disease in absence of signs suggestive of\ndissection n on the fat-suppressed images.\n2. Partial visualization of intracranial left V4 segment due to collateral\nflow but otherwise normal MRA of the head."
        },
        {
            "input": "There is a region of slow diffusion with corresponding FLAIR signal\nhyperintensity in the right cerebellar hemisphere (series 302, image 7) likely\nreflecting an acute/ subacute infarction. There is an additional punctate\nregion of slow diffusion also seen within the left basal ganglia with subtle\ncorresponding FLAIR signal which likely represents an additional tiny\nacute/subacute lacune infarct.\n\nThe ventricles and sulci are enlarged consistent with generalized parenchymal\nvolume loss. There are scattered foci of T2/FLAIR signal hyperintensity in the\nperiventricular, subcortical, and deep white matter which are nonspecific but\nlikely on the basis of chronic small vessel ischemic disease.  There is an\nempty sella which appears elongated in the superior to inferior dimension.\nMajor vascular flow voids are preserved. Patient is status post left lens\nreplacement. There is near-complete opacification of the right maxillary\nsinus. Mucosal thickening/ fluid signal is also noted to a lesser extent in\nthe ethmoids and left maxillary sinus. The mastoid air cells are clear.",
            "output": "1.  Acute/subacute right cerebellar infarct.  Additional tiny acute/subacute\nleft basal ganglia lacunar infarct.  No evidence of hemorrhagic transformation\n\n2.  Generalized parenchymal volume loss and scattered foci of T2/FLAIR signal\nhyperintensity in the periventricular, subcortical, and deep white matter\nlikely on the basis of chronic small vessel ischemic disease.\n\nNOTIFICATION:  These findings were discussed with Dr. ___ by Dr.\n___ on ___ at 10:00 am."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, or infarction.\nThe ventricles and sulci are normal in caliber and configuration. There are\nfew nonspecific scattered foci of T2/FLAIR signal hyperintensity in the\nsubcortical white matter of the bilateral cerebral hemispheres.  Major\nvascular flow voids are preserved. The orbits are unremarkable. The paranasal\nsinuses and mastoid air cells are clear.  No focal encephalomalacia\nidentified.",
            "output": "1. No acute hemorrhage, infarction, or mass effect.\n2. Few scattered nonspecific the bilateral cerebral subcortical white matter\nhyperintensities. Differential consideration includes prior trauma, prior\ninfection, small vessel ischemic changes, demyelinating disease, migraine\nheadache, vasculitis, and Lyme disease.  Recommend clinical correlation.\n3. No focal encephalomalacia or microhemorrhages identified."
        },
        {
            "input": "Multiple foci of restricted diffusion are seen within the cerebellar\nhemispheres bilaterally, the left parietal lobe and throughout the right\ncerebrum. There is a rim enhancing lesion within the left temporal lobe\nposteriorly with associated blood products and mild surrounding edema. Focal\nabnormal leptomeningeal/cortical enhancement is seen overlying the right\nfrontal lobe. There is a punctate focus of enhancement within the left\ncerebellar hemisphere which corresponds to a focus of restricted diffusion.\nSubarachnoid hemorrhage overlies the medial right parietal occipital region\nwith slight sulcal FLAIR hyperintensity associated with the susceptibility in\nthis region. A small focus of susceptibility is present within the inferior\nleft occipital lobe. Linear FLAIR hyperintensity is seen to the right frontal\nlobe as the sequela of the previous infarct seen on the prior examination.\n\nNo mass effect or shifting of the midline structures is present. The\nventricular system is normal in size and configuration. Flow voids for the\nmajor intracranial vessels are preserved.",
            "output": "Multiple foci of restricted diffusion within the posterior fossa and in the\nright cerebral hemisphere.  There is a rim enhancing lesion with a small\namount of associated hemorrhage within the left temporal lobe.  These findings\nare suggestive of septic emboli.\n\nA focus of leptomeningeal/cortical enhancement involving the right frontal\nlobe may represent an additional area of infection, possibly meningitis.\n\nRight parieto-occipital subarachnoid hemorrhage of uncertain chronicity. CT\nhead is recommended."
        },
        {
            "input": "There is mild global parenchymal volume loss.  Areas of signal within the\nsubcortical and periventricular white matter on T2/FLAIR nonspecific, but\nlikely reflect the sequela of mild chronic small vessel disease.  There is no\nevidence of infarction, hemorrhage, or mass effect.  The normal flow voids\nwithin the major intracranial vessels are preserved.\n\nThere are bilateral lens implants.  The orbits are otherwise unremarkable.",
            "output": "1. No evidence of infarction or hemorrhage.\n2. Probable mild chronic small vessel disease."
        },
        {
            "input": "Incomplete exam, only diffusion images were obtained..\n\nThere is suggestion of an area of encephalomalacia in the superior left\ntemporal lobe, consistent chronic infarct, similar.  Small rim of probable\nlate subacute infarct surrounding this.\n\nSuperior to this in the left parietal corona radiata extending slightly into\nthe left posterior centrum semiovale, is a moderate zone of increased signal\non diffusion-weighted images, without definite corresponding ADC low values;\nsome of this area demonstrates high values on ADC map, consistent with T2\nshine through (for example see series 3 and 4, image 19 for both).  This could\nreflect areas of late subacute infarct.\n\nThere are numerous additional bilateral relatively small areas foci of\nhyperintense DWI signal within the cortex and subcortical white matter of the\nfrontal and parietal lobes bilaterally, some of which demonstrate\ncorresponding low signal on ADC map (for example see series 3 and 4, image\n24), compatible with small cortical or subcortical white matter bilateral\nacute infarcts.\n\nSmall focus of left cerebellar mildly hyperintense T2 high signal appears to\nhave a low signal ADC correlate (series 4 and 3, image 6), possible punctate\nacute cerebellar infarct.\n\nThere is no evidence of intracranial mass-effect. The ventricles and sulci are\nprominent, compatible with global parenchymal volume loss.",
            "output": "1. Limited examination, as above.\n2. Chronic infarct left temporal lobe.\n3. Areas of bihemispheric small subacute infarcts, left greater than right,\nand single focus in the left cerebellum.  Consider embolic source."
        },
        {
            "input": "MRI BRAIN:\nPunctate intraparenchymal cerebral foci of susceptibility on GRE likely\nrepresent old microhemorrhages.  A T2 hyperintense lesion in the right centrum\nsemiovale with a rim of FLAIR hyperintensity and a similar T2 hyperintense\nperipherally FLAIR hyperintense lesion in the left postcentral gyrus with\ncorresponding encephalomalacia on the prior CT are compatible with late\nsubacute infarcts.\n\nA small amount of nonenhancing T1 intrinsically hyperintense signal, which\ndemonstrates extensive blooming on GRE is again noted along the anterior\naspect of the pons.  No evidence of aneurysm.\n\nA punctate focus of enhancement in the left external capsule may represent a\nsmall capillary telangiectasia (series 14, image 88) or developmental venous\nanomaly.\n\nNonspecific enhancement in the deep white matter of the left temporal lobe\n(series 14, image 60, series 1400, image 59) likely represents a vascular\nmalformation.  There is no corresponding abnormal signal on additional\nsequences.\n\nAdditional subcortical, periventricular and deep white matter FLAIR\nhyperintensities are nonspecific but likely represent sequela of chronic small\nvessel ischemic disease.\n\nThe ventricles and sulci are normal in morphology.  The dural venous sinuses\nare patent.\n\nThere is a moderate mucous retention cyst in the left sphenoid sinus and a\nsmall mucous retention cyst in the left posterior ethmoid air cells. \nOtherwise, the paranasal sinuses and the mastoid air cells are clear.  The\norbits are unremarkable.\n\nMRA BRAIN:\nThe intracranial vertebral and internal carotid arteries and their major\nbranches appear normal without evidence of stenosis, occlusion, or aneurysm\nformation.\n\nMRA NECK:\nThe common, internal and external carotid arteries appear normal.  There is no\nevidence of internal carotid artery stenosis by NASCET criteria.  The origins\nof the great vessels, subclavian and vertebral arteries appear normal\nbilaterally.",
            "output": "1. Intrinsic T1 hyperintense material, which demonstrates extensive\nsusceptibility on GRE, along the anterior aspect of the pons, compatible with\nhemorrhage.  No underlying vascular malformation or mass.\n2. Right centrum semiovale and left parietal late subacute infarcts.\n3. Multiple small enhancing foci in the left external capsule and the left\ntemporal lobe likely represent vascular malformations, as detailed above.\n4. Nonspecific periventricular FLAIR hyperintense lesions likely represent\nsequela of chronic small vessel ischemic disease.\n5. Foci of susceptibility on GRE likely represent old microhemorrhages."
        },
        {
            "input": "Multiple punctate infarcts in bilateral hemispheric border zone/watershed\nareas ranging up to 15 mm in size in the right middle frontal gyrus/centrum\nsemiovale (series 5, image 24).  Smaller punctate infarcts are seen in\nbilateral parietal, right occipital, right basal ganglia and right temporal\nlobe.\n\nExtensive bihemispheric sulcal FLAIR hyperintensity is nonspecific.  No\nassociated subarachnoid signal abnormality on the other imaging sequences,\nalthough there may be slightly increased T2 hyperintense signal.  Minimally\nincreased FLAIR hyperintense signal of the left greater than right annular\ntear structures.  There may also be minimally increased T1 hyperintense signal\nwithin the sulci along the bilateral convexities on sagittal sequences with\npreservation of the CSF signal within the ventricles.\n\nMultiple small foci of blooming artifact on the gradient echo may represent\nunderlying vasculopathy secondary to hypertension or amyloid.  Chronic\ninfarcts again noted in the right centrum semiovale and left parietal lobe. \nThe pituitary appears normal.  The craniocervical junction appears.  The\nintracranial arteries demonstrate normal T2 flow voids.  Partial opacification\nof the left sphenoid sinus.  The orbits appear normal.",
            "output": "1. Multiple punctate acute infarcts in bilateral hemispheric predominantly\nborder zone/watershed territories as described above.\n2. Extensive bihemispheric sulcal FLAIR hyperintensity is nonspecific.  There\nis also minimally FLAIR hyperintense signal of the inner ear structures.  No\ndefinitive associated subarachnoid signal abnormality on the other imaging\nsequences, although there does seem to be slightly increased T2 hyperintense\nsignal.  No evidence of subarachnoid hemorrhage prior CT head done ___.  In the differential diagnosis consider meningitis, hyper oxygenation\ntherapy, sedatives (propofol) and less likely hemorrhage.  Given stage 4\nkidney disease and use of gadolinium contrast on examination of ___,\nthis could also represent excreted gadolinium contrast material.  Correlation\nwith LP may be performed if clinically indicated.\n3. Multiple small chronic microhemorrhages may represent vasculopathy\nsecondary to hypertension or amyloid.\n4. Chronic right centrum semiovale and left parietal infarcts are again noted\n5. Mild paranasal sinus disease as described above."
        },
        {
            "input": "Multiple small subacute infarcts are identified in both cerebral hemispheres\nright greater than left side.  The infarcts are seen in the periatrial region\nsubinsular and periventricular region and also in the subcortical region of\nboth cerebral hemispheres right greater than left side.  Corresponding FLAIR\nhyperintensities are identified some of which do not demonstrate restricted\ndiffusion for example in the left posterior frontal lobe (11:21) and trans\ncallosal region (11:19)..\n\nFollowing contrast administration no abnormal enhancement is identified within\nthe parenchyma or meninges.  The hyperintensities visualized within the\nconvexity sulci have decreased but mild changes persist.  The hyperintensity\nseen in the region of both cochlea on the previous study has also decreased. \nThis findings explains the hyperintensities due to retained gadolinium from\nkidney disease.",
            "output": "1. Multiple bilateral small infarcts are identified slightly less apparent\ncompared to the prior study due to evolution.\n2. Multiple FLAIR hyperintensities some of which demonstrate no restricted\ndiffusion and are likely due to late subacute to chronic infarcts.\n3. Decreased FLAIR hyperintensities at the convexity along with decreased\nhyperintensities in region of both cochlea on FLAIR images compared to the\nprior study indicates decrease in retained gadolinium in the CSF from renal\ninsufficiency.\n4. No abnormal parenchymal or meningeal enhancement is identified."
        },
        {
            "input": "There are no acute infarcts seen. There is no mass effect, midline or\nhydrocephalus.  The extensive subcortical and deep white matter\nhyperintensities with minimal periventricular hyperintensities indicating\nvelocity is changes of small vessel disease.  Hyperintensities within the pons\nalso indicate small vessel disease.  There is chronic: The left thalamus.\nProminent perivascular spaces are identified. The following gadolinium there\nis no evidence of abnormal parenchymal, vascular and meningeal enhancement\nseen.  There is mild brain atrophy.  There are no chronic micro hemorrhages.\n\nMRA of the head shows normal signal in the arteries of the anterior and\nposterior circulation. No evidence of vascular occlusion stenosis or an\naneurysm greater than 3 mm in size seen.\n\nMRA of the neck shows normal flow in the carotid and vertebral arteries\nwithout stenosis or occlusion or dissection. Arteries at the thoracic inlet\nalso appear normal.",
            "output": "Mild brain atrophy and severe changes of small vessel disease. Chronic\nthalamic lacune. No acute or abnormal enhancement. No significant\nabnormalities on MRI of the head and neck."
        },
        {
            "input": "MRI brain:  There is no evidence of infarction, hemorrhage or mass effect. The\nventricles and basilar cisterns appear normal.\n\nNonspecific T2/FLAIR signal hyperintensity within the subcortical white matter\nof the bilateral cerebral hemispheres is nonspecific though presumably on the\nbasis of sequelae of chronic small vessel ischemic disease.\n\nThe orbits, paranasal sinuses and mastoid air cells appear normal.\n\nMRA head: Evaluation of the intracranial vascular demonstrates no evidence of\nhemodynamically significant stenosis, aneurysm, or vascular malformation. A\nsmall infundibulum is noted projecting inferiorly off of the left M1 segment.\n\nMRA neck: Atheromatous plaque is seen at the origin of the right internal\ncarotid artery without significant stenosis by NASCET criteria. Atheromatous\nplaque narrows the origin of the left internal carotid artery.  There is\ncomplete loss of signal of the left internal carotid artery at its origin\nwhich precludes measurement of lumen diameter.  This signal loss indicates a\nsevere stenosis, but we cannot further assess its severity. There is normal\ncaliber of the internal carotid artery immediately distal to this area of\nstenosis which indicates patency. The vertebral arteries are codominant\nwithout evidence of significant stenosis or occlusion.",
            "output": "1. No evidence of acute intracranial hemorrhage, mass effect, or acute\nischemia.\n2. Severe stenosis at the origin of the proximal left internal carotid artery\nwith distal patency.\n3. No evidence of hemodynamically significant stenosis or aneurysm within the\nintracranial vasculature."
        },
        {
            "input": "There is no intracranial mass, mass effect, or midline shift.  The ventricles\nand sulci are age-appropriate. There is no pathologic intracranial\nenhancement. Multiple foci of T2 and FLAIR prolongation are present within the\nperiventricular, deep a and subcortical white matter. Intracranial flow voids\nare maintained. Visualized paranasal sinuses and mastoid air cells are clear.\nDeformity of the odontoid process of the C2 vertebral body may be due to\nremote trauma.",
            "output": "*No evidence for metastatic disease.\n*Numerous supratentorial white matter signal abnormalities are nonspecific,\nbut in a patient of this age may represent advanced small vessel ischemic\ndisease."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  There is generalized parenchymal volume loss evidenced by ex\nvacuo dilatation of lateral ventricles and expansion of the extra-axial CSF\nspaces.  There is extensive periventricular and deep white matter\npredominantly frontoparietal T2 FLAIR hyperintense signal intensity;\nnonspecific in appearance and could be related to severe form of chronic\nmicroangiopathy.  Also there are increased T2 STIR hyperintense signal\nintensity at bilateral thalami.  There is a pronounced involvement of the both\nexternal capsules.\n\nBoth orbits and globes are normal.  Mild mucosal thickening involving ethmoid\nair cells sphenoid sinuses.",
            "output": "1. No acute intracranial abnormality.\n2. Generalized parenchymal volume loss with extensive white matter abnormal\nsignal intensity predominantly affecting frontoparietal regions, external\ncapsules and bilateral thalami.  Appearance is nonspecific and differential\ndiagnosis includes severe form of chronic microangiopathy and\nleukoencephalopathy of different etiologies."
        },
        {
            "input": "High-resolution images through the internal auditory canals demonstrate\nunremarkable seventh and eighth cranial nerves.  No evidence of abnormal\nenhancement or mass within the internal auditory canal, cerebellopontine\nangle, or membranous labyrinth.  There is normal preserved T2 hyperintense\nsignal within the imaged cochlea and semicircular canals.  No other mass\nlesions are seen in the posterior fossa.\n\nLimited included imaging of the remainder of the brain demonstrates no\nevidence of hemorrhage, edema, masses, mass effect, midline shift or\ninfarction. The ventricles and sulci are normal in caliber and configuration.\nThere is no abnormal enhancement after contrast administration.\n\nNo osseous abnormalities are seen. The paranasal sinuses, mastoid air cells,\nand middle ear cavitiesare unremarkable.  The orbits are unremarkable. The\nvisualized portion of the principle vascular flow voids are preserved.",
            "output": "No evidence of IAC or cerebellopontine angle mass.  Unremarkable examination."
        },
        {
            "input": "MR BRAIN:\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  Intracranial vascular flow voids, including dural venous\nsinuses flow voids are preserved.  Dedicated MR venogram was not obtained.. \nFindings consistent with mild chronic small vessel ischemic changes, similar\nto prior.  Mild prominence of perivascular spaces..  Clear paranasal sinuses,\nmastoids.\n\nMRA brain:\nArtifact versus mild narrowing right M 2 segment MCA.  Otherwise, the\nintracranial vertebral and internal carotid arteries and their major branches\nappear normal without evidence of stenosis, occlusion, or aneurysm formation.",
            "output": "1. No acute intracranial findings.\n2. Essentially normal brain MRA."
        },
        {
            "input": "There is no intracranial mass, edema, pathologic leptomeningeal, parenchymal,\nor pachymeningeal enhancement. Ventricles and sulci are mildly prominent,\nindicative of age related volume loss. Mild, nonspecific periventricular FLAIR\nhyperintensities are likely a sequela of chronic small vessel ischemic\ndisease. The basal cisterns are patent.  No diffusion abnormality to suggest\nan acute infarct.  Principal intracranial vessels enhance normally. Dural\nvenous sinuses are normal without demonstrate filling defects.\n\nThe upper cervical vertebral, clival, and calvarial bone marrow signal is\nnormal. Mild mucosal thickening is noted at the base of the left maxillary\nsinus, otherwise the paranasal sinuses are clear. The orbits and periorbital\nsoft tissues are normal.  No pathologic lymph node enlargement in the\nvisualized cervical soft tissues.",
            "output": "1.  No evidence of metastatic disease within the head.\n2.  There are no pathologic leptomeningeal or pachymeningeal enhancement.\n3.  Normal bone marrow signal, and no pathologic lymph nodes identified."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, or infarction.\nThe ventricles and sulci are normal in caliber and configuration. There is no\nabnormal parenchymal, vascular or meningeal enhancement after contrast\nadministration.  Minimal changes of small vessel disease are again seen.",
            "output": "No significant abnormalities are seen. No enhancing brain lesions are\nidentified."
        },
        {
            "input": "No evidence for acute infarction, hemorrhage, midline shift, mass or mass\neffect.  The ventricles and sulci are within expected limits in size and\nconfiguration.\n\nA T2 and gradient echo hypointense 2 mm round focus the posterior left middle\ntemporal sulcus (series 5, image 10; series 7, image 10) is nonspecific and\ncould represent calcification versus vascular structure.\n\nThe major flow voids are otherwise preserved.  There is mild mucosal\nthickening of the ethmoid sinuses as well as the right maxillary sinus. \nOtherwise, the paranasal sinuses and mastoid air cells are clear the orbits\nare unremarkable.",
            "output": "1. No acute territorial infarction or hemorrhage.  No intracranial mass\nidentified.\n2. A 2 mm T2 and gradient echo hypointense rounded focus centered in the\nposterior left middle temporal sulcus is nonspecific and could represent\ncalcification from prior granulomatous disease versus vascular structure. \nThis could be definitively evaluated with CTA head.\n3. Additional findings described above."
        },
        {
            "input": "Study is moderately degraded by motion, especially on MR angiography imaging.\n\nMR BRAIN:\nNew small intraventricular hemorrhage is noted in the occipital horn left\nlateral ventricle.  (see 09:13).  New hemosiderin staining is noted along the\nleft cerebellar hemisphere (see 9:7).  New subarachnoid blood is noted along\nleft greater than right occipital and left temporal lobes.  The layering\nsubdural blood is noted in the posterior fossa (see 08:12, 09:13, 05:12). \nStable chronic punctate left frontal micro hemorrhages again noted.\n\nThere is no evidence of  edema, masses, mass effect, midline shift or acute\ninfarction.  There is prominence of the ventricles and sulci suggestive\ninvolutional changes.  Periventricular and subcortical T2 and FLAIR\nhyperintensities are noted, which may represent small vessel ischemic changes.\n\nMRA BRAIN:\nThe left vertebral artery is dominant.  The distal right V3 and proximal right\nV4 segments are not visualized on the current study.\nThe intracranial vertebral and internal carotid arteries and their major\nbranches appear normal without evidence of stenosis, occlusion, or aneurysm\nformation.",
            "output": "1. Study is moderately degraded by motion.\n2. New bilateral occipital and right temporal subarachnoid hemorrhage, small\nposterior fossa subdural blood products, and intraventricular hemorrhage\nwithin the left lateral ventricle.\n3. No evidence acute infarct.\n4. Nonvisualization of distal right V3 and proximal right V4 segments, with\nreconstitution of mid right V4 segment.  Differential considerations include\ndistal V3 and proximal V4 occlusion, artifact or distal V3 and proximal V4\nslow flow.  If clinically indicated, head CTA may be obtained for further\nevaluation.\n5. Within limits of study, no definite aneurysm identified.\n\nNOTIFICATION:  The findings were discussed by Dr. ___ with NP ___\n___ on the telephoneon ___ at 3:20 ___, 5 minutes after discovery of\nthe findings."
        },
        {
            "input": "There are multiple small areas of high diffusion signal with corresponding low\nsignal on the ADC map and subtle high signal on FLAIR distributed in the\nsubcortical white matter of the bilateral parietal lobe and in the white\nmatter adjacent to the atrium of the left lateral ventricle (4: 24,22,19,18). \nSusceptibility artifact along the anterior midline corresponds to\ncalcifications of the falx seen on CT.  There is no intra or extra-axial\nhemorrhage.  There is no mass or mass effect.  Prominence of the ventricles\nand sulci is in keeping with global atrophy.  There is mucosal thickening in\nbilateral maxillary sinuses with an air-fluid level on the right.  There is a\nmoderate amount of fluid in the ethmoid air cells.  Mucosal thickening of the\nsphenoid and frontal sinuses and partial fluid opacification of bilateral\nmastoid air cells are also noted.  The orbits are unremarkable.",
            "output": "1. Multifocal small bilateral subcortical late acute/early subacute infarcts\npredominantly distributed in the parietal lobes are suggestive of an embolic\nprocess.\n2. No hemorrhage, edema, mass, or mass effect.\n3. Fluid in the paranasal sinuses and mastoid air cells is likely related to\nintubated status.\n\nNOTIFICATION:  The findings were discussed with ___, M.D. by\n___, M.D. on the telephone on ___ at 1:22 ___, 3 minutes after\ndiscovery of the findings."
        },
        {
            "input": "MRI BRAIN:\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  A few scattered periventricular and subcortical T2/FLAIR white\nmatter hyperintensities in the bilateral frontal lobes and left parietal lobe\n(13:14) are nonspecific but likely reflect a sequela of chronic small vessel\ndisease.  Prominence of the ventricles and sulci are suggestive of age-related\ninvolutional changes.  There is no abnormal enhancement after contrast\nadministration.  The major intracranial flow voids are preserved.  There is\nmoderate mucosal thickening of the ethmoid air cells.  Mild mucosal thickening\nof the remainder the paranasal sinuses is identified.  The orbits are\nunremarkable.  Trace fluid signal is seen in bilateral mastoid tips.\n\nMRA BRAIN:\nThere is moderate attenuation of the M2, M3 and M4 segments of the right\nmiddle cerebral artery, is likely secondary to motion artifact, with component\nof atherosclerotic disease (series 100).  Narrowing of the right A1 segment\nmay be secondary to congenital hypoplasia.  Otherwise, the A2 segments of the\nanterior cerebral arteries, left middle cerebral artery, and posterior\ncerebral arteries (PCA) are without evidence of stenosis or occlusion.  Fetal\ntype PCA is incidentally noted on the left, a normal variant.  Focal\nprominence of the left ophthalmic artery origin is felt to be most likely a\ntorturous turn of the vessel.  The intracranial vertebral and basilar artery\nare within normal limits.\n\nMRA NECK:\nThere is mild atherosclerotic narrowing of the left carotid bifurcation. \nOtherwise, the common, right internal and external carotid arteries appear\nnormal.  There is no evidence of internal carotid artery stenosis by NASCET\ncriteria.  The origins of the great vessels, subclavian and vertebral arteries\nappear normal bilaterally.",
            "output": "1. No acute intracranial abnormality identified.  Specifically, no evidence of\nan acute infarction.\n2. Atrophy and probable chronic small vessel disease.\n3. Moderate narrowing of the right anterior and middle cerebral artery\nbranches, may be secondary to a combination of motion artifact and\natherosclerotic disease.\n4. Mild bulbous appearance at the origin of the left ophthalmic artery, felt\nto be secondary to torturous turn of the vessel.  This could be followed up\nwith MRA to document stability or definitively assessed with CTA.\n5. There is no internal carotid artery stenosis by NASCET criteria.  The\nvertebral arteries are patent, without evidence of stenosis."
        },
        {
            "input": "Please note the study is mildly degraded by motion.\n\nThere is a punctate focus of slow diffusion in the right middle cerebellar\npeduncle.  There is no evidence of hemorrhage, edema, masses, mass effect, or\nmidline shift.  There is prominence of the ventricles and sulci suggestive\ninvolutional changes.  There are multiple stable periventricular subcortical\nT2/FLAIR hyperintensities, greatest in the right periventricular white matter.\nThere is no abnormal enhancement after contrast administration.  A right\nfrontal developmental venous anomaly is seen.\n\nThe major vascular flow voids are preserved.  The orbits and mastoid air cells\nare normal.  Minimal mucosal thickening in the ethmoid sinuses seen.",
            "output": "1. Grossly stable white matter signal abnormality, which is a nonspecific\nfinding and may be secondary to chronic microvascular ischemic changes,\nmigraines, demyelination, or chronic infection/inflammation.\n2. Punctate focus of low diffusion in the middle right cerebellar peduncle,\nmost consistent with an acute infarction.\n3. No evidence for intracranial metastatic disease."
        },
        {
            "input": "MR BRAIN:\nThere is no evidence of acute hemorrhage,edema,masses,mass effect, midline\nshiftor acute infarction.  A prominent T2/FLAIR hyperintensity in the right\nfrontal corona radiata extending to and possibly involving some right frontal\ncortex may relate to old ischemic insult.  Superimposed mild pontine,\nsubcortical and periventricular T2/FLAIR white matter hyperintensities are\nnonspecific but can be seen in setting of chronic small vessel disease.  The\nventricles and sulci are normal in caliber and configuration.\n\nThe major intracranial vascular flow voids are maintained.  The orbits,\nparanasal sinuses and mastoid air cells are normal.\n\nMRA brain: The intracranial vertebral and internal carotid arteries and their\nmajor branches appear normal without evidence of stenosis, occlusion, or\naneurysm formation.",
            "output": "1. No acute intracranial abnormality.\n2. Normal MRA head.\n3. Evidence of a possible small old right frontal lobe ischemic insult.\n4. Mild nonspecific T2/FLAIR white matter hyperintensities can be seen in the\nsetting of chronic small vessel disease."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.\n\nMajor intracranial vessels are patent.  Orbits are unremarkable.  Scattered\nfluid throughout the mastoids bilaterally, nonspecific.",
            "output": "1. Scattered fluid throughout the mastoids bilaterally.\n2. Otherwise normal study."
        },
        {
            "input": "Small early subacute infarct right centrum semiovale is larger or new since\nprior MRI ___.  Other previously seen small right hemispheric\ninfarcts have evolved and are in late subacute stage..  Most of these are in\nthe watershed area..  Atrophy of cerebellar vermis.\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift.\nMild-to-moderate chronic small vessel ischemic changes..  Preserved vascular\nflow voids.  Clear mastoids, paranasal sinuses.",
            "output": "1. Small right centrum semiovale early subacute infarct, new or larger since\n___.\n2. Small right hemispheric watershed distribution late subacute infarcts,\nevolved since prior.\n3. No hemorrhage."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, or infarction.\nThe ventricles and sulci are normal in caliber and configuration.  Major\nintravascular flow voids are preserved.\n\nThe paranasal sinuses and mastoid air cells appear clear. The orbits are\nnormal.",
            "output": "Normal study."
        },
        {
            "input": "No diffusion abnormalities are detected to indicate acute or subacute ischemic\nchanges.  Again congenital abnormalities are re- demonstrated consistent with\ndysgenesis of the corpus callosum and septum pellucidum, the ventricles are\nprominent with no evidence of transependymal migration of CSF. The sulci are\ngrossly unremarkable, the major vascular flow voids are present and\ndemonstrate normal distribution.  The orbits are unremarkable, the paranasal\nsinuses and mastoid air cells are clear.",
            "output": "1.  There is no evidence of acute intracranial process or diffusion\nabnormalities to indicate acute or subacute ischemic changes.\n\n2.  Dysgenesis of the corpus callosum and absence of the septum pellucidum as\ndescribed above, associated with prominent lateral ventricles, likely\ncongenital in nature."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  No parenchymal signal abnormality.  The ventricles and sulci\nare normal in caliber and configuration.\n\nThere is nonspecific fluid in the left greater than right mastoid air cells. \nTrace anterior ethmoid air cell mucosal thickening is noted.  The orbits are\nunremarkable.\n\nProminent adenoidal tissue noted in the nasopharynx as seen on exams dating\nback to ___.  Numerous not pathologically enlarged lymph nodes noted in the\nneck including an 8 mm right lateral retropharyngeal node.",
            "output": "1. No acute intracranial process.\n2. Nonspecific fluid in the left greater than right mastoid air cells."
        },
        {
            "input": "There is a large area of restricted diffusion in the right MCA territory\nincluding the basal ganglia, scratch insula, posterior frontal lobe, superior\nparietal lobe, and temporal lobes, with corresponding increased FLAIR\nintensity, consistent with an acute to early subacute infarction in the right\nMCA distribution (3, 4; 17).  There is associated partial effacement of the\nright lateral ventricle without shift of midline structures.  The third\nventricle is relatively small; its baseline size is not known.  Left lateral\nventricle is normal in size.  Basal cisterns are preserved.  There is no\nevidence for associated blood products.\n\nThere are multiple foci of subcortical, deep, and periventricular white matter\nhyperintensity on T2 and FLAIR, which are nonspecific and likely represent\nchronic small vessel ischemic disease.  There is susceptibility artifact\nrelated to the course bilateral tentorial calcifications seen on the preceding\nCT (series 11, images ___.\n\nMajor vascular flow voids appear grossly preserved. Previously seen dilated\nright superior ophthalmic vein is not well visualized on this study.\n\nThere is moderate opacification of bilateral anterior ethmoid air cells and\nmild mucosal thickening in the bilateral posterior ethmoid air cells, as well\nas in the right greater than left maxillary sinuses.  There is trace fluid\nsignal in the left greater than right mastoid air cells, likely secondary to\nprolonged supine positioning in the inpatient setting.",
            "output": "1. Large acute to early subacute infarct in the right MCA territory with\npartial effacement of the right lateral ventricle, but no shift of midline\nstructures.  No evidence for associated blood products.\n2. T2/FLAIR signal abnormalities in the supratentorial white matter are\nnonspecific but likely sequela of chronic small vessel ischemic disease in\nthis age group..\n3. Paranasal sinus disease.\n\nNOTIFICATION:  The findings were discussed with ___, medical student\nworking with ___, M.D. by ___, M.D. on the telephone on ___\nat 9:21 am, 5 minutes after discovery of the findings."
        },
        {
            "input": "MRA BRAIN:\nThe intracranial vertebral and internal carotid arteries and their major\nbranches appear normal without evidence of stenosis, occlusion, or aneurysm\nformation.  The posterior circulation is also unremarkable.\n\nLimited evaluation of the brain on postcontrast MP-RAGE demonstrates no\nabnormal enhancement or intracranial mass lesions.  Mild mucosal thickening of\nthe paranasal sinuses, most predominantly noted in the ethmoid air cells as\nwell as small mucous retention cyst in the left greater than right mastoid air\ncells.\n\nMRV BRAIN: The superior sagittal sinus, bilateral transverse sinuses, internal\ncerebral veins, ___ and ___ sinus are patent.  The visualized\nportions of the internal jugular veins are patent.\n\nMRA NECK:\nIncidental note is made of an aberrant right subclavian artery.  The right\nvertebral artery arises from the brachiocephalic artery.  The bilateral common\ncarotid arteries are unremarkable.  The bilateral carotid bifurcations and\nright internal carotid artery is unremarkable.  There is no stenosis of the\ncervical internal carotid artery by NASCET criteria.\n\nEccentric 1.7 cm long segment of T1 hyperintense mural signal of the distal\nleft internal carotid artery extending to the very proximal petrous segment is\ncompatible with dissection with mild caliber narrowing without occlusion or\nhigh-grade stenosis.\n\nThe left vertebral artery is dominant, a normal variant.  Otherwise, the\nvertebral arteries are unremarkable.",
            "output": "1. Eccentric 1.7 cm long segment mural thrombus compatible with dissection\nalong the distal left cervical internal carotid artery extending to the very\nproximal petrous segment, resulting in mild caliber narrowing without\nhigh-grade stenosis or occlusion.\n2. Incidental note is made of an aberrant right subclavian artery with the\norigin of the right vertebral artery from the right brachiocephalic artery. \nOtherwise, the remainder of the MRA neck is within expected limits.\n3. Unremarkable MRA of the head.\n4. Unremarkable MRV of the head.\n5. Additional findings described above."
        },
        {
            "input": "There is no acute infarction, intracranial hemorrhage, extracerebral fluid\ncollection, midline shift or mass effect.  Ventricles and extra-axial spaces\nare normal in size.  Flow voids are maintained. Suprasellar and craniocervical\nregions are unremarkable.  No acute infarcts are seen.  No significant\nsubcortical white matter ischemic disease is seen.  Visualized paranasal\nsinuses are clear.",
            "output": "No significant abnormalities are seen on MRI of the brain without gadolinium."
        },
        {
            "input": "MRV:  The left transverse sinus appears hypoplastic, but remains patent. \nOtherwise, there is normal flow signal demonstrated within the superior\nsagittal sinus, straight sinus, right transverse sinus, and sigmoid sinuses.\nThe jugular bulbs and proximal jugular veins are patent. Evaluation of the\ndeep venous systems reveals normal flow signal in the internal cerebral veins.\nThe vein ___ is also unremarkable.",
            "output": "1. Patency of the dural venous sinuses without evidence of stenosis or\nocclusion."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  There is some FLAIR signal abnormality adjacent to the body\nand occipital horn of the right lateral ventricle, with associated volume\nloss, which may represent sequela of a prior injury such as traumatic,\nischemic, or infectious (series 7:  Image 15).\n\nThe ventricles and sulci are normal in caliber and configuration.  The major\nintracranial flow voids are preserved.  The dural venous sinuses are patent. \nThere is no abnormal enhancement after contrast administration.\n\nMild mucosal thickening is noted in the bilateral ethmoid air cells.  The\nremaining paranasal sinuses and mastoid air cells are clear.  The orbits are\nunremarkable.",
            "output": "1. FLAIR signal abnormality is noted in the white matter adjacent to the body\nand occipital horn of the right lateral ventricle, with associated volume\nloss, likely sequela of a prior injury such as traumatic, ischemic, or\ninfectious."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.\n\nThe major vascular flow voids are preserved.  The orbits, paranasal sinuses\nand mastoids are normal.",
            "output": "1. Normal brain MRI.  No acute infarction."
        },
        {
            "input": "There is no acute infarction, intracranial hemorrhage, extracerebral fluid\ncollection, midline shift or mass effect.  No diffusion abnormalities are\ndetected. The cerebral volume is appropriate for the patient's stated age. \nThere is mild T2/FLAIR signal hyperintensity in the periventricular white\nmatter which is nonspecific but likely secondary to chronic small vessel\nischemic the.  The major vascular flow voids are maintained.  There are no\nenhancing parenchymal lesions.  The orbits are unremarkable.  There is mucosal\nthickening within the paranasal sinuses.  There is mild mucosal thickening\nwithin the mastoid air cells.\n\nProminent adenoids and bilateral enlarged cervical lymph nodes are noted.",
            "output": "No evidence of acute or subacute intracranial process\n\nProminent adenoids and bilateral cervical lymphadenopathy."
        },
        {
            "input": "There is gyriform slowed diffusion (series 502 images ___ and T2/FLAIR\nhyperintensity within the medial an anterior left frontal lobe cortex (series\n6, images ___, new from prior MRI on ___. There is no\nassociated contrast enhancement.\n\nThere is slowed diffusion, without corresponding signal abnormality on the ADC\nmap, within the anterior body of the left caudate, new from prior MRI (series\n52, image 17). There is corresponding increased T2/FLAIR signal within the\nanterior body of the left caudate that is new from prior MRI (series 6 image\n14). There is no associated contrast enhancement.\n\nThere are multiple unchanged foci of T2/FLAIR hyperintensity in the corona\nradiata, basal ganglia, and pons, likely sequela of chronic small vessel\nischemic disease, unchanged from MRI on ___. The ventricles and\nsulci are normal in size.\n\nMajor intravascular flow voids are preserved. There is normal enhancement of\nthe major intracranial arteries and dural venous sinuses following contrast\nadministration.\n\nThere is moderate mucosal thickening of the paranasal sinuses, increased in\nthe frontal sinuses since prior MRI.",
            "output": "1. Slowed diffusion and T2 hyperintensity within the anterior and medial left\nfrontal cortex, as well as indeterminate diffusion abnormality in T2\nhyperintensity in the left anterior caudate body, both new compared to ___, without associated enhancement. The left frontal lobe cortical\nsignal abnormality is compatible with a postictal state. However, the left\ncaudate signal abnormality is not typical for a postictal state, and viral or\nprion infection should be  considered.  Subacute infarction in the caudate may\nhave this appearance, but gyriform distribution in the left frontal lobe\nwithout subcortical white matter involvement is atypical for embolic\ninfarction.\n2.  Mucosal thickening of the paranasal sinuses, increased in the frontal\nsinuses compared to prior MRI.\n\nNOTIFICATION:  Findings were discussed by Dr. ___ of radiology with\nDr. ___ at 13:02 on ___."
        },
        {
            "input": "There is faintly increased signal in the anterior body of the left caudate on\ndiffusion tracer images (302:16) without an associated abnormality on the ADC\nmap, decreased in intensity compared to ___.  On FLAIR and T2\nweighted images, abnormal high signal now extends beyond the left caudate and\nincludes the anterior limb of the internal capsule and a portion of the left\nlentiform nucleus.  There is no associated diffusion abnormality in these new\nareas of high T2 signal. There is no evidence for associated blood products on\ngradient echo images.\n\nPreviously noted high T2 signal and high signal on diffusion-weighted\nsequences in the left frontal cortex has resolved.\n\nOther scattered small foci of high signal on T2 weighted and FLAIR images in\nthe corona radiata, basal ganglia and the pons  are unchanged, and likely\nsequela of chronic small vessel ischemic disease. Major intravascular flow\nvoids are preserved.\n\nThere is mild mucosal thickening in the maxillary and ethmoid sinuses.",
            "output": "1. Previously noted area of high T2 signal in the left caudate heads expanded,\nnow also involving the anterior internal capsule and a portion of the left\nlentiform nucleus. There is no new associated diffusion abnormality.\nPreviously noted high signal on diffusion tracer images and a portion of the\nleft caudate has decreased in extent and intensity, and there is no correlate\non the ADC map. Differential considerations include malignancy, particular\nlymph with malignancy, and infection (such as viral or fungal).  Subacute\ninfarction is felt to be less likely given the time course.  Contrast enhanced\nMRI is recommended for further assessment.\n2. No residual signal abnormality in the left frontal cortex."
        },
        {
            "input": "There is no significant change in comparison to the noncontrast MRI brain from\none day prior. There is faintly increased signal in the anterior body of the\nleft caudate on diffusion trace images (302:16) without an associated\nabnormality on the ADC map, decreased in intensity compared to ___, but unchanged from ___. On FLAIR and T2 weighted images,\nabnormal high signal extends beyond the left caudate and includes the anterior\nlimb of the internal capsule and a portion of the left lentiform nucleus,\nunchanged from ___, but new since ___, exerting mild\nmass effect on the frontal horn of the left lateral ventricle. There is no\nassociated diffusion abnormality in these areas of high T2 signal. There is no\nevidence for associated blood products on gradient echo images.  There is no\nassociated enhancement after contrast administration.\n\nOther scattered small foci of high signal on T2 weighted and FLAIR images in\nthe corona radiata, basal ganglia and the pons are unchanged. Major\nintravascular flow voids are preserved.\n\nThere is mild mucosal thickening in the maxillary and ethmoid sinuses as\nbefore.",
            "output": "Abnormal FLAIR and T2 signal in the left basal ganglia without enhancement has\nincreased in size compared to ___ and demonstrates mild mass\neffect on the anterior horn of the left lateral ventricle. These findings may\nrepresent a low-grade neoplasm."
        },
        {
            "input": "Left basal ganglia hyperintense lesion measuring hyperintensity without\nenhancement on post gadolinium images is again identified. There is mass\neffect on the anterior horn of left lateral ventricle as before.  Focus of\nincreased signal within the left side of the pons could be  due to small\nvessel disease or wallerian degeneration.",
            "output": "Left caudate head lesion again identified for surgical planning."
        },
        {
            "input": "The patient is status post a left trans-frontal craniotomy with biopsy track\nextending to the left caudate head. There is residual gradient echo\nsusceptibility blooming artifact at the level of the left caudate head\ncompatible with hemorrhage presumably from the recent biopsy.\n\nWhen compared to the prior exam, there is decreased size and FLAIR\nhyperintense signal of the left caudate.  There is resolution of near-complete\neffacement of the anterior horn and anterior body of the left lateral\nventricle. As on prior exam, there is no significant postcontrast enhancement.\n\nThere is unchanged bilateral periventricular white matter T2/FLAIR\nhyperintensities.\n\nThere is no evidence of acute infarct. Sulci, ventricles cisterns are within\nexpected limits for the patient's age. The dural venous sinuses are patent.\nThe major intracranial flow voids are preserved. Mild mucosal thickening of\nthe paranasal sinuses including a small mucous retention cyst in right\nmaxillary sinus is identified. The orbits are unremarkable. The mastoid air\ncells are clear.",
            "output": "1. The patient is status post a left trans-frontal craniotomy with biopsy\ntrack extending to the left caudate head with new focus of presumed post\nbiopsy hemorrhage.\n2. Compared to the prior exam there is interval decrease in size of the left\ncaudate as well as surrounding FLAIR hyperintense edema pattern with\nresolution of left lateral ventricle effacement.\n3. As before, the lesion does not demonstrate significant postcontrast\nenhancement.\n4. No new lesions are identified.\n\nNOTIFICATION:  The findings were discussed by Dr. ___ with Dr.\n___ on the telephone on ___ at 1 pm, at the time of discovery\nof the findings."
        },
        {
            "input": "There is continued decrease in the FLAIR hyperintense signal in the left basal\nganglia compared to the recent studies of ___ and ___- series\n7, image 13.\nNo significant abnormal enhancement noted.\nBiopsy tract is noted with small foci of mineralization.\nFLAIR hyperintense foci noted in the periventricular and subcortical white\nmatter, frontal more than the parietal lobes and in the sub lentiform location\nand in the pons are grossly similar to the prior study; small foci in the left\nside of the pons are slightly more conspicuous\nNo new foci of abnormal enhancement are noted.\nNo acute infarct or mass effect or suspicious focus of intracranial hemorrhage\nor hydrocephalus. Dominant right vertebral artery and diminutive left\nvertebral artery.\nSmall retention cyst in the right maxillary sinus.",
            "output": "Continued decrease in the FLAIR hyperintense signal in the left basal ganglia,\ncompared to the recent studies  of ___ and ___. .\nNo abnormal enhancement or new lesions.  Other details as above.\nFurther workup or followup as needed."
        },
        {
            "input": "In comparison to ___ study there is interval decrease in FLAIR\nhyperintense signal abnormality in the left basal ganglia (07:12). Along the\nleft frontal region again seen is biopsy tract. No significant change in FLAIR\nhyperintense foci within the periventricular, subcortical, deep white matter\nand left side of pons most consistent with small vessel ischemic disease. \nStable GRE susceptibility within the left caudate is consistent with prior\nhemorrhage (06:13).\n\nThere is no evidence of new hemorrhage, edema, masses, mass effect, or\ninfarction. The ventricles and sulci are normal in caliber and configuration.\nThere is no abnormal enhancement after contrast administration.  A stable 1.1\ncm mucous retention cyst is again seen in the right maxillary sinus. On T2\nweighted imaging vascular flow voids are preserved.",
            "output": "1.  Interval decrease in FLAIR hyperintense signal on the left basal ganglia\nin comparison to ___ study.\n2.  No abnormal enhancement or new lesions.\n3.  Old blood products within the left caudate."
        },
        {
            "input": "There is been a left frontal stereotactic biopsy.  FLAIR signal in the left\ncorona radiata, external capsule, and left mid pons are unchanged from prior\nMRI on ___.  Focal encephalomalacia and blood products within the\nleft caudate, along the biopsy tract, are unchanged.  There is no abnormal\nenhancement on postcontrast imaging.  Additional areas of scattered FLAIR\nsignal in the right corona radiata and external capsule are also unchanged. \nVentricles, sulci, and cisterns are age-appropriate.  Major intravascular flow\nvoids are preserved.  There is normal enhancement of the major intracranial\narteries and dural venous sinuses following contrast administration.\n\nMarrow signal is within normal limits.  There is a mucous retention cyst in\nthe right maxillary sinus.  The paranasal sinuses and mastoid air cells\notherwise appear clear.  The orbits are normal.",
            "output": "Stable post biopsy changes and FLAIR signal in the left basal ganglia,\nexternal capsule, and corona radiata compared to prior MRI from ___.\nNo abnormal enhancement.  No evidence of progressive disease."
        },
        {
            "input": "There changes of a stereotactic biopsy with a left frontal oral and focal\nblood products at the left anterior caudate nucleus consistent with biopsy\nsite.  There is FLAIR signal hyperintensity involving the anterior left corona\nradiata, left external capsule, left caudate, and left putaminal.  There is\nadditional FLAIR signal hyperintensity at the right anterior external and\ninternal capsules in addition to scattered periventricular and central pontine\nlesions, which is relatively unchanged.  There is no evidence acute infarct,\nnew hemorrhage, or mass effect.  There is no abnormal postcontrast\nenhancement.  The ventricles extra-axial spaces are unremarkable.  The\nvasculature is patent.\n\nThere is significant mucosal thickening with air-fluid levels within the\nbilateral maxillary sinuses.  There is bilateral frontal and ethmoid sinus\nmucosal thickening.  The mastoid air cells are clear.  The soft tissues are\nunremarkable.  The orbits are unremarkable.",
            "output": "1. Worsening paranasal sinus disease, as described, with marked mucosal\nthickening and air-fluid levels within the bilateral maxillary sinuses which\nmay be seen with acute sinusitis.\n2. Stable changes following a left-sided stereotactic biopsy.\n3. Stable FLAIR signal hyperintense lesions, as described."
        },
        {
            "input": "A left frontal craniotomy defect is seen.  There is minimal susceptibility in\nthe left caudate head, along the biopsy tract.  Periventricular and\nsubcortical T2 and FLAIR hyperintensities are noted.  There is grossly stable\nconfluent FLAIR hyperintense signal in the left frontal corona radiata.  There\nis no evidence of hemorrhage, masses, mass effect, midline shift or\ninfarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is a focus of contrast enhancement just posterior to\nMeckel's cave which appears to align with the course of the petrosal vein and\nnot definitively associated with the trigeminal nerve.  Otherwise, there is no\nabnormal enhancement after contrast administration.\n\nLayering fluid is noted in the bilateral maxillary and right sphenoid sinuses\nwith mucosal enhancement.  There is ethmoid sinus mucosal thickening.  The\norbits are unremarkable.  The mastoid air cells are clear.  Incidental note is\nmade of a 5 mm Tornwaldt cyst versus mucous retention cyst.",
            "output": "1. Stable abnormal signal in the left frontal corona radiata and scattered\nwithin the white matter, with no abnormal contrast enhancement.\n2. Sinus disease.\n3. There is a focus of more prominent postcontrast enhancement posterior to\nthe left Meckel's cave, most compatible with the course of the superior\npetrosal vein.  However given the patient's clinical history, close attention\non follow up examination is recommended.\n4. Otherwise, no abnormal cranial nerve signal or enhancement."
        },
        {
            "input": "Redemonstrated is susceptibility within the cerebral hemispheres and\ncerebellum compatible with old blood products related to the patient's history\nof septic emboli.  There is evidence of an old small lacunar infarct involving\nthe body of the right caudate nucleus where there is subtle susceptibility\nlikely representing old blood products.  There are a few small old bilateral\ncerebellar infarcts.  No evidence for new septic emboli.  There is no evidence\nof new hemorrhage, edema, masses, mass effect, midline shift or acute\ninfarction.  The ventricles and sulci are normal in caliber and configuration.\nThere is no abnormal enhancement after contrast administration.\n\nMild scattered superimposed subcortical and periventricular white matter\nT2/FLAIR hyperintensities are nonspecific but compatible with small vessel\ndisease.\n\n The major intracranial vascular flow voids are maintained.  The dural venous\nsinuses are patent.  There is mild mucosal thickening of the ethmoid air cells\nand maxillary sinuses.  Otherwise, the paranasal sinuses, mastoid air cells\nand orbits are within expected limits.",
            "output": "1. No acute intracranial abnormality on contrast enhanced MRI brain.  No acute\ninfarct or new hemorrhage.\n2. Sequela of multiple old supra tentorial and infratentorial septic emboli.\n3. Mild white matter small vessel disease.\n4. Additional findings described above."
        },
        {
            "input": "Motion artifact limits evaluation.  Right M1 and proximal right M2 segments\nremain smaller than the left.  Other major intracranial arteries appear patent\nwithout evidence for high-grade stenosis but evaluation for subtle stenosis is\nlimited.  There is artifact from the coil pack in the treated right M2\naneurysm.  There is 1.5 mm round focus of apparent flow at the aneurysm neck,\nimage 2:93.",
            "output": "1. Motion limited exam.\n2. 1.5 mm round focus of apparent flow at the neck of the coiled right M2\naneurysm.\n3. Right M1 and proximal right M2 segments remains smaller than the left."
        },
        {
            "input": "MRI HEAD:\nThere is a large area of right MCA territory chronic infarct.  The remaining\nsubjacent white matter demonstrates FLAIR hyperintensity likely reflecting\ngliosis.  This is new since prior MRI of ___.\n\nMultiple foci of chronic microhemorrhage and small foci of chronic parenchymal\nhemorrhage are noted, including new foci in the right cerebellum (14:7), more\nconspicuous in the right corona radiata (14:15), more conspicuous in the left\nfrontal lobe (14:18 and 19), unchanged in the right occipital lobe (14:15) and\nright frontoparietal region near the vertex (___).  Small areas of chronic\nsuperficial siderosis.\n\nThere is ex vacuo dilatation of the right lateral ventricle.  Background\nventricular and sulcal caliber is consistent with mild global parenchymal\nvolume loss.\n\nSlight FLAIR hyperintense signal in the left frontal lobe (13:18) is more\nconspicuous than on prior but was present in ___, possibly sequelae\nof prior hemorrhage in this area, corresponding to chronic products seen on\nGRE.\n\nNo evidence of acute infarction or hemorrhage, new parenchymal edema, mass\neffect, or extra-axial collection.  Small chronic cerebellar infarcts.  Small\nchronic infarct left middle frontal gyrus.\n\n The visualized paranasal sinuses and mastoids appear clear.\n\n The globes and orbits are unremarkable.\n\n Major intracranial vascular flow voids are preserved.\n\n\nMRA BRAIN:\nLeft dominant vertebral artery, a normal variant.  The right vertebral artery\nis diminutive after the origin of the right posterior inferior cerebral\nartery, very distal aspect not well visualized.  Left vertebral artery widely\npatent.  There is fetal-type configuration bilateral posterior cerebral\narteries with concomitantly diminutive vertebrobasilar system.  Posterior\ncommunicating arteries are widely patent.  2 mm infundibulum, origin of the\nright posterior communicating artery.  Right P1 is diminutive but patent. \nLeft P1 is not well seen, either diminutive or absent.  The P2 and more distal\nbilateral posterior cerebral arteries are patent with normal distal runoff.\n\nSignal void denoting coil pack from previously treated right MCA bifurcation\naneurysm is unchanged.  Minimal flow at the neck.  No evidence of\nrecanalization or residual flow within aneurysm.  The mid and distal right M1\nMCA remains smoothly diminutive in caliber, unchanged.  Distal to the coil\npack, there is unchanged preserved but diminished right MCA territory distal\nrunoff.\n\nBilateral anterior cerebral, left middle cerebral arteries are patent with\nnormal distal runoff.\n\nNo new aneurysm, stenosis, or occlusion.\n\nMRA NECK:\nShort-segment of the horizontal right V3 vertebral artery at the level of C1-2\nis not well visualized, possibly due to in-plane flow on 2D time-of-flight\nimages, as normal flow-related enhancement is seen both proximal and distal to\nthis.  Otherwise, the extracranial vertebral and carotid arteries are widely\npatent throughout their course in the neck.  No ICA luminal narrowing by\nNASCET criteria.",
            "output": "1. No acute intracranial findings.\n2. Chronic large right MCA distribution infarct.  Small chronic cerebellar\ninfarcts.  Small chronic infarct left middle frontal gyrus.\n3. Findings consistent with amyloid angiopathy.\n4. Minimal flow of the treated aneurysm neck, no flow within aneurysm,\nsimilar.\n5. Normal neck MRA."
        },
        {
            "input": "The previously seen multiple enhancing lesions have considerably decreased in\nsize. Surrounding edema has also decreased. There are mild FLAIR signal\nabnormality seen in both frontal lobes lesions and chronic blood products are\nidentified in previously noted lesions. No definite new areas of brain edema\nenhancement seen.  There are no acute infarcts are identified. There is no\nmidline shift or hydrocephalus.",
            "output": "Considerable resolution of previously seen enhancing lesion and surrounding\nedema. No definite areas of new enhancement seen. Mild enhancement is still\nseen surrounding both frontal lobe lesions but there is considerable decrease\nin enhancement in these areas. No new areas of enhancement or brain edema\nseen. Chronic blood products at the site of previous lesions again identified."
        },
        {
            "input": "MR BRAIN: Areas of susceptibility artifact within the cerebral hemispheres and\ncerebellum are consistent with chronic blood products related to the given\nclinical history of septic emboli. There is a small focus of susceptibility\nartifact within the right inferior parietal lobule (series 8, image 15),\nwithout associated signal abnormality on T2/FLAIR.  No slow diffusion is\nidentified to suggest infarct or abscess.  There is no mass effect or midline\nshift.\n\nAdditional areas of white matter signal abnormality within the subcortical and\nperiventricular white matter of the bilateral cerebral hemispheres is\nnonspecific and similar to the prior exam.\n\nMRA brain: The exam is moderately degraded due to motion artifact. The\nintracranial vertebral and internal carotid arteries and their major branches\nappear normal without evidence of stenosis, occlusion, or aneurysm formation.\nThe left posterior cerebral artery is derived from a large left posterior\ncommunicating artery, a normal variant.  The left vertebral artery is\ndominant.",
            "output": "1.  Interval development of a small focus susceptibility artifact within the\nright inferior parietal lobule from the most recent MR head exam dated ___.  Given the lack of associated vasogenic edema, this likely reflects \nchronic microhemorrhage.  No findings to suggest acute septic emboli, infarct,\nor intracranial hemorrhage.\n2.  Moderately degraded MRA due to motion artifact.  Within this confine, no \naneurysm greater than 3 mm is identified."
        },
        {
            "input": "Study is severely degraded by motion.  Within the confines of this study:\n\nAgain seen is a right frontal approach ventriculostomy shunt catheter\nterminating within the left lateral ventricle.  There is redemonstration of\nintraventricular hemorrhage within body of the left lateral ventricle and\nlayering within the atria of bilateral lateral ventricles.  There is\nintraventricular pneumocephalus within the frontal horn of the right lateral\nventricle.\n\nThe ventricles appear slightly decreased in size, which may be related to\ntechnical differences.  Grossly stable left lateral hemisphere convexity and\nleft medial frontoparietal interhemispheric subdural hematomas are again\nnoted.  Right temporal convexity subdural hematoma is also grossly unchanged. \nThere is no definite evidence of acute infarction.\n\nThere is mild right maxillary sinus mucosal thickening.  The bilateral mastoid\nair cells appear clear.  Patient is status post bilateral lens replacement.",
            "output": "1. Study is severely degraded by motion.\n2. No definite evidence of acute infarct.\n3. Intraventricular hemorrhage within lateral ventricles, not significantly\nchanged.\n4. Grossly stable bilateral hemisphere and interhemispheric subdural\nhemorrhages, as described.\n5. Right frontal ventriculostomy catheter with slight interval decrease in\nsize of lateral ventricles.\n6. Paranasal sinus disease , as described."
        },
        {
            "input": "There is a moderate zone of late early subacute infarction within the right\nposterior parietal lobe near the vertex, extending into the temporal\noperculum, posterior right insula, inferior parietal lobule, posterosuperior\nmargin of the right temporal lobe.\nAreas of susceptibility artifact are seen within this infarct, predominantly\nwithin cortex, compatible with petechial microhemorrhage, no evidence of\nparenchymal hematoma.  There is no evidence of parenchymal hematoma on CT from\nyesterday.  1 small area is slightly globular on gradient images, follow-up\nhead CT within 24 hours recommended to exclude development of parenchymal\nhematoma.\nChronic blood products are seen overlying right vertex, about falx cerebri,\nsimilar to MRI ___.\n\nAn additional small focus of restricted diffusion in the right occipital lobe\nis noted, likely representing a second site of early subacute infarct.  No\nevidence of associated hemorrhage within this infarct.\n\nThere are 2 right frontal burr hole is identified, with microhemorrhage\nsurrounding a prior site of external ventricular drain placement.  A more\nrecent right frontal approach external ventricular drain catheter remains in\nplace, unchanged in location from the prior examination.\n\nThe ventricles and sulci are moderately enlarged, but unchanged from the\nprevious exam.  Periventricular and subcortical white matter FLAIR\nhyperintensities are noted, a nonspecific finding that most likely represents\nthe sequelae of chronic small vessel ischemic disease.  Major intravascular\nflow voids are preserved.  Trace bilateral linear dural thickening, improved\nsince prior.\n\nA mucous retention cyst is seen in the right maxillary sinus.  Scattered\nethmoid air cell mucosal thickening is noted.  The remainder of the visualized\nparanasal sinuses, middle ear cavities, and mastoid air cells are well aerated\nand clear.  The patient is status post bilateral lens resections.",
            "output": "1. Large area of early subacute right MCA infarct, with areas of cortical\nmicrohemorrhage.  Follow-up head CT within 24 hours recommended to document\nstability exclude development of parenchymal hemorrhage.\n2. Additional small right occipital lobe early subacute infarct.\n3. Right frontal approach EVD, with stable moderate ventriculomegaly.\n\nRECOMMENDATION(S):  Head CT without contrast within 24 hours."
        },
        {
            "input": "There is laminar necrosis in the left occipital lobe with chronic micro\nhemorrhages indicating a chronic left posterior cerebral artery infarct. In\nthe left medial temporal lobe there is increased signal on diffusion images.\nFollowing gadolinium administration there is diffuse enhancement identified in\nthe medial left temporal lobe but also some gyriform enhancement seen in the\nleft occipital lobe. The findings are indicative of a subacute infarct with a\nmore chronic component in the occipital region. The previously seen hyperdense\narea could reflect blood products but not clearly visualized on the current\nstudy. There is a chronic right frontal lobe cortical infarct seen. Mild to\nmoderate small vessel disease seen. No other areas of abnormal enhancement\nseen.\n\nMRA of the neck shows mild atherosclerotic disease at both carotid\nbifurcations. There is no vascular occlusion or high-grade stenosis seen.\n\nMRA of the head shows nonvisualization of both posterior cerebral arteries\nbeyond the perimesencephalic segment. This may be due to intrinsic disease or\ndue to technical factors.",
            "output": "Number none necrosis and subacute/chronic infarct in the left posterior\ncerebral artery territory with subacute component anteriorly and a chronic\ncomponent posteriorly. MRA shows no definite vascular occlusion in the head or\nneck."
        },
        {
            "input": "A large intraparenchymal hemorrhage centered in the right frontal parietal\nlobes is not significantly changed in size.  Surrounding edema in the right\nfrontoparietal lobes, with sulcal effacement, effacement of the bilateral\nlateral ventricles, right greater than left, and leftward midline shift\nmeasuring up to 8 mm is not significantly changed compared with CT head\nperformed earlier on same day at 10:47.  There is intraventricular extension\nof hemorrhage, with blood layering in the bilateral occipital horns of the\nlateral ventricles, stable.  There is diffuse bilateral subarachnoid\nhemorrhage, similar to prior.  No new intracranial hemorrhage.\n\nThere is a CSF density cystic lesion in the right frontoparietal brain\nparenchyma which measures approximately 4.4 x 2.4 x 2.8 cm, with blood\nproducts layering in the posterior portion (10:18).  There is equivocal\nnodular enhancement along the more inferior aspect of this lesion (12:17). \nAdditionally, a small focus of enhancement along the medial aspect of the\nlesion is possibly vascular in nature (11:205).  There is edema surrounding\nthis cystic lesion.  No definite infarct.\n\nA 7 mm T2 hyperintense nonenhancing lesion in the right posterior pituitary is\nconsistent with a Rathke's cleft cyst. The major intracranial flow voids are\npreserved.  The dural venous sinuses are patent.\n\nThere is mild mucosal thickening in the sphenoid sinuses and ethmoid air\ncells.  There is trace fluid signal in bilateral mastoid air cells.  There is\notherwise no abnormal signal in visualized paranasal sinuses.  The orbits are\ngrossly unremarkable.",
            "output": "1. 4.4 cm intraparenchymal cystic lesion in the right frontoparietal lobes,\nwhich may be CSF collection secondary to compress effect of the hematoma. \nHowever, underlying cystic neoplasm cannot be entirely excluded.  There are\ntwo tiny foci of equivocal nodular enhancement associated with this lesion,\nhowever evaluation for enhancing components is limited by the presence of a\nlarge amount of T1 hyperintense blood products.\n2. No significant change in large right intraparenchymal hemorrhage with\nintraventricular extension and bilateral subarachnoid hemorrhage.\n3. No significant change in mass effect with effacement of the ventricles and\nleftward midline shift measuring up to 8 mm.\n4. A 7 mm cystic pituitary lesion is consistent with a Rathke's cleft cyst.\n\nRECOMMENDATION(S):  Recommend repeat MRI brain with and without contrast\nfollowing resolution of hematoma to document no underlying lesion."
        },
        {
            "input": "-a 0.3 cm enhancing lesion is seen within the left parietal lobe, series 1000,\nimage 125.\n\n-a 0.6 cm enhancing lesion is seen within the right parietal lobe, series\n1000, image 112.\n\n-a 0.6 cm enhancing lesion is seen within the right frontal lobe, series 1000,\nimage 113\n\n-a 0.4 cm enhancing lesion is seen within the left corona radiata, series\n1000, image 104\n\n-a lateral left frontal lobe lesion is seen, series 1000, image 104 measuring\napproximately 0.5 cm.\n\n-a left superior occipital lobe enhancing lesion is seen measuring 0 point 3\ncm, series 1000, image 104.\n\n-a left lateral frontal lobe lesion is seen measuring 0.3 cm, series 1000,\nimage 99.\n\n-a 0.4 cm enhancing lesion is seen within the right caudate nucleus, series\n1000, image 97.\n\n-along the superior right cerebellum, a 0.9 cm x 0.7 cm enhancing lesion is\nseen.  Additional adjacent cluster of lesions are seen within the right\ncerebellum, measuring up to 0.4 cm, series 1000, image 81.\n\n-along the mid right cerebellum, a 0.6 cm enhancing lesion is seen. \nImmediately medial to this a 0.2 cm enhancing lesion is seen, series 1000,\nimage 71.\n\n-along the inferior right cerebellum, a 0.4 cm enhancing lesion is seen series\n1000, image 65.  Along the inferior left cerebellum, a 0.6 cm enhancing lesion\nis seen, series 1000, image 62.\n\nPunctate foci of slow diffusion are seen within the right frontal lobe, left\nfrontal lobe, bilateral parietal lobes, and left cerebellum with associated\nFLAIR signal abnormality.  Punctate focus of low signal on the susceptibility\nweighted images is seen within the right cerebellum, series 7, image 8 which\nmay be secondary to chronic microhemorrhage.  Additional periventricular deep\nsubcortical FLAIR white matter hyperintensities are likely sequelae of chronic\nmicroangiopathy.\n\nMild mucosal sinus thickening is seen involving the ethmoid air cells.  Mucous\nretention cyst is seen within the inferior left maxillary sinus.  The\nremainder the visualized paranasal sinuses, mastoid air cells, and middle ear\ncavities are clear.  The globes are unremarkable.  The principal vascular flow\nvoids appear to be well preserved.",
            "output": "1. Numerous enhancing lesions are seen throughout the bilateral cerebrum and\ncerebellum as described in detail above concerning for metastatic disease.\n2. Punctate bilateral foci of slow diffusion in the bilateral frontal lobes\nand left cerebellum with associated include East FLAIR signal abnormality are\nconcerning for late acute/early subacute infarcts.  No acute intracranial\nhemorrhage.\n\nNOTIFICATION:  The findings were discussed with Dr. ___. by ___\n___, M.D. on the telephone on ___ at 12:55, 5 minutes after\ndiscovery of the findings."
        },
        {
            "input": "There is no evidence of intracranial hemorrhage, mass, mass effect or shifting\nof the normally midline structures. The ventricles and sulci are normal in\nsize and configuration for the patient's age. Few scattered small foci of high\nsignal intensity are seen in the subcortical white matter, mainly on the left\ncerebral hemisphere on FLAIR and T2 weighted images, which are nonspecific,\nlikely consistent with perivascular spaces, and less likely changes due to\nsmall vessel disease (images 15 through 17, series 7). No diffusion\nabnormalities are detected. The major vascular flow voids are present and\ndemonstrate normal distribution. The orbits are unremarkable, the paranasal\nsinuses and the mastoid air cells are clear.",
            "output": "There is no evidence of acute or subacute intracranial process. Small foci of\nhigh signal intensity identified in the subcortical white matte, mainly on the\nleft cerebral hemisphere, which are nonspecific and may represent perivascular\nspaces, this type of findings have been described in patients with chronic\nmigraines and changes due to small vessel disease."
        },
        {
            "input": "There is a 2.1 cm AP x 1.1 cm TV x 1.6 cm SI homogeneously enhancing\ndural-based lesion at the right anterior aspect of the foramen magnum\n(100b:33; 14:113), which demonstrates T2 and T1 isointensity.  This abuts the\norifice of the right hypoglossal canal, without definite intra foraminal\nextension.  There is mild mass effect on the anterior aspect of the medulla,\nwithout vasogenic edema.  There is mild medial displacement of the right\nvertebral artery.  There is no hyperostosis or intrinsic tongue muscle\natrophy.\n\nThere scattered periventricular and subcortical white matter FLAIR\nhyperintense foci, which are nonspecific, but likely secondary to sequela\nchronic microangiopathy.  The parenchymal signal is otherwise unremarkable\nwithout infarct, hemorrhage, or mass effect.  The ventricles and cortical\nsulci are normal in caliber configuration.  The vascular flow voids are\npreserved.\n\nThe orbits are unremarkable.  There is a small low signal excrescence from the\nright frontal calvarium measuring 0.9 x 0.4 cm (14:122).  There is\nhyperostosis frontalis.  There is trace fluid signal within the right anterior\nethmoid sinuses.  There is no abnormal fluid signal within the mastoid air\ncells or middle ears.",
            "output": "1. Enhancing dural-based lesion at the right anterior aspect of the foramen\nmagnum, abutting the orifice of the right hypoglossal canal in causing mild\nmass effect on the adjacent right vertebral artery and brain stem, without\nparenchymal vasogenic edema.  Signal characteristics favor a meningioma with\ndifferential considerations including other dural-based lesion such as\nmetastasis or a mesenchymal tumor.  This is less likely to represent a\nhypoglossal nerve sheath tumor given its T2 isointensity and no definite\nextension into the hypoglossal canal.\n2. Small low signal excrescence from the right frontal calvarium, which may\nrepresent an a small osteoma.\n3. No acute intracranial abnormality."
        },
        {
            "input": "There is no evidence of hemorrhage or mass effect.\n\nThere are normal vascular flow voids.  There is no evidence of acute\ninfarction.  There is brain parenchymal volume loss, greatest within the right\ncerebral hemisphere with persistent enlargement of the supratentorial\nventricular system, with a particularly prominent occipital horn of the right\nlateral ventricle which appears similar when compared to prior exam though\nincreased since ___.  There are similar findings the left, although lesss\nsevere. The etiology of this appearance is unclear although could potentially\nrepresent a chronic vascular insult.  MRA could be considered for further\nevaluation, as clinically warranted.\n\nThe orbits, skull base, and paranasal sinuses are unremarkable.",
            "output": "1. No evidence of hemorrhage or acute infarction.\n2. Enlargement of the supratentorial ventricular system, particularly\ninvolving the occipital horn of the right lateral ventricle with associated\ncortical volume loss.  There are similar, but less dramatic, changes on the\nleft.  The overall appearance is unchanged from the prior exam though\nincreased from ___.  The etiology of this appearance is unclear although\ncould potentially represent a chronic vascular insult.  MRA could be\nconsidered for further evaluation, as clinically warranted.\n\nRECOMMENDATION(S):  MRA could be considered for further evaluation, as\nclinically warranted."
        },
        {
            "input": "Late acute to subacute infarct of the right frontal lobe (series 4, image 22)\nis noted, demonstrating diffusion-weighted and FLAIR hyperintensity with\ncorresponding ADC hypointensity. Additional foci of diffusion-weighted\nhyperintensity in the left frontal lobe and pons are noted, which appear\nhyperintense on diffusion weighted maps, consistent with T2 shine through.\nMultiple foci of prior lacunes are noted. Diffusely scattered and severe\ngradient echo susceptibility artifacts of the pons, basal ganglia and\nperipheral cortex is noted, consistent with microhemorrhages, compatible with\namyloid angiopathy. Superimposed nonspecific subcortical and periventricular\nT2/FLAIR hyperintensities are noted, compatible with small vessel ischemic\ndisease. The sulci, ventricles and cisterns are preserved. No intra or\nextra-axial mass or acute hemorrhage. The major flow voids are preserved.\nMucous retention cyst of the right maxillary sinus is noted. Otherwise the\nparanasal sinuses are essentially clear. The orbits are unremarkable. The the\nmastoids and demonstrate flow signal bilaterally.",
            "output": "1. Late acute infarct of the right frontal lobe. Findings consistent with\namyloid angiopathy with sequela diffuse micro hemorrhages as well as prior\nlacunar infarcts are noted.\n\n2. Superimposed white matter changes as described above, which are\nnonspecific, but compatible with small-vessel ischemic disease."
        },
        {
            "input": "Study is partially degraded due to motion artifact.\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  Apparent FLAIR hyperintensity within the cingulate gyrus (8:\n17) is likely artifactual from motion artifact as it is not seen on the repeat\nFLAIR sequence.  The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.\n\n The major intracranial vascular flow voids are maintained.  There are few\nsmall bilateral mucous retention cyst within the maxillary sinuses measuring\nup to 1.5 cm on the left.  The mastoid air cells and orbits are normal.",
            "output": "1. No acute intracranial abnormality.  Specifically, no structural abnormality\nto account for the patient's headache symptoms.\n2. A few mucous retention cysts of the bilateral maxillary sinuses."
        },
        {
            "input": "There is no intra or extra-axial mass, acute hemorrhage or infarct. The sulci,\nventricles and cisterns are within expected limits for the patient's age. \nThere are no suspicious parenchymal FLAIR signal abnormalities.  No evidence\nof previous microhemorrhages.  There is a partial empty sella.  The major\nintracranial flow voids are preserved.\n\nParanasal sinus mucosal inflammatory changes are mild.  Noting mild elongated\nshape of the globes, presumably representing mild staphyloma, otherwise the\norbits are unremarkable.  Trace fluid signal in the mastoid air cells.  No\nsuspicious marrow signal.",
            "output": "1. No acute intracranial abnormality on noncontrast MRI head.  Specifically no\nevidence of acute infarct or intracranial hemorrhage.  No mass or suspicious\nparenchymal FLAIR signal abnormality.  No evidence of prior microhemorrhages.\n2. There is a partial empty sella, a nonspecific finding, but may be seen in\nthe setting of idiopathic intracranial hypertension.  Clinical correlation\nwith patient's headache is recommended.\n3. Additional findings described above."
        },
        {
            "input": "There is no evidence of acute infarction.  No intracranial hemorrhage.  No\nmass, mass effect, edema or midline shift.\n\nMildly prominent bifrontal extra-axial spaces are noted.  Otherwise, the\nventricles and sulci are normal, without evidence of hydrocephalus. The basal\ncisterns are patent.  There is no evidence of impending, downward herniation. \nThere is gross preservation of the principal intracranial vascular flow voids.\n\nFollowing the administration of intravenous contrast material, there is no\nabnormal enhancement.  The dural venous sinuses appear patent on MP-RAGE\nimagine sequences.\n\nThe visualized paranasal sinuses, middle ear cavities, and mastoid air cells\nare well aerated and clear.  The orbits are within normal limits bilaterally.",
            "output": "1.  No evidence for acute intracranial process.  Specifically, no intracranial\nhemorrhage or meningeal enhancement to suggest meningitis.  No dural\nthickening.  No definite parenchymal signal abnormality.\n2.  Patent dural venous sinuses."
        },
        {
            "input": "Susceptibility artifact in the region of the right ocular globe is likely\nrelated to the high density rounded foreign body, presumably postsurgical seen\non earlier CT head.\n\nThere is tissue loss of the right medial temporal lobe and hippocampus, likely\nsequelae of chronic infarct.  A probable chronic infarct of the right\nsubinsular region is also noted.  There is mild asymmetric right hemi pontine\nand right midbrain volume loss, possibly related to wallerian degeneration. \nThere are minimal periventricular white matter foci of T2/FLAIR signal\nhyperintensity, nonspecific and likely  sequelae of chronic microvascular\ndisease.  There is no evidence of hemorrhage, edema, masses, mass effect,\nmidline shift or acute infarction.  The ventricles and sulci are age\nappropriate in caliber and configuration.\n\nThere is mild mucosal thickening within multiple ethmoid air cells, sphenoid\nand left maxillary sinuses with a small left maxillary mucous retention cyst.",
            "output": "1. No no evidence of hemorrhage, masses, mass effect or recent infarction.\n2. Sequelae of chronic infarction in the right medial temporal lobe,\nsubinsular region and hippocampus.\n3. Asymmetric right hemipontine and right midbrain volume loss, possibly\nrepresenting a component of wallerian degeneration.\n4. Minimal periventricular white matter signal changes, nonspecific and likely\nsequelae of chronic microvascular disease.\n5. Susceptibility artifact related to high density, presumably postsurgical\nforeign body along the right globe"
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration for age.  Scattered periventricular and subcortical white matter\nT2/FLAIR hyperintensities are mild to moderate in severity and nonspecific,\nalthough in a distribution that suggests chronic microangiopathy. In the right\nposterior nasal cavity at the junction with the nasopharynx, a circumscribed\n1.7 x 1.0 cm polypoid nodule demonstrates hyperintense signal on T2 weighted\nimages and isointense signal T1 weighted images (series 9, image 4; series 8,\nimage 14).",
            "output": "1. No evidence infarction.\n2. Mild-to-moderate chronic small vessel changes, as described.\n3. 1.7 cm right nasopharynx mucous retention cyst."
        },
        {
            "input": "MRI Brain:\nAgain seen is diffuse subarachnoid hemorrhage with corresponding hyperintense\nFLAIR signal and slow diffusion (for example, 05:20, 10:13), with small amount\nof fluid in the perimesencephalic cistern.  A T1 hyperintense quadrigeminal\nplate cistern lipoma is seen (02:12) corresponding to hypodensity on prior CT.\nThere is no evidence of acute infarction, mass effect, or midline shift. \nThere is no abnormal enhancement or enhancing mass.\n\nThere is diffuse parenchymal volume loss with commensurate prominence of the\nventricles, sulci, cisterns.  There are nonspecific periventricular\nsubcortical white matter hyperintense T2 and FLAIR signal changes, which may\nbe a sequela of chronic small vessel microangiopathy.\n\nThere is bifrontal extra-axial fluid, right greater than left, with\nhyperintense T2, hypointense T1, with minimal hyperintense FLAIR signal\n(10:15), without intervening vessels, that likely represents late subacute\nsubdural hematoma, with adjacent bifrontal hypointense GRE signal (13:13). \nThe paranasal sinuses and right mastoid air cells appear clear.\n\nMRA brain:  There is an aneurysm at the level of the anterior communicating\nartery, measuring 0.8 x 0.6 cm (11:111).  There is hypoplastic right A1\nsegment of the anterior cerebral artery.  There is patency of the anterior,\nmiddle, and posterior cerebral arteries, without stenosis, occlusion, or other\naneurysm formation.  There is lack of flow related enhancement of the right\nintracranial carotid artery.   There is luminal irregularity of the left\ncavernous internal carotid artery, likely atherosclerotic disease, with mild\nluminal narrowing. There is a right dominant vertebral artery.\n\nMRA neck:  Evaluation of the neck is moderately degraded by patient motion\nartifact, limiting evaluation.  There is luminal irregularity of the distal\nright common carotid artery with moderate narrowing of the proximal right\ninternal carotid artery with nonvisualized flow related enhancement of the\nintracranial segment.  There are vascular calcifications at the left common\ncarotid artery bifurcation, resulting in severe narrowing of the proximal left\ninternal carotid artery, with a nonvisualized portion of the left common and\nproximal internal carotid artery(15:9), likely secondary to extensive vascular\ncalcifications.  There is a right dominant vertebral artery.  The vertebral\narteries appear patent.",
            "output": "1. Diffuse subarachnoid hemorrhage with late subacute bifrontal subdural\nhematoma.\n2. No evidence of acute infarction or edema.\n3. Aneurysm near the anterior communicating artery measuring 0.8 x 0.6 cm.\n4. Nonvisualized flow-related enhancement of the right internal carotid artery\ndistal to its origin, likely related to severe narrowing.  However, motion\ndegradation artifact limits further evaluation.\n5. Severe narrowing at the origin of the left internal carotid artery, with a\nnonvisualized portion of the left common carotid artery bifurcation, likely\nrelated to extensive vascular calcifications.\n\nNOTIFICATION:  The findings were discussed with ___, M.D. by\n___, M.D. on the telephone on ___ at 10:23 AM, 2\nminutes after discovery of the findings."
        },
        {
            "input": "Right frontoparietal mixed density subdural hematoma,  left frontoparietal\nsubdural hematoma with blood layering along the left temporal fossa, and\nassociated mass effect on the bilateral cerebral hemispheres and lateral\nventricles are not significantly changed compared with CT on ___\nallowing for differences in technique.  The lateral ventricles and basal\ncisterns are small, and midbrain appears elongated due to mass-effect.  There\nis no evidence of masses, midline shift or infarction.  There is no abnormal\nenhancement after contrast administration.",
            "output": "1. No evidence of ischemia.\n2. No significant change in bilateral subdural hematomas and associated mass\neffect causing some degree of central herniation unchanged compared with CT\nperformed earlier on same day allowing for differences in technique.\n3. No evidence of brainstem hemorrhage or edema."
        },
        {
            "input": "MRI Brain:  There is a small acute stroke in the inferior pons just slightly\nright to midline (series 8, image 11).  There is a chronic lacunar seen stroke\nin the right internal capsule.  There is T2/FLAIR signal hyperintensity in the\nperiventricular, subcortical, and deep white matter which is nonspecific but\nlikely on the basis of chronic small vessel ischemic disease.  There is a\nfocus of susceptibility artifact in the left basal ganglia likely representing\nchronic microhemorrhage.  There is no evidence of hemorrhage, edema, masses or\nshift of midline.  Ventricles and sulci are normal in caliber and\nconfiguration.  Major vascular flow voids are preserved. The orbits are\nunremarkable.  The paranasal sinuses and mastoid air cells are clear.\n\nMRA brain: The intracranial vertebral and internal carotid arteries and their\nmajor branches appear normal without evidence of stenosis, occlusion, or\naneurysm formation.\n\nMRA neck:  The common, internal and external carotid arteries appear normal. \nThere is no evidence of internal carotid artery stenosis by NASCET criteria. \nA common origin of the brachiocephalic artery and left common carotid artery\nis incidentally noted.\n\nA 8 mm Hypointense nodule is again noted in the right lobe of the thyroid\ngland.  There are smaller regions of low intensity noted in the left thyroid\nwhich also properly represent tiny nodules.",
            "output": "1.  Late acute/early subacute stroke in the inferior pons.\n\n2.  T2/FLAIR signal hyperintensity in the periventricular, subcortical, and\ndeep white matter which is nonspecific but likely on the basis of chronic\nsmall vessel ischemic disease.\n\n3.  Unremarkable MRA of the head and neck."
        },
        {
            "input": "MR BRAIN:\nThere is a focus of slow diffusion with associated T2/FLAIR hyperintensity in\nthe right lateral and right dorsolateral aspect of the medulla, in keeping\nwith acute infarction.  There is no evidence of infarction in the remainder of\nthe brainstem.  There is chronic infarction in the right cerebellar\nhemisphere, with a small amount of adjacent T2/FLAIR hyperintensity.  Chronic\nlacunar infarcts are noted in the thalami and in the corona radiata\nbilaterally.  There are nonspecific bilateral supratentorial T2/FLAIR white\nmatter hyperintensities, which may represent the sequelae of chronic\nmicroangiopathy.  There is no evidence of hemorrhage,masses, mass effect or\nmidline shift.   The ventricles and sulci are normal in caliber and\nconfiguration.  The right lens is been resected.\n\nMRA brain: The intracranial vertebral arteries and basilar artery are\nhypoplastic with large bilateral posterior communicating arteries supplying\nthe posterior cerebral arteries. However, the lack of a flow void in the\ndistal right vertebral artery and basilar artery on the T2 weighted images is\na new finding since ___.  These findings suggest a combination of\nhypoplastic vertebral and basilar arteries due to the large posterior\ncommunicating arteries and severe stenosis or occlusion of the right vertebral\nartery, which is the dominant vessel.  The intracranial internal carotid\narteries and their major branches appear normal without evidence of stenosis,\nocclusion, or aneurysm formation.",
            "output": "1. Acute infarction in the right lateral and right dorsolateral aspect of the\nmedulla.  No evidence of hemorrhage or other recent infarction.\n2. Severe attenuation of the right vertebral artery and the basilar artery, a\nnew finding since the brain MR of ___.  This suggests severe\nstenosis or occlusion of the vertebral artery.\n3. Prominent bilateral posterior communicating arteries supplying the\nposterior cerebral arteries imply underlying hypoplasia of the basilar artery.\n4. The intracranial internal carotid arteries and their major branches appear\nnormal without evidence of stenosis, occlusion, or aneurysm formation.\n5. There is an old infarct in the right cerebellar hemisphere and old lacunar\ninfarcts in the thalami and corona radiata bilaterally.\n6. Nonspecific bilateral supratentorial T2/FLAIR white matter\nhyperintensities, which may represent the sequelae of chronic microangiopathy.\n\nRECOMMENDATION(S):  A CTA of the head and neck is advised for further\nevaluation.\n\nNOTIFICATION:  The findings were discussed with ___, M.D. by ___\n___, M.D. on the telephone on ___ at 11:09 am, 5 minutes after\ndiscovery of the findings."
        },
        {
            "input": "The study is severely degraded by movement artifact.  Allowing for this;\n\nAero digestive tract:\nThere is asymmetry of the true vocal cords, with mild hyperintensity in the\nright true vocal cord on the axial T2 ___ sequence, in keeping with the\nknown right vocal cord palsy.  No associated mass is identified.\nThere no mass.\nIf there is a mass, please insert field choice -->\n\nNeck lymph nodes:\nThere is no adenopathy involving bilateral levels ___.\nThere is no retropharyngeal adenopathy.\n\nExtra nodal tumor spread:\nThere are no findings suggestive of extra nodal extension.\n\nDeep neck muscles, masticator space:\nThere is no muscle invasion.\n\nBones, skull base:\nThere is no bone involvement.\nThere are no findings suggestive of perineural tumor extension.\nJugular foramen, carotid canal,pterygopalatine fossa,infraorbital\nforamen,other skull base foramina are not involved.  There are mild cervical\ndegenerative changes.\n\nVessels:\nThere is loss of the normal flow void in the V2 and V3 segments of the right\nvertebral artery, suggestive of occlusion.\n\nBrachial Plexus:\nThere is no brachial plexus contact or invasion.\n\nThyroid, salivary glands:\nThere is no mass.\n\nOther findings:\nThere is T2 hyperintensity in the right lateral aspect of the medulla, in\nkeeping with the acute infarct identified on the MR head dated the same day. \nOld infarcts are noted in the right cerebellar hemisphere and the thalami\nbilaterally.",
            "output": "Allowing for the movement artifact;\n\n1. Asymmetry of the true vocal cords, with mild hyperintensity in the right\ntrue vocal cord on the axial T2 ___ sequence, in keeping with the known\nright vocal cord palsy.  No associated mass is identified.\n2. T2 hyperintensity in the right lateral aspect of the medulla, in keeping\nwith the acute infarct identified on the MR head dated the same day.\n3. There is loss of the normal flow void in the V2 and V3 segments of the\nright vertebral artery, suggestive of occlusion.\n4. Old infarcts are noted in the right cerebellar hemisphere and the thalami\nbilaterally.\n\nRECOMMENDATION(S):  A CTA head and neck is advised for further evaluation.\n\nNOTIFICATION:  The findings were discussed with ___, M.D. by ___\n___, M.D. on the telephone on ___ at 11:16 am, 5 minutes after\ndiscovery of the findings."
        },
        {
            "input": "There is a 6 mm T1 hypointense T2 hyperintense lesion in the region of the\nleft caudate which suppresses on FLAIR sequences and communicates with the\nfrontal horn of the left lateral ventricle. There is no enhancement associated\nwith this lesion. This imaging appearance is most suggestive of a small\nporencephalic cyst. There is mild surrounding T2/FLAIR hyperintensity\nsurrounding this lesion consistent with mild gliosis.\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, or infarction.\nThe ventricles and sulci are normal in caliber and configuration. There is no\nabnormal enhancement after contrast administration.  Vascular flow voids are\npreserved. The orbits are unremarkable. There is minimal mucosal thickening\nwithin the ethmoid air cells. There is opacification of the right maxillary\nsinus and a small mucous retention cyst in the left maxillary sinus. The\nremaining paranasal sinuses and mastoid air cells are clear.",
            "output": "1.  6 mm T1 hypointense T2 hyperintense lesion which suppresses on FLAIR and\ncommunicates with the frontal horn of the left lateral ventricle .  Findings\nare most compatible with a small porencephalic cyst likely secondary to a\nchronic lacune. .\n\n2.  No enhancing lesions on post-contrast images."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are prominent in an atrophic\npattern.  There are scattered white matter hyperintensities, predominantly\nperiventricular, on the FLAIR images.  These suggest chronic small vessel\nischemia.  There is no abnormal enhancement after contrast administration. \nThere is complete opacification of the right maxillary sinus with mucosal\nthickening but also material that is hypointense on the T2 weighted images\nsuggesting inspissated mucus.\n\nThere is marked narrowing of the upper cervical spinal canal with a disc\nprotrusion at C2-3 deforming the upper cervical spinal cord.",
            "output": "1. No evidence of hemorrhage or infarction\n2. Atrophy and findings suggesting chronic small vessel ischemia\n3. No findings suggesting encephalitis\n4. Narrow cervical spinal canal with disc protrusion at C2-3 deforming the\nspinal cord"
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  There is moderate prominence of the ventricles and sulci\nsuggestive involutional changes.  Areas of periventricular, subcortical and\ndeep white matter T2/FLAIR hyperintensity are in a configuration most\nsuggestive of chronic small vessel ischemic disease.  There is no abnormal\nfocus of slowed diffusion.  The principal intracranial vascular flow voids are\npreserved.\n\nThere is near complete opacification of the right maxillary sinus with central\nmaterial that is T2 hypointense, likely representing mucous inspissation.  The\nremainder the visualized paranasal sinuses are grossly clear.  There are\nchanges from lens replacement surgery on the right.  The orbits are otherwise\ngrossly unremarkable.  There is bilateral mastoid air cell opacification.",
            "output": "1. No hemorrhage, infarct, or findings to suggest encephalitis.\n2. Moderate global atrophy and white matter changes suggesting chronic small\nvessel ischemic disease."
        },
        {
            "input": "There is a punctate focus of slow diffusion in the right parietal lobe,\nconsistent with a an acute infarct.  There are confluent and scattered\nT2/FLAIR hyperintense foci in the periventricular, deep and subcortical white\nmatter of the cerebral hemispheres, nonspecific but likely reflecting sequelae\nof chronic ischemic microvascular disease in this age.  There is similar\nparenchymal volume loss with prominence of the cerebral sulci and ventricles. \nCavum septum pellucidum et vergae is again noted.  There is no evidence of\nhemorrhage,  masses, mass effect or midline shift.\n\nThere is mucosal thickening in multiple ethmoid air cells.  Postsurgical\nchanges related to bilateral lens replacement are again noted.  The major\nintracranial vascular flow voids are maintained.",
            "output": "1. Punctate acute infarct in the right parietal lobe.\n2. Similar advanced parenchymal volume loss and probable chronic small vessel\nischemic changes in the supratentorial white matter."
        },
        {
            "input": "There is no evidence for acute infarction, edema, mass effect, or intracranial\nblood products.  Partially confluent T2/FLAIR hyperintense foci in the\nperiventricular, deep, and subcortical white matter of the cerebral\nhemispheres are grossly unchanged compared to ___, nonspecific but\nlikely sequelae of chronic ischemic microvascular disease in this age.  There\nis unchanged advanced parenchymal volume loss with prominent ventricles and\nsulci.  Cavum septum pellucidum et vergae is again noted.  The major\nintracranial flow voids are maintained.\n\nThere is mucosal thickening within the ethmoid air cells.  Postsurgical\nchanges related to bilateral lens replacement are again noted.\n\nSagittal images again demonstrate incompletely evaluated degenerative changes\nin the included upper cervical spine.",
            "output": "1. No evidence for acute infarction or other acute abnormalities on\nnoncontrast MRI.\n2. Stable appearance of advanced parenchymal volume loss and presumed chronic\nsmall vessel ischemic changes in the supratentorial white matter compared to\n___."
        },
        {
            "input": "There is a mildly heterogeneous right subdural collection, corresponding to\nthe mixed density collection seen on prior CT, increased in size measuring\napproximately 1.5 cm in maximal distance from the inner table.  Within this\ncollection, there is an area with central low and peripheral high signal on T1\nweighted images, and intermediate signal on T2, with slow diffusion (series 4,\nimage 19; series 502, image 23).  There is a smaller but similar focus on the\nslow diffusion in the right paramedian anterior frontal region (series 502,\nimage 21).  These areas may represent acute on chronic hemorrhage versus\nempyema/abscess.  There is also a trace left subdural collection.  There is\ndiffuse pachymeningeal enhancement bilaterally.  The right subdural collection\nresults in mass effect on the adjacent sulci, and approximately 4 mm shift of\nnormally midline structures towards the left, grossly unchanged.  The\nventricles are stable.  There are a few scattered punctate periventricular\nsubcortical white matter foci of FLAIR hyperintense signal which are\nnonspecific but likely sequelae of chronic small vessel ischemic disease. \nThere is no evidence of parenchymal edema adjacent to the hematoma.  There is\nno evidence of acute vascular territorial infarction.  There is no abnormal\nparenchymal enhancement.  The dural venous sinuses are patent on postcontrast\nMP-RAGE sequences.  The major vascular flow voids are present and demonstrate\nnormal distribution, the orbits are unremarkable, the paranasal sinuses and\nmastoid air cells are clear.",
            "output": "1. Increased size of complex right subdural fluid collection, with\nsuperimposed smaller areas of slow diffusion suggesting acute on chronic blood\nproducts versus empyema/abscess.\n2. Grossly unchanged trace left subdural collection.\n3. Diffuse pachymeningeal enhancement is likely reactive.\n4. Mass effect on the sulci and approximately 4 mm shift of normally midline\nstructures to the left is grossly unchanged.\n\nNOTIFICATION:  The findings were discussed with ___ (neurosurgery),\nM.D. by ___, M.D. on the telephone on ___ at 10:31 pm, 60 \nminutes after discovery of the findings."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, mass, mass effect, or infarction. \nA few punctate subcortical white matter foci of FLAIR hyperintense signal are\nnonspecific.  Ventricles and sulci are age-appropriate.  Principal\nintracranial vascular flow voids are preserved.  The orbits are unremarkable.",
            "output": "Normal study."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are patent and prominent in keeping\nwith age-related volume loss.\n\nThere are scattered foci of T2/FLAIR hyperintensity in the subcortical and\nperiventricular white matter, nonspecific, likely secondary to small vessel\nischemic disease. No diffusion abnormalities are detected.\n\nThe orbits are unremarkable.  The visualized paranasal sinuses are clear. \nNonspecific fluid opacification of bilateral mastoid air cells, pool of\nsecretions is visualized in the oro and nasopharynx, the patient is intubated.",
            "output": "1. No acute intracranial abnormality.\n\n2. Age-related volume loss and small vessel ischemic disease."
        },
        {
            "input": "Right-sided craniotomy is again seen. Thin linear right anterior dural\nenhancement is unchanged.  There is an extra-axial enhancing nodule along the\nplanum sphenoidale, measuring 1.7 cm AP x 1.1 cm craniocaudad by 1.8 cm\ntransverse on images 18:89 and 19:37, unchanged dating back to ___.\nAreas of encephalomalacia and gliosis in the anterior frontal lobes, more\nextensive on the right than left, are stable. Ex vacuo enlargement of the\nfrontal horn of the right lateral ventricle is again seen. The ventricles are\noverall stable in size.\n\nAgain seen is expenses susceptibility artifact in the left paracentral scalp,\nlikely related to postsurgical change.\n\nSmall developmental venous anomaly in the left parietal lobe is less well\ndemonstrated than on the prior exams, but remains faintly visible on image\n17:14. Adjacent cavernous malformation is again on images 15:14, 14:14, and\n20:69.\n\nThere is no evidence for new intracranial enhancing lesion. There is no new\nedema, mass effect, or evidence of new blood products in the brain parenchyma.\nThere is no acute diffusion abnormality. A chronic infarct is again seen in\nthe right cerebellar hemisphere.  Major arterial flow voids are grossly\npreserved. Major dural venous sinuses appear patent.\n\nThere is mild mucosal thickening in a right greater than left ethmoid air\ncells.",
            "output": "1. The enhancing extra-axial nodule along the planum sphenoidale, consistent\nwith residual meningioma, is stable dating back to ___.  Right greater\nthan left frontal post-treatment changes are stable.\n2. No evidence for a new intracranial mass.\n3. Developmental venous anomaly and an adjacent cavernous malformation are\nagain seen in the left parietal lobe."
        },
        {
            "input": "Motion artifact mildly limits examination.\n\nThere is no evidence of mass, abnormal fluid collection, or cervical\nlymphadenopathy. The major glandular structures including the parotid glands,\nbilateral submandibular glands, and thyroid gland appear normal. The imaged\nportions of the vascular structures throughout the neck appear unremarkable. \nThere is slight asymmetry of the subcutaneous fat in the region of surface\nmarker in left occipital region but no discrete lipoma is seen.\n\nThere is a chronic right cerebellar infarct. The remaining imaged intracranial\ncontents appear unremarkable.",
            "output": "Examination is limited from motion artifacts.  Slight asymmetry of\nsubcutaneous fat in left occipital region.  Otherwise,  there is no evidence\nof abnormal neck mass, fluid collection, or cervical lymphadenopathy."
        },
        {
            "input": "Again seen are postoperative changes related to prior right-sided craniotomy\nand resection of the olfactory groove meningioma with stable associated\nencephalomalacia and FLAIR signal abnormality.  There is stable ex vacuo\ndilatation of the frontal horn of right lateral ventricle and mild dural\nthickening and enhancement.  There is a residual stable extra-axial enhancing\nnodule on the right olfactory groove measuring 1.5 x 1 cm on image 11:11 with\nassociated slow diffusion, unchanged since ___.\n\nStable susceptibility artifact in the left parieto-occipital scalp, likely\nrelated to prior surgery.\n\nAgain seen is a small developmental venous anomaly in the left parietal lobe\nwithin ages send cavernous malformation as seen on image 15:7 and 11:15.\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are unchanged in configuration.\n\nThe orbits are unremarkable.  Mild mucosal thickening in bilateral ethmoid air\ncells.  The remaining visualized paranasal sinuses are clear.  Minimal\nnonspecific stable fluid opacification of right mastoid air cells.  The\nremaining visualized paranasal sinuses and left mastoid air cells are clear.",
            "output": "1. Stable postoperative changes related to prior right-sided craniotomy and\nresection of the olfactory groove meningioma with associated encephalomalacia,\nFLAIR signal abnormality and dural thickening and enhancement.\n2. Stable residual extra-axial enhancing lesion along the right olfactory\ngroove measuring 1.5 x 1 cm.\n3. Stable left parietal developmental venous anomaly with associated cavernous\nmalformation.\n4. No new lesions are seen."
        },
        {
            "input": "There are multiple foci of susceptibility artifact in the bilateral\nsubcortical white matter, consistent with chronic microhemorrhages in a\ntypical distribution of cerebral amyloid angiopathy, a slightly larger area of\nsusceptibility is noted on the right parietal lobe also suggestive of residual\nblood products from prior chronic hemorrhagic event.  There is no evidence of\nedema, masses, mass effect, midline shift or acute infarct.  There is\nprominence of the ventricles and sulci suggestive involutional changes.. \nSubcortical and periventricular white matter hypodensities are nonspecific,\nhowever likely represent sequela of chronic small vessel ischemic disease. \nThe major intracranial flow voids are preserved.  The paranasal sinuses are\nclear.  The orbits are grossly unremarkable.",
            "output": "1. No evidence of acute infarction.\n2. Multiple foci of susceptibility artifact in the bilateral subcortical white\nmatter are consistent with chronic microhemorrhages in a typical distribution\nof cerebral amyloid angiopathy."
        },
        {
            "input": "A saccular aneurysm arising from the anterior communicating artery is\nunchanged in size compared to prior studies, again measuring approximately 6 x\n5 mm (3:83, 300:18).  The remaining intracranial vertebral and internal\ncarotid arteries and their major branches appear normal without evidence of\nstenosis, occlusion, or aneurysm formation.  Fetal origin of the right\nposterior cerebral artery is incidentally noted.",
            "output": "1. Stable size and appearance of anterior communicating artery aneurysm.\n2. Remaining intracranial arteries are unremarkable."
        },
        {
            "input": "The patient is status post stent assisted coiling of an A-comm aneurysm as\nseen on the previous studies.  There is no nodular flow related enhancement in\nthe region of the coil pack to suggest recanalization.  Evaluation of the\nright A1 and proximal portion of bilateral A2 segments is limited by\nsusceptibility artifact from the coils and stent.  Fetal origin of the right\nposterior cerebral artery is again noted.  The circle of ___ and its major\ntributaries are otherwise within normal limits.  No new aneurysm is\nidentified.",
            "output": "Status post stent assisted coiling of an anterior communicating artery\naneurysm without definite evidence of recanalization."
        },
        {
            "input": "MRI BRAIN:\nThere is no evidence of acute infarction, edema, mass effect, or blood\nproducts.  Normal size of the ventricles, sulci, and basal cisterns.  Cavum\nseptum pellucidum et vergae is a normal variant.  The pituitary gland measures\n7 mm in height with a convex upper margin, which is normal for a ___\nwoman.  Cerebellar tonsils are normally positioned.  Major vascular flow voids\nappear preserved.\n\nMRA NECK:\nThere is a 3 vessel aortic arch.  Common carotid, cervical internal carotid,\nand vertebral arteries appear widely patent.  Specifically, no carotid\nstenosis by NASCET criteria.\n\nMRA CIRCLE OF ___:\nMotion artifact mildly limits evaluation.  The intracranial vertebral and\ninternal carotid arteries and their major branches appear patent without\nevidence of flow-limiting stenosis or aneurysm.\n\nNo fat-suppressed axial T1 weighted images were obtained.",
            "output": "1. No acute infarction or evidence for other acute abnormalities.\n2. Unremarkable MRA of the neck and circle of ___."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There are few scattered subcortical and periventricular\nT2/FLAIR hyperintensities.\n\nThere is fluid-filled opacification the left mastoid air cells.  Minimal fluid\nis seen the right mastoid air cells.  Minimal mucosal thickening of the\nethmoid is seen.  Bilateral cataract extractions are noted.  The major\nvascular flow voids are preserved.",
            "output": "1. No acute intracranial hemorrhage or infarct.\n2. Fluid-filled opacification of the left mastoid air cells which may be\nsecondary to otomastoiditis.  Otherwise, no acute intracranial abnormality.\n3. Few scattered white matter signal abnormalities, likely secondary to\nminimal chronic microvascular ischemic changes."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement.  The cranial nerves are\nsymmetric and normal in signal without abnormal enhancement.\n\nThe left mastoid air cells remain nearly completely opacified.  Several of the\nright posterior mastoid air cells are opacified, unchanged from the prior\nexamination.  There is mild mucosal thickening in the bilateral ethmoid\nsinuses.  The patient is status post bilateral cataract surgery.\n\nThe major intracranial flow voids are preserved.",
            "output": "1. No abnormal enhancement of the cranial nerves.\n2. Unchanged, near complete opacification of the left mastoid air cells and\nmild opacification of the right mastoid air cells, which may represent an\notomastoiditis."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  There are moderate age-related involutional changes with\nprominence of the ventricles and sulci.  Moderate T2 and FLAIR hyperintense\nfoci in the periventricular and deep white matter are nonspecific but likely\nreflect chronic microvascular ischemic gliotic change.  No evidence of\nrestricted diffusion is seen.  There is no abnormal enhancement after contrast\nadministration.\n\nThe orbits and globes appear within normal limits.  The paranasal sinuses and\ntympanomastoid air cells appear clear.",
            "output": "-No evidence of hemorrhage, edema, mass or acute infarction.  No abnormal\nenhancement is seen.\n-Moderate age-related involutional and chronic microvascular ischemic changes."
        },
        {
            "input": "There is mild to moderate generalized brain atrophy seen.  Minimal to  mild\nhippocampal atrophy is identified.  A few punctate foci of FLAIR\nhyperintensity in the white matter indicate early changes of small vessel\ndisease.  There are no territorial infarcts.  There is no midline shift or\nhydrocephalus.  There is no evidence of intra or extra-axial hemorrhage or\nfluid collection.  There are no micro hemorrhages identified.  Mild mucosal\nthickening is seen in the left maxillary sinus.",
            "output": "Mild brain atrophy and minimal to mild hippocampal atrophy.  Early changes of\nsmall vessel disease.  No evidence of mass effect, hydrocephalus or midline\nshift."
        },
        {
            "input": "Enhancing lesion in the left parietal bone appears unchanged compared to the 2\nprior MRI exams. Dural enhancement along the inner margin of the bone lesion\nappears thicker than on ___ but not significantly changed compared to\n___, allowing for motion artifact on ___. No new bone lesions\nor epidural lesion are detected. There is no parenchymal mass .\n\nHemosiderin deposition and mild volume loss is seen at the site of the prior\nhemorrhage in the right basal ganglia and corona radiata. A small focus of\nhigh signal on diffusion tracer sequences in this area, image 6:17, without\nlow signal on the ADC map, is likely related to distortion of the magnetic\nfield by hemosiderin. Otherwise, there is no evidence for an acute infarction.\nThere is no edema or mass effect in the brain parenchyma. There are extensive\nconfluent areas of high T2 signal in the subcortical, deep, and\nperiventricular white matter of the cerebral hemispheres, likely sequela of\nchronic small vessel ischemic disease in a patient of this age. Major arterial\nflow voids are grossly preserved.\n\nLeft frontal burr hole and prior ventriculostomy tract in the left frontal\nlobe are again seen. The ventricles are stable in size compared to the ___ CT, with global mild prominence of the ventricles and sulci due to\nage-related cerebral atrophy, as well as superimpose slight ex vacuo\ndilatation of the frontal horn of the right lateral ventricle.\n\nThere are mucous retention cysts and mucosal thickening in the maxillary\nsinuses. Few left mastoid air cells are opacified.",
            "output": "1. Enhancing lesion in the left parietal bone appear stable. Dural enhancement\nalong its inner margin appears stable compared to ___, though thicker\ncompared to ___. No new bone, epidural, or parenchymal lesions are\nseen.\n2. Mild encephalomalacia at the site of the prior hemorrhage in the right\nbasal ganglia and corona radiata.\n3. Extensive supratentorial white matter abnormalities, grossly unchanged,\nlikely sequela of chronic small vessel ischemic disease in a patient of this\nage."
        },
        {
            "input": "Again noted is an enhancing left parietal temporal bone lesion with dural\nenhancement and thickening and extension through the inner table measuring\napproximately 2.5 x 1.2 x 2.3 cm (AP, TRV, CC), essentially unchanged from\nprior MRIs dated back to ___. No new osseous lesions are identified. \nNo new enhancing lesions are identified. Unchanged appearance of left frontal\nburr hole with a residual ventriculostomy tract.\n\nThere is no evidence of intra-axial mass. Continued evolution of a right basal\nganglia and coronal radiata hemorrhage. Hemosiderin deposition and mild\nencephalomalacia in the region is again identified.  There is no evidence of\nacute infarct or new hemorrhage. Extensive confluent T2/FLAIR nonspecific\nT2/FLAIR subcortical, periventricular and deep white matter hyperintensities\nare noted, likely representing small vessel ischemic disease in a patient this\nage. The major intracranial flow voids are preserved.\n\nMild ex vacuo dilatation of the right lateral ventricle. Otherwise, sulci,\nventricles and cisterns are within expected limits for the degree of\nage-appropriate global cerebral volume loss.\n\nMucous retention cysts are seen in the bilateral maxillary sinuses. Mild\nmucosal thickening of ethmoid air cells is also identified. The patient is\nstatus post bilateral lens replacements. The mastoid air cells are clear.",
            "output": "1. Unchanged appearance of enhancing left parietal temporal bone lesion which\nextends through the inner table resulting in dural enhancement and thickening.\nNo new osseous or parenchymal lesions are identified.\n2. Continued evolution and encephalomalacia of the right basal ganglia and\ncoronal radiata.\n3. Stable confluent white matter changes described above, which are\nnonspecific, but compatible with small-vessel ischemic disease in a patient\nthis age."
        },
        {
            "input": "Punctate focus of likely late acute to subacute infarct of the right\nprecentral gyrus (series 502, image 26) is identified.  No other evidence of\ndiffusion-weighted abnormality is identified.  Very minimal scattered\nsubcortical T2/FLAIR nonenhancing white matter hyperintensities are\nidentified, nonspecific, but commonly seen with sequela of chronic\nmicroangiopathy in a patient of this age.\n\nThere is no intra or extra-axial mass, acute hemorrhage or abnormal\nenhancement.  The sulci, ventricles and cisterns are within expected limits\nfor the patient's age.  The major intracranial flow voids are preserved.  The\ndural venous sinuses are patent on postcontrast MP-RAGE.  There is mild\nmucosal thickening of the ethmoid air cells.  Otherwise the remainder the\nparanasal sinuses are essentially clear.  The orbits are unremarkable. \nMastoid air cells are clear.",
            "output": "1. Punctate focus of likely late acute to subacute infarct of the right\nprecentral gyrus.\n2. Additional findings as described above\n\nNOTIFICATION:  The findings were discussed with ___, M.D. by\n___, M.D. on the telephone on ___ at 1:51 ___, 2 minutes after\ndiscovery of the findings."
        },
        {
            "input": "Few punctate nonenhancing bifrontal and right parietal T2 and FLAIR\nhyperintense lesions, some which are associated with T1 hypointensity are\nnoted (see 13:59-69, 112, 22:55-66).  There is no evidence of hemorrhage,\nedema, masses, mass effect, midline shift or infarction.   The ventricles and\nsulci are normal in caliber and configuration.  There is no abnormal\nenhancement after contrast administration.",
            "output": "1. Supratentorial nonenhancing white matter lesions as described.  Findings\ncompatible with patient's reported history of chronic migraine headaches, with\ndifferential considerations of prior trauma, prior infection, microangiopathic\nchanges, and demyelinating process.\n2.  No acute intracranial abnormality.  No evidence of intracranial mass."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There are few scattered predominately periventricular T2/FLAIR\nhyperintensities as well as a single left frontal subcortical white matter\nhyperintensity.  These are nonspecific though commonly seen in setting of\nchronic small vessel disease.  There is no abnormal enhancement after contrast\nadministration.\n\nBilateral hippocampal formations and mammillary bodies are preserved in signal\nand configuration. There is no disproportionate medial temporal atrophy. There\nis no focal lobar encephalomalacia. There are no focal cortical dysplasias or\ngray matter heterotopia noted.\n\nMucosal thickening noted in the maxillary sinuses, ethmoid air cells, and left\nfrontal sinus.  There is a 1.3 x 1.8 cm FLAIR hyperintense lesion near midline\nthough just to the right at the root of the tongue.  This appears T1\nhypointense.  Postcontrast images did not include this area.",
            "output": "No focal abnormality to explain patient's symptoms.\nA 1.8 x 1.3 cm lesion at the root of the tongue near midline which is\nincompletely characterized.  Consider dedicated MRI of the neck to further\ncharacterize."
        },
        {
            "input": "Just off midline within the right root of tongue and splaying the inferior\naspect of the genioglossus muscles is a 1.7 cm AP x 1.2 cm TV x 1.1 cm SI T2\nhyperintense and T1 isointense lesion, which does not demonstrate definitive\npostcontrast enhancement.  There is suggestion of a T2 nodule along the\ninferior aspect of the lesion or septation without evidence of enhancement\n(series 4, image 19; series 5, image 19).\n\nThere is no evidence of mucosal masse or abnormal lymph nodes.  The neck\nvessels appear patent.  The salivary glands and thyroid appear normal.  No\nsuspicious osseous lesions.\n\nThere are multiple bilateral maxillary sinus mucous retention cysts measuring\nup to 2.1 cm on the left and 1.8 cm on the right.",
            "output": "1. Nonenhancing cystic lesion at the right root of tongue measuring up to 1.7\ncm, with apparent non enhancing small T2 isointense nodule along its inferior\naspects, felt likely to represent a thyroglossal duct cyst.  Additional\nconsiderations include includes dermoid cyst, although no intrinsic T1\nhyperintensity is identified within the lesion.  Follow-up could be performed\nto document stability.\n2. Bilateral maxillary sinus mucous retention cysts.\n3. Additional findings as described above."
        },
        {
            "input": "There is minimal luminal narrowing of the bilateral internal carotid arteries,\npresumably secondary to atherosclerotic disease, demonstrated on prior CT head\nof ___.  Otherwise, the MCAs, ACAS and their major branches are\nunremarkable without evidence of high-grade stenosis, occlusion or aneurysm. \nThe left vertebral artery is dominant, a normal anatomic variation.  There is\nfetal type origin of the right posterior cerebral artery.  The remainder of\nposterior circulation is unremarkable.\n\nIncidental note is made of extra-axial curvilinear T1 hyperintense signal\nalong the left parietal convexity (series 3, image 6), felt to likely\nrepresent signal within a cortical vein, which can be seen on prior CT head. \nT1 hypo intensities of the visualized corona radiata, centrum semiovale and\nbasal ganglia are compatible with perivascular spaces and sequela\nmicroangiopathy previously demonstrated on prior CT head.",
            "output": "1. Allowing for mild atherosclerotic disease of the bilateral internal carotid\narteries and normal anatomic variation, unremarkable MRA of the head.\n2. There is curvilinear extra-axial T1 hyperintense signal along the left\nparietal convexity, felt to represent signal within a cortical vein, which can\nbe seen on prior CT head.\n3. Given the patient's clinical symptoms, dedicated MRI of the head would be\nmore sensitive for evaluation of subtle infarct and microvascular changes.\n4. Additional findings as described above.\n\nRECOMMENDATION(S):  Given the patient's clinical symptoms, dedicated MRI of\nthe head would be more sensitive for evaluation of subtle infarct and\nmicrovascular changes."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  There is prominence of the ventricles and sulci suggestive\ninvolutional changes.   There is no abnormal enhancement after contrast\nadministration.  Periventricular and subcortical T2 and FLAIR hyperintensities\nare noted which may represent small vessel ischemic changes.  Minimal\nbilateral frontal and maxillary sinus and ethmoid air cell mucosal thickening\nis present.\n\nLimited imaging of the cervical spine demonstrates at least mild vertebral\ncanal narrowing at C3-4 (see 9:5), grossly similar compared to prior MRI.",
            "output": "1.  Study is mildly degraded by motion.\n2. No acute intracranial abnormality.\n3. No evidence of acute infarct or mass.\n4. Paranasal sinus disease , as described."
        },
        {
            "input": "There is no evidence of hemorrhage, masses, mass effect, midline shift or\nacute large territorial infarction.  There are postsurgical changes from prior\nright frontal craniotomy.  There is extensive encephalomalacia in the right\nfrontal and parietal lobes.  There is extensive edema in the right parietal\nand occipital lobes which extends across the splenium of the corpus callosum. \nThere is associated sulcal effacement.\n\nThere are a few scattered foci of susceptibility, consistent with blood\nproducts, possibly chronic.\n\nThere is atrophy of the right side of the brainstem, consistent with wallerian\ndegeneration.\n\nThe ventricles and sulci are prominent, consistent with involutional changes. \nThere is periventricular and subcortical white matter hypointensity, likely\nrepresenting chronic microvascular ischemic disease.",
            "output": "1. No acute infarct.\n2. Extensive edema in the right parietal and occipital lobes which extends\nacross the splenium of the corpus callosum, concerning for an infiltrative\ntumor such as a glioma or infiltrative process such as amyloid angiopathy\nrelated inflammation.  Recommend MRI of the brain with contrast for further\nevaluation.\n\nRECOMMENDATION(S):  Repeat MRI of the brain with contrast\n\nNOTIFICATION:  The findings were discussed with ___, M.D. by ___, M.D.\non the telephone on ___ at 2:24 pm, 10 minutes after discovery of the\nfindings."
        },
        {
            "input": "MR BRAIN:\nThere is a large infiltrative mass in the right cerebral hemisphere with\nirregular peripheral contrast enhancement and central nonenhancement,\ninvolving the right parietal, occipital, temporal, and posterior frontal\nlobes, which extends across the splenium and posterior body of the corpus\ncallosum along the atrium and occipital horn of the left lateral ventricle,\nwith a satellite peripherally enhancing lesion in the left occipital lobe. \nThe enhancing portions of the mass demonstrate intermediate T2 signal, with\nhigh T2 and low FLAIR signal of the central nonenhancing portions.  Portions\nof the enhancing components also demonstrate slow diffusion.\n\nThere is high signal on FLAIR images along the bilateral cerebellar folia,\nbrainstem, ventricular ependyma, and right greater than left seventh and\neighth cranial nerves on FLAIR images, suggesting leptomeningeal seeding.\n\nNonenhancing T2/FLAIR hyperintensities in the periventricular and deep white\nmatter of the left frontal and anterior parietal lobes may represent sequela\nof chronic small vessel ischemic disease, though nonenhancing tumor cannot be\nexcluded.\n\nWhere is the anterior aspect of the right lateral ventricle demonstrates ex\nvacuo dilatation from the chronic right middle cerebral artery territorial\ninfarction, the posterior body, temporal horn, and occipital horn are effaced.\nPosterior body of the left lateral ventricle is also slightly effaced compared\nto the ___ head CT, likely due to the enhancing mass in the posterior\ncorpus callosum.  There is only mild leftward shift of midline structures,\nlikely due to the underlying right-sided parenchymal volume loss secondary to\nthe chronic right MCA infarct.\n\nWallerian degeneration is seen within the right brainstem.  There are small\nchronic infarctions in the bilateral pons and left parietal corona radiata\n(14:20), a prominent perivascular space in the left thalamus, and a small\nchronic infarction versus prominent perivascular space in the left midbrain.\n\nThere are small foci of chronic blood products in the right basal ganglia,\nwhich may be secondary to the prior right MCA territory infarct, and within\nthe enhancing mass in the right inferior parietal lobe on image 13:14.  There\nis also mild gyriform low signal on gradient echo images along the right\noccipital lobe corresponding to enhancing tumor.\n\nThere is persistent opacification of the left frontal sinus, mucosal\nthickening within the ethmoid air cells, small mucous retention cyst within\nthe right maxillary sinus, and mild mucosal thickening in the sphenoid\nsinuses.  There is trace fluid within bilateral mastoid air cells.  There is\nalso fluid in the nasopharynx.  The fluid may be secondary to prolonged supine\npositioning in the inpatient setting.\n\nRight craniotomy is again noted with underlying chronic blood products.\n\nMR PERFUSION:\nThe mass demonstrates multiple areas of restricted diffusion, predominantly\nseen along the periphery.  Arterial spin labeling demonstrates numerous areas\nof increased perfusion, including increased perfusion within the left\nsubependymal enhancing nodule.  These findings are also confirmed on the MRI\ncontrast perfusion technique, although less conspicuous.\n\nMR SPECTROSCOPY:\nSingle and multi-voxel MRI spectroscopy demonstrates areas of increased\ncholine and creatine with decreased NAA, particularly affecting the\ninfiltrative portion of the tumor within the right splenium of the corpus\ncallosum.",
            "output": "1. Large, infiltrative mass with peripheral irregular contrast enhancement and\nscattered chronic blood products, involving the right parietal, occipital,\ntemporal, and posterior frontal lobes, and extending across the posterior\nright corpus callosum and along the atrium and occipital horn of left lateral\nventricle, with a satellite lesion in the left occipital lobe.\n2. Arterial spin labeling and contrast perfusion demonstrate multiple areas of\nincreased perfusion, many of which correlate with areas of restricted\ndiffusion on diffusion-weighted imaging.\n3. Single and multi voxel MRI spectroscopy demonstrates areas of decreased NAA\nand increased creatine/choline.\n4. The combination of the above findings suggests a high-grade primary CNS\nneoplasm, most likely a glioblastoma multiforme.\n5. Extensive FLAIR hyperintensity along the cerebellar folia, brainstem, and\nventricular ependyma, as well as along the left greater than right seventh and\neighth cranial nerve complexes, suggesting leptomeningeal malignancy.\n6. Chronic right MCA territory infarction with right frontal and insular\npredominance of volume loss, and Wallerian degeneration in the right\nbrainstem.  Chronic blood products in the right basal ganglia.\n7. Scattered small chronic infarctions in the left parietal corona radiata and\nbilateral pons.  Small chronic infarctions versus prominent perivascular\nspaces in the left thalamus and midbrain."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is an empty sella.  The major vascular flow voids are\npreserved.\n\nThe orbits, paranasal sinuses and mastoid air cells are normal.  The\nvisualized soft tissues are normal.",
            "output": "Normal brain MRI.  No acute infarct."
        },
        {
            "input": "MRI HEAD: The examination is slightly suboptimal secondary to patient motion\nartifact.\nThe patient is status post a right trans frontal ventriculostomy with the\nshunt terminating at the level of the third ventricle. This appears unchanged\nfrom prior CT examination. Interval decrease in size of hydrocephalus. There\nremains pneumocephalus particularly within the anterior horn of the right\nlateral ventricle, improved in size when compared to prior examination.\n\nThe patient is status post onyx embolization and CyberKnife treatment of a\nleft cerebellar AV malformation. The nidus and surrounding FLAIR hyperintense\nsignal involving the left cerebellar hemisphere extending up along the vermis\nand middle cerebellar peduncle into the pons is similar in size and extent\nfrom prior examination allowing for technical differences with the use of a\n1.5 Tesla magnet on today's exam versus the 3 Tesla magnet on the prior\nexamination, measuring approximately 3.3 x 4.6 by 3.6 cm (AP, TRV, CC). There\nremains mass effect on the fourth ventricle and mild rightward midline shift\nof the left cerebellar hemisphere, displacing the cerebellar vermis and right\ncerebellar hemisphere.\n\nThere is no evidence of acute intracranial hemorrhage or infarct. There are\nscattered periventricular and subcortical T2/FLAIR white matter\nhyperintensities, which are essentially unchanged in appearance from prior\nexamination, an commonly seen in the setting of small vessel ischemic disease.\nThe major intracranial flow voids are preserved.\n\nThe paranasal sinuses are essentially clear. The orbits are unremarkable,\nnoting bilateral lens replacements. The mastoid air cells are clear.\n\n\nHEAD MRA: As noted on prior examination the nidus is predominantly fed by a\nposterior inferior cerebellar, anterior inferior cerebellar and left superior\ncerebellar arteries. A large draining vein is identified , similar in\nappearance to prior examination. These appear similar appearance to prior\nexamination allowing for motion artifact.\n\n There is fetal origin of the to the right posterior cerebral artery. The\nright A1 segment is not visualized. Otherwise, the intracranial ICAs, ACAS,\nMCAs and their major branches are unremarkable.",
            "output": "1. The examination is slightly suboptimal secondary to patient motion.\nHowever, the left cerebellar hemisphere AV malformation appears essentially\nunchanged in size from prior MRI examination with blood products and extensive\nenhancement. The dominant draining vein appears unchanged.  AVM has\nconsiderably decrease from earlier CTA.\n2. The patient has undergone interval a right trans frontal ventriculostomy\nwith shunt terminating in the third ventricle. When compared to prior CT\nexamination there is decreased hydrocephalus and degree of pneumocephalus.\n3. Additional chronic findings as described above."
        },
        {
            "input": "Left cerebellar arterial venous malformation for which the patient has\nunderwent prior embolization and CyberKnife treatment has slightly decreased\nin size since the CTA of ___. The nidus currently measures 3.9 x 3.5 x 2.7\ncm (TRV x AP X CC) and previously measured 5.1 x 4.3 x 4.2 cm. The size\ndifference between conventional angiography and imaging studies is likely due\nto surrounding blood products and edema and technical differences.\nThe arteriovenous malformation is fed predominantly by the posterior\ncirculation vessels including the left posterior inferior cerebral artery,\nanterior inferior cerebellar artery and left superior cerebellar artery. \nProminent fluid related aneurysm noted in the medial aspect similar to the\nprior study.\n\nAssessment of contribution from external carotid artery branches is limited on\nthe present study.\nFoci of low signal on gradient echo sequences likely represent a chronic blood\nproducts. Adjacent high signal on FLAIR and T2 weighted sequences likely\nrepresents edema near the nidus. The AVM drains via a deep vein in the to the\nstraight sinus.\nThe left transverse sinus is absent/diminutive.\n\nThere is no right A1 segment, however, there is a robust anterior\ncommunicating artery which supplies both anterior cerebral arteries. There is\na fetal origin of the right posterior cerebral artery. The vertebral arteries\nand internal carotid arteries are widely patent. Subcortical and\nperiventricular foci of high signal on T2 weighted and FLAIR images is\nnonspecific but most likely represents the sequela of chronic small vessel\nischemic disease.",
            "output": "Compared to the prior CTA head of ___, a left cerebellar arterial venous\nmalformation has slightly decreased in size.  The nidus currently measures 3.9\nx 3.5 x 2.7 cm and previously measured 5.1 x 4.3 x 4.2 cm with some\nnonenhancing foci within, which can relate to interval treatment related\nchanges and obliteration of some of the vascular components.\nLimited assessment of the arterial and venous supply on routine MR study.\nCorrelate clinically to decide on the need for further workup or followup."
        },
        {
            "input": "There is a tiny focus of cortical DWI hyperintensity in the primary motor\ncortex (series 450, image 23).  No ADC correlate can be definitively\nidentified.  However, there are no T2/FLAIR lesions to suggest T2 shine\nthrough.\n There are scattered T2/FLAIR hyperintensities in the cerebral hemispheres\nbilaterally, a nonspecific finding and likely related to chronic small vessel\nischemic changes.\n\nThere is no evidence of hemorrhage, edema, masses, mass effect or midline\nshift.   The ventricles and sulci are normal in caliber and configuration.\n\nMajor vascular flow voids are preserved.\nThere is mild mucosal thickening of the ethmoid air cells and right maxillary\nsinus.  The remainder of the visualized paranasal sinuses is clear.  There is\npartial opacification of the inferior left mastoid air cells.  The right\nmastoid air cells are clear.",
            "output": "1. Tiny focus of cortical DWI hyperintensity in the primary motor cortex.  No\nADC correlate visualized, possibly due to its small size.  No corresponding\nT2/FLAIR lesions to suggest T2 shine through.  Therefore, this small focus of\nhyperintensity could represent a tiny infarct.\n2. Scattered white matter lesions in both cerebral hemispheres are nonspecific\nbut suggestive of chronic small vessel ischemic changes."
        },
        {
            "input": "There are punctate foci of mild slow diffusion within the right mid centrum\nsemiovale and anterior and genu of the right internal capsule (___). \nThere are FLAIR signal hyperintense foci within the bilateral central white\nmatter of cerebral central CSF signal which may represent chronic\nmicroangiopathy and/or old lacunar infarcts.  There is no evidence of\nhemorrhage or mass effect.  There is mild prominence of the ventricles.  The\nextra-axial spaces are unremarkable.  The orbits, calvarium, and soft tissues\nare unremarkable.  The vascular flow voids demonstrate a hypoplastic right A1\nsegment, otherwise the flow voids are preserved.  The paranasal sinuses and\nmastoid air cells are clear.",
            "output": "1. Punctate foci of mild slow diffusion within the right mid centrum semiovale\nand anterior and genu of the right internal capsule consistent with acute to\nsubacute infarcts.\n2. Nonspecific FLAIR signal hyperintense foci within the bilateral deep white\nmatter which likely represent sequela of chronic microangiopathy."
        },
        {
            "input": "There are postsurgical changes from left frontotemporal craniotomy and mass\nresection with underlying dural thickening and enhancement, small extra-axial\nfluid collection, small pneumocephalus, and postoperative blood product.  At\nthe superomedial aspect of the resection cavity, there is a residual 22 x 15\nmm focus of nodular enhancement (12:10).  A thin, linear rim of enhancement is\nseen surrounding the remainder of the resection cavity, slightly thick at the\nposterior portion (12:9).  Surrounding FLAIR hyperintensity, with involvement\nand mild expansion of the left medial temporal lobe extending posteriorly is\nessentially unchanged.  High signal on diffusion images in this area\ncorrespond to postoperative blood product.  Otherwise no new enhancing mass is\nseen.\n\nThere is no evidence of midline shift or infarction.   The background\nventricles and sulci are normal in caliber and configuration.  The principal\nintracranial vascular flow voids are preserved.\n\nThe visualized paranasal sinuses are grossly clear.  The orbits are grossly\nunremarkable.  There is minimal opacification of a few left-sided mastoid air\ncells.  The right mastoid air cells are clear.",
            "output": "1. Expected postoperative changes from left frontotemporal craniotomy and mass\nresection with residual 22 x 15 mm focus of nodular enhancement at the\nsuperomedial aspect of the resection cavity, with slightly thickened linear\nrim of enhancement at the posterior aspect of the resection cavity which is\nlikely residual tumor.  FLAIR signal abnormality along the medial temporal\nlobe extending posteriorly also most compatible with residual tumor.\n2. No new enhancing mass."
        },
        {
            "input": "There are evolving postsurgical changes from left frontal temporal craniotomy\nand mass resection, with a small amount of residual postoperative blood\nproducts, underlying dural thickening and enhancement.  Focus of nodular\nenhancement within the superomedial aspect of the surgical cavity has\ndecreased in size, currently measuring 10 x 9 mm (16:9), previously 22 x 15\nmm.  Thin linear rim of enhancement surrounding the remainder of the resection\nsite, with slight thickening along its posterior aspect, is essentially\nunchanged since ___.  Surrounding area of FLAIR hyperintensity,\npredominantly involving the left medial temporal lobe, has decreased in\noverall extent since ___, with interval resolution of left posterior\ntemporal lobe involvement.  There is no slowed diffusion within the resection\ncavity to suggest recurrent or progressive disease.  No new enhancing mass\nidentified.\n\nThere is no evidence of infarction, acute hemorrhage, edema or significant\nmidline shift.  Ventricles and sulci are age-appropriate.  Dural venous\nsinuses are patent on postcontrast MPRAGE images.  Principal intracranial\nvascular flow voids are preserved.\n\nNo osseous abnormalities identified.  Extra-axial soft tissues are\nunremarkable.  The visualized paranasal sinuses are clear.  Trace fluid within\nthe left mastoid air cells, unchanged.  The right mastoid air cells are clear.\nThe orbits are unremarkable.",
            "output": "1. Expected evolution of postsurgical changes from left frontotemporal\ncraniotomy and mass resection, with interval decrease in size of focus of\nnodular enhancement within the superomedial aspect of the resection cavity,\nnow measuring 10 x 9 mm.  Stable slightly thickened linear rim of enhancement\nalong the posterior aspect of resection cavity likely reflects residual tumor.\n2. Interval improvement in FLAIR signal abnormality within the right medial\ntemporal lobe with resolution of posterior component.\n3. No new enhancing lesion."
        },
        {
            "input": "Postoperative changes anterior left temporal lobe.  There is 3.1 cm x 2.8 cm x\n2.9 cm enhancing mass involving anterior left temporal lobe marginating the\nsurgical bed, compared with 2.5 cm x 2.5 cm x 2.8 cm.  Enhancement seen today\nis more confluent compared to prior.  Extra-axial zone of enhancement measures\n2.6 cm x 0.8 cm today, compared with 2.6 cm x 0.8 cm on prior, and is more\nhomogeneous day moderate surrounding nonenhancing T2 signal abnormality\ninvolving anterior left temporal lobe marginating the mass is more prominent. \nThere is minimally restricted diffusion centrally within enhancing component. \nThere are no new blood products.  There is minimal left uncal herniation,\nsimilar to prior, no mass effect on the adjacent vasculature or third cranial\nnerve.  There is no hydrocephalus, no midline shift.  There is linear dural\nthickening about surgical site, similar to prior, postoperative in etiology.\n\nThere is no evidence of hemorrhage, infarction.  Dural venous sinuses are\npatent.  Intracranial vascular flow voids are preserved.",
            "output": "1. Interval mild increase in previously seen anterior left temporal lobe mass,\nwith more homogeneous enhancement today, and worsened surrounding T2\nhyperintensity. Differential considerations tumor progression versus\nposttreatment change. MR spectroscopy, MR perfusion recommended in further\nevaluation.\n\nRECOMMENDATION(S):  MR spectroscopy, MR perfusion recommended in further\nevaluation."
        },
        {
            "input": "There is interval expansion of the area of enhancement within the surgical\nresection bed within the left anterior temporal lobe and progressive vasogenic\nedema within the cerebral hemisphere.  The area of enhancement measures\napproximately 4 cm in diameter, previously 3 cm in a similar transverse\ndimension.  The enhancement now extends into the margin of the left anterior\ntemporal lobe, left uncus and left insular region.  There is no\nintraventricular ependymoma enhancement.  There is 4 mm midline shift and mild\ndisplacement the uncus of the left temporal lobe into the suprasellar cistern,\nwithout downward herniation.  There is narrowing of the left lateral ventricle\nand third ventricle.  The right lateral ventricle appears unchanged.  There is\nno acute infarct or acute intracranial hemorrhage.\n\nThere is a small amount of fluid within left maxillary sinus.  The orbits are\nunremarkable.",
            "output": "1. Interval progression in the degree of thick enhancement and vasogenic edema\nwithin the region of the left temporal lobe surgical resection bed, worrisome\nfor local tumor progression.\n2. 4 mm midline shift and slight narrowing of the left suprasellar cistern,\nwithout downward herniation."
        },
        {
            "input": "The patient is status post left pterional craniotomy and resection of a left\nanterior temporal lobe mass.  Thick peripheral enhancement along the resection\nmargins, measuring 4.0 x 2.4 by 2.7 cm (AP, TRV, SI) as well as surrounding\nwhite matter edema pattern has decreased in size compared to immediate prior\nexamination of ___.  Resolution of mild effacement of the left\nlateral ventricle and left uncal herniation.\n\nThe sulci, ventricles and cisterns are otherwise within expected limits for\nthe patient's age.  Superimposed punctate periventricular and subcortical\nT2/FLAIR white matter hyperintensities are nonspecific, but compatible with\nchronic microangiopathy in a patient of this age.  No acute infarct or new\nhemorrhage.  The major intracranial flow voids are preserved.  The dural\nvenous sinuses are patent.  The visualized paranasal sinuses are essentially\nclear.  The orbits are unremarkable.  No fluid signal is noted in the mastoid\nair cells.",
            "output": "1. Significant interval decreased size thick enhancement along the left\nanterior temporal lobe resection margins as well as associated white matter\nedema pattern.  Resolution of mild effacement of the left lateral ventricle\nand left uncal herniation from prior examination.  No findings to suggest\ndisease progression at this time.\n2. No new enhancing lesion.\n3. Additional findings as described above."
        },
        {
            "input": "Status post left pterional craniotomy for resection of a left anterior\ntemporal lobe mass.  There has been no change to slight decrease in thickness\nof peripheral enhancement surrounding the resection cavity.  The degree of\nabnormal FLAIR signal within the left temporal lobe is not significantly\nchanged from prior.\n\nThe ventricles and sulci are normal in caliber and configuration.  Mild\nsuperimposed subcortical, deep and periventricular white matter T2/FLAIR\nhyperintensities are nonspecific but compatible with chronic small vessel\nischemic disease.  There is no acute infarct or new hemorrhage.\n\nThe major intracranial vascular flow voids are maintained.  The paranasal\nsinuses, mastoid air cells and orbits are normal.",
            "output": "1. Status post left pterional craniotomy for resection of a left anterior\ntemporal lobe mass with no change to slight decrease in peripheral enhancement\nsurrounding the resection cavity.\n2. No significant change in FLAIR signal abnormality within the left temporal\nlobe.\n3. No new enhancing lesions.\n4. No acute infarct or new hemorrhage."
        },
        {
            "input": "There is an irregular peripherally and heterogeneously enhancing mass in the\nleft temporal lobe spanning approximately 2.9 x 2.4 x 2.9 cm which\ndemonstrates some restricted diffusion (900:72, 901:65) with patchy extension\nenhancement along the medial temporal lobe (series 10, image 11).  There is\nsurrounding edema in the left temporal lobe, involving the medial temporal\nlobe including the hippocampus extending to the lingual gyrus (7:11).  There\nis no internal hemorrhage.  There are multiple tiny foci of adjacent\nenhancement (900:76, 901:71).  There is local sulcal effacement and effacement\nof the left lateral temporal horn.  Otherwise, the remainder of the sulci,\nventricles cisterns are within expected limits for the patient's age. The\nmajor intracranial flow voids are preserved.  The dural venous sinuses are\npatent on postcontrast MP-RAGE.\n\nThe paranasal sinuses and mastoid air cells are clear.  The orbits are grossly\nunremarkable.",
            "output": "2.9 cm irregular left temporal lesion with peripheral and heterogeneous\nenhancement, and multiple adjacent tiny satellite lesions, concerning for\nprimary intracranial neoplasm, specifically high-grade glioma, with metastatic\ndisease and abscess much less likely.  There is surrounding edema in the left\ntemporal lobe with involvement of the medial temporal lobe extending to the\nlingual gyrus"
        },
        {
            "input": "Re-identified is a heterogeneously rim enhancing left temporal mass measuring\napproximately 35 x 23 x 26 mm, unchanged compared to recent prior examination.\nMultiple tiny areas of adjacent satellite nodularity are noted, including a 5\nmm area of nodular discontinuous enhancement seen superomedially (03:57). \nPatchy areas of ill-defined surrounding enhancement are also seen. \nSurrounding edema appears overall grossly unchanged.  Adjacent dural\nthickening and enhancement is unchanged.  There remains localized mass effect\nwith effacement of the temporal horn of the left lateral ventricle.  No new\nenhancing lesion is seen.  There is no midline shift.\n\nThe background ventricles and sulci are normal in size and configuration.",
            "output": "1. Unchanged heterogeneously rim enhancing left temporal mass measuring\napproximately 35 x 23 x 26 mm with areas of peripheral satellite nodularity\nand ill-defined patchy enhancement, remaining suspicious for high-grade glial\nneoplasm.\n2. No new enhancing mass.\n3. This examination was performed for pre-surgical planning."
        },
        {
            "input": "MRI BRAIN:\n\nThere is no acute infarction.  There is no evidence for an intracranial mass,\nedema, or blood products.  Multiple small foci of T2 hyperintensity in the\nsubcortical, deep, and periventricular white matter of the cerebral\nhemispheres, as well as mild T2 hyperintensity in the pons, nonspecific but\nlikely the sequela of chronic small vessel ischemic disease in this age group.\nProminence of the ventricles and sulci indicates cerebral atrophy, not\nnecessarily expected at this age.  Major arterial flow voids are grossly\npreserved, and major dural venous sinuses appear patent on postcontrast MP\nRAGE images\n\nMRA NECK:\n\nThere is a 3 vessel aortic arch.  The common, internal and external carotid\narteries are patent.  Minimal irregularity of the proximal right internal\ncarotid artery, without stenosis by NASCET criteria, is likely\natherosclerotic.  Moderate irregularity of the proximal 2 cm of the left\ninternal carotid artery, without a stenosis by NASCET criteria, is likely also\natherosclerotic.  MIPS suggest narrowing at bilateral vertebral artery\norigins, but this could be artifactual.  The remainder of the vertebral artery\ncourses appear widely patent.\n\nMRA BRAIN:\n\nThe intracranial vertebral and internal carotid arteries and their major\nbranches are patent without evidence of stenosis, occlusion, or aneurysm\nlarger than 2 mm. There is fetal origin of the right posterior cerebral\nartery.  There is fenestration of the distal A1 segment of the right anterior\ncerebral artery, as well as a fenestration at the junction of the A1 and A2\nsegments of the left anterior cerebral artery.  The anterior communicating\nartery is either diminutive or absent.",
            "output": "1. No acute infarction.\n2. Extensive supratentorial white matter signal abnormalities, and well of\nmild signal abnormality in the pons, are nonspecific but likely the sequela of\nchronic small vessel ischemic disease in this age group.\n3. Irregularity of the proximal internal carotid arteries, left greater than\nright, presumably atherosclerotic, without stenosis by NASCET criteria.\n4. Bilateral vertebral artery origins appear narrowed, but it is not clear\nwhether this finding is artifactual.\n5. No evidence for flow-limiting intracranial stenosis.\n6. Fenestrations within bilateral anterior cerebral arteries, as detailed\nabove."
        },
        {
            "input": "MR BRAIN:\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  Subtle periventricular and deep subcortical FLAIR white matter\nhyperintensities are likely sequelae of chronic small vessel ischemic disease.\n\nMild mucosal sinus thickening is seen involving the maxillary sinuses and\nmoderate sinus thickening involving the ethmoid air cells.  The previously\nnoted fractures of the right lamina papyracea and orbital floor are not well\nevaluated on this exam, however note is made of fat herniation into the right\nethmoid air cells sequelae of patient's fracture.  The globes are otherwise\nunremarkable.  The principal vascular flow voids appear to be well preserved.\n\nMRA brain: The intracranial vertebral and internal carotid arteries and their\nmajor branches appear normal without evidence of stenosis, occlusion, or\naneurysm formation.",
            "output": "1. No acute intracranial abnormalities identified.  The previously noted\nsubarachnoid hemorrhage on CT is not well seen on this exam and may be\nsecondary to redistribution.  No new hemorrhage is seen.\n2. Mild-to-moderate sinus disease.  The previously noted fractures the right\nlamina papyracea and orbital floor are not well evaluated on this exam however\nthe fat herniation into the right ethmoid air cells sequelae of patient's\nfracture is seen.\n3. Unremarkable MRA of the brain without evidence of aneurysm."
        },
        {
            "input": "There is slow diffusion in the head of the left caudate nucleus, anterior limb\nof the left internal capsule, in the anterior aspect of the left lentiform\nnucleus, in the anterior aspect of the right lentiform nucleus and genu and\nanterior limb of the right internal capsule, in keeping with recent\ninfarction. There is associated T2/FLAIR hyperintensity.  There is no evidence\nof hemorrhagic transformation.  There are a few scattered supratentorial white\nmatter T2/FLAIR hyperintense foci, which are nonspecific and may represent\nmild chronic small vessel ischemic disease.  There is a small old infarct\nadjacent to the trigone of the left lateral ventricle.\n\nThere is no evidence of masses, mass effect or midline shift.   The ventricles\nand sulci are normal in caliber and configuration.",
            "output": "1. Recent infarcts involving thehead of the left caudate nucleus, anterior\nlimb of the left internal capsule, in the anterior aspect of the left\nlentiform nucleus, in the anterior aspect of the right lentiform nucleus and\ngenu and anterior limb of the right internal capsule.  No evidence of\nhemorrhagic transformation.\n2.  Old infarct adjacent to the trigone of the left lateral ventricle."
        },
        {
            "input": "There is no evidence of intracranial hemorrhage, mass, mass effect or shifting\nof the normally midline structures.  The ventricles and sulci are normal in\nsize and configuration.  There is no evidence of abnormal enhancement after\ncontrast administration, no diffusion abnormalities are detected.  The\nhigh-resolution images throughout the posterior fossa demonstrates normal\ncerebellar pontine angles as well as internal auditory canals, the major\nvascular flow voids are present and demonstrate normal distribution.\nSlightly prominent perivascular spaces appear unchanged in the basal ganglia\nbilaterally.\nThe orbits appear normal, the paranasal sinuses, middle ear cavities and\nmastoid air cells are clear.",
            "output": "1. No evidence of intracranial mass lesion.  No abnormal enhancement along the\nV1 distribution.\n2. There is no evidence of acute intracranial process or hemorrhage."
        },
        {
            "input": "There is susceptibility artifact in the right posterior scalp of uncertain\netiology, likely related to hardware outside of the patient.  This limits the\nevaluation, especially on the gradient echo and diffusion-weighted images.\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are patent and prominent in keeping\nwith age-related volume loss.\n\nThere are scattered foci and more confluent areas of T2/FLAIR hyperintensity\nin the subcortical and periventricular white matter, nonspecific, likely\nsecondary to small vessel ischemic disease.\n\nThe orbits are unremarkable.  There is mild mucosal thickening in bilateral\nmaxillary sinuses, bilateral ethmoid air cells and right frontal sinus.  Also\nseen is moderate mucosal thickening in bilateral sphenoid sinuses.  Fluid\nopacification of bilateral mastoid air cells.  Intracranial flow voids are\nmaintained.",
            "output": "1. No acute intracranial abnormality.\n2. Findings of small vessel ischemic disease in age-related involutional\nchanges.\n3. Paranasal sinus disease and fluid opacification of bilateral mastoid air\ncells as described above."
        },
        {
            "input": "2 mm nodular enhancement left IAC fundus, may represent small schwannoma,,\nconsider ___'s palsy, ___ if appropriate.  Metastasis is unlikely in\nthe absence of history of malignancy follow-up exam recommended to document\nstability, exclude other etiologies.  Remainder of the seventh cranial nerve\nis normal.  Left stylomastoid foramen fat pad is preserved, visualized left\nparotid gland is normal.\n\nprominent retrocerebellar CSF space consistent with ___ cisterna magna or\narachnoid cyst, similar to prior.\n\nThere is no evidence of infarction, hemorrhage, edema, mass, or mass effect. \nNo abnormal enhancement.  No evidence of demyelination. The ventricles and\nsulci are normal in caliber and configuration.\n\nA few scattered small periventricular, deep, and subcortical white matter\nFLAIR hyperintensities are nonspecific but are compatible with very mild\nchanges of chronic white matter microangiopathy.\n\nThere is trace fluid layering in the left aspect of the sphenoid sinus. \nRemaining visualized paranasal sinuses, mastoids, appear clear.  The globes\nand orbits are unremarkable.\n\n Major intracranial vascular flow voids are preserved. Major dural venous\nsinuses are patent.",
            "output": "Left IAC fundus 2 mm nodular enhancement, differential considerations\nschwannoma, Bell's palsy, ___ syndrome.  Follow-up exam recommended if\nindicated, especially if there is history of malignancy."
        },
        {
            "input": "Again seen is a 2 mm nodular focus of enhancement within the left IAC (16:43)\nwhich is unchanged in comparison to the previous study dated ___. \nFindings likely reflect small schwannoma.  Otherwise, images through the\ninternal auditory canals demonstrate symmetric appearance of the seventh\neighth nerve complexes.  There is no evidence of abnormal enhancement or mass\nlesion within the right internal auditory canal.  No evidence of abnormal\nenhancement or mass lesion within the cerebellopontine angles or membranous\nlabyrinth.  Again seen is prominence of the retrocerebellar CSF space\nconsistent with ___ cisterna magna versus arachnoid cyst, similar in\nappearance to the ___ CT head.\n\nLimited included imaging of the remainder of the brain demonstrates no\nevidence of hemorrhage, edema, masses, mass effect, midline shift\norinfarction.  There is mild prominence of the ventricles and sulci compatible\nwith involutional changes.  A few periventricular and subcortical T2 and FLAIR\nwhite matter hyperintensities are noted which are nonspecific but compatible\nwith small vessel ischemic changes.\n\nNo osseous abnormalities are seen. The paranasal sinuses, mastoid air cells,\nand middle ear cavitiesare clear. The orbits are unremarkable. The principal\nvascular flow voids are preserved.  The dural venous sinuses are patent.",
            "output": "1. 2 mm nodular focus of enhancement within the left IAC is unchanged in\ncomparison to the previous study dated ___.  Given appearance and\nstability since the prior study, Findings likely reflect small schwannoma.\n2. Ancillary findings, as above."
        },
        {
            "input": "There is restricted diffusion in the left occipital lobe, left thalamus, and\nright cerebellar tonsil associated with T2/FLAIR hyperintense signal.  There\nis no evidence of hemorrhage, edema, masses, mass effect, midline shift. \nScattered foci of T2/FLAIR hyperintensities in the supratentorial white matter\nare nonspecific, but may represent the sequela of chronic small vessel\nischemic disease.  The ventricles and sulci are normal in caliber and\nconfiguration.\n\nLoss of the flow void in the right intradural vertebral artery corresponds to\nthe occlusion seen on recent prior CTA.\n\nThe left maxillary sinus contains a large mucous retention cyst.  The mastoid\nair cells are clear.  The visualized orbits are unremarkable.",
            "output": "1. Acute infarctions of the left occipital lobe, left thalamus, and right\ncerebellar tonsil.\n2. Occlusion of the right intradural vertebral artery.\n\nNOTIFICATION:  The findings were discussed by Dr. ___ with Dr. ___ on the\ntelephone on ___ at 10:20 AM."
        },
        {
            "input": "MRI BRAIN:\nThere is no evidence of intracranial hemorrhage, edema, masses, mass effect,\nmidline shift or infarction.   The ventricles and sulci are normal in caliber\nand configuration.  In comparison with the prior examination dated ___, there is interval progression in the patchy periventricular T2/FLAIR\nhyperintensities, which are nonspecific, however are most likely consistent\nwith chronic microvascular angiopathy.  No diffusion abnormalities are\ndetected.  There is no abnormal enhancement after contrast administration.\n\nMRA BRAIN:\nThe intracranial vertebral and internal carotid arteries and their major\nbranches appear normal without evidence of stenosis, occlusion, or aneurysm\nformation.  There is fetal origin of the right PCA.\n\nMRA NECK:\nThe common, internal and external carotid arteries appear normal.  There is no\nevidence of internal carotid artery stenosis by NASCET criteria.  The origins\nof the great vessels, subclavian and vertebral arteries appear normal\nbilaterally.",
            "output": "1. In comparison with the prior brain MRI examination, dated ___,\nthere is interval progression in the patchy periventricular T2/FLAIR\nhyperintensities, which are nonspecific, however are most likely consistent\nwith chronic microvascular ischemic changes.\n2. There is no evidence of acute intracranial process or hemorrhage.\n3. Essentially normal MRA of the head and neck, with no evidence of flow\nstenotic lesions or aneurysms."
        },
        {
            "input": "Motion graded exam.\n\nRight frontal approach intraventricular catheter remains stable in position\ncoursing through the left lateral ventricle and terminating in the region of\nthe left basal ganglia.  Ventricular system remains mildly enlarged, similar\nin size to prior exam, which could be on the basis of involutional changes and\npossible obstruction from blood products.\n\nRedemonstration of left thalami could intraparenchymal hemorrhage with\nextension intraventriculary, predominately in the left lateral ventricle. \nOverall, amount of hemorrhage is unchanged compared to most recent prior CT\ndated ___ with interval evolution of blood products.  No definite\nevidence of new hemorrhage. Suspected small chronic microhemorrhage in the\nleft frontal lobe (image 14 of series 12).\n\nApparent hyperintense signal abnormality on diffusion-weighted images\ncorresponding to the periphery of the blood products likely relates to\nsusceptibility effects as well as acute compressive changes related to the\nblood products.\n\nPunctate foci of restricted diffusion in the left temporoparietal lobes\n(images 17, ___ series 17) are compatible with acute infarctions.\n\nSmall rounded areas of enhancement in the left thalamic hemorrhage are favored\nto represent focal areas of gadolinium accumulation, possibly related to\nextravasation.  No definite focal underlying mass is identified.  Few punctate\nfoci of superficial distribution chronic microhemorrhage, consistent with\namyloid angiopathy.\n\nModerate mucosal thickening of the paranasal sinuses.  Fluid signal in the\nnasopharynx may relate to nasoenteric tube.  Mild bilateral mastoid\nopacification.  Unremarkable intraorbital contents.",
            "output": "1. Stable 4.2 cm acute parenchymal hematoma centered in the left thalamus,\nwith intraventricular extension, mild hydrocephalus. Small areas of\nenhancement in the left thalamic hemorrhage may represent contrast\nextravasation, vascular malformation. Follow-up to resolution recommended. No\ndefinite mass.\n2. Acute punctate infarctions in the left temporoparietal lobes.\n3. Right frontal ventricular drain, small areas of parenchymal hemorrhage\nalong the drain tract.\n4. Findings consistent with amyloid angiopathy.\n\nRECOMMENDATION(S):  1.  Follow-up head CT without contrast within 24 hours.\n2. Long term follow-up to ensure resolution.\n\nNOTIFICATION:   The findings were discussed with ___, M.D. by ___\n___, M.D. on the telephone on ___ at 2:54 pm, 5 minutes after\ndiscovery of the findings."
        },
        {
            "input": "MRA ___: There is no evidence of intracranial hemorrhage, mass or acute\ninfarct.  Ventricles, cisterns and sulci show symmetric, age-related\nprominence. Scattered FLAIR/T2 hyperintensities likely represent underlying\nmicrovascular changes. The patient is status post left lens surgery. A left\nmaxillary sinus mucus retention cyst is incidentally noted.  \n\nMRA HEAD: There are regions of likely artifactual decreased flow-related\nenhancement within the bilateral carotid siphons, with underlying\natherosclerosis. The more peripheral intracranial arteries show mild\natherosclerotic lumenal irregularity.",
            "output": "1.  No acute infarct, hemorrhage or mass.\n\n2.  Mild intracranial atherosclerosis, with artifact limiting evaluation of\nthe carotid siphons."
        },
        {
            "input": "There is no evidence of flow-limiting stenosis within the neck. \nMild intracranial atherosclerosis is better demonstrated on the MRA of the\nhead.",
            "output": "No flow-limiting stenosis within the neck."
        },
        {
            "input": "There is no evidence of acute intracranial hemorrhage, edema, masses, mass\neffect, midline shift or infarction.  There is no slowed diffusion.  The\nventricles and sulci are mildly prominent, suggestive of involutional changes.\nMild periventricular white matter FLAIR/T2 hyperintensities are nonspecific,\nbut likely sequela of chronic small vessel ischemic disease.  Chronic area of\nencephalomalacia is identified posterior to the right ventricular trigone with\nmild ex vacuo dilatation of the right occipital ventricular horn (image 13,\nseries 6), incidental note is made of a cavum septum pellucidum et vergae, an\nanatomical variant.  Bilateral opacities are visualized in the mastoid air\ncells, more significant on the right, apparently unchanged since the prior\nhead CT dated ___.",
            "output": "1.  No acute intracranial process or other MRI findings to explain the\npatient's encephalopathy.  There is no slow diffusion to suggest infarction.\n\n2.  Age related involutional change and sequelae from chronic small vessel\nischemic disease.\nUnchanged area of encephalomalacia identified posterior to right ventricular\ntrigone as described above.\n\n3.  Persistent opacification of the mastoid air cells, more significant on the\nleft."
        },
        {
            "input": "Study is moderate-to-severely degraded by motion.  Within the confines of the\nstudy, the principal visualized bilateral anterior cerebral arteries, middle\ncerebral arteries, and posterior cerebral arteries appear patent.  The basilar\nartery and bilateral vertebral arteries appear patent.  The bilateral\nintracranial internal carotid arteries appear patent.  There is no definite\nevidence of significant stenosis, occlusion, or aneurysm.",
            "output": "1. Study is moderate to severely degraded by motion.\n2. Within the confines of this study, no definite evidence of stenosis,\nocclusion, or aneurysm."
        },
        {
            "input": "Significantly degraded study due to motion artifact.  Within these confines:\n\nThere is a 1 cm T1 hyperintense focus along the inner table of the right\nparietal calvarium (series 11 image 19) corresponds to the calcification seen\non prior CT head.  There is no evidence of hemorrhage, edema, mass effect,\nmidline shift or infarction.  There are periventricular and subcortical white\nmatter foci of T2/FLAIR signal hyperintensity, nonspecific but likely sequelae\nof chronic microangiopathy.  There is prominence of the ventricles and sulci\nsuggestive of age-related involutional changes.  Abnormal enhancement is\ndifficult to evaluate due to severe image degradation.",
            "output": "1. Significantly degraded study due to motion artifact.\n2. Within these confines, no evidence of hemorrhage or infarction.  Abnormal\ncontrast enhancement is difficult to evaluate due to severe image degradation.\n3. Nonspecific 1 cm T1 hyperintense focus along the inner table of the right\nparietal calvarium corresponding to the calcification seen on prior CT head\nmay represent a meningioma.\n4. Periventricular and subcortical white matter signal changes, nonspecific\nbut likely sequelae of chronic small vessel disease.\n5. Cerebral atrophy."
        },
        {
            "input": "There are periventricular and subcortical white matter foci of T2/FLAIR signal\nhyperintensity, nonspecific but likely sequelae of chronic microvascular\ndisease.  The ventricles and sulci are prominent suggestive of involutional\nchanges.  There is questionable increased signal intensity in the bilateral\nhippocampi.  There is no evidence of hemorrhage, edema, masses, mass effect,\nmidline shift or infarction.  There is no abnormal enhancement after contrast\nadministration.\n\nThere is mucosal thickening within the ethmoid air cells, sphenoid sinus and\nleft maxillary sinus.",
            "output": "1. No infarction, hemorrhage, mass or abnormal enhancement.\n2. Increased FLAIR signal abnormality within the bilateral hippocampi. \nDifferential considerations include postictal changes or encephalitis not\nexcluded.  Continued attention on follow up.\n3. Periventricular and subcortical white matter signal changes, nonspecific\nbut likely sequelae of chronic small vessel disease.\n4. Cerebral atrophy."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.\nThe diffusion images demonstrate several foci of slow diffusion in the parotid\nglands bilaterally.  These are not well characterized on the remainder of the\nstudy.",
            "output": "1. Multiple bilateral small parotid lesions, incompletely characterized.\n2. Otherwise normal brain MRI."
        },
        {
            "input": "DOSE T2 and FLAIR hyperintensity in both frontal lobes extending across the\ngenu of corpus callosum. There is no evidence of blood products seen in this\nregion. Following gadolinium irregular areas of enhancement are seen in both\nfrontal lobes and in the genu of corpus callosum. Additional satellite lesions\nare also identified in both frontal lobes. There is mass effect on the\nanterior on the lateral ventricles. These findings are suggestive of a primary\nneoplasm such as glioma. There is no midline shift or hydrocephalus seen. No\nacute infarcts are identified.\n\nMild mucosal thickening is seen in the maxillary sinuses as well as in the\nethmoid and frontal sinuses.",
            "output": "Bifrontal enhancing lesion involving the genu of corpus callosum indicating a\nprimary neoplasm such as glioma."
        },
        {
            "input": "Please note the study is degraded by motion.\n\nThere is redemonstration of irregular enhancement in by lateral frontal lobes,\nthe genu of the corpus callosum, with additional satellite lesions within\nbilateral frontal lobes. There is also redemonstration of grossly stable\nbilateral ethmoid, maxillary mucosal thickening.",
            "output": "1. Limited imaging for the purposes of pre-surgical planning again demonstrate\nthe patient's previously noted irregular enhancing bifrontal mass with\nextension to the genu of the corpus callosum, with additional satellite\nlesions again seen in bilateral frontal lobes.\n2.  Paranasal sinus disease as described."
        },
        {
            "input": "There are postsurgical changes of right frontal approach stereotactic biopsy\nwith postbiopsy blood products. Enhancing lesions within bilateral frontal\nlobes and genu of the corpus callosum have markedly decreased in size from\nprior MRI on ___.  A residual round enhancing lesion within the\nright frontal lobe measures 1.3 x 1.1 cm (AP x TV), and the residual corpus\ncallosum lesion measures 1.4 x 2.3 cm.  There are other subcentimeter\nenhancing lesions in the subcortical anterior right frontal lobe (series 19,\nimage 67), in the inferior medial right frontal lobe adjacent to the callosal\nlesion (series 17, image 108), and in the left frontal lobe (series 19, image\n79).  No new enhancing lesions are identified.  Right greater than left\nfrontal vasogenic edema has improved from prior MRI, with resolved shift of\nmidline structures and re-expansion of the right lateral ventricle.  There is\nno significant mass effect at this time.  Mildly slowed diffusion associated\nwith the residual enhancing lesions is consistent with a diagnosis of\nlymphoma.\n\nMajor intravascular flow voids are preserved.  There is normal patency of the\nmajor intracranial arteries and dural venous sinuses following contrast\nadministration.\n\nThere is mild mucosal thickening of the ethmoid air cells and right greater\nthan left maxillary sinuses.  There is a tiny amount of fluid in the left\nmastoid air cells.",
            "output": "Multiple enhancing lesions within the frontal lobes and corpus callosum have\nmarkedly decreased in size compared to ___, with decreased edema and\nresolution of mass effect.  No new lesions are seen."
        },
        {
            "input": "A 29 x 13 mm enhancing lesion is identified in the genu of corpus callosum\nwhich has increased in size compared to the previous MRI examination. However,\nif previously seen 13 mm separate enhancing lesion in the right frontal lobe\nadjacent to the genu of corpus callosum has resolved.  Subtle enhancement is\nseen in this region.  In addition, a punctate area of enhancement in the left\nfrontal lobe previously visualized on series 16, image 18 is no longer visible\non the current examination.  A punctate region of enhancement in the right\nfrontal lobe previously seen on series 16, image 16 is also no longer visible.\nThere are no new areas of abnormal enhancement seen.  The edema identified the\nfrontal lobe is unchanged.  A small area of chronic blood products is seen in\nthe frontal lobe.  There is no midline shift seen.  Opacification of the right\nmaxillary sinus has increased from the previous study.",
            "output": "Increase in size of enhancing lesion within the genu of corpus callosum but\nwith resolution of previously seen 13 mm right frontal lobe lesion and\npunctate bifrontal lesions .  No change in frontal FLAIR hyperintensities.  No\nnew enhancing lesions."
        },
        {
            "input": "MRI BRAIN:\nPreviously seen enhancing lesion in the genu of the corpus callosum has\nincreased in size compared to the prior exam, now measuring 3.6 x 1.8 x 2.5\ncm, previously 2.9 x 1.3 x 1.7 cm.  In addition, there is increased\nsurrounding edema and mass effect on the frontal horn of the right lateral\nventricle.  The basal cisterns are patent.\n\nMRA brain: The intracranial vertebral and internal carotid arteries and their\nmajor branches appear normal without evidence of stenosis, occlusion, or\naneurysm formation.",
            "output": "1. 3.6 x 1.8 x 2.5 cm enhancing mass in the genu of the corpus callosum,\nenlarged compared to prior exam with increased surrounding edema and mass\neffect on the frontal horn of the right lateral ventricle.  Patent basal\ncisterns.\n2. No significant stenosis or occlusion of the vessels of the circle of ___\nand its major tributaries.\n\nNOTIFICATION:  The findings were discussed by Dr. ___ with Dr. ___\n___ on the telephoneon ___ at 4:40 ___, 5 minutes after discovery of\nthe findings."
        },
        {
            "input": "Study is mildly degraded by motion.  There is a 0.5 (AP) x 2.3 (TV) x 0.6 (SI)\ncm homogeneously enhancing mass at the genu corpus callosum extending to the\nright forceps minor (see19:74), which has significantly decreased in size as\ncompared to prior study when it measured 1.8 (AP) x 3.6 (TV) x 2.5 (SI) cm. \nThere is bilateral frontal subcortical white matter FLAIR hyperintensity,\nright greater than left, which is decreased in comparison to prior study. \nStable faintly peripherally enhancing approximately 4 x 5 mm right frontal\nlesion is again seen, grossly unchanged (see 19:76 on current study and\n1000:67 on prior exam).\n\nThere is no acute infarct, hemorrhage, or mass effect.  There is mild\nprominence of the ventricles.  The extra-axial spaces are unremarkable.  The\nvasculature is patent.\n\nThe orbits and soft tissues are unremarkable.  There is a right frontal burr\nhole.  There is mild paranasal sinus mucosal thickening.  There are trace\nbilateral mastoid air cell effusions.",
            "output": "1.  Study is mildly degraded by motion.\n2. Interval decrease in size and extent of genu corpus callosum mass an\nadjacent parenchymal signal intensity abnormality, with enhancing mass now\nmeasuring approximately 0.5 x 2.3 x 0.6 cm.\n3. Stable approximately 4 x 5 mm right frontal minimally peripherally\nenhancing lesion as described.\n4. No new enhancing lesions.\n5. Paranasal sinus disease as described."
        },
        {
            "input": "There is a right frontal burr hole from prior biopsy.  There is minimal\nchronic hemorrhage near the burr hole and a few foci in the right frontal lobe\nnear the anterior horn of the right lateral ventricle (06:15), unchanged. \nArea of enhancement in the genu of the corpus callosum extending to the right\nforceps minor (___) measures 2.5x0.8x0.9 cm TRV x AP x CC, overall\nunchanged allowing for differences in slice selection measurement technique. \nA developing central area of nonenhancement may reflect interval necrosis.  A\n7 mm adjacent focus in the right frontal lobe (901b:78) is significantly less\nconspicuous with very faint peripheral enhancement.  Periventricular FLAIR\nhyperintensity, right greater than left, predominantly around the frontal\nhorns is overall unchanged.\n\nThere is no evidence of acute infarct or intracranial hemorrhage size and\nconfiguration of the lateral ventricles is unchanged.  The major intracranial\narterial flow voids are preserved.  The dural venous sinuses are patent. \nThere is worsening mucosal thickening in the right maxillary sinus.",
            "output": "1. Overall unchanged size of enhancing mass in the genu of the corpus\ncallosum.  Evolving central area of nonenhancement may reflect treatment\nrelated necrosis.\n2. Adjacent 7 mm focus in the right frontal lobe is less conspicuous now with\nonly faintly appreciable peripheral enhancement.\n3. Mucosal thickening in the right maxillary sinus has progressed."
        },
        {
            "input": "A right frontal burr hole related to prior biopsy is against.  The foci of\nsusceptibility underlying the burr hole and in the white matter adjacent to\nthe right frontal horn of the lateral ventricle are unchanged.  The enhancing\nlesion with irregular margins in the genu of the corpus callosum appears more\nheterogeneous and has increased in size, measuring 1.8 x 2.9 x 1.7 cm,\npreviously measuring 0.8 x 2.5 x 0.9 cm.  It now abuts a larger surface area\nof the frontal horn of the right lateral ventricle.  The central area of\nnonenhancing T1/T2 hypointense signal within the enhancing mass in the right\nfrontal periventricular white matter has increased in size and likely\nrepresents necrosis.  Surrounding T2 hyperintensity has increased in the right\nfrontal white matter was not significantly changed in the left frontal white\nmatter.\n\nA 7 mm rim enhancing lesion along the right lateral margin of the dominant\nlesion, image 19:98, did not demonstrate rim enhancement on ___,\nbut demonstrate rim enhancement on ___ and ___\n\nNo new enhancing lesions are identified.  There is no evidence for acute\ninfarction or new blood products.  Aside from the right frontal lobe,\nventricles and sulci are normal in size.\n\nThere is minimal mucosal thickening in the right maxillary sinus and mild\nmucosal thickening in the bilateral ethmoid sinuses.\n\nThe major intracranial flow voids are preserved.  Major dural venous sinuses\nappear patent on postcontrast MP RAGE images.",
            "output": "1. Compared to ___, there has been enlargement of the enhancing\nmass in the genu of the corpus callosum with increased extent along the\nfrontal horn of the right lateral ventricle, increased central necrosis, and\nincreased vasogenic edema in the right frontal lobe, with stable vasogenic\nedema in the left frontal lobe.  This is compatible with sequela of radiation\ntherapy, though tumor progression cannot be excluded.\n2. 7 mm rim enhancing lesion along the right lateral margin of the dominant\nlesion is again seen.  It did not demonstrate enhancement on ___,\nbut it was rim enhancing on ___.  This is also compatible with\nsequela of radiation therapy, the tumor progression cannot be excluded.\n3. No new enhancing lesions."
        },
        {
            "input": "MR BRAIN:  A right frontal burr hole related to prior biopsy is unchanged. \nThe foci of susceptibility underlying the burr hole and white matter adjacent\nto the right frontal horn of the lateral ventricle, representing chronic blood\nproducts, are unchanged.  The enhancing lesion with irregular margins and\ncentral necrosis in the genu of the corpus callosum and surrounding the\nfrontal horn of the right lateral ventricle is unchanged from ___,\nbut increased in size from ___.  An adjacent 7 mm rim enhancing\nlesion in the right lateral margin of the dominant lesion is unchanged.  A 9 x\n7 mm rim enhancing lesion in the right anterolateral margin of the dominant\nlesion on 11:19 is more conspicuous in comparison to ___ and new\nfrom ___.  No other enhancing lesions are identified. The\nsurrounding, confluent T2/FLAIR hyperintense signal in the bilateral frontal\nlobes and genu of the corpus callosum is unchanged from ___, but\nslightly increased from ___.\n\nThere is no evidence for acute infarction or new intracranial hemorrhage.\n\nThere is mild mucosal thickening in the bilateral anterior ethmoid sinuses. \nThe bilateral mastoid tips or minimally opacified.  The orbits are\nunremarkable.  The major intracranial flow voids are preserved.\n.\nMR ___: There is no increased cerebral blood flow or blood\nvolume to the area of enhancement in the right frontal lobe and genu of the\ncorpus callosum.\n\nASL Perfusion: There is no increased perfusion to the area of enhancement in\nthe right frontal lobe and genu of the corpus callosum.\n\nMR Spectroscopy: Single and multi voxel spectroscopy were technically\nunsuccessful and nondiagnostic..",
            "output": "1. Interval increase in the size of the irregularly enhancing lesion in the\ngenu of the corpus callosum and along the frontal horn of the right lateral\nventricle with increased central necrosis and increased surrounding T2/FLAIR\nhyperintense signal in the bilateral frontal lobes in comparison to ___.  No increased cerebral blood flow, cerebral blood volume, or ASL\nperfusion to this region.  These findings most likely represent postradiation\nchanges.  Progressive neoplasm cannot be excluded and follow-up is\nrecommended.\n2. Unchanged 7 mm rim enhancing lesion along the right lateral margin of the\ndominant lesion and new 9 mm rim enhancing lesion in the right anterolateral\nmargin of the dominant lesion in comparison to ___, which may also\nrepresent postradiation changes.  Progressive neoplasm cannot be excluded and\nfollow-up is recommended.\n3. Nondiagnostic single and multi voxel spectroscopy."
        },
        {
            "input": "MR BRAIN:  Again seen is a mass in the corpus callosum extending into the\nfrontal white matter bilaterally.  There is extensive surrounding white matter\nedema and resulting mass effect.  The FLAIR images demonstrate hyperintensity\nalong the falx bilaterally, greater on the left than right, in a pattern that\nsuggests leptomeningeal spread of tumor.  The volume of enhancing material has\nincreased substantially since the study of ___.  There is now with a\nlarge area centrally within the mass that does not enhance, presumably\nrepresenting necrosis.\n\nDynamic susceptibility Contrast Perfusion: There is no evidence of increased\nblood volume or blood flow in the anterior corpus callosum in the location of\nthe enhancing lesion.  These findings suggest extensive necrosis..\n\nASL Perfusion: There is no evidence of increased blood flow in the anterior\ncorpus callosum in the location of the lesion and.  This suggests necrosis.\n\n\nMR Spectroscopy: There are multiple areas of marked increased choline in the\nregion of the enhancing lesion.  This is worrisome for viable tumor.\n\nDiffusion: The diffusion throughout the bulk of the lesion is rapid.  However,\nthe area adjacent to the frontal horn of the right lateral ventricle\ndemonstrates slow diffusion, which may represent active tumor.",
            "output": "1. Marked increase in the volume of enhancement in the corpus callosum\nextending into the frontal white matter bilaterally and in the volume of\nedema.\n2. Lobe perfusion and a low blood volume as well as a central nonenhancing\narea suggests necrosis.\n3. Areas of suspected leptomeningeal involvement, choline elevation and slow\ndiffusion within the enhancing lesion are worrisome for active tumor."
        },
        {
            "input": "MR BRAIN:\nAgain seen is a mass in the corpus callosum, extending into the bilateral\nfrontal white matter, right worse than left.  Compared to prior, there is\nincreased amount of hypo intense necrotic central area which is fluid-filled,\nconsistent with history of radiation.  In addition, the peripheral\npostcontrast enhancement have again increased compared to immediate prior in ___ and substantially increased compared to ___.  There is\npersistently large amount of white matter edema, right worse than left with\nmild leftward midline shift and effacement of the right lateral ventricle,\nmildly progressed compared to prior.\n\nMR ___: There is no evidence of increased blood volume or blood\nflow in the location of the enhancing lesion.  This finding is suggestive of\nnecrosis.\n\nASL Perfusion: There is no evidence of increased blood flow in the corpus\ncallosum in the location of the enhancement, suggestive of radiation necrosis.\n\n\nMR Spectroscopy: Again seen are multiple areas of lactate and lipid,\nconsistent with necrosis.  However, in the peripheral area of contrast\nenhancement, there is a trend of rising choline, concerning for local\nrecurrence.",
            "output": "1. Increased overall volume of the previously- treated corpus callosal lesion\ndue to central necrosis.  Multiple findings compatible with central necrosis\ndue to radiation treatment.  However, increased an choline in the periphery\ncorresponding with contrast enhancement is worrisome for local recurrence."
        },
        {
            "input": "MR BRAIN:\nA right frontal burr hole is re-identified.  Peripherally enhancing 3.8 x 1.5\nx 2.7 cm (TRV, AP, SI) mass in the anterior body, genu and rostrum of the\ncorpus callosum with extension into the bifrontal right greater than left\nwhite matter is re-identified demonstrating central hypo enhancement\ncompatible with necrosis.  The degree of peripheral nodular enhancement has\ndecreased from prior exam.  Surrounding of bifrontal white matter FLAIR\nhyperintense edema pattern has also decreased.  Near complete resolution of\npreviously described bifrontal sulcal and ventricular effacement as well as\nleftward midline shift.  The lesion demonstrates unchanged punctate gradient\necho susceptibility artifact compatible with hemorrhage.  Interval mild\nincreased associated diffusion-weighted hyperintense signal.  No new abnormal\nenhancement.\n\nThe major intracranial flow voids are preserved.  Trace mucosal thickening of\nthe paranasal sinuses is identified.  The orbits are unremarkable.  Fluid\nsignal is noted in the bilateral mastoid tips.\n\nASL Perfusion: Decreased perfusion in the region of hypo enhancement,\ncompatible with necrosis.  There is no increased perfusion.\n\nMR Spectroscopy: Single voxel spectroscopy centered over the right genu of the\ncorpus callosum demonstrates paucity of metabolites with increased lactate\npeak, compatible with posttreatment changes.  The remains increased choline to\nNAA ratio consistent with residual tumor.  Multi voxel spectroscopy centered\nover of the abnormal enhancement demonstrates similar findings.",
            "output": "1. Peripherally enhancing 3.8 cm mass in the anterior corpus callosum with\nextension into the bifrontal right greater than left white matter demonstrates\ncentral hypo enhancement, compatible with necrosis.  The degree of peripheral\nnodular enhancement and surrounding white matter FLAIR edema pattern has\ndecreased from prior exam.  There is increased diffusion-weighted hyperintense\nsignal associated with the lesion, likely representing posttreatment effects. \nHowever, close attention on followup is recommended.\n2. No new lesions are identified.\n3. There is no increased perfusion.\n4. MRI spectroscopy demonstrates increased lactate and overall paucity of\nmetabolites compatible with posttreatment changes with increased choline to\nNAA ratio compatible with residual tumor."
        },
        {
            "input": "Again seen is mass centered on anterior corpus callosum, with zone of linear\nperipheral enhancement, and central decreased signal on post gadolinium\nimages.  Overall, mass measures 4.4 cm x 2.7 cm x 1.7 cm today, compared with\n4.4 cm x 2.6 cm x 2.0 cm on ___.  Degree of peripheral enhancement\nhas improved.  Surrounding zone of bifrontal white matter T2 signal\nabnormality has improved, particularly on the left.  Areas of restricted\ndiffusion predominantly within hypoenhancing portion of the tumor is similar,\nlikely representing treatment effect.  There is interval development of subtle\nperipheral linear decreased T1 signal on pre gadolinium images along the edges\nof the treated tumor margin, likely treatment effect.  There is mild linear\ndiffuse pachymeningeal enhancement, which has improved since prior exam. \nThere are no new areas of enhancement.\nThere is right parietal burr hole.  There is stable generalized atrophy of\nanterior bilateral frontal lobes.  There is minimal mucosal thickening of the\nparanasal sinuses, improved since prior exam.  .  Bilateral mastoid air cells\nare patent.  Principal intracranial flow voids are preserved.  There is no\nevidence of midline shift or infarction.  Bilateral orbits are normal.",
            "output": "1. Interval improvement.  There is decreased degree of peripheral enhancement\nsurrounding mass centered on anterior corpus callosum.  There is decreased\ndegree of surrounding edema.  There is decreased degree of pachymeningeal\nenhancement.  No new lesions."
        },
        {
            "input": "MR BRAIN:\n3.8 x 0.9 cm (TRV, AP) peripheral nodular enhancing lesion with associated\nslow diffusion and degree of adjacent bifrontal FLAIR hyperintense white\nmatter edema pattern involving the bilateral genu of the corpus callosum is\noverall similar in appearance to prior examination.\n\nHowever, when compared to examination of ___, there is increased\nsize of left corona radiata periventricular peripheral nodular enhancement\nmeasuring approximately 2.4 x 0.9 cm (AP, TRV; series 11, image 23) with\nassociated slow diffusion and adjacent FLAIR white matter edema pattern\nextending from the corona radiata to the centrum semiovale.\n\nRight trans frontal burr hole and biopsy track is unchanged from prior\nexamination.  Hemorrhage product associated with corpus callosum genu lesion\nis unchanged from prior examination.  There is increased rim of gradient echo\nsusceptibility artifact associated with the bridging left periventricular\nlesion.\n\nThere is no acute infarct.  The major intracranial flow voids are preserved. \nThe dural venous sinuses are patent on postcontrast MP-RAGE.  Partial mucosal\nthickening of the ethmoid air cells with right greater than left mild mucosal\nthickening of the frontal and maxillary sinuses.  Small mucous retention cysts\nin the maxillary sinuses are also identified.  Paranasal sinus disease has\nprogressed from prior examination.  The orbits are unremarkable.  Trace fluid\nsignal is noted in the bilateral mastoid tips.  No suspicious marrow on turbo\nspin echo.\n\nMR ___: No increased perfusion on dynamic susceptibility\ncontrast.\n\nASL Perfusion: No increased perfusion on ASL.\n\nMR Spectroscopy: Single voxel spectroscopy centered over the right genu of the\ncorpus callosum demonstrates overall paucity of metabolites with mildly\nincreased choline to NAA, compatible with posttreatment effect and residual\ntumor.  Similar findings are seen on multi voxel spectroscopy, which also\ndemonstrates elevated lactate on multiple voxels.",
            "output": "1. Overall similar appearance of 3.8 x 0.9 cm peripheral nodular enhancing\nlesion and associated degree of slow diffusion of the bilateral genu of the\ncorpus callosum, without evidence of increased perfusion on ASL or DSC. \nSpectroscopy demonstrates mildly increased choline to NAA ratio with overall\npaucity of metabolites with increased lactate compatible with posttreatment\neffect and residual tumor.\n2. When compared to prior examination of ___, there is\nsignificant interval increase size of left periventricular lesion\ndemonstrating peripheral nodular enhancement measuring 2.4 cm, with associated\nslow diffusion.  Although this may represent posttreatment response, given the\nassociated slow diffusion, pseudo response is a possibility.  Spectroscopy was\nnot performed through this region and close follow-up is recommended with\nspectroscopy through this region.\n3. Additional findings as described above."
        },
        {
            "input": "There is peripheral and nodular enhancing lesion which measures 0.9 x 4.1 cm\n(AP x TV; series 10:14) with associated slow diffusion involving the bilateral\ngenu of the corpus callosum is unchanged in size as compared to MRI head ___.  Degree of enhancement is minimally decreased.  Degree of FLAIR\nhyperintense white matter edema involving the bilateral frontal lobes is\nunchanged.  There are small foci of susceptibility in the right aspect of this\narea of enhancement (series 6:15), unchanged from ___ likely\nrepresenting foci of microhemorrhage.\n\nThere is a focus of peripheral nodular enhancement in the left corona radiata\nand periventricular region which measures 2.5 x 1.9 x 1.6 cm (AP x TV x SI,\nseries 5:18), mildly increased in size from ___, previously\nmeasuring 2.5 x 1.4 x 1.3 cm.  There is associated slow diffusion and white\nmatter edema involving the left corona radiata and centrum semiovale, which\nappears more prominent from ___.\n\nRight frontal burr hole in biopsy track is again noted.\n\nThere is no acute infarction.  Major vascular flow voids are preserved.  Dural\nvenous sinuses are patent on postcontrast MP-RAGE.  There is mucosal\nthickening of the bilateral ethmoid air cells.  Remaining paranasal sinuses\nare patent.  Mastoid air cells middle ear cavities are patent.  Globes are\nunremarkable.",
            "output": "1. Mild interval increase in size of left periventricular lesion with\nperipheral nodular enhancement and associated slow diffusion which measures\n2.5 x 1.9 x 1.6  Cm (series 5:18), previously measuring 2.5 x 1.4 x 1.3 cm on\nMRI head ___. Given the progressive size and associated slow\ndiffusion, further evaluation with MR spectroscopy and perfusion is\nrecommended to exclude progression.\n2. Stable appearance of 4.1 x 0.9 cm peripheral nodular enhancing lesion with\nassociated slow diffusion in the bilateral genu of the corpus callosum.\n3. No definite new intracranial lesion.  Additional findings as described\nabove."
        },
        {
            "input": "The scratch slow diffusion in the splenium and in the left frontal lobe has\nslightly decreased.  A rim of T1 hyperintense pre gadolinium signal in the\nleft frontal lobe is better defined on the current study with slightly\ndecreased enhancement compared to the prior study.  There remains enhancement\nat anterior to the genu of corpus callosum and along the lateral margin of the\nbody of the left lateral ventricle LP at slightly decreased.  The FLAIR\nhyperintensities have also slightly decreased in both frontal lobes.  No new\nareas of abnormal enhancement are identified.",
            "output": "Compared to the previous MRI, diffusion, FLAIR and post gadolinium enhancement\nhave slightly decreased with some persistent abnormalities as described above."
        },
        {
            "input": "Right frontal parietal burr hole is unchanged.  Minimally enhancing bifrontal\nlesion with extension across the genu of the corpus callosum, demonstrating\nspeckled T1 intrinsic hyperintense signal as well as a left cingulate gyrus\nlesion with similar characteristics are unchanged from examination of ___.  Geographic bifrontal FLAIR white matter edema pattern is\nunchanged.\n\nThere is a linear focus of sulcal FLAIR hyperintense signal in the left\nprecuneus ((series 15, image 14 and 15), which appears to correspond to a\ncortical vessel, not seen on prior exams.  Close attention is recommended.\n\nThere is no acute infarct or new intracranial hemorrhage.  The sulci,\nventricles and cisterns are within expected limits.  The major intracranial\nflow voids are preserved.  The dural venous sinuses are patent.  There is now\ninterval complete opacification of the left frontal sinuses, left ethmoid air\ncells and maxillary sinuses, significantly worsened from prior examination. \nMild mucosal thickening of the right ethmoid air cells and maxillary sinuses\nare noted.  The orbits are unremarkable.  Trace fluid signal is seen in the\nmastoid air cells.",
            "output": "1. Unchanged appearance of bifrontal minimally enhancing lesions demonstrating\nspeckled intrinsic T1 hyperintense signal, extending the genu of the corpus\ncallosum.  A left cingulate gyrus lesion is also unchanged.\n2. There is new linear focus of sulcal FLAIR hyperintense signal in the left\nprecuneus, which appears to correspond to a small cortical vessel.  However,\nclose attention on followup is recommended to document resolution or\nstability.\n3. Interval development of complete opacification of the left frontal sinuses,\nleft ethmoid air cells and maxillary sinus.  Clinical correlation is\nrecommended.\n4. Additional findings as described above."
        },
        {
            "input": "Again seen are peripherally enhancing masses in the anterior corpus callosum\nand in the left frontal white matter.  These lesions demonstrate markedly slow\ndiffusion and there is associated edema on FLAIR imaging.  The left frontal\nwhite matter enhancing lesion appears larger than on the study of ___.  The volume of the anterior corpus callosum material also appears to\nhave increased in the interval.  It is unclear whether these changes represent\ntumor progression or tumor response.  No new lesions are identified.  There is\nno evidence of hemorrhage or infarction.  There are inflammatory changes in\nthe maxillary and ethmoid sinuses bilaterally with near complete opacification\nof the left maxillary sinus.  These findings appear similar to the prior\nexamination.",
            "output": "1. Increased volume of the anterior corpus callosum and left frontal white\nmatter peripherally enhancing lesions with strikingly slow diffusion.\n2. The findings are compatible with lymphoma.\n3. The change may represent treatment effect, tumor progression, or both."
        },
        {
            "input": "Peripherally enhancing masses are again seen in the anterior corpus callosum\nand left periventricular frontal white matter.  These have demonstrated\ngradual enlargement with worsening surrounding edema.  For example, the\nsegment extending into the right forceps minor now measures 2.7 x 3 cm (AP by\nSI) where it previously measured 2.4 x 2.8 cm.  There is no evidence of\nhemorrhage or infarction.\n\nThere is moderate chronic maxillary sinus disease involving the right\nmaxillary and bilateral ethmoid sinuses.  There is resolution of the\npreviously seen left maxillary sinus disease.",
            "output": "1. Gradual increase in size of the left frontal and anterior corpus colossal\nmasses with worsening surrounding edema, concerning for tumor progression.\n2. Sinus disease as above."
        },
        {
            "input": "Postsurgical changes remain stable consistent with right frontal burr hole. \nAllowing for the differences in slice selection, no significant changes are\nvisualized in the peripherally enhancing mass lesion, centered in the anterior\ncorpus callosum, with similar pattern of vasogenic edema and asymmetry of the\nright frontal ventricular horn, with punctate foci of magnetic susceptibility\nand areas of slow diffusivity on the DWI and ADC maps (image 15, series 350,\nand series 352).  There is an unchanged ring-enhancing mass lesion in the left\nfrontal subcortical white matter extending towards the cingulate gyrus and\ncorpus callosum, measuring approximately 20 x 25 mm in transverse dimension,\nand approximately 20 x 24 mm in sagittal projection, with similar pattern of\nslow diffusivity, magnetic susceptibility, and vasogenic edema likely\nconsistent with mass lesion, hemorrhagic changes and posttreatment changes. \nFocus of FLAIR high signal intensity in the left percutaneous remains\nunchanged (image 14, series 7), no new areas with abnormal enhancement are\nseen.  The ventricles and sulci are slightly prominent suggesting mild\ncortical volume loss, unchanged since the prior exam.  The major vascular flow\nvoids are present and demonstrate normal distribution.  The orbits are\nunremarkable, the paranasal sinuses are notable for persistent mucosal\nthickening in the frontal sinus, opacification of the right frontoethmoidal\nrecesses and right ethmoidal air cells and opacification of the maxillary\nsinuses, more significant on the right.  The middle ear cavities are clear,\nminimal mucosal thickening is noted in the left mastoid air cells.",
            "output": "1.  Relatively stable peripherally enhancing mass lesion in the anterior\ncorpus callosum as described detail above, with similar pattern of vasogenic\nedema, and also grossly unchanged left frontal subcortical lesion, extending\ntowards the left cingulate gyrus, these lesions demonstrate similar areas of\nslow diffusion, suggestive of residual mass an underlying posttreatment\nchanges.\n\n2.  No new enhancing lesions are seen.\n\n3.  Persistent paranasal sinus disease."
        },
        {
            "input": "There is no evidence of an enhancing mass, edema, acute infarction, or blood\nproducts.  Ventricles and sulci are mildly prominent due to age-related\nparenchymal volume loss.  Periventricular, deep, and subcortical white matter\nT2 hyperintensities are likely sequelae of chronic microangiopathy, similar to\nthe ___ MRI.  Principal vascular flow voids are preserved.  Major dural\nvenous sinuses appear patent on postcontrast MP RAGE images.\n\nA mucous retention cyst is seen within the left maxillary sinus.  Moderate\npolypoid mucosal sinus thickening and dependent inspissated secretions are\nseen within the left sphenoid sinus, similar to the ___ CT.  There is\nevidence of bilateral lens replacement surgery.",
            "output": "1. No evidence for acute intracranial abnormalities, intracranial mass, or\nanother seizure focus.\n2. Left sphenoid sinus disease, unchanged compared to the head CT from ___.  Left sphenoid wall sclerosis seen on the preceding CT indicates chronic\ninflammation."
        },
        {
            "input": "MRI BRAIN:\nPostsurgical changes after right parietal craniotomy are again noted.  The\npatient is also status post embolization of the right middle meningeal artery.\n\nThere is redemonstration of bilateral, right greater than left, subdural\nhematomas with extension along the interhemispheric fissure and with the right\nsubdural hematoma extending inferiorly to the right cerebellar hemisphere. \nThere is no significant change in size of the right subdural hematoma\nmeasuring up to 13 mm in maximum thickness and left subdural hematoma\nmeasuring up to 7 mm in maximum thickness. No significant change of\nmass-effect of predominantly the right subdural hematoma with effacement of\nthe underlying gyri and sulci and unchanged 4.5 mm leftward midline shift with\npartial effacement of the right lateral ventricle.  The basal cisterns remain\nclear.\n\nThere is diffuse FLAIR hyperintensity within the sulci of right cerebral\nhemisphere and left frontal vertex which is favored to represent incomplete\nCSF suppression given no signal abnormality on the GRE and MRA sequences as\nwell as a prior CT to suggest underlying subarachnoid hemorrhage.\n\nThere are scattered foci of DWI hyperintensity in the right corona radiata\n(series 5, image 22 and 23) which demonstrate associated ADC correlates and\nmay reflect small acute infarctions.  There is no evidence of hemorrhagic\ntransformation.\n\nSmall chronic lacunar infarct versus enlarged perivascular space in the left\nputamen.\n\nThe paranasal sinuses appear clear.  There is partial opacification of the\nbilateral mastoid air cells.  The orbits appear grossly unremarkable.\n\n\nMRA BRAIN:\nEvaluation of the intracranial vasculature is degraded by motion artifact.\nIrregularities along both carotid siphons correspond to atherosclerotic\ndisease, previously identified on the CT.  Irregularities along the right A1\nsegment are most likely artifactual given a normal smooth with course and\ncaliber on the prior CTA.  The intracranial vertebral and internal carotid\narteries and their major branches appear otherwise unremarkable without\nevidence of stenosis,occlusion,or aneurysm formation.\n\nMRA NECK:\nNormal 3 vessel aortic arch.  The origins of the great vessels, subclavian and\nleft vertebral arteries appear unremarkable bilaterally.  The common, internal\nand external carotid arteries appear normal.  There is no evidence of internal\ncarotid artery stenosis by NASCET criteria.\nThere is occlusion of the right vertebral artery, shortly after its origin. \nThe right vertebral artery is intermittently visualized throughout its\ncervical course and reconstituted at its V3 segment, likely from muscular\nbranches.",
            "output": "1. Stable postsurgical changes after left parietal craniotomy and embolization\nof the right middle meningeal artery.\n2. No significant change of bilateral, right greater than left subdural\nhematomas with unchanged mass effect and stable leftward midline shift\nmeasuring up to 4.5 mm.\n3. FLAIR hyperintensity in the sulci of the right cerebral hemispheres most\nlikely represent incomplete CSF suppression given no signal abnormality on the\nGRE and MRA sequences as well as on the prior CT.  However, small amount of\nunderlying subarachnoid hemorrhage cannot be entirely excluded.\n4. Scattered small acute infarctions in the right corona radiata.\n5. Occlusion of the proximal right vertebral artery with intermittent\nvisualization throughout its cervical course and reconstitution at its V3\nsegment, likely from muscular branches.\n6. Limited evaluation of the proximal intracranial vasculature due to motion\nartifact.  No definitive high-grade stenosis, vessel occlusion or aneurysm\nformation identified."
        },
        {
            "input": "There is susceptibility artifact in the left superior parietal lobule\ncorresponding to the focus of hyperattenuation seen on same day CT and CTA. \nNo definite enhancement on post gadolinium spin echo images, the some\nintrinsic mildly increased T1 signal on pre gadolinium T1 images.  On MP rage\nimages there is mildly increased peripheral T1 signal which may represent\nmineralization, or possibly mild peripheral enhancement.  No evidence of\ncavernoma.  No adjacent vascular flow voids suggest AVM.  Follow-up to\nresolution recommended.  No adjacent edema.  Associated parenchymal atrophy. \nNo gyral expansion.\n\nPeriventricular and subcortical white matter T2/FLAIR hyperintensities are\nnonspecific but likely sequelae of chronic small vessel ischemic disease.  The\nventricles and sulci are slightly prominent, indicative of chronic\ninvolutional change. The major intracranial flow voids are preserved.  There\nis mild diffuse paranasal sinus mucosal thickening, most prominent in the\ninferior maxillary sinuses.\n\nThere is a 2.0 x 1.1 cm, well-circumscribed, T2 hyperintense, T1 hypointense,\nhomogeneously enhancing lesion in the right temporoparietal scalp which\ndemonstrated simple fluid attenuation on prior CT.  No restricted diffusion. \nNormal adjacent bone.",
            "output": "1. No evidence of intracranial metastasis.\n2. Sequela of probably chronic blood products or mineralization left parietal\nlobe.  No surrounding edema or mass effect.\n3. Indeterminate 2 cm right occipital scalp mass, possibly venous\nmalformation, close clinical or imaging follow-up recommended to ensure\nstability.."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  The ventricles and sulci are normal in caliber and\nconfiguration.  A couple of deep white matter punctate T2 and FLAIR\nhyperintensities are nonspecific, most likely secondary to microangiopathy,\nand of questionable clinical significance.  The pituitary appears normal.  The\ncraniocervical junction appears normal the intracranial arteries demonstrate\nnormal T2 flow voids.  The orbits appear normal.  The paranasal sinuses are\nessentially clear.",
            "output": "Essentially normal brain MRI.\nNo evidence of posterior circulation infarct."
        },
        {
            "input": "Study is moderately degraded by motion.  Within these confines:\n\nMRI BRAIN:\nThere is a right frontal intraparenchymal hematoma demonstrating predominantly\nhypointense T2 with corresponding hyperintense T1 signal suggestive of early\nsubacute infarction measuring 2.0 x 3.7 cm, similar to the prior study.  There\nis no definite abnormal enhancement.  There is surrounding edema with 4 mm\nleftward midline shift, similar to the prior study.\n\nSulcal FLAIR hyperintensities throughout the right cerebral hemisphere and\nquestion within the left occipital lobe are noted.\n\nThere are of few scattered foci of hyperintense DWI signal involving left\nparietal lobe and left occipital lobes (802-19, 11), without definite evidence\nof corresponding hypointense ADC signal.  There is subtle left occipital FLAIR\nhyperintensity (___) corresponding to the left occipital diffusion\nabnormality.\n\nThere is nonspecific left frontal T2 and FLAIR hyperintense focus with slight\nprominence of the adjacent sulcus, possibly related to prior infarction.\n\nThere is mild mucosal thickening of ethmoid and maxillary sinuses.  The\nbilateral mastoid air cells appear clear.  Patient is status post right lens\nreplacement.\n\nMRA BRAIN:\nAgain seen is a small left M1 middle cerebral artery nonocclusive filling\ndefect (___), with slight irregularity of the right M1 middle cerebral artery\n(___).  There is hypoplastic left A1 and mild irregularity of the right A2\nsegments of the anterior cerebral artery.  There is diffuse irregularity of\nthe basilar artery with mild luminal narrowing.  There is hypoplastic left V4\nvertebral artery with continuation to the ___.  There is no definite evidence\nof an arteriovenous malformation.  Otherwise, there is no significant\nstenosis, occlusion, or aneurysm.",
            "output": "1.  Study is moderately degraded by motion.\n2. Scattered left parietal and occipital findings concerning for acute to\nsubacute infarcts.\n3. Right frontal intraparenchymal hematoma with surrounding edema and leftward\nmidline shift, similar to the prior study.  Please note that underlying mass\nis not excluded on the basis of this examination.  Recommend follow-up imaging\nto resolution.\n4. Findings suggestive of right cerebral hemisphere and questioned left\noccipital lobe subarachnoid hemorrhage.\n5. Left frontal lobe encephalomalacia, likely related to prior infarction.\n6. Nonocclusive left M1 MCA intraluminal thrombus again seen.\n7. Multiple areas of luminal irregularity of the intracranial vasculature as\ndescribed above, likely related to atherosclerotic disease.\n8. Findings suggestive left frontal chronic infarct.\n9. Paranasal sinus disease as described.\n\nRECOMMENDATION(S):  Right frontal intraparenchymal hematoma with surrounding\nedema and leftward midline shift, similar to the prior study. Please note that\nunderlying mass is not excluded on the basis of this examination. Recommend\nfollow-up imaging to resolution.\n\nNOTIFICATION:  The findings were discussed with ___, M.D. by ___\n___, M.D. on the telephone on ___ at 1:30 pm, 2 minutes after\ndiscovery of the findings."
        },
        {
            "input": "The study is severely limited by metal artifact from underlying braces. \nSpecifically, the inferior frontal lobes and bilateral temporal lobes cannot\nbe assessed.\n\nThe visualized portions of the brain parenchyma demonstrate no gross\nabnormalities.  No definite evidence of an enhancing mass.  Ventricles and\nsulci are normal in caliber and configuration.  No shift of midline\nstructures.",
            "output": "Limited assessment of the bilateral inferior frontal and temporal lobes. \nWithin these limitations, there is no evidence of an enhancing mass in the\nvisualized portions of the parenchyma."
        },
        {
            "input": "There is significant motion artifact on all sequences, most pronounced on the\npostcontrast MP rage, which degrades spatial resolution.\n\nThere is a 3.2 (AP) x 2.3 (TV) x 2.9 (SI) cm enhancing mass at the left mid\ncentrum semiovale (17:17 ; 18:44) which extends to ependymal surface of\nlateral ventricular body and demonstrates correlate slow diffusion in a\nperipheral rim of T2 hypointensity.  There is a central nonenhancing, T2\nhyperintense , which may represent necrosis.  There is adjacent FLAIR\nhyperintensity.  The enhancing rim demonstrates correlate hyperdensity on\nprior CT.  There is no evidence of internal hemorrhage.\n\nThere is a 1.4 (AP) x 2.5 (TV) x 1.7 (SI) cm enhancing mass at the left side\nof splenium (17:14; 8:7) which demonstrates correlate slow diffusion and mild\nT1 hyperintensity.  There is mass effect with adjacent mild FLAIR\nhyperintensity.  Enhancing lesion demonstrates correlate hyperdensity on prior\nCT.  There is no evidence of internal hemorrhage.\n\nThere is background periventricular and subcortical white matter FLAIR\nhyperintense foci, some of which demonstrate confluence in addition to central\npontine FLAIR hyperintensity, which are nonspecific but likely represents\nsequela of chronic small vessel disease, given patient's age.  There is more\nfocal periventricular FLAIR hyperintense lesion at the anterior left centrum\nsemi ovale measured 1.5 x 1.7 cm (14:18), which may represent additional site\nof microangiopathy, versus nonenhancing FLAIR hyperintense disease.\n\nThere is prominence of the ventricles and cortical sulci consistent with\nvolume loss.  The extra-axial spaces are unremarkable.  The vascular flow\nvoids are preserved.  The bilateral lenses are absent.  There is mucosal\nthickening within the right frontal, right ethmoid, and right maxillary\nsinuses.  There left maxillary sinus mucous retention cysts.  The mastoid air\ncells and middle ears are clear.  There is partially visualized fusion\nhardware at the cervical spine.  The soft tissues are unremarkable.",
            "output": "1. Enhancing lesions at the left mid centrum semi ovale and left splenium\nwhich demonstrate slow diffusion and correlate hyperdensity on prior CT. \nFindings suggest a hypercellular lesion with signal morphology suspicious for\na CNS lymphoma versus a high-grade glioma.  The central nonenhancement at the\nleft mid centrum semi evaluation may represent necrosis, which is atypical for\nCNS lymphoma if immunocompetent patient.  DDx can include tumefactive\ndemyelination, metastatic disease, inflammatory etiology,  less likely\ninfarction, etc\n\n2. Background sequela of chronic small vessel ischemic disease.  More focal\narea FLAIR hyperintensity at the anterior left centrum semi ovale may\nrepresent additional microangiopathy versus nonenhancing FLAIR hyperintense\ndisease.\n3. Significant motion artifact which degrades spatial resolution.\n\nRECOMMENDATION(S):  Clinical correlation; further workup and followup as\nneeded"
        },
        {
            "input": "Images through the internal auditory canal demonstrates symmetric appearance\nof the seventh eighth nerve complexes.  There is a stable 2 mm focus of\ncontrast enhancement in the posterior left internal auditory canal, not\ndefinitively associated with either the vestibular or facial nerve. \nDifferential includes a schwannoma or meningioma given possible origin from\nthe dura.  This is unlikely to represent leptomeningeal inflammation given the\nlack of other findings suggesting this diagnosis.  However, inflammatory\nconditions such as sarcoidosis could produce an isolated focus of dural\nthickening and enhancement.  The stability since ___ argues\nagainst  malignant leptomeningeal involvement.  This is unlikely represent a\nvein given no apparent contiguity with adjacent venous structures.  No other\nmass lesions are seen within the posterior fossa.\n\nLimited included imaging of the remainder of the brain demonstrates no\nevidence of hemorrhage, edema, masses, mass effect, midline shift or\ninfarction. There is prominence of the ventricles and sulci suggestive\ninvolutional changes.  There are few periventricular and subcortical T2 and\nFLAIR hyperintensities, likely secondary to chronic microvascular ischemic\nchanges. Left frontotemporal craniotomy changes are seen with minimal dural\nenhancement underlying the craniotomy site.  Artifact from an aneurysm clip is\nnoted in the left sylvian fissure.\n\nNo osseous abnormalities are seen. The  mastoid air cells, and middle ear\ncavitiesare clear. The orbits are unremarkable. The visualized portion of the\nprinciple vascular flow voids are preserved.  There is an air-fluid level in\nthe right maxillary sinus with mucosal thickening of the ethmoid sinus.\n\nDegenerative changes are partially visualized in the upper cervical spine.",
            "output": "1. Stable 2 mm focus of masslike contrast enhancement in the posterior left\ninternal auditory canal, most likely representing a small meningioma or\nschwannoma, as described above.\n2. Small air-fluid level in the right maxillary sinus with partial\nopacification of the ethmoid sinus.  Recommend correlation for acute\nsinusitis."
        },
        {
            "input": "MR BRAIN:\nThere is a small left frontal T2/T1 hyperintense subdural hematoma measuring\nup to 6 mm in greatest thickness.  Minimal mass effect on the underlying\nparenchyma is seen with no midline shift.  In addition, a small amount of\nsubarachnoid hemorrhage is noted along the frontoparietal convexity.  There is\nno evidence of  edema, masses, mass effect, midline shift or infarction. \nThere is prominence of the ventricles and sulci suggestive involutional\nchanges.   Periventricular and subcortical T2 and FLAIR hyperintensities are\nnoted.  The major vascular flow voids are preserved.\n\nThe the orbits and mastoid air cells are normal.  Minimal mucosal thickening\nof the bilateral maxillary and ethmoid sinuses is seen.  The visualized soft\ntissues are normal.\n\nMRA brain:  Susceptibility is seen in the left MCA bifurcation region\nsecondary to aneurysm clipping.  Disc limits evaluation of the adjacent\nvascular structures.  Otherwise, the remainder of the intracranial vertebral\nand internal carotid arteries and their major branches appear normal without\nevidence of stenosis, occlusion, or aneurysm formation.",
            "output": "1. Stable small left frontal subacute subdural hematoma with mild mass effect\non the underlying parenchyma and no midline shift.  Small high left\nfrontoparietal convexity subarachnoid hemorrhage.\n2. No acute infarct.\n3. Post clipping of the left MCA bifurcation aneurysm with surrounding\nartifact which limits evaluation of the adjacent vascular structures. \nOtherwise, unremarkable MRA of the brain."
        },
        {
            "input": "Redemonstrated is a stable 2 mm enhancing nodule in the posterior superior\nleft IAC, along the intracanalicular portion of the seventh and eighth cranial\nnerves (Series 7, image 9; series 5, image 57).  No new enhancing lesions are\nidentified.  There is no abnormality on diffusion-weighted images.\n\nImages through the internal auditory canal demonstrates symmetric appearance\nof the seventh eighth nerve complexes.  There is no evidence of abnormal\nenhancement or mass lesion within the internal auditory canals,\ncerebellopontine angles or membranous labyrinth. No other mass lesions are\nseen within the posterior fossa.\n\nLimited included imaging of the remainder of the brain demonstrates no\nevidence of hemorrhage, edema, masses, mass effect, midline shift or\ninfarction.  Prominence of the ventricles and sulci is in keeping with\ninvolutional changes.  A few periventricular and subcortical white matter\nhyperintense foci are grossly unchanged and may be related to chronic small\nvessel ischemic changes.\n\nNo osseous abnormalities are seen. The there is moderate mucosal thickening in\nthe ethmoid air cells.  The orbits are unremarkable.  The visualized portion\nof the principle vascular flow voids are preserved.",
            "output": "There is a 2 mm enhancing nodule abutting the posterosuperior wall of the left\nIAC, which is unchanged dating back to at least ___, most likely\nrepresenting a small meningioma or schwannoma as described above.\n\nRECOMMENDATION(S):  Long-term follow-up with MRI of the head with and without\ncontrast, and spatial attention to the left IAC is recommended to demonstrate\nstability or any further changes."
        },
        {
            "input": "The study is degraded by motion artifact.\n\nAgain noted as on prior outside MRI are 2 T1 precontrast hyperintense lesions\nin the right cerebellar hemisphere and left superior frontal gyrus.  The\nlesion in the right cerebellar hemisphere has a fluid fluid level with\nassociated blooming on the gradient echo suggesting a hemorrhagic lesion.  It\nmeasures 12 x 14 mm in the axial plane.  The lesion in the left superior\nfrontal gyrus measures 15 x 14 mm in the axial plane and demonstrates a hypo\nintense rim with associated blooming on the gradient echo suggesting also a\nhemorrhagic nature.  CT head from ___ demonstrated hyperdensity in\nthese lesions consistent with blood products.\n\nThere are innumerable parenchymal enhancing lesions, for example in the medial\naspect of the left thalamus measuring 6 mm in diameter (series 5, image 50) in\nthe posterior lateral aspect of the right thalamus measuring 7 mm in diameter\n(series 5, image 48) in relation to the posterior left parietal operculum\nmeasuring 4 mm in diameter (5, 58), the left superior temporal gyrus measuring\n8 mm diameter (5, 46) left parietal occipital junction measuring 3 mm diameter\n(series 5, image 46), left middle frontal gyrus measuring 5 mm diameter\n(series 5, image 64) adjacent to the falx in the left frontal lobe measuring 6\nmm in diameter (5, image 49) left tail of hippocampus (series 5, image 42)\nmeasuring 2 mm in diameter.\nAdditional enhancing lesions right parietal operculum measuring 2 mm in\ndiameter (series 5, image 57) superior aspect of the right cerebellar\nhemisphere measuring 4 mm diameter (series 5, image 30).  Please note that\nthere are a couple of millimetric areas of apparent enhancement which is\ndifficult to determine whether it is artifactual or secondary to motion\nartifact for example in the left middle frontal gyrus (series 5, image 63).\n\nThere is an indeterminate area of enhancement in the C2 vertebral body (series\n700, image 121) which is not clearly correlated on coronal imaging.\n\nGeneralized cerebral atrophy.  No acute infarct.  Ex vacuo dilatation of the\nventricular system.  The dural venous sinuses are patent.  The orbits appear\nnormal.  The paranasal sinuses are relatively clear.",
            "output": "1. Numerous supra and infratentorial brain metastatic lesions.  The largest 2\nlesions are hemorrhagic in nature and are present in the left superior frontal\ngyrus and right cerebellar hemisphere as described above.\n2. There is an indeterminate area of enhancement in the C2 vertebral body\nsuboptimally evaluated."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.\n\nThe orbits are unremarkable.  There is mild mucosal thickening in bilateral\nethmoid and right maxillary sinus.  The mastoid air cells are clear. \nIntracranial flow voids are maintained.",
            "output": "1. No acute intracranial abnormality.  Essentially unremarkable brain MRI\nwithout evidence for acute infarct."
        },
        {
            "input": "Images are limited by motion artifact, particularly the FLAIR and T2 weighted\nimages.\n\nThere is no evidence of acute infarction.\n\nThere is a large chronic right infarction involving the parietal, posterior\ntemporal, and superior occipital lobes.  There is ex vacuo enlargement of the\nright lateral ventricle.  There are several small chronic infarctions within\nbilateral cerebellar hemispheres, largest on the right.\n\nThere are multiple foci of encephalomalacia in the bilateral basal ganglia and\nadjacent white matter, as well as in the right frontal centrum semiovale on\nimage 6:17.  The largest is located within the right anterior internal capsule\nand corona radiata with ex vacuo enlargement of the frontal horn of the right\nlateral ventricle.  Some of these demonstrate faint siderosis on gradient echo\nimages.  This may represent chronic infarctions and/or sites of prior\nhemorrhage.\n\nExtensive confluent areas and discrete foci of FLAIR hyperintensity in the\nperiventricular, deep, and subcortical white matter of the cerebral\nhemispheres are nonspecific but likely sequela of chronic small vessel\nischemic disease in this age group.  The ventricles and sulci are prominent,\ncompatible with global cerebral atrophy.\n\nMajor vascular flow voids appear grossly preserved.\n\nThere is mild mucosal thickening in the ethmoid air cells.",
            "output": "1. Motion limited exam.\n2. No evidence for acute infarction.\n3. Large chronic right parietal/posterior temporal/superior occipital infarct.\nMultiple small chronic bilateral cerebellar hemisphere infarcts.\n4. Multiple foci of encephalomalacia in bilateral basal ganglia and deep white\nmatter, some of which demonstrate faint siderosis, compatible with chronic\ninfarctions and/or sites of prior hemorrhage.\n5. Extensive signal abnormalities on FLAIR images in the supratentorial white\nmatter are nonspecific but likely sequela of chronic small vessel ischemic\ndisease in this age group."
        },
        {
            "input": "Th no areas of acute diffusion restriction to suggest an acute infarct. \nChronic infarcts noted in the distribution of the right MCA involving the\nright temporal and parietal lobes (with extensive cystic encephalomalacia) as\nwell as right ___ distribution involving the inferior aspect of the right\ncerebellar hemisphere.  Small punctate/lacunar infarcts in the medial aspect\nof the left cerebellum in the left ___ distribution.  Multiple bilateral\nbasal ganglia and centrum semiovale lacunar infarcts.  Periventricular and\ndeep white matter T2 and FLAIR hyperintensities most likely represent sequela\na of microangiopathy.  Generalized cerebral and cerebellar atrophy with ex\nvacuo dilatation of the ventricular system.  The intracranial arteries\ndemonstrate normal T2 flow void.  Mild mucosal thickening involving the\nethmoid air cells.  The orbits appear normal.",
            "output": "1. No acute infarct.\n2. Right MCA and bilateral ___ territory chronic infarcts.\n3. Multiple lacunar infarcts as described above.\n4. Generalized cerebral atrophy with sequela a of microangiopathy.\n5. No intracranial mass or hemorrhage."
        },
        {
            "input": "There are scattered periventricular and subcortical white matter foci of\nT2/FLAIR signal hyperintensity including the area of interest, nonspecific but\nlikely sequelae of chronic small vessel disease.  There is no evidence of\nhemorrhage, edema, masses, mass effect, midline shift or infarction.   The\nventricles and sulci are normal in caliber and configuration.  There is no\nabnormal enhancement after contrast administration.\n\nThere is mucosal thickening within multiple ethmoid air cells and bilateral\nmaxillary sinuses.",
            "output": "1. No acute intracranial abnormality or abnormal enhancement, specifically in\nthe area of interest from the prior CT head.\n2. Periventricular and subcortical white matter changes, nonspecific but\nlikely sequelae of small vessel disease.\n3. Mild paranasal sinus mucosal thickening."
        },
        {
            "input": "The ventricle and basal cisterns appear normal.\n\nThere are normal vascular flow voids. There is no evidence of acute infarct\nbased on diffusion-weighted imaging. There is diffuse brain parenchymal volume\nloss.\n\nThere are punctate foci of subcortical and periventricular T2/FLAIR signal\nhyperintensity which are nonspecific though presumably on the basis of\nsequelae of chronic small vessel ischemic disease.\n\nThere is focal encephalomalacia within the left cerebellum with gradient\nsignal hypointensity likely representing sequelae of prior infarct with\nassociated prior hemorrhage. Additional gradient signal hypointensity within\nthe right parietal lobe may represent remote hemorrhage.\n\nThe orbits, skull base, and paranasal sinuses are unremarkable.",
            "output": "1. No evidence of acute infarct or mass effect.\n2. Probable chronic punctate hemorrhage within the right parietal lobe and\nleft cerebellar hemisphere in association with chronic infarct.\n3. Brain parenchymal volume loss and presumed sequelae of chronic small vessel\nischemic disease."
        },
        {
            "input": "The axial oblique MP-RAGE and FSTIR sequences demonstrates bilateral DBS leads\nextending to the inferior thalamic regions.  Axial FSTIR (series 3) only\nshowed the left-sided DBS lead.  The right-sided deep brain stimulating\nelectrode is new since examination of ___.  Both tips terminate in\nthe expected location of the subthalamic nucleus.  Pneumocephalus is\nidentified overlying the right cerebral hemisphere.\n\nThere is no mass, mass effect, or shift of normally midline structures.  The\ndiffusion-weighted images are degraded by artifact from the hardware.  Within\nthis limitation, there is no evidence of acute infarction.",
            "output": "-Bilateral DBS electrode leads extending to the expected location of the sub\nthalamic nuclei.  The right sided lead is new since prior examination of ___.\n-Mild right sided pneumocephalus."
        },
        {
            "input": "A left-sided DBS electrode terminates in the expected location of the left\nsubthalamic nucleus.  The ventricles and sulci are age-appropriate.  There is\nno mass or mass effect.  A focus of FSTIR hyperintense signal along the DBS\nlead is grossly unchanged compared to the prior examination and consistent\nwith postsurgical change.",
            "output": "Left DBS electrode terminating in the expected region of the left subthalamic\nnucleus."
        },
        {
            "input": "Hardware artifact limits examination. Deep brain stimulator leads are in\nplace.\n\nThere is no evidence of no evidence of infarction, hemorrhage, edema, or mass.\nThe ventricles and sulci are normal in size and configuration.\n\nThere is no evidence of osseous abnormality. The paranasal sinuses, mastoid\nair cells, and middle ear cavities are clear. The orbits are unremarkable.",
            "output": "Deep brain stimulator leads are in place.  No complications."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  Few punctate T2 signal abnormalities brain parenchyma, can be\nseen with chronic migraines, early chronic small vessel ischemic change.  No\ndefinite evidence of demyelination.  Preserved vascular flow voids.  Minimal\nmucosal thickening paranasal sinuses.  Clear mastoids.",
            "output": "1. Essentially normal brain MRI."
        },
        {
            "input": "Study is moderately degraded by motion.\n\nMRI BRAIN:\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  There is prominence of the ventricles and sulci suggestive\ninvolutional changes.   There is no abnormal enhancement after contrast\nadministration.  The sella appears normal.  The craniocervical junction\nappears normal.  Mild mucosal thickening involving the ethmoid air cells.  The\nintracranial arteries demonstrate normal T2 flow voids.  Periventricular FLAIR\nand T2 hyperintense changes are nonspecific.  Prominent Virchow ___ since\nspaces are noted in the left thalamus.\n\nMRA BRAIN:\nThe intracranial vertebral and internal carotid arteries and their major\nbranches appear normal without evidence of marked stenosis, occlusion, or\naneurysm formation.  Fetal origin of the right PCA.  The right vertebral\nartery is dominant.  The left vertebral artery terminates in an AICA. \nMultiple infundibular noted along the course of bilateral M1 segments.\n\nMRA NECK:\n\nPlease note that the origin of the left vertebral and left subclavian\narteries, and aspects of the left V3 and V4 segments were not included in the\nimaging.\n\nQuestion moderate stenosis of the distal cervical segment of the right\ninternal carotid artery versus artifact.\n\nOtherwise, the common, proximal internal and external carotid arteries are\npatent, with no evidence of stenosis at the carotid bulb by NASCET criteria,\nand patent origins of the great vessels, right subclavian and right vertebral\narteries.",
            "output": "1. Study is degraded by motion artifact and evaluation of left vertebral and\nsubclavian artery origins and portions of left V3 and V4 segment are limited\ndue to exclusion outside of field-of-view.\n2. No acute intracranial abnormality, with no definite evidence of acute\ninfarct or intracranial mass.\n3. Mild global volume loss and probable microangiopathic changes, as\ndescribed.\n4. Nonocclusive moderate stenosis of right ICA distal cervical segment versus\nartifact.  If clinically indicated, consider neck CTA for further evaluation.\n5. No evidence of circle of ___ aneurysm, stenosis or occlusion.\n6. No proximal ICA stenosis by NASCET criteria."
        },
        {
            "input": "There is no evidence of intracranial hemorrhage, edema, masses, mass effect,\nmidline shift or infarction.  There is prominence of the ventricles and sulci\nbilaterally, consistent with involutional changes.  Again seen moderate\ncerebellar atrophy, unchanged since MR ___ ___.  Mild\nperiventricular T2/FLAIR hyperintensities are nonspecific, but often seen in\nthe setting of chronic small vessel ischemia.  The major vascular flow voids\nare patent.\n\nThere is mild mucosal thickening of the bilateral ethmoid air cells.  The\nremaining paranasal sinuses are patent.  The mastoid air cells are clear.  The\nmiddle ear cavities are clear.",
            "output": "1. No evidence of infarction.\n2. Moderate cerebellar atrophy, unchanged since ___."
        },
        {
            "input": "The ventricles and extra-axial spaces are normal in size. There is no evidence\nof midline shift, mass effect or hydrocephalus. There are no acute infarcts.\nThere is no evidence of focal abnormalities.  The vascular flow voids are\nmaintained. The visualized paranasal sinuses are clear. Following gadolinium\nadministration there is no evidence of abnormal parenchymal, vascular and\nmeningeal enhancement seen.  Slightly prominent soft tissues in the\nnasopharynx is likely due to lymphoid hyperplasia.",
            "output": "No significant abnormalities are seen on MRI of the brain with and without\ngadolinium."
        },
        {
            "input": "Images are severely motion degraded and essentially nondiagnostic.  There is\nno evidence of large acute infarction or ischemia.  There is no shift of\nnormally midline structures.  Basal cisterns appear patent.  Ventricles and\nsulci appear age appropriate in size and configuration.  Images are otherwise\nessentially nondiagnostic.",
            "output": "Essentially non-diagnostic examination secondary to motion degradation.  No\nevidence of obvious and large acute intracranial abnormality."
        },
        {
            "input": "There is no intra or extra-axial mass, acute hemorrhage or infarct. Sulci,\nventricles and cisterns are within expected limits for the patient's age\nrelated global cerebral volume loss.  Incidental note is made of a partial\nempty sella.  There is no abnormal enhancement.  The major intracranial flow\nvoids are preserved.  The dural venous sinuses are patent.  The paranasal\nsinuses are essentially clear.  The orbits are unremarkable, noting bilateral\nlens replacements.  The mastoid air cells are essentially clear.",
            "output": "Unremarkable contrast-enhanced pre-surgical MRI of the brain."
        },
        {
            "input": "Study is mildly degraded by motion.\n\nMRI BRAIN:\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.\n\nMRV BRAIN:\nThere is normal signal in the major cortical veins, deep veins, and dural\nvenous sinuses, without evidence of occlusion.  The right transverse and\nsigmoid sinus is dominant.\n\nMRA NECK:\nThe common, internal and external carotid arteries appear normal.  There is no\nevidence of internal carotid artery stenosis by NASCET criteria.  The origins\nof the great vessels, subclavian and vertebral arteries appear normal\nbilaterally.",
            "output": "1. No acute intracranial abnormality.\n2. Patent intracranial vasculature without venous sinus thrombosis.\n3. Patent neck vasculature without carotid stenosis by NASCET criteria."
        },
        {
            "input": "There is a confluent area of DWI hyperintensity centered in the left\nparieto-occipital region with extension anteriorly into the left frontal lobe.\nThis area demonstrates corresponding ADC hypointensity and also areas of ADC\nT2 shine through effect, increased FLAIR signal, most consistent with a late\nsubacute infarcts in a watershed distribution, please correlate.\nThere are also linear, gyriform T1 hyperintensities in the left parietal lobe\n(series 3, image 15 and 16, consistent with cortical laminar necrosis.\n\nThere is mild associated edema within the infarct region resulting in partial\neffacement of the left occipital horn, which is uncommon in acute/subacute\nischemic changes, therefore close follow-up is recommended, and if clinically\nwarranted an MRI of the head with and without contrast can be obtained in ___\nweeks or as clinically warranted.\n\nThere are additional scattered T2/FLAIR hyperintensities in the cerebral\nhemispheres bilaterally and in the pons, a nonspecific finding and likely\nrelated to chronic small vessel ischemic changes.  There is no evidence of\nabnormal enhancement after contrast administration.\n\nThere is mild generalized parenchymal volume loss, most likely age related. \nProminence of the ventricular system and extra-axial CSF spaces is consistent\nwith the previously mentioned parenchymal volume loss.\nMajor vascular flow voids appear preserved.  Major dural venous sinuses are\npatent.\n\nThe paranasal sinuses appear clear.  There is minimal opacification of the\ninferior bilateral mastoid air cells.  The orbits appear unremarkable.",
            "output": "1. Late subacute infarct involving the left parieto-occipital region with\nextension in to the left frontal lobe and evidence of cortical laminar\nnecrosis,  in a watershed distribution, please correlate.\n2. Scattered white matter changes in the cerebral hemispheres bilaterally and\nin the pons likely reflect sequela of chronic small vessel ischemic changes.\n\nRECOMMENDATION(S):  There is mild associated edema within the infarcted region\nresulting in partial effacement of the left occipital horn, close follow-up is\nrecommended, if clinically warranted MRI of the head with and without contrast\ncan be obtained in ___ weeks to demonstrate evolution and further changes."
        },
        {
            "input": "Study is severely degraded by motion, especially on postcontrast imaging. \nWithin these confines:\n\nA 1.1 cm x 1.2 cm enhancing mass is re-demonstrated in the pons, demonstrating\nsusceptibility and surrounding edema, consistent with a hemorrhagic metastatic\nlesion.  This is unchanged.\n\nAn 8 mm x 11 mm enhancing lesion is seen in the right thalamus, consistent\nwith a metastatic lesion, unchanged.\n\nA 1.7 cm x 1.9 cm T1 heterogeneously hyperintense, probably enhancing lesion\nis re-demonstrated in the left parietal lobe, demonstrating susceptibility and\nsurrounding edema, consistent with a hemorrhagic metastatic lesion.  This is\nunchanged.\n\nA punctate T1 hyperintense focus is re-demonstrated in the left thalamus,\nunchanged.\n\nA punctate focus of enhancement is seen in the left subependymal third\nventricle (9:75), unchanged.\n\nA right medial temporal intrinsically T1 hyperintense structure suggested to\ncorrespond to hyperintense lesion on T1 postcontrast imaging (see 04:10 and\n10:9) that is not definitely seen on ___ prior study is noted. \nCorresponding lesions are not clearly seen on T2, FLAIR, or MPRAGE imaging.\n\nThe ventricles and sulci are stable in caliber and configuration.  There is no\ndefinite evidence of acute infarct or midline shift.",
            "output": "1.  Study is severely degraded by motion, especially on postcontrast imaging.\n2. Question new punctate right medial temporal lobe lesion versus artifact, as\ndescribed.\n3. Additional grossly stable probable metastatic lesions as described.\n4.  No acute intracranial abnormality, with no definite evidence of acute\ninfarct."
        },
        {
            "input": "Again seen is an enhancing T1 hyperintense 1.2 x 1.1 cm (AP X TR) lesion in\nthe pons (series 5, image 58).  An adjacent 7 mm focus of patchy enhancement\n(series 5, image 61) is new from ___ but likely unchanged from the\nprior exam in ___.\n\nPatchy area of enhancement in the posterior right temporal lobe (series 5,\nimage 81) corresponds to a vessel on the sagittal and coronal reformats.\n\nA small focus of subependymal enhancement in the left aspect of the third\nventricle is unchanged (series 5, image 100).\n\nStable T1 hyperintense 0.7 x 1.0 cm (AP X TR) lesion in the right thalamus\n(series 5, image 105).  Unchanged 3 mm T1 hyperintense focus in the left\nthalamus (series 5, image 110).\n\nThe largest lesion in the left parietal lobe demonstrates increased\nenhancement when compared to the prior MRI from ___ with the\nenhancing component now measuring 2.0 x 2.4 mm (AP X TR) from previously 1.5 x\n1.6 cm.\n\nAn adjacent 7 mm focus of enhancement (series 5, image 137) has increased in\nsize from the prior MRI in ___ now measuring 7 mm from previously 5\nmm.\n\nMultiple (more than 10), additional tiny 2-3 mm enhancing metastatic lesions\nare seen in the cerebellum (series 5, image 49, pons, (series 5, image 57),\nleft occipital lobe (series 5, image 77), anterior inferior left temporal lobe\n(series 5, image 64) left frontal lobe (series 5, image 112, 129, 133, 156),\nright parietal lobe (series 5, image 113), right frontal lobe (series 5, image\n127, 132, 134, 135, 140, 147).\n\nThere is no evidence of acute territorial infarction.\nThe ventricular system is normal in caliber and configuration.  There is no\nmidline shift.\nMajor dural venous sinuses are patent.",
            "output": "1. Multiple partially hemorrhagic infratentorial and supratentorial metastatic\nlesions, some of which are new and others which have increased in size since\nthe prior exam.\n2. A total of 22 intracranial metastatic enhancing lesions identified, some of\nwhich measure 1-3 mm which are difficult to assess due to patient motion and\nsmall size.\n\nNOTIFICATION:  Findings were discussed with Dr. ___ (radiation\noncologist) by Dr. ___ (neuroradiology attending) via telephone on ___ at 09:05 am."
        },
        {
            "input": "The previously seen 3 dominant lesions with blood products in the pons (10:5)\nthe left posterior frontal lobe (10:16) and right posterior thalamus (9:78)\nare again identified with evolution of blood products development of\nwell-defined hemosiderin rim and decreased surrounding FLAIR hyperintensities.\nHowever, a small area of enhancement and blood products is seen at the\nposterior aspect of the pontine lesion (4:5 and 10:5) which presumably is\nsecondary to evolution of blood products.\n\nSeveral small previously noted lesions are either imperceptible or decreased\nin size.  For example the previously seen left parietal lobe lesion (5:139) is\ndecreased in size (9:120) on the current study similarly several small\npunctate lesions are less perceptible or decreased in size.  No definite new\nareas of abnormal enhancement or FLAIR hyperintensities are seen.",
            "output": "1. The previously seen 3 dominant lesions in the pons left frontal lobe and\nright thalamus demonstrate evolution of blood products and slight decrease in\nenhancement and surrounding FLAIR hyperintensities.\n2. Previously noted several small lesions are either decreased in size or\nimperceptible on the current study.\n3. No definite new enhancing lesion is identified or new areas of blood\nproducts seen."
        },
        {
            "input": "There has been interval decrease in size the dominant lesions with blood\nproducts at the pons (series 901 image 87), and left posterior frontal lobe,\n(series 10, image 16).  Again the aforementioned lesions demonstrate evolution\nof blood products the role of well-defined hemosiderin rim and decreased\nsurrounding FLAIR hyperintense. No interval change in size and configuration\nof the enhancing lesion at the right posterior thalamus.  No acute diffusion\nabnormalities are detected.\n\nSeveral small previously noted lesions on imperceptible and decreased in size.\nFor example the previously seen small lesion at the anterior pons, (series 10,\nimage 6).  No definite new areas of abnormal enhancement pole FLAIR\nhyperintensities are seen.\n\nThe ventricles and sulci are normal in caliber and configuration.  The\nvisualized paranasal sinuses are well pneumatized.  There is trace fluid\nopacification of the bilateral mastoid air cells.  The orbits are\nunremarkable.  Major flow voids are preserved.",
            "output": "1. There is been interval decrease in size of dominant lesions in the pons and\nleft frontal lobe which total demonstrated dilution of blood products and\nsurrounding FLAIR hyperintensities.\n2. Previously noted small lesions of with a decreased in size or imperceptible\non current study.\n3. No definite evidence of new enhancing lesions or new areas of blood\nproducts seen."
        },
        {
            "input": "Study is degraded by motion.\n\nAgain seen are numerous (> than 20) small intrinsically T1 hyperintense\nprimarily supratentorial but also infratentorial brain parenchymal lesions\nmostly centered near the cortical gray-white matter junction, compatible with\nmelanoma metastases.  The largest lesions within the pons and left\nfrontoparietal region again show evidence of prior hemorrhage, unchanged,\nmeasuring 1.6 x 1.5 x 1.6 x 1.4 cm, respectively.\n\nMany of the lesions are either new/newly apparent or larger/more conspicuous\ncompared with the prior exam; for example:\n\n-Left frontal 4 mm, previously 2 mm (04:19).\n-High left frontal sub-5 mm, more conspicuous (04:21)\n-Punctate left precentral gyrus, new or newly apparent (on the left 04:18)\n-Punctate high right frontal lobe, new or newly apparent (04:22).\n-Left parieto-occipital 4 mm, previously 3 mm (04:15)\n-Punctate left parietal, new or newly apparent (04:15)\n-New or newly apparent right periventricular white matter (04:14)\n-More conspicuous, sub 5 mm left frontal lobe (04:13)\n-9 x 7 mm right thalamic lesion, previously 8 x 5 mm (04:13)\n-Medial right temporal lobe, 4 mm, previously 3 mm\n-Medial right temporal lobe, punctate, significantly more conspicuous (4:9)\n-Left temporal lobe, more conspicuous (4:9)\n-Right cerebral hemisphere, more conspicuous (4:5)\nFLAIR hyperintensity likely representing vasogenic edema surrounding 4 mm left\nfrontal lesion is increased (07:18 on current study and 07:18 on ___ prior exam).  No other perilesional edema identified.\n\nNo evidence of acute infarct, new hemorrhage, extra-axial collection, or mass\neffect.  The ventricles and sulci are normal in caliber and configuration. \nTrace bilateral mastoid effusions.  Trace ethmoid air cell mucosal thickening\nand sphenoid sinus mucosal thickening.  Globes and orbits are unremarkable. \nMajor intracranial vascular flow voids are preserved.  Major dural venous\nsinuses are patent.",
            "output": "1.  Study is degraded by motion.\n2. Numerous (>20) intrinsically T1 hyperintense supratentorial and\ninfratentorial metastases; numerous lesions are either more conspicuous/larger\nor new/newly apparent compared with ___, although several are\nstable, as above.\n3. Unchanged hemorrhagic lesions in the pons and left frontoparietal region. \nNo new hemorrhage\n4. Interval increased vasogenic edema surrounding a ___ m left frontal lesion. \nOtherwise, within limits of study, no definite evidence of new parenchymal\nedema.\n5. No acute infarct, extra-axial collection, or mass effect."
        },
        {
            "input": "There is a 1.2 x 1.1 cm (AP X TR) lesion in the pons which demonstrates\nintralesional hemorrhage and a small surrounding rim of blood products.  The\nlesion demonstrates intense homogeneous enhancement.\n\nA larger 1.6 x 1.7 cm (AP X TR) lesion in the left parietal region\ndemonstrates partial intrinsic T1 hyperintensity as well as intralesional\nhemorrhage.  Given the hyperintense signal intensity on the noncontrast T1\nsequence, evaluation for enhancement is limited.\n\nThere is a third well circumscribed intrinsic T1 hyperintense lesion in the\nright thalamus which likely demonstrates peripheral enhancement after contrast\nadministration and measures approximately 0.7 x 1.0 cm (AP X TR X SI).\n\nA punctate focus of intrinsic T1 hyperintensity is also seen in the region of\nthe left thalamus (series 13, image 12 and series 14, image 94) which may or\nmay not demonstrate enhancement after contrast administration which is\ndifficult to evaluate given the T1 hyperintense signal on the noncontrast\nsequence.\n\nA punctate focus of enhancement in the subependymal left aspect of the third\nventricle (series 14, image 84; series 101, image 69) may represent an\nadditional lesion.\n\nThe larger lesions in the left parietal lobe and in the pons demonstrate mild\nsurrounding edema.\n\nNone of the lesions demonstrate restricted diffusion.  The DWI hyperintensity\nin the left parietal region is most likely artifactual given the presence of\nblood products.\n\nThe ventricular system and sulci are normal in caliber and configuration.\n\nMajor vascular flow voids are preserved.  Major dural venous sinuses are\npatent.\n\nThere is mild mucosal thickening along the ethmoid air cells.  The remainder\nof the paranasal sinuses and mastoid air cells appears clear.  The orbits\nappear unremarkable.  No suspicious marrow signal.",
            "output": "1. Several hemorrhagic intracranial lesions as detailed above, some of which\ndemonstrate surrounding edema.  Enhancement of the pontine and right thalamic\nlesions.  Enhancement of the remaining lesions is difficult to assess given\nthe intrinsic T1 hyperintensity but felt to be likely present.  Given the\ndifferent age of blood products within the lesions and no restricted\ndiffusion, these lesions less likely represent infarcts and are more\nsuspicious for metastatic disease, possibly in the setting of melanoma or\npotentially germ-cell tumor given the patient's age.\n2. Additional findings described above"
        },
        {
            "input": "MRI BRAIN:\nThere is restricted diffusion in the left cerebellum with associated T2/FLAIR\nsignal hyperintensity, consistent with late acute to subacute infarct.  There\nis mild prominence of the ventricles and sulci suggestive of age-related\ninvolutional changes.  Subcortical and periventricular white matter T2/FLAIR\nsignal hyperintensities are nonspecific, however likely represent sequela of\nchronic small vessel ischemic disease.  There is no abnormal enhancement after\ncontrast administration.\n\nThere is mild mucosal thickening in the ethmoid air cells.  There is otherwise\nno abnormal fluid signal in the remainder of the paranasal sinuses or mastoid\nair cells.  Patient is status post bilateral lens replacement.  The orbits are\notherwise grossly unremarkable.\n\nMRA BRAIN AND NECK:\nThere is a short segment of intraluminal thrombus in the V4 segment of the\nleft vertebral artery, as seen on recent CTA (13:68, 107:1).  There is slow\nflow in the more proximal left vertebral artery.  The thrombus does not extend\nto the basilar artery.  There is no clear evidence to support or refute\ndissection in this region.  Please note that T1 fat saturated images cannot be\nused to evaluate for dissection in the intracranial portion of the vertebral\narteries as there is no fat surrounding these arteries.\n\nThe remainder of the intracranial vertebral and internal carotid arteries and\ntheir major branches appear normal without evidence of stenosis, occlusion, or\naneurysm formation.\n\nThe common, internal and external carotid arteries appear normal.  There is no\nevidence of internal carotid artery stenosis by NASCET criteria.  The origins\nof the great vessels, subclavian and vertebral arteries appear normal\nbilaterally.\n\nThere is a small left consolidation or effusion at the left lung base.  There\nis a left thyroid nodule, as seen on recent CTA.",
            "output": "1. Late acute to subacute infarct in the left cerebellum.\n2. Intraluminal thrombus in the V4 segment of the left vertebral artery, as\nseen on recent CTA.  No clear evidence to support or refute dissection in this\nregion.  There is no evidence of dissection in the neck.\n3. Atrophy and sequela of chronic small vessel ischemic disease."
        },
        {
            "input": "MRI BRAIN:\nThere is no evidence of hemorrhage,edema,masses, mass effect, midline shift or\ninfarction.   The ventricles and sulci are prominent, consistent with global\ncerebral volume loss.  There is no abnormal enhancement after contrast\nadministration.\n\nA 1.2 cm x 1.1 cm by 1 cm homogeneously enhancing dural-based lesion is seen\nalong the left anterior clinoid (27:92, 110:45), most likely representing a\nmeningioma.\n\nThere is atelectasis of the right maxillary sinus.  The mastoid air cells are\nclear.  The patient is status post bilateral cataract surgery\n\n\nMRA BRAIN:\nA 9 mm fusiform aneurysm/dolichoectasia of the cavernous segment of the left\nICA is seen (9:95).\n\nA 2 mm superoposteriorly directed outpouching of the cavernous segment of the\nright ICA is seen (9:98).\n\nLuminal irregularities of the cavernous and supraclinoid segments of the\nbilateral internal carotid arteries are seen, likely secondary to atheromatous\nchange, without stenosis.\n\nOtherwise, the intracranial vertebral and internal carotid arteries and their\nmajor branches appear normal without evidence of stenosis,or occlusion.\n\nMRA NECK:\nThere is moderate focal narrowing of the left distal V3 segment (18:41) with\nsubsequent luminal irregularity distal to this, concerning for a chronic\ndissection/pseudoaneurysm (18:44).  There is patency seen distally.\n\nThe origins of the great vessels, subclavian and vertebral arteries appear\nnormal bilaterally.  The common, internal and external carotid arteries appear\nnormal.  There is no evidence of internal carotid artery stenosis by NASCET\ncriteria.",
            "output": "1. No acute infarct or intracranial hemorrhage.\n2. 1.2 cm enhancing dural-based lesion along the left anterior clinoid\nprocess, most likely representing a meningioma.\n3. 9 mm fusiform aneurysm/dolichoectasia of the cavernous segment of the left\nICA.\n4. 2 mm supra posteriorly directed outpouching of the cavernous segment of the\nright ICA may represent an infundibulum or a small aneurysm.\n5. Luminal irregularity of the distal left V3 segment, concerning for a\nchronic dissection/pseudoaneurysm.  Patency seen distally.\n6. No stenosis or narrowing of the circle of ___ vessels."
        },
        {
            "input": "There is no evidence of intracranial hemorrhage, mass, mass effect or shifting\nof the normally midline structures. The ventricles and sulci are normal in\nsize and configuration for the patient's age. Multiple scattered foci of high\nsignal intensity are identified on T2 and FLAIR sequences, distributed in the\nsubcortical and periventricular white matter, which are nonspecific and may\nreflect changes due to small vessel disease. No diffusion abnormalities are\ndetected. There is no evidence of abnormal enhancement to suggest metastatic\nor leptomeningeal disease. The major vascular flow voids are present and\ndemonstrate normal distribution. The orbits are unremarkable, the paranasal\nsinuses and the mastoid air cells are clear.  Note is made of a tiny soft\ntissue cystic formation in the superior and external left  orbital region,\nmeasuring approximately 6 x 7 mm in coronal projection (image 25, series 901),\nprobably consistent with small sebaceous cyst, please correlate clinically.",
            "output": "1.  There is no evidence of acute intracranial process.\n\n2.  Scattered foci of high signal intensity detected on FLAIR and T2 weighted\nimages, distributed in the subcortical and periventricular white matter, are\nnonspecific and may reflect changes due to small vessel disease.\n\n3.  There is no evidence of abnormal enhancement or evidence of intracranial\nmetastatic disease."
        },
        {
            "input": "This study is limited by motion artifact.  There are multiple bilateral linear\nFLAIR hyperintensities within the sulci of the frontal, parietal and occipital\nlobes (12:22, 12:20, 12:17), as well as FLAIR hyperintensities within the\nsulci of the left cerebellum, with subtle T1 post-contrast enhancement (14:22\nand 14:8).  In the setting of known malignancy, findings are concerning for\nleptomeningeal metastases.\n\nThe ventricles and sulci are normal in caliber and configuration.  There are\nmultiple additional scattered T2 and FLAIR hyperintense foci in the bilateral\nsubcortical and periventricular white matter, nonspecific but compatible with\nsequelae of chronic small vessel ischemic disease.  No diffusion abnormality\nis detected.  Major vascular flow voids are present and demonstrate normal\ndistribution.  The paranasal sinuses and mastoid air cells are clear. There is\nno evidence of hemorrhage, edema, masses, mass effect, midline shift or\ninfarction.",
            "output": "1. Diffuse bilateral sulcal linear FLAIR hyperintensities with subtle T1\npost-contrast enhancement.  In the setting of known malignancy, findings are\nconcerning for leptomeningeal metastasis.  However, the differential includes\ninfection, sarcoidosis, and less likely subtle subarachnoid hemorrhage.\n2. No acute intracranial abnormalities identified.\n3. Chronic small-vessel ischemic disease.\n\nNOTIFICATION:  The findings were discussed with ___, M.D. by ___\n___, M.D. on the telephone on ___ at 10:38 am, 5\nminutes after discovery of the findings."
        },
        {
            "input": "There is a 9 x 6 mm right putamina intraparenchymal hematoma, corresponding to\nhyperdensity on prior CT.  There is mild surrounding FLAIR hyperintensity,\nwith associated susceptibility artifact and slow diffusion.  There is no\ndefinite evidence of corresponding enhancement.\n\nThere is a nonspecific right medial frontal gyrus focus of T2 hyperintensity\nand T1 hypointensity (3:17, 12:17), without corresponding susceptibility\nartifact, slow diffusion, or enhancement.  Given the hypointensity on FLAIR\nimages and similar signal characteristics is CSF, finding may represent a\nporencephalic cyst.\n\nThere is no evidence of acute infarction.  There is mild prominence of the\nventricles and sulci compatible with involutional changes.  There is no mass\neffect or midline shift.\n\nThere is mild bilateral ethmoid and maxillary sinus mucosal thickening.  The\norbits the bilateral mastoid air cells appear clear.  There are nonenhancing\nbilateral FLAIR hyperintense superficial parotid lesions, measuring 7 x 6 mm\non the right and 8 x 6 mm on the left, likely lymph nodes..  Otherwise, the\nvisualized soft tissues appear unremarkable.",
            "output": "1. Right putaminal intraparenchymal hematoma.  No evidence of an underlying\nmass, although follow-up MRI after resolution of the hemorrhage is recommended\nto further assess.\n2. Probable right frontal porencephalic cyst or sequela prior infarct, as\nabove, unchanged since prior exam.\n3. No evidence of acute infarction."
        },
        {
            "input": "Study is moderately degraded by motion.\n\nThe lateral ventricles and third ventricle are enlarged, most likely secondary\nto central greater than peripheral volume loss, given the configuration of the\nextra-axial spaces.  There is no hydrocephalus or mass effect.\n\nThere are trace residual blood products within right lenticular nucleus and\ncaudate nucleus.  There is no acute intracranial hemorrhage or acute infarct. \nSmall areas of hyperintense signal on T2/FLAIR within the subcortical and\nperiventricular white matter are nonspecific, but likely reflect the sequela\nof mild chronic small vessel disease.  A more prominent area of signal\nabnormality within the right cingulate gyrus likely reflects a sequela of a\nremote infarct.  There is no abnormal intracranial enhancement.  The major\nvascular flow voids and\norbits are preserved.\n\nThere is mild diffuse paranasal sinus mucosal thickening. Apparent aerosolized\ndebris within the right sphenoid sinus could reflect a more acute inflammatory\nprocess.",
            "output": "1. Study is moderately degraded by motion.\n2. Nonspecific probable moderate central greater than peripheral parenchymal\nvolume loss, grossly similar to the ___ CT.  Please note the normal\npressure hydrocephalus may have a similar appearance.\n3. No acute infarct, intracranial hemorrhage, mass effect, or hydrocephalus.\nNo abnormal enhancement.\n4. Interval evolution of right lenticular and caudate nucleus blood products.\n5. Probable mild chronic small vessel disease.\n6.  Paranasal sinus disease with findings concerning for acute sinusitis, as\ndescribed."
        },
        {
            "input": "The exam is severely degraded by patient motion.  Within these confines:\n\nAllowing for differences in modality, there is grossly unchanged left temporal\nlobe hemorrhage with extension into the left temporal horn.  Mild expansion of\nthe left temporal horn is noted.  There are few scattered foci of\nsusceptibility in the bilateral cerebral hemisphere and basal ganglia.  No\nevidence of midline shift.\n\nThere are confluent T2/FLAIR hyperintensity in the bilateral periventricular\nand subcortical white matter suggestive of chronic microangiopathy.  There is\nno evidence of an acute infarct.  There is stable prominence of the\nventricles, cortical sulci and basal cisterns, likely representing age-related\ninvolutional changes.  There aerosolized fluid in the right maxillary sinus\nwith mucosal thickening of the ethmoid and bilateral maxillary sinuses.",
            "output": "1. Allowing for differences in modality, unchanged intraparenchymal hemorrhage\nin the left temporal lobe with extension into the left temporal horn.  The\nsusceptibility artifacts noted in the bilateral cerebral hemisphere and basal\nganglia may represent hypertensive microhemorrhages versus microhemorrhages\nfrom cerebral amyloid angiopathy.\n2. Changes of chronic microangiopathy in the periventricular white matter.\n3. No evidence of an acute territorial infarct."
        },
        {
            "input": "There is curvilinear T1 and FLAIR hyperintense signal of the left frontal\noperculum (series 4, image 14 and 15, series 7, image 14) without evidence of\nacute infarct or intracranial hemorrhage.  This may represent slow flow\nthrough a cortical vein versus thrombus.\n\nSulci, ventricles and cisterns are within expected limits for the patient's\nage.  The remainder of the intracranial flow voids are preserved.  The\nparanasal sinuses are clear.  The orbits are unremarkable.  The mastoid air\ncells are clear.",
            "output": "1. Curvilinear T1 and FLAIR hyperintense signal of the left frontal operculum\nwhich may represent slow flow in a cortical vein or developmental venous\nanomaly.  However, thrombosis is not entirely excluded.\n2. There is no associated acute infarct or hemorrhage.\n\nRECOMMENDATION(S):  Point 1:  The findings likely represents a slow flow\nthrough a cortical vein or developmental venous anomaly.  However, small\nthrombus is not entirely excluded.  Recommend further evaulation with contrast\nenhanced MRI head with MRA head.\n\nNOTIFICATION:  The impression and recommendation above was entered by Dr.\n___ on ___ at 09:35 into the Department of Radiology critical\ncommunications system for direct communication to the referring provider."
        },
        {
            "input": "There is moderate artifact through bilateral cavernous segments of ICAs,\nophthalmic arteries, there may be cavernous segment ICA bilateral mild\natheromatous narrowing.  Otherwise, the intracranial vertebral and internal\ncarotid arteries and their major branches appear normal without evidence of\nstenosis, occlusion, or aneurysm formation.  A-comm is probably present and\ndiminutive.  Bilateral PCOM is identified.  Left vertebral artery is dominant.\nNo evidence of AVM.  Left ICA is not aberrant.  There is no flow in the\npreviously seen right frontal operculum developmental venous anomaly.  Dural\nvenous sinuses, cavernous sinus is not opacified.",
            "output": "There is no evidence of AVM, aneurysm or aberrant ICA."
        },
        {
            "input": "MRI Brain: There is no evidence of hemorrhage, edema, masses or infarction.\nVentricles and sulci are prominent, likely due to age related cortical volume\nloss. FLAIR hyperintensities are nonspecific and probably represent small\nvessel disease. There is significant mucosal thickening in the right maxillary\nsinus with heterogeneous signal and an air fluid level.\nMRA brain: The intracranial vertebral and internal carotid arteries and their\nmajor branches appear normal without evidence of stenosis, occlusion, or\naneurysm formation.\nMRA neck: The common, internal and external carotid arteries appear normal.\nThere is no evidence of internal carotid artery stenosis by NASCET criteria.\nThe origins of the great vessels, subclavian and vertebral arteries appear\nnormal bilaterally.",
            "output": "1. No infarction.\n2. Sinus disease in the right maxillary sinus with inspissated secretions.\nFungal colonization is a possibility."
        },
        {
            "input": "A normal appearing right frontal approach VP shunt catheter is seen,\nterminating in the third ventricle, causing a large right-sided susceptibility\nartifact.  The ventricles and sulci are normal in caliber and configuration. \nA cavum septum pellucidum et vergae is seen.\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  There is no abnormal enhancement after contrast\nadministration.\n\n The paranasal sinuses, mastoid air cells and middle ear cavities are clear. \nThe intraorbital contents are normal.",
            "output": "1. Normal appearing right frontal approach VP shunt without evidence of\nventriculomegaly.\n2. No acute intracranial abnormalities."
        },
        {
            "input": "There is a punctate focus of susceptibility in the right posterior temporal\nlobe and posterior limb of the right internal capsule.  There is no signal\nabnormality in the posterior parietal or occipital lobes.  There is no\nevidence of acute hemorrhage, edema, masses, mass effect, midline shift or\ninfarction.   The ventricles and sulci are normal in caliber and\nconfiguration.\n\nThere is trace mucosal thickening in several ethmoid air cells.  The\nvisualized orbits and mastoid air cells are unremarkable.  The major vascular\nintracranial flow voids are maintained.",
            "output": "1. No acute intracranial abnormality, specifically no evidence of signal\nabnormality to suggest PRES.\n2. Punctate foci of susceptibility in the posterior right temporal lobe and\nposterior limb of the right internal capsule, possibly reflecting chronic\nmicrohemorrhage."
        },
        {
            "input": "There is an unchanged appearance of right posterior temporal and right\nputaminal microbleeds.  Otherwise, there is no evidence of hemorrhage, edema,\nmasses, mass effect, midline shift or infarction.   The ventricles and sulci\nare normal in caliber and configuration.\n\nThe orbits appear normal normal.  Mild mucosal thickening involving ethmoid\nair cells.",
            "output": "1. 2 tiny micro bleeds, unchanged.\n2. Otherwise normal study."
        },
        {
            "input": "There is unchanged micro bleed in the right posterior temporal lobe (10:9) and\nright putamina (10:14).  No additional hemorrhages are identified.\n\nThere is no evidence of edema, masses, mass effect, midline shift or\ninfarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.  The visualized major vascular flow voids are grossly\npreserved.  The paranasal sinuses and mastoid air cells are clear.  The globes\nand orbits are unremarkable.  There is no abnormal marrow signal.",
            "output": "1. Stable two small microbleeds in the right posterior temporal lobe and right\nputamina.\n2. Otherwise no acute intracranial abnormalities.  No evidence of an acute\ninfarct, intracranial mass, or new hemorrhage."
        },
        {
            "input": "MRI BRAIN:\nThere is no evidence of new hemorrhage, noedema,masses,mass effect,midline\nshift or infarction.  There are two punctate foci of susceptibility as seen\npreviously along the posterior limb of the internal capsule/putamen on the\nright and within the right temporal lobe posteriorly.  No new foci of\nsusceptibility artifact identified.  The ventricles and sulci are normal in\ncaliber and configuration.\n\nMRA BRAIN:\nThe intracranial vertebral and internal carotid arteries and their major\nbranches appear normal without evidence of stenosis,occlusion,or aneurysm\nformation.\n\nMRA NECK:\nThe origins of the great vessels, subclavian and vertebral arteries appear\nnormal bilaterally.  The common, internal and external carotid arteries appear\nnormal.  There is no evidence of internal carotid artery stenosis by NASCET\ncriteria.",
            "output": "1. No acute intracranial abnormality.\n2. Two prior microhemorrhages, unchanged.\n3. Patent circle of ___ without evidence of stenosis,occlusion,or aneurysm.\n4. Patent bilateral cervical carotid and vertebral arteries without evidence\nof stenosis, occlusion, or dissection."
        },
        {
            "input": "There is no evidence of acute intracranial hemorrhage, edema, masses, mass\neffect, midline shift or acute infarction.  The ventricles and sulci are\nnormal in caliber and configuration.  There is redemonstration of unchanged 2\npunctate foci of signal void at T2 star images in the posterior limb of right\ninternal capsule and right posterior parietal temporal region.\n\nBoth orbits and globes are normal.  Paranasal sinuses and mastoid air cells\nare clear.",
            "output": "1. No acute intracranial abnormality or newly developed abnormal brain\nparenchymal abnormal signal abnormality."
        },
        {
            "input": "Artifact centered in the face, presumably from dental implants, limits\ndetailed evaluation near the skullbase including the inferior frontal lobes\nand brainstem specifically on diffusion, FLAIR and gradient echo sequences.\n\nThere is no intracranial mass, mass effect, or midline shift.  A few scattered\nsubcortical and periventricular white matter T2/FLAIR hyperintensities are\nnoted, nonspecific but compatible with chronic small vessel disease. \nVentricles and sulci are prominent compatible with global volume loss.  There\nis no restricted diffusion to suggest acute infarct. No abnormal\nsusceptibility artifact identified. Major intravascular flow voids are\npreserved including within the major dural venous sinuses.\n\nMucous retention cysts noted in the left maxillary sinus.  No abnormal signal\nnoted in the remaining paranasal sinuses or mastoids.",
            "output": "Artifact near the skullbase.  Within this limitation, in no acute intracranial\nprocess.  Minimal scattered white matter T2/FLAIR hyperintensities, likely\nsequela of chronic small vessel disease."
        },
        {
            "input": "Examination is mildly degraded by motion.  Within these limitations:\n\nThere is encephalomalacia from chronic infarcts in the left occipital lobe and\nbilateral cerebellar hemispheres.  There is no evidence of hemorrhage, masses,\nmass effect, midline shift or acute infarction.  There is prominence of the\nventricles and sulci suggestive involutional changes.   There are\nperiventricular and subcortical lucencies, which may represent small vessel\nischemic changes.   The principal intracranial vascular flow voids are\npreserved.  There is no abnormal focus of slowed diffusion.\n\nThere is complete opacification of the right maxillary sinus.  The remainder\nof the paranasal sinuses are grossly clear.  The orbits are grossly\nunremarkable.",
            "output": "1. Examination is mildly degraded by motion.\n2. Chronic left occipital and cerebellar infarcts.\n3. No acute infarct, hemorrhage or suggestion of mass.\n4. Prominent ventriculomegaly out of proportion to global atrophy, which may\nbe seen in the setting of normal pressure hydrocephalus.\n5. Extensive confluent white matter signal abnormality suggestive of chronic\nsmall vessel ischemia.\n6. Right maxillary sinus disease."
        },
        {
            "input": "As noted on prior studies of ___ including a MRI head without\ncontrast and multiple CT head examinations as while as a CTA head and neck,\nchronic infarcts of the bilateral basal ganglia, left occipital lobe with ex\nvacuo dilatation of the left lateral occipital horn, and multiple bilateral\ncerebellar hemispheric coronary infarcts are unchanged.  Confluent\nperiventricular and subcortical T2/FLAIR white matter hyperintensities are\nnonspecific, but compatible with a combination of small vessel ischemic\ndisease and prior infarcts.  No interval change from examination of 1 day\nprior.  No acute intracranial hemorrhage.  The major intracranial flow voids\nare preserved.  No abnormal postcontrast enhancement.  The sulci, ventricles\nand cisterns are prominent, which may represent involutional changes.\n\nComplete opacification of the right maxillary sinus is noted.  There is mild\nmucosal thickening of the inferior frontal sinuses and ethmoid air cells.  The\norbits are unremarkable, noting bilateral lens replacements.  The mastoid air\ncells are clear.",
            "output": "1. No evidence of acute infarct or intracranial mass.  No acute hemorrhage.\n2. Chronic bilateral basal ganglia, cerebellar and left occipital lobe\ninfarcts."
        },
        {
            "input": "There is no evidence of acute intracranial hemorrhage, mass, mass effect or\nlarge territorial infarction.  Mildly prominent ventricles and sulci are\nlikely related to age related involutional changes.  Periventricular FLAIR\nwhite matter hyper intensities are likely sequelae of chronic microangiopathy.\n\nMild mucosal sinus thickening is seen involving the ethmoid air cells.  The\npatient is status post bilateral lens replacement surgery.  The principal\nvascular flow voids are grossly unremarkable.",
            "output": "1. No acute intracranial abnormalities identified.  Mild chronic\nmicroangiopathy."
        },
        {
            "input": "There is a small area of slow diffusion in the left cerebellum with associated\nT2/FLAIR signal hyperintensity, compatible with acute to subacute infarct\n(5:8).  There is no evidence of hemorrhage, edema, masses, mass effect, or\nmidline shift.  There is prominence of the ventricles and sulci consistent\nwith age related involutional changes.  Subcortical and periventricular white\nmatter T2/FLAIR hyperintensities are nonspecific, however are likely due to\nchronic small vessel ischemic disease in this age group.  T2/FLAIR signal\nhyperintensities in the brainstem additionally are nonspecific, however likely\nrepresent sequela of chronic small vessel ischemic disease.  The major\nintracranial flow voids are preserved.\n\nThere is partial opacification of the bilateral mastoid air cells,\nnonspecific.  The orbits are grossly unremarkable.",
            "output": "1. Acute to subacute infarct in the left cerebellum.\n2. Atrophy and sequela of likely chronic small vessel ischemic disease."
        },
        {
            "input": "MRA brain: The left internal carotid artery is normal.  The left middle\ncerebral artery is normal.  There is normal arborization of the distal left\nMCA vessels.  The right internal carotid artery is normal.  The right middle\ncerebral artery is normal.  There is normal arborization of the distal right\nMCA vessels.  The anterior cerebral arteries are normal.  The vertebral\narteries are normal.  The basilar artery is normal.  There is fetal type\nconfiguration of the bilateral PCAs which are otherwise unremarkable.",
            "output": "1. Unremarkable MRA of the head without evidence of aneurysm or significant\nstenosis."
        },
        {
            "input": "There is no evidence of acute intracranial hemorrhage, or infarction. \nProminence of the ventricles and sulci is likely related to age related\ninvolutional changes.  Periventricular and deep subcortical FLAIR white matter\nhyperintensities are likely sequelae of chronic microangiopathy.  Mild mucosal\nsinus thickening is seen involving the ethmoid air cells.  The remainder the\nvisualized paranasal sinuses, mastoid air cells, and middle ear cavities are\nclear.  Patient is status post bilateral lens replacement surgery.  The\nprincipal vascular flow voids are well preserved.  No concerning enhancing\nlesions are seen.",
            "output": "1. No acute intracranial abnormalities identified.  No concerning enhancing\nlesions seen.\n2. Chronic microangiopathy."
        },
        {
            "input": "There is no evidence of intracranial hemorrhage or acute infarction.  There is\nprominence of the ventricles and sulci related to age-appropriate diffuse\nparenchymal volume loss.  There are nonspecific periventricular and\nsubcortical FLAIR hyperintensities including the pons, likely a sequela of\nchronic small vessel ischemic disease.  There is no mass effect or midline\nshift.  There is mild mucosal thickening of the bilateral ethmoid air cells. \nThe patient is status post bilateral cataract surgery.  Major visualized\narterial vascular flow voids are preserved.  The visualized soft tissues\nappear unremarkable.",
            "output": "1. No evidence of intracranial hemorrhage or acute infarction.\n2. Age-appropriate diffuse parenchymal volume loss.\n3. Nonspecific white matter signal abnormality, likely representing moderate\nchronic small vessel ischemic disease, unchanged from prior exam."
        },
        {
            "input": "Study is moderately degraded by motion.  Within these confines:\n\nAgain identified are a small T1 hyperintense focus in the right cerebellum\n(series 12, image 5) with an additional elongated area of T1 hyperintensity in\nthe more superior right cerebellar hemisphere (series 12, image 6).   The\nassociated FLAIR hyperintensity appears less conspicuous on today's exam which\nmay be due to motion artifact.  However, overall the lesions appear stable\nfrom ___.  Mild enhancement of these lesions is better identified on\ntoday's exam (series 17, image 33 and 37-42).\n\nOtherwise, there is no evidence of hemorrhage, edema, masses, mass effect,\nmidline shift or infarction.  Unchanged scattered T2/FLAIR hyperintensities in\nthe cerebral hemispheres bilaterally, a nonspecific finding and likely related\nto chronic small vessel ischemic changes.\n\n There is grossly stable prominence of the ventricles and sulci suggestive of\ninvolutional changes.   Major vascular flow voids appear preserved.  Major\ndural venous sinuses are patent.\n\nThere is minimal mucosal thickening along the ethmoid air cells.",
            "output": "1.  Study is moderately degraded by motion.\n2. Grossly stable right cerebellar mildly enhancing lesions with less\nconspicuous associated FLAIR hyperintensity, again concerning for metastatic\ndisease, with differential consideration of  developmental venous anomaly. \nRecommend attention on follow-up imaging.\n3. Within limits of study, no definite evidence of new enhancing intracranial\nmass.\n\nRECOMMENDATION(S):  Grossly stable right cerebellar mildly enhancing lesions\nwith less conspicuous associated FLAIR hyperintensity, again concerning for\nmetastatic disease, with differential consideration of developmental venous\nanomaly.  Recommend attention on follow-up imaging."
        },
        {
            "input": "MRI BRAIN:\nExtensive restricted diffusion is seen involving the left temporal, frontal,\nparietal and occipital lobes consistent with patient's known left MCA\ninfarction.  Additional foci of slow diffusion is seen within the right\nfrontotemporal region, likely embolic in etiology.  There is no definite\nevidence of hemorrhagic conversion of the patient's left MCA infarction.\n\nVentricles and sulci are normal in size and configuration.  Periventricular\nFLAIR hyperintensities are likely secondary to chronic microangiopathy.  No\nconcerning enhancing lesions are identified.\n\nMRA brain:  Re demonstrated is an abrupt cut off along the left M2 segment of\nthe MCA, with asymmetric oligemia along the left frontoparietal lobes.  The\nremainder of the circle of ___ is unremarkable.  The posterior circulation\nappears to be well preserved.  The right MCA and bilateral ACA is well\npreserved.  The anterior communicating artery is well seen.  The right PCA\ndemonstrates fetal type configuration.",
            "output": "1. Extensive restricted diffusion involving the left temporal, frontal,\nparietal, and occipital lobes consistent with patient's known left MCA\ninfarction.  Additional foci of slow diffusion within the right frontotemporal\nregion likely embolic in etiology.  No definite evidence of hemorrhagic\nconversion.\n2. Re demonstrated is an abrupt cut off of the left M2 segment of the MCA. \nThe remainder of the circle ___ is unremarkable."
        },
        {
            "input": "There is an area of slow diffusion in the right thalamus that is mildly\nhypodense on the head CT.  This suggests an acute to subacute infarction. \nThere is no evidence of hemorrhage, edema, masses, mass effect or midline\nshift.  Confluent periventricular and subcortical T2/FLAIR hyperintensities\nare likely the sequela of chronic small vessel ischemic disease.  Focal\nhypodensity seen in the left parietal lobe on most recent head CT corresponds\nto an area of increased diffusion reflecting a focal area of chronic\nencephalomalacia (series 5, image 19; series 6, image 20; series 302, image 24\nand series 300, image 24).  There is prominence of the ventricles and sulci\nsuggestive involutional changes.\n\nThere is mucosal thickening of the left ethmoidal air cells.",
            "output": "1. Acute to subacute right thalamic infarction.\n2. Chronic small vessel ischemic disease.\n3. Focal encephalomalacia in the left parietal lobe."
        },
        {
            "input": "Carotid and vertebral arteries demonstrate normal flow signal. There is no\nevidence of vascular, stenosis or dissection. The. The thoracic aorta and its\nmajor branches also demonstrate normal appearances. The vertebral artery\nartery origins are patent.",
            "output": "No significant abnormalities are seen on MRA of the neck."
        },
        {
            "input": "There has been no significant interval change.  Postoperative changes are seen\nin the left parietal convexity region.  No recurrent mass lesion is identified\nin this region.  A small calcific area of susceptibility and T1 hyperintensity\nin the left frontal convexity region with some enhancement is unchanged. \nThere are no other areas of abnormal enhancement seen.  No mass effect seen\nmidline shift identified.  Mild changes of small vessel disease are noted.",
            "output": "Stable appearance of the brain without significant new abnormalities."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor acute infarction.  Unchanged left parietal convexity postoperative changes.\nThere are multiple punctate subcortical and deep white matter T2 and FLAIR\nhyperintensities, similar to prior study, which likely represent sequelae of\nchronic small vessel ischemic disease.  Unchanged left frontal area of\nsusceptibility and T1 hyperintensity.  There is prominence of the ventricles\nand sulci suggestive involutional changes, which is stable.",
            "output": "1. No evidence of acute infarct.\n2. No significant change from prior study when compared to the pre contrast\nimages of the previous study."
        },
        {
            "input": "There are postoperative changes from left parietal craniotomy and mass\nresection with minimal underlying dural thickening and enhancement and chronic\nblood product.  There is no new or nodular enhancement in this area to suggest\nmeningioma recurrence.\n\nA 14 x 8 mm left frontal extra-axial lesion demonstrating susceptibility\nartifact and intrinsic T1 hyperintensity, without definite post-contrast\nenhancement is unchanged since earliest prior examination from ___, appearing heavily calcified on prior CT examination, likely representing\nprominent calcified dural plaque.  Another subtle 5 x 2 mm enhancing left\nfrontal extra-axial lesion (1000:115), is unchanged compared the earliest\nprior examination from ___ (will see series 1000, image 60 on that\nexamination).  No new enhancing mass is seen.\n\nThere is no evidence of hemorrhage, edema, significant mass effect, midline\nshift or infarction.   There is mild prominence of the ventricles and sulci\nsuggestive of involutional change.  There are mild scattered periventricular,\nsubcortical and deep white matter T2/FLAIR hyperintensities in a configuration\nmost suggestive chronic small vessel ischemic disease.  The principal\nintracranial vascular flow voids are preserved.\n\n The visualized paranasal sinuses are grossly clear.  The orbits are grossly\nunremarkable.  The mastoid air cells are clear.",
            "output": "1. Stable postoperative changes from left parietal craniotomy and meningioma\nresection without evidence of residual or recurrent disease.\n2. 5 x 2 mm left frontal extra-axial enhancing lesion is unchanged since ___, representing either tiny meningioma or prominent vascular\nstructure.\n3. 14 x 8 mm calcified left frontal extra-axial lesion without definite\npost-contrast enhancement likely represents a calcified dural plaque.\n4. No new enhancing mass."
        },
        {
            "input": "There is a left anterior parietal parasagittal extra-axial dural-based\nenhancing mass measuring 9 mm AP by 16 mm transverse by 12 mm craniocaudad,\nimages 300:45 and 301:41. The medial aspect of the mass abuts the superior\nsagittal sinus without occlusion. There is no mass effect on the adjacent\nbrain parenchyma. There is no change compared to ___.\n\nThere is another dural-based extra-axial enhancing mass in the left frontal\nregion measuring 15 mm AP x 14 mm transverse by 7 mm craniocaudad, images\n300:33 and 301:79, without mass effect on the adjacent brain parenchyma. There\nis no change compared to ___ allowing for differences in technique.\n\nVentricles and sulci are normal in size for age. Major dural venous sinuses\nappear patent, and major intracranial arteries appear unremarkable.\nComprehensive evaluation of the brain parenchyma is not performed with this\nlimited exam which is targeted for surgical planning.",
            "output": "Left anterior parietal parasagittal and left frontal extra-axial masses,\ncompatible with meningiomas, are again demonstrated for surgical planning."
        },
        {
            "input": "The patient is status post left parietal approach craniotomy, with the\nexpected postsurgical changes. There is no enhancing mass or other evidence of\nresidual tumor at the surgical site. A 1.2 x 1.0 x 0.5 cm calcified mass in\nthe left frontal convexity (9:134, 900:56, 10:20) is unchanged and again\nlikely represents a second meningioma.\nThere is no evidence of hemorrhage, edema, or infarction. The ventricles and\nsulci are normal in caliber and configuration. Periventricular T2/FLAIR\nhyperintensities are suggestive of chronic small vessel ischemic disease.\nThere is no abnormal enhancement after contrast administration.",
            "output": "1. Status post left parietal approach craniotomy with the expected\npostsurgical changes, without evidence of residual or recurrent mass.  No new\nmass identified.\n2. Unchanged calcified mass in the left frontal convexity, likely a second\nmeningioma.\n3. Sequela of chronic small vessel ischemic disease."
        },
        {
            "input": "Postoperative changes are again identified in the left parietal region.  There\nis no recurrent mass or abnormal enhancement seen.  Subtle area of enhancement\nin the left parietal convexity region series 16, image 18 appears to be\nvascular enhancement and is unchanged.  A small left frontal likely calcified\nmeningioma with fatty degeneration is again identified and is unchanged. \nThere are no new areas of abnormal enhancement seen.  Acute infarcts are\nidentified.  A few nonspecific foci of T2 hyperintensity are identified. \nVascular flow voids are maintained.  Suprasellar and craniocervical junctions\nunremarkable.  Visualized paranasal sinuses are clear.",
            "output": "Stable appearance of brain compared to the previous MRI of ___.  No\nevidence of recurrent mass lesion seen or new area of abnormal enhancement\nidentified.  No acute infarct."
        },
        {
            "input": "Small subacute infarct posterior left corona radiata, extending into putamen. \nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift.\nChronic lacunar infarct right pons.  Moderately prominent prevascular spaces\nbasal ganglia, cerebral hemispheres.  Findings consistent with\nmild-to-moderate chronic small vessel ischemic change.  Mild brain parenchymal\natrophy.  Small caliber right vertebral artery, may be from chronic occlusion\nwith back filling from dominant large caliber left vertebral artery.  Clear\nparanasal sinuses, mastoids.",
            "output": "Small subacute infarct left corona radiata, putamen.\nOccluded proximal V4 segment right vertebral artery.  Large caliber dominant\nleft vertebral artery."
        },
        {
            "input": "Evaluation is suboptimal due to motion artifact.  Within this confine:\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  Moderate brain parenchymal atrophy.  The intracranial flow\nvoids are maintained.  There is no abnormal enhancement after contrast\nadministration.  Small chronic right thalamus lacunar infarct.\n\nThere is mild mucosal thickening of the ethmoid sinuses.  There is minimal\nfluid in the bilateral mastoid air cells.  The intraorbital contents are\nnormal.",
            "output": "1. Suboptimal exam due to motion artifact.\n2. No acute intracranial abnormality.\n3. Moderate brain parenchymal atrophy.."
        },
        {
            "input": "Images are moderately degraded by motion artifact.  Within these confines:\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor acute infarction.\n\nSmall chronic bilateral lacunar infarcts are noted.\n\nThere is prominence of the ventricles and sulci suggestive of involutional\nchanges.  Periventricular and subcortical T2 and FLAIR hyperintensities are\nnoted which are nonspecific but compatible with small vessel ischemic changes.\n\nThere is no definite abnormal enhancement after contrast administration.  The\ndural venous sinuses appear grossly patent.  The major intracranial flow voids\nare grossly preserved.  Right thalamic punctate focus of blood products versus\nmineralization is noted (07:12).\n\nThere is opacification of several ethmoid air cells.  Small volume\nnon-specific fluid is noted within the bilateral mastoid air cells.  The\norbits and globes appear within normal limits.",
            "output": "1.  Study is moderately degraded by motion.\n2. No evidence of acute infarct, intracranial hemorrhage, mass or abnormal\nenhancement.\n3. Age-related involutional changes and periventricular/subcortical\nhyperintensities which are nonspecific but compatible with small vessel\nischemic changes.\n4. Right thalamic punctate focus of blood products versus mineralization.\n5.  Paranasal sinus disease and nonspecific bilateral mastoid fluid, as\ndescribed."
        },
        {
            "input": "The examination is slightly motion degraded.  Within these confines:\n\nFoci of high T2 signal in the subcortical, deep, and periventricular white\nmatter of the cerebral hemispheres, including callosal and pericallosal\nlesions, are unchanged.  No there is also an unchanged small lesion in the\nmedial left cerebellar hemisphere at the margin of the left middle cerebellar\npeduncle, images 2:76 and 12:6.  There are no contrast enhancing lesions. \nThere are no lesions with slow diffusion.\n\nThere is no evidence of acute infarction, edema, intracranial mass , or blood\nproducts.  Intracranial arterial flow voids are maintained.  Major dural\nvenous sinuses are patent.\n\nDependent secretions in the right maxillary sinus are similar in appearance to\nprior exam.  Partial opacification of the ethmoid air cells has progressed. \nThere is also unchanged.  Mild mucosal thickening of the left frontal sinus. \nFluid signal in the left mastoid air cells are also similar appearance to\nprior exam.  Visualized nasopharynx is unremarkable.",
            "output": "1. Stable appearance of demyelinating disease without evidence for new or\ncontrast enhancing lesions.\n2. Persistent fluid signal in left mastoid air cells and dependent secretions\nin the right maxillary sinus, and progressed moderate ethmoid air cell\nopacification.  Please correlate with clinical symptoms ."
        },
        {
            "input": "There is no acute infarction, intracranial hemorrhage, extracerebral fluid\ncollection, midline shift or mass effect.  Ventricles and extra-axial spaces\nare normal in size.  Flow voids are maintained. Suprasellar and craniocervical\nregions are unremarkable.  There is a 12 mm simple appearing pineal cyst\nidentified without significant mass effect on the tectum or evidence of\nhydrocephalus.",
            "output": "12 mm simple appearing pineal cyst without significant mass effect on the\ntectum or hydrocephalus.  Otherwise, no significant abnormalities are seen on\nMRI of the brain without gadolinium."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  Periventricular and subcortical FLAIR hyperintensities are\nnonspecific but likely reflect sequela of chronic small vessel ischemic\ndisease.  There is mild prominence of the ventricles and sulci suggestive\ninvolutional changes.  Fluid is seen in the left maxillary sinus.",
            "output": "No acute intracranial process.  No evidence of ischemia or infarct."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, or infarction.\nNo diffusion abnormalities are detected. The ventricles are normal in caliber\nand configuration.  There is mild prominence of the sulci in the parietal\nconvexities, which is a nonspecific finding.\n\nMultiple small nasal polyps versus mucosal retention cysts are identified in\nthe right maxillary sinus.  A large mucosal retention cyst is identified at\nthe left maxillary sinus. The remaining paranasal sinuses and mastoid air\ncells are clear. The orbits are unremarkable.",
            "output": "Mild prominence of the sulci in the parietal convexities, which is a\nnonspecific finding. However, clinical correlation is advised."
        },
        {
            "input": "7.0 x 4.0 cm intraparenchymal hematoma centered at the left basal ganglia is\nstable in size compared to 1 day ago.  Mass effect from the hematoma causes\neffacement of left lateral ventricle and rightward midline shift by 9 mm are\nunchanged.  At least 3 millimetric scattered foci of slow diffusion are\nidentified in the left frontal and temporal regions surrounding the hematoma\n(07:23, 19, 17).  Nonenhancing signal abnormality is noted in the left\ncerebral peduncle (see 12, 13:9.  Cerebellar tonsils are located 6 mm below\nthe foramina magnum, similar to before.  Left frontal calvarial probable\narachnoid granulations or hemangioma are noted (see 100:83; 12, 13:24).\n\nNo mass is identified.  There is no abnormal enhancement after contrast\nadministration.  Mucosal thickening is mild in the ethmoid, sphenoid, and\nmaxillary sinuses.  Mild partial opacification of bilateral mastoid air cells\nis noted.",
            "output": "1. Left basal ganglia intraparenchymal hematoma is stable in size compared to\n1 day ago.  While no definite underlying mass is identified, mass is not\nexcluded on the basis of this examination.  Recommend follow-up imaging to\nresolution.\n2. Several scattered foci of slow diffusion in the left frontal and temporal\nregions surrounding the hematoma are concerning for acute to subacute\ninfarcts.\n3. Probable edema extension into left cerebral peduncle.\n4. Low lying cerebellar tonsils are similar to before.\n5. Paranasal sinus disease and nonspecific bilateral mastoid fluid, as\ndescribed.\n\nRECOMMENDATION(S):  Left basal ganglia intraparenchymal hematoma is stable in\nsize compared to 1 day ago. While no definite underlying mass is identified,\nmass is not excluded on the basis of this examination. Recommend follow-up\nimaging to resolution."
        },
        {
            "input": "There is no focus of slowed diffusion to suggest acute infarction.  No\nevidence of gradient echo susceptibility to suggest the presence of\nintracranial hemorrhage.  There is no evidence of edema, masses, mass effect,\nor midline shift.  Several faint, nonenhancing FLAIR hyperintense foci in the\nscattered cerebral white matter in bilateral frontal lobes and left pons are\nagain seen.  The ventricles and sulci are normal in caliber and configuration\nfor the patient's age.  There is no abnormal enhancement after contrast\nadministration.\n\nThe major intracranial flow voids are preserved.  Dural venous sinuses are\npatent at post contrast MP RAGE imaging.\n\nThe there is mild mucosal thickening in the ethmoidal air cells and maxillary\nsinuses.  The remaining paranasal sinuses are clear.  Trace fluid signal is\nidentified in the bilateral mastoid air cells.  The imaged orbits are\nunremarkable.",
            "output": "1.  No evidence of intracranial metastatic disease,  intracranial hemorrhage,\nor acute or subacute infarction.\n\n2.  Several faint, scattered FLAIR hyperintense foci in the cerebral white\nmatter are nonspecific, but unchanged since the prior study."
        },
        {
            "input": "MRA BRAIN:\nThere is atherosclerotic disease of the left posterior cerebral artery with\nmild-to-moderate stenosis.  Otherwise the remainder of the intracranial\nvertebral and internal carotid arteries and their major branches appear normal\nwithout evidence of stenosis, occlusion, or aneurysm formation.\n\nMRA NECK:\nThere is unchanged linear filling defect at the origin of the left subclavian\nartery (1102, 54), corresponding to known dissection.\n\nThere is severe narrowing (70-80%) of the right proximal internal carotid\nartery at its origin by NASCET criteria.  There are stable atherosclerotic\nchanges of the left proximal internal carotid artery with mild-to-moderate\nstenosis.",
            "output": "1. No evidence of intracranial high-grade stenosis occlusion or aneurysm\nformation.\n2. Somewhat limited neck MRA secondary to delays in acquisition.  Within this\nlimitation, stable severe narrowing (70-80%) of the right proximal internal\ncarotid artery by NASCET criteria."
        },
        {
            "input": "MR BRAIN:  The examination is mildly motion degraded.  Within this confines:\n\nLeft parietal occipital encephalomalacia corresponds to hypodensity described\non prior CT examination.  There is also right middle frontal gyrus cortical\nFLAIR hyperintensity, also likely representing sequela of prior infarct. \nSuperimposed periventricular and subcortical T2/FLAIR white matter\nhyperintensities are nonspecific, but compatible with chronic microangiopathy\nin a patient of this age.  There is no intra or extra-axial mass, acute\nhemorrhage or infarct.  The sulci, ventricles and cisterns are mildly\nprominent, in part secondary to age related senescent global cerebral volume\nloss.  There is also prominence of the temporal horns, which likely represents\na component of mesial temporal atrophy.  The major intracranial flow voids are\npreserved.  The visualized paranasal sinuses are essentially clear.  The\norbits are unremarkable, noting bilateral lens replacements.  Fluid signal\nopacifies the left-greater-than-right mastoid air cells.  Fluid in nasopharynx\nis compatible with intubation.\n\nMRA brain:  The most proximal V4 segments visualize secondary to technical\nfactors.  As such, the origins of the bilateral posterior inferior cerebellar\narteries are not well visualized.  The remainder of the intracranial vertebral\nand internal carotid arteries and their proximal major branches appear normal\nwithout evidence of stenosis, occlusion, or aneurysm formation.  Please note,\nthe more distal segments are also not visualized secondary to technical\nfactors.\n\nOn localizer images, there is a moderate-sized right pleural effusion.",
            "output": "1. No evidence for acute infarct.  Left parietal occipital hypodensity on CT\ncorresponds to encephalomalacia.\n2. Superimposed periventricular and subcortical T2/FLAIR white matter\nhyperintensities are nonspecific, but compatible with chronic microangiopathy\nin a patient of this age.\n3. There are age-related involutional changes as well as prominence of the\ntemporal horns, which may represent mesial temporal atrophy.  Clinical\ncorrelation is recommended.\n4. The proximal V4 segments on noncontrast MRA is not visualize secondary\ntechnical factors.  As such, the bilateral posterior inferior cerebellar\nartery origins cannot be evaluated.  The remainder of the MRA brain is grossly\nunremarkable."
        },
        {
            "input": "There are 2 punctate foci of FLAIR hyperintensity seen within the deep\nsubcortical white matter of the right frontal lobe (05:15), and within the\nleft pericallosal white matter tracts (6:78).  Associated T1 hypointensity is\nnoted involving the pericallosal lesion (19:78).  There is no evidence of\nassociated slow diffusion or contrast enhancement following administration of\nintravenous gadolinium.\n\nThere is no evidence of acute infarction.  No intracranial hemorrhage.  No\nmass, mass effect, edema or midline shift.\n\nThe ventricles and sulci are normal, without evidence of hydrocephalus.  The\nbasal cisterns are patent.  There is no evidence of impending, downward\nherniation.  There is apparent preservation of the principal intracranial\nvascular flow voids.\n\nFollowing the administration of intravenous contrast material, there is no\nabnormal enhancement.  The dural venous sinuses appear patent on MP-RAGE\nimagine sequences.\n\nThe visualized paranasal sinuses, middle ear cavities, and mastoid air cells\nare well aerated and clear.  The orbits are within normal limits bilaterally.",
            "output": "1.  No evidence for intracranial mass, abnormal areas of enhancement,\nhemorrhage, or ischemia/infarction.\n2.  Two punctate foci of FLAIR hyperintensity, identified within the\nsubcortical right frontal lobe and within the left pericallosal deep white\nmatter, which are nonspecific and may represent gliotic foci, which are not in\na typical distribution for demyelinating disease.  No evidence of enhancing\nlesions or slow diffusion to suggest active demyelination."
        },
        {
            "input": "The 13 x 14 left temporal lobe lesion is similar in size and signal\ncharacteristics compared with ___. The lesion has heterogeneous\ninternal T1 signal hyperintensity, T2 and FLAIR signal hyperintensity. There\nis increased diffusion-weighted signal intensity and corresponding reduced\napparent diffusion coefficient. An incomplete rim of peripheral enhancement at\nthe medial and posterior borders is similar. Enhancement and signal\nabnormality continues to extend inferiorly in the left temporal lobe. There is\nheterogeneous signal loss on the gradient echo sequence, again compatible with\ninternal blood products.\n\nIn the mid cerebellum there is a new tiny punctate focus of increased\ndiffusion-weighted signal (402:9) with a rim of FLAIR signal hyperintensity\n(7:7).\n\nAn enhancing retroclival dural-based lesion partially effacing the right pre\npontine cistern is similar (901:40).\n\nThere is no new hemorrhage, other intracranial mass, or midline shift.\nVentricles and sulci are mildly enlarged. There are extensive periventricular\nand deep white matter FLAIR signal hyperintensities compatible with\nsmall-vessel ischemic change.  Principle intracranial flow voids are\nmaintained. There is a small right maxillary sinus mucosal retention cyst. The\nother visualized paranasal sinuses and mastoid air cells are clear. Osseous\nand soft tissue structures are unremarkable.",
            "output": "1. Stable size and appearance of left temporal lobe CNS lymphoma.\n2. Tiny right cerebellar infarction is new since ___.\n3. Stable right retroclival meningioma."
        },
        {
            "input": "MR Head:  This is a limited examination without contrast, due to abnormal low\nEGFR. In comparison with the prior head CT, an extensive area of vasogenic\nedema is re- demonstrated in the left basal ganglia extending in the left\ninsular region, with no evidence of significant mass effect, areas of slow\ndiffusion are demonstrated within this lesion including a focal area of low\nADC signal in the posterior limb of the internal capsule (image 14, series 10\nand 11), which is suspicious for hypercellularity, correlation with MRI with\ncontrast is advised for further characterization.  Unchanged foci of T2 and\nFLAIR high signal intensity are redemonstrated in the subcortical and\nperiventricular white matter bilaterally, which are nonspecific and may\nreflect areas of small vessel disease, there is an unchanged right petroclival\nmeningioma, causing effacement of the right prepontine cistern and extending\ninto the cavernous sinus on the right, however a direct comparison with the\nprior examinations is not possible due to lack of intra the contrast material.\nChronic areas of ischemia are re- demonstrated in the pons and both cerebellar\nhemispheres. The orbits are unremarkable, the paranasal sinuses again\ndemonstrate a small mucous retention cyst on the right maxillary sinus, the\nmastoid air cells are clear.\n\nMRA Head: On the left carotid siphon, there is loss of the vascular signal,\nsuggestive of narrowing and arthrosclerotic disease, there is also moderate\nnarrowing or vascular signal on the right carotid cavernous segment. The\nintracranial vessels are patent with no evidence of critical stenosis\nthroughout the anterior and middle cerebral arteries, the vertebral basilar\nsystem appears patent with no evidence of stenosis throughout the basilar\nartery.\n\nMRA of the neck: The origin of the supraaortic vessels is partially evaluated\nin this examination,. Both common carotid arteries are patent with no evidence\nof stenosis at the carotid cervical bifurcations. The vertebral arteries are\npatent with no evidence of flow stenotic lesions, and both vertebral arteries\nare codominant.",
            "output": "1. A combination of vasogenic edema and slow diffusion is identified in the\nleft basal ganglia as described above, suggestive of hypercellularity, this\nexamination is limited without contrast, correlation with MRI with gadolinium\nis advised for further characterization, the possibility of an underlying mass\nlesion cannot be completely excluded, and given the slow diffusion pattern\nlymphoma is a consideration.\n2. Unchanged right petroclival meningioma, extending into the right cavernous\nsinus.\n3. Narrowing of the cavernous segments of the internal carotid arteries, more\nsignificant on the left, likely atherosclerotic in nature.\n4. Normal MRA of the neck.\nNOTIFICATION:. These findings were discovered and communicated via phone call\nto Dr. ___ by Dr. ___ ___ at 13:15 hr."
        },
        {
            "input": "Left temporal lobe masses are again seen and decreased in size, the 2 largest\ncomponents now measuring 11 x 14 mm (9:11, previously 15 x 16 mm) and the 8 x\n4 mm (9:11, previously 10 x 21 mm).  The masses now demonstrate intrinsic T1\nhyperintensity, possibly treatment-related, without significant enhancement.\nThere is decreased mass effect. Slow diffusion is seen in an area of old\nhemorrhage, likely related to prior biopsy. There is no evidence of\nleptomeningeal or dural enhancement after contrast administration.  No new\nlesion is identified.\n\nThere is no acute infarct or intracerebral hemorrhage. Principal intracranial\nvascular flow voids are preserved. No extra-axial blood or the ventricles and\nfluid collection sulci is present. Are unchanged in size and configuration.\nMultiple FLAIR hyperintensities are similar in appearance.  The brainstem,\nposterior fossa, and cervicomedullary junction are preserved. The petroclival\nmeningioma is unchanged.",
            "output": "Decreased size and enhancement of left temporal lobe masses, without evidence\nof new mass or leptomeningeal involvement."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, or infarction.\nThe ventricles and sulci are normal in caliber and configuration. There is no\nabnormal enhancement after contrast administration.",
            "output": "Normal study"
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are prominent, consistent with\ninvolutional changes.  Compared to ___, minimal interval\nprogression in diffuse periventricular subcortical and deep white matter\nT2/FLAIR hyperintensities which are nonspecific, but likely represent chronic\nmicrovascular ischemic changes.  There is no abnormal enhancement after\ncontrast administration.  There are mucous retention cysts in the right\nmaxillary sinus.  Otherwise, the paranasal sinuses, mastoid air cells and\nmiddle ears are clear.  Major intracranial vascular flow voids are preserved. \nMajor dural sinuses are unremarkable on MPRAGE sequences.",
            "output": "1. No evidence of metastasis, as clinically questioned.\n2. Compared to ___, mild interval progression of involutional\nchanges and likely chronic microvascular ischemic changes."
        },
        {
            "input": "There is no evidence of acute intracranial hemorrhage or mass effect. The\nventricles and basal cisterns appear normal. There is poor FLAIR suppression\nof the anterior cerebral hemispheres which is likely on an artifactual basis.\n\nThere is no evidence of acute ischemia based on diffusion-weighted imaging. \nThere are normal vascular flow voids.  Single T2/FLAIR hyperintense lesion\nadjacent to the body of the right lateral ventricle is unchanged from ___,\nand is nonspecific. No new lesions are seen. There are no areas of abnormal\nbrain parenchymal or leptomeningeal enhancement.\n\nThe orbits, skull base, and paranasal sinuses appear unremarkable.  Minimal\nsoft tissue prominence within the right mastoid air cells may represent mild\ninflammation.",
            "output": "Single T2/FLAIR signal hyperintense lesion along the body of the right lateral\nventricle is unchanged from ___ and is nonspecific."
        },
        {
            "input": "There is no evidence of an intracranial mass, edema, blood products, or\ndiffusion abnormality. There is no abnormal meningeal or parenchymal\nenhancement after contrast administration.  The hippocampal formations appear\nsymmetric in size and signal intensity.  The temporal horn of the right\nlateral ventricle is slightly larger than the left, but the ventricles and\nsulci are overall normal in size. Major intracranial arterial flow voids are\npreserved.  Major dural venous sinuses are patent. The orbits are\nunremarkable.\n\nThere is mild mucosal thickening within the ethmoid air cells and right\nmaxillary sinus.",
            "output": "1. No evidence for an intracranial mass.\n2. The temporal horn of the right lateral ventricle is slightly larger than\nthe left, most likely representing anatomic variation, since the hippocampal\nformations appear normal and symmetric. However, correlation with EEG results\nis recommended."
        },
        {
            "input": "Imaging is mildly motion degraded.\n\nMR BRAIN:\n\nThere are linear foci of slowed diffusion in the left frontal and parietal\nwhite matter with subsequent FLAIR hyperintensity concerning for subacute\ninfarct (series 302, image 21).\n\nThere is a thin curvilinear T1 hyperdensity compared with the surrounding CSF\nthat spans the bilateral hemispheres, right greater than left (series 4, image\n19, 7) consistent with chronic subdural hematoma measuring up to 3 mm.  No\nsignificant mass-effect or evidence of herniation.\n\nThere is no evidence of edema,or mass..  The ventricles and sulci are enlarged\nconsistent with age related involutional changes.  Periventricular and\nsubcortical FLAIR hyperintensities are consistent with chronic small vessel\nischemic changes.  The orbits are unremarkable.\n\n\nMRA brain: Imaging only spans partially through the skull base.  The\nintracranial internal carotidarteries and the distal vertebral arteries are\npatent without evidence of stenosis or dissection.  The proximal portion of\nthe basilar artery is patent without evidence of aneurysm, or large vessel\nocclusion.",
            "output": "1. Linear foci of restricted diffusion in the left frontal and parietal white\nmatter is concerning for subacute infarct.\n2. Better visualized bilateral chronic subdural hematomas spanning the\nbilateral hemispheres without evidence of mass-effect.  No evidence of acute\nhemorrhage.\n3. Incomplete MRA images through the skull base demonstrate no evidence of\nhigh-grade stenosis, dissection or aneurysm in the intracranial ICAs, distal\nvertebral or proximal basilar arteries."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are age-appropriate in caliber and\nconfiguration.  There are few scattered T2/FLAIR hyperintensity in the\nperiventricular subcortical white matter, compatible with chronic\nmicroangiopathy.  The major vascular flow voids are grossly preserved.  There\nis mild mucosal thickening of the ethmoid air cells, otherwise the paranasal\nsinuses and mastoid air cells are clear.  The globes and orbits are\nunremarkable.",
            "output": "1. No evidence of an acute infarct, intracranial mass, or hemorrhage.\n2. Mild nonspecific white matter signal changes most likely reflecting chronic\nsmall vessel disease in this age group."
        },
        {
            "input": "Study is moderately degraded by motion.  Within these confines:\n\nThere is no evidence of acute infarction or intracranial hemorrhage.  The\ndural venous sinuses appear patent.\n\nAlong the medial right tentorium, extending into the perimesencephalic cistern\nand contacting right anterolateral pons, there is a 6 x 5 mm enhancing focus\nthat demonstrates intrinsic T2/FLAIR hyperintensity.  No additional enhancing\nlesions are identified.\n\nThe coronal T2 sequences are moderately motion degraded, but within this\nconfines there is no gross asymmetry in size or signal intensity identified\nwithin the bilateral hippocampi by or para hippocampal gyri.\n\nThere is no disproportionate medial temporal atrophy. There is no definite\nfocal lobar encephalomalacia. There are no focal cortical dysplasias or gray\nmatter heterotopia noted.\n\nThe ventricles, sulci and the principal intracranial vascular flow voids are\ngrossly preserved.",
            "output": "1.  Study is moderately degraded by motion.\n2. No evidence for acute intracranial hemorrhage or infarction.\n3. Motion degraded examination with suboptimal evaluation of the medial\ntemporal lobes and hippocampi.  Allowing for this, there is no definite\nasymmetric medial temporal lobe atrophy, abnormal signal, or focal lobar\nencephalomalacia.\n4. 6 x 5 mm enhancing focus contacting the right tentorium and extending into\nthe perimesencephalic cistern, minimally contacting the right anterolateral\npons.  Diagnostic considerations favor an extra-axial dural-based lesion such\nas meningioma or schwannoma.  Recommend continued attention on follow-up.\n5. If clinically indicated, consider repeat examination when patient can\ntolerate study.\n\nRECOMMENDATION(S):  6 x 5 mm enhancing focus contacting the right tentorium\nand extending into the perimesencephalic cistern, minimally contacting the\nright anterolateral pons. Diagnostic considerations favor an extra-axial\ndural-based lesion such as meningioma or schwannoma.  Recommend continued\nattention on follow-up."
        },
        {
            "input": "Again seen arising from the medial edge of the right tentorium is a 5 x 3 mm\nextra-axial enhancing mass narrowing the perimesencephalic cistern focally and\nlikely touching the mid brain without significant mass effect or resultant\nvasogenic edema (14:70 and 101:80), most compatible with meningioma or\nschwannoma.  This mass is unchanged compared with study of ___.\n\nElsewhere, there is no evidence of acute intracranial infarction, hemorrhage,\nadditional mass, mass effect, or edema.  The ventricles and sulci are within\nexpected limits in caliber and configuration.  There is mild mucosal\nthickening of the ethmoid air cells.  Otherwise, the remainder the visualized\nparanasal sinuses and mastoid air cells appear clear.  Major intracranial\nvascular flow voids are preserved.  The globes and orbits are grossly\nunremarkable.  No suspicious marrow lesions.",
            "output": "1. Stable extra-axial 5 mm mass arising from the medial right tentorium most\ncompatible with meningioma or schwannoma.\n2. Otherwise, no acute intracranial abnormality.  No acute infarct or\nintracranial hemorrhage.  No abnormal parenchymal FLAIR signal abnormality. \nNo imaging findings suggestive of mesial temporal sclerosis, gray matter\nheterotopia or focal cortical dysplasia.\n3. Additional findings as described above."
        },
        {
            "input": "Study is mildly degraded by motion.\n\nGrossly stable approximately approximate 5 x 3 mm homogeneously enhancing\nextra-axial mass narrowing the perimesencephalic cistern focally, arising from\nthe medial and to the right tentorium, without definite focal signal\nabnormality within adjacent pons (see 15:9; 16:9; 12:9 on current study and\n11:9 and 14:70 on ___ prior exam).\n\nNo definite new enhancing mass is identified.\n\nThere is no evidence of hemorrhage, edema, midline shift or infarction.   The\nventricles and sulci are stable in caliber and configuration.  Few bifrontal\nsubcortical T2 and FLAIR hyperintensities are noted which may represent small\nvessel ischemic changes.\n\nMucosal thickening of bilateral maxillary sinuses and ethmoid air cells noted.",
            "output": "1. Study is mildly degraded by motion.\n2. Grossly stable approximately 5 x 3 mm right tentorium probable meningioma\nwith minimal mass effect on adjacent pons as described.\n3. No acute intracranial abnormality.\n4.  Paranasal sinus disease, as described."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  The major intracranial flow voids are preserved.  The sphenoid\nsinus is opacified.  There is mild-to-moderate mucosal thickening of the\nremaining paranasal sinuses.",
            "output": "Normal study"
        },
        {
            "input": "There is no evidence of intracranial hemorrhage, edema, masses, mass effect,\nmidline shift or infarction.   The ventricles and sulci are normal in caliber\nand configuration.  There is no abnormal enhancement after contrast\nadministration.  The dural venous sinuses are patent.  The intracranial\narteries appear patent.  Mild mucosal thickening involving the paranasal\nsinuses with a possible mucous retention cyst on the right maxillary sinus.",
            "output": "1.  No intracranial mass, hemorrhage or infarction.  No abnormal enhancement\nafter contrast administration.\n\n2.  Mild mucosal thickening involving the paranasal sinuses."
        },
        {
            "input": "There is partially normalized slow diffusion at the right frontal operculum,\ninsular cortex, anterior to mid temporal cortex, centrum semi ovale, putamen,\nand caudate body with correlate FLAIR hyperintensity corresponding to the\nright middle cerebral artery territory.  There is no evidence of hemorrhage. \nThere is mild mass effect with sulcal effacement.  There is mild prominence of\nthe ventricles and cortical sulci consistent with mild volume loss.  The\nextra-axial spaces are unremarkable.  The vascular flow voids are preserved.\n\nThe orbits, calvarium, and soft tissues are unremarkable.  The paranasal\nsinuses and mastoid air cells are clear.",
            "output": "1. Early subacute infarction in the right middle cerebral artery territory, as\ndescribed, with mild associated mass effect.  No evidence of hemorrhagic\ntransformation.  No midline shift or downward herniation."
        },
        {
            "input": "Study is degraded by motion.  Within these confines:\n\n There is a 4 mm parasagittal enhancing lesion in the posterior aspect of the\nleft frontal lobe (9:127), with mild surrounding edema.\n\nQuestion additional left anterior parasagittal approximately 2 mm enhancing\nnodule versus volume averaging of vessels (see 9: 85-88; 901:39-40).\n\nMultiple calvarial areas of slow diffusion, with associated minimal\nenhancement are noted (see 500, 502: 22, 25, 28; 9:108, 124, 127, 138).\n\nThere is no evidence of hemorrhage, mass effect, midline shift or infarction. \nPeriventricular and subcortical T2 and FLAIR hyperintensities are noted which\nmay represent small vessel ischemic changes.  There is prominence of the\nventricles and sulci suggestive of involutional changes.  There is a trace of\nfluid in the right mastoid air cells.  Minimal bilateral maxillary sinus\nmucosal thickening is present.  Limited imaging of the parotid glands\ndemonstrate bilateral subcentimeter nonspecific probable lymph nodes.",
            "output": "1.  Study is degraded by motion.\n2. Approximately 4 mm left posterior frontal parasagittal intracranial\nenhancing lesion, with surrounding edema.\n3. Question additional left anterior parasagittal approximately 2 mm enhancing\nnodule versus volume averaging of vessels.\n4. No definite evidence of acute infarct.\n5. Numerous calvarial marrow signal abnormalities with faint enhancement\nconcerning for additional metastatic lesions.\n\nNOTIFICATION:  The impression and recommendation above was entered by Dr.\n___ on ___ at 18:09 into the Department of Radiology critical\ncommunications system for direct communication to the referring provider."
        },
        {
            "input": "MRI BRAIN:\nThere is a mass in the fourth ventricle measuring approximately 22 x 29 x 23\nmm.  This enhances in homogeneously, greater around the periphery than\ncentrally, after contrast administration.  The mass is hyperintense to brain\non the T2 weighted and FLAIR images.  There is no evidence of hemorrhage. \nDiffusion is moderately fast. The ventricles are mildly enlarged as is the\naqueduct but there is no evidence of hydrocephalus.  No other masses are\nidentified and there is no evidence of spread of this lesion beyond the fourth\nventricle.\n\nIt is not clear whether the lesion arises from the choroid plexus or from the\nfloor of the fourth ventricle.  Therefore, the differential diagnosis includes\nchoroid plexus papilloma or  meningioma as well as an ependymoma arising from\nthe pons.  A metastasis to the fourth ventricle, likely to the choroid, is\nanother diagnostic consideration.  There is no edema in the adjacent pons,\nthus if this arose from the floor of the fourth ventricle, it would appear\nmore likely to be a lower grade neoplasm than a metastasis.  The inhomogeneous\nenhancement and lack of a cyst argue against a hemangioblastoma.\n\nThere is no evidence of hemorrhage, edema or midline shift.  There is right\nfrontal tissue loss suggesting old infarction or contusion.  The ventricles\nand sulci are mildly prominent in an atrophic pattern with no evidence of\nhydrocephalus.  There is no other abnormal enhancement after contrast\nadministration.  FLAIR images demonstrate scattered white matter\nhyperintensities.  These are nonspecific but are often attributed to mild\nchronic small vessel ischemia.\n\nMRA BRAIN:\nThe intracranial vertebral and internal carotid arteries and their major\nbranches appear normal without evidence of stenosis, occlusion, or aneurysm\nformation.\n\nMRA NECK:\nThe common, internal and external carotid arteries appear normal.  There is no\nevidence of internal carotid artery stenosis by NASCET criteria.  The origins\nof the great vessels, subclavian and vertebral arteries appear normal\nbilaterally.\n\nIncidentally noted is a 7 mm right thyroid nodule.  Absent risk factors for\nthyroid cancer, the ___ College of Radiology guidelines do not recommend\nfurther evaluation for incidental thyroid nodules of this size.",
            "output": "1. Irregularly enhancing fourth ventricular mass with dilated aqueduct but\nwithout hydrocephalus.  The differential diagnosis includes choroid plexus\npapilloma, meningioma, ependymoma and metastasis.\n2. Normal MRA of the head and neck\n3. Incidental thyroid nodule\n\nNOTIFICATION:  The findings of a fourth ventricular mass or communicated to\nDr. ___ at 23:20 ___ by telephone by Dr. ___ 5 minutes after\nmaking the observations."
        },
        {
            "input": "The patient's previously noted heterogeneously rim enhancing fourth\nventricular mass measuring roughly 24 x 18 x 29 mm, extending inferiorly at\nthe level of the obex is again seen and is unchanged in size (03:36).  There\nis associated dilation of the cerebral aqueduct, though without frank\nhydrocephalus.  The ventricles and sulci are otherwise overall unchanged in\nsize and configuration.  There is a small area of right frontal\nencephalomalacia denoting chronic infarct.  Areas of periventricular,\nsubcortical and deep white matter T1 hypointensity correspond to FLAIR\nhyperintensities as seen on prior examination and are consistent with changes\nfrom chronic small vessel ischemic disease.  There is no new enhancing mass.",
            "output": "1. Unchanged irregularly enhancing 24 x 18 x 29 mm fourth ventricular mass\nwith dilated cerebral aqueduct without frank hydrocephalus.\n2. No new enhancing lesion."
        },
        {
            "input": "Patient is status post suboccipital craniectomy with resection of a previously\nseen intraventricular mass within the fourth ventricle, with expected\npostsurgical changes including extra-axial fluid and blood products along the\nresection cavity, postoperative dural thickening and enhancement, scattered\nintra-axial and extra-axial pneumocephalus, with soft tissue edema along the\nbifrontal and left parietal convexities. There is a small focus of slow\ndiffusion adjacent to the resection cavity, likely representing postoperative\nischemia and hemorrhage product.  There is no evidence of acute territorial\ninfarction.\n\nThere is heterogeneous T2/FLAIR signal intensity within the fourth ventricle\nwith associated susceptibility artifact related to postsurgical change.  In\ncomparison with the preoperative imaging, there is a nodular enhancement along\nthe right posterolateral aspect of the fourth ventricle (100 a: 37). \nOtherwise, there is minimal postoperative enhancement without suggestion of\nresidual mass. There is minimal intraventricular hemorrhage layering within\nthe occipital horns of bilateral lateral ventricles. There is no significant\ninterval change in size of the ventricles dating back to ___.\n\nThere is nonspecific mild hyperintense sulcal FLAIR signal intensity within\nthe right frontal lobe (11:18) without corresponding findings on gradient echo\nimages, which is likely artifactual from vascular enhancement.  There is\nnonspecific hyperintense T2 and FLAIR signal intensity within the\nperiventricular and subcortical white matter, which may be a sequela of\nchronic small vessel microangiopathy.\n\nThere is mild mucosal opacification of bilateral maxillary and ethmoid\nsinuses.  The major dural venous sinuses are patent on post-contrast MPRAGE\nimages.  The major intracranial vascular flow voids are preserved.  Chronic\nappearing left lamina papyracea fracture with herniation of orbital fat is\nidentified.  Otherwise, the remainder of the orbits are unremarkable.  There\nis a 1 cm T2 hyperintense nonenhancing cystic lesion in the right parotid tail\n(series 12, image 4), unchanged from prior examination dating back to ___.",
            "output": "1. Status post suboccipital craniectomy with resection of a previously seen\nintraventricular mass with expected postoperative changes, as described above.\n2. Small nodular focus of enhancement along the right posterolateral aspect of\nthe fourth ventricle.  Finding is nonspecific, most likely postoperative\nsequela; however, possibility of residual tumor is not entirely excluded. \nAttention on follow-up is recommended.\n3. Stable small amount of intraventricular hemorrhage within the bilateral\nlateral ventricles, without evidence of hydrocephalus or midline shift.\n4. 1 cm nonenhancing cystic lesion in the right parotid tail, potentially\nrepresenting a lymphoepithelial cyst versus sialocele.  This could be further\nevaluated with ultrasound."
        },
        {
            "input": "The patient is status post suboccipital craniotomy for resection of a fourth\nventricular mass.  Previously seen immediate postoperative changes have\nresolved.\n\nInterval development of symmetric FLAIR hyperintense signal in the medullary\nolives and small residual hyperintense signal along the dorsal medulla and the\nfourth ventricle bilaterally are likely due to postsurgical changes.  Foci of\nsusceptibility artifact with blooming in the occipital soft tissues and along\nthe resection cavity and areas of cirrhosis along the fourth ventricle are\nconsistent with chronic hemorrhagic products and postsurgical change.  A 6 mm\nnodular focus of enhancement along the resection cavity at the level of the\nright middle cerebellar peduncle is slightly smaller compared to the prior\nexamination (series 19, image 29).  Additional thin linear foci of enhancement\nin this region are likely vascular.  A 3 x 4 mm nodular focus of enhancement\nalong the left lower cranial nerves was likely present prior examination\n(series 19, image 24) and may be venous.\n\nA small area of right frontal encephalomalacia and gliosis with superimposed\nhemorrhagic products adjacent to a burr hole likely related to a prior\nprocedure or possible shunt is unchanged.  Additional periventricular and\nscattered punctate subcortical and deep white matter foci of FLAIR\nhyperintense signal are grossly unchanged and although nonspecific likely\nrepresent sequelae of chronic small vessel ischemic disease.\n\nThe ventricles are stable.  There is no mass effect or shift of normally\nmidline structures.  Principal intracranial vascular flow voids are preserved.\nThe dural venous sinuses are patent on postcontrast MP-RAGE sequences.  There\nare a few opacified mastoid air cells bilaterally.  A defect along the left\nlamina papyracea with herniation of the orbital fat into the left ethmoids is\nunchanged.  The orbits are otherwise unremarkable.\n\nUnchanged appearance of a 1 cm nonenhancing cystic lesion in the right parotid\ntail, potentially representing a lymphoepithelial cyst versus sialocele.",
            "output": "1. Postsurgical changes of suboccipital craniotomy for resection of fourth\nventricular mass as described above.\n2. Interval development of symmetric nonenhancing FLAIR hyperintense signal in\nthe medullary olives is compatible with hypertrophic olivary degeneration,\npresumably postsurgical sequela.\n3. Previously noted nodular focus of enhancement along the resection cavity at\nthe level of the right middle cerebellar peduncle measuring 6 mm, is slightly\nsmaller compared to prior examination and likely represents postsurgical\nchange although continued follow-up is recommended.\n4. A 3 x 4 mm nodule focus of enhancement along the left lower cranial nerves\nwas likely represent on the prior study, but given the presence of more\nextensive postsurgical changes of that study exact comparison is difficult. \nThis probably represents postsurgical change or venous in nature, although\ncontinued follow-up is recommended.\n5. Additional chronic findings as described, including a 1 cm right parotid\ntail cystic lesion, which may represent a lymphoepithelial cyst or sialocele. \nThis could be further evaluated with ultrasound as indicated."
        },
        {
            "input": "There are blood products within the surgical resection bed within the inferior\ncerebellar vermis and suboccipital craniotomy changes.  No acute intracranial\nhemorrhage is identified.\n\nSulcal cisternal hyperintense signal on T2/FLAIR is likely related to\nincreased oxygen tension related to endotracheal intubation.\n\nThere is interval expansion of the hyperintense signal on T2/FLAIR within the\nbrainstem, with more conspicuous infiltration of the bilateral cortical spinal\ntracts, that now approach the internal capsule on the left.  The degree of\nnodular enhancement within the surgical resection bed and medulla are much\nmore conspicuous from the ___ exam, worrisome for interval tumor\nprogression.\n\nNew nonenhancing third ventricular soft tissue density measuring up to 1.2\n(AP) x 0.5 (TV) x 0.5 (SI) cm is noted (see 900:86; 9:123; 07:15), not\ndefinitely seen on ___ prior exam (see 19:55; 17:90 on prior MRI).\n\nThere is no acute infarct.  There is mild global parenchymal volume loss. \nSmall areas of hyperintense signal on T2/FLAIR within the subcortical and\nperiventricular white matter nonspecific, but may reflect the sequela of\nchronic small vessel disease.  An old right frontal ventriculostomy catheter\ntract is noted.\n\nThere is diffuse paranasal sinus mucosal thickening.  The gaze is\ndysconjugate.  There is a concave defect within the left medial orbital wall,\nlikely related to an old fracture.  Incidental note is made of a 6 mm\ndermoid/epidermoid cyst external to the right frontal zygomatic suture (series\n5, image 9).\n\nThe soft palate is prominent, grossly unchanged.",
            "output": "1. Interval expansion of the medulla and pons and nodular enhancement within\nthe inferior cerebellar vermian surgical resection bed and pons from a ___ exam is worrisome for tumor progression.\n2. Question new third ventricular nonenhancing mass versus volume averaging\nartifact as described with grossly stable ventricular size.  Recommend\nattention on follow-up imaging.\n3. There is no acute infarct or acute intracranial hemorrhage.\n4. Paranasal sinus disease , as described.\n\nRECOMMENDATION(S):  Question new third ventricular nonenhancing mass versus\nvolume averaging artifact as described with grossly stable ventricular size. \nRecommend attention on follow-up imaging."
        },
        {
            "input": "The patient is status post resection of the suboccipital bone.  There is no\nacute infarct or intracerebral hemorrhage. Principal intracranial vascular\nflow voids are preserved. No extra-axial blood or fluid collection is present.\nThe ventricles and sulci are normal in size and configuration. There is no\ndiffusion abnormality.  No intracranial mass or pathologic parenchymal\nleptomeningeal, or dural focus of enhancement after contrast administration is\nseen.\n\nThere is mucosal thickening of the bilateral sphenoid sinuses and ethmoid air\ncells. Edema of the right nasal cavity may represent daily cycling of the\nturbinates. Possible posterior nasal polyps are also noted.",
            "output": "1.  Status post suboccipital craniotomy ; otherwise normal MR brain without\nevidence of CSF obstruction or leak.\n\n2.  Possible posterior nasal polyps. Correlate with direct visualization."
        },
        {
            "input": "There is no intra or extra-axial mass, acute infarct or intracranial\nhemorrhage.  The intrinsic T1 hyperintense signal of the bilateral globus\npallidi is compatible with hepatic encephalopathy.  There is nonspecific T2\nhyperintense signal of the caudate, left greater than right anterior putamen\nand left anterior medial temporal lobe without evidence of restricted\ndiffusion, which may be secondary to artifact versus encephalopathy.  No\nabnormal enhancement is identified.  There is prominent right superior frontal\ngyrus, centrum semiovale and coronal radiata white matter hyperintensities as\nwell as a subtle FLAIR hyperintense signal of the left frontal centrum\nsemiovale, which are nonspecific, without associated restricted diffusion to\nsuggest acute process.  These could represent sequela of prior embolic events\nversus inflammatory/demyelinating process.\n\nThe major intracranial flow voids are preserved.  The dural venous sinuses are\npatent.  Mild mucosal thickening of the ethmoid air cells and moderate mucosal\nthickening of the left maxillary sinus is identified.  The orbits are\nunremarkable.  The mastoid air cells are essentially clear.\n\nThere is subtly increased diffusion-weighted hyperintense signal of the\ncalvaria with associated ADC hyperintense signal and T1 hypointense signal on\nsagittal T1 sequences.  The marrow signal of the cervical spine is\nunremarkable.  This is of uncertain clinical significance and may represent\nmarrow reconversion given the history of hepatitis.",
            "output": "1. No evidence of acute infarct acute intracranial hemorrhage or enhancing\nlesion.\n2. Right superior frontal gyrus, centrum semiovale and corona radiata FLAIR\nwhite matter hyperintensities with associated subtle left frontal centrum\nsemiovale lesion, which are nonspecific and without diffusion-weighted\nhyperintense signal to suggest acute process.  These may represent sequela\nprior embolic disease, versus inflammatory/ demyelinating process.\n3. T1 intrinsic hyperintense signal the bilateral globus pallidi compatible\nwith hepatic encephalopathy.  There is also mildly increased FLAIR\nhyperintense signal of the anterior left putamen, bilateral caudate and\npossibly the left anterior medial temporal lobe, which may be artifactual in\nnature versus possible sequela of encephalopathy.\n4. Subtle increased diffusion-weighted hyperintense signal of the calvarial\nmarrow, with associated ADC hyperintense signal and T1 hypointensity on\nsagittal T1 sequences.  This is also nonspecific, but may represent sequela of\nmarrow reconversion given the patient's history of chronic hepatitis. \nAttention on followup examinations is recommended.\n\nNOTIFICATION:  The findings were discussed by Dr. ___ with Dr.\n___ on the telephoneon ___ at 9:19 AM, 5 minutes after discovery\nof the findings."
        },
        {
            "input": "Examination is moderately degraded by patient motion, within this limitation:\n\nThere is redemonstration of a 3.3 x 2.2 cm axially x 2.4 cm SI\nintraparenchymal hematoma in the left occipital lobe, with heterogeneous\nhypointense signal on gradient recalled echo images and intrinsic T1\nhyperintense signal and predominantly T2 hypointense signal.  Evaluation for\nenhancement is limited due to intrinsic T1 hyperintense signal.  There is\nmoderate surrounding edema with slight mass-effect on the occipital horn and\ntrigone of the left lateral ventricle.  There is effacement of the overlying\nsulci.\n\nElsewhere in the brain, there is no evidence of true slow diffusion to suggest\nacute infarction.  Otherwise, the ventricles are age-appropriate in size and\nconfiguration.  There is no appreciable midline shift.  The basal cisterns are\npatent.\n\nThere is minimal mucosal thickening of the ethmoid sinuses.  The intraorbital\ncontents are grossly unremarkable.",
            "output": "Left occipital lobe intraparenchymal hematoma measuring up to 3.3 cm. \nModerate surrounding edema with mass-effect on the occipital horn and trigone\nof the left lateral ventricle and effacement of the overlying sulci. \nEvaluation for an underlying mass is limited by presence of hemorrhage.  Short\ninterval follow-up with contrast after resolution of the hematoma is\nrecommended.\n\nRECOMMENDATION(S):  Evaluation for an underlying mass is limited by presence\nof left occipital lobe intraparenchymal hemorrhage.  Short interval follow-up\nwith contrast after resolution of the hematoma is recommended."
        },
        {
            "input": "Foci of slow diffusion with associated FLAIR signal abnormality are seen\nwithin the bilateral frontoparietal lobes, left frontal lobe, bilateral\noccipital lobes, right cerebellum, measuring up to 2.2 cm in the left frontal\nlobe, series 4, image 19.  There is no evidence of acute intracranial\nhemorrhage.\n\nAdditional periventricular and subcortical FLAIR white matter hyperintensities\nare likely sequelae of chronic microangiopathy.  Mild prominence of ventricles\nand sulci is likely related to age related involutional changes.\n\nMild mucositis thickening seen involving the ethmoid air cells.  The remainder\nthe visualized paranasal sinuses are clear.  Fluid opacification is seen\ninvolving the mastoid air cells bilaterally.",
            "output": "Foci of acute to subacute infarcts are seen within the bilateral\nfrontoparietal lobes, left frontal lobe, bilateral occipital lobes, and right\ncerebellum spanning up to 2.2 cm and left frontal lobe.  Predominantly, the\nfoci are in a watershed distribution although a few of the foci may be embolic\nin etiology.\n\nNo evidence of acute intracranial hemorrhage.\n\nRECOMMENDATION(S):  Neurology consult is recommended for further evaluation.\n\nNOTIFICATION:  The findings were discussed with ___, M.D. by ___\n___, M.D. on the telephone on ___ at 4:09 pm, 10 minutes after\ndiscovery of the findings."
        },
        {
            "input": "MRI BRAIN:\nPreviously noted hyperdense right suprasellar mass corresponds to a 1.7 x 1.6\ncm thrombosed aneurysm which appears to arise from a hypoplastic right A1\nsegment of the anterior cerebral artery.  There is a small amount of linear\nrow flow at the neck of the aneurysm, with peripheral enhancement,\nrepresenting either a thin rim of lumen, or enhancement of the aneurysm wall. \nThe thrombosed aneurysm extends minimally into the sella, and exerts mild mass\neffect upon the pituitary stalk, displacing it to the left.  Additionally,\nthere is mass effect, and displacement of the right optic nerve and right\naspect of the optic chiasm.\n\nThere are scattered areas of right medial frontal slowed diffusion with\nassociated FLAIR hyperintensity, in the right anterior cerebral artery\nterritory.  The larger portion of these areas correspond to hypodensity on\nprior CT examination.\n\nThere is an additional small right inferior frontal extra-axial enhancing mass\nwith broad-based dural attachment measuring 8 x 6 mm, compatible with\nmeningioma (1101:69).\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  There is prominence of the ventricles and sulci suggesting\ninvolutional changes.  There are background scattered areas of\nperiventricular, subcortical and deep white matter T2/FLAIR hyperintensity in\na configuration most suggestive of chronic small vessel ischemic change.  The\nprincipal intracranial vascular flow voids are preserved.  The dural venous\nsinuses are patent on MP rage images.\n\nThe paranasal sinuses are grossly clear.  The orbits are grossly unremarkable.\n\nMRA brain:  There are infundibular origins of the bilateral posterior cerebral\narteries and superior cerebellar arteries with a patulous basilar tip.  There\nis irregularity of a hypoplastic right A1 segment of the anterior cerebral\nartery, adjacent to the large thrombosed aneurysm, with minimal linear flow\nseen within the neck/ base of the aneurysm.  The intracranial vertebral and\ninternal carotid arteries and their major branches appear patent without\nevidence of stenosis, occlusion, or other aneurysm formation.",
            "output": "1. Previously noted hyperdense right suprasellar mass corresponds to a 1.7 x\n1.6 cm thrombosed aneurysm with minimal flow at the neck/base, with either a\nthin rim of flow or vascular wall enhancement.  This exerts mass effect upon\nthe pituitary stalk as well as the right optic nerve and right aspect of the\noptic chiasm, displacing the structures to the left.  Aneurysm appears to\noriginate from a hypoplastic A1 segment of the right anterior cerebral artery,\nwhich appears mildly irregular.\n2. Scattered areas of medial right frontal acute to subacute infarct, in the\nanterior cerebral artery distribution, with appearance compatible with embolic\netiology.\n3. 8 x 6 mm right inferior frontal meningioma.\n4. Otherwise patent intracranial vasculature, without significant stenosis,\nocclusion, or other aneurysm formation.\n\nRECOMMENDATION(S):  Recommend neurosurgical consultation, for possible further\nevaluation with cerebral angiogram.\n\nNOTIFICATION:  The findings were discussed with ___, M.D. by\n___, M.D. on the telephone on ___ at 8:23 AM, 2 minutes after\ndiscovery of the findings."
        },
        {
            "input": "There is no evidence of acute intracranial hemorrhage or mass effect.\n\nThere is slow diffusion with T2/FLAIR signal abnormality within the right\ntemporal lobe compatible with a subacute infarct. There is focal volume loss\nwithin the left occipital and right parietal lobes compatible with chronic\ninfarcts. There is moderate brain parenchymal volume loss. There are normal\nvascular flow voids.\n\nThe orbits, skull base, and paranasal sinuses appear unremarkable.",
            "output": "1. Small, peripheral subacute infarct within the right temporal lobe.\n2. Chronic infarcts of left occipital right parietal lobe."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, or infarction.\nThere is mild widening of the posterior portions of both lateral ventricles\nhyperintensities in the adjacent white matter. The findings are indicative of\nchronic changes of periventricular leukomalacia.\n\nCoronal high-resolution images demonstrate normal appearance of the medial\ntemporal lobe structures. There is no evidence of atrophy or increased signal\nwithin the hippocampal regions.  There is no evidence of migration abnormality\nidentified.\n\nIncidentally noted is a lipoma along the right superior cerebellar hemisphere.",
            "output": "Findings indicating chronic changes of periventricular leukomalacia. No other\nsignificant abnormalities are seen."
        },
        {
            "input": "MRI BRAIN:\nThere is an area of DWI hyperintensity involving the posterior left insular\nregion and the left temporoparietal region.  There are corresponding ADC and\nFLAIR correlates, consistent with a subacute infarct.  There is hemorrhagic\ntransformation.\n\nThere is no abnormal enhancement after contrast administration.\nThere is mild generalized parenchymal volume loss, most likely age related. \nMild prominence of the ventricular system and extra-axial CSF spaces is\nconsistent with the previously mentioned parenchymal volume loss.  There is a\nsmall amount of fluid in the left maxillary and sphenoid sinuses.  The\nremainder of the paranasal sinuses and mastoid air cells appears clear.\n\nOval-shaped structures in the bilateral orbits are again identified with the\nlargest lesion in the right orbit demonstrating mass effect on the right\nmedial rectus muscle.  There appears to be a fluid fluid level which would\nsupport the diagnosis of an intraorbital venolymphatic malformation.\n\nMRA BRAIN:\nThere are mild vessel wall irregularities along both carotid siphons,\nconsistent with the previously noted atherosclerotic changes on the CT, but no\nsignificant stenosis.\n\nThe intracranial internal carotid arteries and their major branches appear\nnormal without evidence of stenosis,occlusion,or aneurysm formation.\n\nThe left V3 and V4 segments are not clearly visualized on the MRA of the head.\nThis is probably due to slow flow, given its opacification of the MRA of the\nneck.\n\nThe right intradural vertebral artery appears unremarkable.  Vertebrobasilar\njunction is normal.  The posterior circulation is otherwise unremarkable.\n\nMRA NECK:\nNormal 3 vessel aortic arch.  There is mild-to-moderate stenosis at the origin\nof the right innominate artery.  Evaluation of the cervical vasculature is\nsignificantly degraded by motion artifact.  Allowing for this limitation,\nthere appears to be severe stenosis at the origin of left vertebral artery. \nThe origins of the great vessels, subclavian and right vertebral arteries\nappear grossly patent.\n\nThe common, internal and external carotid arteries appear grossly\nunremarkable.  Evaluation for internal carotid artery stenosis is limited due\nto motion artifact but there is no high-grade stenosis.",
            "output": "1. Subacute infarction involving the posterior insula and left temporoparietal\nregion with evidence of hemorrhagic transformation.\n2. Limited evaluation of the cervical vasculature due to motion artifact. \nAllowing for this limitation, there is mild-to-moderate stenosis at the origin\nof the right innominate artery and likely severe stenosis at the origin of the\nleft vertebral artery.\n3. Nonvisualization of part of the intracranial course of the left vertebral\nartery is likely due to slow flow.\n4. Otherwise patent intracranial and cervical vasculature.  No intracranial\naneurysm formation.\n5. Redemonstration of oval shaped structures in the bilateral orbits, with the\nlargest in the right orbit demonstrating mass effect on the right medial\nrectus muscle.  Presence of a fluid fluid level would support the diagnosis of\nintraorbital ___ lymphatic malformation.  Ophthalmology consultation and/or a\ndedicated MRI of the orbits with and without contrast is recommended if the\npatient is able to remain still for the exam.\n\nRECOMMENDATION(S):  Further evaluation of the bilateral infraorbital lesions\nwith a an ophthalmology consultation and/or a dedicated MRI of the orbits with\nand without contrast is recommended if the patient is able to remain still for\nthe exam."
        },
        {
            "input": "Study is limited due to patient motion, within this limitation, again\nhyperintense DWI signal involving the posterior left insular and left\ntemporoparietal regions appears similar to prior.  Corresponding FLAIR\nhyperintense and ADC hypointense signal, consistent with a subacute infarct,\nappears similar as well, although there is new associated T1 hyperintense\nsignal consistent with evolution.  Susceptibility artifact related to\nhemorrhagic transformation is stable.\n\nAlthough comparison is limited due to motion artifacts, and lack of\nintravenous contrast, ovoid T2 hyperintense structures in the bilateral orbits\nappear grossly similar with the largest lesion in the right orbit, exhibiting\nmass effect on the right medial rectus muscle.\n\nThere is no evidence of new infarct, hemorrhage, mass effect, or midline\nshift.  Mild generalized parenchymal volume loss, appears similar to prior,\nlikely age-related.  There is no abnormal enhancement after contrast\nadministration.",
            "output": "1. Stable, evolving subacute infarction involving the left posterior insula\nand left temporoparietal regions with similarly stable associated hemorrhagic\ntransformation.  No new acute infarct or hemorrhage.\n2. Although comparison is limited due to motion artifacts, and lack of\nintravenous contrast, persistently enlarged ovoid structures within the\nbilateral orbits appear grossly similar, and better depicted in the prior\nMRI/MRA of the head, if clinically warranted, correlation with dedicated MRI\nof the orbits is recommended.\n\nRECOMMENDATION(S):  Although comparison is limited due to motion artifacts,\nand lack of intravenous contrast, persistently enlarged ovoid structures\nwithin the bilateral orbits appear grossly similar, and better depicted in the\nprior MRI/MRA of the head, if clinically warranted, correlation with dedicated\nMRI of the orbits is recommended."
        },
        {
            "input": "There is a region of left posterior parietal slowed diffusion appearing dark\non ADC with associated FLAIR hyperintensity with some subtle areas of\nenhancement suggesting subacute infarct (12:  16, 17).  There is no evidence\nof hemorrhagic transformation.\n\nThere is no evidence of hemorrhage, masses, mass effect, or midline shift. \nThere is prominence of the ventricles and sulci suggestive involutional\nchanges.  Numerous areas of periventricular, subcortical and deep white matter\nT2/FLAIR hyperintensity are in a configuration most suggestive of chronic\nsmall vessel ischemic disease.  .  There is no abnormal enhancement after\ncontrast administration.  The principal intracranial vascular flow voids are\npreserved.\n\nThe paranasal sinuses and mastoid air cells are clear.  The orbits are grossly\nunremarkable.",
            "output": "1. Subacute left posterior parietal infarct in the MCA territory.\n2. No hemorrhage or enhancing mass.\n3. Mild global atrophy and areas of white matter signal abnormality in a\nconfiguration most suggestive of chronic small vessel ischemic disease.\n\nRECOMMENDATION(S):  The findings were discussed with ___, M.D. by\n___, M.D. on the telephone on ___ at 3:30 ___, 5 minutes after\ndiscovery of the findings."
        },
        {
            "input": "The right common, internal and external carotid arteries appear normal.  There\nis approximately ___ stenosis of the right cervical internal carotid artery\nby NASCET criteria.  There is stenosis of the left internal carotid artery,\napproximately 66 - 68% by NASCET criteria ___ 501c:83; 2c:52).  The\norigins of the great vessels, subclavian, and vertebral arteries appear normal\nbilaterally.\n\nThe left vertebral artery is dominant, however both vertebral arteries are\npatent, with possible tight cut termination of the right vertebral artery.",
            "output": "1.  66 - 68% narrowing of the left internal carotid artery by NASCET criteria.\n\n2.  Approximately ___ stenosis of the right cervical internal carotid\nartery by NASCET criteria."
        },
        {
            "input": "There is no acute infarct, mass effect, hydrocephalus or midline shift.  Mild\nperiventricular and brainstem changes of small vessel disease are seen.  There\nare no micro hemorrhages.  Suprasellar and craniocervical regions are\nunremarkable.  The vascular flow voids are maintained.",
            "output": "No acute abnormalities are seen on MRI of the brain without gadolinium."
        },
        {
            "input": "There is a nonspecific focus of T2/FLAIR hyperintensity within the subcortical\nwhite matter of the left frontal lobe (series 4, image 16).  There is no\nassociated enhancement or slow diffusion.  No additional white matter signal\nabnormalities are identified.  There is no evidence of hemorrhage, edema,\nmasses, mass effect, midline shift or infarction.   The ventricles and sulci\nare normal in caliber and configuration.  There is no abnormal enhancement\nafter contrast administration.",
            "output": "Solitary focus of T2/FLAIR hyperintensity within the subcortical white matter\nof the left frontal lobe (series 4, image 16), without associated abnormal\nenhancement or slow diffusion.  No additional white matter signal\nabnormalities are identified.  Whilst the lesion is nonspecific in nature, a\nsolitary demyelinating lesion could be considered."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.  The paranasal sinuses are clear.  The orbits appear normal. \nThe intracranial arteries demonstrate normal T2 flow voids.  No CP angle\nmasses.  The dural venous sinuses are patent.  The craniocervical junction\nappears normal.  Partially empty sella.",
            "output": "1. Essentially normal brain MRI."
        },
        {
            "input": "MRI BRAIN:\nThere is no evidence of acute infarction or intracranial hemorrhage.  The\nventricles and sulci are normal in size and configuration with no mass effect\nor midline shift.  There is no evidence of abnormal enhancement.\n\nMild mucosal thickening of the ethmoid sinuses.  The mastoid air cells are\nclear.  Intraorbital contents are unremarkable.  MPRAGE images demonstrate\npatent dural venous sinuses with no evidence of filling defects.\n\nMRA BRAIN:\nThe intracranial vertebral and internal carotid arteries and their major\nbranches appear normal without evidence of stenosis, occlusion, or aneurysm\nformation.\n\nMRA NECK:\nThere is a long-segment of T1 hyperintense signal abnormality surrounding the\nV2 segments of the right vertebral artery with associated areas of luminal\nnarrowing consistent with mural hematoma and compatible with dissection\n(images ___ of series 21).\n\nAdditionally, there is a short-segment of T1 hyperintense signal abnormality\nsurrounding the V2 segment of the left vertebral artery also concerning for\nmural hematoma and dissection (images ___ of series 21).\n\nEvaluation of the aortic arch demonstrates an aberrant origin of the right\nsubclavian artery, a normal anatomic variant.  The origins of the great\nvessels, subclavian and vertebral arteries appear normal bilaterally. There is\nnormal flow related enhancement within the common, internal and external\ncarotid arteries.  There is no evidence of internal carotid artery stenosis by\nNASCET criteria.",
            "output": "1. Intramural hematoma with luminal narrowing involving the right vertebral\nartery V2 segment concerning for dissection.\n2. Short-segment intramural hematoma with luminal narrowing involving the left\nvertebral artery V2 segment is also concerning for dissection.\n3. Unremarkable MRI of the brain.  No evidence of acute infarction or\nintracranial hemorrhage.\n4. No evidence of abnormal enhancement."
        },
        {
            "input": "There is no evidence of early filling of the ophthalmic veins or cavernous\nsinus to suggest a carotid cavernous fistula.  The intracranial vasculature\nappears patent without evidence of stenosis, occlusion, or aneurysm",
            "output": "1. Unremarkable MRA without evidence of carotid cavernous fistula."
        },
        {
            "input": "A 2.7 x 2.9 cm (AP, TRV) left orbital frontal extra-axial lesion with\nassociated hyperostosis of the left orbital plate and fovea ethmoidalis\nappears to be minimally increased in size by a few mm from examination of\n___.\n\nA left frontal vertex 1 x 0.9 cm (AP, TRV) extra-axial lesion demonstrating\nunderlying calvarial hyperostosis is also minimally increased in size from\nprior examination.\n\nThe above lesions both demonstrate associated gradient echo susceptibility\nartifact, felt likely to represent calcification.\n\nCorresponding to the new lesion described on PET-CT of ___, is a\nheterogeneously enhancing 0.6 x 1.1 cm (AP, TRV); series 900, image 125)\nlesion which is closely associated with the right postcentral gyrus. \nAssociated gradient echo susceptibility artifact may represent calcification\nversus microhemorrhage.  It is difficult to determine whether this lesion is\ncortically based versus extra-axial, but felt likely to be cortically based. \nIn addition, associated CSF space of the associated sulcus has increased in\nsize when compared to prior examination, potentially representing a cystic\ncomponent to the lesion versus interval enlargement of a arachnoid cyst. \nThere is mild associated FLAIR parenchymal signal abnormality of the\nparacentral lobule (series 7, image 19).\n\nThere is no acute infarct.  There are superimposed periventricular and\nsubcortical T2/FLAIR white matter hyperintensities, which are nonspecific, but\ncompatible with chronic microangiopathy in a patient of this age.  The sulci,\nventricles and cisterns are within expected limits for the patient's age.  The\nmajor intracranial flow voids are preserved.  The dural venous sinuses are\npatent.  There is mild mucosal thickening of the ethmoid air cells.  The\norbits are unremarkable.  No significant fluid signal is noted in the mastoid\nair cells.",
            "output": "1. Corresponding to PET-CT finding of ___, interval development of a\nright paracentral lobule likely cortically based 1 cm heterogeneously\nenhancing lesion, with mild adjacent parenchymal FLAIR edema pattern, not seen\non examination of ___.  Given the patient's history of pulmonary carcinoid,\nthis is highly suspicious for metastatic disease.  The lesion demonstrates\ngradient echo susceptibility artifact, likely representing hemorrhage and/or\ncalcification.\n2. There is interval increase size of CSF space of the adjacent sulcus from\nprior examination of ___, which may represent a cystic component to lesion\nversus superimposed arachnoid cyst.\n3. A left orbital frontal lobe extra-axial lesion with underlying hyperostosis\nof the frontal orbital plate measuring approximately 2.9 cm in greatest\ndimension as well as a left frontal vertex 1 cm extra-axial lesion with\nunderlying calvarial hyperostosis demonstrates millimetric slightly increased\nsize from ___, felt to be most compatible with meningiomas.\n4. Additional findings as described above."
        },
        {
            "input": "Again seen is a right parasagittal enhancing mass that appears to be partially\nin the subarachnoid space at the depth of a sulcus.  However, as on the prior\nstudy, there is a small amount of white matter edema, suggesting that a\ncomponent of this may be intra-axial.  This lesion enhances inhomogeneously\nafter contrast administration and demonstrates marked signal loss on the\ngradient echo images suggesting chronic hemorrhage.  The volume of edema\nappears slightly larger than on the study of ___.  The lesion has\nincreased in size since the prior study in all linear ___.\nThe enlarged subarachnoid space overlying the lesion appears unchanged since\nthe prior study.  Vessels are seen draped around this area again suggesting an\narachnoid cyst.\nAgain seen and unchanged are lesions arising from the floor of the anterior\ncranial fossa on the left, a large mass measuring 31 mm in greatest dimension\nand, slightly more posteriorly, a lesion measuring 7 mm in greatest dimension.\nThese both have a dural bases and are associated with underlying hyperostosis.\nThe most likely diagnosis remains meningiomas.  Also unchanged is a\ndural-based enhancing mass with hyperostosis measuring approximately 6 mm in\ngreatest dimension overlying the left frontal convexity.  This is also\nassociated with hyperostosis and also likely a meningioma.\nThe right cortical and subarachnoid lesion is new since the study of ___. \nThere has been little if any change in the appearance of the presumed\nmeningiomas.\nThe ventricles and sulci are prominent in a mild atrophic pattern.  Unchanged\nsince the study of ___ but progressed since ___ are periventricular\nand subcortical white matter hyperintensities on FLAIR.  Although nonspecific,\nthese are often attributed to chronic small vessel ischemia.  There is a small\nmucous retention cyst in the sphenoid sinus..  No new lesions are identified.",
            "output": "1. Enlargement of right frontal dancing mass that appears to be at least\npartly intra-axial.\n2. Slight increase in the volume of edema associated with this lesion,\nalthough still minimal.\n3. Unchanged appearance of likely arachnoid cyst adjacent to the right frontal\nlesion.\n4. Unchanged appearance of multiple dural-based enhancing masses with\ncalvarial hyperostosis suggesting meningiomas."
        },
        {
            "input": "The previously seen approximately 13 x 10 mm right posterior frontal mass with\nblood products appear to have minimally increased in size and now measuring 16\nx 11 mm.  However, the surrounding edema has not significantly changed.  While\nthe change in size is minimal compared to the immediate prior study, there is\nslight definite increased since the earlier MRI of ___.\n\nPreviously seen meningioma in the left inferior frontal region with\nsurrounding hyperostosis and other small extra-axial enhancement are unchanged\ncompared to the prior study.  No new parenchymal area of abnormal enhancement\nis seen.",
            "output": "1. Minimal increase in size in enhancing hemorrhagic right posterior frontal\nparietal lesion without change in surrounding edema.  Given the minimal change\nin size, this can be further observed on the follow-up examinations.\n2. Unchanged left inferior frontal meningioma and other extra-axial enhancing\nlesions."
        },
        {
            "input": "Examination is moderately degraded by motion.  Within these confines:\n\nThere is a 1.5 x 0.9 cm heterogeneously enhancing lesion along the right\npostcentral gyrus, which is unchanged in size compared to prior exam, but\nincreased in size compared to ___.  Associated gradient echo\nsusceptibility artifact may represent calcification versus microhemorrhage. \nThere is unchanged minimal surrounding edema.  The enlarged subarachnoid space\noverlying the lesion appears unchanged since the prior exam.\n\nThere is an extra-axial left frontal mass which demonstrates heterogeneous\nenhancement along the left orbital plate and left fovea ethmoidalis.  There is\nill-defined hypointensity on gradient recalled echo images.  The mass measures\napproximately 3.7 cm transverse by 1.9 cm craniocaudal by 2.4 cm AP (image 40\nof series 901, image 78 of series 900), unchanged dating back to ___, but mildly increased in size compared to ___.  The mass demonstrates\nslightly irregular margins.\n\nA left frontal vertex 1 x 0.8 cm extra-axial lesion with associated calvarial\nhyperostosis is unchanged compared to ___.  Lesion also\ndemonstrates calcification on gradient echo images.  Allowing for difference\ntechnique, this is grossly unchanged compared to ___ prior exam, although\nevaluation is limited due to lack of thin-section imaging.\n\nPatchy areas of hyperintensity overlying bilateral temporal lobes is noted on\naxial T1 images (see 10:9), with no corresponding abnormality on any other\nsequences including MPRAGE postcontrast imaging, and is likely artifactual.\n\nThere is evidence of acute infarction or intracranial hemorrhage.  The\nventricles and sulci are stable in size and configuration with no mass effect\nor midline shift.  Multiple scattered T2 and FLAIR hyperintense foci in the\nperiventricular and subcortical white matter are nonspecific, but may reflect\nchronic small vessel ischemic changes.\n\nMild mucosal thickening of the left maxillary sinus.  The mastoid air cells\nare clear.  Intraorbital contents are unremarkable.  The major intracranial\narterial flow voids are preserved.  The dural venous sinuses are patent.",
            "output": "1.  Study is moderately degraded by motion.\n2. The right paracentral lobule heterogeneously enhancing lesion with mild\nadjacent parenchymal edema is unchanged compared to prior exam, but slightly\nincreased in size compared to ___, again concerning for metastatic\nlesion.\n3. The left frontal extra-axial mass with heterogeneous enhancement and\nslightly irregular margins is unchanged compared to ___, and mildly\nincreased in size compared to ___, again concerning for atypical meningioma.\n4. Additional left frontal vertex extra-axial lesion is favored to represent a\nmeningioma.\n5. Probable artifacts overlying bilateral temporal lobes on axial T1\npostcontrast imaging as described.\n6. Paranasal sinus disease , as described."
        },
        {
            "input": "Heterogeneously enhancing 3.1 x 2.8 cm left frontal lesion along the left\norbital plate and left fovea ethmoidalis with a broad dural base (series 9,\nimage 8), is unchanged from ___ and is compatible with a meningioma.\n\nA 0.9 x 0.5 cm left frontal vertex lesion with associated calvarial\nhyperostosis is also unchanged from ___.  The lesion again\ndemonstrates calcification on the gradient echo images and is compatible with\na meningioma.\n\nA 1.4 x 1.1 cm enhancing lesion along the right post central gyrus (series 9,\nimage 130), is unchanged in size.  Gradient echo susceptibility, again may\nrepresent calcification versus microhemorrhage.  Surrounding FLAIR signal\nabnormality is moderately increased, without significant mass effect. \nEnlargement of the subarachnoid space overlying the lesion, appears unchanged\nfrom multiple prior examinations.\n\n2 mm punctate enhancing lesion in the right paramedian cerebellum (series 9,\nimage 57) and a 3 mm enhancing lesion in the cerebellar vermis with associated\nFLAIR signal abnormality (series 901, image 109, series 9, image 51) appear\nnew or more conspicuous in comparison the prior examination.  Additional\npunctate cerebellar enhancing lesions, (series 9 image 46, 45, 44, 63), were\nnot definitely seen on the prior examination measuring up to 2 mm.\n\nAdditional periventricular deep white matter FLAIR hyperintensities are\nnonspecific but likely represent sequela of chronic small vessel ischemic\ndisease.  Prominence of the sulci and ventricles, likely represent age related\nchange.\n\nThe orbits are unremarkable.  Two small mucous retention cysts are noted in\nthe left maxillary sinus.  Otherwise, the mastoid air cells and paranasal\nsinuses are clear.",
            "output": "1. 1.4 cm enhancing lesion along the right post central gyrus, is unchanged in\nsize from prior, but demonstrates mild increased surrounding edema.  No mass\neffect or midline shift.  Susceptibility on gradient echo imaging may\nrepresent microhemorrhage or calcification, similar to prior.\n2. Multiple new enhancing bilateral cerebellar punctate lesions measuring up\nto 3 mm are concerning for metastatic disease.\n3. Two left frontal meningiomas measuring up to 3.1 cm are unchanged."
        },
        {
            "input": "Re- identified is an unchanged 26 x 23 mm enhancing extra-axial mass, centered\nalong the left inferior aspect of the tentorial incisura (05:41), with\nsignificant mass effect upon the posterior aspect of the midbrain and pons,\nwith effacement of the adjacent cerebral aqueduct.  There is associated\nmoderate ventriculomegaly with transependymal edema.  No new enhancing mass is\nidentified.",
            "output": "1. Unchanged 26 x 23 mm enhancing extra-axial mass centered along the inferior\naspect of the left tentorial incisura, likely meningioma.\n2. Resultant effacement of the cerebral aqueduct with moderate obstructive\nhydrocephalus and transependymal edema.\n3. Examination was performed with external markers for preoperative planning."
        },
        {
            "input": "The patient is status post suboccipital craniotomy and cranioplasty for\nresection of a tentorial notch meningioma.  Postsurgical changes including\nscalp swelling, hemosiderin deposition, a small extra-axial hematoma and dural\nthickening/enhancement along the craniotomy margin.  The lateral and third\nventricles remain enlarged however hydrocephalus has improved.  A few small\nfoci of DWI hyperintense signal with corresponding low signal on ADC map in\nthe left cerebellum, suggestive of acute infarcts, are consistent with\nposttreatment changes.  There is trace triangular enhancement along the left\nambient cistern (series 13, image 10).  Otherwise, there is no new or residual\nenhancing mass.  Principal intracranial vascular flow voids are preserved and\narteries of the circle of ___ and dural venous sinuses enhance\nappropriately after contrast administration.",
            "output": "1.  Postsurgical changes of suboccipital craniotomy and cranioplasty for\nresection of a tentorial notch meningioma as described above, including a\nsmall extra-axial hematoma along the craniotomy margin.  Mild triangular focus\nof postcontrast enhancement along the left ambient cistern, which may\nrepresent postsurgical sequela.  Close attention on followup is recommended.\n\n2.  A few small foci of acute infarction in the left cerebellum likely reflect\npostsurgical changes.\n\n3.  Improved hydrocephalus."
        },
        {
            "input": "Postsurgical changes are again seen from suboccipital craniectomy and\nresection of a meningioma with a right occipital bone burr hole.  There is no\nevidence for residual or recurrent disease at the resection site.  There is\nminimal asymmetric thickening and enhancement of the left tentorial leaflet\nrelative to the right in the region of the ambient cistern, unchanged\n(901:98).  There has been resolution of previously seen hydrocephalus. \nPreviously seen trace triangular enhancement along the left ambient cistern is\nnot seen on today's study.  No nodular areas of enhancement are identified.\n\nThere are mildly prominent asymmetric vascular structures along the cortical\nsurface of the left parietal lobe (900:116, 105, 117) which are similar\ncompared to the prior MRI from ___ and were not present on the CTA\nof the head and are favored to represent prominent venous structures.\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  The dural venous sinuses are patent on postcontrast MP-RAGE. \nThe major intracranial flow voids are preserved.  There is mild mucosal\nthickening of the ethmoid air cells and left maxillary sinus.  The orbits are\nunremarkable.  Fluid signal is seen in the left mastoid air cells.",
            "output": "Status post suboccipital craniectomy for resection of a tentorial notch\nmeningioma without evidence for recurrent or residual tumor.\n\nMildly prominent asymmetric vascular structures along the cortical surface of\nthe left parietal lobe did not demonstrate arterial enhancement on the CTA of\nthe head from ___ and are similar compared to the prior MRI from\n___ MR, favored to represent mildly prominent cortical veins. \nThis finding can be reassessed on follow-up imaging to exclude small\nmeningioma."
        },
        {
            "input": "Stable postsurgical changes are again seen status post suboccipital\ncraniectomy with meningioma resection, in addition to a right occipital burr\nhole.  There is no evidence for residual or recurrent enhancing mass.\n\nThere is no evidence of acute infarction.  No intracranial hemorrhage.\n\nThe ventricles and sulci are normal, without evidence of hydrocephalus. The\nbasal cisterns are patent.  There is gross preservation of the principal\nintracranial vascular flow voids.\n\n  The dural venous sinuses appear patent on MP-RAGE imagine sequences.\n\nThere is near complete opacification of the left maxillary sinus with mucosal\nthickening and an air-fluid level.  Scattered ethmoid air cells also\ndemonstrate mucosal thickening, bilaterally.  The remainder of the visualized\nparanasal sinuses, middle ear cavities, and mastoid air cells are well aerated\nand clear.  The orbits are within normal limits bilaterally.",
            "output": "1. Stable postoperative changes following suboccipital craniotomy, meningioma\nresection, and right right occipital burr hole.\n2. No evidence for new or residual enhancing mass.  No intracranial hemorrhage\nor infarction.\n3. Paranasal sinus disease, as above, significantly progressed from the prior\nexamination."
        },
        {
            "input": "There has been no significant interval change.  Right occipital burr hole is\nagain noted.  Subtle asymmetry of the tentorial enhancement with slightly more\npronounced enhancement along the left tentorial margin are unchanged.  The\npreviously seen mass in the region of quadrigeminal cistern at the tentorial\nincisura is no longer visible.  No residual or recurrent enhancement is seen. \nThere is no hydrocephalus.  There is no acute infarct.  Mucosal thickening is\nseen and fluid level noted within the left maxillary sinus unchanged from the\nprior study.",
            "output": "Stable appearance compared to the previous MRI study without signs of\nrecurrent mass lesion or enhancement.  Stable left maxillary sinus\ninflammatory changes."
        },
        {
            "input": "There is subtle likely sulcal FLAIR hyperintense signal centered in the right\nsuperior frontal sulcus (series 10, image 18) without evidence of associated\ngradient echo susceptibility artifact.  In addition, there is cortical\ngyriform FLAIR hyperintensity of the left medial parietal lobe (series 10,\nimage 17) and occipital lobe (series 10, image 11), which demonstrates subtle\ndiffusion-weighted hyperintense signal, without ADC hypointensity, suggestive\nof subacute infarct.\n\nThere is no evidence for acute infarct or intracranial mass.  There is no\nmidline shift.  No sulcal effacement.  Sulci, ventricles and cisterns are\nwithin expected limits for the patient's minimal senescent related global\ncerebral volume loss.\n\nThe aneurysm of the left mid M1 segment of the MCA (09:10) is better assessed\non the prior CTA.\n\nExtensive mucosal thickening of the bilateral maxillary sinuses, as well as\nthe anterior ethmoid air cells.  Mild nasal polyposis (series 9, image 4). \nMild fluid within the left mastoid air cells.  The bilateral orbits appear\nunremarkable.  The major intracranial vascular flow voids appear preserved.",
            "output": "1. Subtle likely FLAIR hyperintense signal centered in the right superior\nfrontal sulcus.  Although this is not associated with gradient echo\nsusceptibility artifact, this could potentially represent subarachnoid\nhemorrhage.  If the signal is cortical in nature, this could represent sequela\nof subacute infarct.\n2. Cortical gyriform FLAIR hyperintensity of the left medial parietal lobe and\noccipital lobe, is suggestive of subacute infarct.\n3. No evidence of acute infarct.\n4. The aneurysm of the left mid M1 segment of the MCA is better assessed on\nthe prior CTA.\n5. Extensive mucosal thickening of the bilateral maxillary sinuses and the\nanterior ethmoid air cells, suggestive of paranasal sinus disease.  Mild nasal\npolyposis.\n\nNOTIFICATION:  The findings were discussed with Dr.  ___, M.D.\nby ___, M.D. on the telephone on ___ at 11:40 am, 20 minutes\nafter discovery of the findings."
        },
        {
            "input": "Again seen is a large left parietal and occipital all hematoma.  The lateral\n___ of the hematoma appear to have enlarged since the most recent head\nCT.  There are small peripheral areas of enhancement seen on the postcontrast\nimages that were not displaced on the CTA.  These raise a concern of an\nunderlying vascular abnormality.  In this location, the possibility of a\nmycotic aneurysm should be considered.  Alternatively, it is possible that the\nenhancement seen reflects enlarged veins associated with the hematoma itself\nand peripheral breakdown of the blood-brain barrier due to the hematoma.\nThere is subarachnoid hemorrhage, superficial siderosis, or both over the left\nconvexity in the vicinity of the hematoma and in the parasagittal right sulci.\nAgain seen and unchanged is a small convexity left subdural hematoma,\nunchanged.  Also again seen and unchanged is a small amount of subdural\nhematoma along the falx and along the left tentorium.\nThere is medial displacement of the left uncus with deformity of the adjacent\ncerebral peduncle.",
            "output": "1. Findings concerning for enlargement of the left parietal and occipital\nhematoma.\n2. Several areas of peripheral enhancement that raise concern for possible\nmycotic aneurysm.  Alternatively, this may reflect enhancement or engorged\nveins associated with the hematoma itself.\n3. Subarachnoid hemorrhage, superficial cirrhosis or both in both hemispheres."
        },
        {
            "input": "A 4.9 x 3.4 x 4.9 cm intraparenchymal hematoma is again noted in the left\nparietooccipital region with minimal surrounding edema.  This appears\nrelatively stable compared to the most recent CT, given differences in\nimaging.  There is associated subarachnoid hemorrhage superior to the\nhematoma, unchanged.\n\nA subdural hematoma is seen overlying the left cerebral hemisphere, with the\nbulk of the hematoma overlying the left frontal lobe where it measures up to\n1.5 cm in maximum width.  This is relatively stable since the most recent CT,\nbut increased in size since prior MRI of ___.  There is an\nassociated 1 cm rightward midline shift, unchanged.  There is stable\nsubfalcine herniation.  There is stable medial deviation of the left uncus\nwith mass effect on the left cerebral peduncle.  No evidence of infarct\nallowing for artifact from hemorrhage.\n\nThere is trace subdural hemorrhage along the falx and tentorium.\n\nA stable mucous retention cyst is seen in the left maxillary sinus.  The\nmastoid air cells and middle ear cavities are clear.  The intraorbital\ncontents are normal.",
            "output": "1. Relatively stable large left parieto-occipital intraparenchymal hematoma\nwith trace associated subarachnoid hemorrhage.\n2. Stable left subdural hematoma with stable 1 cm rightward midline shift from\nmost recent head CT head.  The subdural hematoma has increased in size from\nprior MRI of ___.\n3. Allowing for artifact from hemorrhage product, no evidence of new infarct."
        },
        {
            "input": "MRI BRAIN:\nAllowing for differences in technique, there has been further decrease in size\nof the left occipital lobe intraparenchymal hematoma now measuring\napproximately 2.0 x 1.9 x 3.2 cm.  There has also been decrease of the\nsurrounding edema.\nMild pachymeningeal thickening and enhancement adjacent to the hemorrhage is\nmost likely reactive.\n\nThere is no evidence of new hemorrhage, midline shift or infarction.\n\nThe ventricles and sulci are stable in caliber and configuration.\nUnchanged fusiform aneurysm of the left MCA bifurcation.  Major vascular flow\nvoids appear otherwise preserved.  Major dural venous sinuses patent.\n\nThere is mild mucosal thickening in the left frontal sinus.  There is near\ncomplete opacification of the ethmoid air cells.  Moderate to severe mucosal\nthickening is seen in the bilateral maxillary sinuses.  There is partial\nopacification of the left mastoid air cells.\n\nMRA brain: Fusiform aneurysm of the left MCA bifurcation is unchanged.  The\nintracranial vertebral and internal carotid arteries and their major branches\nappear normal without evidence of stenosis or occlusion.  Note is made of a\nprominent right posterior communicating artery.\nThere is no evidence for an underlying vascular malformation in the region of\nthe intraparenchymal hemorrhage.",
            "output": "1. Further decrease in the size of the left occipital lobe intraparenchymal\nhematoma and surrounding edema.\n2. Mild pachymeningeal thickening and enhancement adjacent to the hemorrhage\nis most likely reactive.\n3. No evidence of underlying mass or vascular malformation region of the\nintraparenchymal hemorrhage.\n4. Stable fusiform aneurysm of the left MCA bifurcation."
        },
        {
            "input": "There is no intra or extra-axial mass, acute hemorrhage or infarct. The sulci,\nventricles and cisterns are within expected limits for the patient's age. \nMildly increased T1 hyperintense signal of the bilateral globus paladus may be\nseen in the setting of hepatic encephalopathy given the patient's history of\nalcoholic hepatitis.  No parenchymal FLAIR signal abnormality.  The major\nintracranial flow voids are preserved.  The orbits are unremarkable.  Fluid in\nthe bilateral mastoid air cells and nasopharynx compatible with sequela of\nintubation.  Mild mucosal thickening of the sphenoid sinus, bilateral\nmaxillary sinus and opacification of the right frontal sinus is identified. \nThere is mildly decreased T1 hypointense signal of the calvarial marrow\nsignal, which may be secondary to the patient's renal failure.",
            "output": "1. No acute infarct or intracranial hemorrhage.  No FLAIR signal abnormality.\n2. Subtle T1 hyperintense signal of the bilateral globus paladus may be seen\nin setting of hepatic encephalopathy given the patient's history of alcoholic\nhepatitis.\n3. Additional findings as described above."
        },
        {
            "input": "There is a large chronic left cerebellar infarct with hemosiderin deposition\nalong the margins.  A smaller chronic right cerebellar infarct is also noted. \nThere is no evidence of acute intracranial hemorrhage, edema, mass, mass\neffect, or acute infarction.  The ventricles and sulci are age-appropriate. \nPrincipal intracranial vascular flow voids are preserved.  Small mucous\nretention cyst in a left ethmoid air cells noted.  The remainder the\nvisualized paranasal sinuses are clear.  The orbits are unremarkable noting\nbilaterally elongation of the globes compatible with staphyloma/axial myopia. \nThe mastoid air cells are clear.",
            "output": "1.  Chronic bilateral cerebellar infarcts.\n\n2.  No evidence of acute intracranial hemorrhage or infarction."
        },
        {
            "input": "The study is partially limited due to patient motion. Unchanged bilateral\ncerebellar infarcts, with susceptibility changes on the left suggesting\nresidual blood products. There is no evidence of intracranial hemorrhage,\nmass, mass effect or shifting of the normally midline structures. The\nventricles and sulci are unchanged, with no evidence of hydrocephalus. No\ndiffusion abnormalities are detected to indicate acute or subacute ischemic\nchanges. The major vascular flow voids are present and demonstrate normal\ndistribution. The orbits are unremarkable, the paranasal sinuses and mastoid\nair cells are clear.",
            "output": "Unchanged bilateral cerebellar infarcts with magnetic susceptibility on the\nleft suggesting residual blood products, unchanged since the prior head CT and\nMRI of the brain dated ___."
        },
        {
            "input": "The examination is partially limited due to patient motion. The posterior\nfossa is notable for unchanged bilateral cerebellar infarcts, with\nsusceptibility changes on the left, suggesting residual blood products. There\nis no evidence of diffusion abnormalities to indicate acute infarction,, there\nis no evidence of new intracranial hemorrhage, extracerebral fluid collection,\nmidline shift or mass effect.  The supratentorial cerebral volume is\nappropriate for the patient's stated age.  Flow voids are maintained.",
            "output": "Stable bilateral cerebellar infarcts, with magnetic susceptibility on the\nleft, suggestive of residual blood products as previously described.  There is\nno evidence of acute intracranial hemorrhage or new areas of ischemia.\n\nNOTIFICATION:  The findings were discussed by Dr. ___ with Dr. ___\n___ on the telephone on ___ at 3:50 ___,  minutes after discovery of\nthe findings."
        },
        {
            "input": "There is no acute infarct identified. There is no mass effect midline shift or\nhydrocephalus. Chronic bilateral cerebellar infarcts with chronic blood\nproducts are identified unchanged from prior study.",
            "output": "No acute infarcts. Bilateral chronic cerebellar infarcts."
        },
        {
            "input": "There is encephalomalacia of the bilateral cerebellar hemispheres, left\ngreater than right, secondary to prior infarction.  Stable susceptibility is\nnoted at the site of the prior left cerebellar hemisphere infarction,\nconsistent with chronic blood products.  There is no evidence of hemorrhage,\nedema, masses, mass effect, midline shift or infarction.   The ventricles and\nsulci are normal in caliber and configuration.  The major vascular flow voids\nare preserved.\n\nThere is elongation of the bilateral globes, likely secondary to axial myopia.\nThe paranasal sinuses, mastoids and visualized soft tissues are normal.",
            "output": "1. No acute infarct.\n2. Encephalomalacia of the bilateral cerebellar hemispheres and left\ncerebellar siderosis from prior infarction."
        },
        {
            "input": "There is interval evolution and redistribution of the previously demonstrated\nextra-axial fluid collection/subdural hematoma in the right temporal region\nand right middle cranial fossa with extension along the right cerebral\nconvexity towards the right frontal/supraorbital and right posterior parietal\nconvexity.  Within the right temporal region, the subdural hematoma measures\nup to 2.3 cm in maximal thickness with mass effect on the right temporal lobe.\nThere is no midline shift.  There is a smaller additional right temporal lobe\nintraparenchymal hemorrhage measuring up to 1.3 cm in maximal length.  No new\nintracranial hemorrhage is identified.\n\nEvaluation of the gradient recalled echo images demonstrates no findings to\nsuggest amyloid angiopathy.\n\nMild prominence of the ventricles and sulci is suggestive of involutional\nchanges.  Patchy to confluent areas of T2 and FLAIR hyperintense signal\nabnormalities in the periventricular and subcortical white matter are\nnonspecific, but likely reflect chronic small vessel ischemic changes.  A\nprominent CSF space in the posterior fossa may represent ___ cisterna\nmagna.  Prominent perivascular spaces.\n\nThere is moderate right and mild left pachymeningeal thickening and\nenhancement along the cerebral convexities, likley due to underlying\nhemorrhage.  The major intracranial arterial flow voids are preserved.  The\ndural venous sinuses are patent.\n\nThere is no evidence of slow diffusion to suggest acute infarction.\n\nThere is mild mucosal thickening of the paranasal sinuses.  The mastoid air\ncells are clear.  Unremarkable intraorbital contents.",
            "output": "1. Interval evolution and redistribution of the previously demonstrated\nsubdural hematoma along the right cerebral convexity measuring up to 2.3 cm in\nmaximal thickness.  Localized mass effect on the right temporal lobe.  No\nmidline shift.\n2. No new intracranial hemorrhage identified.\n3. No findings to suggest amyloid angiopathy.\n4. Mild to moderate parenchymal volume loss and chronic small vessel ischemic\ndisease."
        },
        {
            "input": "Study is degraded by motion.  Within these confines:\n\n There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are prominent in caliber and\nconfiguration, reflecting age related involutional changes.  There are\nscattered T2/FLAIR hyperintensity in the periventricular and subcortical white\nmatter compatible with chronic microangiopathy.  Chronic lacunar infarct in\nthe right parietal lobe.\n\nThere is mucosal thickening in the ethmoid air cells and bilateral maxillary\nsinuses.  Trace nonspecific bilateral mastoid fluid is present.  Status post\nbilateral lens replacement.  There is partially visualized multilevel\ndegenerative disc disease of the cervical spine.",
            "output": "1. Study is degraded by motion.\n2.  No acute intracranial abnormality, no definite evidence of acute infarct.\n3. Global volume loss and probable microangiopathic changes as described.\n4.  Paranasal sinus disease and trace bilateral nonspecific mastoid fluid, as\ndescribed."
        },
        {
            "input": "There is extensive global cerebral volume loss, with most severe involvement\nof the bilateral parietal and temporal lobes (including mesial temporal cortex\nand hippocampal formations) and more moderate involvement of bilateral frontal\nand medial occipital lobes.  This is not significantly changed compared to\n___. Nonspecific extensive confluent periventricular white matter T2 size\nFLAIR hyperintensities are noted, similar to periventricular hypodensities on\nCT examinations dating back to ___. Prominent perivascular spaces are also\nagain noted.\n\nThere is no acute infarction, mass, or evidence of blood products. No abnormal\npachymeningeal or leptomeningeal enhancement. The major intracranial flow\nvoids are preserved.  The major dural venous sinuses are patent.\n\nMild mucosal thickening of ethmoid air cells. The mastoid air cells\ndemonstrate right greater than left trace fluid signal.",
            "output": "1. No evidence for mass, acute infarction, or other acute abnormalities.\n2. Extensive global cerebral volume loss, most severe in bilateral parietal\nand temporal lobes, and more moderate in bilateral frontal and medial\noccipital lobes, without significant change since ___.\n3. Extensive periventricular white matter signal abnormalities, similar to\n___, nonspecific but most likely sequela of chronic small vessel ischemic\ndisease in a patient of this age."
        },
        {
            "input": "MRI HEAD:  There is a punctate, subcentimeter, acute lacunar infarct within\nthe right thalamus.  There is no other evidence of interval infarct. \nVentricles, cisterns and sulci are age appropriate.  There is no evidence of\nhemorrhage.  There is no abnormal enhancement.\n\nMRA HEAD:  There is no large vessel occlusion or aneurysm.  Mild regions of\nirregularity are likely atherosclerotic, particularly in the posterior\ncirculation.  Some of this is artifactual as well.\n\nMRA NECK:  The great vessel origins are not well seen, including the vertebral\nartery origins.  There is no evidence of flow-limiting stenosis within the\nneck.",
            "output": "1.  Acute, punctate, subcentimeter lacunar infarct in the right thalamus.\n2.  No definite flow-limiting stenosis within the head or neck.  The posterior\ncirculation within the head is not well evaluated secondary to artifact, but\nthere is no large vessel occlusion."
        },
        {
            "input": "Susceptibility artifact associated with the dental hardware obscures\nvisualization of the adjacent structures.\n\nThere is no enhancing mass or abnormal enhancement.  There is no evidence of\nacute infarction for intracranial hemorrhage.  Incidental note is made of\ncavum velum interpositum.  There is no mass effect or midline shift.  The\nprincipal arterial vascular flow voids are preserved.  The dural venous\nsinuses appear patent on the postcontrast images.\n\nThere is mild mucosal thickening of the bilateral ethmoid air cells.  There is\nmoderate right and mild left nonspecific bilateral mastoid air cell\nopacification.",
            "output": "1. No evidence of enhancing mass or abnormal enhancement to suggest metastatic\ndisease.\n2. No evidence of acute infarction or intracranial hemorrhage."
        },
        {
            "input": "There is a left pontine focus of slow diffusion corresponding to low ADC\nvalues and no significant T2/FLAIR signal hyperintensity.  These findings\nindicate an acute infarction.  There are moderate periventricular and\nsubcortical white matter foci of T2/FLAIR signal hyperintensity, nonspecific\nand likely sequelae of chronic microangiopathy.  There is prominence of the\ncerebral sulci and ventricles suggestive of age-related involutional changes. \nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor other infarction.  There is mucosal thickening within the paranasal sinuses\npredominately the void air cells and sphenoid sinus with inspissated debris in\nthe sphenoid sinus.  Fluid signal intensity is noted in the bilateral mastoid\nair cells.",
            "output": "1. Small acute left pontine infarct.\n2. No no evidence of mass, hemorrhage or other infarction.\n3. Mild periventricular and subcortical white matter signal changes,\nnonspecific and likely sequelae of chronic microangiopathy.\n4. Small amount of bilateral mastoid fluid.\n5. Paranasal sinus disease."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.",
            "output": "1. Normal brain MRI."
        },
        {
            "input": "There is a stable partially empty sella.  There is no evidence of hemorrhage,\nedema, masses, mass effect, midline shift or infarction.  No diffusion\nabnormalities are detected.  The ventricles and sulci are normal in caliber\nand configuration.  The major intracranial flow voids are maintained.\n\nThere is mild mucosal thickening within the ethmoid air cells and sphenoid\nsinus.  Trace fluid signal is noted in the bilateral mastoid air cells.  The\nintraorbital structures are unremarkable.",
            "output": "1. No acute intracranial process or mass given lack of intravenous contrast.\n2. Stable partially empty sella.  No other MR findings to suggest idiopathic\nintracranial hypertension.\n3. Mild paranasal sinus mucosal thickening and trace bilateral mastoid fluid."
        },
        {
            "input": "A 4 mm  focus is seen in the midline parietal bone (9:108), is likely\nrepresenting a benign hemangioma given the T1 hyperintensity on pre gadolinium\nimages (04:16).\n\nThere is no evidence of hemorrhage, edema, mass effect, midline shift or\ninfarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  Patchy subcortical and deep white matter T2 hyperintensities\nare nonspecific but may be sequela of chronic microvascular angiopathy or\nchronic migraines.\n\nThere is mild mucosal thickening of the right sphenoid sinus.  The mastoid air\ncells and middle ear cavities are clear.  The intraorbital contents are\nnormal.",
            "output": "No significant intracranial abnormalities on MRI of the brain with and without\ngadolinium.  No enhancing brain lesions are seen."
        },
        {
            "input": "MRI BRAIN:\n There is no evidence of acute infarction.  there are several T2/FLAIR\nhyperintensities seen involving the right thalamus and right putamen (11:14),\nwithout associated diffusion abnormality.  Additional small white matter FLAIR\nhyperintensities are seen at the high left frontal lobe.  A small chronic\nright cerebellar hemispheric infarcts noted.\n\nThere is no evidence of hemorrhage, mass, mass effect, edema or midline shift.\nThere is a cavum septum pellucidum.  Ventricles and sulci are age appropriate\nin size.\n\nMild mucosal thickening is seen in scattered ethmoid air cells.  There are\nbilateral maxillary mucous retention cysts.  The remainder of the visualized\nparanasal sinuses, middle ear cavities, and mastoid air cells are well aerated\nand clear.  The orbits are within normal limits bilaterally.\n\nMRA BRAIN:\nThe intracranial vertebral and internal carotid arteries and their major\nbranches appear patent without evidence of stenosis, occlusion, or aneurysm\nformation.\n\nMRA NECK:\nThe common, internal and external carotid arteries appear patent.  There is no\nevidence of internal carotid artery stenosis by NASCET criteria.  The origins\nof the great vessels, subclavian and vertebral arteries appear normal\nbilaterally.",
            "output": "1. No evidence of hemorrhage or acute infarction.\n2. Lesions in the right putamen and right pons that may represent subacute to\nchronic infarction.\n3. Chronic right cerebellar hemispheric infarct.\n4. Nonspecific white matter FLAIR hyperintensities are noted, involving the\nsuperior left frontal lobule, right basal ganglia and right thalamus.  No\nassociated diffusion abnormality.  These findings may represent the sequelae\nof late subacute/early chronic infarct, small-vessel ischemic disease, or\npotentially the sequelae of inflammatory/demyelinating disease.\n5. Patent intracranial and cervical vasculature without high-grade stenosis,\nlarge vessel occlusion, or aneurysm."
        },
        {
            "input": "Motion artifact degrades the 3D FLAIR images.\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  Mild asymmetry of the lateral ventricles (left larger than\nright) which is nonspecific.  Periventricular and deep white matter T2 and\nFLAIR hyperintensities are small, nonspecific and not in the typical\ndistribution of MS. ___ is no abnormal enhancement after contrast\nadministration.  The intracranial vessels demonstrate normal T2 flow voids. \nThe paranasal sinuses are clear.  The orbits appear normal.",
            "output": "Periventricular and deep white matter T2 and FLAIR hyperintensities are small,\nnonspecific and not in the typical distribution of MS. ___ these\nlesions are most likely secondary microangiopathy although other demyelinative\ncauses cannot be excluded with certainty."
        },
        {
            "input": "There is no evidence of intracranial hemorrhage, edema, masses, mass effect,\nmidline shift or infarction.  There are few periventricular and deep white\nmatter small punctate FLAIR hyperintensities which are nonspecific. The\nventricles and sulci are normal in caliber and configuration.  Partially empty\nsella.  The craniocervical junction appears normal.  Heterogenously decreased\nbone marrow signal is nonspecific and may be secondary to hemopoietic active\nred marrow or renal osteodystrophy.  Delete the intracranial arteries\ndemonstrates normal T2 flow voids.  The orbits appear normal.  Minimal mucosal\nthickening involving the paranasal sinuses.",
            "output": "1.  No acute intracranial pathology.  No intracranial mass, hemorrhage or\nacute infarct.\n\n2.  Few periventricular and deep white matter FLAIR hyperintense foci are\nnonspecific, and can be seen in multiple entities such as chronic migraines,\nchronic hypertension, sequela of viral infection, demyelination and small\nvessel disease.\n\n3.  Heterogenously decreased bone marrow signal is nonspecific and may be\nsecondary to hemopoietic active red marrow or renal osteodystrophy."
        },
        {
            "input": "Left insula and inferior parietal gyrus restricted diffusion with associated\nT2 and FLAIR hyperintensity and no definite associated increase susceptibility\nis present.\n\nThere is no evidence of hemorrhage, masses, mass effect or midline shift.  \nThere is prominence of the ventricles and sulci suggestive of involutional\nchanges.  Periventricular and subcortical T2 and FLAIR hyperintensities are\nnoted which may represent small vessel ischemic changes.  Chronic left basal\nganglia and right caudate infarcts are again noted.  Right thalamic punctate\nfocus of blood products versus mineralization is noted.\n\nBilateral maxillary sinus and ethmoid air cell mucosal thickening is present. \nBilateral lens replacement postoperative changes are noted.",
            "output": "1. Left MCA distribution insula and inferior parietal frontal gyrus acute to\nsubacute infarcts without definite evidence of hemorrhagic transformation.\n2. Chronic left basal ganglia and right caudate infarcts.\n3. Global volume loss and probable microangiopathic changes as described.\n4. Punctate right thalamic focus of blood products versus mineralization.\n5.  Paranasal sinus disease , as described."
        },
        {
            "input": "The bilateral trigeminal nerves are preserved in course and caliber.  Subtle\nasymmetric enhancement of the V2 segment of the left trigeminal nerve is seen\nat the level of the foramen rotundum (15:35, 14: 8).  The nerve at this level\nappears slightly asymmetrically expanded as compared to the right, without\nnodular component.  The left AICA is seen crossing superiorly to the root\nentry zones/proximal cisternal segment of the left trigeminal nerve (13:47). \nA likely venous structure is seen superior to the cisternal segment of the\nright trigeminal nerve.\n\nImages through the internal auditory canal demonstrates symmetric appearance\nof the seventh eighth nerve complexes.  There is no evidence of abnormal\nenhancement or mass lesion within the internal auditory canals,\ncerebellopontine angles or membranous labyrinth. No other mass lesions are\nseen within the posterior fossa.\n\nLimited included imaging of the remainder of the brain demonstrates no\nevidence of hemorrhage, edema, masses, mass effect, midline shift or\ninfarction. The ventricles and sulci are normal in caliber and configuration. \nFew, scattered areas of nonspecific periventricular and subcortical white\nmatter T2/FLAIR hyperintensity are seen.  There is no abnormal enhancement\nafter contrast administration.  There is no abnormal focus of slowed\ndiffusion.\n\nNo osseous abnormalities are seen.  There is mild polypoid mucosal wall\nthickening in the floors of the maxillary sinuses as well as mild bilateral\nethmoid air cell mucosal thickening.  There is a small mucous retention cyst\nin the left sphenoid sinus.  The remainder of the paranasal sinuses,mastoid\nair cells, and middle ear cavitiesare clear. The orbits are unremarkable. The\nvisualized portion of the principle vascular flow voids are preserved.",
            "output": "1. Subtle asymmetric enhancement and smooth expansion of the V2 segment of the\nleft trigeminal nerve at the level of the foramen rotundum without nodular\ncomponent.  This appearance is nonspecific, and may be inflammatory.\n2. The left AICA is seen contacting the root entry zone/proximal cisternal\nsegment of the left trigeminal nerve without definite compression. \nCorrelation with nature of symptoms is recommended in order to exclude\npossible neurovascular impingement.  The right trigeminal nerve is preserved.\n3. No internal auditory canal or cerebellopontine angle mass.\n4. No infarct, hemorrhage, or enhancing mass lesion."
        },
        {
            "input": "The previously seen left occipital hematoma has considerably decreased in size\nwith decrease in surrounding edema.  The blood products also demonstrate\nevolution with majority of the blood products not demonstrating T1\nhyperintensity and T2 hyperintensity indicative of late subacute blood\nproducts (extra cellular methemoglobin) with a peripheral rim of low signal\n(hemosiderin).  The hemosiderin rim appears continuous and un interrupted. \nThere has been evolution of blood products within the ventricular system. \nWhile there is slight enlargement of the left atrium more than the right side\nindicative of ex vacuo dilatation, the overall ventricular size has also\nslightly increased measuring 37 mm at the level of the ventricle bodies\n(07:14) compared to 28 mm previously (13:15) however, the temporal horn size\nis not significantly changed.  On the postcontrast images there is no definite\nenhancement seen at the site of evolving hematoma or in other parts of the\nbrain.  No abnormal vascular structures are seen.  Mucosal thickening is\nvisualized in the sinuses and small amount of fluid is seen in the mastoid air\ncells as before.",
            "output": "1. Decrease in size of the left temporal hematoma with evolution of blood\nproducts with a continuous surrounding hemosiderin rim, and absence of any\nenhancement indicates that there is no underlying mass lesion present to the\nhematoma.  No abnormal vascular structures are seen.\n2. Slightly increased ventricular size could be related to previous\nintraventricular blood products and need to be assessed on the follow-up.  At\npresent, there are no signs of hydrocephalus."
        },
        {
            "input": "Again seen is a 6.1 x 4.0 cm left temporal occipital intraparenchymal\nhematoma.  There is intraventricular extension of hemorrhage into the body of\nthe left lateral ventricle, as seen previously (07:15).  There is no\nenhancement within the hematoma to suggest an underlying mass.  Intrinsically\nT1 hyperintense blood products are seen within the medial and dependent\naspects of the hematoma (8:12 and 11).  There is sulcal T2/FLAIR\nhyperintensity susceptibility artifact along the left temporal and parietal\nlobes which most likely represent subarachnoid hemorrhage.\n\nThere is mild surrounding white matter vasogenic edema.  Mass effect includes\nleft-sided cerebral sulcal effacement, and 4 mm rightward shift of midline\nstructures which is unchanged.  The basal cisterns are patent, without\nherniation.  No hydrocephalus/ventricular entrapment.\n\nNo acute infarction.  No separate area of hemorrhage.  The ventricles and\nsulci are mildly prominent, compatible with global parenchymal volume loss.\n\nThere is moderate pansinus mucosal thickening worst in the ethmoid air cells\nand left more than right maxillary sinus.  No air-fluid levels.\n\nThe globes and orbits unremarkable.  Major intracranial vascular flow voids\nare preserved.  There are trace bilateral mastoid effusions.  Major dural\nvenous sinuses are patent.",
            "output": "1. Unchanged 6.1 cm left temporoparietal intraparenchymal hematoma with\nintraventricular extension.  Mild amount of adjacent subarachnoid hemorrhage\nalong the left parietal and temporal lobes. No evidence of an underlying mass\nat the site of the hematoma.\n2. Mild surrounding vasogenic edema and mild mass effect including unchanged 4\nmm rightward shift of midline structures. No herniation or ventricular\nentrapment.\n3. Mild global parenchymal volume loss.\n4. Moderate pansinus mucosal thickening.  No air-fluid levels.\n5. Trace bilateral mastoid effusions."
        },
        {
            "input": "Motion artifact limits evaluation on multiple sequences.  There is no evidence\nof an enhancing mass, pathologic leptomeningeal or pachymeningeal contrast\nenhancement, acute infarction, or edema.  Gradient echo images are\nparticularly limited by motion with limited evaluation for chronic blood\nproducts.  Linear hypointensity between the inferior left cerebellar\nhemisphere and vermis on gradient echo images ___ most likely represents a\nprominent blood vessel, though a blood vessel is not clearly visualized on\nmotion limited postcontrast MP RAGE images.  Ventricles and sulci are normal\nin size for the patient's age.  Basal cisterns are preserved.  Major vascular\nflow voids appear grossly preserved.",
            "output": "Motion limited exam. No evidence for acute intracranial mass or acute\nintracranial abnormalities."
        },
        {
            "input": "There is no evidence of intracranial hemorrhage, mass, mass effect or shifting\nof the normally midline structures. The ventricles and sulci are unchanged and\nappear slightly prominent suggesting cortical volume loss. There is an\nunchanged perivascular space in right centrum semiovale. There is no evidence\nof abnormal enhancement. No diffusion abnormalities are detected. The major\nvascular flow voids are present and demonstrate normal distribution.  The\norbits are unremarkable, the paranasal sinuses are notable for persistent\nmucosal thickening and air-fluid level on the right maxillary sinus,\nsuggesting an ongoing inflammatory process.",
            "output": "1. There is no evidence of abnormal enhancement or acute or subacute ischemic\nchanges.  Slightly prominent ventricles and sulci are unchanged, suggesting\ncortical volume loss.\n\n2. Persistent opacity with air-fluid level on the right maxillary sinus,\nsuggesting an ongoing inflammatory process."
        },
        {
            "input": "Post-contrast sequences are severely degraded by motion artifact. No obvious\nintra-axial or extra-axial enhancing lesions are seen.\n\nThere is a punctate focus of high signal on the diffusion tracer sequence in\nthe posterior perisylvian right temporal cortex on image 502:18, without a\ncorrelate on the ADC map or FLAIR images. There is another punctate focus of\nhigh signal on the diffusion tracer sequence in the posterior-most left\nfrontal opercular cortex on image 502:15, with faint associated high signal on\nFLAIR images, image 6:15, and no correlate on the ADC map. These likely\nrepresent small acute infarctions, probably embolic.\n\nFLAIR images demonstrate high signal along the left lateral occipital cortex,\nimages 16:15 and 16:13, high-signal in the left medial occipital sulci, image\n6:11, and high signal in the superior cerebellar vermis bilaterally, image\n6:11. This may be related to to the recent lumbar puncture, but could also\nrepresent infectious meningitis or leukemic infiltration of the meninges,\ngiven the clinical history. Subarachnoid blood products may have a similar\nappearance. Evaluation for blood products is otherwise limited as gradient\necho images are degraded by motion artifacts. Precontrast T1 weighted images\nare also degraded by motion artifacts.\n\nMild global cerebral atrophy with associated prominence of the ventricles and\nsulci is again seen. Major arterial flow voids appear grossly preserved.\n\nThere is persistent fluid in the right maxillary sinus, as well as mucous\nretention cyst and mild mucosal thickening in the right maxillary sinus, and\nmild mucosal thickening in the left maxillary sinus.",
            "output": "1. Punctate foci of abnormal diffusion in the posterior perisylvian right\ntemporal cortex and in the posterior-most left frontal opercular cortex,\nsuggesting small acute infarctions which are probably embolic.\n2. High signal on FLAIR images along the left lateral occipital cortex, in the\nleft medial occipital sulci, and in the bilateral superior cerebellar vermis\nmay be related to the recent lumbar puncture, but could also represent\ninfectious meningitis or leukemic infiltration of the meninges, given the\nclinical history. Subarachnoid blood products may have a similar appearance,\nbut are less likely. Please correlate with lumbar puncture results.\n3. Persistent fluid in the right maxillary sinus may be related to prolonged\nsupine positioning in the inpatient setting. However, please correlate\nclinically with any signs of active sinusitis."
        },
        {
            "input": "MRI HEAD: The punctate diffusion abnormality in the posterior pre-Sylvian\nright temporal region is still present but appears to be located in the\nsubarachnoid space within a sulcus (602:18). The other punctate diffusion\nabnormality in the posterior left frontal opercular cortex has resolved. There\nare bilateral foci of diffusion abnormality in the medial occipital lobes\nwhich are more prominent on today's study (602:14), and, on the left, are\nassociated with sulcal hyperintensity on FLAIR images (9:10). There is no\ncorresponding abnormality on the ADC map. In retrospect, these abnormalities,\nrather than focal infarction, likely represent a subarachnoid process located\nwithin the sulci. More faintly elevated signal on FLAIR images in multiple\nbilateral sulci are not significantly changed. These findings remain\ncompatible with either infectious or leukemic meningitis. There is no\nassociated contrast enhancement. Overall, no abnormal contrast enhancement is\nseen.\n\nOn gradient echo images, there is low signal in several bilateral frontal and\nparietal sulci, which is unchanged as far back as the earliest MRI available\nfor comparison dated ___. A review of multiple prior CTs of\nthe head do not demonstrate any blood products at these locations. These\nabnormalities represent siderosis from chronic blood products originating\nbefore the earliest comparison study, or they may be related to the infectious\nor leukemic meningeal infiltration.\n\nThere is no acute infarction, mass effect, edema, or hydrocephalus. Ventricles\nand sulci are normal in size and configuration.\n\n Fluid in the right maxillary sinus has resolved.  There is residual mild\nmucosal thickening in the bilateral maxillary sinuses. There is a small amount\nof fluid in the left mastoid air cells.  Incidentally noted is mild\nanterolisthesis of C2 on C3.\n\nHEAD MRA: Normal flow related enhancement is seen in the intracranial internal\ncarotid, middle cerebral and anterior cerebral arteries without significant\nmural irregularity or high-grade stenosis. There is normal symmetric\narborization of the MCA branches. There is no aneurysm greater than 3 mm.\nNormal flow related enhancement is seen in the codominant intracranial\nvertebral arteries, the basilar artery, and the bilateral superior cerebellar\nand posterior cerebral arteries.\n\nHEAD MRV: The major dural venous sinuses are patent.\n\nNECK MRA: There is mild  narrowing of the left internal carotid artery at its\norigin, without flow limiting stenosis.  Cervical right carotid system is\nunremarkable.  The left vertebral artery arises directly from the aortic arch,\na normal variant.  No significant vertebral narrowing is seen on either side.",
            "output": "1. No evidence for new acute intracranial abnormalities.\n2. Unchanged mutlifocal bilateral abnormal signal in the sulci on FLAIR\nimages, compatible with either infectious or leukemic meningitis. Persistent\npunctate signal abnormality on diffusion weighted images in the posterior\nperisylvian right temporal region (still present) is located in the\nsubarachnoid space, not in the cortex, and likely related to the underlying\nmeningeal process, and not  infarction .\n3. Previously noted punctate diffusion abnormality in the left posteriort\nfrontal opercular cortex (or subarachnoid space) is no longer seen; it may\nhave been related to infarction or a meningeal process.\n4. Mild non-flow-limiting narrowing of the left internal carotid artery\norigin.\n5. Unremarkable head MRA.\n6. No evidence for major dural venous sinus thrombosis."
        },
        {
            "input": "MR BRAIN:\nThere is a large 5.5 x 4.5 x 4.4 cm (AP, TV and SI directions; respectively),\nintra-axial mass lesion, centered above the left basal ganglia, deviating the\ngenu and body of corpus callosum, and causing approximately 15 mm midline\nshifting of the normally midline structures towards the right.  This mass\nlesion demonstrates heterogenous T2 signal intensity, predominantly isointense\non T2, with thick rim of T2 hypointensity, mild ill-defined slow diffusivity,\nas well as irregular and nodular enhancement at the same peripheral area of T2\nhypointensity.  There is no evidence of intracranial hemorrhage.  More\nanteriorly in the left frontal lobe there is slow diffusivity and effacement,\nwith mild pattern of enhancement after contrast administration (series 28,\nimage 18), measuring approximately 1 x 1 cm in transverse dimension, with no\nsignificant mass effect, however also suggestive of tumoral infiltration.  The\nleft lateral ventricle appears enlarged, with narrowing of the third ventricle\nsuggesting entrapment.  At the medial aspect of the mass on susceptibility\nweighted T2* images; there is a linear signal void along ependyma surface\nlikely related prominent draining vein.  Vague areas of high-signal intensity\nidentified on the FLAIR axial images on the left temporal lobe also suggest\ntumoral infiltration (series 24, image 11).\n\nMR perfusion show corresponding increased relative cerebral blood volume at\nthe periphery of the tumor on the areas of T2 hypointensity and diffusion\nrestriction with corresponding irregular enhancement.\n\nThe major dural venous sinuses appear patent, the orbits are unremarkable. \nParanasal sinuses and mastoid air cells are clear.\n\nMRA brain: The intracranial vertebral and internal carotid arteries and their\nmajor branches appear normal without evidence of stenosis, occlusion, or\naneurysm formation.",
            "output": "1. Left frontal lobe mass lesion, extending above the left basal ganglia as\ndescribed above, with heterogeneous pattern of enhancement likely consistent\nwith a glial neoplasm.\n2. The mass lesion causes rightward midline shift by 1.5 cm.\n3. Apparently there is a smaller satellite lesion, with no evidence of\nnecrosis, however mild enhancement, located midline anterior left frontal lobe\nas described above.\n4. Subtle areas of FLAIR high-signal intensity in the left temporal lobe\nsuggest tumoral infiltration as described above."
        },
        {
            "input": "Study is moderately degraded by motion, especially on postcontrast images. \nWithin these confines:\n\nStatus post left frontal craniotomy for partial section of left frontal\nintra-axial mass lesion centered at left basal ganglia with postoperative\nchanges.\n\nRedemonstration of unchanged persistent rightward midline shift by\napproximately 15 mm with associated subfalcine herniation.  Also there is\nsimilar degree of left lateral ventricle entrapment at the level of the\nforamen ___ and third ventricle with persistent unchanged ipsilateral\nperiventricular edema in keeping with isolated intraventricular system\nincreased pressure on left lateral ventricle.\n\nGrossly stable appearance of satellite lesions with similar signal\ncharacteristics of tumor at medial left frontal lobe and left posterior\ntemporal region.",
            "output": "1.  Study is moderately degraded by motion.\n2. Status post left frontal craniotomy for partial resection of left frontal\ntumor with postoperative changes as described.\n3. Grossly stable rightward midline shift with associated subfalcine\nherniation.\n4. Grossly stable left lateral ventricle entrapment and ipsilateral\nperiventricular edema.\n5. Grossly stable enhancing residual mass and satellite lesions as described."
        },
        {
            "input": "Postsurgical changes are again demonstrated from left frontal craniotomy and\ntumor resection.  The degree of irregular enhancement surrounding the margins\nof the resection cavity has increased since the previous examination\nconcerning for tumor progression.  Irregular enhancement along the septum\npellucidum has increased.  The resection cavity with its worsened peripheral\nenhancement measures 5.9 x 5.0 by 7.1 cm.  There is continued effacement of\nthe frontal horn of the left lateral vent and persistent rightward midline\nshift with subfalcine herniation.  The rightward midline shift measures\napproximately 1.5 cm and does not appear significantly changed.  There is\ncontinued evidence for left lateral ventricle entrapment with periventricular\nT2/FLAIR hyperintensity.  In addition, irregular enhancement along the\nsubependymal margins of the lateral ventricle for example on image 14 of\nseries 9 is demonstrated possibly reflecting tumoral involvement.  This is\nmore conspicuous than previously.  The configuration of the right lateral\nventricle is grossly stable.\n\nThere is increased enhancement associated with the medial left frontal\nsatellite nodule compared to the previous examination. This nodule now\nmeasures approximately 1.5 by 1.0 cm.  This demonstrates a similar extent of\nassociated FLAIR hyperintensity.\n\nThe nonenhancing infiltrative FLAIR hyperintensity in the left posterior\ntemporal lobe is similar to the previous examination.\n\nThere are a few scattered areas of punctate susceptibility in the cerebellum\nwhich could reflect blood products or mineralization, and more conspicuous\nthan on the previous examination although this could be due to technique. \nThere is no evidence of infarction.  The enhancing areas of tumor demonstrated\nslow diffusion in the rim enhancing periphery indicating some\nhypercellularity.\n\nThe major intracranial vascular flow voids are preserved.  Orbits are grossly\nunremarkable.",
            "output": "1. Worsening irregular enhancement surrounding the resection cavity margins as\nwell as increasing enhancement related to the satellite nodule in the medial\nleft frontal lobe worrisome for tumor progression.\n2. Grossly stable associated degree of rightward midline shift and subfalcine\nherniation.\n3. Grossly stable left lateral ventricle enhancement and periventricular\nsignal changes.\n4. More conspicuous nodular enhancement along the margins of the left lateral\nventricle which is worrisome for tumor dissemination.\n5. Stable satellite lesions in the left temporal lobe."
        },
        {
            "input": "Postsurgical changes from left frontal craniotomy and tumor resection.\n\nSusceptibility artifact in the left frontal lobe measuring 2.5 x 1.1 cm\ncorresponds to known hematoma, measuring 2.2 x 1.2 cm on recent CT.  No new\nareas of hemorrhage.\n\nThe resection cavity measures 5.4 x 5.2 by 6.3 cm, 5.9 x 5 x 7.1 cm in\n___.  Persistent slow diffusion in the periphery and most inferior\naspect of the cavity suggests hypercellularity.  The peripheral enhancement\nappears more nodular than on prior, particularly in the superomedial aspect of\nthe cavity (10:14).  There continues to be enhancement of the septum\npellucidum and along the subependymal lining of the left lateral ventricle. \nThe cavity exerts mass effect resulting in midline shift to the right of\napproximately 1.7 cm, unchanged since ___. Similar surrounding\nT2 hyperintensity. Degree of effacement of the frontal horn and enlargement of\nthe temporal horn of the left lateral ventricle, and subfalcine herniation are\nsimilar to prior CT.  The right lateral ventricle configuration is unchanged\nfrom priors.\n\nA satellite lesion in the medial left frontal lobe measures 2.2 cm, and has\nincreased in size from prior, previously measuring 1.4 cm.\n\nNonenhancing infiltrative FLAIR hyperintensities in the left posterior\ntemporal lobe are unchanged (08:12).\n\nNo new enhancing lesions.\n\nMotion artifact limits evaluation of the cerebellum in the GRE sequence.\n\nNo evidence of acute infarct.  The major intracranial vascular flow voids are\npreserved.  Orbits are grossly unremarkable.",
            "output": "1. Increased enhancing nodularity along the margins of the resection cavity\nconsistent with presence of progressive tumor in spite of the slightly smaller\ncavity size.\n2. Similar degree of mass effect, rightward midline shift and subfalcine\nherniation.  Stable ventricular configuration\n3. Slight increase in size of the medial left frontal lobe satellite lesion.\n4. Unchanged left temporal infiltrative FLAIR hyperintensities, concerning for\ntumor.\n5. No new lesions or acute intracranial findings.\n6. Of note, the patient was scanned under a claustrophobia protocol and\ntherefore thin sections are not included."
        },
        {
            "input": "Study is degraded by motion.  There is redemonstration of postsurgical changes\nfrom left frontal craniotomy and tumor resection.\n\nThere is redemonstration of a 6.2 x 5.3 x 5.8 cm (5.4 x 5.2 x 6.3 cm on prior\nMRI) left frontal mass with nodular enhancement compatible with known GBM. \nThe lesion exerts mass-effect, resulting in grossly stable 1.5 cm rightward\nmidline shift (previously measuring 1.7 cm) and stable subfalcine herniation. \nThere is stable effacement of the frontal horn with resulting enlargement of\nthe temporal horn of the left lateral ventricle.\n\nThe left frontal lobe hematoma measures 3.4 x 1.3 cm, previously measuring 2.5\nx 1.1 cm.  There is mild  surrounding vasogenic edema.\n\nThe known left paramedian satellite nodule measures 2.6 x 1.8  cm, previously\nmeasuring 2.2 x 1.8  Cm.\n\nThere are no new enhancing lesions identified.",
            "output": "1.  Study is degraded by motion.\n2. Redemonstration of postsurgical changes from left frontal craniotomy and\ntumor resection.\n3. Left frontal mass measuring 6.2 x 5.3 x 5.8 cm, with persistent 1.5 cm\nrightward midline shift and subfalcine herniation.\n4. Left paramedian satellite nodule measures 2.6 x 1.8 cm.\n5. Left frontal hematoma measuring 3.4 x 1.3 cm, previously measuring 2.5 x\n1.1 cm.\n6. Stable effacement of the frontal horn, with resulting entrapment and\nenlargement of the temporal horn of the left lateral ventricle."
        },
        {
            "input": "Patient is status post interval craniotomy for partial resection of of a left\nfrontal lobe mass, with postsurgical changes including a left frontotemporal\nsubgaleal hematoma, regional dural thickening and enhancement, a 7 mm thick\nsubdural fluid collection along the anterior left frontal lobe as well as\nblood products and air within the resection cavity.  Layering blood products\nare noted within the occipital horn of the left lateral ventricle. Again noted\nis adjacent FLAIR signal abnormality within the left frontal lobe.\n\nResidual tumor is present around the margins of the surgical cavity. \nInfiltrating tumor surrounding the enhancing margin and involving the anterior\ncorpus callosum appears unchanged.\n\nThere is no significant interval change in approximately 1.5 cm left to right\nmidline shift and effacement of the anterior horn of the left lateral\nventricle.  There is no ventriculomegaly or evidence for transependymal CSF\nflow. The basilar cisterns remain patent.\n\nThere is no evidence of infarction.  The major intracranial flow voids are\npreserved. The dural venous sinuses are patent",
            "output": "1. Status post interval craniotomy with partial resection of a left frontal\nmass compatible with known GBMs with expected postsurgical changes.\n2. Residual enhancing tumor and infiltrating tumor..\n3. Stable 1.5 cm left to right midline shift with effacement of the left\nlateral ventricle anterior horn.  The basal cisterns remain patent.\n\nNOTIFICATION:  The findings were discussed with ___, M.D. by ___\n___, M.D. on the telephone on ___ at 12:25 am, 5 minutes after\ndiscovery of the findings."
        },
        {
            "input": "As before, there are postsurgical changes related to partial resection of the\nleft frontal lobe mass, including regional dural thickening and enhancement,\nfluid/blood products within the resection cavity and a left frontal subdural\nfluid collection which is decreased in size, now measuring 4 mm in thickness. \nThere has been interval decrease in the overlying subgaleal hematoma.  The\noverall size of the resection cavity appears slightly increased in comparison\nthe prior study, now nearly completely fluid-filled with only trace\npostsurgical air in the non-dependent portions of the cavity.\n\nIn comparison to the previous study, there is increased peripheral enhancement\nsurrounding the superior aspects of the resection cavity, with persistent\nthick nodular heterogeneous enhancement medially and inferiorly compatible\nwith residual tumor.  Residual tumor is again noted in the region of the\nsplenium of the corpus callosum.\n\nSurrounding FLAIR signal abnormality within the left frontal lobe appears\nunchanged, which may reflect any combination of edema, postsurgical changes\nand residual tumor. Additional nonenhancing FLAIR signal abnormalities within\nthe left temporal lobe (series 16, images 11 and 9) are suspicious for\nadditional tumor foci.\n\nAs before, there is subfalcine herniation, complete effacement of the anterior\nhorn of the left lateral ventricle, and unchanged left to right shift of\nnormally midline structures by approximately 14 mm.  The basilar cisterns\nremain patent.\n\nThe dural venous sinuses are patent.  The major intracranial flow voids are\npreserved.  The orbits appear unremarkable.",
            "output": "1. Redemonstrated postsurgical changes related to partial resection of the\nknown left frontal lobe mass, as above.\n2. Increased peripheral enhancement surrounding the superior aspects of the\nresection cavity is nonspecific and may reflect postsurgical changes. \nHowever, persistent heterogeneously nodular enhancement along the medial and\ninferior aspects of the resection cavity indicates residual tumor.  Residual\ntumor is also noted at the splenium of the corpus callosum.\n3. Surrounding FLAIR signal abnormality appears similar to the prior study,\nwhich may reflect any combination of edema, postsurgical changes and residual\ninfiltrating tumor.\n4. Two smaller nonenhancing FLAIR hyperintense foci in the left temporal lobe\nare suspicious for additional tumor foci.\n5. Mass effect appears similar to the prior study, including unchanged\nsubfalcine herniation with 14 mm left to right shift of normally midline\nstructures.  The basilar cisterns remain patent."
        },
        {
            "input": "Postsurgical changes related to partial resection of the left frontal lobe\nmass, including residual dural thickening and enhancement, fluid/blood\nproducts within the resection cavity and left frontal subdural fluid which are\noverall stable.  The overall size of the resection cavity appears unchanged in\nsize from prior exam and is now completely fluid filled.  There is intrinsic\nT1 shortening at the margins of the cavity consistent with blood products.\n\nThere is increased peripheral enhancement surrounding the resection cavity\nwith a thickened nodular heterogeneous enhancement pattern which may be\nconsistent with residual tumor or radiation necrosis in light of recent\ncompletion of radiation therapy.  There is surrounding T2/FLAIR hyperintensity\nwith some areas of curvilinear slow diffusion.  There is no clear new slowed\ndiffusion compared to the previous study, which there is also a rim of slow\ndiffusion of the cavity margins.  However, the extent of surrounding T2/FLAIR\nhyperintensity has increased since the previous examination it is now also\nseen in the superior right frontal lobe in the centrum semiovale, and has\nincreased on the left side on all margins of the cavity.  There is 5 mm\nenhancing FLAIR signal abnormality within the left temporal lobe (series 17:\nImage 76), not visualized on prior exam, concerning for recurrence. \nAdditional surrounding nonenhancing FLAIR signal abnormalities within the left\ntemporal lobe (series 15: Image 11) are again seen and suspicious for\nadditional tumor foci.  Residual tumor is again noted in the region of the\nsplenium of the corpus callosum.\n\nAs before, there is subfalcine herniation, complete effacement of the anterior\nhorn of the left lateral ventricle, and slightly decreased left-to-right shift\nof normally midline structures to approximately 10 mm, previously 14 mm.  The\nbasilar cistern remains patent.\n\nThe dural venous sinuses are patent.  The major intracranial flow voids are\npreserved.  The orbits appear unremarkable.",
            "output": "1. Increased heterogeneously nodular enhancement along the resection cavity\nmay be consistent with residual tumor or evolving radiation necrosis in light\nof recent completion of radiation therapy.  There has been increase in the\nextent of surrounding FLAIR hyperintensity, with signal changes now seen in\nthe right frontal lobe as well.  There is persistent diffusion change along\nthe cavity margins as well.  The FLAIR and diffusion changes can reflect\nprogressive tumor and/or post treatment changes.  Consider examination further\nassessment with perfusion in spectroscopy.\n2. Nonenhancing FLAIR hyperintense foci in the left temporal lobe again seen,\nsuspicious for additional tumor foci.  There has been increase in enhancement\nin the left temporal lobe, which is concerning for tumor progression.  This\ncould also be further assessed with spectroscopy and perfusion.\n3. Redemonstrated postsurgical changes related to partial resection of known\nleft frontal lobe mass, as above.\n4. Persistent subfalcine herniation with 10 mm of left-to-right shift of\nnormally midline structures, decreased from 14 mm.  The basilar cisterns are\npatent."
        },
        {
            "input": "Again postsurgical changes are seen, the patient is status post partial\nresection of a left frontal intra-axial glial mass lesion, there is persistent\nperipheral and nodular enhancement surrounding the surgical cavity, with\nincreased mass effect and shifting of the normal structures towards the left\nwith approximately 17 mm of deviation, and previously 11 mm, additionally\nthere is narrowing of the left perimesencephalic cisterns with left uncal\nherniation and vasogenic edema in the left cerebral peduncle (series 7 and 8,\nimages 11 and 10).  There is persistent heterogeneous enhancement along the\ngenu of the corpus callosum.  Focal areas of enhancement in the left temporal\nlobe are suggestive of satellite lesions which are slightly more conspicuous\nlarger measuring approximately 6.2 mm in transverse dimension and previously\n5.2 mm (series 10, image 10, series 9, image 67).  The pattern of vasogenic\nedema in the left cerebral hemisphere appears grossly unchanged, however now\nthere is increased extension of the vasogenic edema towards the right centrum\nsemiovale (series 7, image 19).  Multiple vascular flow voids are visualized\nwithin the ventral aspect of the left frontal lesion (series 8, image 13),\nindicating hypervascularity.  Focal area of slow diffusion in the mid aspect\nof the heterogeneous mass lesion is suggestive of ischemic changes (series\n402, image 20, series 400, image 20).\n\nThe orbits are unremarkable, the paranasal sinuses, middle ear cavities and\nmastoid air cells are clear.",
            "output": "1.  In comparison with the most recent examination, the heterogeneous\nenhancing lesion in the left frontal lobe demonstrates increased mass effect,\ncausing displacement of the normally midline structures  with approximately 17\nmm of shifting towards the right, previously 11 mm, associated with underlying\nmild left uncal herniation and edema extending towards the left cerebral\npeduncle as described in detail above.\n\n2. Two satellite enhancing lesions in the left temporal lobe appear slightly\nlarger (series 10, image 10, series 9, image 67).\n\n3.  There is also extension and interval increased of the vasogenic edema\ntowards the right centrum semiovale.\n\nNOTIFICATION:  The findings were discussed with ___, M.D. by ___\n___, M.D. on the telephone on ___ at 3:20 pm, 5 minutes after\ndiscovery of the findings."
        },
        {
            "input": "There is new subependymal FLAIR hyperintense nodular enhancement of the roof\nof the fourth ventricle extending into cerebral aqueduct, bilateral dentate\nnuclei, and along right greater than left foramen of Luschka to the right post\nolivary sulcus (series 8, image 4 through 9), and concerning for disease\nprogression.\n\nThe patient is status post prior left frontal craniotomy and underlying left\nfrontal lobe resection, measuring approximately 7.8 x 6.9 cm (AP, TRV),\nslightly increased in size from prior examination, with peripheral nodular and\nheterogeneous enhancement along the margins, extending across the midline to\nthe right frontal lobe, involving the corpus callosum.  Although the mass\neffect on the right frontal horn of the lateral ventricle has decreased from\nprior examination, the degree of right subependymal enhancing FLAIR\nhyperintensities has increased in prominence.  In addition, the degree of\ndiffusion-weighted hyperintense signal lesion has increased in size.\n\nA left temporoparietal 1.4 by 0.7 cm lesion with surrounding FLAIR edema\npattern is similar to prior exam, although there is increased associated\ndiffusion-weighted hyperintensity (series 502, image 15).\n\nThere is no evidence for acute infarct or new intracranial hemorrhage.  There\nis no hydrocephalus.  FLAIR hyperintense signal involving left cerebral\npeduncle extending into the midbrain and pons is compatible with wallerian\ndegeneration and unchanged.  The major intracranial flow voids are preserved. \nThe dural venous sinuses are patent.  No suspicious marrow signal.  The\nparanasal sinuses demonstrates mild mucosal thickening of the ethmoid air\ncells.  The orbits are unremarkable.  No significant fluid signal is seen\nmastoid air cells.",
            "output": "1. New subependymal FLAIR hyperintense nodular enhancement along the roof of\nthe fourth ventricle extending into the cerebral aqueduct, bilateral dentate\nnuclei, and along right greater than left foramen of Luschka to the right post\nolivary sulcus (series 8, image 4 through 9), and concerning for disease\nprogression with leptomeningeal disease.\n2. Left frontal lobe lesion with extension across the midline, involving the\ncorpus callosum and right frontal lobe appears to have increased in size from\nprior exam (with increased involvement of the right frontal lobe) and\nincreased associated diffusion-weighted hyperintense signal.  This could\nrepresent posttreatment effect, however disease progression is not excluded.\n3. Left temporoparietal lobe 1.4 cm lesion is similar in size to prior\nexamination although there does appear to be increased associated\ndiffusion-weighted hyperintensity.  Close attention on follow-up is\nrecommended to exclude progression given the apparent increased diffusion\nhyperintense signal.\n4. No acute infarct or new intracranial hemorrhage.  Additional findings as\ndescribed above.\n\nNOTIFICATION:  The impression and recommendation above was entered by Dr.\n___ on ___ at 11:22 into the Department of Radiology critical\ncommunications system for direct communication to the referring provider."
        },
        {
            "input": "The patient is status post partial resection of a left frontal lobe\nintra-axial glial mass lesion extending towards the anterior corpus callosum,\nthere is essentially unchanged peripheral and nodular enhancement surrounding\nthe surgical cavity,  with unchanged extensive mass effect and  approximately\n15 mm of rightward midline shifting.  Additionally; there is persistent\nnarrowing of the left perimesencephalic cisterns with left uncal herniation,\nand unchanged vasogenic edema in the left cerebral peduncle.\n\nGrossly unchanged heterogeneous enhancement along the genu of the corpus\ncallosum.\n\nFocal areas of enhancement in the left temporal lobe are suggestive of\nsatellite lesions, which are progressively enlarged, measuring approximately\n12 mm in transverse dimension, previously 6 mm.\n\nThere is mild interval progression and increased T2/FLAIR hyperintensity\ninvolving the left frontotemporal, and anterior parietal regions, as well as\nright frontotemporal region.\n\nThere is no acute infarction or acute intracranial hemorrhage.  There is no\ndefinite newly developed areas of abnormal enhancement.  The ventricular\nsystem are mildly enlarged compared to ___ examination.\n\nThe orbits are unremarkable.  The paranasal sinuses, middle ear cavities and\nmastoid air cells are clear.",
            "output": "1. Grossly unchanged  heterogeneous enhancement and nodularity in the left\nfrontal lobe, anterior corpus callosum as described above, consistent tumoral\nglial infiltration and underlying posttreatment changes.\n2. Mild interval increased in the T2/FLAIR pattern of high-signal intensity\nconsistent with vasogenic edema and posttreatment changes.\n3. Focal areas of enhancement in the left temporal lobe are suggestive of\nsatellite lesions, which are progressively enlarged, measuring approximately\n12 mm in transverse dimension, previously 6 mm.\n4. No evidence of acute territorial infarction or acute intraparenchymal\nhemorrhage."
        },
        {
            "input": "There is no evidence of acute intracranial hemorrhage or mass effect. The\nventricles and basal cisterns appear normal for the stated age.\n\nThere are normal vascular flow voids.\nThere is persistent trigeminal artery onto the left side series 101, image 52.\nThere is no evidence of acute ischemia based on diffusion-weighted imaging.\n\nThere are multiple small foci of T2/FLAIR signal hyperintensity in  the\nsubcortical and periventricular white matter in the frontal and parietal lobes\non both sides a which are nonspecific though presumably on the basis of\nchronic small vessel ischemic disease. There is there probable chronic left\ncerebellar hemisphere lacunar infarct/cystic focus.\nSmall FLAIR hyperintense focus is noted in the right side of the cervical\nmedullary region series 11, image 4 which is not clearly seen on the axial T2\nweighted images due to motion and pulsation artifacts. No abnormal enhancement\nnoted in this location.\nThere is no abnormal brain parenchymal or leptomeningeal enhancement.\nPostcontrast images somewhat limited due to pulsation artifacts.\n\n\nIn the left posterior parietal bone superiorly, there is a small, 1.1x0.8cm, \nfocus of increased FLAIR signal (series 11, image #20) with corresponding slow\ndiffusion and possible mild enhancement, the appearance of which could\nrepresent an osseous lesion-?  Metastasis or a vascular focus.\nRecommend correlation with noncontrast head CT or nuclear medicine imaging for\nfurther evaluation.\n\nThe orbits and paranasal sinuses are unremarkable.\nMinimal ethmoidal mucosal thickening. Sphenoid sinus septation inserts on the\nleft carotid groove.\nMinimal amount of fluid in the right mastoid air cells.\n\nLimited assessment of the upper cervical spine for any focal lesions due to\npulsation artifacts on the postcontrast images.\nDedicated imaging of the cervical spine can be considered if needed.",
            "output": "1. No evidence of acute intracranial hemorrhage, mass effect, or acute\nischemia.  No abnormal enhancement in the brain parenchyma.\n2. Brain parenchymal volume loss and presumed sequelae of chronic small vessel\nischemic disease and prior infarcts.\n3. Small focal encephalomalacia within the superior left frontal lobe which\nmay represent sequelae of prior trauma and/ or prior ischemia.\n4. A small 1.1cm focus of increased FLAIR signal and slow diffusion and\npossible mild enhancement in the superior left parietal bone which could\nrepresent a metastatic or vascular lesion. Recommend correlation with\nnoncontrast head CT or nuclear medicine imaging for further evaluation given\nthe history of known skeletal metastases in the spine.\nLimited assessment of the upper cervical spine for any focal lesions due to\npulsation artifacts on the postcontrast images.\nDedicated imaging of the cervical spine can be considered if needed.\n\nNOTIFICATION:\nThe impression above was entered by Dr. ___ on ___ at 11:15\ninto the Department of Radiology critical communications system for direct\ncommunication to the referring provider."
        },
        {
            "input": "There is no evidence of acute intracranial hemorrhage or mass effect. The\nventricles and basal cisterns appear normal.\n\nNo evidence of acute ischemia based on diffusion-weighted imaging. There are\nnormal vascular flow voids.  A brain parenchymal volume is within normal\nlimits.\n\nThere is no abnormal brain parenchymal or leptomeningeal enhancement.\n\n The orbits, skull base, and paranasal sinuses are unremarkable.",
            "output": "Normal MRI of the brain."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  The ventricles and sulci are normal in caliber and\nconfiguration. There is no abnormal enhancement after contrast administration.\nCerebellar and cerebral parenchyma are unremarkable.  Normal flow voids\nwithout occlusion or dissection of the vascular system.  No abnormalities\ninvolving the 6 nerve are identified.",
            "output": "1.  Normal brain MR without evidence of hemorrhage, mass, fracture or infarct."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are within expected limits in\ncaliber and configuration.  A few scattered T2 and FLAIR hyperintense foci in\nthe periventricular and subcortical white matter are nonspecific, but may\nreflect chronic small vessel ischemic changes.\n\n Images through the internal auditory canal demonstrates symmetric appearance\nof the seventh eighth nerve complexes.  No abnormalities are evident along the\ncourse of the ___ cranial nerves.  There is no evidence of abnormal\nenhancement or mass lesion within the internal auditory canals,\ncerebellopontine angles or membranous labyrinth. No other mass lesions are\nseen within the posterior fossa.\n\nThere is no abnormal enhancement after contrast administration.\n\nThe mastoid air cells and middle ear cavities are clear.  The paranasal\nsinuses are clear to the extent visualized.  The intraorbital contents are\nunremarkable.  The major intracranial arterial flow voids are preserved.  The\ndural venous sinuses are patent.",
            "output": "1. No evidence of abnormal mass or contrast enhancement in the\ncerebellopontine angles or prepontine cisterns.\n2. No evidence of acute infarct.\n3. Additional findings described above."
        },
        {
            "input": "There is no intra or extra-axial mass, acute hemorrhage or infarct. No\nabnormal postcontrast enhancement.  Interval development of a single punctate\nT2/FLAIR hyperintense white matter focus of the right frontal centrum\nsemiovale (series 7, image 17) since examination of ___, nonspecific. \nNo suspicious parenchymal FLAIR hyperintense signal.  The sulci, ventricles\nand cisterns are within expected limits for the patient's age.  No\ndisproportionate mesial temporal volume loss.  Partially empty sella,\nunchanged from prior exam.  The major intracranial flow voids are preserved. \nThe dural venous sinuses are patent.  There is mild mucosal thickening of the\nethmoid air cells.  The orbits are unremarkable.  Trace fluid signal is seen\nin the mastoid air cells.  No suspicious osseous lesions.",
            "output": "1. No evidence of intracranial metastatic disease.  No abnormal enhancement or\nmass.\n2. No acute infarct or intracranial hemorrhage.\n3. Interval development of a single punctate T2/FLAIR hyperintense white\nmatter focus of the right frontal centrum semiovale, nonspecific.  No\nsuspicious FLAIR hyperintense parenchymal lesions.\n4. Additional findings described above."
        },
        {
            "input": "The examination is limited by motion. There is re-demonstration of a solitary\nenhancing lesion within the medial left occipital lobe measuring approximately\n1.8 x 1.6 x 2.0 cm ((series 4, image 92). This lesion demonstrates regions of\nperipheral slow diffusion and surrounding vasogenic edema. The overall\nappearance is similar compared to the outside study dated ___.  No\nnew lesions are seen. No evidence of interval infarction or midline shift. \nDural venous sinuses are patent.",
            "output": "Stable 1.8 cm enhancing lesion within the medial left occipital lobe\nconsistent with metastases. No new lesions are seen within the limitations of\nthe study."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.\n There are scattered T2/FLAIR hyperintensities in the cerebral hemispheres\nbilaterally, a nonspecific finding but unchanged and likely related to chronic\nsmall vessel ischemic changes.\n\nAgain noted is parenchymal volume loss predominantly affecting the sylvian\nfissures, parietal lobes and occipital lobes bilaterally as well as the\nposterior aspect of the corpus callosum.  Stable prominence of the ventricular\nsystem and extra-axial CSF spaces is consistent with the previously mentioned\nparenchymal volume loss.\nUnchanged low lying cerebellar tonsils, approximately 2-3 mm below the level\nof the foramen magnum.\n\nMajor vascular flow voids are preserved\n\nThere is mild mucosal thickening along the ethmoid air cells.  The remainder\nof the paranasal sinuses and mastoid air cells are clear.  The orbits appear\nunremarkable.",
            "output": "1. No significant intracranial abnormality.  No evidence of acute infarction,\nhemorrhage or mass.\n2. Unchanged parenchymal volume loss predominantly affecting the sylvian\nfissures, parietal and occipital lobes bilaterally as well as the posterior\naspect of the corpus callosum.\n3. Unchanged low-lying cerebellar tonsils."
        },
        {
            "input": "Again noted are heterogeneously enhancing lytic lesions in the left frontal\nand left parietal calvarium with regional edema and slow diffusion and post\nbiopsy changes.  The left parietal lobe lesion measures up to 1.4 cm in\nthickness, previously 1.6 mm on ___.  The left frontal calvarium\nlesion appears grossly unchanged.  There is stable mild dural thickening and\nenhancement underlying the left frontal greater than left parietal lesions. \nNo underlying parenchymal enhancement or slow diffusion is noted at either\nlocation on the current study.  No new calvarial lesion is identified.\n\nThere is questionable mild enhancement and increased heterogeneity involving\nthe clivus in comparison the prior study, which may reflect lymphomatous\ninvolvement versus post treatment changes (compare current study 10:32 to the\n___ MRI 9:36).\n\nFLAIR hyperintense white matter signal within the right parietal lobe (8:14)\nappears slightly increased in comparison to the prior study.  Additional\nsmaller periventricular and subcortical T2/FLAIR hyperintense foci appear\nunchanged, and are nonspecific but may reflect chronic sequela of small vessel\nischemic changes.\n\nThere is no evidence of acute infarct, intracranial hemorrhage, mass effect or\nmidline shift.  The ventricles and sulci are normal in caliber and\nconfiguration.  There is no evidence of abnormal brain parenchymal\nenhancement.\n\nThere are mild ethmoid sinus mucosal inflammatory changes.  There is trace\nnonspecific fluid within the left mastoid air cells.  The orbits and globes\nappear unremarkable.",
            "output": "1. Redemonstrated heterogeneously enhancing lytic lesions in the left frontal\nand left parietal calvarium with regional edema and mild slow diffusion as\nwell as post biopsy changes.  The left parietal lobe lesion appears slightly\ndecreased in size and the left frontal calvarium lesion appears unchanged,\nwith stable mild dural thickening and enhancement underlying the left frontal\ngreater than left parietal lesions.  No evidence of brain parenchymal\nenhancement or new calvarial lesion.\n2. Questionable mild enhancement and increased heterogeneity involving the\nclivus in comparison the prior study, which may reflect lymphomatous\ninvolvement versus post treatment changes.\n3. FLAIR hyperintense signal within the right parietal lobe (8:14) appears\nslightly increased in comparison the prior study.  Additional white matter\nT2/FLAIR hyperintensities appear unchanged and are nonspecific but compatible\nwith chronic small vessel ischemic changes.\n4. No acute intracranial hemorrhage, acute infarct or significant mass effect."
        },
        {
            "input": "Again noted are heterogeneously enhancing lesions in the left frontal and left\nparietal calvarium with regional edema,  slow diffusion and post biopsy\nchanges.  There is no significant interval change in the extent of the\ncalvarial signal abnormalities as well as opposing minimal dural thickening. \nNo new calvarial lesion is identified.\n\nThere is redemonstration of clival intrinsic T1 hyperintense signal intensity\nwhich could be related to fatty infiltration related to post therapeutic\nchanges with unchanged associated heterogenous enhancement.\n\nBilateral multifocal predominantly left cerebral hemisphere nonenhancing T2\nFLAIR hyperintensities are unchanged. There is no evidence of acute infarct,\nintracranial hemorrhage, mass effect or midline shift.  The ventricles and\nsulci are normal in caliber and configuration.  There is no evidence of\nabnormal brain parenchymal enhancement.\n\nThere are mild ethmoid sinus mucosal inflammatory changes.  There is trace\nnonspecific fluid within the left mastoid air cells.  The orbits and globes\nare unremarkable.",
            "output": "1. There is no imaging signs to suggest meningitis, abscesses or cerebritis.\n2. Stable appearance of left frontal and left parietal calvarial signal\nabnormalities with opposing minimal dural thickening.\n3. Stable bilateral predominantly left cerebral hemisphere nonenhancing white\nmatter signal abnormalities.\n4. Stable appearance of clival and middle cranial fossa osseous heterogeneity\nlikely related to posttreatment changes."
        },
        {
            "input": "Study is moderately degraded by motion.  MPRAGE images are severely degraded\nby motion.  Within these confines:\n\nGrossly stable heterogeneously enhancing left frontal and parietal calvarial\nosseous lesions with adjacent probable edema and slow diffusion, and\npostoperative changes are again seen.  Nonspecific dural enhancement adjacent\nto these areas is also grossly unchanged compared to ___ prior\nexam.\n\nThere is no evidence of hemorrhage, mass effect, midline shift or\nacute/subacute infarction.  The ventricles and sulci are grossly stable in\ncaliber and configuration, without definite evidence of ventriculomegaly. \nPeriventricular and subcortical T2 and FLAIR hyperintensities are noted which\nmay represent small vessel ischemic and/or treatment related changes.\n\nMinimal left frontal and bilateral maxillary and sphenoid sinus, and bilateral\nethmoid air cell mucosal thickening is present.  Minimal grossly stable\nnonspecific left greater than right mastoid fluid is present.  Previously\nnoted left temporal scalp probable skin tag is partially visualized, though\nevaluation is limited secondary to artifact (see 11:11; 10:68 on current\nstudy; 10:85 on ___ prior brain MRI; and 5:17 on ___\nnoncontrast head CT).",
            "output": "1.  Limited study as described.\n2. No acute intracranial abnormality, with no definite evidence of acute\ninfarct.\n3. Grossly stable left frontal and parietal calvarial osseous lesions and\nprobable postoperative changes as described.\n4. Within limits of study, no definite evidence of new intracranial enhancing\nmass.\n5.  Paranasal sinus disease, as described.\n6.  Additional findings as described above."
        },
        {
            "input": "Re-identified is the T1 hypointense, infiltrative enhancing mass centered in\nthe left frontal calvarium, measuring up to 4.0 x 3.7 x 2.9 cm (TV by AP by\nSI) (10:19 and 900:61).  The lesion demonstrates restricted diffusion (series\n502 and 500, image 17).  The mass appears centered in the left frontal\ncalvarium, which demonstrates a permeative, lytic appearance.  The mass\nextends through the bone both superficial to the calvarium to involve the\nscalp, where there is a prominent, centrally nonenhancing central component\nwhich could represent necrosis (10:19); and also deep to the calvarium to\ninvolve the subjacent dura, which is thickened eccentrically, measuring up to\n8 mm in width (see series 10, image 17 and series 9, image 110).\n\nThere are multiple additional less apparent but similar osseous skull lesions,\nnumber at least 5, for which involve the calvarium, including the left frontal\nand parietal calvarium (502:70), as well as the right parietal skull (502:18);\nthese also demonstrate T1 hypointensity and patchy enhancement, without scalp\nsoft tissue components.  The largest these additional lesions measures up to\n4.8 x 2.1 cm (502:19).\n\nThere is an additional lesion involving the right skull base involving the\nclivus and right sphenoid, extending into the very superior aspect of the\nright pterygoid plate (series 4, images 6, 5, and 4, as well as series 502,\nimage 5; series 10, images ___.  Note that the intracranial ICA/carotid canal\npasses just superior to the involved skullbase (series 900, images 88 and 90).\n\nThe enhancing dural thickening which is thickest just deep to the left frontal\nlesion extends posteriorly to involve the parietal dura, involving much of the\nAP length of the head (see series 10, image 17).\n\nThere is no evidence of infarction, hemorrhage, extra-axial collection, or\nintracranial mass effect. No abnormal brain parenchymal enhancement.\n\n The ventricles and sulci are normal in caliber and configuration.\n\nThere is a focus of deep and subcortical white matter FLAIR hyperintensity in\nthe left parietal lobe (07:13), without enhancement, demonstrating T1\nhypointensity.  Additional background supratentorial periventricular deep\nwhite matter FLAIR hyperintensities are noted elsewhere, left more than right.\n\nThe visualized paranasal sinuses and mastoids appear clear.  The globes and\norbits are unremarkable.  Major intracranial vascular flow voids are\npreserved.  Major dural venous sinuses are patent.",
            "output": "1. Multiple enhancing osseous lesions, numbering at least 6, the two (2)\nlargest of which show permeative changes within the involved bony calvarium,\ninvolving primarily the left frontal and parietal calvarium, but also the\nright parietal calvarium and the right skullbase (clivus, sphenoid).  The\ndominant lesion the left frontal calvarium has a prominent superficially\nextending soft tissue component with central necrosis.  There is a large area\nof enhancing dural thickening contiguous with deep extension of the large left\nfrontal lesion extending over much of the left frontoparietal convexity,\nmeasured 8 mm, consistent with dural extension of disease.  Given\nmultifocality, findings raise concern for metastasis, differential includes\nlymphoma.\n2. No abnormal brain parenchymal enhancement.\n3. Prominent FLAIR hyperintensity in the left parietal subcortical and deep\nwhite matter is nonspecific, and could reflect demyelination.\n4. Mild-to-moderate changes of chronic white matter microangiopathy."
        },
        {
            "input": "Multiple heterogeneously enhancing T1 hypointense lesions are demonstrated\nthroughout the calvarium, some of which are new:\n\n-Heterogeneous enhancement involving the right vertex (9:148, 901: 109) was\nnot clearly seen on the previous study which could be related to differences\nin angulation.\n-More conspicuous right parietal heterogeneous enhancement, similar in size\n(9:128, 901:111).\n-Larger focus of heterogeneous enhancement involving the left parietal cranium\n(9:115, 901:114), demonstrating worse diffusion restriction.\n-Larger focus of heterogeneous enhancement involving the left frontal\ncalvarium (9:129, 901:47), demonstrating unchanged diffusion restriction. \nUnchanged extension into the epidural space, measuring up to 8 mm.  Unchanged\nextension into the scalp.  However, smaller peripherally enhancing collection,\nlikely necrosis, within the scalp extension, now measuring 7 mm x 9 mm,\npreviously 1.3 cm x 1.2 cm.\n-Unchanged heterogeneous enhancement involving the left occipital calvarium\n(9:79, 900:66).\n-Unchanged right clival/sphenoid wing/pterygoid plate enhancement (09:43,\n901:71).\nA previously seen epidural lesion in the right posterior parietal region,\nadjacent to the superior sagittal sinus, measures 8 mm x 10 mm (9:108, and\n101:131), unchanged.  The adjacent superior sagittal sinus appears patent.\n\nThere is larger focus of T2/FLAIR signal abnormality involving the left\nparietal lobe (06:14).  Other foci of T2/FLAIR signal abnormality are\nre-demonstrated in the bilateral frontal and bilateral parietal lobes,\nunchanged.\n\nThe ventricles and sulci are normal in caliber and configuration.  There is no\nhemorrhage or infarct.  The paranasal sinuses, mastoid air cells and middle\near cavities are clear.  The intraorbital contents are normal.",
            "output": "1. Heterogeneously enhancing lesion at the right parietal bone was not\nvisualized on the previous study and could be a new lesion versus better\nvisualization secondary to differences in angulation.\n2. Previously seen left frontal calvarial lesion demonstrates increased\nenhancement within the bony structures and demonstrates worse diffusion\nrestriction.  Unchanged extension into the epidural space and scalp.  Smaller\nperipherally enhancing scalp collection, likely necrosis.\n3. Previously seen left parietal calvarial lesion is larger and demonstrates\nworse diffusion restriction.\n4. Previously seen right parietal lesion appears more conspicuous, similar in\nsize.\n5. Unchanged heterogeneously enhancing lesions in the left occipital calvarium\nand right clivus/sphenoid wing/pterygoid plate.\n6. Unchanged epidural lesion in the right posterior parietal region, adjacent\nto a patent superior sagittal sinus.\n7. Slightly larger focus of FLAIR signal abnormality involving the left\nparietal lobe.  Other foci of abnormal signal involving the bilateral frontal\nand parietal lobes are unchanged.  These are nonspecific and may represent\nareas of demyelination or posttreatment changes.\n8. No acute infarct or intracranial hemorrhage.\n\nNOTIFICATION:   The findings were discussed with ___, M.D. by ___\n___, M.D. on the telephone on ___ at 10:22 am.."
        },
        {
            "input": "Again seen are multiple heterogeneously enhancing T1 hypointense lesions\nthroughout the calvarium involving the right vertex, bilateral parietal, left\noccipital and left frontal calvarium which demonstrate restricted diffusion.\n\nThere has been decrease in size of the epidural extension along the left\nfrontal calvarium which is now reduced to merely thickening of the dura but no\nsoft tissue component (series 9, image 140).\nThe extension into the scalp appears also smaller in size with stable\nappearance of the hypointense, likely necrotic collection.\n\nThe previously seen epidural lesion in the right posterior parietal lesion,\nadjacent to superior sagittal sinus has decreased in size. The superior\nsagittal sinus remains patent.\n\nThere is unchanged heterogeneous enhancement involving the right\nclival/sphenoid wing/pterygoid plate (series 9, image 56 and series 900, image\n88) and measuring 24 x 15 x 17 mm (AP X TR X SI).\n\nStable nonenhancing focus of T2/FLAIR hyperintensity in the left parietal lobe\n(series 7, image 16).  Other nonenhancing foci of T2/FLAIR signal abnormality\nare again identified and appear unchanged.\n\nThere is no evidence of acute infarction or intracranial hemorrhage.\n\nThe ventricles and sulci are normal in caliber and configuration.\n\nThe paranasal sinuses, mastoid air cells and middle ear cavities are clear. \nThe intraorbital contents are normal.",
            "output": "1. Decrease in the size of the right posterior parietal and the left frontal\nlesions which extend into the scalp and dura.\n2. Otherwise, no significant change in the heterogeneously enhancing lesions\nthroughout the calvarium and right clival/sphenoid wing/pterygoid plate.\n3. Stable nonenhancing foci of T2/FLAIR hyperintensity in the frontal and\nparietal lobes."
        },
        {
            "input": "There is redemonstration of multiple areas of heterogeneous infiltrative\nenhancement throughout the calvarium, predominately in the left frontal and\nleft parietal regions as well as the skullbase and clivus.  These regions also\ndemonstrate restricted diffusion.\n\nThere is mild persistent dural thickening and enhancement involving the left\nfrontal region, and to a much lesser extent the left parietal region, slightly\ndecreased compared to prior exam.  No definite epidural soft tissue component.\n\nAdditionally, there has been interval further decrease in size/near resolution\nin the right posterior parietal lesion, adjacent to the superior sagittal\nsinus.\n\nOtherwise, there is no evidence of abnormal parenchymal or leptomeningeal\nenhancement.\n\nThere is no evidence of acute infarction or hemorrhage.  The ventricles and\nsulci are age-appropriate.  No mass effect or midline shift.  The major\nintracranial arterial flow voids are preserved.  The dural venous sinuses are\npatent.\n\nScattered T2/FLAIR hyperintense areas in the periventricular and subcortical\nwhite matter, predominately in the left frontal and left parietal regions, are\nnonspecific, and likely reflect a combination of post treatment changes,\ndemyelination, and/or chronic small vessel ischemic changes.\n\nMinimal mucosal thickening of the ethmoid sinuses.  Mild left and trace right\nfluid signal in the mastoid air cells.  Unremarkable intraorbital contents.",
            "output": "1. Multiple stable heterogeneous infiltrative enhancing lesions throughout the\ncalvarium, predominantly in the left frontal and left parietal regions and\nskullbase.  Mild persistent dural thickening enhancement along left frontal\nand left parietal regions, slightly decreased compared to prior exam.\n2. No evidence of epidural soft tissue tumor, markedly decreased/essentially\nresolved from prior exams.\n3. No abnormal parenchymal or leptomeningeal enhancement.\n4. No acute infarction or intracranial hemorrhage."
        },
        {
            "input": "Study is moderately degraded by motion.  Within these confines:\n\nDiffuse calvarial/skullbase marrow signal abnormalities are again noted.\n\nGrossly stable periventricular and subcortical T2 and FLAIR hyperintensities\nare noted which may represent small vessel ischemic and/or treatment related\nchanges.\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   There is prominence of the ventricles and sulci, unchanged.\n\nMinimal bilateral ethmoid air cell and maxillary sinus mucosal thickening is\npresent.  Nonspecific left mastoid fluid is seen.  An approximately 3 mm left\nfrontal scalp lesion not definitely seen on ___ prior exam is noted\n(see 9:93).",
            "output": "1. Study is moderately degraded by motion.\n2. Redemonstration of patient's known diffuse osseous metastatic disease\ncompared to ___ contrast brain MRI.\n3.  Within limits of study, no definite evidence of enhancing intracranial\nmass.\n4. Left frontal scalp probable sebaceous cyst.  If concern for dermal lesion,\nconsider correlation with direct examination."
        },
        {
            "input": "Again seen are diffuse calvarial/skullbase marrow signal abnormalities. \nPreviously noted focally increased FLAIR signal abnormalities in the left\nfrontal and left parietal calvarium have increased in size and enhancement in\ncomparison to the prior study.  New since the prior study, there is diffuse\npachymeningeal enhancement, which may be reactive from worsening calvarial\nmetastatic disease versus secondary to lymphomatous involvement of the\npachymeninges.  No leptomeningeal enhancement is seen.  No discrete new lesion\nis identified.\n\nNo evidence of acute intracranial hemorrhage, edema, mass effect, midline\nshift or acute territorial infarction.  Stable periventricular and subcortical\nT2/FLAIR hyperintensities are noted which may reflect microvascular ischemic\nchange and/or treatment related changes.\n\nSmall left frontal scalp lesion appears grossly unchanged (9:84). Paranasal\nsinus mucosal thickening and small left mastoid effusion appear unchanged. \nThe orbits and globes appear grossly unremarkable.",
            "output": "1. Redemonstrated diffuse calvarial and skullbase marrow signal abnormalities,\nwith focally increased FLAIR signal and enhancement within the left frontal\nand left parietal calvarium compatible with progression of disease.\n2. New since prior study, diffuse pachymeningeal enhancement is noted which\nmay be reactive from worsening calvarial metastatic disease versus secondary\nto lymphomatous involvement of the pachymeninges. No leptomeningeal\nenhancement.  No discrete new lesion is identified.\n3. Stable periventricular and subcortical T2/FLAIR hyperintensities are noted\nwhich may reflect chronic microvascular ischemic change and/or treatment\nrelated changes.\n\nNOTIFICATION:  The findings were discussed with Dr. ___ by ___\n___, M.D. on the telephone on ___ at 1631 hours, 10 minutes after\ndiscovery of the findings."
        },
        {
            "input": "There is calvarial T2/FLAIR hyperintensity and enhancement in the left frontal\nand parietal bone.  The degree of enhancement and T2/FLAIR hyperintensity\nappear more pronounced when compared to prior MRIs.  There is associated thick\ndural enhancement in the left parietal region (9:122).  These findings could\nbe related to post biopsy changes versus progression of disease.\n\nThe previously noted scattered foci of T2/FLAIR hyperintensity in the left\ncerebral hemisphere appear to be stable in size when compared to most recent\nMRI dated ___, but demonstrate slight progressive increase since MRI\ndated ___.  These focal lesions do not demonstrate enhancement. \nOtherwise no new lesions identified.\n\nThere is no evidence of an acute infarct or intercranial hemorrhage.  The\nventricle, sulci, and cisterns are symmetric and age-appropriate.  The\nvisualized flow voids are preserved.  The pituitary, suprasellar cistern,\nbrainstem, and posterior fossa are unremarkable.  Unchanged effusions in the\nbilateral mastoid air cells, greater on the left.",
            "output": "1. Interval increase of T2/FLAIR hyperintensity, calvarial enhancement, and\nadjacent pachymeningeal enhancement involving the left frontal and parietal\nbone which could be related to post biopsy changes versus progression of\ndisease.\n2. Stable scattered foci of T2/FLAIR hyperintensity in the left cerebellar\nhemisphere when compared to most recent MRI, but progressively increased since\nMRI dated ___.\n3. Additional findings as described above."
        },
        {
            "input": "As before, there is calvarial T2/FLAIR hyperintensity, enhancement and slowed\ndiffusion involving the left frontal and parietal bones in the region of prior\ncraniotomies.  Underlying dural thickening and enhancement in both of these\nregions appears grossly similar in comparison the prior study, which may be\nreactive versus secondary to neoplastic involvement.  Increasing enhancing\ntissue within the left parietal calvarium demonstrates increased mass effect\non the underlying dura, now with a convex appearance, suggesting tumor\nprogression with soft tissue breakthrough.  Several other patchy regions of\ncalvarial enhancement are again seen, the largest of which is in the right\nhigh parietal lobe, which appears slightly more prominent in comparison to the\nprior study with the suggestion of slow diffusion.\n\nQuestion mild enhancement involving the skullbase at the clivus and right\nsphenoid, which appears grossly unchanged in comparison to previous MRIs.\n\nThere is no evidence of hemorrhage, midline shift or acute infarction.  A\nfocus of deep and subcortical white matter FLAIR hyperintensity in the left\nparietal lobe without enhancement appears grossly unchanged, given differences\nin technique.  Additional scattered left greater than right periventricular\ndeep white matter FLAIR hyperintensities also appear stable and are\nnonspecific but may be related to treatment related changes and/or chronic\nmicroangiopathy.  No evidence of hydrocephalus.\n\nMajor intracranial flow voids are present.  The internal venous sinuses are\npatent.\n\nThe paranasal sinuses appear grossly clear.  There is a small left mastoid\neffusion.  The orbits and globes appear within normal limits.",
            "output": "1. Again seen is calvarial metastatic disease, most prominent in the left\nfrontal and left parietal skull.\n2. Grossly stable underlying dural thickening and enhancement may be reactive\nversus secondary to neoplastic involvement.\n3. Increasing enhancing tissue within the left parietal calvarium with\nincreased mass effect on the underlying dura, now convex, suggesting tumor\nprogression with soft tissue breakthrough.\n4. Several other patchy regions of calvarial enhancement are again seen, the\nlargest of which is in the right high parietal lobe, which appears slightly\nmore prominent with the suggestion of slow diffusion.\n5. White matter FLAIR hyperintensity in the left parietal lobe without\nenhancement appears grossly unchanged, given differences in technique.\nAdditional scattered left greater than right periventricular deep white matter\nFLAIR hyperintensities are nonspecific but appear stable."
        },
        {
            "input": "ORBITS: The bony orbits and preseptal soft tissues are normal. The globes are\nintact and appear normal in appearance. The optic nerves and complex are\nnormal, without edema or abnormal enhancement after contrast administration. \nThe extraocular muscles are uniform in size and normal in signal. The lacrimal\napparatus is normal. Retrobulbar soft tissues are normal.\n\nOTHER FINDINGS: \n\nThere is redemonstration of left frontal and parietal calvarial T2/FLAIR\nsignal hyperintensity and enhancement in the region of the prior craniotomy\nsites with similar underlying dural thickening and enhancement, unchanged\nsince the prior study.  There is similar soft tissue enhancement in the left\nparietal calvarium with persistent convex appearance of the inferior margin\nand resulting mass effect on the underlying dura.  There is redemonstration of\nseveral additional areas of ill-defined calvarial contrast enhancement with\nthe largest area in the high right parietal region, not significantly changed\nsince the prior study.  There is question enhancement is seen in the right\nclivus and sphenoid, slightly less pronounced in the right clivus compared to\nthe previous study.\n\nThe remaining imaged portion of the brain demonstrate foci of T2/FLAIR signal\nhyperintensity in the deep and subcortical white matter predominantly in the\nleft frontal and left parietal lobes, partially evaluated and similar to the\nprior study.  Additional scattered periventricular white matter FLAIR signal\nhyperintensities are again noted, nonspecific and may be related to treatment\nrelated changes and or chronic microangiopathy. The cavernous sinuses are\nunremarkable. The imaged paranasal sinuses and mastoid air cells are clear.",
            "output": "1. No definite intraorbital mass lesion, edema or abnormal enhancement.\n2. Similar calvarial metastatic disease, most pronounced in the left frontal\nand parietal calvarium with unchanged mass effect on the underlying dura of\nthe left parietal lesion suggesting soft tissue breakthrough.  Superimposed\ninfection cannot be excluded in the appropriate clinical setting.  Correlate\nclinically for further evaluation.\n3. Persistent underlying dural thickening and enhancement, possibly reactive\nchanges versus secondary to neoplastic involvement.\n4. No significant interval change in appearance of several ill-defined areas\nof calvarial enhancement, predominately in the high right parietal lobe."
        },
        {
            "input": "Study is mildly degraded by motion.\n\nThe pre-existing calvarial lesions in the left parietal and frontal bone are\nagain noted.  The lesion in the left parietal bone demonstrate slight interval\nincrease in size, now measuring 3.9 x 2.1 x 4.1 cm (AP, transverse, SI), as\ncompared to 3.6 x 1.7 x 3.2 on MR dated ___. There is persistent\nindentation on the adjacent thickened dura, resulting in mild mass effect on\nthe adjacent brain parenchyma. This lesion shows interval decreased internal\nenhancement, has intermediate T1 and T2 signal and diffusion restriction.\n\nThe left frontal calvarial lesion continues to demonstrate patchy enhancement,\nand grossly unchanged since MRI dated ___.\n\nThe previously noted patchy contrast-enhancement in the right parietal bone is\ngrossly unchanged.  Stable questionable diffuse enhancement involving the\nclivus and the sphenoid bone.\n\nThere is no intracranial enhancement.  There is no evidence of an acute\ninfarct, midline shift, or hemorrhage. The ventricles and sulci are stable in\ncaliber and configuration.  The visualized vascular flow voids are grossly\npreserved.  The paranasal sinuses are clear.  Stable small effusion in the\nleft mastoid air cells.\n\nLeft frontal scalp probable skin tag is again seen (see 9: 84 on current study\nand 9:88 on ___ prior exam).",
            "output": "1.  Study is mildly degraded by motion.\n2. Minimal interval increase in size of the right parietal calvarial lesion\nwith associated a mass-effect on the adjacent thickened dura and the\nunderlying brain parenchyma.  This finding may be secondary to neoplastic\ninvolvement; however infectious process cannot be excluded.\n3. The remaining calvarial lesions are grossly stable since MRI dated ___.\n4.  Within limits of study, no definite evidence of enhancing intraparenchymal\nmasses."
        },
        {
            "input": "The pre-existing calvarial lesions in the left parietal and frontal bone are\nessentially unchanged in signal characteristics.  The lesions again show T1\nhypointensity, T2 hyperintensity with corresponding heterogenous postcontrast\nenhancement and increased DWI signal intensity.  The right frontal lesion is\ndifficult to accurately assess given poorly defined margins though is grossly\nunchanged in size.  The left parietal calvarial lesion may be marginally\nsmaller measuring up to 1.6 cm in thickness (901:111), previously 1.8 cm. \nAdditionally, the degree of associated dural thickening of appears decreased.\n\nThe previously noted patchy contrast-enhancement in the right parietal bone is\nunchanged with minimal persistent unchanged residual increased DWI signal\nintensity.  Essentially unchanged questionable diffuse enhancement involving\nthe clivus and the sphenoid bone.\n\nThere is no intracranial enhancement.  There is no evidence of an acute\ninfarct, midline shift, or hemorrhage. The ventricles and sulci are stable in\ncaliber and configuration. No acute intracranial hemorrhage or infarct is\nidentified. Periventricular and subcortical white matter T2/FLAIR\nhyperintensities are nonspecific but likely sequelae of chronic small vessel\nischemic disease.  The T2/FLAIR hyperintense left parietal lesion (7, 8:14) is\nunchanged given differences in technique in similar appearance overall\ncompared to more remote exam from ___.  Of note, some of this\nregion did not demonstrate the visualized vascular flow voids are grossly\npreserved.\n\nMucosal thickening noted in the ethmoid air cells.  Stable small effusion in\nthe left mastoid air cells.",
            "output": "1. Essentially unchanged left frontal calvarial lesion with unchanged\nquestionable subtle findings in the right parietal calvarium as seen\npreviously.  No new lesion.\n2. Minimal decrease in overall size and associated underlying degree of dural\nthickening of the left parietal calvarial lesion compared to prior.\n3. No acute intracranial abnormality or abnormal new intracranial enhancement."
        },
        {
            "input": "There is redemonstration of heterogenously enhancing T1 hypointense lesions in\nthe left frontal and parietal calvarium with regional edema and slow\ndiffusion, grossly unchanged since the prior study from ___. \nThe left parietal lesion measures 1.6 cm in thickness, unchanged in size since\nthe prior study.  The irregular left frontal calvarial lesion is difficult to\nmeasure and appears unchanged in size.  There is similar dural thickening and\nenhancement underlying the calvarial lesions.  There is similar mild patchy\nenhancement ill-defined enhancement along the posterior right parietal bone\nwith minimal associated slow diffusion (series 9, image 127) is much less\nappreciated.  There is minimal enhancement along the right clivus (series 9,\nimage 34).  There is similar scattered subcortical and periventricular FLAIR\nsignal hyperintensity, nonspecific but likely sequelae of chronic small vessel\ndisease.  The T2/FLAIR signal hyperintensity in the left parietal lobe is\nunchanged.  There is no evidence of hemorrhage, edema, mass effect, midline\nshift or infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.\n\nThere is diffuse mucosal thickening throughout the frontal sinus, sphenoid and\nmultiple ethmoid air cells.  Trace fluid signal intensity is noted in the\nbilateral mastoid air cells.",
            "output": "1. No significant interval change and left frontal and parietal lesions \ncompared with ___.\n2. Similar dural thickening and enhancement underlying the calvarial lesions.\n3. Essentially unchanged nonspecific FLAIR signal abnormality in the left\nparietal lobe compared with the prior study from ___.\n4. No acute intracranial process or new lesions.\n5. Paranasal sinus disease and trace bilateral mastoid fluid."
        },
        {
            "input": "There is no intracranial hemorrhage. There is a 3 mm focus of hyperintensity\non diffusion-weighted images within the left cerebellum (series 502, image 9).\nThis focus does not demonstrate hypo intensity on ADC weighted images. It is\nbright on T2 and FLAIR images and does not demonstrate contrast enhancement.\n\nThe ventricles and sulci are normal in caliber and configuration. Major\nintravascular flow voids are preserved. There is normal opacification of the\nmajor intracranial arteries and dural venous sinuses following contrast\nadministration.\n\nThe paranasal sinuses and mastoid air cells are clear. The orbits are normal.",
            "output": "1. No evidence of metastatic disease.\n2. Small 3 mm focus of high FLAIR hyperintensity within the left cerebellum.\nThis focus is hyperintense on diffusion weighted images, although this may be\ndue to T2 shine through as no corresponding hypointensity is seen on ADC\nweighted images. This lesion is nonenhancing. This focus may be a subacute or\nold infarct."
        },
        {
            "input": "Tumor:\nThere is a large, intra-axial, heterogeneously enhancing mass centered on left\ntemporal lobe., Extending into the left inferior insula, mass-effect on\ndisplacement of the basal ganglia.  Moderate edema extends into frontal,\ntemporal, inferior parietal lobes.\nTumor measures 6.1 x 4.7 x 4.4 cm (14:12, 100:80), predominantly enhancing,\nwith cystic components.  Small area of restricted diffusion within the tumor.\nRightward midline shift measuring approximately 7 mm.  Left uncal herniation,\neffaced left perimesencephalic cistern, mass-effect on the upper left\nmidbrain, cerebral peduncle.  No hydrocephalus, no ventricular trapping. \nSmall area of mineralization of the posterior aspect of the tumor and punctate\nfoci of increased signal on gradient images.  Mass effect on and medial\ndeviation of the left optic pathways.\nMild asymmetric enhancement along the dura left anteromedial middle cranial\nfossa, likely from prominent vasculature, no definite direct tumor extension. \nPatent left cavernous sinus, with tumor abutting its lateral wall.\nTumor is similar compared with CT head ___.\nTumor abuts left M1, M 2, M3 branches.  Patent and probably moderately\nnarrowed P 2, P3 segment left PCA secondary to uncal herniation..  Partially\neffaced prepontine cistern, suprasellar cistern.  No tonsillar herniation.\n\nOther findings:\nMild-to-moderate opacification bilateral mastoids.  Preserved vascular flow\nvoids.  No other brain lesions, no bone lesions..  No acute infarct.  Patent\ndural venous sinuses.",
            "output": "1. 6.1 cm mass left temporal lobe, moderate surrounding edema.  Small areas of\nintratumoral mineralization.  Findings likely represent high-grade glioma,\npossibly solitary metastasis.\n2. 7 mm midline shift, left uncal herniation, moderate narrowing left P3 PCA\nsegment."
        },
        {
            "input": "There are expected interval postoperative changes from left sided craniotomy\nand resection of the previously demonstrated temporal lobe mass.\n\nThe vast majority of the previously demonstrated enhancing left temporal lobe\nlesion is no longer identified.  There is a small amount of thickened,\nenhancing soft tissue at the very deep, posteromedial aspect of the resection\ncavity, which measures up to 6 mm in thickness, involving the deepest,\nposteromedial quadrant of the resection cavity, likely small volume residual\ntumor.\n\nElsewhere, surrounding the resection cavity, there is thin, linear\npostsurgical enhancement and a thin rim of devitalized tissue, within expected\nrange.\n\nFLAIR hyperintense signal in the white matter surrounding the resection cavity\nis stable.\n\nMass-effect is mildly improved, including 4 mm of rightward shift of midline,\npreviously 6-7 mm.  There remains mild left uncal herniation, although less\npronounced than on the prior.  There is no hydrocephalus or ventricular\nentrapment.\n\nElsewhere, there is no unexpected hemorrhage, parenchymal edema, acute\ninfarction, new mass or abnormal enhancement.\n\nThe visualized paranasal sinuses are clear.  There are partial bilateral\nmastoid effusions, unchanged.\n\n The globes and orbits are unremarkable.\n\n Major intracranial vascular flow voids are preserved.  Major dural venous\nsinuses are patent.",
            "output": "1. Vast majority of the previously demonstrated left temporal lesion has been\nresected.\n2. Probable small volume residual tumor at the very deep resection cavity\nmargin/quadrant within the temporal lobe, 6 mm in width.\n3. Stable primarily left frontotemporal peritumoral white matter FLAIR\nhyperintensities.\n4. New, expected postoperative changes from interval left craniotomy.  No\nadditional unexpected acute intracranial abnormality identified.\n5. Partial bilateral mastoid effusions, unchanged."
        },
        {
            "input": "Study is mildly degraded by motion.  There is no evidence of acute\nintracranial hemorrhage, mass, mass effect or territorial infarction. \nVentricles and sulci are age appropriate.  Few scattered periventricular deep\nsubcortical FLAIR white matter hyperintensities are nonspecific however may be\nsequelae of chronic microangiopathy.  No concerning enhancing lesions are\nseen.\n\nMild mucosal sinus thickening is seen involving the ethmoid air cells.  The\nremainder the visualized paranasal sinuses, mastoid air cells, and middle ear\ncavities are clear.  The globes are unremarkable.  The principal vascular flow\nvoids appear to be well preserved.  Limited imaging of the cervical spine\nsuggests probable degenerative changes (see 03:11).",
            "output": "1.  Study is mildly degraded by motion.\n2. No evidence of acute infarct or acute intracranial hemorrhage.\n3. Mild chronic microangiopathy.\n4.  Within limits of study, no definite evidence of intracranial metastatic\ndisease.\n5.  Paranasal sinus disease , as described."
        },
        {
            "input": "The ventricles, sulci, and cisterns are age appropriate.  There is no\nparenchymal signal abnormality or abnormal enhancement.  The hippocampal\nformations appear symmetric.  There is no acute infarct, intracranial\nhemorrhage, or mass effect.\n\nThere is a small mucous retention cyst within the alveolar recess of the right\nmaxillary sinus.",
            "output": "No acute infarct, intracranial hemorrhage, parenchymal signal abnormality or\nabnormal enhancement."
        },
        {
            "input": "MRI BRAIN:\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  Few prominent perivascular spaces.  There is no abnormal\nenhancement after contrast administration.\n\nThe patient is post bilateral cataract surgery.  The paranasal sinuses,\nmastoid air cells and middle ear cavities are clear.  Dural venous sinuses are\npatent.\n\nMRA brain:\nThere is mild-to-moderate narrowing cavernous segment right ICA, and mild\nnarrowing left cavernous segment ICA and probably moderate narrowing\nsupraclinoid left ICA.\nProbable mild narrowing right M3, left M2 segments.\n\nOtherwise, intracranial internal carotid arteries and their major branches\nappear normal without evidence occlusion, or aneurysm formation.\n\nDominant right vertebral artery.  Small caliber left vertebral artery in upper\nleft neck and intracranially.  There is no flow in left vertebral artery V4\nsegment, distal to the left ___ takeoff may be from narrowing,, or strain\nsequela of low neck left vertebral artery abnormality seen on CTA ___.  Negative susceptibility vessel sign on gradient images.  There is no\nevidence of intracranial dissection on fat-suppressed axial T1 images.  The\nright vertebral and basilar arteries and their major branches are patent.",
            "output": "1. Intracranial atherosclerotic disease, with areas of narrowing anterior\ncirculation.\n2. Absent flow V4 segment left vertebral artery, distal to the left ___\ntakeoff.  This may be downstream sequela of low neck left vertebral artery\nabnormality seen on comparison CTA, or atherosclerotic disease combined with\nvessel decreasing in caliber after ___ takeoff\n3. No acute infarct."
        },
        {
            "input": "A small focus of restricted diffusion in the right cerebellar hemisphere\n(series 302, image 3), with corresponding signal hypointensity on ADC map,\nlikely reflects a small acute right cerebellar hemispheric infarct.  There is\nno evidence of infarction elsewhere.  There is no evidence of edema, mass, or\nhemorrhage.  Bilateral subcortical and periventricular white matter T2 FLAIR\nsignal hyperintensities are likely sequelae of chronic small vessel ischemic\nchange.  Prominence of the ventricles and sulci is compatible with age-related\ninvolutional change.  There is partial opacification of the right mastoid air\ncells; otherwise the imaged paranasal sinuses and mastoid air cells are clear.\nPatient is status post bilateral lens removal.",
            "output": "1. Small right cerebellar hemispheric acute infarct.  No hemorrhage, mass, or\nedema.\n2. Chronic findings including white matter small vessel ischemic changes and\nglobal involutional change."
        },
        {
            "input": "Punctate focus of left posterior temporal lobe restricted diffusion with\nassociated FLAIR hyperintense signal (series 6, image 15; series 11, image 14)\nmay represent late acute to subacute infarct.\n\nThere are scattered periventricular and subcortical punctate T2/FLAIR white\nmatter hyperintensities, which are nonspecific, but compatible with chronic\nmicroangiopathy in a patient of this age.  The sulci, ventricles and cisterns\nare otherwise within expected limits for the patient's age related global\ncerebral volume loss.\n\nA single punctate gradient echo susceptibility of the left temporal lobe\n(series 10, image 12) may represent sequela of prior microhemorrhage.\n\nThe major intracranial flow voids are preserved.  The dural venous sinuses are\npatent on postcontrast MP-RAGE.  The orbits are unremarkable noting bilateral\nlens replacements.  Mild mucosal thickening of the ethmoid air cells is noted.\nThe remainder the paranasal cells are clear.  Fluid signal is noted in the\nright mastoid air cells.",
            "output": "1. Punctate focus of left posterior temporal lobe restricted diffusion with\nassociated FLAIR hyperintense signal may represent late acute subacute\ninfarct.\n2. Sequela of prior punctate microhemorrhage in the left temporal lobe is also\nidentified.\n3. No evidence of signal abnormality of the bilateral medial temporal lobes to\nsuggest HSV encephalitis.\n4. Periventricular and subcortical T2/FLAIR white matter hyperintensities,\nwhich are nonspecific, but compatible with chronic microangiopathy in a\npatient of this age.\n\nNOTIFICATION:  The findings were discussed with ___, M.D. by\n___, M.D. on the telephone on ___ at 3:24 ___, 5 minutes after\ndiscovery of the findings."
        },
        {
            "input": "MRI HEAD:  There is no intra or extra-axial mass, acute hemorrhage or infarct.\nSulci, ventricles and cisterns are within expected limits. The major flow\nvoids are preserved. The paranasal sinuses are clear. The orbits are\nunremarkable. The mastoid air cells are clear. Incidental note is made of a\nmetopic suture.\n\nHEAD MRA:  Normal flow related signal is seen in the intracranial internal\ncarotid, middle cerebral and anterior cerebral arteries without significant\nmural irregularity or stenosis. There is normal symmetric arborization of the\nMCA branches. There is no aneurysm greater than 3 mm. Normal flow related\nenhancement is seen in the intracranial vertebral arteries, the basilar\nartery, and the bilateral superior cerebellar and posterior cerebral arteries.\nThese left vertebral artery is dominant.\n\nNECK MRA: There is a normal 3 vessel takeoff from the aortic arch. The\ncervical common carotid, internal carotid and external carotid arteries are\nnormal in course, caliber and contour. They demonstrate normal enhancement\nwithout mural irregularity, stenosis or evidence of dissection. The roughly\ncodominant vertebral arteries are normal in course, caliber and contour. They\ndemonstrate normal enhancement without mural irregularity, stenosis or\nevidence of dissection.\n\nMRV:  There is diminished flow related signal on time-of-flight MRV of the\nright transverse and sigmoid sinus as well as diminutive contrast enhancement\nof the visualized portions of the right transverse and sigmoid likely\nrepresenting hypoplastic right transverse and sigmoid sinus given its smooth\ntapered appearance versus slow flow.  In addition, given the normal MRI of the\nhead, potential thrombus is much lower in likelihood, tho not entirely\nexcluded.",
            "output": "1. Normal MRI of the head.\n2. Normal MRA of the head and neck.\n3. Uniformly diminished flow related signal and contrast enhancement of the\nright transverse and sigmoid sinuses and proximal internal jugular vein, most\nlikely representing congenital hypoplasia with superimposed slow flow;\nthrombus is considered much less likely."
        },
        {
            "input": "There is no evidence of acute intracranial hemorrhage, or infarction. \nVentricles and sulci are age appropriate.  Mild mucosal sinus thickening is\nseen involving the ethmoid air cells.  There is complete opacification of the\nright maxillary sinus.  The left maxillary sinus is clear.  The mastoid air\ncells, and middle ear cavities are clear.  The principal vascular flow voids\nare well preserved.  The globes are unremarkable.",
            "output": "1. No acute intracranial infarction.  Complete opacification of the right\nmaxillary sinus."
        },
        {
            "input": "An area of subacute hematoma is seen in the left basal ganglia region with\nincreased T1 and T2 signal in the center and surrounding hemosiderin rim.  The\narea demonstrates restricted diffusion secondary to blood products.  Several\nareas of diffusion hyperintensity are visualized in the left periventricular\n(350:15 and 350:19) as well as in the right frontal lobe without definite low\nsignal on ADC map could be due to subacute infarcts. Extensive changes of\nsmall vessel disease are identified.  Chronic blood products are seen within\nboth occipital horns.  A small area of micro hemorrhages are seen seen in the\nright temporal lobe as well as right frontal lobe.  There is no midline shift\nor hydrocephalus.",
            "output": "1. Subacute hematoma in the left basal ganglia.  While in absence of contrast\nenhanced study it is difficult to exclude underlying mass lesion, given the\nwell-defined surrounding hemosiderin rim and evolution of the blood products,\nit is less likely to be due to an underlying mass lesion.\n2. Foci of hyperintensity on diffusion images could be due to subacute\ninfarcts.\n3. Severe changes of small vessel disease and moderate brain atrophy.\n4. Areas of micro hemorrhages could be related to amyloid angiopathy or\nhypertension."
        },
        {
            "input": "MRA: The major intracranial arteries appear normal with no evidence of\nstenosis, occlusion, or aneurysm formation.\n\nMRI BRAIN:\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline\nshiftor infarction. The ventricles and sulci are normal in caliber and\nconfiguration.  Gray-white matter differentiation is preserved.  The basal\ncisterns remain patent.\n\nNo osseous abnormalities are seen.  A mucous retention cyst is noted within\nthe right maxillary sinus.  The remainder of the paranasal sinuses, mastoid\nair cells, and middle ear cavities are clear. The visualized portion of the\norbits are unremarkable. The visualized portion of the vascular flow voids are\npreserved.",
            "output": "Unremarkable noncontrast-enhanced MRI/MRA brain without evidence of\nintracranial mass, ischemia, or hemorrhage."
        },
        {
            "input": "MR BRAIN:\nAgain seen is a partially empty sella ___ with no evidence of residual or\nrecurrent pituitary mass.  There is no evidence of hemorrhage, edema, masses,\nmass effect, midline shift or infarction.   The ventricles and sulci are\nenlarged in an atrophic pattern.  There are extensive periventricular white\nmatter hyperintensities on the T2 and FLAIR images.  Although nonspecific,\nthese are often attributed to chronic small vessel ischemia..\n\nMRA brain: Again seen is irregularity of the distal left M1 segment and\nproximal M2 segments of the middle cerebral artery.  This is unchanged. \nOtherwise, the intracranial vertebral and internal carotid arteries and their\nmajor branches appear normal without evidence of stenosis, occlusion, or\naneurysm formation.",
            "output": "1. Partially empty sella ___, unchanged.\n2. Irregularity and mild narrowing of the distal left middle cerebral artery\nM1 segment and proximal M 2 segments.\n3. No evidence of mass, hemorrhage or infarction.\n4. White matter changes suggesting chronic small vessel ischemia."
        },
        {
            "input": "There is no acute intracranial infarction, hemorrhage, edema, mass, or mass\neffect. The ventricles and sulci are prominent, compatible with global\nparenchymal volume loss. Bilateral periventricular and in areas confluent deep\nwhite matter foci of T2/FLAIR signal hyperintensity are nonspecific but\ncompatible with moderate changes of chronic white matter microangiopathy,\nunchanged from prior.\n\nMajor intracranial vascular flow voids are preserved.  Globes and orbits are\nunremarkable.  Visualized paranasal sinuses and mastoids appear clear.",
            "output": "1. No acute intracranial abnormality.  No acute infarction.\n2. Stable chronic findings including global parenchymal volume loss and\nmoderate changes of chronic white matter microangiopathy."
        },
        {
            "input": "There is no intra or extra-axial mass, acute hemorrhage or infarct. The sulci,\nventricles and cisterns are within expected limits for the patient's age. \nThere are very few punctate periventricular and subcortical T2/FLAIR white\nmatter hyperintensities, which are nonspecific, but compatible with chronic\nmicroangiopathy in a patient of this age.  The major intracranial flow voids\nare preserved.  The dural venous sinuses are patent.  Partial opacification of\nmultiple ethmoid air cells, moderate mucosal thickening of the left frontal\nsinus and mild mucosal thickening of the remainder of the visualized paranasal\nsinuses is noted.  The orbits are unremarkable.  The mastoid air cells are\npoorly pneumatized.\n\nIncidental note is made of a small right cerebellar hemisphere developmental\nvenous anomaly.  Otherwise, no abnormal postcontrast enhancement.",
            "output": "1. Essentially unremarkable contrast-enhanced MRI brain.  No evidence of\nintracranial mass, or parenchymal signal abnormality.\n2. There is no evidence of disproportionate lobar or mesial temporal volume\nloss to suggest etiology of patient's symptoms.\n3. Very few punctate periventricular and subcortical T2/FLAIR white matter\nhyperintensities are nonspecific, but may be seen in setting of chronic\nmicroangiopathy in a patient of this age.  Differential considerations include\nsequela of migraine headache, prior infectious/inflammatory etiology or\ntrauma.\n4. Sinus disease as described above."
        },
        {
            "input": "There is no infarct, hemorrhage, mass effect or abnormal enhancement. The\nventricles, sulci and cisterns are appropriate for age.  There is ___\ncisterna magna. The principal intracranial flow voids are present.\n\nThe orbits, and visualized soft tissues are unremarkable. There is mild\nethmoid mucosal thickening. There is a sphenoid sinus mucous retention cyst\nwith inspissated secretions.  Incidentally noted is minimal fluid within the\nleft mastoid air cells.\n\nThere is diffusely decreased bone marrow signal which may relate to patients\nleukemia or post treatment changes.",
            "output": "No evidence of infarct, hemorrhage, mass, mass effect or abnormal enhancement.\n\n Uniformly hypointense regional bone marrow signal, likely reflecting\nunderlying leukemia or its treatment.\n\nIncidentally noted  minimal fluid within air cells at the left mastoid apex,\nand paranasal sinus inflammatory disease; correlate clinically."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  Few scattered T2/FLAIR hyperintensities are detected in the\nsubcortical white matter (for example image 16, series 15), which are\nnonspecific and may reflect changes due to small vessel disease.  There is no\nabnormal enhancement after contrast administration, no diffusion abnormalities\nare detected.\nThe major vascular flow voids are present and demonstrate normal distribution.\n There is a small amount of fluid within the right maxillary sinus (image 32,\nseries 18), otherwise, the orbits, paranasal sinuses, and mastoids are within\nnormal limits.",
            "output": "1.  There is no evidence of acute or subacute intracranial process, there is\nno evidence of abnormal enhancement.\n\n2.  Scattered foci of T2/FLAIR high signal intensity are demonstrated in the\nsubcortical white matter as described above, which are nonspecific and may\nreflect changes due to small vessel disease."
        },
        {
            "input": "Study is mildly degraded by motion.\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.\n\n There is prominence of the ventricles and sulci suggestive involutional\nchanges.  Periventricular and subcortical T2 and FLAIR supratentorial\nhyperintensities are noted, which may represent small vessel ischemic changes,\ngrossly unchanged.\n\nThere is no abnormal enhancement after contrast administration.",
            "output": "1. Study is mildly degraded by motion.\n2.  Within limits of study, no definite evidence of intracranial metastatic\ndisease.\n3. No evidence of acute infarct."
        },
        {
            "input": "A large area of intraparenchymal hemorrhage centered within the right frontal\nlobe is noted with a fluid fluid level and surrounding edema causing mild\nlocal mass effect on the adjacent sulci and minimally displacing the normally\nmidline structures to the left by approximately 1-2 mm.  Overall, the\nappearance of this is unchanged from the previous examination CT ___ 19:00.  Small volume extra-axial subdural hemorrhage is also noted along\nthe right anterior falx.\n\nAdditional areas of chronic left frontal lobe blood products are noted with\nadjacent cortical subcortical encephalomalacia, unchanged from previous\nexamination MRI ___.  There is hemosiderin staining along the\nbifrontal sulci, left greater than right.  A focus of susceptibility within\nthe right pons (10:7) is noted, without evidence of associated T2 FLAIR\nabnormality or enhancement, and stable from at least ___.\n\nRestricted diffusion surrounding the dominant right frontal intraparenchymal\nhemorrhage is most likely nonischemic, and secondary to hemorrhagic blood\nproducts.  Otherwise, no convincing evidence for acute infarction.\n\nThe ventricles and sulci are mildly prominent, compatible with age related\natrophic changes.  Areas of chronic encephalomalacia are noted within the left\nfrontal and left parietal lobes, from distant chronic infarcts. \nPeriventricular and subcortical white matter T2 hyperintensities are noted,\nlikely the sequelae of chronic small vessel ischemic disease.  The basal\ncisterns are patent.  There is no evidence of impending, downward herniation. \nThere is gross preservation of the principal intracranial vascular flow voids.\nThere is small chronic bilateral cerebellar infarcts, similar compared with ___\n\nPostcontrast images demonstrate scattered punctate and curvilinear areas of\nenhancement adjacent to the right frontal lobe intraparenchymal hemorrhage\n(for example 100:86), and adjacent to a second site of prior hemorrhage within\nthe left precentral gyrus (100:90).  No discrete underlying enhancing mass is\nseen.  Mild diffuse pachymeningeal enhancement is noted.  The dural venous\nsinuses appear patent on MP-RAGE imagine sequences.\n\nThe visualized paranasal sinuses, middle ear cavities, and mastoid air cells\nare well aerated and clear.  The orbits are within normal limits bilaterally.",
            "output": "1. Unchanged large intraparenchymal hemorrhage centered in the right frontal\nlobe with surrounding edema causing mild local mass effect and minimal\nleftward midline shift.  Several punctate areas of adjacent enhancement are\nlikely secondary to hemorrhage, there is no discrete mass identified. \nRecommend follow-up imaging following the resolution of this hemorrhage, CT\nwithout contrast follow-up may be sufficient in this clinical setting.\n2. Multiple additional areas of chronic hemorrhage, encephalomalacia involving\nthe left frontal lobe, parietal lobe, chronic cortical siderosis.\n3. Curvilinear focus of susceptibility artifact within the right pons, stable\nsince prior, appearance on T2 is not consistent with cavernoma, and is likely\nsequela of chronic hemorrhage or chronic infarct.\n4. Mild diffuse pachymeningeal enhancement without associated nodularity,\nlikely reactive in the absence of symptoms of infection."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  The ventricles and sulci are normal in caliber and\nconfiguration.\nThere is one non specific small focus of FLAIR hyperintensity in the left\nfrontal lobe (see 10:15).\nThere is mild mucosal thickening and partial opacification of bilateral\nethmoid air cells, bilateral frontal, sphenoid and bilateral maxillary\nsinuses. The mastoid air cells are clear. The orbits are unremarkable. \nOsseous structures are unremarkable.  Intracranial flow voids are maintained.",
            "output": "1. No acute intracranial abnormality.\n2. Paranasal sinus disease as described above."
        },
        {
            "input": "Study is mildly degraded by motion.  There is no evidence of edema, masses,\nmass effect, midline shift or infarction.  There is prominence of the\nventricles and sulci suggestive involutional changes.  Periventricular\nT2/FLAIR hyperintensities likely represent chronic small vessel ischemic\ndisease.  Chronic right basal ganglia and left external capsule infarct with\nhemosiderin staining are noted.  Additionally, 3 left cerebellar punctate\nchronic micro hemorrhages are noted.\n\nThere is a mucous retention cyst in the right maxillary sinus.  Mucosal\nthickening is seen in bilateral frontal and maxillary sinuses and the ethmoid\nair cells.  The mastoid air cells, and middle ear cavities are clear.",
            "output": "1.  Study is mildly degraded by motion.\n2. No acute intracranial abnormality.\n3. No evidence of intracranial mass or acute infarct.\n4.  Paranasal sinus disease as described.\n5. Chronic right basal ganglia and left external capsule infarcts as\ndescribed."
        },
        {
            "input": "There is no evidence of hemorrhage or infarction.  The ventricles and sulci\nare age-appropriate.  No mass effect or midline shift.\n\nThere is no abnormal enhancement after contrast administration. The major\nintracranial arterial flow voids are preserved.  The dural venous sinuses are\npatent.\n\nSmall mucous retention cysts are noted in the maxillary sinuses.  There is\nmild mucosal thickening of the paranasal sinuses.  The globes and orbits are\nunremarkable.",
            "output": "1. Mild paranasal sinus inflammatory changes.\n2. Otherwise normal study."
        },
        {
            "input": "Hardware artifact limits examination.\n\nThere is no evidence of infarction, hemorrhage, edema, or mass. The ventricles\nand sulci are normal in size and configuration. There is no abnormal\nenhancement on post contrast images.  Major intracranial vascular flow voids\nare intact.\n\nThere is no evidence of osseous abnormality. The paranasal sinuses, mastoid\nair cells, and middle ear cavities are clear. The orbits are unremarkable.",
            "output": "Unremarkable limited brain MRI."
        },
        {
            "input": "Hardware and motion artifact limits examination. Deep brain stimulator leads\nare in place.\n\nThere is no evidence of no evidence of infarction, hemorrhage, edema, or mass.\nThe ventricles and sulci are normal in size and configuration.",
            "output": "Deep brain stimulator leads in place.  No acute intracranial abnormality on\nthis limited examination."
        },
        {
            "input": "The ventricles and extra-axial spaces are normal in size.  There is no midline\nshift mass effect or hydrocephalus.  No focal signal abnormalities or acute\ninfarcts are seen.  Vascular flow voids are maintained.  The visualized\nparanasal sinuses are clear.\n\nNote is made of slightly low position of the cerebellar tonsils 3 mm below the\nlevel of foramen magnum.  This finding is unchanged from the previous MRI\nstudy.  However, given the history of chronic headaches, clinical correlation\nis recommended to exclude pseudotumor cerebral.",
            "output": "1. No significant abnormalities are seen on MRI of the brain without\ngadolinium.\n2. Nonspecific finding of slightly low but normal position of the cerebellar\ntonsils which could be seen in conjunction with pseudotumor cerebral. \nClinical correlation recommended."
        },
        {
            "input": "Right thalamic intraparenchymal hematoma is again noted measuring 24 x 35 mm. \nAssociated subarachnoid blood present in the occipital horns of the lateral\nventricles bilateral.  No underlying vascular malformation or enhancing mass. \nMild surrounding edema.\n\nT2 and FLAIR hyperintense signal changes with associated facilitated diffusion\nand mild volume loss in the left peritrigonal area appear similar compared to\nprior CT most likely represents a prior/old insult.  The intracranial arteries\ndemonstrate normal T2 flow void.  No CP angle masses.  The orbits appear\nnormal.  Mild mucosal thickening involving the ethmoid air cells.  Partially\nempty sella.\nSmall calcification or minimal blood products right parafalcine high parietal\n(series 10, image 22).",
            "output": "Right thalamic intraparenchymal hematoma is again noted.  Minimal associated\nsubarachnoid blood products present in the occipital horns the lateral\nventricles.\n\nNo underlying vascular malformation or enhancing mass visualized.\n\nChronic left peritrigonal insult as described above."
        },
        {
            "input": "Examination is moderately motion degraded.\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  There is mild prominence of the ventricles and sulci\nsuggestive of age-related involutional change.  Mild periventricular white\nmatter T2/FLAIR hyperintensities likely reflect the sequela of chronic small\nvessel ischemic disease.  There is no abnormal enhancement after contrast\nadministration.  There is no abnormal focus of slowed diffusion.  The\nprincipal intracranial vascular flow voids are preserved.\n\nImages through the internal auditory canal demonstrates symmetric appearance\nof the seventh eighth nerve complexes. There is no evidence of abnormal\nenhancement or mass lesion within the internal auditory canals,\ncerebellopontine angles or membranous labyrinth.  Smaller amounts of\nenhancement masses would be missed on this study due to motion artifact.  The\nremainder of the posterior fossa also appears normal\n\nThere is mild mucosal wall thickening in the floors of the maxillary sinuses\nbilaterally along with a small mucous retention cyst on the left.  There is a\nsmall amount of layering fluid in the left sphenoid sinus with background mild\nmucosal wall thickening.  The remainder the visualized paranasal sinuses are\ngrossly clear.  The orbits are grossly unremarkable.  There is near complete\nleft and moderate right opacification of the mastoid air cells.  There is\napparent extension of opacification into the left middle ear cavity and\npossibly to a lesser degree on the right.",
            "output": "1. No evidence of intracranial metastatic disease.  No hemorrhage, infarct, or\nenhancing mass identified.\n2. No IAC or cerebellopontine angle mass.\n3. Left-greater-than-right mastoid air cell and middle ear cavity\nopacification, suggestive of otomastoiditis which may account for hearing\nloss."
        },
        {
            "input": "MRI BRAIN:\nThere is no evidence of hemorrhage,edema,masses, mass effect, midline shift or\ninfarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.  Hardware in the right oral cavity produces artifact and\nlimits evaluation of this area.\n\nMRA BRAIN:\nThe intracranial vertebral and internal carotid arteries and their major\nbranches appear normal without evidence of stenosis,occlusion,or aneurysm\nformation.\n\nMRA NECK:\nThe origins of the great vessels, subclavian and vertebral arteries appear\nnormal bilaterally.  The common, internal and external carotid arteries appear\nnormal.  There is no evidence of internal carotid artery stenosis by NASCET\ncriteria.",
            "output": "1. No evidence of hemorrhage, infarction or mass.\n2. No evidence of dissection, aneurysm formation or large occlusion of the\nhead or neck vessels."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  No evidence of demyelination.  Paranasal sinuses, mastoids are\nclear.  Intracranial vascular flow voids are preserved.  Normal visualized\nskull-base.",
            "output": "1. Normal brain MRI."
        },
        {
            "input": "There is linear encephalomalacia centered in the left lentiform nucleus, with\nextension into the internal capsule on corona radiata, at the site of the\nprior hemorrhage.  There is associated susceptibility artifact from\nhemosiderin deposition.  There is no underlying enhancing mass, and no\nenhancing mass elsewhere in the intracranial compartment.  There are no other\nsites of intracranial blood products.\n\nThere is no acute infarction or edema.  Multiple small foci of high T2 signal\nare again seen in the subcortical, deep, and periventricular white matter of\nthe cerebral hemispheres, as well as in the pons, nonspecific but likely\nsequela of chronic small vessel ischemic disease in a patient of this age.  A\nprominent perivascular space is again seen in the medial left temporal lobe. \nVentricles and sulci are mildly prominent due to parenchymal volume loss, as\nbefore.\n\nMajor intracranial arterial flow voids are grossly preserved.  Major dural\nvenous sinuses appear patent on postcontrast MP RAGE images.\n\nThere is a small mucous retention cyst in the right maxillary sinus.",
            "output": "1. Linear encephalomalacia at the site of the prior hemorrhage in the left\nlentiform nucleus, internal capsule, and corona radiata.\n2. No evidence for a mass at the site of prior hemorrhage or elsewhere in the\nintracranial compartment.  No other sites of intracranial blood products."
        },
        {
            "input": "There is no acute infarct identified.  There is no mass effect midline shift\nor hydrocephalus.  A few scattered nonspecific foci of FLAIR hyperintensity\ncould indicate early changes of small vessel disease.  Suprasellar and\ncraniocervical regions are unremarkable.  Vascular flow voids are maintained.",
            "output": "No acute infarcts are identified."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  Moderate prominence of the ventricles and sulci is suggestive\nof involutional changes.  Patchy to confluent areas of T2 and FLAIR\nhyperintense signal abnormalities in the periventricular and subcortical white\nmatter are nonspecific, but likely reflect chronic small vessel ischemic\nchanges.\n\nAreas of GRE hypointensity at level of basal ganglia are consistent with\nmineralization as seen on the CT head without contrast dated ___.\n\nThere is mild mucosal thickening of the ethmoid and right greater than left\nmaxillary sinuses.  The mastoid air cells are clear.  The intraorbital\ncontents are unremarkable.  The intracranial arterial flow voids are grossly\npreserved.",
            "output": "1. No evidence of acute infarction or intracranial hemorrhage.\n2. Moderate cerebral atrophy and chronic small vessel ischemic disease.\n3. Paranasal sinus disease as described above."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are prominent, likely related to\nage-appropriate volume loss.  No diffusion abnormalities are detected. \nNumerous foci of T2/FLAIR hyperintensities in the periventricular,\nsubcortical, and deep white matter are nonspecific, but may represent the\nsequela of chronic small vessel ischemic disease.\nThe major intracranial flow voids are preserved and demonstrate normal\ndistribution.\nThe paranasal sinuses and mastoid air cells are clear.  The patient is status\npost bilateral cataract surgery.",
            "output": "1. No evidence of a mass lesion, or mass effect on this limited examination\nwithout intravenous contrast.\n2. Nonspecific supratentorial white matter lesions, which may represent the\nsequela of chronic small vessel ischemic disease."
        },
        {
            "input": "The sagittal T1 weighted images are completely degraded by motion and are\nnondiagnostic.\n\nWhile diffusion-weighted images are also motion limited, the demonstrate a\nfocus of slow diffusion in right pons measuring 10 x 9 mm, consistent with an\nacute infarct.\n\nMarked ventriculomegaly, out of proportion to the size of the sulci and\ncisterns, is unchanged compared to the prior MRI from ___.",
            "output": "1. Limited incomplete exam.\n2. Acute infarct involving the right pons.\n3. Marked ventriculomegaly out of proportion to the size of the sulci and\ncisterns is again demonstrated, compatible with communicating hydrocephalus in\nan appropriate clinical setting.\n\nNOTIFICATION:  The findings were discussed by Dr. ___ with Dr.\n___ on the ___ ___ at 9:28 AM, immediately after discovery\nof the findings."
        },
        {
            "input": "MRI Brain:\n\nEncephalomalacia in the right pons relates to a chronic infarct.  There is no\nslow diffusion to suggest acute infarction. Confluent periventricular and\nscattered subcortical white matter foci of T2/FLAIR hyperintense signal\nwithout associated slow diffusion are nonspecific, but likely sequelae of\nchronic microangiopathy in a patient of this age.  Marked ventriculomegaly,\nout of proportion to the size of the sulci and cisterns, is unchanged compared\nto the prior examinations.  There is no evidence of hemorrhage, edema, mass,\nor mass effect.  Moderate mucosal thickening of the left maxillary sinus is\nunchanged.\n\nMRA brain: The intracranial vertebral and internal carotid arteries and their\nmajor branches appear normal without evidence of stenosis, occlusion, or\naneurysm formation.\n\nMRA neck:  Evaluation of the aortic arch and the proximal common carotid and\nvertebral arteries is limited by motion artifact and the noncontrast\ntechnique.  The common, internal and external carotid arteries appear normal. \nThere is no evidence of internal carotid artery stenosis by NASCET criteria.",
            "output": "1.  Chronic pontine infarct.  No evidence of acute infarction or intracranial\nhemorrhage.\n\n2.  Marked ventriculomegaly out of proportion to the size of the sulci and\ncisterns is unchanged and could represent communicating hydrocephalus in the\nappropriate clinical setting.\n\n2.  Unremarkable head MRA.\n\n3.  Unremarkable neck MRA.  No internal carotid artery stenosis by NASCET\ncriteria."
        },
        {
            "input": "There is no acute infarction, edema, mass effect, or evidence for blood\nproducts.  Ventricles, sulci, and basal cisterns are normal in size.  Either\nprominent perivascular spaces or cysts are seen in the medial temporal lobe,\nmeasuring up to 6 mm on image 9:10.  Major intravascular flow voids are\ngrossly preserved.\n\nThere is a small mucous retention cyst and probably also a small amount of\nfluid in the left maxillary sinus.  There is a small mucous retention cyst in\nthe right maxillary sinus.",
            "output": "1. No acute infarction and no evidence for other acute intracranial\nabnormalities.\n2. Prominent perivascular spaces versus cysts in the medial temporal lobe.\n3. Probable small amount of fluid in the left maxillary sinus, adjacent to a\nmucous retention cyst.\n\nRECOMMENDATION(S):\n\n1. Non urgent brain MRI with and without contrast is suggested for better\nassessment of the possible medial left temporal lobe cysts.\n2. Please correlate clinically whether the patient has symptoms of left\nmaxillary sinusitis.\n\nNOTIFICATION:  The recommendation for additional imaging was emailed to the ED\nQA nurses list by Dr. ___ at 11:30 on ___."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  Multifocal areas of facial, pre malar subcutaneous tissue\nnodularity, better seen on CTA, can be seen in the setting of prior cosmetic\nprocedure, unlikely inflammatory process, clinically correlate.  0.8 cm left\nparotid tail or periparotid nodule..  Findings consistent with mild chronic\nsmall vessel ischemic change.  Moderately prominent prevascular spaces.. \nPreserved vascular flow voids",
            "output": "1. No acute intracranial findings.\n2. 0.8 cm left parotid tail lesion.\n3. Remainder as above."
        },
        {
            "input": "The study is limited by motion artifact.\n\nAgain seen is soft tissue edema in the right ___ and infraorbital edema\nsuggesting periorbital cellulitis/preseptal edema. No evidence of extension\nposterior to the orbital septum to suggest orbital cellulitis. No abnormal\nenhancement of the optic nerves.\n\nThe cavernous sinus appears normal.  No evidence of cavernous sinus\nthrombosis.\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.  No diffusion abnormalities are detected.  The major vascular\nflow voids are present and demonstrate normal distribution.  Partially empty\nsella.  The craniocervical junction appears normal.",
            "output": "1.  Findings in keeping with periorbital cellulitis/preseptal edema.\n2.  No evidence of extension posterior to the orbital septum to suggest\norbital cellulitis.  3.  No abnormal enhancement of the globe to suggest\nendophthalmitis.  No evidence of cavernous sinus thrombosis."
        },
        {
            "input": "There is no acute infarction, intracranial hemorrhage, extracerebral fluid\ncollection, midline shift or mass effect.  Ventricles and extra-axial spaces\nare normal in size.  Flow voids are maintained. Suprasellar and craniocervical\nregions are unremarkable.  The vascular flow voids are maintained.  The\nvisualized paranasal sinuses are clear.",
            "output": "No significant abnormalities are seen on MRI of the brain without gadolinium."
        },
        {
            "input": "There is enhancing nodular dural-based structure measuring 1.5 x 1.4 cm with\nan immediately adjacent cystic mass filled with CSF in the right frontal lobe\nwhich measures 3.7 x 3.3 cm (7; 21, 19; 21).  The structure could represent 2\nseparate entities or 1 mixed component structure. The solid component is\nheterogeneous and isointense on T1 and T2 and homogeneously enhances after\ncontrast administration. There is a dural tail anterior to the mass, which\nsuggests possible meningioma origin.  The combined structure causes local mass\neffect on the parenchyma of the right frontal lobe and to its adjacent\nstructures.  There is no evidence of surrounding edema in the underlying\nbrain.  There is no evidence of midline shift.\n\nOtherwise, there is no other abnormal enhancement after contrast\nadministration. There is no evidence of large territory infarction or\nhemorrhage.  The ventricles and sulci are normal in caliber and configuration.\nFlow voids on T2 are preserved.\n\nThere are multiple bilateral extracranial subcutaneous structures that most\nlikely correspond with epidermoid inclusion cysts (4; 9, 12).\n\nThere is partial opacification of the right mastoid air cells, most likely\ncontaining fluid.  There is mucosal thickening of the right sphenoid sinus and\nethmoid air cells.  The visualized portion of the orbits is normal.",
            "output": "1. 1.5 x 1.4 cm enhancing nodular  lesion with an adjacent 3.7 x 3.3 cm cystic\nmass, not entirely certain whether this is an intra or extra-axial lesion, but\nprobably extra-axial predominantly as the nodular component appears to have a\ndural tail.  This could represent a meningioma with associated cystic\ncomponent, uncertain whether the latter cystic component is intra or\nextra-axial, or possibly 2 separate lesions with an arachnoid cyst adjacent to\na meningioma.  Local mass effect on the underlying right frontal lobe but no\nparenchymal signal alteration.\n2. No evidence of midline shift or surrounding edema.\n3. Multiple bilateral extracranial subcutaneous structures are likely\nepidermal inclusion cysts (sebaceous cysts)."
        },
        {
            "input": "The patient's previously noted right frontal enhancing dural-based mass with a\nprominent surrounding cyst is again seen.  There is local mass effect but no \nmidline shift.",
            "output": "1. Preoperative localization for surgical resection.\n2. No change in the appearance of the right frontal nodular enhancing and\ncystic lesion."
        },
        {
            "input": "Status post right frontal craniotomy and resection of a previously seen \ncystic and enhancing nodular extra-axial mass lesion, expected residual blood\nproducts are seen at the surgical bed, postsurgical pneumocephalus, thin right\nsubdural collection/hematoma measuring approximately 1 mm in thickening and\nextracranial collection involving the right calvarium convexity with maximum\nthickness 9 mm.\n\nThere is no surgical cavity definite nodular enhancing component to suggest\nresidual disease, however long-term follow-up is advised.\n\nThere is persistent effacement of the superior sagittal sinus at the surgical\nsite with small focus of slow diffusion in the left frontal lobe suggesting\nvenous ischemic changes (5:25, 6:25), otherwise; other major vascular flow\nvoids is within normal limits.  No evidence of newly developed\nintraparenchymal hemorrhage.\n\nBoth orbits and globes are normal.  Paranasal sinuses are clear.  Moderate\nright and mild left fluid signal intensity in both mastoid air cells.",
            "output": "1. Status post right frontal craniotomy and resection of the previously seen\nright frontal cystic enhancing nodular mass lesion as described above.\n2. No imaging signs to suggest residual tumor, however long-term follow-up is\nrecommended.\n3. Persistent asymmetry and narrowing of the anterior aspect of the superior\nsagittal sinus at the surgical site, with small area of slow diffusion in the\nleft frontal lobe suggesting acute venous ischemic changes."
        },
        {
            "input": "MR BRAIN:\nThere are very extensive areas of slowed diffusion most pronounced in the\nbilateral cerebral white matter and bilateral basal ganglia There is no\nevidence of hemorrhage, masses, mass effect, or midline shift.  The ventricles\nand sulci are normal in caliber and configuration.\n\nOrbits are within normal limits.  There is mucosal thickening of the bilateral\nethmoid air cells, sphenoid sinuses, and left maxillary sinus.  Fluid is also\nnoted within the mastoid air cells bilaterally.\n\nMRA brain: The intracranial vertebral and internal carotid arteries and their\nmajor branches appear normal without evidence of stenosis, occlusion, or\naneurysm formation.",
            "output": "Very extensive areas of slowed diffusion predominantly involving the bilateral\ncerebral white matter and globus pallidi, a pattern that can be seen in the\nsetting of \"chasing the dragon\" induced encephalopathy or late stage hypoxic\nischemic encephalopathy."
        },
        {
            "input": "There are multiple small foci 2 patchy areas of slow diffusion in the right\ngreater than left cerebral hemispheres and to a lesser extent in the left\ncerebellum. The largest of these are in the right parietal lobe (302:22), and\nthe right periventricular white matter (302:18).  There are corresponding\nareas of hypointense signal on the ADC map.  The findings are most consistent\nwith acute infarction, most likely embolic.\n\nThere is no evidence of hemorrhage.  The ventricles and sulci are\nage-appropriate in size and configuration with no mass effect or midline\nshift.  Patchy to confluent areas of T2 and FLAIR hyperintense signal\nabnormalities in the periventricular and subcortical white matter have a right\nangle orientation with respect to the lateral ventricles and raise the\npossibility of demyelinating disease.  The alternative is chronic small vessel\nischemia.\n\nThere is mild mucosal thickening of the right greater than left ethmoid air\ncells and bilateral maxillary sinuses.  The mastoid air cells are clear.  The\nintraorbital contents are unremarkable.  The major intracranial arterial and\nvenous flow voids are preserved.",
            "output": "1. Multifocal areas of infarction in the cerebral hemispheres and left\ncerebellum.  Findings are most consistent with an embolic infarction.\n2. No evidence of hemorrhage.\n3. White matter FLAIR hyperintensities that may represent chronic small vessel\nischemic disease but raise the possibility of demyelinating disease."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor acute infarction.  Encephalomalacia is identified along the right straight\ngyrus of the right frontal lobe, with no evidence of diffusion abnormalities\nto indicate acute ischemic changes.  There is prominence of the ventricles and\nsulci suggestive age related involutional changes.  The major intracranial\nflow voids are patent.  The paranasal sinuses are clear.  The orbits are\nunremarkable.",
            "output": "1.  There is no evidence of acute intracranial process.\n2.  Area of encephalomalacia is identified along the straight gyrus of the\nright frontal lobe as described above, this finding is nonspecific and may\nrepresent sequela of prior insult such as trauma."
        },
        {
            "input": "There is area of mildly restricted diffusion, with normalized ADC values in\nthe right parietal operculum, posterosuperior right insula, with smaller\npunctate foci of infarct involving medial right precentral gyrus.  If with\nassociated mild gyriform enhancement, cortical laminar necrosis a small area\nof cortical microhemorrhage.  Findings consistent with late subacute infarct,\napproximately 7 to 10-day-old.  No parenchymal hematoma.\n\nArea of mildly restricted diffusion, with normalized ADC values involving left\nmiddle frontal gyrus, frontal operculum, with cortical laminar necrosis, few\npunctate foci of cortical microhemorrhage, and minimal gyriform enhancement. \nSuggestion of mild volume loss.  Findings consistent with late subacute\ninfarct, probably greater than 10-day-old.  No parenchymal hematoma.\n\nNo acute infarcts.\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift.\nGeneralized brain parenchymal atrophy, most prominent at the sylvian fissures.\nFindings consistent with mild chronic small vessel ischemic changes. \nIntracranial vascular flow voids are preserved.  Paranasal sinuses, mastoids\nare clear.  Dural venous sinuses are patent.",
            "output": "1. Right MCA distribution subacute infarct, approximately 7 to 10-day-old.\n2. Left MCA distribution subacute infarct, greater than 10-day-old.\n3. Areas of cortical laminar necrosis within above described bilateral MCA\ninfarcts, few punctate foci of cortical microhemorrhage, no parenchymal\nhematoma.\n4. Brain parenchymal atrophy."
        },
        {
            "input": "Study is slightly motion limited.  There are a few scattered subcortical and\nperiventricular white matter T2/FLAIR hyperintensities.  No associated\nenhancement or diffusion restriction is seen.  Similar signal abnormality is\nseen within the pons.  There is no evidence of hemorrhage, edema, masses, mass\neffect, midline shift or infarction.   The ventricles and sulci are normal in\ncaliber and configuration.  There is no abnormal enhancement after contrast\nadministration.  Hyperostosis frontalis is re-identified.",
            "output": "1. No evidence of metastatic involvement of the brain or acute intracranial\nabnormality.\n2. Mild nonenhancing white matter T2/FLAIR hyperintensities are nonspecific\nbut may represent microvascular ischemic change"
        },
        {
            "input": "There are bilateral symmetrical periventricular and deep white matter T2 FLAIR\nabnormal hyperintense signal intensity at posterior frontal and parietal\nregion sparing the subcortical U fibers.  There is no corresponding\npostcontrast enhancement, microhemorrhage or diffusion restriction.  In\nretrospect; the white matter abnormality was very subtle and moderately\nprogressed since ___.  Described findings are nonspecific and may\nrepresent changes due to chronic small vessel disease, however given the\nclinical history, changes related to chemotherapy-induced toxic\nleukoencephalopathy cannot be completely excluded.\n\nThere is a focal left hippocampal T2/FLAIR hyperintensity with facilitated\ndiffusion anteriorly (series 7 and 8, image 9); could be explained as a result\nof postictal status, please correlate.\n\nThere few scattered bilateral foci of subcortical T2/FLAIR high-signal\nintensity; nonspecific in appearance and could be related to post therapeutic\nchanges versus chronic microangiopathy.\n\nThere is no abnormal intracranial enhancement after contrast administration. \nThere is no evidence of intracranial hemorrhage, edema, masses, mass effect,\nmidline shift or infarction.\n\nThe previously suggest left frontal hypodensities not visualized in the recent\nMRI and likely a result of beam hardening artifact from hyperostosis\nfrontalis; a normal variant.\n\nBoth orbits and globes are unremarkable.  Paranasal sinuses and mastoid air\ncells are unremarkable.",
            "output": "1. Bilateral symmetrical posterior frontal and parietal white matter abnormal\nsignal intensity; findings are nonspecific and may reflect changes due to\nchronic small vessel disease, however given the clinical history,\nchemotherapy-induced toxic encephalopathy is also consideration.\n2. Left hippocampal T2/FLAIR hyperintensity is also nonspecific and can be\nseen in patients with postictal status, please correlate.\n3. There is no abnormal intracranial enhancement after contrast\nadministration."
        },
        {
            "input": "There are similar pontine and symmetric bilateral periventricular and deep\nwhite matter T2/FLAIR signal hyperintensities involving the frontal and\nparietal lobes with sparing the subcortical U-fibers in a similar pattern and\ndistribution compared to the prior MR dated ___.  There is similar\nT2/FLAIR hyperintensity within the pons (8:7) and left hippocampus.  No new\nareas of signal abnormality are identified.  There is no abnormal enhancement\nafter contrast administration.  There is no evidence of hemorrhage, masses,\nmass effect, midline shift or infarction.   The ventricles and sulci are\nnormal in caliber and configuration.  The major intracranial vessels and dural\nvenous sinuses are patent.\n\nThere is mild mucosal thickening in the ethmoid air cells.  No significant\nfluid signal is seen in the mastoid air cells.  The visualized orbital\nstructures are unremarkable.",
            "output": "1. No significant interval change in bilateral symmetric white matter T2/FLAIR\nsignal abnormality involving the frontal and parietal lobes; findings remain\nnonspecific and may reflect sequelae of chronic small vessel ischemic disease.\nHowever given clinical history, chemotherapy-induced toxic encephalopathy\nremains in the differential.\n2. Similar left hippocampal T2/FLAIR signal abnormality, nonspecific and may\nbe seen in a variety of conditions including postictal status.\n3. No new areas of signal abnormality or abnormal enhancement to suggest\ndisease progression or metastasis.  No acute infarction or hemorrhage."
        },
        {
            "input": "Hyperostosis frontalis interna is again noted.  There is no intraparenchymal\nabnormality corresponding to the apparent hyperdensity noted in the right\nsuperior frontal gyrus on prior CT, which is related to beam artifact from the\nadjacent thickened calvarium.\n\nThere is no abnormal enhancement after contrast administration.\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.\n\nThe paranasal sinuses and mastoid air cells are clear.  The globes and orbits\nappear normal.  There is no abnormal marrow signal.",
            "output": "1. Normal study.  The earlier study identified on the prior CT appears to be\nartifact.\n2. No evidence of metastatic disease, infarct, or hemorrhage."
        },
        {
            "input": "Motion artifact limits evaluation.\n\nThere is no evidence of an intracranial mass, edema, acute infarction, or\nblood products.  The ventricles and sulci are normal in size for the patient's\nage.  Mild foci of T2/FLAIR hyperintensity in the supratentorial white matter\nand pons are nonspecific but compatible with mild chronic small vessel\nischemic changes in this age.  The dural venous sinuses are patent.  The\nprincipal intracranial flow voids appear preserved. Again noted is\nhyperostosis frontalis interna.",
            "output": "1. Motion limited exam.\n2. No evidence of intracranial metastatic disease or acute intracranial\nabnormalities."
        },
        {
            "input": "There is slow diffusion in bilateral occipital cortices and, to a lesser\nextent, bilateral parietal cortices, compatible with a pattern of lobe hypoxic\nischemic injury or seizure activity.  There is no associated cortical\nswelling.  No slow diffusion is seen in the basal ganglia or brainstem.\n\nA moderate-sized infarct in the superior right cerebellar hemisphere is new\ncompared to the ___ MRI.  It demonstrates volume loss, fast rather\nthan slow diffusion, and enhancement on postcontrast images, indicating that\nis late subacute.\n\nExtensive confluent T2 hyperintensity in the supratentorial white matter is\nagain seen, nonspecific but likely sequela of chronic small vessel ischemic\ndisease in this age group.  There is moderate enlargement of the ventricles,\nparacentral and parietal sulci, and sylvian fissures, a mild enlargement of\nother cerebral sulci, similar to prior and compatible with parenchymal volume\nloss.\n\nMajor arterial flow voids appear grossly preserved.  Major dural venous\nsinuses appear patent on postcontrast MP RAGE images.\n\nThere is fluid and mild mucosal thickening in the ethmoid air cells and\nmaxillary sinuses.  Right frontal sinus is hypoplastic.  Left frontal sinus\ndemonstrates no signal abnormalities.  There is trace fluid and a\nmoderate-sized mucous retention cyst in the left sphenoid sinus.  The right\nsphenoid sinus is hypoplastic due to asymmetric insertion of the sphenoid\nseptum, and it is completely or nearly completely opacified.  There is trace\nfluid in bilateral mastoid air cells.  This is similar to the prior CTs dating\nback to ___ and may be related to endotracheal intubation.\n\nThere is evidence of right cataract surgery.\n\nSagittal images demonstrate degenerative changes in the included cervical\nspine with disc pathology plus/minus endplate osteophytes remodeling the\nventral spinal cord at C4-C5.",
            "output": "1. Slow diffusion in bilateral occipital cortices and, to a lesser extent,\nbilateral parietal cortices, is compatible with a pattern of global hypoxic\nischemic injury or seizure activity.  No associated cortical swelling.\n2. Moderate-sized late subacute infarct in the superior right cerebellar\nhemisphere with associated contrast enhancement.\n3. Grossly stable extensive supratentorial white matter signal abnormalities,\nnonspecific but likely sequela of chronic small vessel ischemic disease in\nthis age group.\n\nRECOMMENDATION(S):  Follow up MRI with and without contrast is recommended in\napproximately 8 weeks to confirm the expected resolution of contrast\nenhancement in the superior right cerebellar hemisphere."
        },
        {
            "input": "FLAIR images were repeated with motion reducing technique due to motion on the\ninitial images.  FLAIR sequence 8 is used for interpretation.\n\nPreviously noted slow diffusion in bilateral occipital cortices, bilateral\nparietal cortices, and bilateral posterior temporal cortices has markedly\ndecreased if not completely resolved.  There is new cortical hyperintensity on\nFLAIR images in the same distribution.  This is consistent with expected\nevolution of hypoxic ischemic injury.\n\nThere is no new diffusion abnormality.\n\nModerate sized infarction in the right superior cerebellar hemisphere is\nsimilar to ___ but new compared to ___.  In the absence of\nintravenous contrast, it is not possible to reassess the previously visualized\ncontrast enhancement, which was attributed to the late subacute nature of the\ninfarct on the ___ exam.\n\nThere is extensive confluent periventricular, deep, and subcortical white\nmatter T2 hyperintensity, nonspecific likely secondary to chronic small vessel\nischemic disease in this age.  There is also T2 hyperintensity within the\nright anterior aspect of the upper medulla, consistent with a chronic infarct.\nThese findings are unchanged dating back to ___.\n\nThere are chronic microhemorrhages in the bilateral cerebellar hemispheres,\nsimilar to ___ but new compared to an earlier MRI dated ___.  2 chronic micro hemorrhages within the right thalamus have been present\nsince ___.\n\nThere is a cavum septum pellucidum et vergae, a normal variant.  There is\nunchanged prominence of the ventricles and cortical sulci consistent with\nvolume loss, which is most pronounced in the parietal and mesial temporal\ncortices.\n\nThe major vascular flow voids are preserved.\n\nThere is a circumscribed T1 and T2 hyperintense lesion in the posterior left\nparasagittal parietal calvarium, likely representing a hemangioma or another\nnonaggressive fat containing lesion (4:10). There is evidence of right\ncataract surgery.\n\nThere is mild mucosal thickening within the paranasal sinuses.  There is\nlayering fluid within the bilateral maxillary and left sphenoid sinuses, as\nwell as fluid filling the asymmetrically small right sphenoid sinus.  There\nare bilateral mastoid air effusions.  There is fluid layering within the\npharynx.  This may be related to endotracheal intubation and prolonged supine\npositioning in the inpatient setting.",
            "output": "1. Compared to ___, there is neo hyperintensity on FLAIR images\nwith markedly decreased, if not completely resolved, slow diffusion within\nbilateral occipital, parietal, and posterior temporal cortices.  This is\nconsistent with expected evolution of hypoxic ischemic injury.\n2. Moderate-sized infarct in the right superior cerebellar hemisphere is\nstable in size compared to ___.  In the absence of intravenous\ncontrast, it is not possible to reassess the associated contrast enhancement,\nwhich was attributed to the late subacute nature of the infarct on ___.\n3. Chronic infarct in the right anterior aspect of the upper medulla is\nunchanged compared to ___.\n4. Chronic micro hemorrhages in bilateral cerebellar hemispheres are unchanged\ncompared to ___.  Chronic micro hemorrhages in the right thalamus\nare unchanged dating back to ___."
        },
        {
            "input": "MRI Brain:\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  The ventricles and sulci are normal in caliber and\nconfiguration.\n\nMRA brain: The intracranial vertebral and internal carotid arteries and their\nmajor branches appear normal without evidence of stenosis, occlusion, or\naneurysm formation.\n\nMRA neck: The common, internal and external carotid arteries appear normal.\nThere is no evidence of internal carotid artery stenosis by NASCET criteria.\nThe origins of the great vessels, subclavian and vertebral arteries appear\nnormal bilaterally.  Please note that the V3 and proximal V4 segments of the\nvertebral arteries cannot be well evaluated on this exam secondary to the 2D  \ntime-of-flight technique.  The remainder of the V4 segments of the vertebral\narteries however appear to be unremarkable.",
            "output": "1. No acute intracranial abnormalities identified.\n2. Unremarkable circle of ___ without evidence of significant stenosis or\naneurysm.\n3. No evidence of internal carotid artery stenosis by NASCET criteria."
        },
        {
            "input": "Study is mildly degraded by motion.\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are preserved in caliber and\nconfiguration.  Minimal nonspecific low-lying cerebellar tonsils approximately\n3 mm extension inferior for magnum is noted (see 2:12).\n\nQuestion asymmetric increased enhancement in the left canalicular segment of\nthe facial nerve (21:57; 101:68; series 15) versus artifact, with normal\nenhancement of the geniculate, tympanic and mastoid segment of the facial\nnerve.\n\nThere is no abnormal intra-axial enhancement after contrast administration.\n\nThere is small layering fluid in the sphenoid sinus.  Limited imaging of the\nparotid glands demonstrate bilateral subcentimeter nonspecific probable lymph\nnodes.",
            "output": "1.  Study is mildly degraded by motion.\n2. Question asymmetric increased enhancement of left facial nerve as described\nversus artifact.  If not artifactual, finding is nonspecific, but may be seen\nin the setting of Bell's palsy.\n3. Otherwise, within limits of study, no definite evidence of intracranial\nlesion or enhancing intracranial mass.\n4.  No acute intracranial abnormality.\n5.  Paranasal sinus disease with findings concerning for acute sinusitis, as\ndescribed.\n6. Nonspecific low-lying cerebellar tonsils as described."
        },
        {
            "input": "There is slow diffusion in the right posterior frontal lobe with involvement\nof the pre motor and motor strip.  Associated T2 prolongation.  No evidence of\nhemorrhage.\n\nThere are multiple chronic infarcts in the bilateral cerebellar hemispheres,\nand possible subtle chronic infarct in the pons.  There is extensive confluent\nand patchy T2 prolongation throughout the white matter which probably reflects\nchronic small vessel disease at this age.  Chronic lacunar infarct noted in\nthe medial left thalamus.\n\nGlobal prominence of the ventricle and sulci reflecting volume loss is noted. \nThere is no extra-axial collection or mass effect.  No shift of midline\nstructures or basal cistern effacement.\n\nLoss of the left vertebral artery flow void is noted, with occlusion of the\nleft vertebral artery noted on the preceding CTA as described on the MRI\ncervical spine exam.  Bilateral lens replacements are noted.  There is mild\nmucosal thickening scattered throughout the paranasal sinuses.",
            "output": "1. Acute infarction in the right posterior frontal lobe involving the motor\nand pre motor areas.\n2. Multiple chronic infarcts including in both cerebellar hemispheres, the\nleft thalamus, and the pons.\n3. Extensive white matter signal changes which most likely reflect chronic\nsmall vessel disease at this age.\n4. Loss of the left vertebral artery flow void as described on the cervical\nspine MRI, with known occlusion seen on previous CT angiography."
        },
        {
            "input": "The study is mildly limited by motion artifact.  Redemonstrated is an evolving\nright basal ganglia hemorrhage measuring 26 x 27 mm with surrounding vasogenic\nedema.  Mild mass effect on the body of the right lateral ventricle and the\ninsula and minimal shift of normally midline structures to the left is\nunchanged.  There is persistent slow diffusion surrounding the hemorrhage. \nThere is no new hemorrhage.  The ventricles are stable in size and\nconfiguration.\nMajor intracranial vascular flow voids are preserved.  The dural venous\nsinuses are patent.  There is a mucous retention cyst in the right maxillary\nsinus.",
            "output": "1.  Evolving right basal ganglia hemorrhage with surrounding vasogenic edema\nand stable mass effect on the right lateral ventricle and the adjacent brain\nparenchyma.  No new hemorrhage.\n\n2.  There is no vascular or masslike enhancement in the region of the\nhemorrhage.  However, an underlying lesion masked by the hemorrhage cannot be\nexcluded."
        },
        {
            "input": "Only scout images were obtained which are severely motion degraded and are\nnondiagnostic.  Known right basal ganglia hemorrhage is partially visualized.",
            "output": "Incomplete nondiagnostic examination.\n\nRECOMMENDATION(S):  Consider repeating the examination when the patient is\nbetter able to tolerate."
        },
        {
            "input": "And complex study again demonstrates a hemorrhage in the right basal ganglia\nwith surrounding edema.  Mild renal surrounding slow diffusion is seen which\ncould be due to compression of the adjacent parenchyma.  There is no\nhydrocephalus or midline shift.",
            "output": "Incomplete study right basal ganglia hemorrhage is seen.  Examination can be\nrepeated if indicated with anesthesia or conscious sedation."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  Mild periventricular T2/FLAIR signal hyperintensities are\nwound nonspecific, but likely related to chronic small vessel ischemic\ndisease.  No diffusion abnormalities are detected.  Intravascular flow voids\nare patent.  There is no abnormal enhancement after contrast administration.",
            "output": "1.  No acute intracranial pathology.\n2.  Mild chronic small vessel ischemic changes in the periventricular white\nmatter."
        },
        {
            "input": "No evidence of infarction, hemorrhage, edema or mass .  There is proportional\nprominence of the ventricles and sulci consistent with age-related parenchymal\natrophy. A cavum septum pellucidum  is unchanged. Scattered areas of mucosal\nthickening are noted in the ethmoidal air cells and frontal/sphenoid sinuses.\nThere is a mucous retention cyst in left maxillary sinus. Fluid is seen within\nthe left greater than right mastoid air cells. Trace secretions are seen\npooling in the nasopharynx. The orbits appear normal.  On the sagittal T1\nsequence there is a punctate T1 hypointensity within the posterior aspect of\nthe pituitary, favored to be artifactual (series 9, image 12).",
            "output": "1. No evidence of infarction, hemorrhage, mass or edema.\n2. Mild paranasal sinus disease as described above. Fluid is seen within left\ngreater than right mastoid air cells, nonspecific but sometimes seen during\nprolonged supine positioning."
        },
        {
            "input": "Again seen are multiple foci of white matter signal abnormality, some with a\nclose Ill and pericallosal distribution, compatible with the patient's given\nhistory of multiple sclerosis. No new lesion is identified.  A lesion present\nwithin the left cerebellar hemisphere on the previous examination is not as\nobvious compared to the prior examination, while a lesion within the right\ncerebellar hemisphere is slightly more conspicuous compared to the prior.\nThere is no enhancement or decreased diffusion associated with any of the\nlesions to suggest active inflammation.\n\nThe ventricles, cerebral sulci and cisterns are age appropriate without\nevidence of significant cerebral atrophy. There is no acute infarct or\nintracranial hemorrhage.",
            "output": "Multiple foci of white matter signal abnormality consistent with the patient's\ngiven history of multiple sclerosis. There is no new lesion or evidence of\nenhancing lesion."
        },
        {
            "input": "Grossly stable numerous nonenhancing supratentorial and infratentorial\nperiventricular and subcortical white matter lesions, some which are\nassociated with T1 hypointensity, are noted.  No lesions are associated with\nrestricted diffusion or susceptibility.  No definite new lesions are\nidentified.\n\nThere is no evidence of hemorrhage, midline shift or infarction.   The\nventricles and sulci are normal in caliber and configuration.  There is no\nabnormal enhancement after contrast administration.",
            "output": "1. Nonenhancing grossly stable white matter lesions compatible with clinical\nhistory of multiple sclerosis, as described.\n2. No definite new white matter lesions identified.\n3.  No acute intracranial abnormality."
        },
        {
            "input": "The patient is status post right pterional craniotomy for resection of an\nolfactory groove meningioma, with interval involution of the surgical\nbed/resection cavity.  When compared to prior exam, there is more confluent\ndural thickening (measuring approximately 8 mm thick) and enhancement along\nthe bilateral cribriform plate as well as punctate curvilinear enhancement\nwithin the superior margins of the resection cavity.  Encephalomalacia\ninvolving the right rectus gyrus and right anterior temporal lobe is noted. \nDural thickening underlying the craniotomy is within expected limits.  No\nother abnormal enhancement.  Significant improvement in degree of right\nfrontal lobe FLAIR edema pattern with resolution of rightward midline shift.\n\nThere is no acute infarct or intracranial hemorrhage.  The sulci, ventricles\nand cisterns allowing for above described encephalomalacia is within expected\nlimits for the patient's age.  There are mild superimposed periventricular and\nsubcortical T2/FLAIR white matter hyperintensities, which are nonspecific, but\ncompatible with chronic microangiopathy in a patient of this age.  The major\nintracranial flow voids are preserved.  Dural venous sinuses are patent.  Mild\nmucosal thickening of the ethmoid air cells.  The orbits are unremarkable. \nTrace fluid signal is seen in the right mastoid tip.",
            "output": "1. Expected evolution of right pterional craniotomy and resection of an\nolfactory groove meningioma, including resolution of leftward midline shift,\ndecreased right frontal lobe white matter edema pattern, as well as right\nrectus gyrus and right anterior temporal lobe encephalomalacia.\n2. There is now residual enhancing dural/soft tissue thickening along the\ncribriform plate measuring approximately 8 mm in thickness, as well as\ncurvilinear punctate enhancement within the superior margins of the resection\ncavity.  This is likely post surgical sequela and granulation tissue, however\nresidual lesion cannot be excluded and interval follow-up is recommended.\n3. No acute infarct or intracranial hemorrhage.  Additional findings described\nabove."
        },
        {
            "input": "The patient is status post right pterional craniotomy for resection of an\nolfactory groove meningioma.  The previously seen thickening along the dura of\nthe cribriform plate is again seen, measuring approximately 8 mm, unchanged. \nThere is encephalomalacia of the right rectus gyrus and right anterior\ntemporal lobe, unchanged.  Minimal enhancement is seen along the superior\nmargin of the resection cavity, likely representing granulation tissue,\nunchanged.  T2 signal abnormality is again seen within the right frontal lobe,\nunchanged.\n\n  The ventricles and sulci are normal in caliber and configuration.  The\nparanasal sinuses, mastoid air cells and middle ear cavities are clear.  The\nintraorbital contents are normal.",
            "output": "1. Status post right pterional craniotomy for resection of an olfactory groove\nmeningioma with expected postsurgical changes, unchanged.  No evidence of\nworsening enhancement suggestive of tumor progression or new lesions are seen."
        },
        {
            "input": "Homogeneously enhancing 3.1 x 2.3 x 2.4 cm (AP, TRV, SI) lesion arising from\nthe cribriform plates, eccentric to the right with associated hyperostosis, is\nre-identified exerting prominent mass effect on the right orbitofrontal lobe\nwith resulting edema pattern of the right frontal lobe extending to the middle\nfrontal gyrus, most compatible with an olfactory groove meningioma.  There is\nminimal mass effect on left rectus gyrus without evidence of underlying\nparenchyma FLAIR signal abnormality.\n\nThere is no acute infarct or intracranial hemorrhage.  The remainder of the\nsulci, ventricles and cisterns are within expected limits for the patient's\nage.  Very mild superimposed periventricular and subcortical T2/FLAIR punctate\nwhite matter hyperintensities are nonspecific, but compatible with chronic\nmicroangiopathy in a patient this age.  The major intracranial flow voids are\npreserved.  The dural venous sinuses are patent.  T2 hyperintense nodules in\nthe bilateral left-greater-than-right visualized parotid glands likely\nrepresent lymph nodes.\n\nThere is minimal mucosal thickening of the ethmoid air cells.  The orbits are\nunremarkable.  No significant fluid signal is seen the mastoid air cells.",
            "output": "1. 3.1 cm olfactory groove meningioma, eccentric to the right with mass effect\non the right orbital frontal lobe with resultant parenchymal edema pattern\nextending to the right middle frontal gyrus.  Minimal mass-effect on the left\nrectus gyrus without evidence of underlying parenchymal edema pattern.\n2. No other enhancing lesions are identified.\n3. Additional findings as described above."
        },
        {
            "input": "The patient's previously noted 3.1 x 2.3 x 2.4 cm olfactory groove meningioma\nis again seen, with surrounding edema in the right frontal lobe.  Effacement\nof adjacent orbital frontal gyri, stable.  Area of calcification on its base\nbetter seen on CTA ___.  No definite area of tumor extension in the\nnasal cavity or cyst ethmoid sinus.",
            "output": "1. Again seen is extra-axial olfactory groove mass most consistent with\nmeningioma."
        },
        {
            "input": "The patient is status post resection of olfactory bulb meningioma, with\npostsurgical changes including extracranial air and fluid overlying the right\nfrontal lobe.  At the site of resection, there is increased T1, T2 and FLAIR\nsignal, likely representing edema and blood products.  Edema within the right\nfrontal lobe is similar in extent to that seen prior to surgical intervention.\nPostoperative restricted diffusion is seen at the margin of the surgical site.\nA separate punctate focus of restricted diffusion chest superior to the\nsurgical site may represent an area of ischemia (4:16).  The ventricles and\nsulci are normal in caliber and configuration.",
            "output": "1. Status post resection olfactory bulb meningioma, with no residual nodular\narea of enhancement identified.\n2. A punctate focus of restricted diffusion at the superior margin of the\nsurgical site may represent adjacent ischemia."
        },
        {
            "input": "The examination is limited by patient motion.\n\nSlow diffusion involving mainly the left anterior thalamus extending along of\nthe left cerebral peduncle to the left aspect and midline of the brainstem\njust inferior to the floor of the fourth ventricle is noted. In addition,\nthere is slow diffusion of the anterior right cerebellar hemisphere as well as\nof the bilateral occipital lobes. Subtle focus of slow diffusion of the left\ncerebellar hemisphere (series 4, image 7) is also demonstrated. These lesions\ndemonstrate associated FLAIR hyperintense signal. The findings are compatible\nwith late acute to subacute infarct in the bilateral PCA and SCA\ndistributions. Although evaluation is limited secondary to patient motion, no\nclear evidence of acute intracranial hemorrhage.\n\nSulci, ventricles and cisterns are within expected limits for the patient's\nage. Mucosal thickening of the paranasal sinuses are noted. The orbits are\nunremarkable. Fluid signal is seen in the right mastoid tip.",
            "output": "1. There are late acute to subacute infarcts of the left thalamus extending to\nthe brainstem, bilateral cerebellar hemispheres and bilateral occipital lobes\nin a distribution compatible with known basilar tip thrombus.  Extending to\nthe bilateral P1 segments and proximal SCAs.\n2. No evidence of hemorrhage, although this evaluation is limited secondary to\npatient motion."
        },
        {
            "input": "There is redemonstration of a large area of encephalomalacia involving the\nright MCA territory.  There is no evidence of acute infarction.  There is an\narea of hemorrhage in the right cerebellar hemisphere with minimal adjacent\nedema.  This lesion measures approximately 3.0 x 2.2 x 3.3 cm and shows\npartial enhancement on postcontrast images (series 13, image 9).  There is\npersistent mass effect on the right aspect of the quadrigeminal plate cistern.\nThere is no evidence of midline shift.\n\nProminence of ventricles and sulci is consistent with age related involutional\nchanges.  A small mucous retention cyst is noted in the right maxillary sinus.",
            "output": "1. Right cerebellar hemorrhage with surrounding edema and minimal enhancement.\nThe etiology of the hemorrhage is uncertain.\n2. Encephalomalacia involving the right MCA territory, compatible with known\nprior infarction.\n3. No evidence of acute infarction."
        },
        {
            "input": "When compared to examination of ___, there is a new nonenhancing more\nconfluent right superior frontal gyrus FLAIR hyperintense 2.3 x 1.7 cm focus\n(series 9, image 18) lesion demonstrating a prominent T1 dark hole. \nSuperimposed periventricular, subcortical, cerebellar and pontine white matter\nT2/FLAIR hyperintensities are similar in configuration and number from the\nprior exam.  Cervical white matter lesions are better evaluated on dedicated\ncervical spine MRI performed on the same day.  There is no abnormal\nenhancement.  There is global cerebral volume loss greater than would be\nexpected for the patient's age.  The sulci, ventricles and cisterns are within\nexpected limits given the degree of volume loss.\n\nThere is no acute infarct or intracranial hemorrhage.  The major intracranial\nflow voids are preserved.  The right orbit is unremarkable.  There is a left\nprosthetic globe.  There is opacification of the frontal sinuses with T2\nhypointense focus which may represent inspissated secretions versus fungal\ncolonization small mucous retention cyst is noted in the right maxillary\nsinus.",
            "output": "1. New from examination of ___ is a 2.3 cm right superior frontal gyrus\nnonenhancing FLAIR hyperintense lesion.  There are superimposed unchanged\nperiventricular, subcortical, cerebellar and pontine white matter FLAIR\nhyperintensities, compatible with demyelinating plaques given the history of\nmultiple sclerosis.\n2. No enhancement to suggest active process.\n3. FLAIR hyperintense lesions of the cervical spine is better evaluated on\ncontrast enhanced MRI cervical spine performed the same day."
        },
        {
            "input": "There are several foci of slow diffusion with DWI hyperintensity and\ncorresponding ADC hypointensity in the bilateral cerebellar hemispheres, left\nparieto-occipital lobe, right parietal lobe, left frontoparietal lobe, right\nfrontal lobe and high left parietal lobe.  Most of these infarcts are in\ncortical and subcortical location.\nNo evidence of hemorrhagic transformation.\n\nAdditional small and scattered T2/FLAIR hyperintense foci in the\nperiventricular white matter and centrum semiovale are nonspecific but may\nrepresent migraine related white matter changes or early small vessel ischemic\nchanges/microangiopathic changes. Alternatively, these white matter lesions\ncould represent at an autoimmune/inflammatory process.  Distribution pattern\nof the white matter lesions does not suggest an underlying demyelinating\ncondition.\n\nThe ventricles and sulci are normal in caliber and configuration.\n\nThere is minimal opacification of the inferior left mastoid air cells, likely\nunchanged.  The right mastoid air cells are clear.  There is mild mucosal\nthickening in both maxillary sinuses, unchanged.  The orbits are normal.",
            "output": "1. Acute/subacute infarcts in predominantly cortical and subcortical locations\nof the left parieto-occipital lobe, left frontoparietal lobe and high left\nparietal lobe as well as in the right parietal lobe, right frontal lobe and\nbilateral cerebellar hemispheres.  No evidence of hemorrhagic transformation.\n2. Additional nonspecific scattered periventricular white matter changes may\nbe migraine related or represent early small vessel ischemic\nchanges/microangiopathic changes.  Alternatively, they could represent an\nautoimmune/inflammatory process.  The distribution pattern does not suggest an\nunderlying demyelinating condition."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor acute infarction.  The ventricles and sulci are globally prominent\nsuggestive of involutional changes with no definite focal atrophy seen.  In\nthe left lentiform nucleus, there is focal T2 hyperintensity without definite\nhemorrhage, slowed diffusion, or mass-effect, but which incompletely\nsuppresses on the FLAIR sequence.  There are patchy T2/FLAIR hyperintensities\nthroughout the subcortical and periventricular white matter which are\nnonspecific but most likely reflect chronic small vessel disease at this age.\n\nThe major intracranial vascular flow voids are preserved. Left intraocular\nlens replacement is noted. The visualized extracranial soft tissues are\nunremarkable.",
            "output": "1. Global volume loss suggestive of involutional changes, but no definite\nfocal atrophy.\n2. Nonspecific white matter signal changes most likely reflecting chronic\nsmall vessel ischemia in this age group.\n3. T2 hyperintensity in the left basal ganglia which incompletely suppresses\non the FLAIR sequence.  This most likely reflects an evolving late subacute or\nchronic lacunar infarct, but consider short-term follow-up in ___ weeks to\nassess stability.\n\nRECOMMENDATION(S):  T2 hyperintensity in the left basal ganglia which\nincompletely suppresses on the FLAIR sequence. This most likely reflects an\nevolving late subacute or chronic lacunar infarct, but consider short-term\nfollow-up in ___ weeks to assess stability."
        },
        {
            "input": "There are scattered punctate foci of increased signal intensity on the\ndiffusion-weighted images predominantly along the gray/white matter junction\nof the left frontal, left parietal and right occipital lobes, and in the left\ncerebellar hemisphere, with several foci demonstrating decreased signal on ADC\nand corresponding FLAIR hyperintensity, for example series 502, image 24 and\nimage 22 correspond to series 8 image 19 and 17).  These foci likely represent\nacute or subacute infarcts, with the distribution suggesting embolic etiology.\n\nThere is are scattered 2 mm enhancing foci at the gray/white matter junction\nof the left middle frontal gyrus (___), left postcentral gyrus\n(11:19, 10:26, 1001:111), in the superior left parietal lobe (10:05,\n1001:113), right occipital lobe (11:10, 1000:109) and in the right caudate\nhead (11:14, 101:84), with corresponding FLAIR hyperintensity.  These\ndemonstrate high signal on FLAIR images, and some of them also demonstrate\nhigh signal on diffusion tracer images, possibly subacute infarcts.\n\nThere are multiple additional small periventricular, deep, and subcortical\nwhite matter foci of T2/FLAIR hyperintensity without corresponding slow\ndiffusion or contrast enhancement, nonspecific in this age group.\n\nThere is FLAIR hyperintensity in the right greater than left parietal sulcal,\nas well as right occipital and temporal sulci (series 8, images ___ without\nevidence for corresponding signal abnormality on gradient echo diffusion\nweighted images, and without leptomeningeal contrast enhancement. No\nhyperdensity on the preceding CT.  Diagnostic considerations include nonacute\nsubarachnoid hemorrhage versus inflammation/meningitis.\n\nMRV based on postcontrast MP RAGE images:\nThere is an irregular, incompletely occlusive filling defect in the distal\nleft transverse sinus extending to the proximal sigmoid sinus (series 10 image\n48) on the postcontrast images which demonstrates heterogenous signal\nintensity on T2/FLAIR images (series 8 images ___ and slightly hyperintensity\non the diffusion-weighted images (series 502, image 10).  There is slightly\nasymmetric prominence of the left vein ___ which is patent.  There is a\nrounded filling defect in the superior sagittal sinus (series 10, image 108),\nwith corresponding hyperintensity on T2 weighted images, most likely an\narachnoid granulation.  Otherwise normal contrast opacification is\ndemonstrated within the superior sagittal sinus, straight sinus, right\ntransverse sinus and sigmoid sinuses. The jugular bulbs and proximal jugular\nveins are patent. Evaluation of the deep venous systems reveals normal flow\nsignal in the internal cerebral veins. The vein ___ is also unremarkable.\n\nThere is FLAIR hyperintensity in several small cortical veins of the bilateral\nvertex (series 8, images ___ without corresponding susceptibility artifact\nor filling defect on post-contrast images, and with cortical venous patency\ndemonstrated on the preceding CTA, possibly representing slow venous flow.\n\nMajor arterial flow voids are grossly preserved.\n\nSagittal images demonstrate incompletely evaluated degenerative changes in the\nincluded upper cervical spine.",
            "output": "1. Irregular, incompletely occlusive filling defect in the distal left\ntransverse sinus extending to the proximal sigmoid sinus, consistent with\nthrombosis.\n2. Several cortical veins at the bilateral vertex demonstrate high signal\nT2/FLAIR images, likely related to slow flow, since these veins appear patent\non the postcontrast MP RAGE images, as well as on the preceding CTA.\n3. Multiple small acute to early subacute infarcts, mostly at the gray/white\nmatter junction of the bilateral cerebral hemispheres and in the left\ncerebellum, suggesting embolic etiology.  Sequela of vasculitis may also have\na similar appearance, but there is no evidence of active vasculitis on the\npreceding head CTA.\n4. Multiple small 2 mm enhancing foci with T2/FLAIR hyperintensity plus/minus\ndiffusion signal abnormality, mostly at the gray/white matter junction of the\nbilateral cerebral hemispheres, and also in the right caudate head, suggesting\nsubacute infarctions, once again with likely embolic distribution.\n5. Additional small nonenhancing T2/FLAIR hyperintense foci in the\nsupratentorial white matter are nonspecific in this age group.  Diagnostic\nconsiderations include migraine related lesions, sequelae of\ninfection/inflammation, sequela of vasculitis (though no evidence for active\nvasculitis is seen on the preceding CTA), or sequela of chronic ischemic\nmicrovascular disease if the patient has longstanding cardiovascular risk\nfactors such as hypertension, diabetes or smoking.\n6. FLAIR hyperintensity in the right greater than left cerebral sulci, with\nparietal predominance, without hyperdensity on CT or contrast enhancement. \nDiagnostic considerations include non acute subarachnoid blood products,\nversus inflammation/meningitis.  LP has already been performed.\n\nRECOMMENDATION(S):  Recommend follow up MRI with and without contrast in\napproximately 1 month for reassessment of the small enhancing foci.\n\nNOTIFICATION:  Preliminary findings were discussed with ___, M.D. by\n___, M.D. on the telephone on ___ at 11:57 pm, 5 minutes\nafter discovery of the findings."
        },
        {
            "input": "Mild prominence of sulci and ventricles indicating brain atrophy.  A few\nscattered foci of FLAIR hyperintensity indicate mild changes of small vessel\ndisease.  No acute infarcts are seen.  There are no cortical or subcortical\ninfarcts identified.  There is no evidence of inappropriate medial temporal\natrophy.  Following gadolinium administration, there is no evidence of\nabnormal parenchymal, vascular or meningeal enhancement seen.  No micro\nhemorrhages are identified.  Visualized paranasal sinuses are clear.",
            "output": "Mild brain atrophy and small vessel disease.  No other significant\nabnormalities.  No specific atrophy pattern identified or chronic cortical or\nsubcortical infarcts are seen.  No enhancing brain lesions."
        },
        {
            "input": "The ventricles and extra-axial spaces are normal in size. There is no evidence\nof midline shift, mass effect or hydrocephalus. There are no acute infarcts. \nA few scattered nonspecific foci of FLAIR hyperintensity are seen which could\nindicate early changes of small vessel disease.  .  The vascular flow voids\nare maintained. The visualized paranasal sinuses are clear. Following\ngadolinium administration there is no evidence of abnormal parenchymal,\nvascular and meningeal enhancement seen.",
            "output": "Early changes of small vessel disease, otherwise, no significant abnormalities\nare seen on MRI of the brain with and without gadolinium."
        },
        {
            "input": "Multiple small foci of abnormal enhancement are seen along the juxtacortical\nwhite-gray matter junction within the bilateral parietal lobes (for example,\n900:117, 120).  No significant T2 abnormalities associated with these foci of\nenhancement.\n\nAdditionally, there is a subtle region of gyriform enhancement along the right\nparasagittal cingulate gyrus (900: 110-113).\nA solitary focus of slow diffusion within the inferior left occipital lobe\n(500/502:10), demonstrating increased associated T2 signal, but without\ndiscrete contrast enhancement at this location.\n\nThere is no evidence of acute, territorial infarction.  No intracranial\nhemorrhage.\n\nThe ventricles and sulci are prominent, compatible with global cerebral\natrophic changes.  Incidentally noted is a cavum septum pellucidum et vergae. \nThe basal cisterns are patent.  There is no evidence of impending, downward\nherniation.   The dural venous sinuses appear patent on MP-RAGE imagine\nsequences.\n\nThe visualized paranasal sinuses, middle ear cavities, and mastoid air cells\nare well aerated and clear.  The orbits are within normal limits bilaterally.",
            "output": "1. Several punctate foci of abnormal enhancement at the gray-white matter\njunction of the bilateral parietal lobes, concerning for parenchymal\nmetastatic disease.\n2. Gyriform pattern of enhancement within the right cingulate gyrus,\nsuspicious for leptomeningeal metastatic disease or evolving infarct.\n3. Solitary focus of slow diffusion within the left occipital lobe,\ndemonstrating associated increased T2/FLAIR signal but without associated\nenhancement.  Findings may represent an additional focus of metastatic\ndisease, although the lack of enhancement would be atypical.  Differential\nconsiderations include a small focus of ischemia not conforming to a vascular\nterritory.\n4. Global cerebral atrophic changes and findings of chronic small vessel\nischemic disease."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  Scattered, mild periventricular foci of T2/FLAIR\nhyperintensity are nonspecific but grossly similar and likely the sequela of\nchronic small vessel ischemic changes.  Small hypointense focus in the\nanterior right frontal lobe on gradient echo imaging appears grossly similar\nand may represent an old cavernoma.  There is no abnormal enhancement after\ncontrast administration.  The paranasal sinuses are grossly clear.",
            "output": "No evidence of brain metastases."
        },
        {
            "input": "MR BRAIN:\nRestricted diffusion in the left caudate head and left putamen is associated\nT2/FLAIR hyperintense signal.  There is a focal calcification in the left\nglobus pallidus.  There is no evidence of hemorrhage, masses, mass effect,\nmidline shift or extra-axial fluid collection.   The ventricles and sulci are\nnormal in caliber and configuration.\n\nThe paranasal sinuses and mastoid air cells are clear.  The orbits are\nunremarkable.\n\nMRA brain:  There is reconstitution of flow in the left distal M1 and proximal\nM2 segments with mild narrowing and irregularity of the inferior division of\nthe left proximal M2 segment.  The remainder of the vessels of the circle\n___ are patent without evidence of stenosis or occlusion.  A 2 mm aneurysm\nof the left cavernous internal carotid artery projects medially on 5:74.",
            "output": "1. Acute infarction in the left caudate head and putamen without evidence of\nhemorrhagic conversion.\n2. Reconstitution of flow in the left distal M1 and proximal M2 segments.\n3. Mild narrowing and irregularity of the inferior division of the left\nproximal M2 segment likely represents residual nonocclusive thrombus.\n4. Two mm aneurysm of the left cavernous internal carotid artery."
        },
        {
            "input": "The patient's previously noted bilateral enhancing cerebral metastases are\nagain seen, measuring 3.1 x 2.8 cm in the left occipital lobe abutting the\nsplenium of the corpus callosum, and the right occipital-parietal region\nmeasuring 2.6 x 1.8 cm.  Also noted is a 0.2-0.3 cm enhancing lesion in the\nposterior right frontal lobe along the cortical-subcortical gray-white matter\njunction (05:37, 6:20, 503:74), likely an additional small metastasis.\n\nThere is no midline shift and mild regional mass-effect in the region of the\nmass is consisting of slight effacement of the atrium of the left lateral\nventricle without entrapment, and right sided sulci near the right\nparieto-occipital mass.\n\nNo evidence of extra-axial collection.  There is opacification of the right\nmaxillary sinus and right-sided ethmoid air cells likely due to sinus\ninflammation.\n\nThere is an indeterminate subgaleal lesion, right frontal region measuring 1.8\nx 0.8 cm (06:18), possibly sequelae of resolving subgaleal hematoma given\nfindings from head CT from ___.",
            "output": "1. Three (3) enhancing cerebral metastases, largest left occipital lobe\nmeasuring 3.1 cm, smallest in the posterior right frontal lobe measuring\n0.2-0.3 cm, as above.\n2. 1.8 cm probable evolving right frontal subgaleal hematoma, not fully\nevaluated on this study.\n3. Right maxillary and ethmoid air cell sinus inflammation."
        },
        {
            "input": "2.5 x 2.7 x 2.6 cm (AP, TRV, SI) enhancing rounded mass of the left\nparietooccipital lobe is slightly smaller when compared to examination of ___.  A 1.4 x 2.3 x 1.5 cm right parietal lobe lesion is also smaller. \nUnchanged gradient echo susceptibility artifact compatible with intratumoral\nhemorrhage.  The degree of associated white matter edema pattern has improved.\nA previously described punctate focus of enhancement in the right precentral\ngyrus is no longer noted.  No additional enhancing lesions identified.\n\nThere is no evidence of acute infarct or new intracranial hemorrhage. \nAllowing for mild mass-effect on the left lateral ventricle and local sulcal\neffacement, the sulci, ventricles and cisterns are within expected limits for\nthe patient's mild to moderate senescent related global cerebral volume loss. \nSuperimposed periventricular and subcortical T2/FLAIR white matter\nhyperintensities are nonspecific and mild, but compatible with chronic\nmicroangiopathy in a patient this age.  Sequela of prior lacunar infarcts of\nthe bilateral basal ganglia is also unchanged.\n\nThe major intracranial flow voids are preserved.  The dural venous sinuses are\npatent.  Moderate to severe paranasal sinus disease has slightly progressed\nfrom prior examination.  Orbits appear unremarkable, allowing for bilateral\nlens replacements.  No suspicious marrow signal.",
            "output": "1. Dominant left parietooccipital 2.7 cm and right parietal lobe 2.3 cm\nenhancing lesions appear smaller when compared to prior exam.  The associated\nwhite matter edema pattern has also improved.\n2. A punctate lesion of the right precentral gyrus is no longer noted.  No new\nenhancing lesions are identified\n3. Slightly worsening paranasal sinus these.  Additional findings described\nabove."
        },
        {
            "input": "Study is mildly degraded by motion.\n\nAgain is noted intra-axial enhancing mass of the left parietoccipital lobe\nwhich shows interval decrease of enhancement and significant interval increase\nof surrounding T2 FLAIR abnormal hyperintensity.  The mass lesion is stable in\nsize measuring 25 x 24 x 27 mm (AP, TRV, SI directions; respectively).  There\nhas been interval progression of mass effect on adjacent brain sulci and\noccipital horn of the left lateral ventricle with no definite evidence of\nhydrocephalus.\n\nAgain is noted cortical based intra-axial right parietal lobe lesion which\nshow also interval decrease of enhancement and interval increased surrounding\nT2 FLAIR hyperintensity.  The mass lesion is grossly stable in size measuring\n16 (AP) x 27 (TV) x 17 (SI) mm.\n\nInterval increase of the gradient echo susceptibility artifact is suggestive\nintratumoral hemorrhage versus mineralization.\n\nNew two right frontal lobe cortical based approximately 2 mm enhancing lesions\n(series 9, image 124 and 107).\n\nThere is no evidence of acute infarct or new other intracranial hemorrhage.\n\n Periventricular and subcortical T2 and FLAIR hyperintensities are noted which\nmay represent small vessel ischemic and/or treatment related changes.  Sequela\nof prior lacunar infarcts of the bilateral basal ganglia is also unchanged.\n\nThe major intracranial flow voids are preserved.  The dural venous sinuses are\ngrossly patent.\n\nThere is interval progression of moderate to severe paranasal sinuses disease\ninvolving both maxillary sinuses; worse on the left side; as well as anterior\nmode air cells and left frontal sinus.",
            "output": "1.  Study is mildly degraded by motion.\n2. Redemonstration of left parieto-occipital and right parietal intra-axial\nmetastatic lesions with interval decrease of enhancement and stable size.\n3. Interval increase of surrounding T2 FLAIR signal abnormality with\nlocoregional mass effect as described.\n4. New cortical based tiny abnormal enhancement as described, concerning for\nnew metastatic lesions.\n5. New right frontal cortical based approximately 2 mm metastatic lesions as\ndescribed.\n6.  Paranasal sinus disease , as described."
        },
        {
            "input": "When compared to ___ MR head, there has been overall interval\nimprovement of intracranial metastatic disease, as evidenced by interval\ndecrease in size of the lesions as well as decreased contrast enhancement and\nperilesional T2/FLAIR hyperintense parenchymal edema.  The left\nparietooccipital lobe parasagittal lesion now measures 2.2 x 1.7 x 1.9 cm,\npreviously measuring 2.7 x 2.5 x 2.4 cm in ___ (901:116, 9:98). The\nright cortically based parietal lobe lesion now measures 2.5 x 1.2 x 1.8 cm,\npreviously measuring 2.7 x 1.7 x 1.6 cm ___ (901:129, 9:100).  Both\nlesions continues to demonstrate gradient echo susceptibility artifact,\nsimilar to prior studies.  Previously seen 2 cortically based 2 mm enhancing\nlesions within the right frontal lobe are not identified in the postcontrast\nimages today, suggesting interval significant decrease in size/resolution.  No\nnew enhancing lesions are identified.\n\nThere is no evidence of midline shift or infarction.  Scattered\nperiventricular and deep subcortical white matter T2/FLAIR hyperintensities\nare nonspecific and may represent chronic small vessel disease, overall\nsimilar to prior.  The ventricles and sulci are normal in caliber and\nconfiguration.\n\nBilateral maxillary and ethmoidal paranasal sinus disease has improved in the\ninterim: Left ethmoidal and left maxillary sinusitis has resolved, there is\nresidual moderate right maxillary mucosal thickening with air-fluid levels and\nmild mucosal thickening of the right ethmoid air cells.  Major intracranial\nflow voids are preserved.",
            "output": "1. When compared to ___ head MR there has been overall interval\nimprovement of intracranial metastatic disease, as evidenced by decreased size\nof the lesions as well as decreased contrast enhancement and perilesional\nT2/FLAIR hyperintense parenchymal edema.\n2. No new metastatic lesions identified.\n3. Moderate right ethmoidal and maxillary sinus disease."
        },
        {
            "input": "In comparison with the most recent MRI examination dated ___, the\npreviously seen left parieto-occipital hemorrhagic metastatic lesion has\ndecreased in size from 22 mm x 19 mm, to 15 mm x 12 mm (series 8, image 16),\nhowever the peripheral pattern of enhancement appears slightly thicker and now\nmeasures 7 mm a previously 4 mm (series 10, image 16).  The right cortical\nbased parietal lobe lesion appears slightly larger and measures 30 x 19 mm in\ntransverse dimension and previously 24 x 16 mm (series 10, image 16).  Similar\nareas of T2/FLAIR high-signal intensity are visualized surrounding the\nhemorrhagic metastatic lesions, likely consistent with posttreatment changes. \nChronic lacunar infarcts are again seen in the basal ganglia bilaterally and\nappear unchanged.  The ventricles and sulci are slightly prominent suggesting\nmild cortical volume loss, unchanged.  The major vascular flow voids are\npresent and demonstrate normal distribution.\n\nThe orbits demonstrate bilateral lens replacement, otherwise are unremarkable.\nThe paranasal sinuses demonstrate persistent mucosal thickening in the right\nethmoidal air cells, and increased opacification of the right maxillary sinus\nwith heterogeneous signal suggesting an ongoing inflammatory process, the\npossibility of fungal colonization is also a consideration.",
            "output": "1.  In comparison with the most recent brain MRI examination dated ___, there is mild interval enlargement and persistent heterogeneous\nenhancement in the cortically based right parietal lobe lesion hemorrhagic\nmetastatic lesion, with similar pattern of vasogenic edema suggestive\nposttreatment change.\n\n2.  The left parieto-occipital hemorrhagic metastatic lesion has decreased in\nsize from 22 mm x 19 mm, to 15 mm x 12 mm (series 8, image 16), however the\nperipheral pattern of enhancement appears slightly thicker and now measures 7\nmm a previously 4 mm (series 10, image 16).\n\n3.  There is no evidence of new areas with abnormal enhancement.\n\n4.  Persistent paranasal sinus disease, with interval worsening in the\nopacification of the right maxillary sinus, suggesting an ongoing inflammatory\nprocess, the possibility of underlying fungal colonization is also\nconsideration."
        },
        {
            "input": "When compared to most recent MRI of ___, the previously noted\nhemorrhagic metastatic lesion in the left parieto-occipital lobe demonstrates\ninterval decrease in size, measuring 1 cm x 1 cm.  Similarly, the pre-existing\nnodular enhancement in the anterior aspect of the hemorrhagic lesion also\ndemonstrate interval decrease in size measuring approximately 6 mm x 9 mm x 6\nmm (AP, TV, SI).  There is also interval decrease of surrounding T2/FLAIR\nhyperintensity in the left parieto-occipital lobe.\n\nAdditionally, the previously noted cortically based hemorrhagic lesion in the\nright parietal lobe also demonstrate interval decrease in size, measuring\napproximately 2.0 cm x 1.0 cm.  There is also interval decrease of enhancement\nand T2/FLAIR hyperintensity surrounding this hemorrhagic lesion.\n\nNo new lesions are identified.\n\nThere is no evidence of mass effect, midline shift or infarction.   The\nventricles and sulci are prominent in caliber and configuration, likely\nreflecting age-related involutional changes.  There are scattered T2/FLAIR\nhyperintensity in the periventricular and subcortical white matter compatible\nwith chronic microangiopathy in this age.  Chronic lacunar infarcts are again\ndemonstrated in the bilateral basal ganglia.\nThe major vascular flow voids are present and appear normal, the major dural\nvenous sinuses enhance normally.\n\nAgain seen is complete opacification of the right maxillary sinus with mucosal\nthickening of the ethmoid air cells and heterogeneous signal, the possibility\nof fungal colonization is a consideration.  The mastoid air cells are clear. \nStatus post bilateral lens replacement.",
            "output": "1. Interval decrease in size of the hemorrhagic metastatic left\nparieto-occipital lobe lesion, and the adjacent anterior nodule enhancement,\nwhen compared to MRI of ___.  Additionally, surrounding perilesional\nvasogenic edema also demonstrates interval decrease in size of, likely related\nto posttreatment changes.\n2. Interval decrease in size of the cortically based hemorrhagic lesion in the\nright parietal lobe and the surrounding vasogenic edema, likely compatible\nwith posttreatment changes.\n3. No new lesions are identified.\n4. Persistent paranasal sinus disease with opacification of the right\nmaxillary sinus, suggesting continued inflammatory processes.  Underlying\nfungal colonization is a consideration."
        },
        {
            "input": "There is no evidence of acute intracranial hemorrhage or mass effect.  The\nventricles and sulci are slightly prominent for the patient's age, this\nfinding is not specific, however suggest mild cortical volume loss, please\ncorrelate clinically, note is made that this finding is more significant on\nthe parietal regions.  No focal lesions are noted throughout the brain\nparenchyma or diffusion abnormalities to indicate acute or subacute ischemic\nchanges.  The major vascular flow voids are present and demonstrate normal\ndistribution.  The orbits are unremarkable, paranasal sinuses are notable for\nmucosal thickening on the right maxillary sinus, consistent with mucous\nretention cyst",
            "output": "1.  There is no evidence of acute intracranial process.\n\n2.  Slightly prominent sulci for the patient's age, which is nonspecific,\nhowever suggest cortical volume loss, more notable in the parietal\nconvexities.\n\n3.  Mucous retention cyst identified on the right maxillary sinus."
        },
        {
            "input": "There is an approximately 4.5 x 4 cm irregular rim enhancing lesion in the\nright temporal lobe with extensive surrounding edema and mass effect on the\nright lateral ventricle.  There is no hydrocephalus.  Susceptibility images\ndemonstrate small areas of blood products.  No evidence of intrinsic\nrestricted diffusion seen within the mass.  No other areas of abnormal\nenhancement are seen.  No acute infarcts are identified.",
            "output": "Right temporal lobe mass with appearance most consistent with an aggressive\nglial neoplasm."
        },
        {
            "input": "Study is moderately degraded by motion.  Within these confines:\n\nPatient is status post right craniotomy for temporal lobe mass resection. \nMinimal nodular enhancement (see 4,10:11) and ischemic changes are noted at\nthe resection margin.  No residual mass is identified.  Small amount of\npneumocephalus is noted.  Leftward midline shift by 9 mm is stable.  Soft\ntissue swelling overlying craniotomy is increased than before.  Subdural fluid\nis noted deep to the craniotomy site and in the surgical cavity.  Expansile\nwhite matter FLAIR hyperintensity in left basal ganglia and temporal region is\nsimilar to before.  The ventricles and sulci are unchanged in caliber and\nconfiguration.",
            "output": "1. Study is moderately degraded by motion.\n2. Patient is status post right temporal mass resection with expected\npostoperative findings.  Minimal nonspecific restricted diffusion along\nresection margin may represent postoperative changes.\n3. Minimal nonspecific nodular enhancement along resection cavity as\ndescribed.  While finding may represent postoperative changes, residual tumor\nis not excluded on the basis of this examination.  Recommendation attention on\nfollow imaging.\n4. Leftward midline shift is unchanged compared to 1 day ago.\n5. Soft tissue swelling overlying the right temporal craniotomy is increased\ncompared to 1 day ago.\n\nRECOMMENDATION(S):  Minimal nonspecific nodular enhancement along resection\ncavity as described.  While finding may represent postoperative changes,\nresidual tumor is not excluded on the basis of this examination. \nRecommendation attention on follow imaging.\n\nNOTIFICATION:  The impression and recommendation above was entered by Dr.\n___ on ___ at 21:45 into the Department of Radiology critical\ncommunications system for direct communication to the referring provider."
        },
        {
            "input": "MRI BRAIN:\n There is no evidence of acute infarction.  There is a small chronic infarct\nin the left cerebellar hemisphere.  No intracranial hemorrhage. No mass, mass\neffect, edema or midline shift.\n\nThe ventricles and sulci are normal, without evidence of hydrocephalus. There\nis gross preservation of the principal intracranial vascular flow voids.\n\nThe visualized paranasal sinuses, middle ear cavities, and mastoid air cells\nare well aerated and clear.  The orbits are within normal limits bilaterally.\n\n\nMRA BRAIN:\nThe intracranial vertebral and internal carotid arteries and their major\nbranches appear grossly patent without evidence of stenosis, occlusion, or\naneurysm formation.  Mild irregularity is noted in the bilateral cavernous\ninternal carotid arteries, better characterized on the recent CT examination.\n\n\nMRA NECK:\nThe entirety of the left V1, V2, and V3 segments are not visualized.  Minimal\nflow related signal is seen within the distal left V4 segment, likely due to\nretrograde filling from the basilar artery.\n\nT1 fat saturated sequences demonstrate the absence of a left-sided vertebral\nartery flow void, but without focal increased T1 signal to suggest an\nintramural hematoma/dissection.\n\nThe right vertebral artery is widely patent.  Similarly, the bilateral common\nand internal carotid arteries are patent without high-grade stenosis by NASCET\ncriteria.",
            "output": "1. No evidence for acute intracranial hemorrhage or infarction.\n2. Grossly patent intracranial vasculature without high-grade stenosis or\nvessel occlusion.\n3. No appreciable flow related signal seen throughout the course of the left\nvertebral artery, similar to findings seen on recent CT examination.  However,\nno focal increased signal on T1 fat saturation sequences to suggest a hematoma\nor dissection.  These findings may be congenital in nature vs less likely\nsecondary to a chronically thrombosed vessel, and correlation with earlier\nimaging is recommended if available."
        },
        {
            "input": "MR BRAIN:\nThere is no acute infarction, edema, evidence for blood products, or other\nsignal abnormalities on the images provided.  Ventricles, sulci, and basal\ncisterns are normal in size.  Cerebellar tonsils are normally positioned. \nPituitary gland is grossly normal in size on the sagittal T1 weighted images,\nthough not evaluated in detail in the absence of dedicated high-resolution\nimages.\n\nMRA BRAIN:\nImages are mildly limited by motion artifact.  The intracranial vertebral and\ninternal carotid arteries and their major branchesappear widely patent without\nevidence for flow-limiting stenosis or aneurysm.\n\nDural venous sinuses are not adequately assessed in the absence of\npostcontrast MP RAGE images.",
            "output": "1. No acute infarct and no evidence for other abnormalities in the brain\nparenchyma on noncontrast MRI.\n2. Unremarkable MRA of the circle of ___.\n3. Dural venous sinuses are not adequately assessed in the absence of\npostcontrast MP RAGE images."
        },
        {
            "input": "The origin of right vertebral artery appears normal.  Distal to this, the\nvessel is very poorly seen, as is the course of this vessel through most of\nthe neck on post-contrast images.  The distal cervical portion of the vessel\nand intracranial portion both appear normal.  Prominent vessels, perhaps\nearly-enhancing veins, obscure images of the mid cervical portion of the right\nvertebral artery, however the pre-contrast 2D time-of-flight images\ndemonstrate this portion of the right vertebral artery to be widely patent. \nAlthough overall findings suggest a right vertebral artery to be widely\npatent, findings also raise the possibility of a right vertebral-venous\narteriovenous shunt with early opacification of spinal veins in this location.\n\nThe common, internal and external carotid arteries appear normal bilaterally. \nThere is no evidence of ICA stenosis by NASCET criteria. The visualized\norigins of the great vessels, subclavian, andleft vertebral arteries appear\nnormal bilaterally.  The common carotid bifurcations appear normal. There is\nno evidence of dissection.",
            "output": "1. Although the right vertebral artery appears widely patent, findings also\nraise the possibility of a right vertebral-venous arteriovenous shunt, which\ncould be traumatic in etiology.\n2. Normal appearance of the bilateral carotid and left vertebral arteries.\n\nRECOMMENDATION(S):  Neurology or neurosurgical consultation is recommended for\nfurther assessment as to the clinical relevance of the above indeterminate\nimaging findings regarding the right vertebral artery, with consideration of\nmore advanced imaging (e.g. time-resolved MRA or CTA), if clinically\nappropriate.\n\nNOTIFICATION:  The impression and recommendation above was entered by Dr.\n___ on ___ at 16:41 into the Department of Radiology\ncritical communications system for direct communication to the referring\nprovider."
        },
        {
            "input": "Arterial phase of MRA neck ___ head significant venous contamination\nsecondary to technique, and less than ideal arterial phase.\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.  Preserved vascular flow voids.  Mild paranasal sinus disease,\nsecretions in the sphenoid sinus.  Clear mastoids.  No abnormal intracranial\nvasculature.  No MRI evidence of AVM or dural AV fistula.  Small developmental\nvenous anomaly left cerebellum.  Patent dural venous sinuses.",
            "output": "1. No evidence of vascular malformation.\n2. Suggestion of mild acute sphenoid sinusitis."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  Minimal subcortical T2/FLAIR white matter hyperintensity in\nthe right frontal lobe is nonspecific (6:15), and could be due to a sequela of\nchronic microangiopathic disease.  Major intracranial vascular flow voids are\npreserved.  There is a mucous retention cyst in the right maxillary sinus.\nOrbits are unremarkable.",
            "output": "No acute process."
        },
        {
            "input": "There is an area of restricted diffusion which is dark on the ADC in the left\ntemporoccipital lobe (04:18) compatible with acute infarction.  Additional\nareas of restricted diffusion dark on the ADC seen are seen along the left\ntemporal cortex compatible.  These areas demonstrate increased FLAIR signal\nabnormality.  There is no evidence of masses, mass effect, or midline shift. \nThe ventricles and sulci are normal in caliber and configuration.",
            "output": "Acute infarction in the left temporooccipital lobe.  Additional areas of\nrestricted diffusion along the left temporal cortex may represent additional\nareas of infarction, however findings may also be associated with seizure."
        },
        {
            "input": "MRI Brain:\nThere are several scattered deep white matter infarcts within bilateral\ncerebral hemispheres, some of which  appear acute/subacute, for example in the\nleft frontoparietal lobe (302:22).  Old lacunes and a hemorrhagic focus are\nseen within the pons (9:8), unchanged from ___.  Diffuse microhemorrhages are\nagain noted, which could be due to amyloid angiopathy.  Extensive bilateral\nperiventricular, subcortical and deep white matter T2/FLAIR hyperintensities\nare nonspecific, but suggestive of chronic small vessel disease.  There is no\nevidence of masses, mass effect or midline shift.  Ventricles and sulci are\nprominent, suggestive of age related involutional changes.\n\nMRA brain:  There is diffuse narrowing of the bilateral M1 and M2 segments of\nthe middle cerebral artery, as well as the A1 segment of the left anterior\ncerebral artery (Se 60___: Im4), an appearance that is suggestive of severe\natheromatous disease.  However, given their normal appearance on the prior CTA\ndated ___, it is unclear if this may partially be due to artifact. \nRemainder of the circle of ___ vessels, intracranial internal carotid and\nvertebral arteries are without evidence of stenosis, occlusion, or aneurysm\nformation.\n\nMRA neck:  Please note that the 2D time-of-flight images are limited. \nHowever, common, internal and external carotid arteries appear normal on the\n3D reformations. There is no evidence of internal carotid artery stenosis by\nNASCET criteria. The origins of the great vessels, subclavian and vertebral\narteries appear normal bilaterally.",
            "output": "1.  Several scattered deep white matter infarcts, some of which are\nacute/subacute in the left frontoparietal lobe.\n2.  Diffuse microhemorrhages as noted previously, which could be due to\namyloid angiopathy.\n3.  Old pontine lacunes and hemorrhage, unchanged from ___.\n4.  Diffuse narrowing of bilateral M1 and M2 segments, and the left A1 segment\nan appearance that is suggestive of severe atheromatous disease. However,\ngiven normal appearance of these vessels on the ___ CTA, this may\npartially be due to artifact.\n5. No aneurysm in the circle ___."
        },
        {
            "input": "MRI Brain:  Motion degraded exam.  There is no evidence of acute infarction. \nAsymmetrically increased signal within the vessels overlying the right\ncerebral hemisphere indicate slow anterograde flow.  Mild to moderate chronic\nmicroangiopathic ischemic changes in the periventricular and subcortical white\nmatter.  No signs of intracranial hemorrhage.  Absent right intracranial\ninternal carotid artery flow void.\n\nBilateral lens replacements.  Paranasal sinuses and mastoid air cells appear\nclear.  Fluid layering dependently in the nasopharynx.\n\nMRA brain:  Loss of normal anterograde flow related enhancement of an in the\nright intracranial internal carotid artery.  Asymmetrically decreased, but\nanterograde flow within the right middle cerebral artery and branches is from\nthe left ICA via the anterior communicating and patent right A1 segments. \nLeft intracranial internal carotid artery, middle cerebral artery, and\nbilateral anterior cerebral arteries show normal flow related enhancement. \nBilateral posterior communicating arteries are present.\nNon dominant posterior circulation.  Normal flow related enhancement in\nbilateral intracranial vertebral arteries, basilar artery, and posterior\ncerebral arteries.  Both posterior cerebral arteries are partially fistulae\nreplaced.\n\nMRA neck:  Antegrade flow in the right common carotid artery is asymmetrically\ndecreased.  There is absent antegrade flow in the right internal carotid\nartery.  Preserved antegrade flow in the right external carotid artery.\n\nPreserved, anterograde flow related enhancement within the left common,\ninternal, and external carotid arteries.\n\nThere is absence of the antegrade flow in the nondominant proximal left\nvertebral artery, which is likely artifactual.  There remaining cervical\nvertebral arteries demonstrate antegrade flow.\n\nBilateral pleural effusions.",
            "output": "1. No evidence of acute infarction, acute hemorrhage, mass effect, or\nhydrocephalus.\n2. Absence of flow within the right cervical and intracranial internal carotid\nartery.  Asymmetrically decreased antegrade flow within the right common\ncarotid artery.  CTA is recommended to establish sites of inflow disease.\n3. Absence of flow within the nondominant proximal cervical left vertebral\nartery is likely artifactual, but can also be evaluated with CTA.\n4. Prominent, chronic microangiopathic ischemic changes.  Generalized volume\nloss."
        },
        {
            "input": "There is focal T2 hyperintensity in the left frontal lobe posteriorly, which\nwas not present on the MR head scan from ___ if this ___ represent an\ninterval, chronic focal infarct.  There is no evidence of hemorrhage, edema,\nmasses, mass effect, midline shift or acute infarction.  There is expected\nsusceptibility artifact related to the left ICA stent.  The ventricles and\nsulci are normal in caliber and configuration.",
            "output": "1. No mass, hemorrhage or recent infarction.\n2. New interval T2 hyperintense focus in the posterior left frontal lobe, not\npresent on the MRI performed in ___, this ___ represent an interval,\nchronic infarct.\n3. Expected susceptibility artifact from the left ICA stent."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  The ventricles and sulci are normal in caliber and\nconfiguration.  The inferior, intracranial portion of the right internal\njugular vein is mildly prominent (19:21), but without focal mass with an\nassociated right jugular diverticulum (series 18, image 79) measuring\napproximately 1.6 cm.  However, there is a 1.3 x 0.5 x 0.7 cm enhancing lesion\nnoted within the right occipital bone, immediately posterior to the right\ntransverse sinus (17:138, 19:29).  The adjacent transverse sinus remains\npatent.  No additional foci of abnormal intracranial enhancement are\nidentified.\n\nThere is preservation of gray-white matter differentiation. The basal cisterns\nremain patent.  No overt osseous lesion is identified. The left mastoid air\ncells are partially opacified.  There is mild mucosal thickening of the\nethmoid air cells and sphenoid sinuses.  The remainder the paranasal sinuses,\nmiddle ear cavities, and mastoid air cells are otherwise clear. The bilateral\norbits are unremarkable in appearance. The major intracranial flow voids are\npreserved.",
            "output": "1. No mass lesion in the right jugular foramen is noted.  The right jugular\nvein is dominant with an inferiorly projecting right jugular diverticulum.\n2. 1.3 x 0.5 x 0.7 cm enhancing mass within the right occipital bone, noted\nimmediately posterior to the right transverse sinus.  Findings likely\nrepresent an intraosseous hemangioma.\n3. Otherwise, the brain is essentially unremarkable.\n\nRECOMMENDATION(S):  Point 2:  Correlation with prior imaging if available is\nrecommended to document stability."
        },
        {
            "input": "There is no acute infarction, intracranial hemorrhage, extracerebral fluid\ncollection, midline shift or mass effect.  Ventricles and extra-axial spaces\nare normal in size.  Flow voids are maintained. Suprasellar and craniocervical\nregions are unremarkable.",
            "output": "No significant abnormalities are seen on MRI of the brain without gadolinium."
        },
        {
            "input": "Evaluation is suboptimal due to motion artifact.  Within this confine:\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  The ventricles and sulci are prominent, consistent with global\ncerebral volume loss.  Etat crible is noted.  A partially empty sella is seen.\nA subcentimeter old infarct is seen involving the left anterior corona\nradiata.\n\nThere is mild mucosal thickening of the left sphenoid sinus.  Otherwise, the\nparanasal sinuses, mastoid air cells and middle ear cavities are clear.  The\nintraorbital contents are normal.",
            "output": "1. No acute intracranial abnormality."
        },
        {
            "input": "There is no evidence of intracranial hemorrhage, edema, masses, mass effect,\nmidline shift or acute infarction.  Mild prominent ventricles and sulci,\nsuggesting mild cortical volume loss, slightly more pronounced towards the\nfrontoparietal convexity.  Few scattered ill-defined T2/FLAIR periventricular\nand subcortical white matter hyperintensities are nonspecific but likely\nsecondary due to chronic sequela of small-vessel ischemic disease.  There is\nno abnormal enhancement after contrast administration.\n\nThe major intracranial arterial flow voids are preserved.  There are\npostsurgical changes in the paranasal sinuses, moderate mucosal thickening is\nseen in the frontal sinuses, left greater than right.  There is near complete\nopacification of the anterior ethmoid air cells.  The mastoid air cells and\nmiddle ear cavities appear grossly clear.  The orbits are unremarkable.",
            "output": "1. No acute intracranial abnormalities.  Specifically, no evidence of tumor or\nfindings to indicate multiple sclerosis.  There is no evidence of abnormal\nenhancement after contrast administration.\n2. Slightly prominent ventricles and sulci suggesting mild cortical volume\nloss.\n3. Few scattered foci of T2/FLAIR high-signal intensity are nonspecific and\nmay reflect chronic microvascular ischemic disease.\n4. Moderate paranasal sinus disease, as detailed above."
        },
        {
            "input": "There is restricted diffusion in the posterior limb of the left internal\ncapsule extending into the left corona radiata and associated with T2/FLAIR\nhyperintense signal.  Chronic infarctions are noted within the anterior limb\nof the right internal capsule, right putamen, right caudate, and left\nthalamus.\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, or midline\nshift.   The ventricles and sulci are normal in caliber and configuration. \nThere is no abnormal enhancement after contrast administration.\n\nThere is mild mucosal thickening in the bilateral ethmoid sinuses.  The\nmastoid air cells are clear.  The orbits are unremarkable.",
            "output": "1. Acute infarction in the posterior limb of the left carpus internal capsule\nand left corona radiata without evidence of hemorrhagic conversion.\n2. Chronic right basal ganglia and left thalamus infarcts.\n3.  Paranasal sinus disease as described.\n\nNOTIFICATION:  These findings were documented in the in Neurology progress\nnote on ___ at 10:33 A.M. by Dr. ___."
        },
        {
            "input": "Study is slightly motion limited.  Previously seen focus of diffusion\nrestriction within the right temporoparietal junction is no longer evident. \nAdditional questionable punctate focus seen in the right cerebellum is no\nlonger identified.  No new focus of diffusion restriction is evident.  Focus\nof susceptibility abnormality in the left posterior frontal lobe/precentral\ngyrus (6; 20) is similar.  Vascular enhancement involving in the right frontal\ncentrum semiovale is re-identified in consistent with developmental venous\nanomaly.  Ventricles, sulci and cisterns demonstrate similar mild involutional\nchanges.  Mild predominantly periventricular and a few scattered subcortical\nwhite matter T2/FLAIR hyperintensities are similar and suggestive of\nmicrovascular ischemic change.\n\nThere is no evidence of acute hemorrhage, edema, masses, mass effect, midline\nshift or acute infarction.  The ventricles and sulci are normal in caliber and\nconfiguration.\n\nApproximately 4.7 CC x 2.0 AP x 6.0 TRV cm fat intensity lesion in the\nsubcutaneous soft tissues at the posterior base of the neck is similar. \nApproximately 1.5 cm (3; 3) ovoid focus within the left neck is incompletely\nimaged, but likely a level 1 lymph node.  Minimal ethmoid air cell mucosal\nthickening is noted.",
            "output": "1. No evidence of metastatic involvement of brain or acute intracranial\nabnormality.\n2.  Similar appearance of focus susceptibility abnormality posterior right\nfrontal lobe.\n3. Left upper limits of normal left cervical lymph node.  Clinical correlation\nsuggested, given history of malignancy.\n\nRECOMMENDATION(S):  Left upper limits of normal left cervical lymph node.\nClinical correlation suggested, given history of malignancy.\n\nNOTIFICATION:\n The impression and recommendation above was entered by Dr. ___ on\n___ at 10:16 into the Department of Radiology critical communications\nsystem for direct communication to the referring provider."
        },
        {
            "input": "There are few scattered foci of T2/FLAIR hyperintensity in the periventricular\nand subcortical white matter without associated enhancement, nonspecific. \nThere is mild FLAIR hyperintensity in the splenium of the corpus callosum\nwithout associated enhancement.  There is a focus of susceptibility in the\nright precentral gyrus (7:20) without enhancement (21:120), possibly related\nto a microhemorrhage.  There is no evidence of hemorrhage, edema, masses, mass\neffect, midline shift or acute infarction.  The ventricles and sulci are age\nappropriate caliber and configuration.  There is no abnormal enhancement after\ncontrast administration.\n\nThere is mild mucosal thickening in the ethmoid air cells.  No significant\nfluid signal is noted in the mastoid air cells.  The visualized orbits are\nunremarkable.",
            "output": "1. Punctate focus of susceptibility in the right precentral gyrus likely\nreflecting a microhemorrhage.\n2. Few scattered foci of T2/FLAIR hyperintensity in the periventricular and\nsubcortical white matter, nonspecific but likely reflect sequelae of chronic\nmicroangiopathy.  This pattern of distribution is not typical for\ndemyelinating disease and there is no associated enhancement to suggest active\ndemyelination.\n3. Otherwise no acute intracranial abnormality, mass or abnormal enhancement."
        },
        {
            "input": "There is a 38 x 29 mm lesion identified within the right cerebellar hemisphere\nwith intrinsic restricted diffusion and peripheral rim of subacute to chronic\nblood products.  There is T1 hypointensity and T2 and FLAIR hyperintensity in\nthe central portion of the lesion.  There is extensive susceptibility related\nlow signal within the midbrain extending to the right middle cerebellar\npeduncle indicative of a cavernous malformation.  Multiple other areas\nsuggestive of cavernous malformations are seen in both cerebral hemispheres. \nMass effect is identified on the fourth ventricle.  There is no hydrocephalus\nseen.",
            "output": "1. The right cerebellar hematoma has increased in size considerably since the\nprevious CT.  There are no intervening examinations.  The signal\ncharacteristics of the hematoma are unclear and could represent new blood\nproducts or cellular debris within the hematoma.\n2. Further evaluation with CT is recommended.  If  acute blood products are\nnot identified on CT, further evaluation with contrast-enhanced brain MRI is\nrecommended."
        },
        {
            "input": "There is redemonstration of innumerable supra and infratentorial partially\nenhancing presumably cavernous malformation.  There is interval evolution of\nlarge right medial cerebellar hemisphere hemorrhagic component with residual\nlocoregional hemosiderin staining.  There is a pronounced cerebellar\nhemispheres and brainstem structures atrophy.\n\nThere is no definite enlarging or new edematous changes. There is no evidence\nof mass effect, midline shift, brain or acute infarction.  The ventricles and\nsulci are stable in caliber and configuration.  Patent dural venous sinuses. \nUnremarkable major intracranial vascular flow voids.\n\nBoth orbits are unremarkable.  Mucosal thickening involving paranasal sinuses.\nRight maxillary sinus retention cyst.  trace fluid signal intensity at right\nmastoid air cells.",
            "output": "1. Redemonstration of innumerable supra and infratentorial partially enhancing\npresumably cavernous malformations.\n2. Interval evolution of large right medial cerebellar hemisphere hemorrhagic\ncomponent with residual locoregional hemosiderin staining.\n3. No definite enlarging or new edematous changes."
        },
        {
            "input": "Again seen are numerous supratentorial, infratentorial and brainstem cavernous\nmalformations with varying degrees of chronic internal hemorrhage and\ncalcification, not significantly changed in number in comparison to prior MRI\nperformed ___.  A small cavernoma is also partially visualized in the\nlateral aspect of the upper cervical spinal cord (7:1).  Findings are\ncompatible with familial multiple cavernous malformation syndrome.\n\nAs noted on the prior CT, one of the larger lesions which is located in the\nright cerebellar peduncle extending into the right pons demonstrates recent\nhemorrhage contributing to local mass effect including partial effacement of\nthe fourth ventricle on the right, for which DTI tractography was requested\nfor potential preoperative planning.\n\nDTI tractography: Artifact from hemorrhage in the region of the right\ncerebellar peduncle obscures evaluation of white matter tracts.  However,\nthere is lateral deviation of the white matter tracts along the right lateral\naspect of the cerebellar peduncle hemorrhagic cavernoma.  Additional lateral\ndeviation of the major bilateral white matter tracts is noted around a second,\nmore inferior pontine cavernoma.\n\nThere is mild diffuse prominence of the sulci compatible with involutional\nchanges.  Cerebellar atrophy appears similar in comparison to the previous\nMRI.  No evidence of acute territorial ischemic infarct.  No evidence of\nmidline shift.\n\nThere are mild paranasal sinus inflammatory changes.  There is a small right\nmaxillary sinus mucosal retention cyst.  The mastoid air cells appear clear. \nThe visualized globes and orbits appear within normal limits.",
            "output": "1. Numerous cavernous malformations in the supra and infratentorial brain as\nwell as within the brainstem and upper cervical spinal cord appear similar in\nnumber when compared to prior MRI performed ___.  Findings compatible\nwith familial multiple cavernous malformation syndrome.\n2. As seen on the prior CT, one of the most prominent cavernomas centered in\nthe right cerebellar peduncle extending into the right pons demonstrates\nrecent hemorrhage with local mass effect including partial effacement of the\nright anterior fourth ventricle.  This lesion demonstrates lateral deviation\nof the major white matter tracts on DTI tractography, as described above.\n3. Additional findings, as above.\n\nNOTIFICATION:  The findings were discussed with Dr.  ___ by Dr.\n___ in person on ___ at 12:00 pm, 10 minutes after discovery of\nthe findings."
        },
        {
            "input": "An acute to subacute intracranial infarction is seen in the left\nfrontoparietal region in the territory of the left M2, corresponding to the\narea of decreased density on the prior CTA from 06:00 on the same day.  A\npunctate focus of restricted diffusion is also seen in the left frontal lobe,\nnear the vertex, series 4, image 29 and along the anterior inferior frontal\nlobe, series 4, image 17, are likely secondary to an embolic foci of\ninfarction.  Extensive FLAIR signal abnormality is seen surrounding the left\nfrontoparietal region, with extension of the cytotoxic edema to the left\noccipital lobe.  Extensive T2/FLAIR signal abnormality in the periventricular\nand deep subcortical white matter is likely secondary to chronic small vessel\nischemic disease.  Mild prominence of ventricles and sulci is secondary to\nglobal atrophy.\n\nNo definite susceptibility artifact within the region of the left\nfrontoparietal infarction to suggest hemorrhage is identified.  Cut off of the\nleft M3 segment flow void, is similar to the prior CTA.\n\nEncephalomalacia is seen involving the left cerebellum, likely from prior\nsurgical intervention given overlying craniotomy changes.  No other marrow\nsignal abnormalities are identified.  The visualized paranasal sinuses,\nmastoid air cells, and middle ear cavities are clear.  The globes are\nunremarkable.",
            "output": "1. Acute to subacute left frontoparietal infarction in the left M2 territory. \nNo definite underlying hemorrhage is identified.  Additional punctate foci of\nrestricted diffusion within the left vertex and inferior left frontal lobe\n(4;17,29),  suggestive of foci of acute infarction.  Extensive surrounding\ncytotoxic edema.\n2. Postsurgical changes with encephalomalacia within the left cerebellum,\nstatus post prior left cerebellar craniotomy.\n3. Cut off of the left M3 segment flow void, similar to the prior CTA from ___."
        },
        {
            "input": "There is right caudate body and posterior lentiform nucleus diffusion\nrestriction with corresponding very subtle T2/FLAIR hyperintensity in keeping\nwith hyperacute to acute infarction.  There is no acute intracranial\nhemorrhage.\n\nThere is extensive periventricular and deep white matter as well as central\npontine confluent T2 FLAIR hyperintense signal intensity; nonspecific in\nappearance and could be related to moderate to severe form of chronic\nmicroangiopathy.  Multiple bilateral cerebral hemispheres and basal ganglionic\nlacunar infarcts.\n\nThere is no evidence of masses, mass effect or midline shift.   The ventricles\nand sulci are normal in caliber and configuration.\n\nStatus post lens removal surgery.  Otherwise both orbits are normal.  Minimal\nfluid signal intensity involving both mastoid air cells; worse on the left\nside.  Paranasal sinuses are essentially clear.",
            "output": "1. Right corpus striatum acute infarction with no acute intracranial\nhemorrhage.\n2. Background of moderate to severe form of chronic microangiopathy as well as\nbilateral lacunar infarctions.\n3. Additional findings as described above."
        },
        {
            "input": "There is no acute infarct mass effect midline shift or hydrocephalus.  The\nventricles and extra-axial spaces are normal in size.  A few scattered\nnonspecific foci of FLAIR hyperintensity are seen.\n\nIn absence of contrast-enhanced images evaluation for facial nerve enhancement\ncould not be performed given the history of Bell's palsy.\n\nAn expansile right frontal sinuses identified with fluid and scalloping of the\nadjacent frontal bone with high intensity on pre gadolinium images. \nSuggestive of a frontal sinus mucocele with inspissated secretions.\n\nExtensive mucosal thickening soft tissue changes are identified in the\nremaining sinuses including fluid in the sphenoid sinus with low intensity\nmaterial on T2 weighted images suggestive of inspissated secretions or fungal\ncolonization.  Additionally, there is a small low signal seen at the margin of\ncavernous sinus along the bony structures which could be due to hyperostosis. \nHowever, extension cavernous sinus is not completely excluded.  There is no\ndilatation of the superior ophthalmic veins seen, however.\n\nThere is a soft tissue changes seen within the right mastoid air cells and\nmiddle ear likely secondary to obliteration of the eustachian duct.",
            "output": "1. Right frontal mucocele with inspissated secretions.  Further evaluation\nwith sinus CT recommended.\n2. Chronic inspissated secretions or fungal colonization in the sphenoid sinus\ndue to chronic sinusitis.  Extension to the cavernous sinuses is not excluded\nalthough no dilatation of the superior ophthalmic veins is seen.  Further\nevaluation with cavernous sinus MRI is recommended.\n3. Enhancement of the facial nerves can be assessed on the cavernous sinus MRI\nfor visualization of the internal auditory canals.\n4. Fluid within the right mastoid air cells and middle ear as well as\nextensive soft tissue changes in the sinuses due to chronic sinus inflammatory\ndisease.\n5. No acute infarcts mass effect hydrocephalus within the brain.\n\nRECOMMENDATION\n1. Sinus CT for further evaluation of frontal sinus mucosal.\n2. Cavernous sinus gadolinium enhanced MRI to evaluate cavernous sinuses as\nwell as internal auditory canals."
        },
        {
            "input": "Severe diffuse mucosal thickening is identified in the nasal cavity and\nparanasal sinuses.  Altered sinus anatomy is suggestive of prior sinus\nsurgery.\n\nRight frontal sinus is completely opacified and dilated, measuring 29 (AP) x\n29 (TV) x 34 (SI) mm , unchanged in size compared to CT from ___. the\nwalls along the inner table of the frontal sinus is thinned and likely\ndehisced (series 6, image 9).  The contents of dilated right frontal sinus\ncontains T1 hyperintense material and does not enhance, consistent with a\nmucocele.  The frontal the dilated right frontal sinus displaces the right\nfrontal lobe and right intra orbital contents, including the right superior\nrectus.  There is no evidence of underlying brain parenchymal signal\nabnormality.  Left sphenoid sinus is similarly completely opacified and\ndilated, measuring 26 (AP) x 18 (TV) x 23 (SI) mm , stable in size and also\nconsistent with a mucocele.  The dilated left sphenoid sinus displaces the\nleft cavernous internal carotid artery slightly posteriorly and effaces medial\naspect of the left cavernous sinus, which is asymmetrically smaller compared\nto the right.  There appears to be mass effect on the left orbital apex and\nthe sphenoid mucocele appears to efface the left rotundum (series 13, image\n23; series 8, image 23).\n\nLeft superior ophthalmic vein is asymmetrically enlarged compared to the\nright.  The vessel is T2 hyperintense, which likely reflects slow flow,\nwithout evidence of filling defect on postcontrast images.  The cavernous\nsinuses appear patent bilaterally without evidence of defect, or expansion of\nthe lateral walls to suggest thrombosis.\n\n\nThere is no evidence of intracranial mass or acute infarct.  The ventricles\nand sulci are normal in caliber and configuration.  There is no abnormal\nintracranial enhancement after contrast administration.\n\nThe right mastoid air cells are fluid opacified.",
            "output": "1. 23 mm left sphenoid sinus mucocele causes asymmetric narrowing of the left\ncavernous sinus and left orbital apex.  In addition, the lesion effaces the\nleft foramina rotundum, presumably impinging on the V2 segment.  Correlation\nwith patient facial numbness is recommended.\n2. Left ophthalmic vein is asymmetrically dilated with slow internal blood\nflow, which may be due to the narrowing of the left cavernous sinus and\norbital apex.  This could be further evaluated with CTA/CTV as clinically\nindicated.  There does not appear to be cavernous sinus thrombosis.\n3. 34 mm right frontal sinus mucocele displaces right frontal lobe and right\nperiorbital structures.  No abnormal dural enhancement is identified to\nsuggest dural invasion.  Review of prior CT sinus from ___ is\nsuggestive of intracranial bony dehiscence.\n4. Diffuse severe mucosal thickening is noted in the nasal cavity and\nparanasal sinuses.  Fluid opacification of the right mastoid air cells."
        },
        {
            "input": "MRI BRAIN:\nThere is no evidence of intracranial hemorrhage, edema, masses, mass effect,\nmidline shift or infarction.  Prominence of the ventricles and sulci is\nsuggestive of involutional changes.  There is T2/FLAIR hyperintensities within\nthe periventricular white matter that may be nonspecific but may represent\nchronic microvascular ischemia.  There is no abnormal enhancement after\ncontrast administration.\n\nThere is mild mucosal thickening of the bilateral ethmoid air cells.  The\nmastoid air cells are clear.\n\nMRA BRAIN:\nThe intracranial vertebral and internal carotid arteries and their major\nbranches appear normal without evidence of stenosis, occlusion, or aneurysm\nformation.\nMRA NECK:\nThe common, internal and external carotid arteries appear normal.  There is no\nevidence of internal carotid artery stenosis by NASCET criteria.  The origins\nof the great vessels, subclavian and vertebral arteries appear normal\nbilaterally.",
            "output": "1. No acute intracranial process, most specifically no findings on MRI brain\nfindings to explain patient's symptoms.\n2. Normal MRA brain and neck with no evidence of internal carotid stenosis by\nNASCET criteria."
        },
        {
            "input": "There are areas of left cerebellar, left occipital and left parietal\nencephalomalacia with areas of bifrontal corona radiata and centrum semiovale\nencephalomalacia, as well as punctate areas of right cerebellar\nencephalomalacia suggestive of prior infarcts.  There is also left temporal\nvolume loss, which may suggest another prior infarct in this region.  There is\nex vacuo dilatation of the left lateral ventricle.  There is no evidence of\nhemorrhage, edema, masses, mass effect, midline shift or infarction.  Other\nbackground areas of periventricular, subcortical, deep and pontine white\nmatter T2/FLAIR hyperintensities are in a configuration most suggestive of\nchronic small vessel ischemic disease.  There is severe prominence of the\nventricles and sulci suggestive of involutional change.  There is also\ndisproportionate severe left hippocampal atrophy.  There is no abnormal focus\nof slowed diffusion.  The principal intracranial vascular flow voids are\npreserved.\n\nThere is a punctate  linear focus of magnetic susceptibility artifact in the\nleft posterior parietal lobe, suggestive of chronic microhemorrhage.\n\nThere is trace mucosal wall thickening in the bilateral anterior ethmoid air\ncells.  The remainder of the visualized paranasal sinuses are otherwise clear.\nThere are changes from left lens replacement surgery.  The orbits are\notherwise grossly unremarkable.  There is fluid in a single left mastoid air\ncell.  The mastoid air cells are otherwise clear.\n\nDegenerative pannus is seen around the dens, also with ligamentum flavum at\nthis level producing moderate spinal canal narrowing.  Limited view of the\ncervical spine demonstrates disc bulges, endplate osteophytes and ligamentum\nflavum thickening producing at least mild spinal canal narrowing at the C3-C4\nand C4-C5 levels.",
            "output": "1. Numerous scattered chronic infarcts with associated ex vacuo dilatation of\nthe left lateral ventricle, as described.\n2. Severe global atrophy as well as disproportionate severe left hippocampal\natrophy, which may be due to volume loss from prior infarcts.\n3. No acute infarct, hemorrhage, or suggestion of mass.\n4. Partial characterization of upper cervical spine degenerative change, with\nspinal canal narrowing at multiple levels, which can be further evaluated with\ndedicated cervical spine MR if clinically indicated"
        },
        {
            "input": "Patient is status post right parietal craniectomy and resection of a right\nparietal calvarial lesion, with postoperative changes including trace amount\nof hemorrhagic contents and fluid deep to the craniectomy site measuring 7 mm,\nwith adjacent dural thickening and enhancement, and soft tissue swelling with\nfluid.  There is no evidence of residual right parietal calvarial lesion.\n\nThere is a new peripherally enhancing right parietal intraparenchymal fluid\ncollection measuring 3.0 x 2.2 cm (10:16), demonstrating internal isointense\nT1, hyperintense T2 signal, with peripheral slow diffusion and surrounding\nFLAIR hyperintensity, without associated hypointense GRE signal.  This exerts\nmass effect with partial effacement of the right lateral ventricle with 6 mm\nleftward midline shift.  There is no evidence of hydrocephalus, although the\ntemporal horn of the right lateral ventricle is slightly prominent.\n\nThere is no evidence of infarction.  The paranasal sinuses and bilateral\nmastoid air cells appear clear.  The visualized vascular flow voids are\npreserved.  The visualized dural venous sinuses appear patent.",
            "output": "1. Status post right parietal craniectomy and resection of previously seen\nright parietal calvarial lesion.  No evidence of residual tumor.\n2. Right parietal lobe fluid collection, with signal characters described\nabove although not typical may be compatible with an abscess or late\ncerebritis, measuring 3.0 x 2.2 cm.\n3. Nonspecific pachymeningeal thickening and enhancement deep to the\ncraniectomy site.  Finding is nonspecific and may be postoperative in\netiology, although possibility of infection is not entirely excluded.\n4. Surrounding edema with mass effect on the right lateral ventricle and 6 mm\nleftward midline shift.\n\nNOTIFICATION:  The findings were discussed with ___, M.D. by\n___, M.D. on the telephone on ___ at 11:33 ___, 1 minutes after\ndiscovery of the findings."
        },
        {
            "input": "Postsurgical changes right parietal abscess evacuation are noted including 2.0\nx 1.4 cm and 1.1 x 2.0 cm collections within the evacuation cavity with\nminimal associated rim enhancement (series 12, image 16; series 12, image 15).\nA small amount of pneumocephalus is expected.  There is intrinsic T1\nhyperintense signal and susceptibility within the evacuation cavity,\nconsistent with postoperative blood products.  Surrounding the evacuation\ncavity are small linear regions of slowed diffusion.  There is also a region\nof enhancement measuring 13 x 9 mm along the superior aspect of the evacuation\ncavity (series 14, image 18).  There remains extensive surrounding vasogenic\nedema causing mass effect on the right lateral ventricle, mildly improved\ncompared to the preoperative MRI from ___.  There remains mild dilation\nof the temporal of the right lateral ventricle.  Also mildly improved is the\ndegree of midline shift to the left, previously 6 mm, now 5 mm.  Subdural\ndrain is better identified on same-day head CT.\n\nPostsurgical changes from prior right parietal craniectomy and resection of a\nright calvarial lesion are again noted.  Intracranial flow voids are\npreserved.  Dural venous sinuses are patent.  The paranasal sinuses are clear.\nThe orbits are unremarkable.",
            "output": "1. Post treatment changes in the right parietal lobe from abscess evacuation,\nwith small amount of blood product in the evacuation cavity.  Two adjacent\nfluid collections in the evacuation cavity, with mild associated rim\nenhancement and more focal enhancement superiorly, also likely postsurgical. \nHowever, attention on follow-up is recommended to exclude residual abscess.\n2. Mildly improved mass effect on the right lateral ventricle and midline\nshift to the left.  Persistent surrounding vasogenic edema, grossly unchanged.\n3. Mild slow diffusion along the evacuation cavity, likely post procedural,\nattention on followup.\n\nRECOMMENDATION(S):  Follow-up with MRI of the head without where contrast\nrecommended as clinically warranted to demonstrate residual or recurrent\nabscess formation."
        },
        {
            "input": "Right parietal craniectomy, postoperative changes adjacent right inferior\nparietal lobe.  T2 signal abnormality surrounding surgical cavity has improved\nsince prior.  Enhancement marginating parenchymal surgical cavity has\nimproved, with minimal residual enhancement..  There are no new fluid\ncollections.  There is no new area of restricted diffusion.  There is no\nevidence of acute hemorrhage, midline shift or infarction.  The ventricles and\nsulci are normal in caliber and configuration.  Intracranial vascular flow\nvoids are preserved.  Paranasal sinuses, mastoid air cells, middle ear\ncavities are clear.",
            "output": "Interval improvement at the surgical bed."
        },
        {
            "input": "Right parietal craniectomy is again seen.  A previously noted small right\nparietal fluid collection contiguous with the craniectomy has decreased in\nsize, now 2.0 x 0.7 cm on image 19:76.  It demonstrates persistent thin\nperipheral contrast enhancement, most likely related to postsurgical change,\nsimilar to mild dural enhancement along the right posterior convexity. \nSurrounding parenchymal T2 hyperintensity has markedly decreased, and\nassociated mass effect has resolved.  No new fluid collection or enhancing\nlesion is seen.  There is no acute infarction and no new blood products. \nVentricles and sulci are normal in size.  Major vascular flow voids are\npreserved.  There is mild mucosal thickening in the ethmoid air cells.",
            "output": "Previously noted small right parietal fluid collection contiguous with the\ncraniectomy has decreased in size, with decreased surrounding edema. \nPersistent thin peripheral contrast enhancement likely represents postsurgical\nchange, similar to mild dural enhancement along the right convexity.  No new\nfluid collection or enhancing lesion."
        },
        {
            "input": "The patient is status post right parietal craniectomy, as seen previously. \nMild linear contrast enhancement along the dura near the craniectomy site is\nunchanged.  Mild linear contrast enhancement along the prior surgical track in\nthe right parietal lobe is stable.  Mild T2/FLAIR hyperintensity surrounding\nthe right parietal surgical bed has slightly decreased in extent.  There is no\nevidence for a new enhancing collection or mass.  There is no edema acute\ninfarction, or evidence for new blood products. Ventricles, sulci, and basal\ncisterns are age-appropriate.  Major vascular flow voids are grossly\npreserved.  Dural venous sinuses appear patent on postcontrast MP RAGE images.\n\nThere is mild mucosal thickening in the ethmoid air cells.",
            "output": "Stable linear contrast enhancement at the right parietal surgical site with\nslightly decreased mild surrounding T2 hyperintensity.  No evidence for new\nintracranial abnormalities."
        },
        {
            "input": "Within the right parietal bone, there is a well-circumscribed 2.6 x 1.4 cm\nexpansile lesion, expanding both the inner and outer table more which\ncorrespond to the abnormality on the prior CT and radiographs.  It\ndemonstrates low signal on precontrast T1 weighted images, slightly\nheterogenous high signal on T2 weighted images, and contrast enhancement on\npostcontrast T1 weighted and MP RAGE images.  There is no slow diffusion. \nThere is linear dural and subgaleal contrast enhancement at the level of the\nlesion, but not extending beyond the level of the lesion.  This lesion\ndemonstrates a ground-glass matrix on the preceding CT, without periosteal\nreaction.\n\nNo other calvarial lesions are identified.  There is no evidence for an\nintra-axial or extra-axial intracranial mass.  There is no evidence for edema,\nabnormal diffusion, blood products, or other signal abnormalities in the brain\nparenchyma.  Ventricles, sulci, and basal cisterns are normal in size.  Major\narterial flow voids are grossly preserved.  Major dural venous sinuses appear\npatent on postcontrast MP RAGE images.",
            "output": "Well-circumscribed 2.6 x 1.4 cm expansile lesion in the right parietal bone\ndemonstrates nonspecific signal characteristics on MRI without evidence for\nfat.  It appears to have a ground-glass matrix on CT.  Fibrous dysplasia or\nother nonaggressive etiology is most likely, given the patient's age.\n\nRECOMMENDATION(S):  If no intervention is planned, recommend follow up by MRI\nto monitor stability."
        },
        {
            "input": "Minimal interval increase in a 2.4 x 1.7 x 3.2 cm (11:21) (previously 2.5 x\n1.6 x 3 cm) T2/FLAIR heterogeneous, T1 hypo intense, well-circumscribed,\nheterogeneously enhancing lesion expanding to both the inner and outer table\nof the right parietal bone without intra-axial extension or surrounding bony\nchanges.  The lesion mildly restricts on diffusion-weighted imaging.  There is\nmass effect along the right posterior parietal lobe which is similar to prior\nexamination.  Again seen is periosteal enhancement primarily along the outer\ncortex of this lesion.  No significant pachymeningeal enhancement.   No\nparenchymal edema.  No new enhancing lesion identified.\n\nThere is no evidence of hemorrhage, edema, midline shift or infarction.   The\nventricles and sulci are normal in caliber and configuration.  There is no\nabnormal enhancement after contrast administration.",
            "output": "1. Minimal increase in a 3.2 cm well-circumscribed expansile lesion in the\nright parietal bone demonstrates mild restricted diffusion.  Given the CT\nfindings of a expansile osseous lesion with internal matrix in combination\nwith the MR findings, the lesion is mildly aggressive and atypical for fibrous\ndysplasia. Differential includes aggressive hemangioma and Langerhans cell\nhistiocytosis, however metastatic lesion cannot be excluded.\n\nRECOMMENDATION(S):  Consider nuclear medicine RBC scan to further assess for\nhemangioma.\n\nNOTIFICATION:   The impression and recommendation above was entered by Dr.\n___ on ___ at 14:14 into the Department of Radiology critical\ncommunications system for direct communication to the referring provider."
        },
        {
            "input": "External stereotactic markers are identified.  Expansile right parietal\nepiploic 2.5 x 1.9 x 2.9 cm (AP, TRV, SI) enhancing lesion demonstrating\nspeckled appearance, with remodeling of the inner and outer table is unchanged\nfrom prior examination, resulting and mild underlying mass effect of the\nadjacent parietal lobe.  Mild adjacent periosteal enhancement is identified. \nNo other enhancing lesions are identified.  The major intracranial flow voids\nare preserved.  .",
            "output": "1. On this pre-surgical planning MRI, unchanged appearance of a 2.9 cm\nenhancing right parietal calvarial lesion with speckled appearance expanding\nthe inner and outer table."
        },
        {
            "input": "Study is mildly degraded by motion.\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are preserved in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.  The dural venous sinuses are patent.\n\nMaxillary sinus mucosal thickening is present.  Right maxillary sinus probable\nmucous retention cyst is seen.  Minimal bilateral ethmoid air cell mucosal\nthickening is present.  Bilateral frontal sinus mucosal thickening is present.",
            "output": "1.  Study is mildly degraded by motion.\n2. No acute intracranial abnormality.\n3. Within limits of study, no definite evidence of intracranial mass or\nlesion.\n4. Paranasal sinus disease , as described.\n5.  Within limits of study, no definite evidence of venous sinus thrombosis."
        },
        {
            "input": "There is a small focus of T2 hyperintensity in the right frontal deep white\nmatter (03:113).  There is no abnormal enhancement or slow diffuse\ncorresponding to this focus.  There is trace periventricular linear FLAIR\nhyperintensity, a nonspecific finding which is frequently seen in asymptomatic\npatients.  There is no evidence of an intracranial mass, acute infarction,\nedema, or blood products.  Parenchymal volume is normal for age, with normal\nsize of the ventricles, sulci, and basal cisterns.  Cerebellar tonsils are\nnormally positioned.  Major arterial flow voids are grossly preserved.  Major\ndural venous sinuses appear patent on postcontrast MP RAGE images.  Prominence\nof the pituitary gland is within normal limits for the patient's age and\ngender.\n\nMild mucosal thickening is seen in the right maxillary sinus and right ethmoid\nair cells",
            "output": "1. Single small discrete focus of T2 hyperintensity in the right frontal deep\nwhite matter is a nonspecific finding, which may sometimes be seen in\nasymptomatic patients.  Diagnostic possibilities include a focus of\ndemyelination, prior infection/inflammation, or a migraine related lesion.\n2. No evidence for at acute intracranial abnormality, an intracranial mass, or\nother structural abnormalities."
        },
        {
            "input": "The patient terminated the study after the T1 postcontrast images due to\nclaustrophobia.\n\nThere are postsurgical changes of left temporal lobe biopsy. The left temporal\nhorn remains dilated, unchanged from preoperative MRI on ___.  There\nis enhancement within the dilated temporal horn, most of which appears to be\nchoroid plexus. There is a focus of enhancement in the left temporal horn\nlaterally that may be distinct from the choroid plexus and due to the known\nmass versus enhancement due to the choroid plexus (series 10, image 11). There\nis a small amount of blood in the left temporal horn consistent with recent\npost biopsy change (series 10, image 10). There is no increased perfusion in\nthe left temporal lobe operative bed or surrounding areas on arterial spin\nlabeling images or postcontrast perfusion images.  The basal cisterns are\npatent and symmetric. No new lesion is identified.\n\nThere is no acute infarct. There is no extra-axial fluid collection. Major\nintravascular flow voids are preserved.\n\nThe paranasal sinuses and mastoid air cells are clear. The orbits are normal.",
            "output": "1. Persistently dilated left temporal horn due to a known left temporal lobe\nmass, unchanged from preoperative MRI. The known mass is difficult to\ndistinguish by imaging with only a small focus of enhancement in the left\ntemporal horn that may be due to the mass versus choroid plexus. No increased\nperfusion on ASL images.\n2. Postsurgical changes of left temporal lobe biopsy with trace blood in left\ntemporal horn."
        },
        {
            "input": "As seen on the recent MRI head study, there is a cystic lesion versus moderate\ndilation of the left temporal horn along with 2 small foci of enhancement, 1\nlocated posteriorly and superiorly series 3, image 54 and another another\nfocus series 3, image 49 located anteriorly and and of inferiorly. The\nappearance is not significantly changed compared to the recent study and\nbetter seen compared to the motion limited study of ___ from ___.\nNo new lesions are noted elsewhere.\nThe rest of the ventricular system appears normal.\nThe cerebral sulci and cerebellar folia are normal.\nThere is a small cyst/calcific focus in the pineal gland subcentimeter in\nsize.\nNo mass effect.\nMildly prominent adenoids.",
            "output": "A cystic lesion versus moderate dilation of the left temporal horn along with\n2 small foci of enhancement, demonstrated for treatment planning.\nPlease see prior studies for details"
        },
        {
            "input": "There is a left parietal/temporal craniotomy. There is a small underlying\nextra-axial collection at the level of the left temporal lobe, containing\nblood, fluid, and foci of air, which mildly indents and displaces the left\ntemporal parenchyma. Slightly expanded medial left temporal lobe effaces the\nleft aspect of the perimesencephalic cistern, new compared to the preoperative\nMRI. There is dural thickening and contrast enhancement along the left\ntemporal, parietal, and frontal convexity, consistent with postsurgical\nchange. Small foci of susceptibility artifact at the left frontal vertex may\nrepresent mild residual extra-axial pneumocephalus, not optimally assessed by\nMRI, rather than blood products.\n\nThere are T1 hyperintense blood products in the left temporal surgical bed,\nwith associated blooming artifact on gradient echo images.  No definite\nsuperimposed contrast enhancement is seen in the surgical bed, but there is\nmild linear contrast enhancement along the temporal horn of the left lateral\nventricle. High T2 signal in the medial left temporal lobe is similar to\npresurgical exams. In addition, there are small foci of high T2 signal and\nslow diffusion along the anterior margin of the left temporal surgical bed on\nimages 6:13, 6:12, 11:11, and extending towards lateral margin of the left\nlentiform nucleus on images 6:15 and 11:13, which may represent postsurgical\ncontusions or infarctions.\n\nTemporal horn of the left lateral ventricle and other components of the left\nlateral ventricle are smaller than the right, as before.\n\nMajor arterial flow voids are grossly preserved. Major dural venous sinuses\nappear patent on postcontrast MP RAGE images.",
            "output": "1. Allowing for T1 hyperintense blood products within the left temporal\nsurgical bed, no evidence for residual enhancing tumor is seen, but follow up\nis needed after blood products resolve. Linear contrast enhancement along the\ntemporal horn of the left lateral ventricle could be postsurgical. Persistent\nhigh T2 signal in the medial left temporal lobe is similar to presurgical\nexams.\n2. Small collection of blood, fluid, and the air underlying the left\ncraniotomy, which indents on displaces the left temporal parenchyma. Slightly\nexpanded medial left temporal lobe mildly effaces the left perimesencephalic\ncistern, more than on the presurgical exams.\n3. Small foci of slow diffusion along the anterior margin of the left temporal\nsurgical bed and extending towards the lateral margin of the left lentiform\nnucleus, which may represent postsurgical contusions or small infarctions."
        },
        {
            "input": "There are postoperative changes of a prior left temporal craniotomy with\nchronic underlying blood products and postoperative dural enhancement.  There\nare no additional areas of abnormal brain parenchymal or leptomeningeal\nenhancement.\n\nThere is no evidence of acute intracranial hemorrhage or mass effect.  The\nventricles and basal cisterns appear normal.  There are normal vascular flow\nvoids.  There is no evidence of acute infarct based on diffusion-weighted\nimaging.  The brain parenchymal volume is within normal limits.\n\nThe orbits, skull base, and paranasal sinuses are unremarkable.  Residual\nT2/FLAIR signal hyperintensity within the left temporal lobe appears unchanged\nwhen compared to prior exam.",
            "output": "1. Postoperative change of left temporal craniotomy with subjacent resection\ncavity, chronic underlying blood products, postoperative dural enhancement.\n2. Stable T2/FLAIR signal hyperintensity around the resection cavity.\n3. No new areas of enhancement or other evidence of residual/recurrent\ndisease."
        },
        {
            "input": "There has been slight interval decrease in size of the residual solid and\ncystic mass in the right superior cerebellum. Currently the mass measures 21 x\n12 mm. There is stable edema and gliosis in the right cerebellum.  There are\nchronic blood products noted on the gradient echo images.  There is gliosis in\nthe left frontal lobe from a prior shunt tract. There are chronic small vessel\nischemic changes in the white matter.  The ventricles are prominent but\nunchanged in size.\n\nIntracranial flow voids are maintained.  There is mild right frontal sinus\nopacification.",
            "output": "Slight interval decrease in enhancing right superior cerebellar mass. \nFindings an compatible with patient's history of hemangioblastoma."
        },
        {
            "input": "There has been no significant interval change. Again postoperative changes are\nidentified in the posterior fossa. An approximately 2.5 x 1 cm enhancing\nlesion identified at the superior aspect of the right cerebellum with\nsurrounding hemosiderin.  There is no change in size and surrounding FLAIR\nhyperintensities. No new areas of enhancement seen. Mild prominence of frontal\nextra-axial spaces again noted along with a shunt catheter extending to the\nanterior horn of the left lateral ventricle.",
            "output": "Unchanged appearance of enhancing lesion in the superior aspect of the right\ncerebellar hemisphere since the previous MRI examination. No definite new\nlesions are seen."
        },
        {
            "input": "Residual enhancing mixed solid and cystic mass in the superior right\ncerebellum has not significantly changed compared to the prior examination\nmeasuring 21 x 11 mm (1001b: 66). Minimal localized mass effect and edema in\nthe right cerebellum has not significantly changed. This lesion is associated\nwith a bloom artifact being on gradient echo images compatible with chronic\nblood products, unchanged. There is no midline shift. Ventricles and sulci\nremain prominent suggestive of age related atrophy. A left frontal approach\nventriculoperitoneal shunt catheter remains with its tip in the frontal horn\nof the left lateral ventricle. Associated postsurgical changes are noted. Note\nis made of nonspecific scattered prominent perivascular spaces. Scattered\nareas of periventricular, subcortical and deep white matter T2/FLAIR\nhyperintensities which appear similar to the prior study. There is no abnormal\nfocus of slowed diffusion. There is mild mucosal wall thickening in bilateral\nmaxillary sinuses, at bilateral anterior ethmoid air cells as well as the\nfrontoethmoidal recesses. Intracranial flow voids are maintained. The mastoid\nair cells are clear.",
            "output": "1. Interval stability of an enhancing superior right cerebellar mass with\nassociated surrounding edema.\n2. Stable scattered foci of nonspecific white matter T2/FLAIR\nhyperintensities, likely the sequelae of chronic small vessel ischemia ."
        },
        {
            "input": "The residual enhancing, mixed solid-cystic mass in the superior right\ncerebellum has not changed since the prior examination, now measuring 1.9 x\n1.0 cm (19:43), previously 2.1 x 1.1 cm. There is continued minimal localized\nmass effect edema in the right cerebellum. Blooming artifact on GRE images is\ncompatible with chronic blood products, also unchanged. There is no midline\nshift.\n\nThere is no evidence new mass or infarction. The ventricles and sulci are\nprominent, suggesting age-related volume loss. The left frontal approach\nventriculoperitoneal shunt catheter appears unchanged in position. Scattered\nnonspecific periventricular subcortical white matter T2 for and FLAIR\nhyperintensities are unchanged. There is no abnormal enhancement after\ncontrast administration.\n\nMild mucosal thickening of the bilateral maxillary sinuses is unchanged.\nMastoid air cells are clear.",
            "output": "1.  Interval stability in size in appearance of the enhancing, superior right\ncerebellar mass.\n\n2.  No new mass identified."
        },
        {
            "input": "There is redemonstration of an enhancing mixed solid and cystic lesion which\ncontains chronic blood products in the superior right cerebellum, measuring\napproximately 1.9 x 1.0 cm, previously measuring 1.9 x 1 1.0 cm (series 1000,\nimage 78).  There is stable mild surrounding edema.\n\nThere are no new enhancing lesions identified. There is no evidence of midline\nshift or large territorial infarction.\n\nA left frontal approach ventricular catheter drainage remains in unchanged\nposition, terminating the third ventricle.  There is surrounding T2/FLAIR\nhyperintensity along the course of the catheter intracranially.   Prominence\nof ventricles and sulci is consistent with age related involutional changes.\nConfluent T2/FLAIR hyperintensities within the subcortical, periventricular\nand deep white matter are nonspecific but likely the sequela of chronic small\nvessel ischemic disease.\n\nThere is mild mucosal thickening of the ethmoidal air cells. There is partial\nopacification of the mastoid air cells bilaterally.  The intracranial flow\nvoids are preserved.  The dural venous sinuses are patent.  The orbits are\nunremarkable.",
            "output": "1. Stable size and appearance of an enhancing superior right cerebellar mass.\n2. No new mass identified."
        },
        {
            "input": "MR BRAIN:\n Moderate motion degradation, limiting assessment. Within these confines:\n\nScattered foci of sulcal based FLAIR hyperintensity likely reflect interval\nredistribution of previously demonstrated acute subarachnoid hemorrhage, for\nexample left parieto-occipital region (12:20), right parietal region (series\n12 images 15 and 17).\n\nSubarachnoid hemorrhage is seen within the right aspect of the quadrigeminal\nplate cistern.  Acute subarachnoid blood products are again seen in the\nposterior fossa just posterior to the cerebellopontine angles bilaterally\n(17:8), unchanged.\n\nThere is layering intraventricular hemorrhage in the occipital horns\nbilaterally.\n\nThere is a focus of chronic microhemorrhage in the right cerebellum (17:8).\n\nThere is a faint focus of hyperintense signal on diffusion-weighted images in\nthe right parafalcine parietal lobe which appears parenchymal, without clear\nADC correlate (06:23), mildly FLAIR hyperintense.  This could reflect a\nsubacute infarct (06:23, 12:19).\n\nNo evidence of extra-axial collection.  No mass effect.\n\nThe ventricles and sulci are prominent, compatible with global parenchymal\nvolume loss, stable.\n\nBilateral periventricular and deep white matter foci of T2/FLAIR signal\nhyperintensity are nonspecific but compatible with mild changes of chronic\nwhite matter microangiopathy.  Component of periventricular edema is possible.\nMild hydrocephalus.  Severe prominence perivascular spaces.\n\nMild right ethmoid air cell and left maxillary sinus mucosal thickening. \nRemaining visualized paranasal sinuses, mastoids, appear clear.  Left globe\nprosthesis is noted.  Right globe and orbit is notable only for right lens\nremoval.  Major intracranial vascular flow voids are preserved.  Major dural\nvenous sinuses are patent.\n\nMRA BRAIN:\n Severe motion degradation, limiting assessment. Within these confines:\n\nCalcified atheromatous plaque causes severe right cavernous intracranial ICA\nluminal narrowing, at least moderate left cavernous intracranial ICA luminal\nnarrowing (series 10, images 66, 60).  Areas of luminal irregularity of the\nintracranial circle of ___ vasculature may represent areas of mild or\nmoderate luminal narrowing, however this appearance is difficult to separate\nfrom the effects of severe motion degradation.  Mild narrowing left P1\nsegment.\nNo other area of severe luminal narrowing identified.  No large vessel\nocclusion.  No large aneurysm identified.",
            "output": "1. No intracranial mass.\n2. Interval redistribution of subarachnoid, intraventricular hemorrhage.\n3. Mild hydrocephalus, suggestion mild periventricular edema.\n4. Severe chronic small vessel ischemic change.  Component of brainstem edema\ncannot be excluded, is less likely.  Exclude low likelihood of central pontine\nmyelinolysis.\n5. Possible small right parietal lobe subacute infarct.\n6. No aneurysm.\n7. Motion degraded MRA.  Severe right and moderate left cavernous, paraclinoid\natherosclerotic ICA narrowing."
        },
        {
            "input": "Multiple of foci of gradient echo susceptibility involving bilateral thalami,\nright basal ganglia extending up along the right coronal radiata and cerebral\nperipheral gray-white junction is noted compatible with hemorrhages.  Although\nthe hemorrhages centered in the basal ganglia and could potentially represent\nhypertensive in etiology, the more peripheral nature of the cerebral micro\nhemorrhages would suggest amyloid angiopathy. There is no abnormal T2 signal\nwith popcorn or Mulberry like appearance of the hemorrhages to suggest\nunderlying cavernoma.\n\nThere is no evidence of acute infarct. Sulci, ventricles and cisterns are\nwithin expected limits given the degree of the patient's age appropriate\nglobal cerebral volume loss. There are diffuse confluent subcortical and\nperiventricular FLAIR/ T2 white matter hyperintensities, which are\nnonspecific, but compatible with small-vessel ischemic disease in a patient of\nthis age. The major intracranial flow voids are preserved, with suggestion of\ndolichoectasia of the basilar artery. The paranasal sinuses are essentially\nclear. The orbits are unremarkable. The mastoid air cells are clear.",
            "output": "1. Multiple foci of micro hemorrhages involving the bilateral thalamotomy,\nright basal ganglia and the peripheral cerebral subcortical white matter in a\npattern suggestive of amyloid angiopathy.\n2. No underlying findings to suggest cavernoma.\n3. No acute infarcts.\n4. Confluent white matter changes described above compatible with small vessel\nischemic disease."
        },
        {
            "input": "There is no abnormal parenchymal, leptomeningeal, or pachymeningeal contrast\nenhancement. There is no edema, mass effect, abnormal diffusion, evidence of\nold blood products, or white matter lesions in the brain parenchyma. Stable\nsulci, ventricles, and basal cisterns are normal in size. Cerebellar tonsils\nare normally positioned.\n\nThe pituitary gland has a height of 8 mm with a convex upper margin. Its size\nand morphology could be within normal limits for a woman of this age. The\ninfundibulum is midline. The gland does not appear to exert mass effect on the\noptic chiasm, but it may contact the prechiasmatic left optic nerve, image\n101:47.",
            "output": "1. Normal appearance of the brain parenchyma without evidence for intracranial\nmanifestations of Lyme disease. No abnormal leptomeningeal contrast\nenhancement.\n2. Prominent pituitary gland is within normal limits for the patient's age and\ngender. It does not appear to exert mass effect on the optic chiasm, but it\nmay contact the prechiasmatic left optic nerve.  Given the patient's visual\nsymptoms, further evaluation by a dedicated MRI of the pituitary is suggested."
        },
        {
            "input": "MRI BRAIN:\nAgain seen is extensive left temporal lobe tissue loss as well as bifrontal\ntissue loss.  The distribution suggests a chronic contusion.  There is no\nevidence of edema or mass effect.  There is marked enlargement of the adjacent\ntemporal and frontal horns of the lateral ventricles.  There is no evidence of\nhemorrhage.\nAgain seen are several areas of slow diffusion superficially in the right\nhemisphere.  These appear similar, although not identical, to the finding on\n___.  It would be quite unusual for acute infarction to maintain this\nslow diffusion for an extended period of time.  Given the history of\nmeningitis, an alternate possibility is that these areas represent foci of pus\nin the subarachnoid space, rather than acute embolic infarction.  There\npersistence also argues against infarction as a consequence of meningitis.\nMRA BRAIN:\nThe intracranial vertebral and internal carotid arteries and their major\nbranches appear normal without evidence of stenosis, occlusion, or aneurysm\nformation.\nMRV Brain: There is no evidence of dural venous sinus occlusion.  The left\ntransverse sinus is smaller than the right, a normal variant\n\nMRA NECK:\nThe common, internal and external carotid arteries appear normal.  There is no\nevidence of internal carotid artery stenosis by NASCET criteria.  The origins\nof the great vessels, subclavian and vertebral arteries appear normal\nbilaterally.",
            "output": "1. Superficial areas of slow diffusion in the right hemisphere may represent\nfoci of pus in the subarachnoid space, rather than cortical infarctions.\n2. Bifrontal and left temporal tissue loss suggesting chronic contusions\nappears unchanged since the prior study."
        },
        {
            "input": "MR BRAIN:\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There are no chronic small vessel ischemic changes.  The\nparanasal sinuses, mastoid air cells are patent.  Visualized orbits are\nnormal.  Intracranial flow voids are preserved.\n\nMRA brain: The intracranial vertebral and internal carotid arteries and their\nmajor branches appear normal without evidence of stenosis, occlusion, or\naneurysm formation.  Bilateral intracranial vertebral arteries are patent, and\nleft vertebral artery is mildly dominant, appearance is unchanged since prior.\nBilateral PCOM, A-comm are patent.  The right A1 segment is hypoplastic. \nThere is no evidence of intramural hematoma within vessels of the visualized\nupper neck, head.\n2D time-of-flight images of the neck demonstrate mildly diminished flow in the\nV 2 segment of the left vertebral artery in the mid neck, and moderately\ndiminished flow within V2 segment of right vertebral artery in the low neck,\nsimilar compared to prior.",
            "output": "1. There are no infarcts.\n2. Intracranial MRA is normal."
        },
        {
            "input": "The common, internal and external carotid arteries appear normal.  There is no\nevidence of stenosis by NASCET criteria. The origins of the great vessels,\nsubclavian, and vertebral arteries appear normal bilaterally.  The common\ncarotid bifurcations appear normal.\n\nPlease refer to the concurrent MR brain for full description of the mass\ninvading the clivus.",
            "output": "1. Normal MRA neck.  No evidence of dissection.\n2. Please refer to the concurrent MR brain for full description of the mass\ninvading the clivus."
        },
        {
            "input": "There is a large clival and right sphenoid wing mass, which should be compared\nto any available prior studies.  The mass invades the clivus with abnormal\nsignal intensity throughout the structure.  The mass also extends along the\ndorsum sella and along the posterior aspect of the clivus into the pontine\ncistern.  The mass grossly enlarges the right cavernous sinus and appears to\nfill the left cavernous sinus as well.  The mass encases the right internal\ncarotid artery in the carotid canal and in the cavernous sinus.  There is a\npunctate focus of T1 hyperintensity centrally, best evaluated by comparison\nwith prior studies (series 8, image 13).\n Bilateral cavernous carotid artery flow voids appear preserved.\n\nThe mass nearly completely fills the sphenoid sinus bilaterally with a small\namount of fluid present anteriorly.  The lesion also involves the right\npetrous apex.  The mass extends into the suprasellar cistern on the right,\nelevating the optic chiasm.  The lesion extends into the right orbital apex\nand appears to compromise the optic nerve.\n\nThere has been a prior craniotomy for resection of some component of this\nlesion.  There is right temporal lobe tissue loss underlying the craniotomy\nsite.  Extensive white matter hyperintensity on the FLAIR and T2 weighted\nimages may be entirely due to the tissue loss.  However, the possibility of\nsuperimposed edema cannot be evaluated without comparison to prior studies.\n\nThere is a small focus of chronic hemorrhage in the left cingulate gyrus. \nThere is no evidence of midline shift or of infarction.  Mild predominantly\nperiventricular T2/FLAIR white matter hyperintensities are nonspecific, but\nlikely represent the sequela of chronic microvascular ischemia.  Prominence of\nthe ventricles and sulci suggest age-related involutional changes.\n\nPatient is status post lens resection on the right.  Small volume fluid within\nthe mastoids bilaterally.",
            "output": "1. No acute intracranial abnormalities.\n2. Patient is status post resection of a right sphenoid wing meningioma.  A\nlarge clival, petrous apex and right sphenoid wing mass likely represents a\nmeningioma, however comparison with any available prior imaging and\ncorrelation with treatment history is recommended.\n3. Encephalomalacia within the right temporal lobe with ex vacuo dilatation of\nthe right temporal horn, however superimposed edema from prior treatment or\nfrom the adjacent mass cannot be excluded.\n4. Solitary left cingulate micro bleed.\n\nRECOMMENDATION(S):  Comparison with any available prior imaging and\ncorrelation with treatment history.\n\nNOTIFICATION:  The impression and recommendation above was emailed to the ED\nQA nurses by Dr. ___ on ___ at 10:07."
        },
        {
            "input": "The previously noted left frontal metastatic lesion is minimally decreased in\nsize with there is marked interval decrease in the surrounding edema.  The\nlesion measures 6.9 mm compared to prior measurement of 8.5 mm.  No new\nlesions is seen. There are scattered periventricular and subcortical\nhyperintense foci which are nonspecific regarding etiology but likely\nrepresent sequela of small vessel ischemic disease in a patient of this age\ngroup.\n\nThere is no intracranial mass, mass effect, or midline shift.There ventricles\nand sulci are age-appropriate.  There is no hydrocephalus or acute ischemia.\nIntracranial flow voids are maintained. Visualized paranasal sinuses and\nmastoid air cells are clear.",
            "output": "Decreased size of left frontal metastatic lesion and decreased surrounding\nedema."
        },
        {
            "input": "The enhancing lesion within the left frontal lobe mass slightly increased in\nsize now measuring 10 x 8 mm versus 8 x 7 mm. The FLAIR hyperintensity\nsurrounding this lesion has markedly increased compared prior study. There are\nno other enhancing lesions identified.\n\nThere is no infarct, hemorrhage, or midline shift. The ventricles, sulci and\ncisterns are normal in size and configuration.  The other nonspecific\nscattered pontine and periventricular and subcortical white matter FLAIR\nhyperintensities are unchanged.\n\nThere is a small amount of fluid in bilateral mastoid air cells.",
            "output": "Left frontal lobe enhancing lesion has slightly increased in size now\nmeasuring 10 x 8 mm versus 8 x 7 mm. The FLAIR hyperintensity surrounding this\nlesion has markedly increased. There are no other enhancing lesions\nidentified.\n\nThere is no infarct or hemorrhage."
        },
        {
            "input": "Again seen is an enhancing lesion within the left frontal lobe, measuring\napproximately 11 mm AP x 10 mm TR by 12 mm SI, which is slightly increased\ncompared to prior study of ___. FLAIR hyperintensities surrounding\nthe mass also demonstrates interval increase compared to prior study. There is\nmild local mass effect with effacement of the adjacent sulci but no evidence\nof midline shift. There is no evidence of associated hemorrhage.\n\nThere is a new enhancing focus within the most superior aspect of the right\nanterior insula, measuring approximately 6 mm AP x 7 mm TR x 6 mm SI (12A-70),\nwith also surrounding FLAIR hyperintensity, compared to prior study of ___.\n\nNo other focus of new enhancement or mass effect is identified. There is no\nhemorrhage or extra-axial fluid collections.  There is no slow diffusion to\nsuggest acute infarct. Ventricles and sulci are otherwise stable. The basilar\ncisterns are within normal limits.\n\nThere are scattered foci of FLAIR hyperintensity within the deep and\nperiventricular white matter, as well as in the pons, nonspecific. These may\nrepresent sequela of treatment and/or microvascular ischemic disease.\n\nIntracranial flow voids are maintained. Visualized paranasal sinuses are\nclear. Again seen is a small amount of fluid in the bilateral mastoid air\ncells.  The orbits and soft tissues are grossly unremarkable.",
            "output": "1. Interval mild increase in size of enhancing lesion within the left frontal\nlobe, as well as associated FLAIR hyperintensity, resulting in local mass\neffect but no evidence of midline shift or herniation.\n2. New enhancing focus at the most superior aspect of the right anterior\ninsula, with new associated FLAIR hyperintensity. No other focus of abnormal\nenhancement or mass effect is seen. Findings are concerning for progression of\ndisease.\n3. No acute infarct or hemorrhage."
        },
        {
            "input": "Again seen are enhancing lesions with surrounding edema representing\nmetastatic disease. The degree of edema has decreased surrounding the left\nfrontal lesion and increased surrounding the right insular lesion. Both the\nfoci have enlarged by a 1-2 mm in their enhancing volumes.  These changes may\nreflect tumor progression or treatment response. If the distinction remains\nunclear on follow-up imaging, spectroscopy and perfusion studies may be\nhelpful.\n\nThere is no evidence of hemorrhage.  No new metastases are identified.  There\nis no hydrocephalus.",
            "output": "Reduction in edema associated with the left frontal lesion and increasing\nedema associated with the right insular lesion. The volume of enhancing\nmaterial has increased slightly surrounding both metastases. These changes may\nreflect tumor progression or treatment effect."
        },
        {
            "input": "There is a 0.5 x 0.6 cm enhancing mass in the left cerebellum that is new from\nprior MRI on ___ (series 10, image 8). There is surrounding edema\nwith mild mass effect on the left lateral wall of the fourth ventricle. There\nis focal FLAIR signal abnormality in the high left parietal lobe, new from\nprior MRI (series 7, image 20). This is suspicious for an underlying\nmetastasis even though no enhancing lesion can get be identified at this site.\nSimilarly, there is new FLAIR signal abnormality in the high left parasagittal\nfrontoparietal white matter (series 7, image 23), also concerning for an\nunderlying metastasis that is not yet identifiable on contrast enhanced\nimages.\n\nThe left frontal gyrus enhancing mass is less conspicuous on the prior study\nwith a smaller area of enhancement (series 10, image 18). The right frontal\nlobe enhancing lesion demonstrated on prior MRI is no longer identified.\n\nThere are numerous foci of increased FLAIR signal in the periventricular white\nmatter.\n\nThe ventricles are normal in size. Major intravascular flow voids are\npreserved. No osseous lesions are identified. The paranasal sinuses are clear.\nThere is fluid in the dependent mastoid air cells. The orbits are normal.",
            "output": "1.  Progressive disease with a new enhancing metastasis and adjacent edema in\nthe left cerebellar hemisphere.\n2.  In addition, there are two new foci of FLAIR-signal abnormality without\nenhancement in the high left parietal lobe and high left parasagittal\nfrontoparietal lobe. These are suspicious for metastases that are currently\ntoo small to be detected on post-contrast imaging.\n3.  Previously present metastases show some improvement, with the known left\nfrontal lobe metastasis smaller than on the prior study, and the known right\nfrontal metastasis no longer  seen."
        },
        {
            "input": "When compared to prior, there has been interval increase in size and number of\nthe enhancing metastatic foci. Specifically, there is a new subcortical white\nmatter 6 mm enhancing focus (901 b, 36) in the right frontal lobe, new\nbilateral occipital lobe and left temporooccipital enhancing foci (901 B, 68)\nas well as in the left temporal lobe enhancing lesion. There is a new 4 mm\nfocus of enhancement in the left insula (901 B, 60) with increased surrounding\nFLAIR hyperintensity. Increased FLAIR signal abnormality at the left frontal\nvertex now demonstrates an enhancing 6 mm nodule (901 b, 20). There is an\nadjacent new 6 mm nodule of enhancement in the left frontal lobe (901 B, 31)\nwhich was not present on prior.  Enhancing lesion in the left frontal lobe\nwhich had demonstrated ill-defined enhancement and surrounding FLAIR signal\nabnormality on ___ which had decreased since prior, now\nsubsequently has increased in size, currently measuring 11 x 12 mm, similar to\nexam from ___. There has not been dramatic interval change in the\nenhancing lesion in the left cerebellar hemisphere although the degree of\nsurrounding vasogenic edema has increased.\n\nThere is no acute infarct. Ventricular configuration essentially stable. The\nmajor intravascular flow voids are preserved.",
            "output": "Interval increase in size and number of parenchymal metastases as above."
        },
        {
            "input": "As compared to the prior study many of the previously seen enhancing foci\nwithin the brain are no longer visualized; however, multiple new enhancing\nlesions are noted. For example the previously seen left frontal vertex, right\nsubcortical frontal lobe, left occipital and left temporal lesions are no\nlonger visualized.  New enhancing foci are seen including a 4 mm left\nsubcortical frontal lobe lesion (20:90), 1 mm subcortical frontal lesion (20:\n89), 5 mm right parietal subcortical lesion (20:66), 5 mm right frontal\nsubcortical lesion (20:87), 3 mm right occipital lesion (20:44) and 3 mm right\ntemporal lesion (20:45).\n\nThe enhancing lesion in the left frontal lobe with ill-defined enhancement and\nsurrounding FLAIR abnormality appears unchanged from prior measuring 10 x 14\nmm (20:79). A enhancing lesion in the left cerebellar hemisphere has slightly\ndecreased in size now measuring 7 x 4 mm previously 11 x 6 mm (20:31) and the\nsurrounding FLAIR hyperintensity has decreased.\n\nThere is no evidence of acute hemorrhage or infarction. The ventricles and\nsulci are normal in caliber and configuration.  The major intracranial flow\nvoids are preserved.",
            "output": "Multiple previously seen enhancing lesions are no longer visualized likely\nrelated to interval CyberKnife treatment. However, multiple new parenchymal\nmetastases are seen as described above.  The left temporal enhancing lesion is\nunchanged and the left cerebellar enhancing lesion has decreased in size."
        },
        {
            "input": "There are multiple enhancing intraparenchymal lesions with surrounding\nvasogenic edema again noted consistent with history of metastatic disease.\n\nThere has been a slight interval increase in size of a right occipital lobe\nenhancing lesion previously measuring 3 mm and now measuring 4 mm (series\n901b, image 75) with questionable slight interval increase in associated FLAIR\nsignal.\n\nThere has been a slight interval decrease in the size of the left cerebellar\nlesion today measuring 5 mm x 3 mm (previously 7 mm x 4 mm) with an associated\ninterval decrease in surrounding FLAIR signal (series 901b, image 88, series\n7, images 7).\n\nThere is a new 2 mm region of enhancement in the right parietal lobe in a\nregion of previously seen FLAIR signal hyperintensity (series 901b, image 38).\n\nThere is an additional new 2 mm enhancing lesion in the right parietal lobe\nwith subtle FLAIR hyperintensity (901b, image 49, and series 7, image 15).\n\nThere is a questionable new tiny 1 mm enhancing lesion in the right frontal\nlobe (series 9030b, image 42) although there is no definite FLAIR signal\nabnormality in this region.\n\nA previously identified 1 mm enhancing lesion in the right frontal lobe\nsubcortical white matter lobe is not definitely visualized although there is\nnew FLAIR signal abnormality within this region on today's exam.\n\nAll other lesions appear relatively stable in size, specifically the left\nfrontal lobe lesion measuring 9 x 13 mm (901b image 43),a 4 mm left frontal\nlobe lesion (901 b: 30), a 4 mm right frontal lesion (901 b: 36) and a right\ntemporal lobe lesion measuring 5 mm (901 b: 55). Stable punctate focus of\nenhancement in the anteriomedial right temporal lobe (901b:76) is again seen\nwith questionable increased surrounding FLAIR hyperintensity.\n\nThe ventricles and sulci are normal in caliber and configuration.  There is no\nshift of midline. There is no evidence of acute hemorrhage or infarction.\nThere are additional scattered foci of T2/FLAIR signal hyperintensity in the\nperiventricular and deep white matter which are nonspecific but likely\nsecondary to the chronic small vessel ischemic disease. Similar increased\ncentral T2/FLAIR signal intensity is seen in the central pons which is also\nlikely reflective of chronic small vessel ischemic disease. Vascular flow\nvoids are preserved. The orbits are unremarkable. The paranasal sinuses and\nmastoid air cells are clear.",
            "output": "Multiple enhancing bilateral intraparenchymal lesions consistent with history\nof metastatic disease as described in detail above.\n\nThere has been interval decrease in the size of left cerebellar lesion.\n\nInterval increase in size of a right occipital lobe lesion as described above.\n\nThere are 2 new small enhancing lesions in the right parietal lobe with\nassociated FLAIR signal abnormality, new enhancement within a previously seen\nFLAIR signal abnormality, and a questionable new enhancing lesion (versus\nartifact) in the right frontal lobe without associated FLAIR signal\nabnormality."
        },
        {
            "input": "When compared to most recent prior from ___, there is 1 new lesion\nidentified within the ventrolateral aspect of the pons on the left (19:35).\nThere is mild surrounding FLAIR hyperintensity without significant mass\neffect. There is no other definite new lesion identified.\n\nThere are multiple enhancing lesions which have demonstrated progressive\ninterval decrease in size over the past 2 exams, specifically a 2 mm enhancing\nright frontal lesion (19:87), and a 2 mm left frontal lobe lesion in the\nprecentral gyrus (19:90). These lesions are associated with mild FLAIR\nhyperintensity which has decreased since exam from ___.\n\nThere are several additional lesions which are essentially unchanged\nInvolving the cerebellum on the left (19:31) which measures 4 mm, a right\ntemporal lobe lesion measuring 3 mm (19:65) is similar compared to most\nprevious exam and likely slightly decreased since ___. The dominant\nleft frontal lesion measuring 1.3 x 1.1 cm is unchanged over multiple exams.\n\nA 4 mm right temporoccipital lesion (19:45) is essentially unchanged in size\nsince most recent exam although slightly larger when compared to ___\nand demonstrates mild increased surrounding FLAIR hyperintensity compared to\n___. The leptomeningeal lesion involving the right parietal region\n(19:71) measures approximately 4 mm and is unchanged since most recent exam\nalthough increased since ___. FLAIR hyperintensity surrounding this\nlesion has also increased. These changes could be due to radiation.\n\nThere is FLAIR hyperintensity in the right frontal subcortical white matter\n(15:19) which has slightly increased in size over this past few exams without\nassociated enhancement.\n\nThere is no acute infarct or hemorrhage. Major intravascular flow voids are\npreserved.\n\nMucosal thickening seen within the ethmoid air cells and there is mild T2\nhyperintensity within the left mastoids.",
            "output": "1.  Single new 4 mm enhancing lesion within the pons on the left worrisome for\nnew metastatic lesion.\n2.  Increased surrounding FLAIR hyperintensity surrounding the right parietal\nand the right temporoccipital enhancing lesions which have not enlarged,\npotentially post treatment related.\n3.  Other numerous enhancing metastatic foci which have not changed since the\nmost recent exam, several which have decreased since the exam before that.\n4. Slight interval increase in the subcortical FLAIR hyperintensity in the\nright frontal lobe without abnormal enhancement which should be followed on\nsubsequent exams."
        },
        {
            "input": "When compared to the most recent examination of ___, interval\nincrease in size of left pontine 7 x 8 mm (TRV, AP; series 19, image 36).)\nenhancing lesion, with increased prominence of surrounding FLAIR hyperintense\nsignal, resulting in mild mass effect and expansion of the pons. The lesion\npreviously measured 4 mm.\n\nMultiple additional enhancing punctate lesions throughout the cerebral and\ncerebellar hemispheres are decreased to stable in size. For example, a left\nprecentral gyrus punctate enhancing focus (series 19, image 93) is barely\nperceptible on the current exam. Some of these lesions demonstrate surrounding\nFLAIR edema pattern, decreased from prior exam. No definite new enhancing\nlesions are identified.\n\nA left frontal peripherally enhancing 1.4 x 8 0.8 cm (AP, TRV) with\nsurrounding FLAIR hyperintense signal is similar in size compared to the prior\nexam.\n\nFLAIR hyperintense signal of the right frontal subcortical white matter has\ncontinued to increase in size without evidence of underlying enhancement\n(series 15, image 19).\n\nThere is no acute intracranial hemorrhage or infarct. Sulci, ventricles and\ncisterns are within expected limits for the patient's age. The major\nintracranial flow voids are preserved. The paranasal sinuses are clear. The\norbits are unremarkable. Fluid signal is seen in the right mastoid tip.",
            "output": "1. increased size of a left pontine 7 x 8 mm enhancing lesion with increased\nsurrounding FLAIR hyperintense edema pattern with mild mass effect and\nexpansion of the pons, which previously measured 4 mm.\n2. There is continued increased size of right frontal white matter\nhyperintense focus without underlying enhancement. While this may represent\nposttreatment changes, continued followup is recommended.\n3. The remainder of the previously noted lesions are stable to slightly\nsmaller in size.\n\nNOTIFICATION:  The impression and recommendation above was entered by Dr. ___\n___ on ___ at 17:31 into the Department of Radiology critical\ncommunications system for direct communication to the referring provider."
        },
        {
            "input": "Multiple enhancing supratentorial and infratentorial lesions with surrounding\nedema are again seen consistent with provided history of metastatic disease. \nA left frontal peripherally enhancing lesion has decreased in size compared to\nprior study now measuring 10 mm AP by 8 mm TV, previously measured 14 mm AP x\n8 mm TV (AP, TRV).  A left pontine lesion has also decreased in size and now\nmeasures 6 mm AP x 5 mm TV (previously 9 mm AP x 7 mm TV).  Previously seen\nleft temporal lobe and left middle cerebellar peduncle lesions are less\nconspicuous on today's exam.  Other enhancing lesions are unchanged.  No new\nenhancing lesions are identified.\n\nFLAIR hyperintense signal in the right frontal subcortical white matter\nwithout underlying enhancement appears slightly less prominent than on prior\nstudy (series 7, image 19).\n\nT2/FLAIR signal hyperintensity is also noted in the periventricular,\nsubcortical, and deep white matter as well as in the central pons likely\nreflecting combination of chronic small vessel ischemic disease and or post\ntreatment change.\n\nThere is no acute intracranial hemorrhage or infarct. Sulci, ventricles and\ncisterns are within expected limits for the patient's age. The major\nintracranial flow voids are preserved. The paranasal sinuses are clear. The\norbits are unremarkable.  Trace fluid signal is again seen in the right\nmastoid tip.",
            "output": "Multiple enhancing supratentorial and infratentorial lesions consistent with\nhistory of metastatic disease.  Multiple lesions have decreased in size or\nappear less conspicuous on today's exam as described in detail above.  No\ndefinite new enhancing lesions are seen."
        },
        {
            "input": "MR BRAIN:\nThere is no intra or extra-axial mass effect, acute hemorrhage or infarct. \nThe sulci, ventricles and cisterns are within expected limits for the\npatient's age.  There are 2 nonspecific subcortical left frontal FLAIR white\nmatter hyperintensities (series 7, image 16), which are nonspecific in a\npatient of this age, but may be seen in setting of chronic headache, prior\ntrauma or infectious/ inflammatory etiology.  The major intracranial flow\nvoids are preserved.  There is a left maxillary sinus mucous retention cyst. \nOtherwise, the remainder the paranasal sinuses are essentially clear.  The\norbits are unremarkable.  The mastoid air cells are clear.\n\nMRV brain: Normal flow signal is demonstrated within the superior sagittal\nsinus, straight sinus, transverse sinuses, and sigmoid sinuses. The jugular\nbulbs and proximal jugular veins are patent. Evaluation of the deep venous\nsystems reveals normal flow signal in the internal cerebral veins. The vein of\n___ is also unremarkable.",
            "output": "1. No acute infarct, intracranial hemorrhage or evidence of intracranial mass.\n2. 2 nonspecific subcortical left frontal FLAIR white matter hyperintensities,\nwhich are entirely nonspecific in a patient of this age.  This could represent\nsequela of chronic headache such as migraine.  Prior trauma, infectious/\ninflammatory etiology are also differential considerations.\n3. Unremarkable MRV, demonstrating patent dural venous sinuses."
        },
        {
            "input": "Areas of slow diffusion are seen within the left parietotemporal lobes, with\nassociated FLAIR signal abnormality consistent with an subacute infarction. \nThere is no evidence of underlying hemorrhage.  No acute intracranial\nhemorrhage is identified.  Focus of low susceptibility signal in the right\nfrontal lobe may be sequelae of mineralization or prior chronic hemorrhage.\n\nMild mucosal sinus thickening is seen involving the ethmoid air cells.  The\nremainder the visualized paranasal sinuses, mastoid air cells, and middle ear\ncavities are unremarkable.  The globes are unremarkable.  The principal\nvascular flow voids appear to be well preserved.",
            "output": "1. Subacute infarction in the left parietotemporal lobe.  No evidence of acute\nintracranial hemorrhage."
        },
        {
            "input": "The T2/FLAIR hyperintense signal within the right precentral gyrus is less\nconspicuous than on prior study. Also the two foci of enhancement in this\nregion are no longer appreciated. Findings likely reflect if a subacute\ninfarct.\n\nThere is no acute infarct, hemorrhage, mass effect or abnormal enhancement. \nThere is a chronic lacunar infarct in the left caudate head. The ventricles,\nsulci and cisterns are appropriate for age. There are scattered nonspecific\nperiventricular and subcortical white matter FLAIR hyperintensities, likely\nrepresenting sequela of chronic small vessel ischemic disease. The principal\nintracranial flow voids are present.\n\nThere are post radiation changes in the cervical spine with increased T1\nsignal in the bone marrow.\n\nThere is mild ethmoid and bilateral maxillary sinus mucosal thickening. There\nis minimal fluid in bilateral mastoid air cells.",
            "output": "The T2/FLAIR hyperintense signal within the right precentral gyrus is less\nconspicuous than on prior study and the prior associated enhancement in this\nregion is no longer appreciated. Findings likely reflect evolution of a\nsubacute infarct."
        },
        {
            "input": "Study is mildly degraded by motion.   There is no evidence of acute\ninfarction.  No intracranial hemorrhage. No mass, mass effect, edema or\nmidline shift. There is no abnormal enhancement.  The dural venous sinuses\nappear patent.\n\nThe ventricles and sulci are mildly prominent.  Periventricular and\nsubcortical white matter FLAIR hyperintensities are noted, a nonspecific\nfinding that most likely represents the sequelae of chronic small vessel\nischemic disease.   There is gross preservation of the principal intracranial\nvascular flow voids.\n\nMucosal thickening is seen in scattered ethmoid air cells bilaterally.  The\nmiddle ear cavities, and mastoid air cells are well aerated and clear.  The\npatient is status post bilateral lens replacement.  Limited imaging of\ncervical spine demonstrates at least mild vertebral canal narrowing at C3-4\n(see 10:122).",
            "output": "1.  Study is mildly degraded by motion.\n2. Within limits of study, no evidence for acute intracranial hemorrhage or\ninfarction.\n3. Mild-to-moderate global parenchymal volume loss and evidence of chronic\nsmall vessel ischemic disease.\n4. Limited imaging of cervical spine demonstrates at least mild vertebral\ncanal narrowing at C3-4.  If clinically indicated, consider dedicated cervical\nspine MRI for further evaluation.\n5. Paranasal sinus disease, as described."
        },
        {
            "input": "NON-CONTRAST HEAD CT:  There is no evidence of hemorrhage, infarct or mass. \nThe ventricles, cisterns and sulci are age-appropriate.\n\nCTA HEAD:  The intracranial internal carotid arteries have normal course,\ncaliber and branching pattern.  The right A1 segment is slightly dominant. \nThe anterior and middle cerebral arteries have otherwise normal course,\ncaliber and branching pattern.  The distal vertebral arteries, basilar artery,\nand posterior cerebral arteries have normal course, caliber and branching\npattern.  A right posterior communicating artery is patent.  No posterior\ncommunicating artery is identified on the left.\n\nCTV BRAIN:  The dural venous sinuses and major intracranial veins are patent.",
            "output": "Normal CTA, CTV of the brain."
        },
        {
            "input": "Image quality is severely degraded by motion artifact\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, or infarction.\nThe ventricles and sulci are normal in caliber and configuration. \nPost-contrast images are severely limited by motion artifact. Within this\nconfine, no definite enhancing mass lesions are identified. Major vascular\nflow voids are preserved. The orbits are unremarkable. The paranasal sinuses\nand mastoid air cells appear grossly clear.\n\nThe T2 weighted images demonstrate fluid in the left posterior oropharynx.\nThis is not present on other images, suggesting the fluid has been swallowed.\nIf there is clinical concern of a mucosal retention cyst in this area, direct\nexamination would be most helpful.",
            "output": "1. Exam severely limited by motion artifact\n\n2.  No definite evidence of acute infarction, hemorrhage, or enhancing mass\nlesion."
        },
        {
            "input": "Postcontrast MP RAGE images are mildly limited by motion artifact.  Axial spin\necho precontrast and postcontrast images are somewhat limited by pulsation\nartifact in the posterior fossa.\n\nThere is no evidence for an enhancing intra-axial or extra-axial mass.  There\nis a small developmental venous anomaly in the left cerebellar hemisphere. \nThere is no evidence for edema, blood products, or acute infarction. \nScattered small foci of high T2 signal in the subcortical, deep, and\nperiventricular white matter of the cerebral hemispheres are nonspecific but\nlikely sequela of chronic small vessel ischemic disease in this age group. \nVentricles and sulci are age-appropriate.  Extra-axial spaces in the posterior\nfossa are mildly prominent, indicating mild volume loss.  Major vascular flow\nvoids are preserved.  Dural venous sinuses are patent on postcontrast MP RAGE\nimages.\n\nExtracranial soft tissues of the scalp and skullbase are not optimally\nassessed on this exam in the absence of fat suppression.  There is evidence of\nbilateral cataract surgery.  There is mild mucosal thickening in the ethmoid\nair cells and trace opacification of bilateral mastoid tip air cells.",
            "output": "1. No evidence for acute infarction or other acute abnormalities.\n2. No evidence for intracranial metastatic disease.  Extracranial soft tissues\nof the scalp and skullbase are not optimally assessed on this exam in the\nabsence of fat suppression."
        },
        {
            "input": "Motion artifact mildly limits evaluation on postcontrast T1 weighted and MP\nRAGE images.\n\nThere is a large developmental venous anomaly coursing through the right\ncerebellar hemisphere and vermis, which courses along the roof of the fourth\nventricle and cerebral aqueduct, then coursing posteriorly and draining into\nthe great vein of ___.  There is a punctate focus of low signal on gradient\necho images in the right inferior cerebellar hemisphere along the\ndevelopmental venous anomaly, image 7:5, which may reflect a cavernous\nmalformation versus calcification versus punctate focus of chronic venous\nthrombus.  Acute venous thrombus is unlikely as there is no corresponding\nsignal abnormality on T1 or T2 weighted images.\n\nThere is no evidence for an enhancing intracranial mass, nor pathologic\nleptomeningeal or pachymeningeal contrast enhancement, to suggest intracranial\nmetastatic disease.  There is no acute infarction or edema.  Mild confluent\nFLAIR hyperintensity along the lateral ventricles, and scattered small foci of\nFLAIR hyperintensity in the subcortical and deep white matter of the cerebral\nhemispheres, are nonspecific but likely sequela of minimal chronic small\nvessel ischemic disease in this age group.  There is mild age-related\nprominence of the ventricles and sulci.\n\nMajor arterial flow voids appear grossly preserved.  Dural venous sinuses\nappear patent on postcontrast MP RAGE images.\n\nThere is mild mucosal thickening in the ethmoid, frontal, and possibly also\nmaxillary sinuses.  A tiny mucous retention cyst along the floor of the left\nsphenoid sinus near the septum is seen on MP RAGE images 9:77 and 3:13.\n\nThe nasopharyngeal soft tissues are enlarged and heterogenous with several\napparent nodules of mixed signal intensity.",
            "output": "1. No evidence for intracranial metastatic disease.\n2. Large developmental venous anomaly in the right cerebellum, coursing\nthrough the superior fourth ventricle and cerebral aqueduct and draining into\nthe great vein of ___.\n3. Punctate hypointense focus on gradient echo images in the right inferior\ncerebellar hemisphere, along the developmental venous anomaly, may reflect a\ncavernous malformation versus calcification versus punctate focus of chronic\nvenous thrombus.  Acute venous thrombus is unlikely as there is no\ncorresponding signal abnormality on T1 and T2 weighted images.\n4. Enlarged nasopharyngeal soft tissues with several apparent heterogenous\nnodules.  These may reflect mucous retention cysts plus/minus a Thornwaldt\ncyst, but other pathology is not excluded.\n\nRECOMMENDATION(S):  Recommend direct ENT visualization of the nasopharyngeal\nsoft tissues.\n\nNOTIFICATION:  The impression and recommendation above were entered by Dr.\n___ on ___ at 11:44 into the Department of Radiology critical\ncommunications system for direct communication to the referring provider."
        },
        {
            "input": "7 mm focus of enhancement, series 16, image 9, in the left upper pons with\nassociated T2 signal abnormality and mildly restricted diffusion, has\nincreased compared with ___ when enhancing lesion measured 5 mm, on ___ it measured 4.4 mm.  Lesion seen in the inferior left pons on ___ is not seen today.\n\nNew focus of faint cortical and subcortical enhancement posterior left frontal\nlobe, in the pre motor strip, series 16, image 20, series 17, image 135, is\nstable compared with ___, is new since ___.\n\nPunctate focus of enhancement left caudate head is stable since ___.\n\n2 mm lesion anterior left temporal lobe series 17, image 68, new since ___\n\nFew punctate foci of cerebellar enhancement, some a worrisome for metastases,\nsome may represent imaging artifact, there best seen on MP rage images example\nseries 17, image 49, largest measures 3 mm,; spin echo series 16, image 4,\nmeasuring 4 mm; they are more prominent compared to prior ___ findings\nare likely cortical, no linear enhancement to suggest leptomeningeal disease.\n\nThere is no evidence of hemorrhage, scratched midline shift or infarction. \nDegenerative changes cervical spine, minimal anterolisthesis C3-C4, C4-C5\nlevels.  Mild generalized brain parenchymal atrophy.  Dural venous sinuses are\npatent.  Vascular flow voids are preserved.",
            "output": "1. Brain metastases, mildly worsened since prior.\n\nNOTIFICATION:  The impression and recommendation above was entered by Dr.\n___ on ___ at 09:07 into the Department of Radiology\ncritical communications system for direct communication to the referring\nprovider."
        },
        {
            "input": "There is no evidence of acute intracranial hemorrhage or mass effect. The\nventricles and basal cisterns appear normal.\n\nThere is no evidence of acute ischemia based on diffusion-weighted imaging.\nThere are normal vascular flow voids. There is no abnormal brain parenchymal\nor leptomeningeal enhancement.\n\nThe orbits, skull base, and paranasal sinuses are unremarkable.",
            "output": "No evidence of intracranial metastatic disease."
        },
        {
            "input": "Study is mildly degraded by motion.  There is mild global parenchymal volume\nloss.  Small areas of hyperintense signal on T2/FLAIR within the subcortical\nand periventricular white matter are nonspecific, but likely reflect the\nsequela of mild chronic small vessel disease.  There is no acute infarct,\nintracranial hemorrhage, mass effect, or abnormal enhancement.  The major\nvascular flow voids are preserved.\n\nThe orbits are grossly unremarkable.\n\n3 mm anterolisthesis of C4 on 5 appears worse from the ___ MRI. \nThis is likely related to degenerative disc disease.",
            "output": "1. Study is mildly degraded by motion.\n2.  Within limits of study, no evidence of intracranial metastasis.\n3. 3 mm anterolisthesis of C4 on C5 is likely secondary to degenerative disc\ndisease and appears worse from the ___ MRI."
        },
        {
            "input": "There is a new 2 mm enhancing focus in the left lower pons, images 17:60 and\n19:74, with associated high signal on FLAIR image 16:6; no definite associated\nslow diffusion.  There is also a new 3 mm focus with thin rim of enhancement\nin the left superior pons, images 17:74 and 19:76, with high signal on FLAIR\nand diffusion tracer images, but no definite low signal on the ADC map.  There\nis no associated mass effect or blood products.\n\nMinimal periventricular T2 hyperintensity is unchanged, nonspecific but likely\nsecondary to mild chronic small vessel ischemic disease in this age group.  No\nevidence for intracranial blood products.  Parenchymal volume is within normal\nlimits for age.  Major arterial flow voids are grossly preserved.  Dural\nvenous sinuses appear patent on postcontrast MP RAGE images.\n\nSagittal images included upper cervical spine, again demonstrating minimal\nanterolisthesis of C3 on C4 and of C4 on C5, with disc protrusions at these\nlevels, incompletely evaluated.",
            "output": "New 3 mm rim enhancing focus in the left superior pons with high signal on\nFLAIR and diffusion tracer images, without signal abnormality on the ADC map. \nNew 2 mm homogeneous enhancing focus in the left lower pons with high signal\non FLAIR images, but no evidence for diffusion signal abnormality. These are\ncompatible either with metastases or subacute infarcts.\n\nRECOMMENDATION(S):  Follow up MRI in several weeks (in order to assess for\nevolution in contrast enhancement and diffusion signal) may be helpful to\ndifferentiate between metastases and subacute infarcts.\n\nNOTIFICATION:  The impression and recommendation above were entered by Dr.\n___ on ___ at 10:51 into the Department of Radiology critical\ncommunications system for direct communication to the referring provider."
        },
        {
            "input": "Re-identified is a ring-enhancing 3-4mm lesion in the left superior pons\ndemonstrating diffusion-weighted hyperintense signal, increased in size from\nprior exam.  Associated diffusion-weighted hyperintense signal is unchanged. \nAssociated FLAIR signal is more prominent.  Addition, a 2-3 mm punctate\nenhancing left pontine lesion at the level of the brachium pontis demonstrates\nincreased conspicuity of enhancement.  Associated FLAIR signal is similar. \nThis lesion does not demonstrate diffusion-weighted hyperintense signal.\n\nNo other enhancing lesions are identified.  No new parenchymal FLAIR signal\nabnormality.  The sulci, ventricles and cisterns are within expected limits\nfor the patient's age.  The major intracranial flow voids are preserved.  The\ndural venous sinuses are patent.  No acute infarct or intracranial hemorrhage.\nThe orbits are unremarkable.  No significant fluid signal seen in the mastoid\nair cells or paranasal sinuses.  No suspicious osseous lesion.",
            "output": "1. Re-identified is a 3-4 mm left superior pontine ring-enhancing lesion,\ndemonstrating increased associated FLAIR and enhancement.  Associated\ndiffusion-weighted signal abnormality seen on prior examination is unchanged. \nA 2-3 mm punctate enhancing left pontine lesion at the level of the brachium\npontis demonstrates increased conspicuity of enhancement, with unchanged FLAIR\nsignal.  Overall, given increasing enhancement of both lesions and increasing\nFLAIR signal abnormality of the dominant left pontine lesion, metastatic\ndisease is preferred over the previously discussed differential consideration\nof subacute infarcts.\n2. No new enhancing lesions are identified.  No new FLAIR signal abnormality.\n3. Additional findings as described above."
        },
        {
            "input": "Study is mildly degraded by motion.\n\nGrossly stable approximately 3 mm left superior pons minimally peripherally\nenhancing lesion with restricted diffusion and minimal associated T2 and FLAIR\nhyperintensity is again noted (see 10:117; 550, 552:11; 7, 8:9 on current\nstudy and 17:16 on prior exam).\n\nQuestion minimal residual enhancement of patient's previously noted left\nbrachium pontis enhancing lesion decreased compared to prior exam, versus\nartifact (see 9:6 on current study and 18:7 on prior exam).  Minimal residual\nFLAIR hyperintensity versus artifact in this region is suggest (see 7:6 on\ncurrent study and 15:7 on prior exam).\n\nThere is no evidence of hemorrhage, midline shift or infarction.   The\nventricles and sulci are stable in caliber and configuration.",
            "output": "1. Study is mildly degraded by motion.\n2. Grossly stable 3 mm peripherally enhancing left superior pons lesion with\nsuggested minimal edema.\n3. Previously noted left brachium pontis with question minimal residual\nenhancement, decreased compared to prior exam, with minimal residual\nparenchymal signal intensity abnormality as described.\n4.  Within limits of study, no definite new enhancing intracranial mass\nidentified."
        },
        {
            "input": "MRA brain: The intracranial vertebral and internal carotid arteries and their\nmajor branches appear normal without evidence of stenosis, occlusion, or\naneurysm formation.  The blood supply of the left posterior cerebral artery is\nprimarily from a left posterior communicating artery.\n\nMRA neck: The common, internal and external carotid arteries appear normal. \nThere is no evidence of stenosis by NASCET criteria.  The left common carotid\nshows a common origin with the right brachiocephalic artery compatible with a\nbovine arch.  There are mild atherosclerotic changes at the distal right\ncommon carotid artery and proximal right internal carotid artery without\nstenosis.  The origins of the subclavian, and vertebral arteries appear normal\nbilaterally.  The common carotid bifurcations appear normal.",
            "output": "1. Mild atheromatous change at the distal right common carotid and proximal\nright internal carotid arteries.\n2. Otherwise normal normal head and neck MRA."
        },
        {
            "input": "There is no evidence of intracranial hemorrhage, mass, mass effect or shifting\nof the normally midline structures. The ventricles and sulci are normal in\nsize and configuration for the patient's age. Few scattered small foci of high\nsignal intensity are identified on FLAIR and T2 weighted images, distributed\nin the subcortical white matter, which are nonspecific and may reflect changes\ndue to small vessel disease, these type of findings have been described in\npatients with chronic migraines, sequela of viral infection. No diffusion\nabnormalities are detected, there is no evidence of abnormal enhancement.  The\nmajor vascular flow voids are present and demonstrate normal distribution. \nThe orbits are unremarkable, the paranasal sinuses and the mastoid air cells\nare clear.",
            "output": "Few scatter small foci of high signal intensity identified on FLAIR and T2\nweighted images, distributed in the subcortical white matter, which are\nnonspecific and may reflect changes due to small vessel disease, otherwise,\nthere is no evidence of acute or subacute intracranial process, there is no\nevidence of abnormal enhancement."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration for patient's age.  Periventricular and deep subcortical FLAIR\nwhite matter hyperintensities are likely sequelae of chronic small vessel\nischemic disease.  There is no abnormal enhancement after contrast\nadministration.  Incidentally noted is a right frontal developmental venous\nanomaly, a normal variant.\n\nMild mucosal sinus thickening is seen involving the ethmoid air cells as well\nas a mucous retention cyst within the left maxillary sinus.  The remainder of\nthe visualized paranasal sinuses, mastoid air cells, and middle ear cavities\nare clear.  The globes are unremarkable.  The principal vascular flow voids\nappear to be well preserved.  Degenerative changes noted at the right\ntemporomandibular joint with subchondral cyst within the condyle.",
            "output": "No acute intracranial abnormalities identified.  No concerning enhancing\nlesions seen.  A few scattered white matter T2/FLAIR hyperintensities, likely\nsequela of chronic small vessel disease."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, or midline\nshift.  The ventricles and sulci are normal in caliber and configuration for\nage.  An area of encephalomalacia in the left occipital lobe is unchanged from\nrecent studies.  Mild scattered foci of T2 and FLAIR hyperintensity are\nnonspecific but likely represent the sequelae of chronic microvascular\ndisease.\n\nA small focal area of decreased diffusivity within the splenium of the corpus\ncallosum most likely represents an area of acute infarction (402:15, 400:15). \nAn area of mildly increased signal on the trace image with minimally decreased\nADC values within the brainstem is felt less likely to be related to\ninfarction and more likely represents artifact ___, 400:12).  While this\narea is perfused by the recently occluded basilar artery, an infarction\noccurring 4 days ago should have a correlation on T2 and FLAIR, which this\ndoes not.  An area of hyperacute infarction could have no correlate on T2 or\nFLAIR, but typically would have lower diffusivity and would be unlikely across\nthe midline.  If the possibility of infarction in the pons remains a clinical\nconcern, follow-up imaging should clarify the question.",
            "output": "1. Small focal acute infarction within the splenium of the corpus callosum.\n2. Mild age-appropriate involutional changes and nonspecific T2 and FLAIR\nhyperintensities likely representing the sequela of chronic microvascular\ndisease.\n\nNOTIFICATION:  The findings were discussed with ___, M.D. by ___\n___, M.D. on the telephone on ___ at 5:13 pm, 45 minutes after\ndiscovery of the findings."
        },
        {
            "input": "Study is moderately degraded by motion, especially on postcontrast imaging. \nWithin these confines:\n\nThere is encephalomalacia from chronic appearing right posterior parietal\ninfarct.\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor acute infarction.  There is prominence of the ventricles and sulci\nsuggesting involutional changes.  Confluent areas of periventricular,\nsubcortical and deep white matter T2/FLAIR hyperintensity are nonspecific,\nmost likely representing chronic small vessel ischemic disease.  There is no\nabnormal enhancement after contrast administration.  There is no abnormal\nfocus of slow diffusion.  The principal intracranial vascular flow voids are\npreserved.\n\nThe paranasal sinuses are grossly clear.  The orbits are grossly unremarkable.",
            "output": "1.  Study is moderately degraded by motion.\n2.  Within limits of study, no evidence of intracranial metastatic disease.\n3. Chronic right posterior parietal infarct.\n4.  No acute intracranial abnormality."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  Stool generalized mild brain parenchymal atrophy.  Findings\nconsistent with mild chronic small vessel ischemic changes. Prominent\nperivascular spaces.  Intracranial vascular flow voids are preserved.  Minimal\nopacification paranasal sinuses, mastoids.  There is fluid in the posterior\nnasopharynx, likely from intubation.  Punctate focus of superficial\nmicrohemorrhage right frontal lobe is stable since prior.",
            "output": "1. No acute intracranial findings.\n2. Brain parenchymal atrophy.  Mild chronic small vessel ischemic changes."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration for age.  Periventricular white matter T2 and FLAIR\nhyperintensities most likely represent microangiopathy.  The intracranial\narteries demonstrate normal T2 flow voids.  The orbits appear normal.  Minimal\nmucosal thickening involving the right maxillary sinus. partially empty sella\nis nonspecific.  No other findings to suggest hydrocephalus.  The\ncraniocervical junction is normal.",
            "output": "No evidence of mass, hemorrhage or infarct.  Specifically no cerebellar\nischemia.\n\nPeriventricular white matter T2 and FLAIR hyperintensities are most likely\nsecondary to microangiopathy."
        },
        {
            "input": "The exam is moderately degraded due to motion artifact.\n\nThere is no evidence of infarction, hemorrhage, mass effect.  Postcontrast\nimages are severely degraded by motion artifact.  However, there is no\nevidence of abnormal enhancing\n\nThe ventricles, sulci, and cisterns appear normal.  Small foci of hyperintense\nsignal in the subcortical and periventricular white matter nonspecific, but\nlikely reflect the sequela of mild chronic small vessel disease.  The major\nvascular flow voids are preserved.\n\nThe orbits are unremarkable.  There is a mucous retention cyst within the left\nmaxillary sinus.",
            "output": "1. Moderately degraded exam due to motion artifact.  No evidence of\ninfarction, hemorrhage, mass effect, or abnormal enhancement.\n2. Probable mild chronic small vessel disease."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal focus of slowed diffusion.  The principal\nintracranial vascular flow voids are preserved.  Trace periventricular white\nmatter T2/FLAIR hyperintensity most likely reflects the sequela of chronic\nsmall vessel ischemic disease.\n\nThere are small mucous retention cyst in the floor of the left maxillary sinus\nalong with mild mucosal wall thickening in the left sphenoid and bilateral\nethmoid air cells.  The remainder of the visualized paranasal sinuses are\notherwise clear.  The orbits are grossly unremarkable.  The mastoid air cells\nare clear.",
            "output": "1. No hemorrhage, infarct, or suggestion of mass.\n2. Trace white matter signal abnormality most likely suggestive of chronic\nsmall vessel ischemic disease."
        },
        {
            "input": "There is no evidence of intracranial hemorrhage, mass, mass effect or shifting\nof the normally midline structures. The ventricles and sulci are normal in\nsize and configuration for the patient's age.  Multiple scattered foci of high\nsignal intensity are identified on T2 and FLAIR sequences, distributed in the\npons, subcortical and periventricular white matter, which are nonspecific and\nmay reflect changes due to small vessel disease. No diffusion abnormalities\nare detected. There is no evidence of abnormal enhancement after contrast\nadministration.  The major vascular flow voids are present and demonstrate\nnormal distribution. The orbits are unremarkable, the paranasal sinuses and\nthe mastoid air cells are clear.",
            "output": "1.  There is no evidence of acute intracranial process or hemorrhage.\n\n2.  Scattered foci of high signal intensity detected on FLAIR and T2 weighted\nimages, distributed in the subcortical and periventricular white matter, are\nnonspecific and may reflect changes due to small vessel disease.\n\n3.  There is no evidence of abnormal enhancement after contrast\nadministration."
        },
        {
            "input": "There are postprocedural changes of a prior right-sided craniotomy recent\ndural and deep electrode placement along the right cerebral hemisphere\nincluding a right frontal, parietal, temporal, and occipital lobe. There is\nassociated postoperative pneumocephalus with layering subdural fluid and blood\nwithin the right cerebral convexity. There is unchanged volume loss within the\nright temporal lobe. The ventricles are stable in size.\n\nThe orbits, skull base, and paranasal sinuses are unremarkable.",
            "output": "1. Postprocedural changes of dural and deep electrode placement along the\nright cerebral hemisphere with associated postoperative pneumocephalus,\nextra-axial fluid, and blood products.\n2. Unchanged chronic volume loss within the right temporal lobe."
        },
        {
            "input": "Patient is again noted to be status post right temporal craniotomy and\nlobectomy.  Postoperative pneumocephalus with layering of subdural fluid and\nblood within the right cerebral convexity is again noted.  On FLAIR images,\nthere is increased signal intensity seen in sulci in the right frontal and\nparietal lobe likely representing postoperative subarachnoid hemorrhage.  This\nappears similar to recent prior CT when accounting for differences in\nmodality.  There has been interval further resection of the right anterior\ntemporal lobe.   The ventricles and sulci are stable in size and\nconfiguration.  There is no evidence of acute territorial infarction.  There\nis no shift of midline.  Major vascular flow voids are preserved.  The orbits\nare unremarkable.  There is minimal mucosal thickening within the ethmoid air\ncells.  The remaining paranasal sinuses and mastoid air cells are clear.",
            "output": "Patient is status post right craniotomy and right anterior temporal lobectomy.\nThere are expected postoperative changes as detailed above.  There is no\nevidence of acute territorial infarction."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  Mild prominence of the ventricles and sulci is likely related\nto age related involutional changes.  There is no abnormal enhancement after\ncontrast administration.\n\nMild mucosal sinus thickening is seen involving the ethmoid air cells.  The\nremainder the visualized paranasal sinuses, mastoid air cells, middle ear\ncavities are clear.  The globes are unremarkable.  The principal vascular flow\nvoids appear to be well preserved.",
            "output": "1. No acute intracranial abnormalities identified.  No concerning intracranial\nlesions seen."
        },
        {
            "input": "The visualized aspect of the aortic arch appears unremarkable, there is normal\nappearance and origin of the supraaortic vessels with 3 branching pattern. \nBoth common carotid arteries as well as the vertebral arteries are patent with\nno evidence of flow stenotic lesions or dissection the visualized intracranial\nstructures are partially evaluated, however grossly there is no evidence of\nflow stenotic lesions.",
            "output": "1. The major arterial vessels of the neck appear patent with no evidence of\ndissection or stenotic lesions."
        },
        {
            "input": "Study is moderately degraded by motion, especially on FLAIR imaging.\n\nThere is no evidence of acute hemorrhage, edema, masses, mass effect, midline\nshift or infarction.  A punctate focus of susceptibility in the right\ncerebellar hemisphere in 12:5 likely represents chronic microhemorrhage.  The\nventricles and sulci are normal in caliber and configuration.\n\nThe paranasal sinuses and mastoid air cells are clear.  The orbits are\nunremarkable.\n\nThe major intracranial flow voids are preserved.",
            "output": "1.  Study is moderately degraded by motion, as described.\n2. No acute intracranial abnormality.\n3. No evidence of acute infarct."
        },
        {
            "input": "Study is mildly degraded by motion.\n\nCentered in the right temporal lobe, there is a 1.0 x 0.6 x 0.8 cm\nring-enhancing, centrally T1 hypointense, T2 hyperintense, without definite\ncentral restricted diffusion mass with extensive surrounding parenchymal FLAIR\nhyperintensity (13:9, 14:76, 100:84, 101:92).  The peripherally enhancing,\nsolid portion of the mass demonstrates slowed diffusion (05:11, 06:11) and\nminimal increase susceptibility (see 10:9; 14:74), and may correspond areas of\nhigh density on previous day outside noncontrast head CT (see 02:11 on prior\nexam).\n\nThere is minimal brain parenchymal edema, without definite midline shift.  Is\nno definite evidence of herniation or ventricular entrapment.\n\nNo additional masses or abnormal enhancement is seen.  There is no evidence of\nacute infarct, additional definite areas of hemorrhage, or extra-axial\ncollection.\n\nThe ventricles and sulci are grossly preserved in caliber and configuration.\n\nThere is mild left maxillary sinus and ethmoid air cell mucosal thickening. \nThe visualized portion of major intracranial vascular flow voids are grossly\npreserved.  Major dural venous sinuses are grossly patent.  The globes and\norbits are grossly preserved.",
            "output": "1. Study is mildly degraded by motion.\n2. Ring-enhancing 1 cm mass in the right temporal lobe with surrounding\nextensive parenchymal FLAIR hyperintensity. Differential includes high-grade\nglioma, metastasis, tumefactive demyelination, and CNS lymphoma or atypical\ninfection (e.g.  Cryptococcus) if known to be immunocompromised."
        },
        {
            "input": "Infiltrative FLAIR hyperintense lesion involving the right inferior temporal\nlobe measuring a conglomerate 7.2 x 4.0 cm is overall unchanged in size and\nconfiguration from examination of ___.  There is mild associated hazy\ngradient echo susceptibility hypointensity without blooming, compatible with\nminimal calcifications associated with a more central region of hazy\nenhancement measuring 1 cm (series 9, image 60) also unchanged.  The lesion\ndemonstrates mild mass effect with local sulcal effacement and mild effacement\nof the right perimesencephalic cistern.  No significant midline shift.  No\nhydrocephalus.\n\nThere is no evidence for acute infarct or acute intracranial hemorrhage.  The\nsulci, ventricles cisterns are otherwise within expected limits for the\npatient's age.  The intracranial flow voids are preserved.  Dural venous\nsinuses are patent.  There is mucosal thickening of the paranasal sinuses with\napparent mucous retention cysts in the left maxillary sinus alveolar recess. \nThere does appear to be mild increased enhancement associated with dental\nroots (series 901, image 43).  No significant fluid signal is noted in the\nmastoid air cells.  The orbits appear unremarkable allowing for overlying\nmetallic artifact.\n\nOtherwise, no suspicious marrow signal.",
            "output": "1. Infiltrative FLAIR hyperintense 7.2 cm right inferior temporal lobe lesion\nwith a central region of 1 cm enhancement and associated calcification is\nunchanged in appearance from examination of ___.  Overall given the\nstability in appearance over 1 month, this is felt to be most compatible with\na neoplastic process such as high-grade glioma rather than infectious process.\n2. There is mucosal thickening of the left maxillary sinus with regions of\nenhancement which appears to be associated with dental roots.  Clinical\ncorrelation for odontogenic sinusitis is recommended.\n3. Additional findings described above."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, midline shift or recent infarction.\nThere is a focus of tissue loss in the right cerebellar hemisphere that likely\nrepresents a chronic lacune.  The ventricles and sulci are enlarged in an\natrophic pattern.  There is a right middle cranial fossa arachnoid cyst. \nThere is a small nonenhancing left frontal ependymal or subependymal nodule\nadjacent to the corpus callosum, seen on image 114 of series 9, image 15 of\nseries 7, image 15 of series 8 and image 95 of series 900.\nThere are scattered white matter hyperintensities on the FLAIR images.  These\nare often seen in patients of this age and are usually attributed to chronic\nsmall vessel ischemia.\nThere is partial opacification of a right ethmoid air cell.  The lenses have\nbeen resected.  There is no abnormal enhancement after contrast\nadministration.",
            "output": "1. No evidence of hemorrhage or infarction.\n2. Mild changes suggesting chronic small vessel ischemia.\n3. Left frontal subependymal nonenhancing nodule.\n4. Chronic right cerebellar hemispheric lacune"
        },
        {
            "input": "The left parafalcine enhancing mass measuring 2.6 x 5.1 x 3.1 cm best seen on\nseries 5002b, image 74 and series 103, image 84.  Extension into the overlying\ncalvarium and abutting the superior sagittal sinus.  Associated mass effect on\nthe adjacent frontal parietal cortex with edema.  No significant midline\nshift.    7 x 4 x 5 mm extra-axial dural-based mass at the right parietal\nconvexity best seen on series 100p image 69 and series 2, image 67.  9 x 4 x 6\nmm extra-axial mass overlying the right cerebellar cortex best seen on series\n103, image 94 and series 5002b, image 119.  Prominent ventricles, normal for\nage.",
            "output": "1. Left parafalcine enhancing mass, as described, with extension into the\noverlying calvarium and abutting the superior sagittal sinus.  Associated mass\neffect and edema within the underlying frontal parietal cortex. Findings\nlikely represent a meningioma.\n2. Small extra-axial dural-based masses at the right parietal convexity and\nright cerebellar cortex.\n3. Finding relatively unchanged in comparison to outside prior MR of the\nbrain."
        },
        {
            "input": "Interval high parietal craniotomy status post partial resection and left\nparafalcine mass.  Residual enhancing mass at the left parasagittal resection\ncavity measuring 1.0 x 2.2 x 3.3 cm best seen on series 14, image 92 and\nseries 100b, image 86. Associated scattered foci of gradient echo\nsusceptibility consistent with blood products.  Diffuse mild dural\nenhancement.  Slow diffusion within the anterior parasagittal left parietal\ncortex extending minimally into the precentral or gyrus seen on series 5,\nimage 26 which may represent acute infarction versus postsurgical changes.\n\nNumerous additional punctate foci of slow diffusion throughout cortical\nsurface of the bilateral frontal and occipital cortices, left greater than\nright. Additional foci within the left insula are left parietal, left\ntemporal, and right cerebellar cortices.  Smaller number of small areas of\nslow diffusion within the deep white matter.  Findings correspond to multiple\nvascular territories. No evidence of hemorrhagic conversion.  FLAIR signal\nhyperintensity within the left parietal and occipital cortices without\nsignificant mass effect.\n\nFilling defect within the mid to posterior superior sagittal sinus consistent\nwith meningioma.  The remainder of the venous sinuses are patent.\n\nAgain seen are small homogeneously enhancing extra-axial masses, presumably\nmeningiomas, at the right posterior cranial fossa measuring 6 mm (series 100b,\nimage 96) and at the lateral right parietal convexity measuring 6 mm (series\n100b, image 82).\n\nNormal ventricular size for patient age.  Preserved vascular flow voids.  Mild\nmucosal thickening within the left ethmoid maxillary and sphenoid sinuses. \nBilateral mastoid air cell effusions.  Skin staples with expected\nsusceptibility within the scalp.",
            "output": "1. Postsurgical changes with partial resection of the left parasagittal\nextra-axial mass with small parafalcine site of residual disease, as\ndescribed.\n\n2. Confluent slow diffusion within the the superior post central parietal\ncortex which may represent postsurgical change versus acute infarction,\npossibly of venous etiology.\n3. Numerous additional punctate infarcts throughout the bilateral cerebral\ncortices, left greater than right, as described corresponding to multiple\nvascular territories suggestive of embolic etiology.  Thrombus within the mid\nto posterior superior sagittal sinus.\n4. Unchanged small enhancing extra-axial masses within the right posterior\ncranial fossa and lateral right parietal convexity likely representing small\nmeningiomas.\n\nNOTIFICATION:  Results discussed with Dr ___ by Dr ___ 30 minutes\nfollowing discovery via phone at ___ on ___"
        },
        {
            "input": "There is no evidence of hemorrhage, edema, mass, mass effect, or acute\ninfarction.  Scattered periventricular, subcortical, and deep white matter\nFLAIR hyperintense foci without associated slow diffusion are nonspecific but\nlikely sequelae of chronic microangiopathy in a patient of this age.  The\nventricles and sulci are age-appropriate.  Principal intracranial vascular\nflow voids are preserved.  There is mild mucosal thickening and small mucous\nretention cyst in the sphenoid, frontal, and sphenoid sinuses.  The orbits are\nunremarkable.",
            "output": "No evidence of hemorrhage or acute infarction."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  Mild prominence of the ventricular system size and brain sulci\nare likely age-related involutional changes.\n\nThe lenses have been resected bilaterally.  Otherwise, the orbits appear\nnormal.  Paranasal sinuses and mastoid air cells are clear.",
            "output": "1. No evidence of mass, hemorrhage or infarction."
        },
        {
            "input": "Study is mildly degraded by motion.   There is no evidence of acute\ninfarction.  No intracranial hemorrhage. No mass, mass effect, edema or\nmidline shift.  Incidentally noted is a partially empty sella, unchanged\ncompared to ___ exam.  Grossly stable low-lying cerebellar tonsils are again\nnoted, with extensive approximately 2 mm inferior to the foramen magnum (see\n03:12 on current study and 7:119 on prior exam).\n\nThe ventricles and sulci are diffusely prominent.  Periventricular and\nsubcortical white matter FLAIR hyperintensities are noted, a nonspecific\nfinding that most likely represents the sequelae of chronic small vessel\nischemic disease.  There is gross preservation of the principal intracranial\nvascular flow voids.\n\nThe visualized paranasal sinuses, middle ear cavities, and mastoid air cells\nare well aerated and clear.  The patient is status post bilateral lens\nreplacement.",
            "output": "1.  Study is mildly degraded by motion.\n2. No evidence for acute intracranial hemorrhage or vascular territorial\ninfarction.\n3. Global parenchymal volume loss and probable chronic small vessel ischemic\ndisease, progressed compared to ___ prior exam.\n4. Grossly stable nonspecific low-lying cerebellar tonsils compared to ___\nprior exam, with approximately 2 mm inferior extension to the foramina magnum."
        },
        {
            "input": "There is a small focus of restricted diffusion in location of the right\nthalamus and internal capsule posterior limb (4:16, 3:16), with small small\nassociated T2 and FLAIR hyperintensity.  There is no evidence of hemorrhage,\nmass effect, or midline shift.  There is an area of T2 hyperintensity with\ncomponents that are FLAIR hypointense and without evidence of restricted\ndiffusion in the left caudate body and corona radiata consistent with a\nchronic infarct, new since ___ (9:15, 10:15).\n\nThere is prominence of the ventricles and sulci suggestive involutional\nchanges.  Major arterial flow voids are grossly preserved.\n\nThere is a small left ethmoid air cell mucous retention cyst.  The other\nparanasal sinuses are grossly clear.  There is partial left mastoid air cell\nopacification.  The right mastoid air cells are clear.",
            "output": "1. Acute to subacute infarct of the right thalamus and right internal capsule\nposterior limb without evidence of hemorrhagic conversion.\n2. Chronic left caudate body and corona radiata infarct.\n3.  Paranasal sinus disease as described.\n\nNOTIFICATION:  The findings were discussed by Dr. ___ with Dr.\n___ on the telephoneon ___ at 12:48 ___, less than 5 minutes\nafter discovery of the findings."
        },
        {
            "input": "There are bilateral foci of slow diffusion demonstrating mild T2/FLAIR\nhyperintense signal, consistent with multifocal acute infarcts, most numerous\nin the right frontal lobe (302:23) but also seen within the right temporal\nlobe (302:18), the bilateral occipital lobes (302: 24 and 25), as well as the\nright cerebellar hemisphere (302:6).  There is no evidence of hemorrhage\nassociated with these infarcts, or elsewhere intracranially.\n\nThere are multiple small foci of enhancement seen based in the cortex,\ncortical gray-white matter junction, and subcortical white matter bilaterally,\nmost numerous in the right occipital lobe but also seen on the left and in the\nright parietal lobe (for example see series 9, images 110, 113, 117, 112, and\n103, as well as series 901, images 118 and 121 and 81).  Otherwise, no\nabnormal enhancement is seen elsewhere.  The ventricles and sulci are mildly\nprominent, consistent with global involutional changes.  Scattered bilateral\nperiventricular and deep white matter foci of T2/FLAIR signal hyperintensity\nare nonspecific but compatible with mild changes of chronic white matter\nmicroangiopathy.\n\nThe major dural venous sinuses are grossly patent.  Major intracranial\nvascular flow voids are grossly preserved.  The globes are unremarkable.",
            "output": "1. Multifocal bilateral right greater than left supra- and infratentorial\nacute infarcts, most numerous in the right frontotemporal region.  No\nintracranial hemorrhage.\n2. Multiple small bilateral cortically- and subcortically-based subcentimeter\nfoci of enhancement.  Although nonspecific, given history of pancreatic\nadenocarcinoma, early small metastases are difficult to exclude.  Attention on\nfollow-up.\n3. Chronic findings include global involutional changes and mild changes of\nchronic white matter microangiopathy.\n\nNOTIFICATION:  The findings were discussed with ___, M.D. by ___\n___, M.D. on the telephone on ___ at 01:00."
        },
        {
            "input": "There are multiple subacute infarcts, some have associated enhancement,\ninterval evolution since prior.  Area of subacute infarct in the right centrum\nsemiovale, corona radiata has mildly progressed since prior.  It contains\nsmall focus of hemorrhage, seen on gradient images measures approximately 5\nmm..  No definite new infarcts.  Areas of enhancement are most consistent with\nsubacute infarcts.  Previously seen small foci of enhancement right parietal\nlobe have resolved.\n\nNo acute infarct.  No hydrocephalus, midline shift.  Mild generalized brain\nparenchymal atrophy.  Vascular flow voids are preserved.  Paranasal sinuses,\nmastoids are clear",
            "output": "1. Interval evolution of infarcts.  One subacute area of infarct is mildly\nincreased, contains 5 mm focus of hemorrhage.\n2. Areas of enhancement are typical of subacute infarcts.\n3. No definite metastases.\n\nNOTIFICATION:  The impression and recommendation above was entered by Dr.\n___ on ___ at 13:32 into the Department of Radiology\ncritical communications system for direct communication to the referring\nprovider."
        },
        {
            "input": "Encephalomalacia underlying the left parietal craniectomy are seen. Although\nthe configuration of the surrounding white matter T2/FLAIR hyperintensity\nsurrounding the postoperative bed appears slightly more extensive, this is\nlikely due to evolution of the postsurgical changes and the relatively new\nconfiguration of the brain parenchyma which is now occupying the craniectomy\ndefect. There is mild enhancement overlying the surgical bed center (series\n101a, image 112) which is similar when compared to prior. The enhancing\nportion of the calvarium seen on exam from ___ has been removed.\nEnhancement along the margins of remote prior craniotomy (series 101a, image\n100) is not unexpected but should be followed on subsequent exams.\n\nElsewhere, there is no parenchymal signal abnormality. There is mild\nenlargement of the atrium of the left lateral ventricle. Ventricles and sulci\nare otherwise symmetric and unremarkable. There is no region of restricted\ndiffusion nor unexpected susceptibility artifact. Major intravascular flow\nvoids are preserved. Postoperative changes from FESS are seen.",
            "output": "Postoperative changes of resection of left parietal calvarium lesion. \nEnhancement surrounding the postoperative bed and along the prior remote\ncranioctomy site, not unexpected but to be followed at future exams."
        },
        {
            "input": "In comparison with the most recent examination, again postsurgical changes are\nre- demonstrated, consistent with left parietal craniotomy, there is expected\nmild enhancement overlying the surgical area, with no evidence of tumor\nrecurrence or new areas with abnormal enhancement,. The FLAIR sequence is\nnotable for an unchanged area of encephalomalacia in the surgical site,\ncausing mild ex vacuo dilatation of the left ventricular trigone, there is no\nevidence of hydrocephalus. No diffusion abnormalities are detected. The major\narterial vascular flow voids are present and demonstrate normal distribution.\nThe orbits are unremarkable, the paranasal sinuses and the mastoid air cells\nare clear.",
            "output": "1. In comparison with the most recent examination, again expected postsurgical\nchanges are re- demonstrated in the left parietal region, consistent with\ncraniotomy an mild enhancement overlying the surgical bed, with no evidence of\ntumor recurrence or new areas with abnormal enhancement, long-term followup is\nadvised to demonstrate stability.\n\n2. There FLAIR images again shows encephalomalacia in the left parietal\nregion, and unchanged mild ex vacuo dilatation of the left ventricular\ntrigone."
        },
        {
            "input": "Please note the study is degraded by motion.\n\nThere are stable postsurgical changes related to the patient's prior left\nparietal lobe grade 2 meningioma resection.\n\nThere is no acute intracranial hemorrhage, abnormal extra-axial fluid\ncollection, midline shift, or acute territorial infarction. The ventricles and\nsulci are preserved. The mastoid air cells are preserved. There is no abnormal\nenhancement on post-contrast imaging.   There is a new left maxillary sinus\nmucous retention cyst versus polyp. There is redemonstration of postsurgical\nchanges related to bilateral ethmoidectomies.",
            "output": "1. Please note the study is degraded by motion.\n2. No definite new or recurrent mass identified.\n3. Stable postoperative change related to prior left parietal lobe grade 2\nmeningioma resection.\n4. Stable changes related to prior sinus surgery.\n5. Paranasal sinus disease as described."
        },
        {
            "input": "Left posterior parietal craniotomy changes are seen.  There is stable FLAIR\nhyperintense signal in the left parietal lobe, under the craniotomy site.  No\nsignificant dural enhancement is noted at the surgical site to suggest\nrecurrent disease.\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.\n\nMinimal left maxillary and ethmoid sinus mucosal thickening is seen.  Small\nfat deposit or hemangioma in the C3 body, similar to the prior studies.",
            "output": "1. Stable postsurgical changes from a left parietal convexity meningioma\nresection with no evidence of residual or recurrent disease."
        },
        {
            "input": "The patient is status post left parietal craniotomy and resection of an\nextra-axial mass.  Left parietal lobe white matter edema pattern,\nencephalomalacia and postsurgical findings in the resection bed are unchanged\nfrom prior examination of ___.  There are very few superimposed\npunctate periventricular and subcortical white matter hyperintensities, which\nare nonspecific, but compatible with chronic microangiopathy in a patient of\nthis age, also unchanged.  No increasing nodular enhancement within the\nresection bed to suggest disease progression or recurrence.\n\nThere is no acute infarct or intracranial hemorrhage.  No new enhancing\nlesions are identified.\n\nThe major intracranial flow voids are preserved.  The dural venous sinuses are\npatent on postcontrast MP-RAGE.  Partial opacification of the ethmoid air\ncells and dependent fluid in the right maxillary sinus with mild mucosal\nthickening of the left maxillary sinus is identified, progressed from\nexamination of ___.  The mastoid air cells are clear.  The orbits\nare unremarkable.",
            "output": "1. Stable postsurgical changes from left parietal convexity meningioma\nresection without evidence of residual or recurrent disease."
        },
        {
            "input": "There is a 0.7 x 0.9 x 1.2 cm (AP x TV x SI) homogeneously enhancing mass\nwithin the foramen of Magendie (measured on series 901b, image 98 and series\n900b, image 89), unchanged compared to the prior MRI.  There is calcification\nwithin the mass, as seen on the concurrent head CTA, with corresponding mild\nsusceptibility artifact on the present MRI. There is no hydrocephalus.  Basal\ncisterns are normal in size.  No other masses are seen.  There is no edema,\nabnormal diffusion, or evidence for blood products in the brain parenchyma.\n\nMajor intravascular flow voids are preserved.  There is normal enhancement of\nthe major  dural venous sinuses following contrast administration.",
            "output": "Approximately 1.2 cm homogeneously enhancing mass, calcified mass within the\nforamen of Magendie, without hydrocephalus.  Its appearance is most suggestive\nof an ependymoma.  Other, less likely considerations include a meningioma\n(though these are more common in the lateral ventricles), a choroid plexus\npapilloma (though these are usually associated with hydrocephalus), and a\nmetastasis."
        },
        {
            "input": "Since the previous MRI examination, the patient has undergone suboccipital\ncraniectomy for removal of fourth ventricular neoplasm.  There is no acute\ninfarcts seen.  There is pachymeningeal enhancement identified and\npneumocephalus seen which are postoperative in nature.  There is no residual\nenhancement seen in the posterior fossa and the fourth ventricle at the site\nof previously identified tumor.  No other areas of abnormal enhancement seen. \nThere is no hydrocephalus.",
            "output": "Status post resection of posterior fossa  fourth ventricular tumor.  No\nresidual enhancement seen.  No acute infarcts mass effect or hydrocephalus."
        },
        {
            "input": "Patient is status post suboccipital craniotomy and resection of a choroid\nplexus papilloma in the foramen of Magendie.  There is no residual enhancement\nat the resection site.  Interval resolution of postoperative left frontal\npneumocephalus.  No new foci of abnormal enhancement.\n\nThere is no evidence of hemorrhage, edema, mass effect, midline shift or\ninfarction.   The ventricles and sulci are normal in caliber and\nconfiguration.",
            "output": "1. Patient is status post suboccipital craniotomy and resection of a choroid\nplexus papilloma in the foramen of Magendie.  No evidence of local recurrence.\n2. No evidence of acute infarction."
        },
        {
            "input": "Study is mildly degraded by motion, especially on postcontrast imaging. \nWithin these confines:\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration. Periventricular and subcortical T2 and FLAIR hyperintensities\nare noted, which may represent small vessel ischemic changes.  Bilateral\nmaxillary sinus mucous retention cysts versus polyps are noted.  Sphenoid\nsinus mucosal thickening is present.\n\nBilateral hippocampal formations and mammillary bodies are preserved in signal\nand configuration. There is no disproportionate medial temporal atrophy. There\nis no focal lobar encephalomalacia. There are no focal cortical dysplasias or\ngray matter heterotopia noted.",
            "output": "1. Study is mildly degraded by motion.\n2.  No acute intracranial abnormality.\n3. Within limits of study, no definite intracranial mass or lesion identified.\n4.  Paranasal sinus disease as described."
        },
        {
            "input": "There is no intracranial mass, mass effect, or midline shift.  There is no\nevidence of acute infarction. A frontoparietal developmental venous anomaly is\nnoted on the left, a normal variant. A foci of FLAIR hyperintensity\nsurrounding the frontal horn of the left ventricle is stable from prior.\nVentricles and sulci are age-appropriate. There is no pathologic intracranial\nenhancement. Intracranial flow voids are maintained. Visualized paranasal\nsinuses and mastoid air cells are clear.",
            "output": "Normal MRI of the brain.  No evidence of intracranial metastases or sinus\ndisease."
        },
        {
            "input": "No acute infarct, suspicious focus of intracranial hemorrhage, mass effect,\nshift of normally midline structures or hydrocephalus.\nThere are multiple small T2 FLAIR hyperintense foci in the cerebral white\nmatter in the frontal and parietal lobes and a few in the pons, nonspecific in\nappearance.\nThe ventricles, extra-axial CSF spaces, cerebral sulci and cerebellar folia\nare normal, except for mild asymmetry in the size of the lateral ventricles,\nleft slightly larger than right which can be developmental.\n\nNo focus of abnormal enhancement noted in the brain parenchyma to suggest a\nmetastatic lesion.\nA subtle slightly prominent venous tributary is noted in the left frontal\nlobe, similar to the prior study representing variant appearance.\nLinear enhancement noted noted in left cerebellar hemisphere slightly more\nconspicuous compared to the prior study can relate to a venous tributary- se\n9, im 83.\n\nSella, pineal gland and the craniocervical junction regions are unremarkable.\nThe major intracranial arterial flow voids are noted.\nVenous sinuses are unremarkable\n\nMild ethmoidal mucosal thickening.\nThe mastoid air cells are clear.\nThe bone marrow signal is unremarkable.",
            "output": "No focus of abnormal enhancement in the brain parenchyma to suggest a mass\nlesion.\nLinear enhancement in the left cerebellar hemisphere slightly more conspicuous\ncompared to the prior study can be vascular.\nStable appearance of slightly prominent venous tributary in the left frontal\nlobe.\nFollow-up as needed."
        },
        {
            "input": "There is no intracranial hemorrhage. Diffusion weighting imaging does not\ndemonstrate evidence of acute infarct. The major intracranial vessels exhibit\nthe expected signal void related to vascular flow.  Gray white matter\ndifferentiation is maintained. Ventricles and extra axial CSF spaces are\nwithin normal limits.\n\nThere is no abnormal parenchymal, leptomeningeal, or dural focus of\nenhancement. The sella turcica, craniocervical junction, and orbits are\nunremarkable. The paranasal sinuses and mastoid air cells demonstrate normal\nsignal.",
            "output": "Normal MRI of the brain. No evidence of intracranial metastatic disease."
        },
        {
            "input": "The gray-white matter signal is normal without evidence of infarct,\nhemorrhage, mass, or mass effect.  There is a normal variant developmental\nvenous anomaly at the superior left post central gyrus (901:86).  There is no\nabnormal postcontrast enhancement.  The vasculature is patent.  The ventricles\nand extra-axial spaces are unremarkable.  The orbits, calvarium, and soft\ntissues are unremarkable.  The paranasal sinuses and mastoid air cells are\nclear.",
            "output": "Normal brain MRI.  No evidence of metastatic disease."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.\n\nThere are numerous scattered foci of T2/FLAIR hyperintensity in the\nsubcortical and periventricular white matter, which are nonspecific, and may\nreflect changes due chronic small vessel ischemic disease.\n\nThe orbits are unremarkable.  There is mild mucosal thickening in bilateral\nfrontal and ethmoid sinuses.  The remaining visualized paranasal sinuses and\nmastoid air cells are clear.  Intracranial flow voids are maintained.",
            "output": "1. No acute intracranial abnormality.\n2. Findings of small chronic vessel ischemic disease."
        },
        {
            "input": "There is a punctate superior right frontal acute to subacute infarct (see\n4:23) with associated FLAIR signal abnormality (see 10:18).  No corresponding\nsusceptibility on gradient echo imaging is seen.  No other acute infarcts are\nseen.\n\nThere is no evidence of masses, mass effect, midline shift.  There is\nprominence of the ventricles and sulci suggestive involutional changes.\n\nThere are scattered foci of T2/FLAIR hyperintensity in the subcortical and\nperiventricular white matter, nonspecific, likely secondary to small vessel\nischemic disease.\n\nThere are multiple punctate foci of micro hemorrhages in bilateral cerebral\nand cerebellar hemispheres.\n\nThere is mild mucosal thickening in bilateral anterior ethmoid air cells.  The\nremaining visualized paranasal sinuses and mastoid air cells are clear. \nIntracranial flow voids are maintained.  The orbits are unremarkable.",
            "output": "1. Right frontal punctate acute to subacute infarct as described.\n2. Findings of age-related involutional changes with small vessel ischemic\ndisease.\n3. Nonspecific bilateral hemisphere both deep and superficial distribution\nsupratentorial and infratentorial chronic microhemorrhages, concerning for\namyloid angiopathy, with differential consideration of hypertensive\nmicrohemorrhages."
        },
        {
            "input": "Again seen is artifact from the right frontal VPS catheter, most pronounced on\nMPRAGE and gradient echo images. The catheter terminates in the frontal horn\nof left lateral ventricle, as before. The ventricles are stable in size.\n\nThere is an increased number of subcentimeter enhancing intracranial lesions\ncompared to ___, indicating disease progression. There are multiple new\nlesions in the cerebellum and pons bilaterally, left frontal lobe  ,  right\nposterior inferior temporal lobe (best seen on coronal MPRAGE images), between\nthe left temporal and occipital lobes, and in the left temporal lobe.\nPreexisting cerebellar, left frontal, left posterior temporal lobe are not\nsignificantly changed. None of the lesions demonstrate significant edema or\nmass effect.\n\nLeft craniotomy is again noted. Underlying T2 hyperintensity in the left\nfrontal lobe, without contrast enhancement, is stable and consistent with post\ntreatment changes. Stable T2 hyperintense areas without mass effect, also\nsuggesting post treatment changes, are also again seen in the medial left\nfrontal lobe at the vertex and in the anterior right frontal lobe.\n\nDiffuse dural enhancement along the convexities and tentorium is again seen,\nunchanged from prior exam, consistent with pachymeningeal carcinomatosis.\n\nThere is no abnormal diffusion or evidence for new blood products. Major\nintratracranial flow voids are maintained.",
            "output": "1. Interval progression of metastatic disease with multiple subcentimeterl\nenhancing lesions in the supratentorial and infratentorial compartment.  No\nsignificant edema or mass effect.  Preexisting small enhancing lesions are not\nsignificantly changed.\n\n2. Unchanged diffuse dural contrast enhancement, suggesting pachymeningeal\ncarcinomatosis.\n\n3. Stable posttreatment changes in bilateral frontal lobes."
        },
        {
            "input": "In comparison with the most recent MRI examination, again numerous infra and\nsupratentorial enhancing foci are re- demonstrated which are similar in size\nand configuration, there is an new focus of enhancement in the left temporal\nlobe (image 10, series 11), measuring approximately 2 by 3 mm in transverse\ndimension. There is persistent and unchanged dural enhancement along the\nconvexities and the tentorium. Susceptibility artifact is re- demonstrated in\nthe right frontal region related with VPS catheter, with the tip terminating\nin the left frontal ventricular horn. Left frontal craniotomy is re-\ndemonstrated with underlying posttreatment changes and vasogenic edema in the\nleft and right frontal subcortical white matter.  No diffusion abnormalities\nare detected to suggest acute or subacute ischemic changes Unchanged mucosal\nthickening is noted on the right mastoid air cells. The orbits are\nunremarkable, the major vascular flow voids are present.",
            "output": "1. In comparison with the most recent MRI examination, numerous infra and\nsupratentorial nodular enhancing foci are re- demonstrated, with similar size\nand distribution. There is a small new focus of enhancement in the left\ntemporal lobe as described in detail above.\n\n2. Relatively stable posttreatment changes in bilateral frontal lobes. No\ndiffusion abnormalities are detected to indicate acute or subacute ischemic\nchanges.\n\n3. Unchanged diffuse dural enhancement along the convexities and the tentorium"
        },
        {
            "input": "There is no evidence of acute infarction or intracranial hematoma. There are\nnonspecific periventricular and subcortical white matter FLAIR\nhyperintensities, some of which appear perpendicular to the ependymal surface.\nThere is FLAIR hyperintensity within the bilateral cerebellar hemispheres\n(6:7).  There are multiple foci of susceptibility artifact within the right\ncaudate body and along the right periventricular white matter, possibly\nrelated to micro hemorrhages.\n\nThe ventricles are normal in size without mass effect or midline shift.   The\nprincipal visualized arterial vascular flow voids are preserved.  There is\nmild mucosal thickening of the ethmoid air cells.  There is partial\nopacification of the bilateral mastoid air cells.  The orbits appear\nunremarkable.",
            "output": "1. No evidence of acute infarction intracranial hematoma.\n2. Mild FLAIR signal abnormality within the bilateral posterior fossa, which\nmay be related to PRES given the history of hypertension.\n3. Nonspecific additional bilateral white matter FLAIR signal abnormality,\nsome of which appear perpendicular to the ependymal surface, and may be\nrelated to multiple sclerosis in a patient of this age.  Recommend clinical\ncorrelation.\n4. Probable foci of micro hemorrhages along the right periventricular white\nmatter.  Recommend correlation with outside imaging."
        },
        {
            "input": "There is no abnormal focus of slow diffusion.  In the right posterior temporal\nlobe, corresponding to the hyperdensity seen on CT, there is a curvilinear\nfocus of low signal on T1/T2 weighted images that demonstrates blooming on the\ngradient echo sequence.  The curvilinear signal abnormality appears to extend\nto the junction of the right transverse and sigmoid sinuses, but the exact\nlocation intra versus extra-axial is unclear.  If extra-axial, it may\nrepresent a chronically thrombosed cortical vein although a vein would be\nexpected to be more tubular on CT.  If intraparenchymal, it could represent\nhemorrhage.  However, lack of adjacent edema would be in favor of chronic\nhemorrhage or an occult vascular malformation.\n\n\nThere is no evidence of hemorrhage, edema, mass, mass effect, or infarction. \nThe ventricles and sulci are age-appropriate.  Principal intracranial vascular\nflow voids are preserved. The dural venous sinuses are patent on postcontrast\nMP-RAGE sequences.",
            "output": "1. Hyperdensity along the periphery of the right posterior temporal lobe seen\non recent CT, corresponds to a focus of susceptibility artifact without\nassociated edema or enhancement on MRI.  As discussed above, this may\nrepresent a focus of chronic parenchymal hemorrhage, an occult vascular\nmalformation, or a chronically thrombosed cortical vein.\n2. No evidence of hemorrhage, infarction, or mass.\n3. The dural venous sinuses are patent."
        },
        {
            "input": "There is no acute infarction on diffusion-weighted images.  FLAIR in T2\nweighted images demonstrate no signal abnormality in the internal capsules,\nthalami or elsewhere in the brain parenchyma to suggest a chronic infarction.\nThere is no edema, mass effect, or evidence for blood products. Ventricles and\nsulci are normal in size. Cerebellar tonsils are normally positioned. Major\narterial flow voids appear grossly preserved, allowing for hypoplasia of the\nintracranial right vertebral artery.",
            "output": "No evidence for acute or chronic infarction.  No source of the patient's\nsymptoms is detected on noncontrast MRI."
        },
        {
            "input": "Findings are stable compared with head CT ___.\nThere is abnormality of right cerebellum, with 3.0 cm zone of T2 signal\nabnormality, peripherally mildly restricted diffusion, and surrounding edema\nwhich extends into the right middle cerebellar peduncle.  There is no central\nrestricted diffusion findings are worrisome for underlying mass or\nposttreatment change. Post gadolinium images would be helpful in further\nevaluation.  Findings are not consistent with infarct or abscess.\nMild mass effect on the fourth ventricle which is patent.  Cerebellar tonsils\nextend to the level of foramen magnum, there is mild crowding at foramen\nmagnum, without herniation below.  Superior cerebellar cistern is preserved. \nEffaced pre pontine cistern.\nExtensive subcortical and deep white matter FLAIR hyperintensity involving\nbilateral cerebral hemispheres, with areas of subcortical T2 signal\nabnormality at the right frontal, anterior basal left frontal, both temporal\nlobes.  Findings may represent severe chronic small vessel ischemic changes,\nsequela of prior radiation therapy this has been performed.  Underlying\nsubcortical metastases cannot be excluded, post gadolinium images would be\nhelpful in further evaluation.  Patient age and lack of infarcts  makes\ncadasil  unlikely.\nThere is no evidence of hemorrhage, midline shift or acute infarction.  The\nventricles and sulci are normal in caliber and configuration.  Prominent\nbenign prevascular spaces.  Intracranial vascular flow voids are preserved\nparanasal sinuses, mastoids are clear.  No intracranial hemorrhage.",
            "output": "Stable exam compared to outside CT from ___.\nNo acute infarcts.\nExtensive edema in the right cerebellar hemisphere, suggestion of underlying\nmass,, metastasis, or posttreatment change, with local mass effect, mild\ntonsillar crowding at foramen magnum..  Post gadolinium images would be\nhelpful.\nExtensive confluent deep white matter, subcortical cerebral T2 signal\nabnormalities, may be sequela of chronic small vessel ischemic changes,\nposttreatment change.  Subcortical metastases could be obscured.  Post\ngadolinium images would be helpful.\n\nRECOMMENDATION(S):  Post gadolinium brain MRI, also to include pre gadolinium\naxial T1."
        },
        {
            "input": "The right cerebellum, there is extensive enhancement identified the site of\nFLAIR abnormality extending to the cerebellar folia both superiorly as well as\ninferiorly.  There is mass effect on the right side of the fourth ventricle\nbut there is no hydrocephalus.  No other areas of abnormal enhancement are\nseen.  No leptomeningeal enhancement is seen.",
            "output": "Extensive enhancement is seen at the site of previously seen FLAIR\nabnormality.  The pattern of enhancement as well as previously seen pattern on\nthe pre gadolinium images are suggestive of metastatic disease."
        },
        {
            "input": "MRI BRAIN:\nThere is no acute infarction, edema, mass effect, or evidence for blood\nproducts.  There is 8 mm elongated focus of T2 hyperintensity in the left\ncorona radiata on image 13:15, and scattered smaller, nearly punctate foci of\nT2 hyperintensity in the subcortical, deep, and periventricular white matter\nof the frontal and parietal lobes, which are nonspecific.  Ventricles, sulci,\nand basal cisterns are normal in size.\n\nMajor intravascular flow voids are grossly preserved.  There is complete\nopacification of a right posterior ethmoid air cell, as well as mild mucosal\nthickening in other bilateral ethmoid air cells and bilateral maxillary\nsinuses.\n\nMRA NECK:\nTiming of the scan relative to the contrast bolus is suboptimal.  Evaluation\nof the great vessel origins, common carotid arteries, carotid bulbs, and\nproximal vertebral arteries is limited.  No definite carotid stenosis by\nNASCET criteria and no definite vertebral stenosis is seen.\n\nMRA BRAIN:\nPulsation artifact limits evaluation of the carotid siphons, M1 and M2\nsegments of the middle cerebral arteries, and A1 segments of the anterior\ncerebral arteries.  The intracranial arteries are better assessed on the\npreceding CTA.  There is no evidence for flow-limiting stenosis or aneurysm.",
            "output": "1. No acute infarction.\n2. Scattered foci of high T2 signal in the supratentorial white matter are\nnonspecific in this age group.  Diagnostic considerations include accelerated\nchronic small vessel ischemic disease if the patient has longstanding\nhypertension or diabetes, sequela of prior demyelination, infection, or\ninflammation, sequela of vasculitis, and migraine related lesions.\n3. Technically limited gadolinium-enhanced brain MRA demonstrates no definite\nstenosis.  Please note that axial fat suppressed T1 weighted images for\ndetection of intramural hematoma/dissection were not obtained.\n4. Unremarkable, slightly limited brain MRA.  The intracranial arteries were\nbetter assessed on the preceding CTA."
        },
        {
            "input": "Within confines of noncontrast:\n\nAero digestive tract: There no mass.\n\nIf there is a mass, please insert field choice -->\n\nNeck lymph nodes: There is no adenopathy involving bilateral levels ___. There\nis no retropharyngeal adenopathy.  Right-sided level 2A lymph nodes are\nslightly more prominent by 1-2 mm compared to the left but this may be\nreactive in nature.\n\nExtra nodal tumor spread: Not applicable.\n\nDeep neck muscles, masticator space: Unremarkable.\n\nBones, skull base:\nThere is no suspicious osseous signal.\nJugular foramen, carotid canal, pterygopalatine fossa, infraorbital foramen,\nother skull base foramina are unremarkable.\n\nVessels: The visualized flow voids are unremarkable.\n\nBrachial Plexus: Unremarkable.\n\nThyroid, salivary glands: The thyroid is unremarkable.  There is asymmetric\nenlargement of the right submandibular gland underlying an external marker\nindicating the patient's region of palpable interest measuring 2.6 x 2.4 x 3.6\ncm (AP, TRV, SI), without definitive underlying lesion.  There does appear to\nbe mild increased T2 hyperintense signal relative to the left gland and with\nmild surrounding subcutaneous edema.  There is also a 7 mm T2 and T1\nhypointense focus centered in the right sublingual space (series 5, image 14),\nwhich could potentially represent a sialolith.\n\nThe bilateral parotid and left submandibular glands are unremarkable.\n\nOther findings: Incompletely visualized are biopsy pulmonary nodules measuring\nup to 2.8 cm (dominant lesion on the left), which likely corresponds to known\ncalcified lesions seen on prior chest CT dating back to ___.",
            "output": "1. Underlying an external marker indicating the patient's palpable region of\ninterest is an a enlarged right submandibular gland measuring approximately\n3.6 cm in greatest dimension without definitive underlying lesion.  There does\nappear to be mild increased T2 hyperintense signal of the gland relative to\nthe left submandibular gland with mild surrounding subcutaneous edema.  A 7 mm\nT2 and T1 hypointense focus centered in the right sublingual space could\npotentially represent sialolith.  Thus the findings could represent right\nsubmandibular sialoadenitis.  This could be confirmed with CT neck with\ncontrast.\n2. Minimal prominence of right level 2A lymph nodes, likely reactive in\nnature.\n3. Additional findings as described above.\n\nRECOMMENDATION(S):  Further evaluation with CT neck with contrast is\nrecommended."
        },
        {
            "input": "MRA head: The left carotid terminus is significantly narrowed as is the M1\nsegment of the left middle cerebral artery. There is abrupt cut off of the\ndistal left M1 segment, and no distal branches of the left middle cerebral\nartery are visualized.\n\nIrregularity of both carotid siphons is likely secondary to atherosclerotic\ndisease. The cavernous intracranial right internal carotid artery is narrowed\nthrough the right carotid terminus.  Motion artifact is present, but the right\nmiddle cerebral artery and its branches appear to be significantly narrowed as\nwell.\n\nThe V4 segment of the right vertebral artery is hypoplastic.  Both posterior\ncommunicating arteries visualized. The posterior cerebral arteries are\nirregular.  The A1 segments of the anterior cerebral arteries are not well\nseen, and may be narrowed as well, though these arteries are difficult to\nevaluate secondary to motion artifact.\n\nThere is a new shifting of the midline structures to the right by\napproximately 4 mm.\n\nMRA neck:  The aortic arch demonstrates a normal branching pattern. The\norigins of the great vessels are grossly patent. The bilateral common carotid,\ninternal carotid and external carotid arteries are patent. There is mild\nirregularity of the proximal right internal carotid artery, likely secondary\nto atherosclerotic disease.  The right internal carotid artery is noted to\nhave a retropharyngeal course. As seen previously, the right vertebral artery\nis occluded at its origin with through the mid V2 segment with reconstitution\ndistally.",
            "output": "1. Increased shift of the midline structures to the right by approximately 4\nmm.\n2. Severe narrowing of the left carotid terminus and proximal left middle\ncerebral artery with occlusion of the M1 segment of the left middle cerebral\nartery distally and its branches.\n3. Multifocal intracranial narrowing, as described, likely secondary to\natherosclerotic disease.\n4. Chronic occlusion of the right vertebral artery."
        },
        {
            "input": "There is a confluent region of slow diffusion within the territory of the left\nmiddle cerebral artery with corresponding FLAIR-signal abnormality.  There is\nlocal mass effect with effacement of the involved cerebral sulci, and partial\neffacement of the left lateral ventricle, but no shifting of the midline\nstructures.  No intracranial hemorrhage is identified. Flow voids of the major\nintracranial vessels are preserved.\n\nElsewhere within the brain parenchyma, there are scattered foci of\nperiventricular, subcortical and deep white matter FLAIR hyperintensity which\nare nonspecific, but likely represent the sequelae of chronic small vessel\nischemic disease.\n\nMucosal thickening is seen in the inferior aspect of the right maxillary\nsinus. Endotracheal and enteric tubes are noted. The visualized orbits and\nsoft tissues are unremarkable.",
            "output": "1. Large left middle cerebral artery territorial infarction, with no evidence\nof hemorrhagic transformation.\n2. Principal intracranial vascular flow-voids preserved\n3. Multifocal white matter signal abnormality, non-specific, but likely the\nsequelae of chronic small vessel ischemic disease.\n\nNOTIFICATION:  Findings were discussed with Dr. ___ by Dr. ___ by phone\nat 03:00 hr, approximately 5-minutes after discovery."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, or infarction.\nThe ventricles and sulci are dilated likely related to parenchymal volume\nloss.  There is focal volume loss with gliosis in the anterior right temporal\nlobe with associated enlargement of the temporal horn of the right lateral\nventricle.  There is susceptibility artifact noted in the right parietal lobe\n(series 5, image ___ possibly related to prior trauma or alternatively  to\ncavernous malformation.  There is scattered foci of T2/FLAIR signal\nhyperintensity in the periventricular, subcortical, and deep white matter\nwhich are nonspecific but likely reflective of chronic small vessel ischemic\ndisease.  The bilateral hippocampal structures are symmetric and of normal\nsignal intensity.  There is no abnormal enhancement after contrast\nadministration.  The orbits are unremarkable.  The paranasal sinuses and\nmastoid air cells are clear.",
            "output": "1.  No evidence of acute hemorrhage, acute infarction, or enhancing mass\nlesion.  No evidence of mesial temporal sclerosis.\n\n2.  Focal volume loss and gliosis in the right anterior temporal lobe.\n\n3.  Chronic blood products in the right parietal lobe could be related to\nprior trauma are to cavernous malformation.  The patient has prior MRI studies\ncomparison would be helpful.\n\n3.  Scattered foci of T2/FLAIR signal hyperintensity in the periventricular,\nsubcortical, and deep white matter which are nonspecific but likely on the\nbasis of chronic small vessel ischemic disease."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.\n\nThe visualized vascular flow voids are grossly preserved.  The paranasal\nsinuses and mastoid air cells are clear.  The intraorbital contents are\nunremarkable.  No abnormal marrow signal.",
            "output": "1. Normal study."
        },
        {
            "input": "Aero digestive tract: There is no mass.\n\nThere is no abnormality in the base and floor of the tongue to correspond to\nthe FDG uptake seen on prior PET-CT.\n\nNeck lymph nodes: There is no adenopathy involving bilateral levels ___. \nThere is no retropharyngeal adenopathy.\n\nExtra nodal tumor spread: There are no findings suggestive of extra nodal\nextension.\n\nDeep neck muscles, masticator space: There is no muscle invasion.\n\nBones, skull base:\nThere is no bone involvement.\nThere are no findings suggestive of perineural tumor extension. Jugular\nforamen, carotid canal, pterygopalatine fossa, infraorbital foramen, other\nskull base foramina are not involved.\n\nVessels: There is no vascular invasion.\n\nBrachial Plexus: There is no brachial plexus contact or invasion.\n\nThyroid, salivary glands: There is no mass.\n\nOther findings: There are no lung nodules.",
            "output": "1. No abnormality to correspond to the FDG uptake seen on prior PET-CT.\n2. Normal MRI of the neck without mass or lymphadenopathy.\n\nNOTIFICATION:  Findings discussed ___, MD  ___ ___ by\n___, MD via phone on ___ at 09:24 a.m."
        },
        {
            "input": "The patient is status post thrombectomy of the left middle cerebral artery\nthrombus.  Several punctate areas of restricted diffusion are seen at the left\nfrontal and parietal lobe.  Additional punctate areas of restricted diffusion\nare seen in the right cerebral hemisphere left occipital lobe and left\ncerebellum.  Findings are suggestive of multiple supra and infratentorial\ninfarcts.  There is prominence of ventricles and sulci with extensive small\nvessel disease in the white matter.  There is no evidence of micro\nhemorrhages.",
            "output": "Multiple punctate acute infarcts predominantly in the left middle cerebral\nartery region but also involving the right cerebral hemisphere, left occipital\nlobe and left cerebellar hemisphere."
        },
        {
            "input": "MRI head: The images are degraded by motion artifact. Several punctate foci of\nincreased diffusion signal are present, some of which are equivocal, and some\nof which appear to have corresponding ADC and FLAIR signal abnormalities, and\nlikely represent puncate infarcts.  There is no evidence of hemorrhage.  No\nmass, mass effect or midline shift is present. There are confluent and patchy\nregions of T2 and FLAIR prolongation within the subcortical, periventricular\nand deep white matter which likely or represent the sequela of chronic small\nvessel ischemic disease. The ventricles, cerebral sulci and cisterns are age\nappropriate.\n\nMRA head: Images are degraded by motion artifact. Within these limtations,\nthere is possible narrowing of the left middle cerebral artery.  Fetal origin\nof both posterior cerebral arteries is noted.\n\nMRA neck: The images are degraded by motion artifact. Common origin of the\ninnominate and left common carotid artery is noted. There is no evidence of\nstenosis by NASCET criteria. The origins of the vertebral arteries, common\ncarotid arteries, external carotid arteries and internal carotid arteries\nappear patent.",
            "output": "Several punctate foci of increased diffusion signal are present, some of which\nare equivocal, and some of which appear to have corresponding ADC and FLAIR\nsignal abnormalities, and likely represent puncate infarcts.  No intracranial\nhemorrhage.  No definite embolic source is identified, though MRA images are\nsignificantly degraded by motion.  If no etiology for embolic infarcts is\nknown, repeat imaging to better determine the infarct distribution and\nevaluate for an embolic source is recommended.\n\nAdvanced small vessel ischemic disease. No MR evidence for posterior\nreversible encephalopathy syndrome."
        },
        {
            "input": "There is an 8 mm focus of DWI hyperintensity in the posterior limb of the\nright internal capsule which demonstrates hypointensity on the ADC sequence. \nThe focus is hypointense on T1 and bright on the FLAIR sequence.  There is\nenhancement after contrast administration and no surrounding edema is\nidentified.  Constellation of findings is therefore most consistent with a\nlate subacute infarct.\nThere is no evidence of hemorrhagic transformation.\n\nThere is an old lacunar infarct in the left pons.\nThere are scattered T2/FLAIR hyperintensities in the cerebral hemispheres\nbilaterally, a nonspecific finding and likely related to chronic small vessel\nischemic changes.\n\nThe ventricles and sulci are age appropriate.\nMajor vascular flow voids appear preserved.  Major dural venous sinuses are\npatent.\n\nThere is mild mucosal thickening along the ethmoid air cells and right\nmaxillary sinus.  There is partial opacification of bilateral mastoid air\ncells.  The orbits appear unremarkable.",
            "output": "1. Late subacute infarct in the posterior limb of the right internal capsule\nwithout evidence of hemorrhagic transformation.\n2. Old lacunar infarct in the left pons.\n3. Additional nonspecific scattered white matter changes in the cerebral\nhemispheres bilaterally, likely sequela of chronic small vessel ischemic\nchanges.\n4. Mild paranasal sinus disease, and partial bilateral mastoid air cell\nopacification."
        },
        {
            "input": "Study is moderately degraded by motion.\n\nMRV: Normal flow signal is demonstrated within the superior sagittal sinus,\nstraight sinus, transverse sinuses, and sigmoid sinuses. The jugular bulbs and\nproximal jugular veins are patent. Evaluation of the deep venous systems\nreveals normal flow signal in the internal cerebral veins. The vein ___\nis also unremarkable.\n\nMRI BRAIN:  There is no abnormal enhancement on postcontrast imaging. There is\nno midline shift,  or mass. The ventricles and sulci are normal in caliber and\nconfiguration.  Diffuse subarachnoid space FLAIR hyperintensities noted on\nboth non motion corrected and motion corrected FLAIR imaging (see series 9 and\n13), not definitely seen on prior outside brain MRI (see series 8 on prior\nexam) is noted.  No definite corresponding to GRE abnormality is identified. \nNo definite corresponding subarachnoid hemorrhages noted on head CT study\nperformed 20 hr earlier.  There is no definite evidence of acute infarct.\n\nMinimal bilateral ethmoid air cell mucosal thickening is present.  Small\nbilateral nonspecific mastoid fluid is present.",
            "output": "1. Study is moderately degraded by motion.\n2. No evidence of venous sinus thrombosis.\n3. Within limits of study, no definite leptomeningeal enhancement identified.\n4. New nonspecific diffuse subarachnoid signal abnormality, as described. \nWhile finding is compatible with meningitis, differential considerations\ninclude subarachnoid hemorrhage, leptomeningeal carcinomatosis, sequelae of\nhyperoxygenation therapy or artifact.  If clinically indicated, noncontrast\nhead CT may be obtained to evaluate for presence of new subarachnoid\nhemorrhage since ___ noncontrast head CT prior exam.\n5. Paranasal sinus disease as described."
        },
        {
            "input": "No acute infarcts are identified.  There is no mass effect midline shift or\nhydrocephalus.  No evidence of micro hemorrhages.  There are patchy and\nconfluent areas of FLAIR hyperintensity predominantly in the deep white matter\nof both cerebral hemispheres with minimal involvement in the periventricular\nwhite matter consistent with moderate to severe changes of small vessel\ndisease.  Vascular flow voids are maintained.  Craniocervical region is\nunremarkable.",
            "output": "1. Moderate to severe changes of small vessel disease.\n2. No evidence of acute infarcts mass effect midline shift or hydrocephalus."
        },
        {
            "input": "The exam is slightly degraded by motion artifact.  Within these confines:\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is a nonspecific focus of T2/FLAIR hyperintensity in the\nleft external capsule without associated diffusion restriction, likely\nsequelae chronic ischemic disease.  The visualized vascular flow voids are\ngrossly preserved.  There is mild thickening of the ethmoid air cells and\nbilateral maxillary sinuses.  The mastoid air cells are clear.  The globes and\norbits are unremarkable.  There is no abnormal marrow signal.",
            "output": "1. Unremarkable noncontrast brain MRI.  No evidence of an acute infarct,\nintracranial mass, or hemorrhage."
        },
        {
            "input": "Images are mildly compromised secondary to patient motion.\n\nRedemonstrated is a lesion within and expanding the sella, with blood products\nwithin the lesion which are best seen on gradient images, thin rim of\nperipheral enhancement, and complete absence of enhancement within majority of\nthe lesion.  Lesion measures up to 2.4 cm.  Normal pituitary parenchyma is not\nvisualized.  This is more completely characterized on the dedicated MRI\nprotocol performed ___.  There is mild mass effect on the\nundersurface of the optic chiasm with superior displacement.  Cystic\ncomponents extend medially into the cavernous sinuses; there is normal\nenhancement of the remainder of the cavernous sinuses.\n\nThere is soft tissue thickening and enhancement posterior to the clivus with\nassociated T2 signal abnormality, measuring 0.5 cm in maximum thickness,\nsimilar to prior, and pachymeningeal linear thickening and enhancement at the\nCP angles and foramen magnum, with preservation of the underlying marrow\nsignal.\n\nVisualized parotid glands, stylomastoid foramen are normal, no evidence of\nmass.  Suggestion of mild asymmetric linear enhancement of the mastoid segment\nleft seventh cranial nerve, axial MP rage image 26, 27.  Otherwise, no other\nareas of abnormal seventh cranial nerve enhancement.  No definite abnormal\nenhancement of cranial nerves ___ cisternal segments.\nTemporal lobes, insula are normal bilaterally.\nThere is no evidence of parenchymal hemorrhage, edema,, midline shift or\ninfarction.  Dural venous sinuses are patent.  Intracranial vascular flow\nvoids are maintained.\n.  The ventricles and sulci are normal in caliber and configuration.  Orbits\nand mastoid air cells are normal.  There are no brain parenchymal changes. \nThere is mild mucosal thickening of the sphenoid sinus.",
            "output": "1. 2.4 cm centrally necrotic and hemorrhagic sellar mass, with sellar\nexpansion, most consistent with pituitary macroadenoma, causing mild mass\neffect on the optic chiasm, with partial extension into the medial margin of\nboth cavernous sinuses.  Appearance is consistent with either\nnecrotic/hemorrhagic pituitary macroadenoma or pituitary apoplexy within\npre-existing macroadenoma if this fits clinically given fairly acute clinical\npresentation.\n2. Soft tissue enhancement posterior to the clivus, and pachymeningeal\nenhancement in the posterior fossa extending into the foramen magnum.  While\nthese findings may represent prominent venous plexus secondary to above\nfindings, it is more extensive than would be expected, and differential\nconsiderations include subacute subdural hematoma, meningioma, infection,\nneoplasm such as lymphoma, dural metastases, and inflammatory process\nincluding sarcoid.\n3. There is no brain parenchymal abnormality.\n4. Suggestion of asymmetric linear enhancement of mastoid segment left seventh\ncranial nerve.\n\nNOTIFICATION:  The findings were discussed with ___, M.D. by\n___, M.D. on the telephone on ___ at 11:50 am, 10 minutes after\ndiscovery of the findings."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor new infarction.  An old left occipital lobe infarct is seen.  A\nsubcentimeter old infarct is seen in the right centrum semiovale.  The\nventricles and sulci are normal in caliber and configuration.  Patchy\nperiventricular T2 hyperintensities are most consistent with chronic\nmicrovascular angiopathy.\n\nA large mucous retention cyst is seen in the left maxillary sinus.  The\nmastoid air cells and middle ear cavities are clear.  The intraorbital\ncontents are normal.",
            "output": "1. No evidence of hemorrhage or recent infarction.\n2. Old infarcts involving the left occipital lobe and right centrum semiovale.\n3. Left maxillary sinus disease."
        },
        {
            "input": "There is encephalomalacia and gliosis in the right occipital lobe from a\nchronic infarction, similar to ___ but new compared to ___,\nwith gyriform T1 hyperintensity on T1 weighted images indicating pseudolaminar\nnecrosis.  Gradient echo images demonstrate no evidence for associated\nhemosiderin deposition.\n\nDiffusion-weighted images demonstrate no acute infarction.  In the right\ncentrum semiovale at the level of the paracentral lobule, there is an area of\nfaintly elevated signal on diffusion tracer images (B1000) without definite\nsignal abnormality on the ADC map, 302:22 and 300:22, and with high signal on\nT2 weighted and FLAIR images.  This demonstrates low density on the ___ CT, suggesting that the diffusion signal abnormality is related to T2\nshine through, rather than a subacute infarct.\n\nThere are other confluent areas and small discrete foci of high T2 signal in\nthe subcortical, deep, and periventricular white matter of the cerebral\nhemispheres, progressed since the ___ I, which are nonspecific but likely\nsecondary to chronic small vessel ischemic disease in this age group. \nVentricles, sulci, and basal cisterns are normal in size.  Major arterial flow\nvoids are grossly preserved.\n\nThere is mild mucosal thickening in the ethmoid air cells and the left\nmaxillary sinus.  Again seen is a circumscribed lesion with intermediate T2\nsignal posterior/inferior to the left maxillary sinus, image 5:3, likely\nrepresenting an odontogenic cyst.",
            "output": "1. No acute infarction.\n2. Small area of faintly elevated signal on diffusion tracer images and high\nsignal on T2 weighted/ FLAIR images in the right paracentral centrum\nsemiovale, without signal abnormality on the ADC map, demonstrates low density\non the ___ CT, suggesting T2 shine through rather than a subacute\ninfarct.\n3. Chronic left occipital infarction with pseudolaminar necrosis.\n4. Extensive supratentorial white matter signal abnormalities, progressed\nsince the MRI from ___, are nonspecific but likely sequela of chronic\nsmall vessel ischemic disease in this age group."
        },
        {
            "input": "There is an area of restricted diffusion seen centered within the right\ncentrum semiovale, with associated FLAIR hyperintense signal.  These findings\nare compatible with a late acute to early subacute infarction.\n\nNo additional sites of acute infarction are identified.  There is no\nintracranial hemorrhage.  Chronic infarction with encephalomalacia seen\ninvolving the medial left occipital lobe.\n\nThe ventricles and sulci are mildly prominent compatible with global\nparenchymal volume loss.  Periventricular and subcortical white matter FLAIR\nhyperintensities are noted, a nonspecific finding that most likely represents\nthe sequelae of chronic small vessel ischemic disease.   There is gross\npreservation of the principal intracranial vascular flow voids.\n\nMucosal thickening is seen throughout the ethmoid air cells and within the\nleft maxillary sinus.  An unchanged circumscribed lesion with heterogeneous T2\nsignal is seen posterior and inferior to the left maxillary sinus, likely\nrepresenting an unchanged odontogenic cyst.\n\n  The remainder of the visualized paranasal sinuses, middle ear cavities, and\nmastoid air cells are well aerated and clear.  The orbits are within normal\nlimits bilaterally.",
            "output": "1. Late acute to early subacute infarction within the right centrum semiovale.\n2. No additional sites of infarction.  No acute intracranial hemorrhage.\n3. Mild global parenchymal volume loss and evidence of chronic small vessel\nischemic disease.\n4. Chronic encephalomalacia of the medial left occipital lobe.\n5. Additional findings, as above."
        },
        {
            "input": "Sagittal T1 weighted sequence is mildly limited by motion.  There is no\nevidence of hemorrhage, edema, masses, mass effect, midline shift or\ninfarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.",
            "output": "Normal brain MRI."
        },
        {
            "input": "MRI of the brain:\nThere is a 5.1 x 4.2 x 4.2 cm right frontotemporal intra-axial mass associated\nwith moderate effacement of the anterior and temporal horns of the right\nlateral ventricle and mild ~6 mm leftward shift of midline structures, and\nalso mild narrowing of the right perimesencephalic cistern (series 9, image\n10), the nonenhancing mass is T1 hypointense, T2/FLAIR hyperintense and has a\nsmall central restrictive focus on DWI. Two punctate hypointensities on GRE\nmay represent small hemorrhagic foci versus punctate calcifications (07:12). \nFindings concerning for low-grade glioma.\nThe orbits are unremarkable, the paranasal sinuses are notable for bilateral\nmucosal thickening with mucous retention cysts in both maxillary sinuses, no\nair-fluid levels are seen, there is mild mucosal thickening in the ethmoidal\nair cells, the middle ear cavities and mastoid air cells are clear.\n\nMRA brain:\nThe intra-axial mass lesion described in the MRI of the head is surrounding\nthe right middle cerebral artery, causing mild narrowing of the distal M1 and\nproximal M2 segments of the right MCA. Otherwise, the intracranial vertebral\nand internal carotid arteries and their major branches appear without\nsignificant stenosis, occlusion, or aneurysm formation.",
            "output": "1.  5.1 x 4.2 x 4.2 cm right frontotemporal intra-axial mass associated, with\nno evidence of abnormal enhancement after contrast administration, causing\neffacement of the anterior and temporal ventricular horns as described above,\nas well as approximately 6 mm of leftward shift of the normally midline\nstructures.  Findings are concerning for low-grade astrocytoma, a possible\noligodendroglioma is a consideration.\n\n2.  There is mild narrowing of the distal M1 and proximal M2 segments of the\nright MCA. Otherwise, the intracranial vertebral and internal carotid arteries\nand their major branches appear without significant stenosis, occlusion, or\naneurysm formation."
        },
        {
            "input": "MRI BRAIN:\nThere is evidence of a subacute infarct within the right frontotemporal lobe\nwith associated cortical laminar necrosis, without definite postcontrast\nenhancement.  There is evidence of chronic infarct more posteriorly in the\nright parietal lobe.  Superficial siderosis outlining the right\nfrontoparietotemporal sulci is noted.  There is no evidence of acute\nhemorrhage or masses.   The ventricles and sulci are mildly prominent\nsuggestive of involutional changes.  There is mild mucosal thickening of the\nethmoid air cells.  The remaining paranasal sinuses and mastoid air cells\nappear clear. The orbits are unremarkable.  There is no definite abnormal\nenhancement after contrast administration.  The major intracranial flow voids\nare preserved.  The dural venous sinuses are patent.\n\nMRA brain: There is evidence of coiling of the right MCA at the M2 bifurcation\nwithout evidence of residual flow within the aneurysm.  There is mild\nirregularity and narrowing of the right M2 segment.  Mild narrowing of the\nright A1 segment which is likely secondary to hypoplasia as appears unchanged\ncompared to prior exam.  The left vertebral artery appears hypoplastic distal\nto the left ___, unchanged compared to prior exam.  The remaining\nintracranial vertebral and internal carotid arteries and their major branches\nappear normal without evidence of stenosis, occlusion, or aneurysm formation.",
            "output": "1. Evolving subacute right MCA infarct, with associated cortical laminar\nnecrosis/mineralization.  No definite postcontrast enhancement is identified.\n2. Coil pack within the right M2 without evidence of residual flow.\n3. Mild narrowing of the right M2 segment.\n4. Additional findings as described above."
        },
        {
            "input": "Post embolization changes right MCA aneurysm chronic cortical, subcortical\ninfarct right superior temporal gyrus, anterior temporal tip, frontoparietal\noperculum, and few small chronic infarcts right centrum semiovale, corona\nradiata, stable compared with ___.  Right temporal lobe atrophy,\ndilatation of the right temporal horn, likely secondary to atrophy.  Mild\ndilatation of the lateral ventricles, third ventricle, similar to ___.  Findings consistent with mild-to-moderate chronic small vessel ischemic\nchanges.  Postoperative changes of prior right frontal ventriculostomy tract. \nSuperficial siderrhosis minimal periventricular FLAIR hyperintensity about\nlateral ventricles, improved compared with MRI ___. \nIntracranial vascular flow voids are preserved.  Trace mucosal thickening\nparanasal sinuses.  Clear mastoids.  Superficial siderosis overlying right\nhemisphere, sequela of prior subarachnoid hemorrhage.\nThere is no evidence of acute hemorrhage, mass, mass effect, midline shift or\ninfarction.",
            "output": "1. Postsurgical changes.\n2. Stable chronic right MCA distribution infarcts.\n3. Superficial siderosis, sequela of prior hemorrhage.  No acute hemorrhage.\n4. Mildly dilated ventricular system, stable since ___."
        },
        {
            "input": "Limited evaluation of the brain on sagittal and axial T1 weighted images which\nare markedly motion degraded.  No gross intracranial hemorrhage or T1 signal\nabnormality is seen.  .",
            "output": "1. Markedly limited evaluation of the brain given the motion artifact and\nlimited imaging.  If clinically indicated repeat study can be performed at a\nlater time."
        },
        {
            "input": "Small focus of increased signal within ventral pons on diffusion images series\n4, image 10, is likely artifact given appearance of the pre pontine cistern on\ndiffusion images, there is no low ADC correlate, subacute infarct is less\nlikely in the absence of focal clinical symptoms.  There is no associated\nFLAIR or T2 abnormality.  There are no other areas of diffusion signal\nabnormality.  There is no evidence of hemorrhage, edema, masses, mass effect,\nmidline shift.  There is mild generalized brain parenchymal atrophy.  There\nare moderate chronic small vessel ischemic changes, similar to prior.  There\nare multifocal areas of intracranial arterial narrowing, including right\nsupraclinoid ICA, bilateral MCA, left P2 segment PCA, better seen on CTA from\nyesterday, similar to MRA ___.  Intracranial vascular flow voids\nare preserved.",
            "output": "1. Small focus of diffusion signal in the ventral pons is likely artifact\ngiven adjacent pre pontine abnormality, late subacute infarct is unlikely\nunless clinically suspected\n2. No MRI evidence of PRES.\n3. There are multifocal areas of arterial intracranial narrowing, similar to\n___."
        },
        {
            "input": "MR BRAIN:\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are patent and prominent in keeping\nwith age-related volume loss.\n\nIncidentally seen is cavum septum pellucidum.\n\nThere are scattered foci of T2/FLAIR hyperintensity in the subcortical,\nperiventricular and deep white matter, nonspecific, likely secondary to small\nvessel ischemic changes.\n\nThe orbits are unremarkable.  The visualized paranasal sinuses and mastoid air\ncells are clear.\n\nMRA brain:  As described on the prior CTA, there are multiple areas of contour\nirregularity and luminal narrowing involving bilateral vertebral and internal\ncarotid arteries, likely secondary to atherosclerotic plaque.  The previously\nseen focal outpouching of the V4 segment of left vertebral artery and right A2\nartery is not well appreciated on the MRA.\n\nThe intracranial vertebral and internal carotid arteries and their major\nbranches appear otherwise underwithout evidence of  occlusion, or aneurysm\nformation.\n\nIncidentally seen is dominant left vertebral artery.  The right vertebral\nartery terminates in posterior inferior cerebellar artery.",
            "output": "1. No acute intracranial abnormality.\n2. Intracranial atherosclerosis with focal luminal narrowing and irregularity\ninvolving bilateral vertebral and internal carotid arteries."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, mass, or infarction.  The\nventricles and sulci are age-appropriate.  No mass effect or midline shift. \nMidline structures are within normal limits.  Minimal tonsillar ectopia\nmeasuring approximately 2-3 mm.\n\nThe paranasal sinuses, mastoid air cells, and intraorbital contents are\nunremarkable.  The major intracranial arterial and venous flow voids are\npreserved.",
            "output": "1. Unremarkable MRI of the brain with no acute findings.\n2. Additional findings described above."
        },
        {
            "input": "There is moderate motion artifact on several sequences.  There is no evidence\nof hemorrhage, edema, masses, mass effect, or infarction. The ventricles and\nsulci are normal in caliber and configuration. There is no abnormal\nenhancement after contrast administration.  The cerebellum is normal in size\nand configuration without evidence of atrophy.  The cerebellar tonsils are\nnormal in position.  The cervicomedullary junction is normal.\n\nMajor intravascular flow voids are maintained.  There is normal enhancement of\nthe major intracranial arteries and dural venous sinuses following contrast\nadministration.\n\nThere is scattered mucosal thickening of the ethmoid and left maxillary\nsinuses.  The mastoid air cells appear clear.  The orbits are normal.",
            "output": "Normal brain without infarct, hemorrhage, or mass lesion.  Specifically, there\nare no cerebellar lesions or cerebellar atrophy."
        },
        {
            "input": "There is no intracranial hemorrhage. There is no acute infarct or other acute\nprocess on water diffusion or ADC weighted images. There are multiple foci of\nincreased T2/FLAIR signal scattered in the subcortical, deep, and\nperiventricular white matter. These are nonspecific but are commonly due to\nchronic small vessel ischemic disease. There is no mass effect or midline\nshift. Ventricles and sulci are age-appropriate.  Basal cisterns are patent\nand symmetric.\n\nIntracranial flow voids are maintained.\n\nThere is a retention cyst in the left maxillary sinus. The paranasal sinuses\nand mastoid air cells otherwise appear clear.",
            "output": "1.  No acute infarct, intracranial hemorrhage, or evidence of a mass lesion.\n2.  Multiple foci of increased T2/FLAIR signal scattered in the supratentorial\nwhite matter, nonspecific but consistent with mild chronic small vessel\nischemic disease.  Additional diagnostic considerations in the appropriate\nclinical setting are demyelinating disease or prior infectious/inflammatory\ndisease."
        },
        {
            "input": "There is no intra or extra-axial mass, acute hemorrhage or infarct. Again\nnoted are scattered subcortical and periventricular white matter nonspecific\nFLAIR/ T2 hyperintensities, and is supratentorial distribution, which may be\nseen in setting of small vessel ischemic disease in a patient of this age\nunchanged from prior exam. No abnormal enhancement. The major intracranial\nflow voids are preserved. Mild mucosal thickening of the paranasal sinuses.\nThe orbits are otherwise unremarkable. The mastoid air cells are clear.",
            "output": "1. Nonspecific white matter T2/FLAIR nonenhancing hyperintensities, unchanged\nin configuration and number from prior exam of ___ which may be\nseen in setting of small vessel ischemic disease. Demyelinating process is a\nconsideration, however clinical correlation is recommended.\n2. No evidence of acute infarct."
        },
        {
            "input": "MR BRAIN:\nThere is no evidence of infarction, intracranial hemorrhage, edema, mass, or\nmass effect.\n\nThe ventricles and sulci are normal in caliber and configuration.\n\nThe visualized paranasal sinuses and mastoids appear clear.  Major\nintracranial vascular flow voids are preserved.  The globes and orbits are\nunremarkable.\n\nMRA HEAD:\nThe intracranial internal carotid arteries and principal intracranial branches\nincluding the bilateral anterior and middle cerebral arteries are patent with\npreserved distal runoff.  Widely patent vertebrobasilar system.  Patent\nbilateral posterior cerebral arteries with normal distal runoff.  No aneurysms\nare seen.\n\nMRV HEAD :\nMajor dural venous sinuses are patent.  No evidence of dural venous sinus\nthrombosis.",
            "output": "1. No evidence of dural venous sinus thrombosis.  Unremarkable MRV head.\n2. Unremarkable MRI head.  Patent circle of ___ vasculature.  No aneurysm,\nstenosis, or occlusion.\n3. Normal MRI brain."
        },
        {
            "input": "There is no hemorrhage or infarction.  There is no mass lesion, mass effect,\nmidline shift on this unenhanced study.  There is a small focus of reduced\nsignal (magnetic susceptibility), on gradient echo images within the right\nfrontal lobe (11:19), suggestive of hemosiderin.  There is mild diffuse\nparenchymal volume loss with commensurate prominence of the ventricles, sulci,\nand cisterns.  There is mild mucosal opacification of the bilateral ethmoid\nsinuses, with small mucosal retention cysts are partial opacification of\nbilateral maxillary sinuses.  The visualized portions of the major\nintracranial flow voids are preserved.",
            "output": "1. No hemorrhage, infarction, or midline shift.\n2. Nonspecific small focus of microhemorrhage within the right frontal lobe,\nwhich can be seen with hypertension or amyloid angiopathy.\n3. Paranasal sinus disease as above."
        },
        {
            "input": "Limited examination due to patient motion, within this limitation, grossly\nthere is no evidence of intracranial hemorrhage, edema, masses, mass effect,\nmidline shift or infarction.  The ventricles and sulci are prominent,\nconsistent with global cerebral volume loss.  No diffusion abnormalities are\ndetected.  An unchanged punctate focus of mineralization is seen in the right\nfrontal lobe, representing microhemorrhage versus calcification.  The\nintravascular flow voids are maintained.\n\nThe paranasal sinuses, mastoid air cells and middle ear cavities are clear. \nThe patient is status post bilateral lens replacement.",
            "output": "1. No evidence of acute intracranial process or hemorrhage."
        },
        {
            "input": "This study is degraded by motion.\n\nKnown layering right hemispheric subdural hematoma measures up to 10 mm in\ndiameter (07:14).  There is approximately 6-7 mm leftward shift of midline\nstructures, unchanged from the prior study (07:15).  Numerous additional\nscattered areas of intraparenchymal hemorrhage are noted.  No evidence of\ninfarction.\n\nThere is mass effect on the right lateral ventricle and chronic enlargement of\nthe left lateral ventricle.  Bilateral periventricular and subcortical\nT2/FLAIR white matter hyperintensities are nonspecific, but likely reflect\nchronic small vessel disease.  There has been prior lens replacement on the\nleft.  Orbits are otherwise unremarkable.",
            "output": "1. No evidence of infarction.\n2. No significant interval change in 10 mm right hemispheric subdural\nhematoma, with 6-7 mm leftward shift of midline structures.\n3. Numerous scattered areas of intraparenchymal hemorrhage, which may reflect\ndiffuse axonal injury in the setting of trauma, or amyloid angiopathy.\n\nNOTIFICATION:   The findings were discussed with ___, M.D. by ___\n___, M.D. on the telephone on ___ at 5:30 ___, 20 minutes after\ndiscovery of the findings."
        },
        {
            "input": "The patient is status post prior right parietal craniotomy for evacuation of a\nsubdural hematoma.  There remains a right hemispheric convexity subdural mixed\nage hematoma measuring up to 1.0 cm in greatest thickness, slightly improved\nin size from prior examinations.  There is FLAIR hyperintense signal\ninterdigitating the right frontal parietal convexity sulci, which may\nrepresent subarachnoid hemorrhage product.\n\nRe-identified are diffuse punctate foci of gradient echo susceptibility\ninvolving the peripheral cortex, basal ganglia, brainstem and cerebellar\nhemispheres compatible were chronic micro hemorrhages potentially representing\ncombination of amyloid angiopathy and hypertensive etiology.  No new\nhemorrhages are identified.\n\nWhen compared to prior examination there is decreased leftward midline shift\n(measuring 3 mm compared to previously measured 8 mm) with improved effacement\nof the right lateral ventricle.  There remains left lateral ventricle\nventriculomegaly, similar to prior examination.\n\nThere is no evidence for acute infarct.  Confluent periventricular and\nsubcortical T2/FLAIR nonenhancing white matter hyperintensities are unchanged\nfrom prior exam, nonspecific, but compatible with chronic microangiopathy in a\npatient of this age.  There is partial empty sella.\n\nThe major intracranial flow voids are preserved.  There is mild mucosal\nthickening of the a nasal sinuses diffusely.  There is left lens replacement. \nOtherwise the orbits are are unremarkable.  Fluid signal is noted in the right\nmastoid air cells.\n\nDiffuse cortical thickening and heterogeneity of the marrow may represent\nrenal osteodystrophy, unchanged from prior exam.",
            "output": "1. No evidence of acute infarct or new hemorrhage.\n2. A right hemispheric convexity subdural mixed age hematoma measuring up to\n1.0 cm greatest thickness is slightly improved in size from prior examination.\n3. There is improved leftward midline shift now measuring approximately 3 mm\ncompared to previously measured 8mm, with decreased effacement of the right\nlateral ventricle.  There remains left lateral ventricle ventriculomegaly comm\nsimilar to prior exam.\n4. Additional findings described above."
        },
        {
            "input": "MR BRAIN:\nMultiple sequences are limited by motion artifact.\n\nAn approximately 5 mm ovoid focus of slow diffusion is seen within the left\noccipital deep white matter (402:12).  It is not clear whether there is\nassociated signal abnormality on T2 weighted/FLAIR images.\n\nExtensive confluent periventricular, deep, and subcortical FLAIR white matter\nT2 hyperintensities are grossly unchanged, nonspecific but likely sequela of\nchronic small vessel ischemic disease in this age group.  Prominent ventricles\nand sylvian fissures are unchanged compared to ___, compatible with\nsequela of age-related parenchymal volume loss.  Prior MRI demonstrated\nnumerous chronic microhemorrhages, with distribution compatible with a\ncombination of amyloid angiopathy and hypertensive etiology, but these are not\nwell seen on this exam in the absence of gradient echo images.  The principal\nvascular flow voids appear to be well preserved.\n\nThe patient is status post prior right parietal craniotomy. Diffuse calvarial\nthickening and heterogeneity of the bone marrow, which may represent renal\nosteodystrophy, are again noted.\n\nMild mucosal sinus thickening is seen involving the ethmoid air cells.  The\npatient is status post left lens replacement surgery.\n\nMRA BRAIN:\n\nImages are limited by motion artifact.  The right vertebral artery is\ndominant.  The intracranial internal carotid and vertebral arteries, and the\nproximal courses of their branches, are patent without evidence for high-grade\nstenosis.  P2 segments of the posterior cerebral arteries appear to\ndemonstrate diminished flow bilaterally, but this is probably artifactual.  No\nlarge aneurysm is seen.  Evaluation for small aneurysm is limited.",
            "output": "1. Motion limited brain MRI demonstrates a 5 mm focus of slow diffusion within\nthe left occipital white matter, compatible with an acute to early subacute\ninfarct.\n2. Motion limited MRA of the circle of ___ demonstrates no evidence for\nmajor arterial occlusion or high-grade stenosis. P2 segments of the posterior\ncerebral arteries appear to demonstrate diminished flow bilaterally, but this\nis probably artifactual.\n\nNOTIFICATION:  The presence of the acute to early subacute infarct was\ndiscussed with Dr. ___ by Dr.  ___ on the telephone on ___ at\n8:30 am, 5 minutes after discovery of the findings."
        },
        {
            "input": "Evaluation is limited by patient motion.\n\nMR BRAIN:\nThere is a 2.5 x 3.4 cm focus of hemorrhage, centered around the right\nthalamus.  Bowing of the septum to the left by 8 mm is persistent.  Dilation\nof the occipital horn of the bilateral lateral ventricles are stable. \nLayering blood products in the ventricles are stable and likely redistributed\nhemorrhage from the right thalamic hemorrhage.  There is no new focus of\nintracranial hemorrhage.\nPachymeningeal dural thickening along the right convexity is likely related to\nprior right craniotomy.\nDiffuse blooming artifacts in the cerebellum, mid brain, throughout the\ncortex, especially in the bilateral thalami and subinsular regions are related\nto prior hemorrhage.  There is hemosiderin deposition around the bilateral\nparietal sulci, similar in distribution compared to ___.\nThe paranasal sinuses and the middle ear cavities are clear.  There is partial\nopacification of the right mastoid air cells.\nThere is diffuse heterogeneous signal in the calvarium, which is also\nthickened.\n\nMRA brain:\nThe study is limited by patient motion.  There is diminutive caliber of the\nleft M3 branch of the MCA with reconstitution of the left M4 branches. \nOtherwise, within limits of the study, the intracranial vertebral and internal\ncarotid arteries and their major branchesappear patent.  There is no evidence\nof aneurysm formation.  The dural sinuses are patent.",
            "output": "1. Right thalamic hemorrhage with bone of the septum to the left.  There is\ntrace postcontrast enhancement, likely venous.  No definite underlying mass\nlesion identified.  However, follow-up examination after resolution of\nhemorrhage can be performed to document resolution of enhancement.\n2. Dilation of the occipital horns with layering blood products, similar in\nsize and distribution.\n3. Diminutive caliber of left M3 branch of the MCA with reconstitution of the\nM4 branches.  This is felt to be most likely artifactual in nature as this\nfinding was not visualized on prior examination of ___.  Otherwise,\nunremarkable MRA head.\n4. Sequela prior micro hemorrhages in the basal ganglia and bilateral\ncerebellar hemispheres, potentially secondary to hypertension.\n5. Diffuse heterogeneous signal of the calvarium which is thickened,\npotentially representing renal osteodystrophy or possibly fibrous dysplasia."
        },
        {
            "input": "Multiple sequences are limited by motion artifact.\n\nRight thalamic hematoma has not significantly changed in size since the most\nrecent head CT from ___ allowing for differences in modalities.  It\ndemonstrates a thick rim of hyperintensity on T1 weighted images without clear\nevidence for masslike contrast enhancement.  No enhancing mass is seen\nelsewhere in the intracranial compartment.  There is unchanged leftward shift\nand compression of the third ventricle.  Dilatation of the lateral ventricles\ndoes not appear significantly changed from the ___ head CT allowing\nfor differences in patient head position.  Blood products are again seen along\nthe prior left frontal ventriculostomy track.\n\nGradient echo images again demonstrate numerous chronic micro hemorrhages in\nthe cerebellum, brainstem, basal ganglia, and gray/white matter junction.\n\nThere is no acute infarction.\n\nThe calvarium is diffusely thickened and heterogenous, as before, likely\nsecondary to renal osteodystrophy given the patient's history.",
            "output": "1. No significant change in right thalamic hematoma compared to the ___ head CT allowing for differences in modalities.  Allowing for thick rim\nof T1 hyperintense blood products, there is no evidence for an underlying\nmass.\n2. Stable compression of the third ventricle and stable dilatation of the\nlateral ventricles.\n3. Blood products are again seen along the prior left frontal ventriculostomy\ntract.\n4. Numerous chronic microhemorrhages are again demonstrated in the cerebellum,\nbrainstem, basal ganglia, and gray/white matter junction, compatible with a\ncombination of hypertensive etiology and amyloid angiopathy.\nCOMMENT:\nSince no evidence for right thalamic mass was seen on the ___ MRI,\nand given the presence of numerous above-described chronic micro hemorrhages,\nthe present right thalamic hemorrhage is likely related to hypertension rather\nthan an underlying mass."
        },
        {
            "input": "There is minimally gyriform and cortically based increased diffusion-weighted\nhyperintense signal with ADC hypointensity throughout the parietal and\noccipital cortices.  Diffusion-weighted hyperintense signal of the bilateral\nbasal ganglia is also noted, with subtle minimally decreased ADC\nhypointensity.  There is associated with T1 hyperintensity along the cortex. \nExtensive T2/FLAIR hyperintensity throughout the bilateral frontal parietal\ncortices with increased subcortical white matter involvement has increased in\ncomparison with ___, with associated T2 shine through on\ndiffusion-weighted sequence.\n\nAs demonstrated on ___, as there is extensive susceptibility artifact\nin both hemispheres, the brainstem, and cerebellar hemispheres that are\nessentially unchanged.  At that time, there was an acute right thalamic\nhemorrhage, which has evolved and is now manifested as susceptibility artifact\non the GRE sequence (11:15).  Blood products are also seen along the course of\na prior left frontal approach ventriculostomy catheter.  No acute hemorrhage\nis demonstrated.\n\nThere is stable prominence of the ventricles and sulci, likely related to\ninvolutional changes.\n\nThe calvarium is diffusely thickened with heterogeneous signal, likely related\nto renal osteodystrophy, and is unchanged.  There is fluid within the\nbilateral mastoid air cells.  There is moderate mucosal thickening of the\nanterior ethmoid air cells.  T2 hyperintense material in the left globe is\nunchanged.  A left lens replacement is noted.  The right orbit is\nunremarkable.",
            "output": "1. Subtle diffusion-weighted hyperintense signal of the parietal and occipital\ncortices and basal ganglia with slightly hypointense ADC signal, with\nassociated T1 hyperintensity is suggestive of evolving subacute hypoxic brain\ninjury with cortical laminar necrosis.\n2. Interval increase in white matter signal abnormality primarily in the\nfrontal lobes with normalization of ADC values may be related to a more\nchronic hypoxic insult.\n3. Chronic blood products throughout the basal ganglia and thalami, brainstem\nand cerebellar hemispheres are likely related to prior hypertensive\nhemorrhage.  More peripheral blood products could also be related to\nhypertension, or amyloid angiopathy.  No acute hemorrhage is demonstrated.\n\nNOTIFICATION:  The findings were discussed with ___, M.D. by ___\n___, M.D. on the telephone on ___ at 4:10 pm, 5 minutes after\ndiscovery of the findings."
        },
        {
            "input": "Postcontrast MP-RAGE sequences are motion degraded.  Within these confines:\n\nRe-identified are periventricular and subcortical confluent white matter\nT2/FLAIR nonenhancing hyperintensities in a pattern compatible with\ndemyelinating plaques given the history of multiple sclerosis.  No new lesions\nare identified.\n\nThere is no evidence of acute infarct, hemorrhage or intra or extra-axial mass\neffect.  Sulci, ventricles and cisterns are unchanged and slightly prominent\nfor the patient's age.  The major intracranial flow voids are preserved.  The\ndural venous sinuses are patent.  The frontal sinuses are poorly pneumatized,\notherwise the paranasal sinuses are essentially clear.  The mastoid air cells\nare clear.",
            "output": "1. T2/FLAIR white matter hyperintensities are unchanged in number and\nconfiguration from prior exam, in a distribution compatible with demyelinating\nplaques given the history of multiple sclerosis.\n2. No new lesions.  No abnormal enhancement."
        },
        {
            "input": "Innumerable periventricular and subcortical confluent white matter T2/FLAIR\nnonenhancing hyperintensities are seen in a pattern compatible with\ndemyelinating plaques, extending radially from the corpus callosum.  No\ndefinite new lesions are identified.  There is no evidence of abnormal\ncontrast enhancement.  There is no evidence of acute intracranial hemorrhage,\nmass, mass effect or large territorial infarction.  Prominence of the\nventricles and sulci is likely related to age related involutional changes.\n\nThe principal vascular flow voids are well preserved.  The visualized\nparanasal sinuses, mastoid air cells, and middle ear cavities are clear.",
            "output": "1. Grossly stable white matter lesions compared to ___ prior\nexamination, compatible with patient's diagnosis of multiple sclerosis.\n2. No definite new lesions or abnormal enhancement identified.\n3.  No acute intracranial abnormality."
        },
        {
            "input": "No gross change in the innumerable periventricular and subcortical confluent\nwhite matter T2/FLAIR nonenhancing hyperintensities.  These lesions extend\nradially from the corpus callosum in a pattern compatible with demyelinating\nplaques.  No definite new lesions are identified.  There is no evidence of\nabnormal contrast enhancement.  No evidence of acute intracranial hemorrhage,\nacute infarction, mass or mass effect.  Redemonstrated is prominence of the\nventricles and sulci likely related to age-related changes.\n\nMajor vascular flow voids are preserved.  The visualized orbits, paranasal\nsinuses and mastoid air cells are unremarkable.",
            "output": "1. No gross change in innumerable periventricular and subcortical white matter\nlesions compared to ___. findings are compatible with patient's\nhistory multiple sclerosis.\n2. No definite new or enhancing lesions.\n3. No acute intracranial abnormality."
        },
        {
            "input": "MR brain: Innumerable subcortical, deep white matter and periventricular FLAIR\nhyperintense lesions are grossly similar to ___.  No restricted\ndiffusion or abnormal enhancement to suggest active demyelination.\n\nProminence of the ventricles and sulci likely represent atrophic changes,\nsimilar to prior.\n\nThe paranasal sinuses and mastoid air cells are clear.  The orbits are\nunremarkable.\n\nMR brain ___: Multiple patchy T2 hyperintense lesions scattered throughout\nthe cervical spine are suspicious for demyelination.  No abnormal enhancement\nfollowing the administration of contrast.  Degenerative changes throughout the\ncervical spine are minimal.",
            "output": "1. Subcortical, deep white matter and periventricular FLAIR hyperintense\nlesions are grossly similar to ___. No restricted diffusion or\nabnormal enhancement to suggest active demyelination.\n2. Evaluation is limited by motion.  Numerous patchy T2 hyperintense lesions\nthroughout the cervical cord are suspicious for myelomatous involvement.  No\nabnormal enhancement following the administration of contrast."
        },
        {
            "input": "There is similar size and extent of numerous juxtacortical, periventricular\nand deep white matter FLAIR hyperintense lesions compared to the prior study\nfrom ___.  There are similar scattered FLAIR hyperintense lesions in the\nbilateral middle cerebellar peduncles and right cerebellar hemisphere.  There\nis no associated restricted diffusion or abnormal enhancement.  There is no\nassociated low signal on the GRE images.  There is similar prominence of the\nventricles and sulci suggestive of atrophic changes, not significantly changed\nsince the prior exam.  There is no evidence of hemorrhage, mass effect,\nmidline shift or infarction.  There is no abnormal enhancement after contrast\nadministration.\n\nThere is mild mucosal thickening in the ethmoid air cells.  The mastoid air\ncells are clear.  The visualized orbits are unremarkable.  The major\nintracranial vascular flow voids are preserved.",
            "output": "1. Similar extent of FLAIR hyperintense lesions in the supratentorial and\ninfratentorial white matter compared to ___.  No associated\nrestricted diffusion or abnormal enhancement to suggest active demyelination.\n2. No evidence of infarction or hemorrhage."
        },
        {
            "input": "The anterior inferior cerebellar arteries are not visualized bilaterally, and\nmay be hypoplastic. The intracranial vertebral and internal carotid arteries\nand their major branches  otherwise appear normal without evidence of\nstenosis, occlusion, or aneurysm formation.",
            "output": "Nonvisualization of the bilateral anterior inferior cerebellar arteries, may\nbe small in size and not visualized on the MRA.  Otherwise normal MRA of the\nbrain.  No abnormal vascular structures are seen within the internal auditory\ncanals."
        },
        {
            "input": "Aero digestive tract: There is no mass.\n\nNeck lymph nodes: Prominent but subcentimeter bilateral level 2 lymph nodes\nare seen.  There is no retropharyngeal adenopathy.\n\nExtra nodal tumor spread: There are no findings suggestive of extra nodal\nextension.\n\nDeep neck muscles, masticator space: There is no muscle invasion.\n\nBones, skull base:\nThere is no bone involvement.\nThere are no findings suggestive of perineural tumor extension. Jugular\nforamen, carotid canal, pterygopalatine fossa, infraorbital foramen, other\nskull base foramina are not involved.\n\nVessels: There is no vascular invasion.\n\nBrachial Plexus: There is no brachial plexus contact or invasion.\n\nThyroid, salivary glands: There is no mass.\n\nOther findings: There are no lung nodules.  There is unchanged moderate to\nsevere opacification of the maxillary and ethmoid sinuses with T1 moderately\nintense foci, representing inspissated material versus fungal colonization.",
            "output": "1. No lesion or abnormal enhancement.\n2. Prominent but subcentimeter bilateral level 2 lymph nodes, not concerning\nfor malignancy.\n3. Maxillary and ethmoid sinuses with inspissated material versus fungal\ncolonization."
        },
        {
            "input": "There are multiple subcentimeter foci of T2/FLAIR hypertensities in the\nsubcortical and periventricular white matter.  The largest focus is noted in\nthe left periventricular white matter measuring up to 0.7 cm.  No abnormal\nenhancement or slowed diffusion is noted of these lesions.\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.  The principal flow voids are preserved.  The orbits are\nunremarkable.  There is mucosal thickening of bilateral maxillary and ethmoid\nsinuses.  There is opacification of the left frontal sinus as well as a tiny\nair-fluid level within the right sphenoid sinus.",
            "output": "1. Multiple T2/FLAIR hyperintensities in the subcortical and periventricular\nwhite matter which can be seen in the setting of demyelinating disease or\nsmall vessel disease.  Clinical correlation recommended.\n2. No abnormal enhancement or slow diffusion is seen.\n3. Acute on chronic sinus disease."
        },
        {
            "input": "Again seen are multiple bilateral FLAIR hyperintense white matter foci\ncentered within the pericallosal, deep and periventricular white matter, some\nwhich are linearly-oriented perpendicular to the long axis of the lateral\nventricles.  These lesions are not appreciably changed in appearance.  There\nare no new lesions. There are no enhancing lesions.  No lesions demonstrate\nreduced diffusion.  No infratentorial or brainstem lesions identified.\n\nElsewhere, there is no abnormal enhancement, mass effect, edema, infarction or\nhemorrhage.  The ventricles and sulci are normal in caliber and configuration.\n\nThere is complete opacification of left frontal sinus.  There is mild right\nfrontal, bilateral maxillary sinus, ethmoid air cell mucosal thickening. \nTrace sphenoid sinus mucosal thickening.  No air-fluid levels.  This is\nunchanged.\n\n The globes and orbits are unremarkable.  Major intracranial vascular flow\nvoids are preserved. Major dural venous sinuses are patent.",
            "output": "1. Stable exam.  Bilateral supratentorial pericallosal and deep white matter\nFLAIR hyperintense foci without enhancement or restricted diffusion,\nunchanged.  Appearance is nonspecific, and although there is no cerebellar nor\nbrainstem involvement, morphology of a few of the lesions raises suspicion for\ndemyelination; differential again includes early changes of chronic white\nmatter microangiopathy.  No enhancing lesions.\n2. No new acute intracranial abnormality.\n3. Pansinus mucosal thickening, unchanged."
        },
        {
            "input": "Please note the study is moderately degraded by motion.\n\nThere is a 0.7 cm TR x 0.4 cm AP T2 hypo intense, contrast enhancing lesion in\nthe left internal auditory canal, with the distal portion approximately 3 mm\nfrom the cochlea, with no extension beyond the porous acoustics into the\ncerebellopontine angle.  In addition, there is a dural based, extra-axial, 1\ncm x 0.4 cm T2 hypo intense, contrast enhancing lesion in the right\ncerebellopontine angle, anterior to the right porous acusticus with no\ndefinite mass effect on the seventh or eighth cranial nerves is seen on series\n7, image 7 and series 5 image 52.\n\nLimited included imaging of the remainder of the brain demonstrates no\nevidence of hemorrhage, edema, mass effect, midline shift or infarction. \nThere are two 1.2 cm left parafalcine dural based, extra-axial masses, series\n3, image 22 and series 9, image 19.  In addition, there is a 1 cm AP x 1 cm TR\nx 0.6 cm SI dural-based, extra-axial mass, superior to the left anterior\nclinoid process.  A third, partially visualized 1.3 cm AP x 0.9 cm TR,\ncontrast enhancing olfactory groove extra-axial appearing lesion is seen. \nThere is prominence of the ventricles and sulci suggestive involutional\nchanges.   Periventricular and subcortical T2 and FLAIR hyperintensities are\nnoted.\n\nNo osseous abnormalities are seen. The  mastoid air cells, and middle ear\ncavitiesare clear. The orbits are unremarkable. The visualized portion of the\nprinciple vascular flow voids are preserved.  There is opacification of the\nright sphenoid sinus.",
            "output": "1. A 0.7 cm left internal auditory canal vestibular schwannoma.  In addition,\nat least 5 small dural based extra-axial lesions, as described above, some of\nwhich are partially visualized, most consistent with meningiomas.  No\nsignificant mass effect or midline shift.  Given the vestibular schwannoma and\nmultiple probable meningiomas, this may represent neurofibromatosis type 2. \nCorrelate with clinical history.\n2. Senescent volume loss and white matter signal abnormality, likely secondary\nto chronic microvascular ischemic changes.\n3. Opacified sphenoid sinus with inspissated secretions."
        },
        {
            "input": "Evaluation is limited due to motion.\n\nThere has been interval surgical resection of the right posterior fossa\nextra-axial solid and cystic mass demonstrated on MRI from ___.\nThere is ill-defined enhancement in the right cerebellum that may be\npostoperative in nature, however, minimal residual enhancing tumor cannot be\nexcluded (series 10, image 6). Mass effect and edema within the posterior\nfossa are unchanged. There is no acute infarct. There is enhancement within\nthe right internal auditory canal that was not present on preoperative MRI,\nlikely reflecting postsurgical change (series 10, image 7). There are foci of\ngradient susceptibility in the right posterior fossa and right frontoparietal\nextra-axial space consistent with postoperative change. Ventricles and sulci\nare normal in size for age. There is no midline shift.\n\nMajor intravascular flow voids are preserved. The paranasal sinuses are clear.\nThere is scattered fluid in the mastoid air cells.",
            "output": "Postoperative changes of interval right posterior fossa extra-axial mass\nresection. Minimal residual enhancement within the right cerebellum is likely\npostoperative but minimal residual enhancing tumor cannot be excluded. Edema\nand mass effect are not significantly changed from preoperative MRI."
        },
        {
            "input": "There is a large intra-axial cystic mass with areas of heterogenous\nenhancement centered within the right cerebellum which produces associated\nmass effect on the basilar cistern and brainstem.  Additionally, there are\nvascular flow voids within the mass. Given the patient's age and overall\nimaging characteristics, would favor the appearance of hemangioblastoma versus\nvascular metastasis. There is adjacent edema within the cerebellum and\nbrainstem\n\nThere is no evidence of acute intracranial hemorrhage. There is no evidence of\nacute ischemia based on diffusion-weighted imaging. There are no other\nabnormal areas of brain parenchymal or leptomeningeal enhancement.\n\nThe orbits, skull base, and paranasal sinuses are otherwise unremarkable.",
            "output": "1. Large intra-axial cystic mass with heterogenous, nodular enhancement and\nvascular flow voids centered within the right cerebellum favoring the\nappearance of hemangioblastoma versus vascular metastasis.\n2. There is associated mass effect on the basilar cistern and brainstem. \nThere is deformity of the fourth ventricle. Mild ventricular dilatation is\nseen."
        },
        {
            "input": "Again demonstrated is a right cystic mass in the right cerebellum with an\nenhancing nodule. Enlarged vascular structures are also seen inferior to the\nmass. These findings are essentially unchanged from the prior study. There is\nmass effect cistern as before. There is no hydrocephalus.",
            "output": "Pre-surgical MRI demonstrates no evidence of interval change since the\nprevious MRI.  Examination was performed with surface markers for surgical\nplanning."
        },
        {
            "input": "There is no evidence of territorial infarction, hemorrhage, or edema.  The\nventricles are normal in size without midline shift.  The major visualized\narterial vascular flow voids are preserved.\n\nPlease note, there is moderate motion degradation artifact limiting evaluation\nof the postcontrast MPRAGE images.  There is no definite enhancing mass or\nabnormal enhancement within the confines of the study.  The major visualized\ndural venous sinuses appear patent on post-contrast images.\n\nThe paranasal sinuses and bilateral mastoid air cells appear clear.  The\norbits appear unremarkable.",
            "output": "1. No evidence of infarction, hemorrhage, or edema.\n2. Within the confines of moderate motion degraded postcontrast MPRAGE images,\nno definite enhancing mass or abnormal enhancement."
        },
        {
            "input": "There is no evidence of acute intracranial hemorrhage, edema, masses, mass\neffect, midline shift or infarction.   The ventricles and sulci are prominent,\nsuggestive of involutional changes.  Faint periventricular T2/FLAIR\nhyperintensities are nonspecific, likely sequela of chronic small vessel\nischemic disease.  There is no abnormal enhancement after contrast\nadministration.  Major intracranial flow voids are preserved.  Dural venous\nsinuses are patent on post contrast MP-RAGE images.\n\nIncidental note is made of a T1 and T2 hyperintense, circumscribed 2.1 x 0.7\ncm subcutaneous collection adjacent to the left parietal calvarium (9:13,\n4:13, 10:13) and measuring 1.2 by 0.6 cm in the left suboccipital region\n(series 4, image 4).  There is no internal enhancement.\n\nThere is moderate mucosal thickening and aerosolized secretions in the\nbilateral maxillary sinuses, with an air-fluid level in the left maxillary\nsinus, suggesting a component of acute sinusitis.  Mild mucosal thickening is\nidentified in the ethmoidal air cells.  The remaining paranasal sinuses are\nclear.  Trace fluid signal is identified in the bilateral mastoid air cells. \nThe imaged orbits are unremarkable.",
            "output": "1.  No evidence of intracranial metastasis at this time.\n\n2.  Findings suggestive of acute maxillary sinusitis.  Clinical correlation is\nrecommended\n\n3.  2 left parietal and left suboccipital subgaleal lipomas.\n\n4.  Additional findings described above."
        },
        {
            "input": "There is no mass effect, hydrocephalus or midline shift. Bilateral deep brain\nstimulators are identified. The tips extending towards the anterior basal\nganglia region. No evidence of significant surrounding edema seen.",
            "output": "Examination performed for DBS evaluation demonstrates bilateral stimulator\nextending toward the inferior thalamic regions."
        },
        {
            "input": "Interval removal of left-sided deep brain stimulator lead with tract defect\nidentified.  The right deep brain stimulator lead is in place with right tip\nin the right cerebral peduncle (04:52).  There is no evidence of hemorrhage,\nedema, masses, or infarction.  Mild prominence of the ventricles and sulci are\nconsistent with age-related cortical volume loss and unchanged in appearance\nsince previous examination dated ___.",
            "output": "1.  Right deep brain stimulator lead in right cerebral peduncle/inferior\nthalamic region.\n2.  Status post removal of left-sided deep brain stimulator."
        },
        {
            "input": "MRI HEAD: No evidence of intra or extra-axial mass, hemorrhage or acute\ninfarct. There are scattered punctate nonenhancing T2/FLAIR subcortical and\nperiventricular white matter hyperintensities, which are nonspecific. There is\nprominence of the ventricles, greater than would be expected for the degree of\nsulcation and brain volume. In addition, there is asymmetry of the lateral\nventricles (the right being larger than the left). These findings appear\nchronic and likely congenital as there is no evidence for transependymal flow\nto suggest acute hydrocephalus and the cisterns and cerebral aqueduct are\nwidely patent.  The major intracranial flow voids are preserved. No regions of\nabnormal enhancement. Mild mucosal thickening of the maxillary sinuses,\nfrontal sinuses and ethmoid air cells. Sphenoid sinuses are clear. The orbits\nare unremarkable. The mastoid air cells demonstrating very mild fluid signal\ninferiorly.",
            "output": "1. Nonspecific subcortical T2/FLAIR nonenhancing white matter changes, not in\nthe usual distribution of demyelinating disease, although this is not\nexcluded. Such findings may also be seen in a broad range of setting such as\nsmall vessel ischemic disease or chronic migraine.\n2. No evidence of intracranial hemorrhage."
        },
        {
            "input": "There is slow diffusion in the right frontal lobe in a watershed distribution\nwith associated FLAIR hyperintensity.  Additional numerous punctate areas of\nslow diffusion are noted throughout the year right frontal and right parietal\nlobe as well as another punctate focus in the right caudate head with\nassociated FLAIR hyperintensity.\n\nThere is no evidence of hemorrhage, masses, mass effect, or midline shift. \nThere is prominence of the ventricles and sulci suggestive involutional\nchanges.  Confluent areas of periventricular, subcortical, deep and pontine\nwhite matter T2/FLAIR hyperintensity are in a configuration suggestive of\nchronic small vessel ischemic disease.  The principal intracranial vascular\nflow voids are preserved.\n\nThe visualized paranasal sinuses are grossly clear.  The orbits are grossly\nunremarkable.  .",
            "output": "1. Acute to subacute right frontal infarct in a right MCA/ACA watershed\ndistribution.\n2. Numerous scattered punctate areas of slow diffusion in the right frontal\nand right parietal lobes as well as the right caudate head compatible with\nacute to subacute infarct, in a thromboembolic distribution.\n3. No hemorrhage or suggestion of mass.\n4. Mild global atrophy and areas of white matter signal abnormality in a\ndistribution suggestive of chronic small vessel ischemic disease.\nNote that reported prior imaging from ___ dated ___ is not available for review.\n\nNOTIFICATION:  Neurology was aware of findings at time of dictation.  A wet\nread was provided by Dr. ___ on ___ at 06:59 stating \"Areas of\nslow diffusion is identified at the right frontal lobe and caudate head, in\nwatershed distribution. The affected area demonstrates FLAIR hyperintensity.\nFindings are suggestive of late acute/subacute infarct.\nperiventricular white matter FLAIR hyperintensities are nonspecific.\""
        },
        {
            "input": "Focal area of slow diffusion is identified in the splenium of the corpus\ncallosum (image 19, series 702), which is also visible on T2 and FLAIR\nsequences, likely consistent with a subacute ischemic area.  There is no\nevidence of hemorrhagic transformation.  The ventricles and sulci are\nprominent, suggesting cortical volume loss, this finding is more significant\nin the temporal lobes and parietal convexity.  Subcortical and periventricular\nareas of high-signal intensity detected on FLAIR and T2 weighted images are\nnonspecific and may reflect changes due to small vessel disease.  The major\nvascular flow voids are present and demonstrate normal distribution",
            "output": "1.  Focal area of slow diffusion identified in the splenium of the corpus\ncallosum, visible on T2 FLAIR and diffusion weighted maps, these likely\nconsistent with subacute ischemic event.\n\n2 Multiple subcortical and periventricular areas of high-signal intensity on\nFLAIR and T2 weighted sequence, are nonspecific and may reflect changes due to\nsmall vessel disease.\n\n3.  Prominent ventricles and sulci, more significant in the temporal parietal\nlobes suggesting cortical volume loss.\n\nNOTIFICATION:  The findings were discussed by Dr. ___ with NP ___ on\nthe telephone on ___ at 12:04 ___, 5 minutes after discovery of the\nfindings."
        },
        {
            "input": "There is slow diffusion and sulcal effacement in the left middle cerebral\nartery territory, involving the frontal, parietal, and temporal lobes, the\ninsula, and the basal ganglia.  There is associated sulcal effacement, as well\npartial effacement of the frontal horn and anterior body of the left lateral\nventricle.  There is no significant shift of midline structures, uncal\nherniation, or mass effect on the basal cisterns.  The extent of infarction is\nsimilar to the diffusion-weighted images from 1 day earlier, but the above\ndescribed mass effect is new.\n\nThere are multiple areas of encephalomalacia/gliosis and siderosis in the\ninferior left parietal lobe, image 17 of series 5, 6, and 7, and image 302:20,\nwithin the the right basal ganglia and adjacent white matter (image 5:14),\nwithin the supraorbital right frontal lobe (image 5:14), and within the right\nmiddle frontal gyrus (image 5:16).  These are compatible with with prior\ninfarcts with hemorrhagic transformation, though the cortical abnormalities\nare also compatible with sequela of amyloid angiopathy.\n\nSusceptibility artifact in bilateral globus pallidus corresponds to dense\ncalcifications on the prior CT.\n\nThere also multiple small foci of high T2 signal in the supratentorial white\nmatter, likely sequela of chronic small vessel ischemic disease.\n\nRight lateral ventricle and right hemispheric sulci are prominent due to mild\nparenchymal volume loss.  There is superimposed ex vacuo dilatation of the\nfrontal horn of the right lateral ventricle secondary to the encephalomalacia\nin the right basal ganglia.\n\nMajor intravascular flow voids appear grossly preserved.\n\nLeft maxillary sinus is completely opacified and atelectatic, consistent with\nchronic sinusitis.  Right mastoid air cells are opacified.\n\nDysconjugate gaze is noted.",
            "output": "1. Large evolving acute infarction in the left middle cerebral artery\nterritory, as detailed above, with partial effacement of the frontal horn and\nanterior body of the left lateral ventricle.  The extent of infarction is\nsimilar to the MRI from 1 day earlier, but the mass effect is new.\n2. Multiple areas of encephalomalacia/ gliosis in siderosis in the left\nparietal lobe, right frontal lobe, and right basal ganglia, compatible with\nprior infarcts with hemorrhagic transformation, though the cortical\nabnormalities are also compatible with sequela of amyloid angiopathy.\n3. Chronic left maxillary sinusitis with atelectasis of the left maxillary\nsinus."
        },
        {
            "input": "There is no intra or extra-axial mass, acute hemorrhage or infarct. The sulci,\nventricles and cisterns are within expected limits for the patient's age.  One\nor two subcortical T2/FLAIR punctate hyperintensities are nonspecific in a\npatient of this age, but within expected limits, potentially sequela of\nchronic microangiopathy.  The major intracranial flow voids are preserved. \nThe orbits are unremarkable.  There is mild mucosal thickening of the\nparanasal sinuses.  No suspicious marrow signal.",
            "output": "1. Unremarkable noncontrast MRI head.  Specifically no acute infarct."
        },
        {
            "input": "MRI Brain:\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.\n\nMRA brain: The intracranial vertebral and internal carotid arteries and their\nmajor branches appear normal without evidence of stenosis, occlusion, or\naneurysm formation.\n\nMRA neck:  The common, internal and external carotid arteries appear normal. \nThere is no evidence of internal carotid artery stenosis by NASCET criteria. \nThe origins of the great vessels, subclavian and vertebral arteries appear\nnormal bilaterally.",
            "output": "Normal MRI and MRA brain and MRA neck."
        },
        {
            "input": "Study is limited by motion degradation.\n\nMRI HEAD:\nThere is right temporal lesion which abuts the communicating segment of the\nright internal carotid artery and measures 3.9 x 2.4 cm (image 17:11),\ndemonstrating extensive susceptibility artifact on gradient echo imaging with\nmarkedly low signal on T2 weighted images, consistent with a giant aneurysm. \nThere is peripheral hyperintensity on T2 weighted and T1 weighted images\nwithin the aneurysm, compatible with thrombus.  There is surrounding edema in\nthe right temporal lobe, extending into the right external capsule and\nsubcortical white matter of the right insula, as well as into the posterior\nright internal capsule.  The right medial temporal lobe effaces the right\nambient cistern but does not deform the midbrain.  Temporal horn of the right\nlateral ventricle is effaced.  The remainder of the ventricles are\nage-appropriate.  There is mild sulcal enlargement compatible with global\nparenchymal volume loss.\n\nThere is heterogeneously enhancing sellar/suprasellar mass which measures 1\n2.1 cm transverse, 1.6 cm AP, 2.3 cm craniocaudad (108:67, 16:94, 16:98).  The\nmass abuts the optic chiasm.  Optic chiasm signal is not adequately assessed\nin the absence of dedicated high-resolution images through the sella the mass\nextends into the left cavernous sinus, image 108:67.\n\nThere is encephalomalacia and gliosis in the right frontal operculum and\nsupraorbital right frontal lobe, compatible with sequela of prior infarction\nor trauma.  There is a moderate size chronic infarction in the right posterior\ninferior cerebellar hemisphere.  There are periventricular, deep, and\nsubcortical white matter T2/FLAIR hyperintense foci, nonspecific but likely\nsequela of chronic small vessel ischemic disease in this age group.\n\nThere is no acute infarction. Dural venous sinuses appear patent on\npostcontrast MP RAGE images.\n\nThere is a non-enhancing circumscribed T2 hyperintense focus with slow\ndiffusion in the subcutaneous tissues in over the right nose extending into\nthe medial canthus, which measures 1.3 x 1.3 cm (17:9), likely a sebaceous\ncyst.\n\nParanasal sinus disease with osseous remodeling is better assessed on the\npreceding head CT.  Complete opacification of the right maxillary sinus, near\ncomplete opacification of right anterior ethmoid air cells, and mucosal\nthickening in the right frontal sinus are again seen.  Partial opacification\nof left ethmoid air cells and mild mucosal thickening in the left frontal\nsinus are also again seen.  Mucosal thickening and secretions are likewise\nagain seen in the right sphenoid sinus.  Polypoid mucosal thickening is again\nseen in the left posterior ethmoid.  Aerosolized secretions are again noted in\nthe left concha bullosa.\n\nMRA HEAD:\n\nDue to motion artifact, intracranial arteries are better assessed on the\npreceding CTA.  There is a giant aneurysm of the communicating segment of the\nright internal carotid artery, as detailed above.  Flow is seen only in the\nneck of the aneurysm, spanning 9 x 5 mm on image 104:12.  The right middle\ncerebral artery is elevated by mass effect from the right temporal giant\naneurysm.  There is no evidence for flow-limiting stenosis.  Non dominant\nright vertebral artery is hypoplastic distal to right ___.",
            "output": "1. Motion limited exam.\n2. 3.9 x 2.4 cm thrombosed giant aneurysm of the communicating segment of the\nright internal carotid artery, projecting into the right temporal region, with\n9 x 5 mm area of flow in the aneurysm neck.  Associated edema in the right\ntemporal lobe, right insula, right external capsule, and posterior limb of the\nright internal capsule.\n3. Sellar/suprasellar mass with mass effect on the optic chiasm extension to\nthe left cavernous sinus, which most likely represents a pituitary\nmacroadenoma, and less likely a craniopharyngioma given a small peripheral\ncalcification on preceding CT.\n4. Right frontal operculum/supraorbital encephalomalacia and gliosis, likely\nsecondary to chronic infarct or prior trauma.\n5. Moderate-sized chronic infarct in the right posterior inferior cerebellar\nhemisphere.\n6. 1.3 cm probable sebaceous cyst over the right nose extending into the\nmedial canthus.\n7. Extensive sinus disease, better characterized on the preceding head CT."
        },
        {
            "input": "Study is moderate degraded by motion.\n\nThere is no diffusion involving essentially the entire right middle cerebral\nartery territory including the frontal, parietal, and temporal lobes as well\nas the basal ganglia in insula.  There a few areas of slow diffusion at the\nboundary of the right middle cerebral artery and posterior cerebral artery\nterritories in the posterior temporal lobe as well as the medial temporal\nlobe.  In addition, there are chronic infarcts involving the right cerebellar\nhemisphere, and there is encephalomalacia in both inferomedial frontal lobes,\nright greater than left.\n\nElsewhere, there are scattered areas of nonspecific T2/FLAIR hyperintensity in\nthe subcortical and periventricular white matter most reflecting chronic\nmicroangiopathy in this age group.  There is prominence of the ventricles and\nsulci reflecting volume loss.  Edema related to the large right MCA territory\ninfarct causes partial effacement of the right lateral ventricle, but no\nleftward midline shift demonstrated.  Enlarged pituitary measures 2 cm.\n\nLarge signal void projecting laterally from the right ICA terminus\ncorresponding to the known aneurysm is noted.  Orbits are grossly\nunremarkable.  There is a T2 hyperintense 1 cm rounded focus overlying the\nright nasal bone which probably has associated slowed diffusion, any similar\nsmaller structure on the left (images 11 and 13 of series 5).  Right posterior\nparietal epidermal inclusion cyst.  This may reflect epidural inclusion\ncyst/epidermoid.  There is patchy fluid signal in the bilateral mastoid air\ncells, mild scattered mucosal thickening throughout the paranasal sinuses.",
            "output": "1. Acute infarction involving the entire right MCA territory and some areas at\nthe junction of the MCA and PCA territories.\n2. Areas of chronic encephalomalacia in the right cerebellar hemisphere as\nwell as in both inferior frontal lobes.\n3. Enlarged pituitary gland, not assessed in detail by this examination, which\ncan be correlated for history of pituitary adenoma.  This abuts the\nundersurface of the optic chiasm, but is not assessed 12 on this motion\ndegraded brain MRI protocol study.\n4. Epidermoid versus epidermal inclusion cyst in the facial soft tissues\nmedial to the orbits, larger on the right which can be correlated with direct\ninspection.\n5. Large signal void related to the known right ICA aneurysm post pipeline\nstent placement.  Patency of the aneurysm is not assessed by this examination."
        },
        {
            "input": "The examination is motion degraded, particularly the MPRAGE postcontrast\nsequences.  Within these confines:\n\nThe 7.1 by 3.6 x 4.3 cm left temporo-occipital intraparenchymal hematoma is\nunchanged in size from the prior examination.  The local mass effect with\neffacement of the adjacent sulci and atrium and occipital horn of the left\nlateral ventricle is unchanged.  This hematoma demonstrates an outer\nperipheral rim of T1 and T2 hypointense signal with susceptibility and an\ninner peripheral rim of T1 hyperintense signal.  This hematoma demonstrates\nrestricted diffusion.  The central portions of this hematoma are T1\nhypointense and T2/FLAIR hyperintense.  There is no enhancement within or\nsurrounding the hematoma.  Minimal surrounding T2/FLAIR hyperintense signal is\nconsistent with edema.\n\nFaint, curvilinear T1 hyperintense signal with susceptibility in the sulci of\nthe right frontal lobe represents chronic subarachnoid hemorrhage, related to\ntrauma as seen on the CT head ___.\n\nNo new hemorrhage is identified.  Punctate micro hemorrhages of the right\nputamen, posterior right parietal lobe and right cerebellar hemisphere are\nnoted.\n\nThere is no evidence of midline shift or infarction.T2/FLAIR hyperintensities\nin the periventricular, subcortical, and deep white matter are nonspecific,\nbut may represent the sequela of chronic small vessel ischemic disease.  There\nis no abnormal enhancement after contrast administration.\n\nThe paranasal sinuses and mastoid air cells are clear.  The orbits are\nunremarkable.\n\nThe left mid and distal intradural vertebral artery enhances and is patent,\nimproved from the CTA head ___, where no contrast opacification\nwas visualized.  The 3 mm aneurysm of the proximal basilar artery on 100b:30\nis unchanged.",
            "output": "1. Unchanged left temporo-occipital intraparenchymal hematoma with local mass\neffect and no evidence of enhancement.  Follow-up to resolution is\nrecommended.\n2. Chronic subarachnoid hemorrhage in the right frontal lobe.\n3. No new hemorrhage.\n4. Unchanged 3 mm aneurysm of the proximal basilar artery."
        },
        {
            "input": "There is no acute infarction.\n\nThe previously noted left parietal/occipital/posterior temporal hematoma has\ndecreased in size compared to ___.  Compression of the occipital\nhorn of the left lateral ventricle has partially improved.  Other ventricles\nare stable in size, prominent due to underlying age-related parenchymal volume\nloss.\n\nSiderosis from prior subarachnoid hemorrhage is again seen in the right\ncentral sulcus.\n\nThere are multiple punctate chronic micro hemorrhages at the gray/white matter\njunction of the occipital lobe, in the right posterior inferior cerebellar\nhemisphere, and in the right putamen, which are unchanged.\n\nExtensive confluent T2 hyperintensity in the periventricular, deep, and\nsubcortical white matter of the cerebral hemispheres is grossly unchanged,\nnonspecific but likely sequela of chronic small vessel ischemic disease in\nthis age group.\n\nAxial FIESTA images through the brainstem demonstrate no evidence for\nstructural abnormalities related to the cranial nerves.\n\nMajor intravascular flow voids appear grossly preserved, allowing for\ndiminutive caliber of the posterior circulation as demonstrate previously, but\nthe blood vessels were better assessed on the preceding CTA.",
            "output": "1. No acute infarction.\n2. Decreased left parietal/ occipital/ posterior temporal hematoma compared to\n___.  Decreased effacement of the occipital horn of the left\nlateral ventricle.\n3. Unchanged siderosis in the right central sulcus related to prior\nsubarachnoid hemorrhage.  Unchanged scattered punctate microhemorrhages in the\nbrain parenchyma, with distribution compatible with a combination of\nhypertensive etiology and amyloid angiopathy."
        },
        {
            "input": "There is no evidence of acute intracranial hemorrhage or mass effect. \nIncidental note is made of cavum septum pellucidum et vergae. The ventricles\nare otherwise normal in appearance.\n\nThere are punctate foci of slow diffusion within the right precentral gyrus\ncompatible with acute to subacute ischemia. There is a large area of\nencephalomalacia within the left medial frontal lobe which is compatible with\na chronic infarct.  There are chronic lacunar infarcts within the right basal\nganglia and left cerebellum. There is additional scattered foci of subcortical\nand periventricular T2/FLAIR signal hyperintensity which is presumably on the\nbasis of chronic small vessel ischemic disease. There is mild brain\nparenchymal volume loss.  There are normal vascular flow voids.  There is an\nunchanged focus of gradient blooming within the region of the right thalamus\nwhich could represent mineralization or chronic blood products. There is an\nadditional punctate focus of gradient blooming within the right parietal lobe\nmay represent chronic microhemorrhage and is unchanged prior exam.\n\nThere is thickening of the transverse ligament identified ay the\ncraniocervical junction due to degenerative changes which is unchanged from\nthe previous MRI. Otherwise, The orbits, skull base, and paranasal sinuses are\nunremarkable.",
            "output": "1. Punctate foci of slow diffusion within the right precentral gyrus\ncompatible with acute to subacute ischemia.\n2. No evidence of acute intracranial hemorrhage or mass effect.\n3. Left medial frontal lobe encephalomalacia compatible with chronic infarct.\n4. Brain parenchymal volume loss and additional presumed sequelae of chronic\nsmall vessel ischemic disease.\n\nNOTIFICATION:   The impression above was entered by Dr. ___ on\n___ at 11:08 into the Department of Radiology critical communications\nsystem for direct communication to the referring provider."
        },
        {
            "input": "Cystic encephalomalacia in the superior paramedian and inferolateral left\nfrontal lobe from remote infarcts, dates back to at least ___. \nThere are confluent and multiple isolated foci of DWI hyperintense signal with\nassociated low signal on the ADC map and high T2/FLAIR signal, predominantly\ninvolving the watershed zones of the right frontoparietal lobes with an\nadditional focus of similar signal characteristics in the watershed zone of\nthe right parietotemporo occipital lobes.  A single punctate focus of DWI\nhyperintense signal is also present in the left posterior parietal lobe. \nThese are consistent with late acute/early subacute infarcts.  Additional\nconfluent periventricular and scattered punctate subcortical white matter\nT2/FLAIR hyperintensities without associated slow diffusion, most of which\nwere present on the prior study of ___, are nonspecific but likely\nsequelae of chronic microangiopathy in a patient this age.\n\nLayering hypointense signal on T2 weighted images in the occipital horn of the\nleft lateral ventricle demonstrating blooming on gradient echo images is\nconsistent a small amount of intraventricular hemorrhage, similar to the prior\nCT (08:14).  Hypointense signal in the atrium of the right lateral ventricle\non gradient echo images may also represent a small amount of hemorrhagic\nproducts in this region (06:15).  Hypointense gradient echo signal in the\nright posterolateral  thalamus/tail of caudate is consistent with old micro\nhemorrhages (06:15).  Prominence of the ventricles and sulci is in keeping\nwith age related involutional changes.  Ventricles are stable in size and\nconfiguration.  Cavum septum pellucidum et vergae anatomic variant is again\nnoted.  There is mild attenuation of the normal right M1 bifurcation (series\n8, image 12), which may be artifactual versus slow flow/thrombus.  The\nremainder the major intracranial flow voids are preserved.\n\nMild mucosal thickening in the axillary and ethmoid sinuses is noted. \nPartially empty sella is unchanged.  The patient is status post right cataract\nextraction.  The orbits are otherwise unremarkable.",
            "output": "1. Late acute/early subacute right cerebral hemisphere infarcts involving the\nright ACA/MCA/PCA watershed zones as described above, although the infarcts to\nextend to the cortical surface in the right frontal parietal lobes.  A single\npunctate focus of acute/subacute infarct is also present in the left posterior\nparietal lobe.\n\n2.  Suggestion of mild attenuation of normal right M1 bifurcation flow void,\nwhich may be artifactual versus potentially thrombus.  Although the infarcts\nare in a predominately watershed distribution (although right hemispheric\npredominant), MRA could be performed for further evaluation.\n\n3.  Small intraventricular hemorrhages, similar to the prior CT.\n\n4.  Cystic encephalomalacia from chronic infarcts in the superior paramedian\nand inferolateral left frontal lobe.\n\nNOTIFICATION:  The findings were discussed with ___, M.D. by ___\n___, M.D. on the telephone on ___ at 10:43 AM, 5 minutes after\ndiscovery of the findings."
        },
        {
            "input": "Leptomeningeal FLAIR hyperintense signal, enhancement is seen involving the\nbilateral cerebellar and cerebral hemispheres, most prominently in the\noccipital lobes pre findings concerning for leptomeningeal metastasis. \nInfection, inflammatory process could have similar appearance.  No abnormal\nparenchymal or parenchymal enhancement is seen.  Small areas of cortical edema\nadjacent to area of leptomeningeal enhancement.  No evidence of hemorrhage on\ngradient images today or head CT from ___.\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  The intracranial flow voids are maintained.\n\nClear paranasal sinuses.  Mild opacification left mastoids, and trace\nopacification right mastoids.",
            "output": "1. Leptomeningeal enhancement, differential considerations metastases,\ninfection, inflammatory process.  Few adjacent areas of mild parenchymal\nedema."
        },
        {
            "input": "Study is mildly degraded by motion.\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  There is prominence of the ventricles and sulci suggestive of\ninvolutional changes.  Few periventricular and subcortical T2 and FLAIR\nhyperintensities are noted which may represent small vessel ischemic changes.\n\nThere are postsurgical changes of bilateral lens replacement.  There is mild\nmucosal thickening of the ethmoid sinuses.  The mastoid air cells are clear. \nThe major intracranial arterial flow voids are preserved.",
            "output": "1. Study is mildly degraded by motion.\n2.  No acute intracranial abnormality, with no definite evidence of acute\ninfarct.\n3. Global volume loss and minimal probable microangiopathic changes as\ndescribed.\n4.  Paranasal sinus disease , as described."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.",
            "output": "1. Normal brain MRI."
        },
        {
            "input": "MRV: Normal flow signal is demonstrated within the superior sagittal sinus,\nstraight sinus, transverse sinuses, and sigmoid sinuses with slightly\npreferential flow to the right transverse sinus, a common variant.  The\njugular bulbs and proximal jugular veins are patent. Evaluation of the deep\nvenous systems reveals normal flow signal in the internal cerebral veins. The\nvein ___ is also unremarkable.\n\nMRI BRAIN:  Patient is status post suboccipital craniotomy with decompression\nof the posterior fossa.  There is susceptibility artifact in the region of the\ncraniotomy compatible postoperative change.\n\nThere is significant crowding of the posterior fossa with narrowing of the pre\npontine and cerebellar cisterns.  The quadrigeminal and suprasellar cisterns\nare effaced.  The cerebellum appears elongated in the craniocaudal dimension\nand the cerebellar tonsils are low-lying.  The pons appears deformed and\nflattened anteriorly.  The fourth ventricle is small, the pituitary gland\nappears prominent, there is narrowing of the suprasellar cistern.\n\nOn the FLAIR sequence there are thin, likely subdural, collections/effusions\nalong the cerebral convexities bilaterally.  There is no convincing evidence\nof parenchymal edema.  However, following contrast administration there is\ndiffuse symmetric mild supratentorial and infratentorial pachymeningeal\nenhancement.  There is no evidence of mass, infarct or acute hemorrhage.  The\nmajor intracranial arterial flow voids are preserved.",
            "output": "1. There is severe crowding of the posterior fossa in this patient status post\nposterior fossa decompression.  The cisterns and fourth ventricle are very\nsmall.  The cerebellum is elongated and the cerebellar tonsils are low lying. \nThe pons is flattened.  There is no definite evidence of brain edema.\n2. There is mild symmetric bilateral supratentorial and infratentorial\npachymeningeal enhancement of unknown chronicity.\n3. There are thin subdural collections layering along the bilateral cerebral\nconvexities, possibly chronic postoperative subdural hematomas or hygromas.\n4. The dural venous sinuses are patent.\nComparison to prior outside studies including preoperative studies would be\nmost helpful to ascertain the chronicity of these findings.  The constellation\nof findings could reflect intracranial hypotension possibly secondary\npostoperative CSF leak.  Continued close clinical follow-up and neurosurgical\nconsultation is recommended\n\nRECOMMENDATION(S):  Correlation with prior MRIs of the head is recommended, to\nidentified interval changes in the configuration of the posterior fossa\nstructures.\n\nNOTIFICATION:  These findings were discovered and discussed in person with Dr.\n___ by Dr. ___ at 14:45 on ___."
        },
        {
            "input": "MR BRAIN:\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline\nshiftoracute large territory infarction.  The ventricles and sulci are\nprominent, suggestive of involutional changes.  There are scattered\nperiventricular and subcortical white matter T2/FLAIR hyperintensities,\nnonspecific but suggestive of moderate chronic small vessel ischemia.  No\nabnormal postcontrast enhancement.\n\nMRA brain: The intracranial vertebral and internal carotid arteries and their\nmajor branches appear normal without evidence of stenosis, occlusion, or\naneurysm formation.",
            "output": "1. No acute intracranial abnormality.  Specifically, no intracranial\nhemorrhage.\n2. The major vessels of the brain appear patent and without high-grade\nstenosis, occlusion, or aneurysmal change.\n3. Involutional and moderate chronic small vessel ischemic changes."
        },
        {
            "input": "Patient motion moderately degraded images.  Diffusion-weighted images are\ndiagnostic.  There is no evidence of hemorrhage, edema, masses, mass effect,\nmidline shift or infarction.  Probable benign perivascular space right basal\nganglia.  There are no chronic small vessel ischemic changes..  The ventricles\nand sulci are normal in caliber and configuration.  Intracranial vascular flow\nvoids are preserved.  Air-fluid level in the right maxillary sinus, secretions\nin the nasopharynx, partial opacification right mastoids, likely related to\nintubation.",
            "output": "1. No acute infarcts.\n2. Opacified paranasal sinuses, mastoids, nasopharynx, likely from intubation."
        },
        {
            "input": "The examination is mildly motion degraded.  Within this confines:\n\nThere is no evidence of infarction, hemorrhage, edema, mass, or mass effect.\n\nNo abnormal enhancement.  No suspicious parenchymal FLAIR/T2 signal\nabnormality.\n\nThe ventricles and sulci are prominent, compatible with global parenchymal\nvolume loss.\n\nMinimal periventricular and a few small deep white matter foci of T2/FLAIR\nsignal hyperintensity are nonspecific but compatible with mild changes of\nchronic white matter microangiopathy.\n\n The visualized paranasal sinuses and mastoids appear clear.\n\n Aside from right lens extraction, the globes and orbits are within normal\nlimits.\n\n Major intracranial vascular flow voids are preserved.\n\n Major dural venous sinuses are patent.",
            "output": "On mildly motion degraded examination:\n\n1. No acute intracranial abnormality on contrast enhanced MRI head.  No mass\nor abnormal enhancement.\n2. No definite suspicious parenchymal FLAIR/T2 signal abnormality.\n3. Additional findings described above.  If there remains high close suspicion\nfor imaging sequela of Wernicke's encephalopathy or pontine myelinolysis,\nrepeat examination may yield additional formation."
        },
        {
            "input": "There is diffuse leptomeningeal enhancement, both supra and infratentorially.\nThis includes nodular enhancement of the cerebellar hemispheres and vermis.\nThe bilateral internal auditory canals and left trigeminal nerve are also\ninvolved (100a:41).  There are also several intraparenchymal enhancing lesions\n(101a:33,38). There is no edema. The calvarial bone marrow shows normal signal\nand there is no evidence of osseous metastasis. The ventricles and extra-axial\nspaces are normal in size. There is no shift of normally midline structures,\nmass effect or hydrocephalus. There is no acute infarct. The vascular flow\nvoids are maintained. The visualized paranasal sinuses are clear.",
            "output": "Diffuse leptomeningeal enhancement and several parenchymal lesions consistent\nwith metastatic disease.  No evidence of osseous metastasis in the calvarium."
        },
        {
            "input": "MRI BRAIN:\nThere are multiple foci of slow diffusion within the inferior right cerebellum\nand cerebellar tonsils with associated mild increased T2/FLAIR hyperintensity\n(series 8, image 5, 6) compatible with acute/subacute infarcts in ___\ndistribution (series 400 image 5, 7).  No other areas of slow diffusion.\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, or midline\nshift.  The ventricles and sulci are normal in caliber and configuration. \nThere is no abnormal enhancement after contrast administration.\n\nMRA BRAIN:\nThe intracranial vertebral and internal carotid arteries and their major\nbranches appear normal without evidence of stenosis, occlusion, or aneurysm\nformation.\n\nMRA NECK:\nThe right vertebral artery is diminutive throughout its course, with areas of\nirregularity and near occlusion of the V2 and V3 segments, as seen on the CTA\nhead and neck with the same date.  In addition, there is circumferential\nintrinsic T1 hyperintensity within the wall of the right vertebral artery\nthroughout its course (series 14, image 1 and series 13, image 23), compatible\nwith a long segment right vertebral artery dissection.  The left vertebral\nartery is patent and otherwise unremarkable in appearance.\n\nThe common, internal and external carotid arteries appear normal.  There is no\nevidence of internal carotid artery stenosis by NASCET criteria.  The origins\nof the great vessels, subclavian and vertebral arteries appear normal\nbilaterally.",
            "output": "1. Multiple foci of acute/subacute infarct within the inferior right\ncerebellum and cerebellar tonsils, ___ distribution.  No evidence of\nhemorrhage.\n2. Diminutive right vertebral artery throughout its course with areas of\nirregularity and near occlusion of the V2 and V3 segments.  Circumferential\nintrinsic T1 hyperintensity throughout the length of the right vertebral\nartery, compatible with long segment dissection.\n\nNOTIFICATION:   The findings were discussed with ___, M.D. by ___\n___, M.D. on the telephone on ___ at 4:47 pm."
        },
        {
            "input": "There are postoperative changes and soft tissue changes secondary to extensive\nright-sided trauma. Diffusion abnormalities are seen in the anterior right\ntemporal lobe and inferior right frontal lobe as well as marrow abnormalities\nindicative of contusions. Foci of gradient blooming are seen within the right\ncerebellar hemisphere and left temporal lobe which may indicate punctate foci\nof hemorrhage from recent trauma. There is no additional evidence of new\nintracranial hemorrhage or mass effect.  The ventricles and basal cisterns\nappear normal.\n\nThere is no evidence of acute ischemia based on diffusion-weighted imaging. \nThere are normal vascular flow voids.\n\nThere is bilateral mastoid fluid and bilateral maxillary sinus fluid.  There\nis a large right parietal scalp hematoma.  Fluid is seen in the right temporal\nair cells which could be related to trauma.\n\nThere is lack of flow related enhancement within the right distal transverse\nand sigmoid sinus with intrinsic T1 hyperintensity which most likely indicates\na thrombosis. The superior sagittal sinus and left transverse sinu appear\nnormal. The remaining and dural venous structures appear normal. The\nvasculature of the neck including the bilateral vertebral arteries, internal\ncarotid arteries, and common carotid arteries appear normal.",
            "output": "1. Changes secondary to recent trauma as described above.  The right temporal\nand inferior frontal contusions.\n2. Lack of flow related enhancement with suggestion of T1 hyperintensity\nwithin the right transverse and sigmoid sinus likely indicate focal\nposttraumatic thrombosis.\n\nNOTIFICATION:  Discussed with Dr. ___ at 1200 by Dr. ___ telephone\non ___."
        },
        {
            "input": "MRI BRAIN:\nThere is no evidence of acute intracranial hemorrhage, or infarction. \nVentricles and sulci are age appropriate.  Mild mucosal sinus thickening is\nseen involving the ethmoid air cells.  A mucous retention cyst is seen within\nthe left maxillary sinus.  The remainder of the visualized paranasal sinuses,\nmastoid air cells, and middle ear cavities are clear.  The globes are\nunremarkable.\n\nMRA BRAIN:\nThe left internal carotid artery is normal.  The left middle cerebral artery\nis normal.  There is normal arborization of the distal left MCA branches.  The\nright internal carotid artery is normal.  The right middle cerebral artery is\nnormal.  There is normal arborization of the distal right MCA branches.  The\nA1 segments of the anterior cerebral arteries are normal.  There is a normal\nanterior communicating artery complex.  The vertebral arteries are normal. \nThe right vertebral artery is dominant.  There is a fetal type right posterior\ncerebral artery which appears to be patent.  The left PCA is normal.\n\nMRA NECK:\nThe left vertebral artery demonstrates segmental narrowing with surrounding T1\nfat-sat hyperintensity spanning from C2 through C6 with significant\nattenuation of flow, concerning for a dissection (image 18, series 109, and\nimage 14, series 20).  Subtle flow related enhancement is seen through the\ncervical segment of the left vertebral artery.\n\nThe right common carotid, and internal carotid arteries are normal.  There is\nno evidence of internal carotid artery stenosis by NASCET criteria.  The left\ncommon carotid, and internal carotid artery is normal.  There is no evidence\nof internal carotid artery stenosis by NASCET criteria.  The right vertebral\nartery is normal.",
            "output": "1. Acute dissection of the left vertebral artery spanning from C2 through C6\nwith significant attenuation of flow.\n2. No acute intracranial abnormalities identified.\n3. Unremarkable circle of ___ without evidence of aneurysm or significant\nstenosis.\n4. No evidence of internal carotid artery stenosis by NASCET criteria."
        },
        {
            "input": "MRA brain:\nFetal origin of the right posterior cerebral artery is again noted.  The\nintracranial vertebral and internal carotid arteries and their major branches\nappear normal without evidence of stenosis, occlusion, or aneurysm formation.\n\nMRA neck:\nThe distal V2 and V3 segments of the vertebral arteries are excluded from the\ncontrast enhanced images, but demonstrate appropriate flow voids and flow\nrelated enhancement.\n\nPreviously noted wall irregularity and luminal narrowing along the mid V2\nsegment of the left vertebral artery has substantially improved.  The\nvertebral arteries are patent bilaterally.\n\nThe common, internal and external carotid arteries appear normal.  There is no\nevidence of stenosis by NASCET criteria. The origins of the great vessels,\nsubclavian, and vertebral arteries appear normal bilaterally.  The common\ncarotid bifurcations appear normal.",
            "output": "1. Previously noted wall irregularity and luminal narrowing along the mid V2\nsegment of the left vertebral artery has substantially improved. The carotid\nand vertebral arteries are patent bilaterally.\n2. Unremarkable head MRA."
        },
        {
            "input": "MRI BRAIN:\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  The ventricles and sulci are prominent, consistent with global\ncerebral volume loss.  Patchy periventricular T2 hyperintensities are most\nconsistent with chronic microvascular ischemic disease.  There is no abnormal\nenhancement after contrast administration.  A subcentimeter chronic infarct\ninvolving the left cerebral hemisphere is seen.  Thinning of the bilateral\nlenses likely due to prior cataract surgery.  The visualized paranasal sinuses\nand mastoid air cells are clear.\n\nMRA BRAIN:\nThe patient is post clipping of a right MCA aneurysm.  Evaluation of this\nregion is suboptimal due to from the aneurysm clip.  Contrast flow seen in the\nright M2 segment and distally.\n\nStable 4 mm and 3 mm aneurysms are seen at the left MCA bifurcation.\n\nThere is stable mild narrowing of the left P2 segment, likely due to\natherosclerotic disease.\n\nThe remaining intracranial vessels and their major branches appear normal\nwithout evidence of stenosis, occlusion, or aneurysm formation.\n\nMRA NECK:\nThe common, internal and external carotid arteries appear normal.  There is no\nevidence of internal carotid artery stenosis by NASCET criteria.  The origins\nof the great vessels, subclavian and vertebral arteries appear normal\nbilaterally.",
            "output": "1. Status post clipping of a right MCA aneurysm. Evaluation for\nintra-aneurysmal flow is suboptimal due to susceptibility artifact. Contrast\nflow seen in the right M2 segment and distally.\n2. Stable 4 mm and 3 mm aneurysms involving the left MCA bifurcation.\n3. Subcentimeter chronic infarct involving the left cerebellar hemisphere.\n4. Normal MRI of the neck without significant narrowing or occlusion."
        },
        {
            "input": "A syrinx is noted within the upper cervical spinal cord.\n\nThere is no evidence of acute intracranial hemorrhage or mass effect.  There\nis symmetric T1 hyperintensity within the frontal horns of the lateral\nventricles -- overall signal skull characteristics are compatible with fat. \nSmall fat deposits are identified in the inferior portion of the fourth\nventricle.  These findings can be seen with prior ruptured dermoid cyst. \nThere are no other fat deposits within the cisterns are subarachnoid spaces. \nThe ventricles are normal in size.\n\nThere are normal vascular flow voids.  There is no evidence of acute infarct\nbased on diffusion-weighted imaging.  There is mild diffuse brain parenchymal\nvolume loss.  There is minimal subcortical and periventricular T2/FLAIR signal\nhyperintensity which likely represent sequelae of chronic microangiopathy.\n\nThere is no abnormal brain parenchymal or leptomeningeal enhancement.\n\nThere is a right mastoid effusion.  There is a right maxillary sinus mucosal\nretention cyst.  The orbits appear unremarkable.",
            "output": "1. Symmetric fat within the frontal horns of the bilateral lateral ventricles\nand inferior fourth ventricle, the findings of which can be seen with prior\nruptured dermoid cyst.  Also this could be associated with prior surgery or\nspinal trauma.  The ventricles are normal in size and there are no other areas\nof fat deposition seen within the subarachnoid spaces are cisterns.\n2. No hemorrhage, mass effect, abnormal enhancement, or acute infarct.\n3. Upper cervical spinal cord syrinx.\\."
        },
        {
            "input": "MR HEAD: There is no abnormal signal on diffusion weighted imaging to suggest\nacute infarction. Minimal periventricular white matter hyperintensities on\nFLAIR are nonspecific but may be sequela of early small vessel disease. There\nis no intracranial mass, mass effect, or midline shift. Ventricles and sulci\nare age-appropriate. Intracranial flow voids are maintained.  There is mucosal\nthickening of the right maxillary sinus. The mastoid air cells and middle ear\ncavities are clear.\n\nMRA HEAD/NECK:  The left vertebral artery is hypoplastic with poor\nvisualization of its origin. The left vertebral artery ends in the ___.  The\nright vertebral artery is unremarkable.  There is no flow limiting stenosis in\nthe cervical and intracranial internal carotid arteries and their major\nbranches. There is no evidence of craniocervical dissection or aneurysm\ngreater than 3 mm.",
            "output": "1. No evidence of acute infarction.\n2. Hypoplastic left vertebral artery. Otherwise, unremarkable MRA of the head\nand neck."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, or infarction.\nThe ventricles and sulci are normal in caliber and configuration. There is no\nabnormal enhancement after contrast administration. There are scattered white\nmatter hyperintensities on FLAIR that likely reflect a dilated perivascular\nspaces.",
            "output": "Normal study."
        },
        {
            "input": "There is a 0.9 (TV) x 1.4 (AP) x 1.3 (CC) cm parafalcine mass which is\nisointense to gray matter on T1 weighted images, hypo intense to gray matter\non T2 weighted images and shows homogeneous contrast enhancement on\npost-contrast sequences (series 101, image 97; series 13, image 100).  Imaging\ncharacteristics are most consistent with a meningioma.  No additional\nenhancing lesions are identified.  There is no evidence of hemorrhage, edema,\nmidline shift or infarction.  Mild prominence of ventricles and sulci is\nconsistent with age related involutional changes.  Tiny scattered T2/FLAIR\nhyperintensities within the subcortical and deep white matter are nonspecific,\nbut likely the sequela of chronic small vessel ischemic disease.\n\nThere is mild to moderate mucosal thickening of the ethmoidal air cells. \nThere is complete opacification of the left maxillary sinus.  There is a small\namount of fluid in the left mastoid air cells.  Otherwise, the remaining\nvisualized paranasal sinuses and right mastoid air cells are clear.  The\norbits are unremarkable.  The intracranial flow voids are preserved.  The\ndural venous sinuses are patent on MPRAGE sequences.",
            "output": "1. No evidence for metastatic disease.\n2. A 1.3 cm parafalcine mass with imaging characteristics most consistent with\na meningioma.\n3. Sinus inflammatory disease."
        },
        {
            "input": "MRI Brain:\nThere is a large area of slow diffusion in the right middle and posterior\ncerebral artery distribution involving the right frontal, parietal, temporal\nand occipital lobes with associated FLAIR hyperintensity in keeping with an\nacute stroke.  Also seen is susceptibility within the right basal ganglia\ninvolving the caudate head and putamen in keeping with superimposed\nintraparenchymal hemorrhage.  There is associated mass effect with mild\neffacement of the right lateral ventricle and sulci.  No midline shift is\nseen.\n\nThe ventricles, cisterns and sulci are otherwise prominent in keeping with\nvolume loss.  There are scattered and confluent areas of FLAIR hyperintensity\nin the periventricular white matter, likely secondary to small vessel ischemic\nchanges.\n\nMucosal thickening in bilateral ethmoid air cells with mucosal thickening in\nbilateral maxillary sinuses.  The mastoid air cells are clear.  The orbits are\nunremarkable noting prior left cataract surgery.\n\nMRA brain:  There is an abrupt cut off of the right carotid terminus just\nproximal to the origin of the right middle cerebral artery without any flow\nrelated enhancement involving the right MCA.  Also seen fetal origin of\nbilateral posterior cerebral arteries with marked luminal narrowing and\nirregularity, likely secondary to atherosclerotic calcification.  There is\ndecreased distal arborization of the right posterior cerebral artery compared\nto the left in the Ambient cistern.\n\nThere is marked luminal irregularity and narrowing of the left middle cerebral\nartery and bilateral A1 segments of anterior cerebral artery, likely secondary\nto atherosclerotic narrowing.\n\nThere is absence of flow related enhancement involving bilateral V4 segments\nof the vertebral artery as well as the proximal basilar artery.  This is\neither secondary to slow flow because of marked luminal narrowing secondary to\natherosclerosis or because of complete occlusion.  However, given the presence\nof distal flow, this is likely secondary to marked luminal narrowing.\n\nNo aneurysms are seen.\n\nMRA neck:  There is some luminal irregularity involving bilateral common and\ninternal carotid arteries, likely secondary to atherosclerosis without\nsignificant stenosis by NASCET criteria.  The common, internal and external\ncarotid arteries appear otherwise unremarkable.   The origins of the great\nvessels, subclavian and vertebral arteries appear normal bilaterally.",
            "output": "1. Large infarct in the right middle cerebral and posterior cerebral artery\ndistribution with superimposed hemorrhage involving the right basal ganglia as\ndescribed above.  Associated edema and mass effect with effacement of right\nlateral ventricle and and sulci.\n2. Abrupt cut off of the right carotid terminus just proximal to the origin of\nright middle cerebral artery with decreased arborization of the distal\nbranches of right posterior cerebral artery in the ambient cistern.\n3. Luminal irregularity and narrowing of left middle cerebral artery, left\nposterior cerebral artery and bilateral A1 segments of anterior cerebral\nartery, likely secondary to atherosclerosis.\n4. Absence of flow related enhancement involving bilateral V4 segments of the\nvertebral artery on head MRA but visualization on the gadolinium enhanced neck\nMRA likely secondary to atherosclerotic disease and slow flow.\n5. Luminal irregularity of bilateral common and internal carotid arteries near\nthe bifurcation, likely secondary to atherosclerosis without significant\nstenosis by NASCET criteria."
        },
        {
            "input": "Study is mildly degraded by motion.\n\nThere is linear FLAIR hyperintensity in the central gyrus on the right side as\nseen on image 7:18 with associated susceptibility on gradient echo imaging. \nThis likely corresponds to the hyperdensity seen in the recent prior MRI in\nkeeping with subarachnoid hemorrhage.  There is associated mild intrinsic T1\nhyperintensity.  No new hemorrhage is seen.\n\nThere is no evidence of edema, masses, mass effect, midline shift or\ninfarction.   The ventricles and sulci are patent and prominent in keeping\nwith age-related volume loss.\n\nThere are scattered foci and more confluent areas of T2/FLAIR hyperintensity\nin the subcortical and periventricular white matter, nonspecific, likely\nsecondary to small vessel ischemic disease.\n\nLeft pontine, left cerebellar, and left temporal punctate foci of increased\ndiffusion signal without associated ADC hypointensity, with increased FLAIR\nsignal, are noted (see 402:11, 17, 7:8, 12).\n\nThere are multiple foci of susceptibility in keeping with microhemorrhages in\nbilateral cerebral hemispheres, especially in bilateral parietal lobes and a\npunctate focus in the right cerebellar hemisphere.  These are nonspecific,\nlikely secondary to amyloid angiopathy.\n\nThere is a prosthetic left globe.  The right orbit is unremarkable.  There is\nmild mucosal thickening in bilateral anterior ethmoid air cells.  The\nremaining visualized paranasal sinuses and mastoid air cells are clear. \nIntracranial flow voids are maintained.",
            "output": "1.  Study is mildly degraded by motion.\n2. Stable subarachnoid hemorrhage in the right central gyrus.  While no\ndefinite mass  identified, underlying mass is not excluded on the basis of\nthis examination.  Recommend followup imaging to resolution.\n3. Multiple nonspecific punctate microhemorrhages in bilateral cerebral\nhemispheres and left cerebellar hemisphere, concerning for amyloid angiopathy.\n4. Findings of age-related involutional changes and small vessel ischemic\ndisease.\n5. No definite acute intracranial infarct is seen.  Please note that left\npontine, left cerebellar, and left temporal punctate foci of increased\ndiffusion signal without associated ADC hypointensity may represent small\nareas of blood products, however subacute infarcts are not excluded on the\nbasis of this motion degraded examination.  Recommend attention on followup\nimaging.\n\nRECOMMENDATION(S):\n\n1. Stable subarachnoid hemorrhage in the right central gyrus.  While no\ndefinite mass  identified, underlying mass is not excluded on the basis of\nthis examination.  Recommend followup imaging to resolution.\n2. No definite acute intracranial infarct is seen. Please note that left\npontine, left cerebellar, and left temporal punctate foci of increased\ndiffusion signal without associated ADC hypointensity may represent small\nareas of blood products, however subacute infarcts are not excluded on the\nbasis of this motion degraded examination. Recommend attention on followup\nimaging."
        },
        {
            "input": "There is a large lobulated mass in the suprasellar region which appears to be\narising from the sella and extending superiorly and anteriorly.  The mass also\nextends inferiorly with invasion of the clivus and sphenoid sinus.  The mass\nextends also within the sphenoid sinus along its lateral recess (12:5). \nSeveral cystic areas are identified in the anterior superior portion of the\nmass.  The anterior cerebral artery is elevated superiorly and the A2 segments\nare splayed.  The mass extends near the foramen ___ with dilatation of the\nlateral ventricles a right greater than left side with prominence of temporal\nhorns indicative of obstructive hydrocephalus.  There is no periventricular\nedema seen.  No acute infarcts are identified.\n\nThe mass measures 7 x 6 x 5.5 cm in the superior inferior by\nanterior-posterior by right to left ___.  The pattern of the\nenhancement, and displacement of surrounding structures as well as enlargement\nof the sella are suggestive of a sellar or region of the mass most likely a\npituitary macro adenoma.\n\nThere is downward displacement of the cerebellar tonsils.  This is secondary\nto mass effect.",
            "output": "Large sellar and suprasellar mass with invasion of the clivus and sphenoid\nsinus as well as superior extend to the foramen ___ with displacement of the\noptic chiasm and optic nerves (which are difficult to identify) suggestive of\npituitary macroadenoma."
        },
        {
            "input": "The exam is for pre-operative planning.  Skin surface markers are noted.\n\nThe large, lobulated, heterogeneous cystic and solid enhancing sellar and\nsuprasellar mass is overall unchanged in size and appearance since ___,\nmeasuring 6.9 x 6 x 5.5 cm (cc x trv x ap) (series 3, image 51; series 300,\nimage 88).  The mass extends superiorly and anteriorly with displacement of\nthe lateral ventricles, markedly narrowing outflow at the level of the foramen\n___ resulting in right greater than left obstructive hydrocephalus, the\ndegree of which is overall similar to the prior exam.  The mass also extends\ninferiorly, expanding the sella and invading the sphenoid sinus and clivus\n(e.g., series 3, image 40, 31). The degree of associated downward displacement\nof the cerebellar tonsils is overall similar.  The mass is seen within the\nregion of the optic chiasm which is difficult to fully appreciate on this\nlimited exam (series 3, image 44).  The mass encases anterior cerebral\narteries and displaces the A2 segments laterally (series 3, image 56, 47, 48).\nThe major dural venous sinuses appear patent.  Mucosal thickening in the\nethmoidal air cells is mild.",
            "output": "Overall unchanged, large heterogeneous lobulated sellar and suprasellar mass,\ninvading the clinoid and sphenoid sinus inferiorly and causing obstructive\nhydrocephalus superiorly at the level of the foramen of ___, imaging\nfeatures most suggestive of a pituitary macroadenoma."
        },
        {
            "input": "Since the previous MRI examination the patient has undergone resection of a\nlarge sellar and suprasellar mass.  Expected postsurgical changes with\npneumocephalus and fluid in the frontal region at the craniectomy site are\nidentified.  Blood products are seen at the surgical site.  The tumor has been\nresected except for lesion posterior to the anterior cerebral artery near the\nhypothalamus.  There is approximately 70% resection of the sellar and\nsuprasellar mass.  There remains signal changes within both cavernous sinuses\nand the clivus indicative of invasion by tumor.  The ventricular size has \ndecreased.  There is area of restricted diffusion in the left periventricular\nregion (06:20) which likely indicates an acute infarct in the left basal \nganglia and periventricular region in lenticulostriate territory.  Small\namount of blood products are seen in the occipital horn of the right lateral\nventricle.",
            "output": "Postsurgical changes with subtotal resection of the sellar and suprasellar\nmass identified as detailed above.  Acute infarcts are seen in the left basal\nganglia region.  Decreased ventricular size."
        },
        {
            "input": "Study is mildly degraded by motion.\n\nPatient is status post repeat resection of previously noted sellar/suprasellar\nmass.\n\nNew areas of slow diffusion consistent with acute infarct is identified in the\nright genu and body of corpus callosum and in the left occipital lobe.  These\nare new since the MRI from 1 day prior.  The 2 punctate foci of infarct in the\nleft occipital lobe measure 4 mm and 3 mm respectively (6:___).\n\nSlow diffusion is identified in the right caudate head, left caudate and\nlentiform nucleus, and fornix, similar in size compared to 1 day ago although\nincreased in signal, consistent with interval evolution of acute infarct.  A\n1.1 x 0.4 cm area of in far in the left frontal lobe is also unchanged in\nsize.\n\nRight lateral ventricle is slightly larger compared to the CT from 1 day ago. \nThe posterior horn of right lateral ventricle measures 11 mm in width (800b:\n68), larger from before (previously 8 mm).\n\nResidual suprasellar mass is smaller than before measuring 1.1 (AP) x 2.8 (TV)\nx 1.8 (SI) cm (800b:59, 801b:76).\n\nSmall bilateral subdural hematomas appear similar in size compared to  1 day\nago.  The hematoma at the resection bed appear similar to the CT from 1 day\nago.\n\nThe parenchymal defect in the right frontal lobe along the tract of prior\nventriculostomy catheter is larger than prior MRI but stable from prior CT. \nBifrontal subgaleal hematoma with air-fluid levels is noted.  Air-fluid level\nis noted in the sphenoid sinus.  Partial opacification of bilateral ethmoid\nand mastoid air cells is noted.",
            "output": "1.  Study is mildly degraded by motion.\n2. Acute infarct at the corpus callosum and left occipital lobe are new since\nexamination 1 day prior.\n3. Acute infarct at bilateral caudate, left lentiform nucleus, fornix, and\nleft frontal lobe are stable in size compared to 1 day ago.\n4. Right lateral ventricle is larger compared to the postop CT from 1 day ago,\nwith redemonstration of tract communicating from right lateral ventricle to\nsubdural space overlying right frontal lobe, similar to recent head CT exam.\n5. Bifrontal subdural hemorrhage and the hemorrhage at the mass resection bed\nappear similar to the CT from 1 day ago.\n6. Evolving bifrontal subgaleal hematoma with air-fluid levels.\n7. Interval reduced size of residual enhancing suprasellar mass as described.\n\nNOTIFICATION:  The findings were discussed with ___, N.P. by ___\n___, M.D. on the telephone on ___ at 11:40 AM, 5 minutes after discovery\nof the findings."
        },
        {
            "input": "There is increased T2/FLAIR signal in the right genu and body of the corpus\ncallosum with associated volume loss, high signal on diffusion with pseudo\nnormalization on ADC compatible with subacute infarct.  Areas of T2/FLAIR\nhyperintensity are noted in the bilateral caudate, left putamen, fornix, left\ninferior frontal lobe and 2 punctate areas in the left occipital lobe with\nincreased signal on diffusion and ADC compatible with late subacute infarct. \nAgain, there are postsurgical changes from bifrontal craniotomy with evolution\nof appearance.  Small bifrontal fluid collections has intervally decreased in\nsize compared to the prior exam.  There is some superficial soft tissue\nthickening and edema at the level of the recent left frontal craniotomy with\nsome areas obscured by hardware artifact, though with a small 2.2 x 0.5 cm\nleft frontal subgaleal fluid collection.  Again, there is postsurgical change\nand volume loss of the right frontal lobe from the surgical tract which\ncommunicates with the right lateral ventricle.\n\nThere is a new punctate signal in the left cerebral peduncle (7:13, 6:13) this\nextends superiorly.  There is no new hemorrhage, or new mass.  The ventricles\nhave slightly expanded compared the prior examination with persistent\nasymmetry with a larger right lateral ventricle.\n\nResidual enhancing suprasellar mass on coronal images measuring up to 13 x 8\nmm on the right (100b:90) and 17 x 13 mm on the left (100b:85) is unchanged\ncompared to the prior examination.  Areas of enhancement are noted in the\ncorpus callosum, right caudate head and left basal ganglia infarcts.\n\nThere is persistent fluid opacification of the sphenoid air cells and a small\namount of fluid in the left frontal sinus.  The principal intracranial\nvascular flow voids are preserved.",
            "output": "1. Punctate new signal abnormality within left cerebral peduncle which extends\nsuperiorly and likely represents acute wallerian degeneration.\n2. Interval evolution appearance of postsurgical changes from bifrontal\ncraniotomy with decreased bifrontal subdural fluid collections.  Superficial\nsoft tissue thickening and edema is noted in the area of left frontal\ncraniotomy, with a small 2.2 x 0.5 cm left frontal subgaleal fluid collection.\n3. Evolving appearance of subacute to late subacute infarcts in the corpus\ncallosum, fornix, right caudate head, left basal ganglia, left frontal lobe\nand left occipital lobe.  Some of the new enhancement in the area appears to\nbe due to subacute infarcts.  However, this can be further evaluated on\nfollowup examinations\n4. Stable residual enhancing suprasellar mass.\n5. Mild interval expansion of the ventricular system with persistent\nasymmetric enlargement of the right lateral ventricle which communicates with\nthe right frontal surgical tract.\n\nNOTIFICATION:  The findings were discussed with ___, N.P. by\n___, M.D. on the telephone on ___ at 11:00 AM, 5 minutes after\ndiscovery of the findings."
        },
        {
            "input": "Examination is limited by areas of left frontal calvarial susceptibility\nartifact.  Study is mildly degraded by motion.\n\nThere are evolving postsurgical changes from bifrontal craniotomy and sellar\nand suprasellar mass resection.  Bifrontal subdural fluid collections appear\nto have resolved.  Areas of left inferior frontal encephalomalacia and a tract\nof right frontal encephalomalacia leading to the frontal horn of the right\nlateral ventricle is unchanged, likely postsurgical in nature.\n\nThere is evolving encephalomalacia of the right genu and body of the corpus\ncallosum as well as punctate areas in the left basal ganglia, compatible with\nevolving, now chronic infarcts.  There is no acute infarct.  The ventricles\nand sulci appear stable in size and configuration.\n\nAgain there is a prominently expanded sella.  A rim of mildly enhancing tissue\nwithin the expanded sella measuring up to 12 mm in thickness on the left which\nappear to partially encase the bilateral cavernous internal carotid arteries,\nappears unchanged compared to the prior examination (501:110).  .  Suprasellar\ncomponents of enhancing soft tissue, encasing the anterior cerebral arteries\nalso appear unchanged.  This measures up to 17 x 10 mm on the left (501:110)\nand 15 x 9 mm on the right (501:103).  No new enhancing masses noted.",
            "output": "1. Examination is limited by areas of susceptibility artifact overlying the\nleft frontal calvarium, and mild motion.\n2. Unchanged sellar and suprasellar enhancing soft tissue components\ncompatible with residual macro adenoma, as described.\n3. Evolving postsurgical changes from bifrontal craniotomy and\nsellar/suprasellar mass resection.\n4. Unchanged bifrontal encephalomalacia, likely postoperative.\n5. Evolving encephalomalacia of the right genu and body of the corpus\ncallosum, and left basal ganglia compatible with now chronic infarcts."
        },
        {
            "input": "Postsurgical changes of bifrontal craniotomy for resection of a large\nsellar/suprasellar mass including a large tract extending from the cortex to\nthe right lateral ventricle and encephalomalacia and in the left frontal lobe\nare grossly unchanged compared to the prior examination.  Residual enhancing\nsuprasellar components measuring approximately 7 x 11 x 8 mm and 10 x 16 x 13\nmm are grossly stable compared to the most recent prior examination (series 8,\nimages or 9 and 10).  Deviation of the pituitary stalk to the right is\nunchanged.  There is no new area of nodular enhancement.  The major vascular\nflow voids are preserved.\n\nImages of the pituitary appear normal. The pituitary signal intensity appears\nnormal before and after contrast administration. No masses are identified. The\nsuprasellar cistern and cavernous sinuses appear normal. The limited portion\nof the brain included on this study appears normal.",
            "output": "1.  Post treatment changes are overall unchanged compared to the prior\nexamination.\n\n2.  Stable size of residual suprasellar enhancing tumor as compared to prior\nexamination."
        },
        {
            "input": "MR Head:  There is no evidence of acute intracranial hemorrhage, mass, mass\neffect or shifting of the normally midline structures. Multiple scattered foci\nof high signal intensity on FLAIR and T2 weighted sequences are demonstrated\nin the subcortical and periventricular white matter, which are nonspecific and\nmay reflect areas of small vessel disease.  No diffusion abnormalities are\ndetected to indicate acute or subacute ischemic changes. The ventricles and\nsulci are prominent, suggesting atrophy, unchanged since the prior head CT and\nthe prior MRI in ___. The orbits are unremarkable, persistent mucosal\nthickening is noted in the ethmoidal air cells and frontal ethmoidal recesses\nbilaterally, suggesting chronic inflammatory changes, the mastoid air cells\nare clear.\n\nMRA Head: Normal flow signal is noted in the petrous, cavernous, and\nsupraclinoid portions of the internal carotid arteries. The anterior and\nmiddle cerebral arteries are normal. The anterior communicating artery region\nis normal.\n\nThe posterior cerebral arteries and basilar artery are unremarkable.  The\nsuperior cerebellar arteries are normal. The intradural segments to both\nvertebral arteries are patent; the right vertebral artery is dominant. Normal\nbilateral posterior communicating arteries are identified.  No arterial\nstenosis, saccular aneurysm, or AVM is identified. .\n\nMRA of the neck: The origin of the supraaortic vessels is partially evaluated.\nBoth common carotid arteries are patent with persistent narrowing at the right\ncervical carotid bifurcation, correlation with carotid ultrasound is\nrecommended for further characterization. The left cervical carotid\nbifurcation appears patent. The vertebral arteries are patent with dominance\nof the right vertebral artery.",
            "output": "1. There is no evidence of acute or subacute intracranial process.\n2. Normal MRA of the head with no evidence of flow stenotic lesions or\naneurysms.\n3. Unchanged narrowing on the right cervical carotid bifurcation, correlation\nwith carotid ultrasound is recommended for further characterization."
        },
        {
            "input": "The filling defect reported in the left transverse and sigmoid sinus is not\ndefinitely appreciated on post-contrast MPRAGE  images, and likely represents\nan artifact.  No evidence of dural thrombosis.\n\nThere is no evidence of an acute infarct, intracranial mass, or hemorrhage.\nNo diffusion abnormalities are detected.  There is prominence of the\nventricles, sulci, and cistern, reflecting involutional changes.  Subcortical\nand periventricular areas of T2 FLAIR high-signal intensity are nonspecific\nand may reflect changes due to chronic small vessel disease.  The vascular\nflow voids are preserved.  The pituitary, suprasellar cistern, or brainstem,\nposterior fossa are unremarkable.  The major vascular flow voids are present\nand master normal distribution.  The orbits are unremarkable, the paranasal\nsinuses demonstrates mild mucosal thickening in the ethmoidal air cells with\npossible concha bullosa on the left.",
            "output": "1. No acute intracranial abnormality, specifically no acute infarct,\nintracranial mass, hemorrhage\n2. The reported filling defect in the left transverse and sigmoid sinus is not\nappreciated on this exam, and likely represent an artifact.  No evidence of\ndural thrombosis specifically in the left transverse and sigmoid sinuses."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  The ventricles and sulci are enlarged in an atrophic pattern. \nNonspecific periventricular and deep white matter T2 FLAIR hyperintensities;\nlikely related to chronic small vessel disease.\n\nMinimal mucosal thickening of left sphenoid sinus.  Otherwise; paranasal\nsinuses and mastoid air cells are unremarkable.",
            "output": "1. No evidence of mass, hemorrhage or infarction.\n2. Atrophy with findings suggesting chronic small vessel ischemia.."
        },
        {
            "input": "MRI Brain:  There is no evidence of hemorrhage, edema, masses or infarction. \nVentricles and sulci are normal in caliber and configuration.  Vascular flow\nvoids are preserved. The orbits are the bulb. There is mild mucosal thickening\nwithin the ethmoid air cells. The remaining paranasal sinuses and mastoid air\ncells are clear.\n\nMRA neck:  The common, internal and external carotid arteries appear normal. \nThere is no evidence of stenosis by NASCET criteria.  The origins of the great\nvessels, subclavian and vertebral arteries appear normal bilaterally.",
            "output": "1. No evidence of acute infarction or hemorrhage.\n\n2.  Unremarkable MRA of the neck without evidence of stenosis by NASCET\ncriteria."
        },
        {
            "input": "There is no evidence of acute intracranial infarction, hemorrhage, brain\nedema, mass, or mass effect.  There is prominence of the ventricles and sulci\nin keeping with global involutional changes.  Minimal periventricular and a\nfew scattered white matter T2/FLAIR signal hyperintense foci (11:15 for\nexample) are nonspecific but compatible with minimal changes of chronic white\nmatter microangiopathy.\n\nCentered in the right petrous apex, there is an approximately 18 x 12 mm\nintrinsically T1 hyperintense, T2/FLAIR hyperintense focus which does not\ndemonstrate appreciable enhancement, and additionally appears to have a focus\nof susceptibility in its central component (14:56 and 10:6).  The focus does\nnot show restricted diffusion.  Abnormality corresponds to partially opacified\npneumatized petrous apex on CT of ___.\n\nIntrinsically T1 hyperintense, T2 hypointense opacification of the ___\nthe right maxillary sinus (12:4) with expansion of the sinus and peripheral T2\nhyperintense mucosal thickening is consistent with a mucocele.  There is\nmucosal thickening of the right ethmoid air cells. The globes are\nunremarkable.  Major intracranial vascular flow voids are preserved.  Dural\nvenous sinuses are patent.",
            "output": "1. 1.8 x 1.2 cm nonenhancing T1 and T2 hyperintense right petrous apex focus\nwith internal susceptibility, suggestive of accumulating proteinaceous\nsecretions/developing cholesterol granuloma.\n2. Right maxillary sinus mucocele.\n3. No other acute intracranial abnormality identified.\n4. Chronic findings include mild global involutional changes and minimal\nchanges of chronic white matter microangiopathy."
        },
        {
            "input": "There is a well-circumscribed nonenhancing homogeneously T2 hyperintense, T1\nhypointense lesion within the left parotid tail measuring 2.9 cm TV x 2.6 cm\nAP x 3.4 cm SI (6:9; 10:21).  This lesion can be seen on prior PET CTs dating\nback to ___.  There is no associated internal or rim enhancement. \nThe remainder of the parotid gland is  unremarkable.  The right parotid,\nsublingual, and bilateral submandibular salivary glands are unremarkable.\n\nThere is a micronodular appearance of the thyroid gland, with the largest T2\nhyperintense nodule within the left thyroid lobe measuring 4 mm (07:16). \nThere is equivocal asymmetric mucosal enhancement of the right oropharynx\n(series 8, image 11), on axial sequences, not confirmed on coronal sequences. \nThe remainder of the visualized aerodigestive tract is within expected limits.\nThe visualized intracranial structures are unremarkable.  There are no\nsuspicious lymph nodes by size or morphology.  The marrow signal is\nunremarkable.  There are central disc protrusions at C2-C3, C3-C4, C4-C5, and\nC5-C6 causing up to mild spinal canal narrowing, greatest at C3-C4 (03:13). \nThe uppermost segment of the patient's gastro esophageal pull-through is noted\n(series 7, image 27).",
            "output": "1. 2.9 x 2.6 x 3.4 cm nonenhancing unilocular cyst within the left parotid\ntail which may represent a benign lymphoepithelial lesion, sialocele, with\nfirst branchial cleft cyst a consideration although considered slightly less\nlikely given patient's age.  This lesion can be seen on prior PET-CT of ___ where does not demonstrate FDG avidity.  Given the lack of\nnodular components and FDG avidity, lesion such as Warthin's tumor or cystic\nnecrotic lymph node are considered much less likely.\n2. Mild asymmetric enhancement of the right oropharynx, which may represent\nsequela of patient's recent pharyngitis per clinical notes.  Clinical\ncorrelation is recommended."
        },
        {
            "input": "Study is mildly degraded by motion.  There is no evidence of hemorrhage,\nedema, masses, mass effect, midline shift or infarction.  There is prominence\nof the ventricles and sulci suggestive involutional changes.  Multiple left\nprecentral gyrus punctate chronic hemosiderin staining is noted (see 11:18). \nBilateral maxillary and left frontal sinus mucosal thickening is present. \nPostsurgical changes related to bilateral cataract surgeries noted.",
            "output": "1. Study is mildly degraded by motion.\n2.  No acute intracranial abnormality.\n3.  Paranasal sinus disease as described.\n4. Chronic left precentral gyrus hemosiderin staining.  Question history of\nprior trauma or infarct.  Recommend clinical correlation."
        },
        {
            "input": "Study is moderately degraded by motion,/stent postcontrast imaging.  There is\nno evidence of hemorrhage, edema, masses, mass effect, midline shift or\ninfarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  Few nonenhancing periventricular and subcortical T2 and FLAIR\nhyperintensities with no associated restricted diffusion, T1 hypointensity or\nincreased susceptibility are noted.  There is no abnormal enhancement after\ncontrast administration.",
            "output": "1. Study is moderately degraded by motion.\n2.  No acute intracranial abnormality.\n3. Within limits of study, no definite evidence of intracranial mass.\n4. Few nonenhancing white matter lesions as described, likely representing\nmicroangiopathic changes, with differential considerations including sequelae\nof prior trauma or infection, history of migraine headaches, and demyelinating\nprocess."
        },
        {
            "input": "A large left thyroid mass is seen, measuring approximately 8.4 cm x 7 cm by\n11.6 cm, resulting in severe deviation of the trachea to the right,\ndisplacement of the left common carotid and internal jugular veins laterally\nas well as contiguity with the prevertebral soft tissues.  Additional\nenhancing tissue is seen anteriorly and right anterolaterally to the trachea,\nseries 701, image 26 with extension to the submandibular region.  Inferiorly,\nthis lesion extends to the level of the clavicular heads, at the\nsternoclavicular joint.  Prominent vasculature is seen coursing through the\nlarge left thyroid mass.\n\nThe nasopharynx appears to be unremarkable.  Mildly prominent lingual tonsils\nare seen causing effacement of the airway.  Asymmetry of the right vocal fold,\nmay be secondary to patient's known vocal cord paralysis.\n\nNo significant cervical lymphadenopathy is identified.  The visualized\nparanasal sinuses, mastoid air cells aside from mild fluid within the right\nmastoid air cell, and middle ear cavities are clear.  The globes are\nunremarkable.  The vascular flow voids otherwise appear to be well preserved.",
            "output": "1. Large left thyroid mass measures up to 11.6 cm in craniocaudal dimension\nwith severe deviation of trachea to the right, displacement of the left common\ncarotid artery, internal carotid artery and internal jugular veins laterally. \nThe lesion extends inferiorly to the level of the sternoclavicular joint. \nAdditional enhancing tissue is seen anterolaterally to the trachea, with\nextension to the submandibular region which may be secondary to residual\nthyroid tissue from patient's prior procedure.\n2. Mildly prominent lingual tonsils, are seen causing effacement of the\nairway.  Mild asymmetry is seen of the right vocal fold.\n3. Nasopharynx appears to be unremarkable."
        },
        {
            "input": "MR BRAIN:\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline\nshiftor acute infarction.  The ventricles and sulci are within expected limits\nin caliber and configuration.  The major flow voids are preserved.  There is\nmild mucosal thickening of the paranasal sinuses.  The orbits are\nunremarkable.  Fluid signal is seen in the bilateral mastoid air cells.\n\nMRA brain: The intracranial vertebral and internal carotid arteries and their\nmajor branches appear normal without evidence of stenosis, occlusion, or\naneurysm formation.\n\nMRV brain: There is hypoplastic appearance of the left transverse and sigmoid\nsinuses, likely congenital.  Otherwise, the dural venous sinuses appear\npatent.",
            "output": "1. No acute intracranial abnormalities on noncontrast MRI brain.  No\nintracranial hemorrhage or acute infarct.  No suspicious parenchymal FLAIR\nsignal abnormality.\n2. The left transverse and sigmoid sinus is hypoplastic without evidence of\nsignal abnormality.  Otherwise, unremarkable noncontrast MRV of the brain.\n3. Unremarkable MRA of the brain."
        },
        {
            "input": "Limited study with a single motion degraded sagittal sequence of the head. \nThere partially visualized postsurgical changes along the right frontal lobe\nwith regional edema.",
            "output": "1. Incomplete limited study due to early termination related to patient's\ninability to cooperate.\n2. Single motion degraded sagittal sequence of the head demonstrates partially\nvisualized postsurgical changes of the right frontal lobe with regional edema."
        },
        {
            "input": "There is redemonstration of multiple predominantly right-sided enhancing\nsupratentorial lesions not substantially changed compared to prior study dated\n___ as follows:\n\n1.8 x 1.4 x 1.7 cm (TRV x AP x SI) lesion in the posterior right occipital\nlobe (3:94 and 300:109).\n1.7 x 1.1 x 2.1 cm (TRV x AP x SI) lesion in the lateral right occipital lobe\n(3:99 and 300:76).\n1.1 x 0.9 x 0.9 cm (TRV x AP x SI) lesion in the superior right frontal lobe\n(3:148 and 300:128).\nThere are multiple additional subcentimeter lesions in the right parietal lobe\n(3:119, 3:137), right occipital lobe (3:101, 3:120), left frontal lobe\n(3:147), and left lateral occipital lobe (3:191).\n\nThere is extensive vasogenic edema in the right cerebral hemisphere with\napproximately 4 mm of leftward midline shift, previously measuring 5 mm on\nhead CT dated ___.  There are stable postoperative changes status\npost right frontal craniotomy and mass resection.",
            "output": "1. Multiple enhancing lesions predominantly in the right cerebral hemisphere,\nas described above.\n2. Extensive vasogenic edema with approximately 4 mm of leftward midline\nshift, slightly decreased from prior study.\n3. Stable postoperative changes status post right frontal craniotomy and mass\nresection."
        },
        {
            "input": "Some of the sequences have been degraded by movement artifact.\n\nThere are multiple enhancing lesions, predominantly in the right cerebral\nhemisphere.\n\nThe largest lesions are as follows:\n\n-Right posterior frontal lobe, parasagittal:  9 mm (AP) x 10 mm (TV) x 12 mm\n(SI)\n-Lateral aspect of right frontal lobe: 9 mm (AP) x 14 mm (TV) x 8 mm (SI), and\nanterior to this, 14 mm (AP) x 17 mm (TV) x 15 mm (SI).\n-Lateral aspect of right parietal lobe: 15 mm (AP) x 10 mm (TV) x 23 mm (SI).\n-The right occipital lobe: 14 mm (AP) x 17 mm (TV) x 20 mm (SI), and\nanteromedial to this, 9 mm (AP) x 9 mm (TV) x 12 mm (SI).\n-There are several addition small foci of enhancement, within the right\nfrontal lobe, right occipital lobe and in the posterior aspect of the left\nfrontal lobe, in a parasagittal location.\n-There is no pathological leptomeningeal enhancement.\nMany of these lesions demonstrate slow diffusion.  There is vasogenic edema\nsurrounding the right cerebral hemispheric lesions, which is unchanged\ncompared with the prior CT head.  There is mass-effect, with partial\ncompression of the right lateral ventricle, most marked in the trigone,\noccipital and temporal horns.  There is mild midline shift to the left (4 mm)\nwhich is unchanged.\n\nThere is no evidence of hemorrhage.  No definite infarct.\n\nThere is fluid within the right sphenoid sinus.  Paranasal sinuses and mastoid\nair cells are otherwise clear.  Normal appearance of the orbits.",
            "output": "-Multiple enhancing supratentorial lesions, predominantly in the right\ncerebral hemisphere, with surrounding vasogenic edema, which is unchanged. \nFindings are in keeping with multiple intracranial metastases.\n-Mass-effect with partial compression of the right lateral ventricle and mild\nmidline shift to the left (4 mm), unchanged."
        },
        {
            "input": "Motion artifact limits evaluation.\n\nAgain demonstrated are multiple predominantly right-sided enhancing\nsupratentorial lesions, some of which demonstrate slowed diffusion.  The\nlargest lesions are:\n\n-2.1 x 2.2 x 1.6 cm (SI by TRV by AP; 5002:189; 08:42) lesion in the right\noccipital lobe.\n-2.3 x 1.9 x 0.9 cm (SI by AP by TRV; ___, 8:46) lesion in the\nlateral right occipital lobe.\n-1.5 x 1.4 x 1.6 cm (TRV by AP by SI; 8:60, 5003:143) lesion in the right\nfrontal lobe.\nAdditional several smaller enhancing lesion in the right frontal lobe, right\noccipital lobe, and left frontal lobe are also again demonstrated.  Vasogenic\nedema surrounding the right cerebellar hemispheric lesions is not appreciably\nchanged compared to the prior exam.  There is stable mass effect with partial\neffacement of the right lateral ventricle.  Minimal leftward midline shift is\npoorly evaluated on this motion degraded study and was better assessed on the\nprior MR examination.\n\nPlease note that comprehensive evaluation of the brain parenchyma is otherwise\nnot performed with this exam which is limb.",
            "output": "Motion limited exam.  Multiple enhancing lesions, mostly in the right cerebral\nhemisphere, are again demonstrated for surgical planning."
        },
        {
            "input": "MR BRAIN:\nThis is a markedly limited study with only diffusion-weighted images provided.\nBifrontal pneumocephalus and bilateral hemorrhagic extra-axial collection is\nbetter evaluated on the recent noncontrast CT scan.  Right greater than left\nfrontal contusions are noted.  DWI hyperintense signal along the anterior\ninferior frontal lobes bilaterally is likely due to presence of hemorrhage in\nthis region.  There is a focus of slow diffusion in the dorsal midbrain along\nthe midline, likely representing an acute or early subacute infarct (04:11).\n\n\nMRA brain:\nEvaluation subtle abnormality is or small aneurysm is limited by moderate\nmotion artifact.  The circle of ___ and its major tributaries are grossly\npatent.",
            "output": "1.  Markedly limited study as described above.\n\n2.  Known intracranial hemorrhages are better evaluated on the noncontrast CT\nfrom ___.\n\n3.  Focal region of slow diffusion in the dorsal midbrain likely represents an\nacute or early subacute infarct.\n\n4.  MRA is moderately degraded by motion artifact.  The circle of ___ and\nits major tributaries are grossly patent."
        },
        {
            "input": "MRI Brain:\nThere are multiple foci of slow diffusion involving the left insula, posterior\nleft frontal and parietal lobes.  There is corresponding increased signal on\nT2/FLAIR and low signal on the ADC map.  Superimposed scattered subcortical\nand periventricular white matter T2/FLAIR hyperintensities are nonspecific but\ncan be seen in the setting of chronic small vessel disease.  There is no\nevidence of acute hemorrhage, edema, masses, mass effect or midline shift. \nThe ventricles and sulci are normal in caliber and configuration.\n\nMRA brain: There is narrowing at the origin of the left MCA M1 segment.  There\nis decreased arborization of the left M3 and M4 segments of the middle\ncerebral artery, overall similar in appearance compared to the prior CTA.  The\nintracranial vertebral arteries and their major branches appear otherwise\nnormal without evidence of stenosis, occlusion, or aneurysm formation.  The\npara and supraclinoid left MCA appears to be significantly attenuated, with\nattenuation of the flow within the left MCA, likely secondary to\nreconstitution from the contralateral side.  A small vascular infundibulum is\nseen at the origin of the right posterior communicating artery.\n\nMRA neck:\n\nThe left common and internal/external carotid arteries are severely attenuated\ncompatible with occlusion of the proximal left common carotid artery. \nReconstitution occurs at the level of the left supraclinoid ICA.  The right\ncommon and internal and external carotid arteries appear normal.  There is no\nevidence of internal carotid artery stenosis by NASCET criteria on the right. \nThe origins of the great vessels, subclavian and vertebral arteries appear\nnormal bilaterally.",
            "output": "1. Multiple acute to subacute infarcts involving the left insula and\nsubinsular cortex, posterior left frontal lobe and left parietal lobe.\n2. Evidence of occlusion of the proximal left common carotid artery with\nreconstitution intracranially at the level of the left supraclinoid ICA.\n3. Narrowing of the origin of the left MCA M1 segment, with decreased\narborization of the left M3 and M4 segments of the MCA.\n4. Mild scattered nonspecific subcortical and deep white matter T2/FLAIR\nhyperintensities can be seen in the setting of chronic small vessel disease.\n\nRECOMMENDATION(S):  The findings were discussed with ___, M.D. by\n___, M.D. on the telephone on ___ at 10:22 pm, 2 minutes after\ndiscovery of the findings."
        },
        {
            "input": "In the left deep white matter, in the area of the centrum semiovale and corona\nradiata, in the area previously noted acute to subacute infarcts, again seen\nis increased signal on the isotropic diffusion weighted imaging with\ncorresponding isointensity on ADC mapping and increased intensity on T2/FLAIR\nconsistent with evolving subacute infarct.  Previously seen areas of\ninfarction in the left frontal lobe and parietal lobe are not appreciated on\nthis exam. No new areas of slowed diffusion to suggest new, acute infarction. \nAgain seen are superimposed scattered subcortical and periventricular white\nmatter T2/FLAIR hyperintensities, which are nonspecific, but can be seen in\nthe setting of chronic small vessel disease.\nThere is no evidence of hemorrhage, edema, masses, mass effect, or midline\nshift. The ventricles and sulci are normal in caliber and configuration. \nVasculature is better assessed on recent CTA from ___.",
            "output": "Expected evolution of subacute infarction of the left deep white matter in the\narea of the centrum semiovale and corona radiata without evidence of acute\ninfarction.  No evidence of hemorrhagic conversion."
        },
        {
            "input": "The ventricles, sulci, and cisterns appear normal.  There is no intracranial\nhemorrhage, mass lesion, or abnormal enhancement.  The major vascular flow\nvoids are preserved.  The major cortical veins and dural venous sinuses are\npatent.  The orbits are unremarkable.",
            "output": "Normal contrast enhanced MRI of the head."
        },
        {
            "input": "There is a large heterogeneous enhancing 4.3 x 5.6 x 7.7 cm (AP x TV x SI)\nthyroid mass which wraps circumferentially around the trachea without definite\nfat plane in between to exclude invasion (201:33 and 3:28).  The mass extends\nposteriorly to abut the esophagus with associated mass effect, with loss of\nfat plane which may suggest invasion.\n\nMultiple enlarged and necrotic cervical lymph nodes are noted.  For example, a\nrepresentative cervical conglomerate in the left level 2A/2B measures\napproximately 7.2 x 4.1 cm (201:19) and abuts the cervical vasculature.  A\ndominant necrotic right cervical level 2A lymph node measures approximately\n2.5 cm (02:18).  In enlarged left supraclavicular lymph node measures 1.8 cm\n(02:35).\n\nThere is extensive subcutaneous edema along the anterior soft tissue of the\nneck extending inferiorly to the chest.  Patient is status post tracheal\nstenting, which appears patent.  The neck vessels appear grossly patent.  Note\nis made of mucous retention cysts in both maxillary sinuses.  Please refer to\nthe dedicated MR chest for full description intrathoracic findings.",
            "output": "1. Large heterogeneous enhancing 4.3 x 5.6 x 7.7 cm thyroid mass wraps\ncircumferentially around the trachea and extends posteriorly to abut the\nesophagus with loss of normal fat plane, which may suggest edema versus\ntumoral invasion.  Again demonstrated are multiple enhancing, necrotic\ncervical lymph nodes, similar to prior study from ___.\n2. Tracheal stent is in situ, and appears patent."
        },
        {
            "input": "There is a large area of slow diffusion within the vascular territory of the\nleft middle cerebral artery with narrowing of the left lateral ventricle and 3\nmm left to right midline shift.  The basilar cisterns are patent.  There is\nsubtle low signal intensity on gradient recalled echo images within the region\nof the left precentral gyrus and superior parietal lobule (series 7, image 17)\nthat likely reflects early petechial hemorrhagic transformation.  Linear\nblooming on gradient recalled echo images within the left M1 and M2 segments\nis consistent with thrombus.\n\nSmall areas of hyperintense signal on T2/FLAIR within the subcortical and\nperiventricular white matter are nonspecific, but likely sequela of mild\nchronic small vessel disease.\n\nThe orbits are grossly unremarkable.",
            "output": "Left MCA occlusion with a large acute to subacute infarct.  The infarct\nextends to involve the medial cortex of the left frontal lobe which may\nindicate an associated ACA infarct.  Subtle low signal intensity on gradient\nrecalled echo images likely reflects early petechial hemorrhagic\ntransformation."
        },
        {
            "input": "There is re-demonstration of a now subacute infarction involving the left\nmiddle cerebral artery and left anterior cerebral artery territories, overall\nsimilar in extent as compared to the prior examination dated ___,\nthough with increased edema and mass effect.  There is increased partial\neffacement of the left lateral ventricle and increased rightward shift of\nmidline structures, 7 mm compared to 3 mm previously.  There is partial\neffacement of the perimesencephalic cisterns without frank uncal herniation.\n\nGyriform T1 hyperintensity in infarcted territory is consistent with\npseudolaminar necrosis.  T1 hyperintensity is also seen in the left basal\nganglia.  Though there is no associated low signal on gradient echo images,\nsubacute blood products cannot be excluded.  There are lines of low signal in\nthe distal left sylvian fissure on gradient echo images, suggesting thrombosis\nor slow flow in left MCA branches, unchanged.\n\nMild T2 hyperintensity along the right lateral ventricle, as well as foci of\nT2 hyperintensity in the deep and subcortical white matter of the right\ncerebral hemisphere, are again seen, nonspecific but likely sequela of chronic\nsmall vessel ischemic disease in this age group.\n\nThere is mild mucosal thickening involving the bilateral ethmoid air cells.",
            "output": "1. Evolving large left MCA and left ACA territory subacute infarction with\nincreased partial effacement of the left lateral ventricle and increased\nrightward shift of midline structures compared to ___.  Partial\neffacement of the perimesencephalic cisterns without uncal herniation.\n2. Extensive gyriform T1 hyperintensity in the infarcted territory is\nconsistent with pseudolaminar necrosis.  Additional T1 hyperintensity in the\nleft basal ganglia, without corresponding signal abnormality on gradient echo\nimages, may represent subacute hemorrhage versus mineralization.\n3. Lines of low signal in the distal left sylvian fissure on gradient echo\nimages suggest thrombosis or slow flow in the left MCA branches, unchanged.\n\nRECOMMENDATION(S):  Noncontrast head CT to better assess for intracranial\nhemorrhage.\n\nNOTIFICATION:  The preliminary interpretation, which stated that there was\nhemorrhagic transformation of the left-sided infarction, was discussed with\n___, M.D. by ___, M.D. on the telephone on ___ at\n10:28 pm, 2 minutes after discovery of the findings.\n\nThe final interpretation and the recommendation for head CT scratch were\ndiscussed with ___, M.D. by ___, M.D. on the telephone on\n___ at 12:39 pm, 20 minutes after discovery of the findings."
        },
        {
            "input": "Interval evolution of large left hemispheric predominantly MCA distribution\ninfarct, with small component ACA distribution, with extension into the basal\nganglia.  Interval volume loss.  Previously seen midline shift has resolved. \nSmall area of mineralization or hemorrhage at the left vertex, stable since\nprior.  The areas of cortical laminar necrosis.  Again seen is mineralization\nin the left basal ganglia.  Susceptibility vessel sign in the left MCA M2, M3\nbranches, consistent with vessel thrombosis, also seen on prior.  Interval\nvolume loss left midbrain, pons.\n\nThere is no evidence of hematoma, masses, midline shift or new infarction.  No\nhydrocephalus.  Minimal paranasal sinuses.  Patent mastoid air cells.  Loss of\nflow void in the left ICA is similar to prior consistent with occlusion. \nPreserved flow voids in the posterior circulation and the right ICA system. \nMild chronic small vessel ischemic changes elsewhere.",
            "output": "1. Large left MCA, ACA infarct from left ICA occlusion is in late subacute\nphase, with areas of mineralization and/or microhemorrhage.  Resolved midline\nshift.  No hematoma.  Parenchymal atrophy left brainstem."
        },
        {
            "input": "The patient is status post partial embolization of a left temporal lobe AVM.\nCentered in the lower aspect of the left temporal lobe is a tubular and\nspeckled enhancement with associated tubular hypodensities, slightly less\nprominent when compared to prior exam, clear representing a combination of\nresidual nidus and post embolization sequela. Previously seen hemorrhage in\nthe left temporal lobe measuring up to 1.7 cm, has resolved.\n\nNo other lesions are noted.  Sulci, ventricles and cisterns are within\nexpected limits allowing for mild sulcal effacement in the region of the\nlesion.  The paranasal sinuses are clear. The orbits are unremarkable. The\nmastoid air cells are clear.",
            "output": "The patient is status post partial embolization of the left temporal lobe AVM.\nThere remains a enhancing nidus, less prominent when compared to prior exam.\nPreviously seen left temporal lobe hemorrhage has resolved. ."
        },
        {
            "input": "MRI Brain:\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.  The paranasal sinuses are clear.  The orbits are\nunremarkable.  The mastoid air cells are clear.\n\nMRA brain:  1 mm superiorly oriented left proximal M1 segment outpouching is\nidentified (series 4, image 54), which appears to be an infundibulum on\npostcontrast MRA images of the neck.  There is fetal type origin of the right\nposterior cerebral artery.  Otherwise, the intracranial vertebral and internal\ncarotid arteries and their major branches appear normal without evidence of\nstenosis, occlusion, or aneurysm formation.\n\nMRA neck:  The common, internal and external carotid arteries appear normal. \nThere is no evidence of internal carotid artery stenosis by NASCET criteria. \nThe origins of the great vessels, subclavian and vertebral arteries appear\nnormal bilaterally.",
            "output": "1.  No acute infarct or hemorrhage.\n2.  A 1 mm superiorly oriented left proximal M1 segment outpouching, most\nlikely an infundibulum on postcontrast MRA sequences of the neck, otherwise,\nunremarkable MRA of the neck."
        },
        {
            "input": "Images through the internal auditory canal demonstrates symmetric appearance\nof the seventh eighth nerve complexes.  There is no evidence of abnormal\nenhancement or mass lesion within the internal auditory canals,\ncerebellopontine angles or membranous labyrinth.\n\nThere is slight relative thinning of the cisternal segment of the left\ntrigeminal nerve.  There is a small vessel abutting the lateral aspect of the\nleft trigeminal nerve root entry zone, of uncertain clinical significance.  No\nother mass lesions are seen within the posterior fossa.\n\nLimited included imaging of the remainder of the brain demonstrates no\nevidence of hemorrhage, edema, masses, mass effect, midline shift\norinfarction.  There is a small left parietal DVA.  The ventricles and sulci\nare normal in caliber and configuration. There is no abnormal enhancement\nafter contrast administration.\n\nNo osseous abnormalities are seen. The paranasal sinuses, mastoid air cells,\nand middle ear cavitiesare clear. The orbits are unremarkable. The visualized\nportion of the principle vascular flow voids are preserved.",
            "output": "1. No evidence of IAC or cerebellopontine angle mass.\n2. Slight relative thinning of the cisternal segment of the left trigeminal\nnerve, nonspecific but may relate to a long-standing history of left\ntrigeminal neuralgia.\n3. A small vessel abuts the lateral aspect of the left trigeminal nerve root\nentry zone, of uncertain clinical significance.\n4. No acute infarction or intracranial hemorrhage."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  There are nonspecific bilateral supratentorial T2/FLAIR white\nmatter hyperintensities, which may represent the sequelae of chronic\nmicroangiopathy.  The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.\n\nThere is mild mucosal thickening in the ethmoid air cells and maxillary\nsinuses.  There is a trace of fluid in left mastoid air cells.  Left-sided\nantrostomy and turbinatectomy noted.",
            "output": "1. No acute intracranial abnormality is identified.\n2. Nonspecific bilateral supratentorial T2/FLAIR white matter\nhyperintensities, which may represent early changes of chronic\nmicroangiopathy.\n3. No enhancing brain lesions."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.  Patent dural venous sinuses.\n\nThere is expanded partially empty sella turcica.  There are bilateral focal\nluminal narrowing at sigmoid and transverse sinuses junction (series 100,\nimage 138).  Mild expansion of bilateral perioptic nerves sheath CSF space. \nNo cerebellar tonsillar herniation.  Described appearance suggestive of\nidiopathic increased intracranial pressure.\n\nBoth orbits otherwise are unremarkable.  Mild mucosal thickening involving\nparanasal sinuses.  Mastoid air cells are essentially clear.",
            "output": "1. No acute intracranial abnormality or abnormal intracranial enhancement\nincluding brainstem structures.\n2. Expanded partially empty sella turcica, bilateral focal luminal narrowing\nat sigmoid/transverse dural venous sinus junction and mild prominence of\nbilateral perioptic nerve sheath CSF space may suggest idiopathic \nintracranial hypertension."
        },
        {
            "input": "There is no acute intracranial infarct, hemorrhage or mass.  Prominence of the\nventricles and the sulci are likely due to involutional changes. \nPeriventricular, and subcortical T2/FLAIR hyper intensities are nonspecific\nbut likely due to small vessel ischemic disease.  Previously described cystic\nexpansion of the spinal cord is again seen.  The foramen of Magendi is patent\nand there is no hydrocephalus.  The craniocervical cystic expansion measures\napproximately 1.5 x 1.7 cm in axial ___ and 1.9 cm in craniocaudal\ndimension, with approximately 1.4 cm of no significant expansion followed by\n2.5 cm of cystic expansion spanning lower C2 and C3.  The surrounding spinal\ncord demonstrates postcontrast enhancement.  There is anterior spinal canal\nnarrowing, indenting the thecal sac at C3-4 due to posterior osteophytosis,\nwhich also narrows the cystic lesion at that level.\nThe paranasal sinuses and the mastoid air cells are clear.",
            "output": "1. Cystic expansion of the craniocervical and upper cervical spinal cord with\npostcontrast enhancement.  Differentials include spinal cord glioma and\nhemangioma, as well as metastatic disease.  MRI of the cervical, thoracic and\nlumbar spine is recommended for complete evaluation.\n\n2. Spinal canal narrowing at C3-4 due to posterior osteophyte, indenting the\nthecal sac and narrowing the cystic expansion of the cord.\n\nRECOMMENDATION(S):  MRI of the cervical, thoracic and lumbar spine is\nrecommended for complete evaluation.\n\nNOTIFICATION:  The findings were discussed with ___, M.D. by\n___, M.D. on the telephone on ___ at 6:03 ___, 10 minutes after\ndiscovery of the findings."
        },
        {
            "input": "Small area of linear and nodular enhancement in the subarachnoid space at\ninferior left central and inferior postcentral sulcus, left frontal operculum.\nGiven patient history, findings are most consistent with meningitis.  There is\nno evidence of hemorrhage on today's MRI or CT ___ in this area.. \nNo definite evidence of adjacent cortical diffusion abnormality, edema or\nenhancement, or hippocampal edema to suggest infection extension or postictal\nchange.  There is mild ventricular prominence, similar to prior.  Linear areas\nof mild periventricular T2 signal abnormality abutting lateral ventricles,\ncorresponding to low-attenuation changes on prior CT, may represent sequela of\nmild chronic small vessel ischemic changes, component of mild periventricular\nedema cannot be excluded.  No evidence of ventriculitis.  There is no\nrestricted diffusion within ventricular system.  There is no abnormal\npachymeningeal enhancement.\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  There is mild paranasal sinus disease, with areas of\nsecretions within the sphenoid sinus, similar, suggestive of acute sinusitis. \nClear mastoid air cells.  Dural venous sinuses are patent.  Intracranial\nvascular flow voids are preserved.",
            "output": "1. Small areas of leptomeningeal enhancement, most consistent with meningitis\ngiven patient history.  Other etiologies, including inflammatory or neoplastic\nprocess could have similar appearance.\n2. No evidence of subarachnoid hemorrhage on MRI or CT.\n3. Stable, borderline ventricular size.  Linear linear periventricular T2\nsignal abnormality, likely represents mild chronic small vessel ischemic\nchanges, component of mild periventricular edema cannot be excluded.  No\nventriculitis.\n4. Paranasal sinusitis.\n\nNOTIFICATION:  The findings were discussed with ___ , M.D.\nby ___, M.D. on the telephone on ___ at 10:54, 20 minutes\nafter discovery of the findings."
        },
        {
            "input": "Again seen is a right cerebellar mass with surrounding edema and minimal\ndeformity of the inferior fourth ventricle.  The mass enhances avidly after\ncontrast administration and extends to the subarachnoid space surrounding the\nright cerebellum.  The mass measures approximately 31 mm in maximum dimension.\nOverall, these findings strongly suggest a metastasis with leptomeningeal\nspread of tumor.\nNo other masses are identified.  There is no evidence of hemorrhage or\ninfarction.  The third and lateral ventricles appear normal in caliber and\nconfiguration.",
            "output": "1. 31 mm right cerebellar hemisphere enhancing mass with surrounding edema and\nleptomeningeal spread of tumor.\n2. Mild deformity of the inferior fourth ventricle without hydrocephalus."
        },
        {
            "input": "The patient's previously noted right cerebral mass is again seen.  Adjacent\nextensive area of leptomeningeal enhancement.  Findings most consistent with\nmetastasis.  Other etiologies, including infection/inflammatory process is\nless likely.  Mild local mass effect.\n\nFourth ventricle is patent.  No hydrocephalus.  Preserved pre pontine cistern,\nforamen magnum.  Local mass effect and mild effacement of the right transverse\nsinus.  Small short-segment filling defect in the superior margin right\ntransverse sinus likely represents arachnoid granulation.\n\nNo other masses.",
            "output": "1. Stable right cerebellar mass most consistent with metastasis with adjacent\nleptomeningeal disease.  Inflammatory/infectious process is less likely."
        },
        {
            "input": "Postoperative changes status post right suboccipital craniotomy for right\ncerebellar tumor resection.  A small amount of intrinsic T1 hyperintensity\nwithin the resection bed is compatible subacute blood products. There is\nexpected postoperative thin peripheral high signal on diffusion weighted\nimaging.  The amount of peripheral FLAIR signal abnormality is slightly\ndecreased from ___.  Enhancement along the lateral greater than\nmedial aspects of the resection bed is compatible with residual leptomeningeal\ndisease.  There is mild postoperative dural thickening/enhancement underlying\nthe craniotomy site.  The resection bed abuts the right transverse sinus\nwithout definite evidence of dural venous sinus invasion.\n\nNo acute infarction.  The ventricles and sulci are normal in caliber and\nconfiguration.\n\n The major intracranial vascular flow voids are maintained.  There is a trace\namount of fluid within the bilateral mastoid air cells.  The paranasal sinuses\nand orbits are normal.  FLAIR hyperintensity within the bilateral temporalis\nmuscles is nonspecific and possibly artifactual.",
            "output": "1. Status post right suboccipital craniotomy for right cerebellar tumor\nresection with residual enhancement along the lateral greater than medial\naspect of the resection bed is compatible with residual leptomeningeal\ndisease."
        },
        {
            "input": "Diffusion-weighted images demonstrate a small focus of hyperintense signal in\nthe right posterior mid brain (image 13 of series 6) that is likely due to\nartifact associated with adjacent hemorrhage.\n\nGradient recalled echo images demonstrate multiple diffusely scattered rounded\nareas of hypointense signal in the bilateral cerebral and cerebellar\nhemispheres.  More focal rounded areas of GRE hypointense signal in the left\nparietal lobe, right pons, and medulla are hypointense were hyperintense on T1\nweighted images, reflecting hemorrhage.\n\nPostcontrast images demonstrate areas of enhancement in the left parietal lobe\ncorresponding to the site of hemorrhage.  There is also a small focus of\nenhancement in the right parietal lobe corresponding to an additional area of\nGRE hypointensity.\n\nThe constellation of findings may represent multiple cavernous malformations\ngiven the areas of GRE hypointensity are of varying sizes and in a seemingly\nrandom distribution.  Additionally, postcontrast images demonstrate rounded\nareas of contrast accumulation which are favored to represent draining venous\ncomplexes.  Alternately, cerebral amyloid angiopathy is a consideration for\nthe majority of the lesions, however this would not explain the bilateral\nparietal lesions that include hyperintensity on the T1 weighted images.\nThe patient's age is considerably younger than the typical amyloid angiopathy\npatient.\nThe major intracranial arterial flow voids are preserved.  The dural venous\nsinuses are patent.\n\nProminence of the ventricles and sulci is suggestive of involutional changes. \nThere is no mass effect or midline shift.\n\nThere is mild to moderate mucosal thickening of the ethmoid sinuses and left\ngreater than right maxillary sinuses. The intraorbital contents are\nunremarkable.",
            "output": "1. Redemonstration of left parietal, right pons, and medulla intraparenchymal\nhemorrhage, not substantially changed compared to recent CT.\n2. The constellation of findings throughout the brain are favored to be due to\nmultiple cavernous malformations, especially given the varying sizes and\nrandom distribution and post-contrast appearance.  The alternative is a\ncombination of several cavernous malformations as well as cerebral amyloid\nangiopathy.\n3. Mild cerebral atrophy.\n4. Paranasal sinus disease as described above."
        },
        {
            "input": "Again seen are innumerable white matter hyperintensities on FLAIR imaging\ncompatible with a history of multiple sclerosis.  No new lesions are\nidentified.  No areas demonstrate abnormal slow diffusion.\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal for age in caliber and\nconfiguration.",
            "output": "1. No change in multiple white matter lesions compatible with multiple\nsclerosis.\n2. No evidence of new lesions."
        },
        {
            "input": "Numerous areas of nonenhancing periventricular, subcortical and deep white\nmatter T2/FLAIR hyperintense lesions with additional involvement of the left\ncerebral peduncle are unchanged compared the prior examination.  There is no\ndefinite new lesion nor is there associated enhancement.  Many of these\nlesions demonstrate T1 hypo intensity.\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.  There is no abnormal focus of slowed diffusion.  The\nprincipal intracranial vascular flow voids are preserved.\n\nThe paranasal sinuses are grossly clear.  The orbits are grossly unremarkable.\nMildly expansile 14 x 4 mm nonenhancing T1 and T2 hyperintense lesion within\nthe right temporal calvarium is unchanged (14:9)",
            "output": "1. Stable numerous nonenhancing white matter lesions, compatible with given\nhistory of multiple sclerosis.\n2. No definite new lesion or enhancing lesion.\n3. Stable right temporal calvarial lesion, nonspecific, which may represent\nhemangioma or dermoid."
        },
        {
            "input": "The study is degraded by motion artifact.\n\nNumerous bilateral punctate supra and infratentorial acute infarctions.  There\nis a single focus right parietal micro bleed best seen on image 14 of series\n12.  This does not correspond to an area of infarction demonstrated on the\ndiffusion images and is likely chronic\n\n\nNo intracranial masses.  Generalized cerebral atrophy with ex vacuo dilatation\nof the ventricular system.  Moderate severe periventricular deep as well as\npontine white matter T2 and FLAIR hyperintense changes are most likely sequela\nof microangiopathy.  The intracranial arteries demonstrate normal T2 flow\nvoids.  Calcification present in the right globe which appear similar compared\nto prior study.  The paranasal sinuses are essentially clear.  The\ncraniocervical junction appears normal.",
            "output": "Numerous bilateral punctate supra and infratentorial acute infarcts are most\nlikely embolic in nature.\nThere is a single chronic-appearing microhemorrhage.\n\nGeneralized cerebral atrophy with moderate to severe white matter\nmicroangiopathic changes.\n\nNOTIFICATION:  The findings were discussed by Dr. ___ with\nDr. ___ on the ___ ___ at 1:36 pm, 10 minutes after\ndiscovery of the findings."
        },
        {
            "input": "Again seen is a left thalamic hematoma, unchanged since the prior head CT.  As\nbefore, there is intraventricular extension into the left lateral ventricle.\nOn pre-contrast images there is scant hyperintensity around the periphery\nhowever there appears to be more peripheral hyperintensity on post-contrast\nimages suggesting some degree of enhancement. There is no definite evidence of\na feeding or draining vein to suggest an arteriovenous malformation.  There is\nsubstantial edema surrounding the hematoma.  There is minimal associated mass\neffect. There are no new areas of hemorrhage. There is a degree of\nsubarachnoid hemorrhage in the right occipital lobe (9:9).\nAlthough a faint peripheral enhancement and edema arise in reaction to a\nhematoma, this usually requires several days.  This study is true 24 hours of\nthe hematoma, the level of enhancement and edema are worrisome for and\nunderlying lesion, rather than a simple hypertensive hematoma.\n\nVentricles and sulci are unchanged in size or configuration than are\nappropriate for the patient's age. No evidence of hydrocephalus.  Few foci of\nperiventricular and subcortical white matter hyperintensity are nonspecific\nbut may reflect sequelae of chronic small vessel ischemic disease. Major T2\nflow voids are preserved.  The dural venous sinuses appear patent. Visualized\nparanasal sinuses unremarkable.  The visualized orbits are unremarkable.",
            "output": "1. Left thalamic hematoma with infra ventricular rupture appears similar to\nthe prior head CT.\n2. Faint enhancement and substantial surrounding edema seem greater than\nexpected within 24 hours of the initial bleeding.  These findings raise a\nconcern of an underlying lesion as the etiology.  The alternative would be\nmore than a single episode of hemorrhage.  Please note that evaluation is\nsomewhat limited as no T1 pre contrast images were obtained.\n3. No evidence of hydrocephalus."
        },
        {
            "input": "The left thalamic signal abnormality is consistent with late subacute/chronic\nhemorrhage measuring 24 x 11 mm which has considerably decreased compared to\nthe MRI of ___ when it measured 27 x 19 mm. The central high\nintensity on T1 and T2 weighted images indicates late subacute hemorrhage in\nthe surrounding rim of low signal with blooming on the susceptibility images\nis suggestive of hemosiderin deposition.  The hemosiderin rim is un\ninterrupted, a feature usually seen in hemorrhages without underlying\nmalignant lesion.  Otherwise the examination is unchanged with mild changes of\nsmall vessel disease.  There is no midline shift or hydrocephalus..",
            "output": "Decrease in size of left thalamic hemorrhage with the appearance suggestive of\na late subacute/chronic hematoma."
        },
        {
            "input": "There has been interval decrease in size of the left thalamic parenchymal\nhemorrhage.  It now measures approximately 1.5 x 0.7 cm, previously 2.0 by 1.1\ncm in ___.  Though there are several areas of subtle intrinsic T1\nhyperintensity both centrally and at the periphery of this hemorrhage, there\nis also possible superimposed focus of enhancement measuring 5 x 3 mm at the\nposterior margin of the hematoma in the subependymal region (17:91).\n\nScattered periventricular and subcortical white matter T2/FLAIR\nhyperintensities are similar to prior similar in distribution and appearance\nwhen compared to prior.  There is no acute infarct.  No mass effect.  Besides\nwhere detail the above, no abnormal parenchymal or meningeal enhancement. \nThere is no intracranial mass, mass effect, or midline shift. Ventricles and\nsulci are age-appropriate.  Major intravascular flow voids are preserved.\n\nMucosal thickening is noted within the ethmoid air cells.",
            "output": "Continued interval decrease in size of the left thalamic hemorrhage. \nIntrinsic T1 hyperintensity with suspected area of enhancement at the\nposterior margin of the hematoma, potentially related to the hemorrhage though\ncontinued follow-up suggested in several months to ensure expected\ndecrease/resolution."
        },
        {
            "input": "Further slight decrease in size of the left thalamic hemorrhage now measuring\n13.9 x 5.9 mm from previously 15 x 7.4 mm. There is no abnormal enhancement\nafter contrast administration.\n\nScattered T2/FLAIR hyperintensities along the periventricular white matter are\nnonspecific but unchanged from prior and most likely represent chronic small\nvessel ischemic changes.\n\nThere is no evidence of new hemorrhage, edema, masses, mass effect, midline\nshift or acute infarction. The ventricles and sulci are normal in caliber and\nconfiguration for patient's age.",
            "output": "1. Further slight decrease in size of the left thalamic hemorrhage.  No\nabnormal contrast enhancement identified."
        },
        {
            "input": "Postsurgical changes are again demonstrated from right temporoparietal\ncraniotomy and tumor resection.  Enhancement at the surgical site appears\nthicker and more nodular than on the most recent previous examination, and\nthere has been prominent increase in the degree of nodular enhancement and\nFLAIR hyperintensity in the CSF spaces including along the margin of the\ninferior thalamus, right cerebral peduncle, quadrigeminal plate cistern,\nadjacent to the tectum, and now also seen along left-sided parietal sulci and\noverlying the left lateral cerebellar hemisphere as well as a focus of nodular\nenhancement along the cisternal segment of the right trigeminal nerve.  On the\nFLAIR sequence, these findings are more extensive, with suggestion of\nleptomeningeal disease, bilateral sylvian fissures, and temporoparietal sulci.\nNew enhancing nodules along the left thalamus.\n\nFLAIR hyperintensity in the right temporal lobe and periatrial white matter is\nsimilar in extent compared to the most recent previous exam.\n\nStable ventricular configuration with no evidence of worsening hydrocephalus.\n\nScattered areas of susceptibility likely reflecting chronic microhemorrhage\nagain noted without change.  Stable to decreased in extra-axial fluid\ncollection subjacent to the craniotomy site with no significant mass effect.\n\nThe major intracranial vascular flow voids are preserved.  Orbits are\nunremarkable.",
            "output": "1. Worsened FLAIR hyperintensity and enhancement in the basilar cisterns and\nCSF spaces, now also including areas overlying the left parietal lobe, left\nlateral cerebellum, and the right trigeminal nerve cisternal segment, with\nsuggestion of leptomeningeal disease overlying the bilateral sylvian fissures\nand temporoparietal region and new enhancing nodules along the left thalamus. \nThis is worrisome for worsening disease dissemination in the CSF spaces.\n2. Nodular enhancement at the surgical site also appears slightly increased\nalthough the surrounding FLAIR hyperintensity is stable.\n\nNOTIFICATION:  The impression and recommendation above was entered by Dr. ___\n___ on ___ at 11:39 into the Department of Radiology critical\ncommunications system for direct communication to the referring provider."
        },
        {
            "input": "In comparison with the most recent examination dated ___, again\npostsurgical changes are seen consistent with right temporoparietal craniotomy\nfor tumor resection, right frontal burr hole remains unchanged with Ommaya\nreservoir in place, the ventricular catheter terminates in the inferior aspect\nof the left lateral ventricle.  The previously described pattern of\nenhancement in the basilar cisterns and CSF spaces appears more conspicuous\nand worsened since the most recent exam, with increased signal in the folia as\ndetected on FLAIR (series 15, images 5 and 6), and multiple foci of increased\nenhancement  in the supravermian cistern, as well as perimesencephalic\ncisterns, persistent pattern of enhancement along the cisternal segment of the\nright trigeminal nerve (17:53), suggesting worsened neoplastic disease\ndissemination in the CSF spaces.  Overall multiple infra and supratentorial\nenhancing lesions appear larger, for example:\n\nIn the posterior fossa there is a larger focus of enhancement measuring\napproximately 4 mm above the right cerebellar tonsil (17:47).\n\nMore superiorly foci of enhancement adjacent to the cerebellar nodule and in\nthe area of the fourth ventricle are also more conspicuous measuring\napproximately 5.8 mm, foci of enhancement in the lateral aspect of the pons\nappears slightly larger (17:62).\n\nFocus of enhancement in the right temporal fossa measures approximately 6.8 mm\nand previously 2 mm (17:59).\n\nSmall focus of enhancement adjacent to the cortex of the air right frontal\nlobe measuring approximately 2 x 2 mm in transverse dimension is slightly more\nconspicuous (17:105).\n\nAt the level of the thalamus, there are larger areas of enhancement involving\nthe left pulvinar, measuring approximately 15 x 10 mm and previously 4 x 6 mm\n(17:86), more medially towards the subependymal region at the level of the\nthird ventricle larger lesions measuring up to 3 x 5 mm in transverse\ndimension (17:90).\n\nNew focus of enhancement is identified posterior to the corpus callosum\ntowards the left centrum semiovale measuring approximately 9 x 5 mm in\ntransverse dimension (17:112).\n\nNo diffusion abnormalities are detected to indicate acute or subacute ischemic\nchanges.  The major vascular flow voids are present and demonstrate normal\ndistribution.  The orbits are unremarkable, the middle ear cavities and\nmastoid air cells are clear.",
            "output": "1.  In comparison with the most recent MRI examination dated ___,\nthere is interval progression, and worsened pattern of enhancement in the\nbasilar cisterns, and increased in size and more conspicuous multiple infra\nand supratentorial focal areas of enhancement, suggesting neoplastic disease\nprogression.\n\n2. Persistent pattern of enhancement along the cisternal segment of the right\ntrigeminal nerve.\n\n3.  On FLAIR sequences, there is increased enhancement in the cerebellar\nfolia, and perimesencephalic cisterns, concerning for worsened neoplastic\ndisease dissemination in the CSF spaces.\n\n4.  No diffusion abnormalities are detected."
        },
        {
            "input": "Patient is status post right parietal craniotomy for tumor resection. \nCompared to the most recent prior study from ___, there is continued\ndecreased linear enhancement along the right temporoparietal surgical tract\nand with interval decrease in enhancement along the posterior aspect of the\nleft thalamus, with possible punctate focus of residual enhancement (14:81).\n\nThere is continued decreased enhancement of multiple metastatic lesions\npreviously noted on the study from ___, for example a right posterior\ncerebral peduncle lesion (14; 72) with persistent increased FLAIR hyperintense\nsignal (137:10) and left foramen of Luschka lesion (187:6)..\n\nBilateral subependymal FLAIR hyperintense signal is similar to the prior study\nalong the frontal horns of the lateral ventricles as well as bilateral centrum\nsemiovale.\n\nRight frontal approach ventriculostomy catheter is again seen with tip\nterminating in the left lateral ventricle.\n\nThere is no evidence of acute infarction.  There is redemonstration of\nmultifocal gradient echo susceptibility blooming artifacts compatible with\nmicrohemorrhages, similar to prior.  There is cavum septum pellucidum.  The\nventricles and sulci are normal in caliber and configuration.  The major\nintracranial flow voids are preserved.  Dural venous sinuses appear patent. \nParanasal sinuses are essentially clear.  The orbits appear unremarkable.",
            "output": "1. There is continued decreased enhancement along the right temporoparietal\nsurgical tract and posterior to the left thalamus as well as in multiple\npreviously seen foci of enhancement including focus in the right posterior\ncerebellar peduncle, but with continued persistent focal increased FLAIR\nhyperintense signal of these lesions, attention on follow-up.\n2. There is no acute infarct or new intracranial hemorrhage.  No new\nenhancement.\n3. Additional findings as described above."
        },
        {
            "input": "When compared to prior examination, there is resolution of diffuse\nleptomeningeal enhancement, including the trigeminal nerves and seventh eighth\ncranial nerve complexes.  There remains linear enhancement along the right\ntemporoparietal surgical tract and along the posterior edge of the left\nthalamus although the degree of enhancement is significantly decreased. \nSubependymal enhancement of the left thalamic pulvinar has resolved.  There is\nsignificantly decreased leptomeningeal FLAIR hyperintense signal.\n\nHowever, bilateral subependymal FLAIR hyperintense signal appears slightly\nmore conspicuous and thickened when compared to prior exam particularly along\nthe frontal horns of the lateral ventricles.  In addition, there are regions\nof FLAIR hyperintense signal which are more conspicuous when compared to the\nprior exam, for example: Right posterior cerebral peduncle (series 8, image\n10), left posterior hippocampus (series 8, image 10), left foramen of Luschka\n(series 8, image 6), bilateral centrum semiovale (series 8, image 17).\n\nA right frontal approach ventriculostomy catheter with tip terminating in the\nleft lateral ventricle is unchanged.\n\nThere is no evidence of acute infarct.  Multifocal gradient echo\nsusceptibility blooming artifact compatible with microhemorrhages are\nunchanged from prior exam.  The major intracranial flow voids are preserved. \nThe dural venous sinuses are patent.  The paranasal sinuses are essentially\nclear.  The orbits are unremarkable.  Trace fluid signal is seen in the\nmastoid air cells.",
            "output": "1. Resolution of diffuse leptomeningeal enhancement including involvement of\nthe trigeminal nerves and seventy-eighth cranial nerve complexes.  Significant\ndecreased leptomeningeal FLAIR hyperintense signal although there remains\nprominent FLAIR signal abnormality involving the cerebellum.\n2. There is residual enhancement along the right temporoparietal surgical\ntract and along the posterior left thalamus.\n3. Although leptomeningeal enhancement and FLAIR hyperintense signal has\nimproved, there are regions of increased subependymal FLAIR signal abnormality\ninvolving the frontal horns of the lateral ventricles and nodular FLAIR\nhyperintense signal of the right midbrain, left hippocampus, left cerebellum\nand bilateral centrum semiovale.  Close attention on follow-up is recommended\nto these regions.\n4. Additional findings as described above."
        },
        {
            "input": "Study is degraded by motion.  Within these confines:\n\nGrossly stable postsurgical changes related to right parietal craniotomy and\nmass resection are again noted.  Grossly stable T2 and FLAIR hyperintensity\nadjacent to the surgical bed and extending along the right lateral ventricle\nis grossly unchanged.  Grossly stable linear enhancement along the surgical\ntract is again noted.  Grossly stable right frontal approach ventriculostomy\ncatheter with tip in region of left lateral ventricle anterior horn with\nprobable Ommaya reservoir is again seen.  Grossly stable foci of blood\nproducts versus mineralization are again noted throughout the surgical bed.\n\nThere has been interval progression of left temporal T2 and FLAIR hyperintense\nenhancing lesion (see 13, 15, 19:10 on current study and 13, 18, 19:11 on\nprior study).\n\nRight cerebral peduncle T2 hyperintense nonenhancing lesion is slightly\ndecreased in size compared to prior exam (see 13, 18, 19:10 on current study\nand 13, 18, 19: 10 on prior study).\n\nNew approximately 8 mm left hippocampal body T2 and FLAIR hyperintense,\nenhancing lesion is seen with slowed diffusion (see 7, 8:12; 15, 19:9; 16:61).\n\nNew right temporal T2 and FLAIR hyperintensities are seen adjacent to interval\nprogression of enhancing lesion (see 13, 15, 19:8; 16:52 on current study and\n14:53; 19:7 on prior exam).\n\nNew Right frontal T2 and FLAIR hyperintensity without definite enhancement is\nnoted (see 13, 15, 19:13).\n\nNew right cerebellar T2 and FLAIR hyperintensity with interval progression of\nenhancement compared to ___ prior exam is noted (see 13, 15, 19:7;\n16:46 on current study and 18, 19:7; 14:47 on prior study).\n\nNew punctate left cerebellar focus of enhancement with corresponding T2 and\nFLAIR hyperintensity are noted (see 13, 15, 19:8; 16:53 on current study and\n18, 19: 8; 14:54 on prior exam).\n\nLeft cerebellar foci of T2 and FLAIR hyperintensity are again seen, now\ndemonstrating enhancement (see 13, 15, 19: ___ on current study and 18, 19:8\non prior study).\n\nThere is no evidence of midline shift or infarction.   The ventricles and\nsulci are normal in caliber and configuration.  There is no abnormal\nenhancement after contrast administration.\n\nLimited imaging of the parotid glands demonstrate bilateral subcentimeter\nnonspecific probable lymph nodes.",
            "output": "1. Study is degraded by motion.\n2. Grossly stable postsurgical changes compared to ___ prior exam.\n3. Interval new and progressed parenchymal signal intensity abnormalities,\nwith enhancement compared to ___ prior exam as described.  While\nfindings may represent treatment related effects or radiation necrosis, tumor\nprogression is not excluded on the basis examination.  Recommend attention on\nfollow-up imaging.\n\nRECOMMENDATION(S):  Interval new and progressed parenchymal signal intensity\nabnormalities, with enhancement compared to ___ prior exam as\ndescribed. While findings may represent treatment related effects or radiation\nnecrosis, tumor progression is not excluded on the basis examination.\nRecommend attention on follow-up imaging."
        },
        {
            "input": "In comparison with the most recent brain MRI examination dated ___,\nthere are new few foci of slow diffusion along the body of the corpus callosum\nand apparently in the superior aspect of the left choroid plexus (6:19, 7:18,\n19), additionally, a focal area of low attenuation is identified in the mid\naspect of the corpus callosum, better seen in the sagittal T1 weighted\nsequence (11:13), suspicious for acute/subacute ischemic changes.\n\nSimilar periventricular FLAIR hyperintensity signal is identified suggestive\nof posttreatment changes.\n\nThere is a new focus of FLAIR hyperintensity in the left postcentral central\nsulcus (15:18), with no evidence of enhancement after contrast administration,\nprobably consistent with posttreatment change, close attention in this area is\nadvised.\n\nThere is a grossly unchanged focus of T2/FLAIR hyperintensity in the right\ncerebral peduncle (15:11, 13:11).\n\nFocal areas of enhancement in the left temporal lobe appear less conspicuous\nin the current exam and remain visible on the axial FLAIR sequence (15: 10,\n11).  Focus of enhancement in the right temporal lobe appears smaller and also\nsmaller on the axial FLAIR (17:55, 15:9).\nNew focus of enhancement detected on the axial FLAIR postcontrast measuring\napproximately 9 x 7 mm (15:11).\n\nHyperintensity signal in the thalamic pulvinar more significant on the left\nremains unchanged, also slightly more conspicuous FLAIR hyperintensity signal\nin the frontal lobes, probably consistent with posttreatment changes, however\ntumoral infiltration cannot be completely rule out an attention in follow-up\nexams in this areas is recommended.\n\nPostsurgical changes consistent with right parietal craniotomy and resection\nin the right thalamic region remain grossly unchanged with similar pattern of\nenhancement along the surgical tract (16:14), no evidence of new areas of\nenhancement are seen in this region.\n\nIn the posterior fossa bilateral FLAIR hyperintense lesion at remain\nunchanged, with mild decrease in size of previously seen right cerebellar\nenhancing lesion (17:50), the previously seen focus of enhancement in the\nlateral aspect of the vermis on the left is not longer seen.\n\nMagnetic susceptibility along the surgical bed and right occipital lobe remain\ngrossly unchanged consistent with residual blood products.\n\nThere is no evidence of acute intracranial hemorrhage or shifting of the\nnormally midline structures.  Left frontal ventricular shunt appears unchanged\nentering via right frontal burr hole.\n\nThe major vascular flow voids are present demonstrate normal distribution. \nThe orbits are unremarkable, the paranasal sinuses, middle ear cavities and\nmastoid air cells are clear.",
            "output": "1.  New few foci of slow diffusion along the body of the corpus callosum and\napparently in the superior aspect of the left choroid plexus (6:19, 7:18, 19),\nadditionally, a focal area of low attenuation is identified in the mid aspect\nof the corpus callosum, better seen in the sagittal T1 weighted sequence\n(11:13), suspicious for acute/subacute ischemic changes, and less-likely\ntumoral infiltration since there is no evidence of enhancement after contrast\nadministration in this areas.\n\n2.   Similar periventricular FLAIR hyperintensity signal is identified\nsuggestive of postt"
        },
        {
            "input": "Stable redemonstration of postsurgical changes related to right parietal\ncraniotomy for the resection of the underlying mass, with grossly unchanged\nT2/FLAIR hyperintensity surrounding the surgical cavity, and extending into\nthe right lateral ventricle.  There is no abnormal enhancement adjacent to the\nsurgical bed to suggest recurrence in this region.  Similarly, there is stable\nT2/FLAIR hyperintensity in the periventricular region compatible with\nposttreatment changes.\n\nStable foci of slow diffusion along the body of the corpus callosum suggestive\nof evolution of subacute infarct.  Subacute infarct involving the right\nthalamus appears new (7; 12).\n\nThere is interval increase in size of the pre-existing enhancing FLAIR\nhyperintense lesion at the anterior pole of the right temporal lobe, measuring\n15 mm x 15 mm x 15 mm (20:83, 15:10), with new enhancement.\n\nAdditionally, when compared to MRI of ___, there is increased\nenhancement and FLAIR signal intensity of the lesions in the left pulvinar\n(20:92, 15:12), left inferior frontal lobe (20:83, 15:10), right inferior\nfrontal lobe (20:97, 15:13), within the left parietooccipital sulcus (20:126,\n15:17), left hippocampal body (20:74, 15:9).\n\nSimilarly, there is diffuse interval increase of FLAIR hyperintense lesions in\nthe bilateral supratentorial brain and posterior fossa.  For instance,\ninterval increase in FLAIR hyperintensity lesions are noted in the left\ncerebellar, although none of this lesion demonstrates enhancement.  Increased\nFLAIR hyperintensity is also demonstrated along bilateral medial frontal\nlobes, left greater than right with extension into the genu of the corpus\ncallosum (15:13).\n\nStable position of the right frontal approach ventriculostomy catheter with\nthe tip terminating in the left anterior horn of the lateral ventricle.\n\nStable scattered susceptibility throughout the surgical bed, likely reflecting\npostsurgical changes.\n\nThere is no evidence of a large intracranial hemorrhage, mass effect, midline\nshift or new infarction.  The ventricles and sulci are stable in caliber and\nconfiguration.  The paranasal sinuses and mastoid air cells are clear.  The\nglobes and orbits are unremarkable.",
            "output": "1. When compared to MRI of ___, there have been interval increase of\nhyperenhancing lesions with associated FLAIR signal intensity, such as in the\nleft pulvinar, bilateral inferior frontal lobes, anterior pole of the right\ntemporal lobe, and left hippocampal body.  Similarly, there is diffuse\ninterval increase of non-enhancing FLAIR hyperintense lesions in the\nsupratentorial and infratentorial brain.  These findings are worrisome for\nprogression of disease.\n2. Continued evolution of subacute infarct along the body of the corpus\ncallosum.  Subacute infarct in the right thalamus appears new.\n3. Stable postsurgical changes of right parietal craniotomy without\nenhancement in the surgical bed to suggest local recurrence.\n4. Stable position of the right frontal approach ventriculostomy catheter\n5. Additional findings as described above.\n\nNOTIFICATION:  The impression and recommendation above was entered by Dr.\n___ on ___ at 15:23 into the Department of Radiology critical\ncommunications system for direct communication to the referring provider."
        },
        {
            "input": "Some of the images are limited by motion artifact.\n\nThe patient is status post right parietal craniotomy with postoperative\nchanges, including local pachymeningeal thickening and chronic blood products\nnear the surgical bed.\n\nThere is significant interval increase in size of multiple (about 30)\nsupratentorial and infratentorial, intra-axial and leptomeningeal enhancing\nlesions and, some of which demonstrate restricted diffusion for example; the\nleft frontal basal region measuring now 19 x 14 mm and previously about than 8\nx 4 mm.  Also there is interval increase of surrounding T2 FLAIR abnormality. \nThe ventricular system are stable in size without hydrocephalus.  There is no\nshift of midline structures.\n\nNo evidence for an acute infarction.  Expected evolution of the previously\nseen tiny infarct in the right posterior thalamus compared to ___. \nDural venous sinuses appear patent on postcontrast MP RAGE images.\n\nThere is trace fluid in the left mastoid air cells.",
            "output": "Interval increase in size and surrounding T2 FLAIR abnormality of multiple\n(about 30) supratentorial and infratentorial intra-axial and leptomeningeal\nenhancing lesions, consistent with tumor progression.  No shift of midline\nstructures or herniation."
        },
        {
            "input": "Re-identified are postsurgical changes from recent right parietal craniotomy\nand resection, including calvarial defect, linear surgical approach tissue\nloss extending from the parietal craniotomy site medially to the atrium of the\nright lateral ventricle.  Small-volume blood products are seen in and\nimmediately adjacent to the resection cavity and along the surgical approach,\nas well as subjacent to the craniotomy.  Subgaleal fluid has markedly\ndecreased from the prior CT, now trace.  There is right temporoparietal\npachymeningeal thickening and enhancement, likely postsurgical.\n\nIntrinsically T1 hyperintense blood products are seen along the deep margin of\nthe surgical approach and resection site, adherent to the posterior surface of\nthe remaining right thalamic head (12:12).\n\nSurrounding this intrinsic T1 hyperintensity, is infiltrative, mass-like\nenhancing tissue (e.g., series 16, image 12), which extends inferiorly and\nposteriorly along the posterior surface of the right-more-than-left tectal\nmidbrain into the quadrigeminal cistern (series 16, image 11), as well as\nsuperomedially into the body of the right lateral ventricle (16:14), either\nrepresenting postsurgical granulation tissue or residual tumor.  There are\nareas of restricted diffusion within this area of enhancement.\n\nLateral to this, enhancement along and surrounding the linear surgical\napproach in the right temporoparietal lobe (16:13) has a similar differential.\n\nEnhancement centered primarily within the body of the right lateral ventricle\non the outside hospital MRI dated ___ is not as apparent on this\nstudy.\n\nFLAIR signal hyperintensity extends into the right aspect of the splenium of\nthe corpus callosum, and surrounds the surgical approach and resection cavity,\ninvolving the remaining posterior aspect of the right thalamus and the medial\nright occipital lobe.\n\nElsewhere, there is no evidence of infarction, new area of hemorrhage, edema,\nor mass effect.  The quadrigeminal plate cistern is effaced in filled by\nprobable residual tumor, as above; the remaining basilar cisterns are patent.\n\nThe visualized paranasal sinuses and mastoids appear clear.  Major\nintracranial vascular flow voids are preserved.  Major dural venous sinuses\nare patent.",
            "output": "1. Enhancing material at the resection site centered in the atrium of the\nright lateral ventricle and the quadrigeminal cistern along the dorsal surface\nof the midbrain tectum, extending superomedially into the body of the right\nlateral ventricle.  Additionally, there is enhancement along the linear\nsurgical approach in the right temporoparietal lobe.  Differential includes\nresidual tumor versus postoperative enhancing granulation tissue.  Delineation\nbetween these entities would be helped by confirmation of the timing of the\nprior outside hospital MRI from ___ compared with the date/time\nof surgery (e.g. immediately postoperative or several days following surgery).\nFurther evaluation with MR perfusion/spectroscopy could be performed, if\nclinically indicated.\n2. FLAIR signal abnormality is seen surrounding the surgical approach,\nresection cavity, and portions of the enhancing remaining tumor, involving the\nposterior margin of the remaining right thalamus and the medial right\noccipital lobe.\n3. Patent basal cisterns.  No midline shift.  No hydrocephalus.\n4. No evidence of infarction or new area of hemorrhage or edema"
        },
        {
            "input": "There are expected postsurgical changes from prior right temporoparietal\ncraniotomy and resection, including surgical tract through the left temporal\nlobe leading to the right thalamus at the site of the previously demonstrated\nmass.  FLAIR hyperintensity and enhancement aligning the surgical tract, as\nwell as seen posterior to midbrain tectum within the quadrigeminal plate\ncistern, and extending anterosuperiorly into the remaining medial right\nthalamus, is significantly less conspicuous, decreased in extent and\nintensity, compared with the prior exam from ___ (series 9: And\n11:11, 13, 14).\n\nThere is no new abnormal enhancement.\n\nThere is no new FLAIR hyperintense parenchymal signal or parenchymal edema.\n\nThere is no acute infarction, new unexplained area of hemorrhage, or\nextra-axial collection.\n\n The ventricles and sulci are within expected limits in caliber and\nconfiguration allowing for postsurgical findings.\n\n The visualized paranasal sinuses and mastoids appear clear.\n\n The globes and orbits are unremarkable.\n\n Major intracranial vascular flow voids are preserved.  Major dural venous\nsinuses are patent.",
            "output": "1. Interval decrease in enhancement and FLAIR hyperintense signal within and\nalong the right temporal surgical tract leading to the right thalamus, along\nwith similar signal changes within the quadrigeminal plate cistern.  This\ncould reflect resolving post-treatment changes, however a component of\nresidual tumor would be difficult to exclude.  Attention to this area on\nfollow-up.\n2. No new enhancement or FLAIR signal abnormality.\n3. No new acute intracranial abnormality."
        },
        {
            "input": "Stable postsurgical changes after right temporoparietal craniotomy for\nresection of a glioblastoma.  The surgical tract is again identified extending\nthrough the left temporal lobe to the right thalamus.  There is unchanged\nFLAIR hyperintensity and enhancement aligning the surgical tract.  There is a\nsubcentimeter enhancing nodule along the inferior right thalamus and superior\nright cerebral peduncle (series 17, image 79), which is unchanged from prior. \nPreviously noted enhancement posteriorly to the midbrain tectum and\nquadrigeminal plate cistern appears less conspicuous on today's exam.\nThere is a stable thickening and enhancement of the dura along the right\nconvexity, most likely postsurgical.\nThere is no new abnormal enhancement.  There is no new FLAIR hyperintense\nparenchymal signal or parenchymal edema.\n\nNo evidence of acute infarction, new intracranial hemorrhage or extra-axial\ncollection.\n\nThe ventricles and sulci are within expected limits in caliber and\nconfiguration allowing for postsurgical changes.\nMajor intracranial vascular flow voids appear preserved.  Major dural venous\nsinuses are patent.\n\nThe visualized paranasal sinuses and mastoid air cells appear clear.  The\norbits appear unremarkable.",
            "output": "1. Stable postsurgical changes after right temporoparietal craniotomy with\nunchanged enhancement in FLAIR hyperintense signal along the surgical tract.\n2. Stable to less conspicuous appearance of enhancement in the right\nthalamus/right cerebral peduncle, midbrain tectum and quadrigeminal plate\ncistern.  No new abnormal enhancement identified."
        },
        {
            "input": "Small 3 mm thick right parietal extra-axial fluid collection, likely subacute\nsubdural hematoma, slightly more prominent since prior..  Postsurgical change\nright posterior temporal lobe, minimal linear enhancement, consistent with\nposttreatment change.  Right periatrial deep white matter edema extending into\nthe adjacent corpus callosum, temporal and occipital lobes adjacent to the\nventricles, similar, likely posttreatment change.\n\nNo new lesions.  No infarct, mild generalized brain parenchymal atrophy. \nClear paranasal sinuses, mastoids.  Preserved vascular flow voids.  Dural\nvenous sinuses are patent.",
            "output": "1. Posttreatment change.\n2. Small subacute subdural hematoma, more prominent.  Follow-up head CT\nrecommended to document stability/resolution..\n\nRECOMMENDATION(S):  Follow-up head CT within 4 weeks to document stability or\nresolution of subdural collection."
        },
        {
            "input": "Again seen are postoperative changes after glioblastoma resection.  The degree\nof enhancement along the surgical site is gradually decreasing over time,\nsuggesting that much of this may have represented postoperative change.  The\nwhite matter hyperintensity on FLAIR surrounding the occipital horn of the\nright lateral ventricle and to a much lesser extent the occipital horn of the\nleft lateral ventricle has been gradually increasing over time.  This may\nrepresent treatment effect.  However, the possibility of nonenhancing tumor\nprogression cannot be excluded.\nNo other abnormalities are detected.  There is no evidence of other masses or\nof infarction.",
            "output": "1. Gradual reduction of enhancement at the surgical site, suggesting the this\nrepresented postoperative change.\n2. Gradual increase in FLAIR abnormality surrounding the occipital horns of\nthe lateral ventricles, greater on the right than left.  This may be treatment\neffect.  However, cannot exclude the possibility of nonenhancing tumor\nprogression."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.\n\nThe visualized vascular flow voids are grossly preserved.  The paranasal\nsinuses are clear.  There is moderate effusion in the bilateral mastoid air\ncells, right greater than left.  The orbits and globes are unremarkable.  No\nabnormal marrow signal.",
            "output": "1. Unremarkable brain MRI.  No evidence of infection, infarct, hemorrhage, or\nintracranial mass.\n2. Moderate effusion in the right mastoid air cells."
        },
        {
            "input": "Multiple images are significantly limited by motion artifact.\n\nImages through the internal auditory canal demonstrates symmetric appearance\nof the seventh eighth nerve complexes.  There is no evidence of abnormal\nenhancement or mass lesion within the internal auditory canals,\ncerebellopontine angles or membranous labyrinth. No other mass lesions are\nseen within the posterior fossa.\n\nThe sella is again noted to be expanded with small pituitary gland and\nposterior displacement of the infundibulum, grossly unchanged compared to\nprior studies and consistent with postsurgical changes, but not evaluated in\ndetail due to motion artifact and absence of dedicated images through the\nsella.\n\nLimited included imaging of the remainder of the brain demonstrates no\nevidence of acute infarction,edema, or mass.  FLAIR images again demonstrate\nnumerous small foci of high signal in the subcortical, deep, and\nperiventricular white matter of the cerebral hemispheres, nonspecific but\nlikely sequela of chronic small vessel ischemic disease in this age group. \nThere is no pathologic leptomeningeal contrast enhancement.  Age-related\nbronchiole volume loss with prominent ventricles and sulci is again seen. \nMajor dural venous sinuses appear patent on postcontrast MP RAGE images.",
            "output": "1. Motion limited exam.\n2. No evidence of IAC or cerebellopontine angle mass or other abnormality.\n3. Grossly stable appearance of the sella with postsurgical changes, allowing\nfor motion artifact."
        },
        {
            "input": "There is a linear area of slow diffusion in the left corona radiata associated\nwith slight T2/FLAIR hyperintense signal.  There are also 2 adjacent punctate\nfoci of slow diffusion within the adjacent left corona radiata.  Chronic\ninfarctions are noted in the right caudate and putamen.\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor extra-axial fluid collection.   The ventricles and sulci are prominent,\nlikely related to age-appropriate volume loss.  T2/FLAIR hyperintensities in\nthe periventricular, subcortical, and deep white matter are nonspecific, but\nlikely represent the sequela of chronic small vessel ischemic disease.\n\nThe paranasal sinuses and mastoid air cells are clear.  The patient is status\npost bilateral cataract surgery.",
            "output": "Acute infarctions in the left corona radiata.\n\nNOTIFICATION:  The findings of acute infarctions in the left corona radiata\nwere discussed with Dr.  ___, M.D. by ___, M.D. on the telephone on\n___ at 8:30 AM, 5 minutes after discovery of the findings."
        },
        {
            "input": "MRI BRAIN:\nPostcontrast MP RAGE images are degraded by motion artifact, but they do\nadequately demonstrate patent major dural venous sinuses.\n\nThere are multiple small acute infarctions in the left corona radiata with\nsome extension into the left frontal subcortical white matter, demonstrating\nslow diffusion and faint high signal on FLAIR images, which have increased in\nnumber and extent compared to approximately 20 hr earlier on ___. \nThere is no evidence for associated blood products or contrast enhancement. \nThere is no mass effect.\n\nThere is no evidence for an intracranial mass.  Numerous foci of high T2\nsignal in the subcortical, deep, and periventricular white matter of the\ncerebral hemispheres are again seen, nonspecific but likely sequela of chronic\nsmall vessel ischemic disease in this age group.  Ventricles and sulci are\nprominent due to age-related parenchymal volume loss, as seen previously.\n\nThere is evidence of bilateral cataract surgery.  There is mild mucosal\nthickening in the ethmoid air cells.  Frontal sinuses are not pneumatized.\n\nMRA NECK:\nThere is a 3 vessel aortic arch.  Bilateral common carotid, cervical internal\ncarotid, and cervical vertebral arteries appear patent without evidence for\nflow-limiting stenosis.  Specifically, there is no carotid stenosis by NASCET\ncriteria.\n\nMRA BRAIN:\nThe 3D time-of-flight MRA is limited by motion artifact.  The multiple foci of\nstenosis in bilateral M2 branches of the middle cerebral arteries, including\nthe severe stenosis of the superior division branch 3 mm distal to its origin\nwith distal reconstitution, are better demonstrated on the gadolinium enhanced\nneck MRA than on the 3D time-of-flight MRA.  No substantial change is seen\nallowing for differences in modalities.\n\nMultiple foci of at least moderate stenosis are again seen in P1 and P2\nsegments of bilateral posterior cerebral arteries, as seen on the recent CTA. \nThe right ___ is not visualized.  The prior CTA better demonstrates right\nAICA and left ___ branches supplying the right ___ territory.\n\nThere is no evidence for an aneurysm on limited evaluation",
            "output": "1. Multiple small acute infarctions in the left corona radiata with some\nextension into the left frontal subcortical white matter, slightly increased\nin number and extent compared to approximately 20 hr earlier on ___. \nNo associated mass effect or evidence for blood products.\n2. No evidence for flow-limiting stenosis in the cervical arteries.\n3. Technically limited brain MRA.  On the gadolinium enhanced neck MRA, the\nmultiple foci of stenosis in bilateral M2 branches of the middle cerebral\narteries, including the severe stenosis of the superior division branch 3 mm\ndistal to its origin with distal reconstitution, do not appear significantly\nchanged compared to the recent CTA allowing for differences in modalities."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, intra-axial masses/mass effect,\nmidline shift or acute territorial infarction.  Moderate subcortical, deep,\nand periventricular white matter T2/FLAIR hyperintensities nonspecific, but\nlikely reflect chronic microvascular ischemia, and appear to have progressed\ncompared to ___.  There is a chronic lacunar infarct within the right\nputamen, unchanged.  Prominence of the ventricles and sulci suggests\ninvolutional changes.\n\n13 mm extra-axial mass overlying the right temporal lobe is similar to\nslightly increased in size since ___, where it demonstrated homogeneous\nenhancement and a dural tail, compatible with a small sphenoid wing\nmeningioma.\n\nPatient is status post bilateral lens resections.  Otherwise, orbits are\nunremarkable in appearance.  Major intracranial flow voids are preserved. \nMild mucosal thickening of the paranasal sinuses.",
            "output": "1. No evidence of acute territorial infarction or hemorrhage.\n2. Moderate chronic microvascular ischemic changes, progressed compared to\n___.  Unchanged chronic right putaminal lacunar infarct.\n3. 13 mm right sphenoid wing meningioma, similar to slightly increased in size\nfrom prior exam."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no parenchymal signal abnormality.  There is no\nabnormal enhancement after contrast administration.  There is no abnormal\nfocus of slowed diffusion.  The principal intracranial vascular flow voids are\npreserved.\n\nThere is a tiny amount of aerosolized fluid in the right sphenoid sinus.  The\nremainder of the visualized paranasal sinuses are otherwise clear.  The orbits\nare grossly unremarkable.  The mastoid air cells are clear.",
            "output": "1. No evidence of intracranial hemorrhage, infarct, or enhancing mass.\n2. Small amount of aerosolized fluid in the right sphenoid sinus, nonspecific,\nwhich can be seen in setting of acute sinusitis in the appropriate clinical\ncontext."
        },
        {
            "input": "There is nonspecific scalp swelling over posterior parietal lobe (02:14).\n\nThere are focal areas diffusion restriction noted involving the bilateral\nfrontoparietal and occipital lobes (06:11, 20, 23, 24) with corresponding ADC\nhypointensity and mild FLAIR hyperintensity.  Equivocally, there is increased\nDWI signal in the caudate bodies but this does not clearly have a ADC\ncorrelate and could be artifactual.  No evidence of acute hemorrhage.  A few\npunctate areas of susceptibility may reflect chronic microhemorrhage.\n\nThe ventricles and sulci are normal in caliber and configuration.  There is\nmore diffuse vascular enhancement than expected, especially towards the\nvertex, that may be consistent with postictal state.  Attention on follow-up\nimaging is recommended.\n\nMajor vascular flow voids are preserved.  Small mucous retention cyst noted in\nthe right maxillary sinus (04:13).  The orbits appear unremarkable.",
            "output": "1. Diffuse focal areas of cortical diffusion restriction with surrounding\nedema and prominent enhancement, which may be consistent with recent seizure\nactivity.  However, differential also includes hypoxic ischemic injury,\nmetabolic disturbance such as hypoglycemia, or in the appropriate clinical\nsetting, infection.\n2. There is no evidence of acute hemorrhage.\n\nRECOMMENDATION(S):  Follow-up brain MRI is recommended once patient is seizure\nfree.\n\nNOTIFICATION:   The findings were discussed with Dr. ___. by\n___, M.D. on the telephone on ___ at 3:39 pm, 3 minutes after\ndiscovery of the findings."
        },
        {
            "input": "There is leptomeningeal enhancement noted within the subarachnoid spaces of\nthe cerebellum. No evidence of susceptibility artifact is seen on gradient\nimages to suggest hemorrhage.\n\nThere is no acute infarction, intracranial hemorrhage, extracerebral fluid\ncollection, midline shift or mass effect. No diffusion abnormalities are\ndetected. The cerebral volume is appropriate for the patient's stated age.\nThere are a few scattered foci of T2/FLAIR signal hyperintensity in the\nbilateral subcortical and deep white matter of the frontal and parietal lobes\nwhich are nonspecific. There is no abnormal enhancement identified on\npost-contrast images. The major vascular flow voids are maintained. The orbits\nare unremarkable, the paranasal sinuses and mastoid air cells are clear",
            "output": "Leptomeningeal enhancement in the cerebellar subarachnoid space. This finding\nis felt most likely be secondary to an inflammatory or infectious etiology.\nHemorrhage is considered far less likely due to the lack of susceptibility\nartifact on gradient images"
        },
        {
            "input": "Enhancing lesion in the left temporo-occipital region is compatible with a\naneurysm arising from left PCA.  Enhancement at the the inferior left\noccipital lobe is compatible with patient's known AV malformation is less\nconspicuous on today's exam, likely result of interval post treatment changes.\nOld right lentiform nucleus infarct is again noted.  There is no other\nabnormal enhancement.  There is no mass effect or midline shift.",
            "output": "Interval decrease in degree of enhancement in the left occipital lobe AVM,\nlikely post treatment related.  Persistent left PCA aneurysm."
        },
        {
            "input": "The patient is status post embolization of a known left occipital\narteriovenous malformation and occipital/suboccipital craniotomy with\nsurrounding gliosis/encephalomalacia.\n\nThere is restricted diffusion within the left thalamus (04:16) with\ncorresponding hyperintense T2/FLAIR signal intensity.  There is no evidence of\nintracranial hemorrhage.  Chronic infarction is seen within the right basal\nganglia and corona radiata.  The ventricles are normal in size without midline\nshift.  There is minimal nonspecific periventricular and subcortical white\nmatter hyperintense T2/FLAIR signal abnormality, which may be a sequela of\nchronic small vessel microangiopathy.\n\nThere is interval decrease in size of an aneurysm arising from the distal left\nposterior cerebral artery (102a: 87), measuring 3 x 3 mm (previously 7 x 6 mm)\nwith a prominent branch of the left posterior cerebral artery proximal to the\naneurysm.  A short segment occlusion/high grade narrowing  of the proximal P2\nsegment of the left posterior cerebral artery is better seen on the recent\nCTA.  Otherwise, there is no abnormal enhancement.  The visualized paranasal\nsinus and bilateral mastoid air cells appear unremarkable.",
            "output": "1. Status post coil embolization/ resection of left occipital arteriovenous\nmalformation and occipital/suboccipital craniotomy with stable surrounding\ngliosis and encephalomalacia.\n2. Acute/subacute infarction within the left thalamus.  No intracranial\nhemorrhage.\n3. Distal left posterior cerebral artery aneurysm seen on MRI of ___ is no longer visible.\n4. Short segment of high-grade narrowing/occlusion of the proximal P2 segment\nof the left posterior cerebral artery is better seen on the recent CTA and is\nnew from the previous CT angiography of ___.\n\nNOTIFICATION:  The findings were discussed with ___, M.D. by ___\n___, M.D. on the telephone on ___ at 9:40 AM, 3 minutes after\ndiscovery of the findings."
        },
        {
            "input": "There is a suprasellar mass identified adjacent to the hypothalamus. The mass\nshows foci of T1 hyperintensity on pre gadolinium images with susceptibility\nextending to the region of both optic tracts.  The mass is seen adjacent to\nthe infundibulum of the pituitary gland and posterior to the optic chiasm.\nMild enhancement of the mass is identified. No evidence of restricted\ndiffusion seen.  There is no midline shift mass effect or hydrocephalus. A few\nscattered nonspecific foci of T2 hyperintensity are. There are no other foci\nof abnormal parenchymal vascular or meningeal enhancement seen.",
            "output": "Suprasellar and hypo thalamic mass J-tube a signed area measuring\napproximately 1.5 cm in size. The appearance is most likely due to a\ncraniopharyngioma."
        },
        {
            "input": "In comparison with the prior MRI examinations in ___, there is a persistent\nright periatrial white matter FLAIR hyperintensity area pole extending to the\nsubependymal region (images 14, 15, series 6), with mild and unchanged\ndilation and asymmetry of the right ventricular trigone, suggestive of chronic\nmild myelomalacia, no new lesions are identified and the remaining gray/ white\nmatter areas demonstrate normal signal intensity.  There is no evidence of\nacute intracranial hemorrhage or mass effect, no diffusion abnormalities are\ndetected.  The sulci appear slightly prominent, however grossly unchanged,\nsuggesting mild cortical volume loss.  The major vascular flow voids are\npresent.  The orbits are unremarkable, the paranasal sinuses and the mastoid\nair cells are clear.",
            "output": "1.  Unchanged mild dilation of the right ventricular trigone, and stable focal\narea of increased FLAIR signal intensity in the right posterior periatrial\nregion, suggestive of chronic focus of ischemia versus encephalomalacia, no\nnew lesions are identified, given the stability pattern in this lesion and no\nevidence of new subcortical abnormalities, the possibility of demyelination is\nremote, however cannot be completely excluded.\n\n2.  The sulci are slightly prominent, suggesting mild cortical volume loss,\nthis finding appears also unchanged and is nonspecific.\n\n3.  There is no evidence of acute or subacute intracranial process."
        },
        {
            "input": "There is no acute infarction, intracranial hemorrhage, extracerebral fluid\ncollection, midline shift or mass effect.  Ventricles and extra-axial spaces\nare normal in size.  Subtle hyperintensities in the white matter may indicate\nearly changes of small vessel disease.  Flow voids are maintained. Suprasellar\nand craniocervical regions are unremarkable.  There is no evidence of Chiari\nmalformation seen.\n\nMRV of the head demonstrates normal flow signal in the superior sagittal and\ntransverse sinuses as well as in the deep venous system.  There is no evidence\nof dural venous sinus thrombosis.",
            "output": "No significant abnormalities are seen on MRI of the brain without gadolinium. \nNo significant abnormalities on MRV of the head.  No evidence of dural venous\nsinus thrombosis."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There are no diffusion or susceptibility abnormalities.  The\nmajor vascular flow voids are preserved.  There are scattered bilateral\npredominantly subcortical white matter hyperintensities, which are nonspecific\nbut may represent chronic small vessel ischemic disease, inflammatory changes,\nor demyelination.\n\nThe visualized paranasal sinuses, mastoid air cells, and orbits are\nunremarkable.",
            "output": "1. No evidence of infarction, hemorrhage, or mass.\n2. Multiple predominantly subcortical bilateral white matter hyperintensities\nof uncertain clinical significance."
        },
        {
            "input": "There are foci of restricted diffusion with associated T2 and FLAIR signal\nhyperintensity consistent with subacute infarcts in the right prefrontal gyrus\nand adjacent corona radiata (series 6, images ___.  There is curvilinear\nsusceptibility artifact along the distribution of the pulvinar of the right\nthalamus, not corresponding to identifiable vessel on the current MR or\npreceding CTA.  No associated T2/FLAIR signal abnormality or diffusion\nrestriction.  Chronic lacunar infarct of the left cerebellar hemisphere. \nPeriventricular and subcortical white matter T2/FLAIR hyperintensities are\nnonspecific but likely sequelae of chronic small vessel ischemic disease.\nThere is no abnormal enhancement after contrast administration.\n\nThe major intracranial flow voids are preserved.  The dural venous sinuses are\npatent.  There is mild mucosal thickening of the visualized paranasal sinuses.\nMild leftward nasal septum deviation anteriorly. The orbits are unremarkable. \nTrace fluid signal is seen in the mastoid tips.",
            "output": "1. Subacute right prefrontal gyrus and corona radiata infarcts.\n2. Susceptibility artifact in the right thalamus probably reflects chronic\nsequela of prior hemorrhagic infarct.\n3. Chronic lacunar infarct of the left cerebellar hemisphere.\n4. Additional findings described above.\n\nNOTIFICATION:  The findings were discussed with ___, M.D. by\n___, M.D. on the telephone on ___ at 10:07 am, less than 15\nminutes after discovery of the findings."
        },
        {
            "input": "There are multiple areas of slow diffusion involving the right frontal and\ntemporal lobes as well as the basal ganglia in the expected distribution of\nthe right anterior and posterior MCA territories with associated T2/FLAIR\nhyperintensity compatible with subacute ischemia.  There is a petechial\nhemorrhage in the right putamen (11:13).  There is minimal mass effect.  There\nare other scattered areas of periventricular and subcortical white matter\nhyperintensities without slow diffusion which are nonspecific, but likely\nreflect sequelae of chronic small vessel ischemic disease. Slight prominence\nof the ventricles and sulci suggest age related parenchymal atrophy.  Major\nintracranial vascular flow voids, including the right middle carotid artery,\nare preserved.  However, high signal within the right Sylvian fissure vessels\nlikely represent collateral flow versus slow flow.\n\nThere is mucosal thickening in the bilateral maxillary sinuses as well as the\nethmoid air cells likely related to intubation. The mastoid air cells are\nclear. The globes are unremarkable.",
            "output": "1.  Subacute infarcts involving the right frontal and temporal lobes as well\nas the basal ganglia in the expected distribution of the right anterior and\nposterior MCA territories.\n\n2.  Small amount of petechial hemorrhage in the right lentiform nucleus.\n\n3.  Persistent slow flow or collateral flow of the right MCA."
        },
        {
            "input": "Patient is status post left suboccipital craniotomy for hematoma evacuation\nwith appropriate post surgical changes including peripheral ischemic changes\nlikely secondary to manipulation.  Pneumocephalus around the surgical site is\ndecreased.  Large areas of increased T2/FLAIR signal intensity in the left\ncerebellar hemisphere likely reflect sequela of recent trauma and surgical\nintervention.  Foci of susceptibility artifact in the surgical site are\ncompatible with hemorrhage products.  Asymmetric left greater than right\ndiffuse dural enhancement/FLAIR hyperintensity may be post procedural in\netiology.  Abnormal FLAIR signal in the right temporal lobe may be secondary\nto gliosis.\n\nA punctate focus of restricted diffusion along the left temporal lobe\ncorresponds to an area of subarachnoid hemorrhage (6:12), as seen on priors. \nPreviously noted tentorial subdural hematoma is less well appreciated on the\ncurrent study.\n\nThere is no evidence of new acute hemorrhage, masses, midline shift or acute\ninfarction.  The ventricles and sulci are age-appropriate.\n\nThe major intracranial vascular flow voids are preserved.  The dural venous\nsinuses are patent.\n\nFluid and severe mucosal thickening in the right maxillary sinus is similar. \nThere is mild mucosal thickening of the ethmoid air cells and right frontal\nsinus.  The mastoid air cells are well aerated and clear.  The orbits are\nunremarkable.",
            "output": "1. Appropriate post surgical changes status post left suboccipital craniotomy.\nNo evidence of acute territorial infarction.\n2. Paranasal sinus disease."
        },
        {
            "input": "Study is mildly degraded by motion.\n\nLarge left temporoparietal subacute intraparenchymal hematoma measuring 7.0 x\n3.2 x 4.1 cm (AP x TRV x CC) is stable in size compared to ___. \nMild surrounding vasogenic edema and minimal surrounding enhancement is noted.\nMild rightward midline shift by 3 mm and small left uncal herniation are\nunchanged.  Dilation of left lateral ventricle temporal horn is unchanged. The\nventricles and sulci are stable in caliber and configuration. Several small\nscattered foci of white matter T2/FLAIR hyperintensities likely reflect\nchronic small vessel disease.\n\nFour at least partially small enhancing foci are identified in left parietal\nand occipital lobes.  Largest lesion in the left parietal lobe measures 7 mm\nwhich appears to connect to a prominent vein (1000:125).  Other foci are\nsmaller (1000:  94, 119, 120).\n\nPunctate right occipital focus of blood products versus mineralization is\nnoted (see 6:9).\n\nThere is no evidence of new infarction.  Small amount of fluid is noted in the\nleft maxillary sinus.",
            "output": "1.  Study is mildly degraded by motion.\n2. Large left temporoparietal subacute intraparenchymal hematoma with mass\neffect on left lateral ventricle, small left uncal herniation and dilated left\nlateral ventricle temporal horn are stable compared to ___.\n3. No new hemorrhage or definite mass is identified.  Recommend follow-up\nimaging to resolution to evaluate for presence of underlying mass.\n4. Nonspecific left parietal and occipital foci of enhancement may represent\nevolving subacute infarcts with differential consideration of enhancing areas\nof intraparenchymal hemorrhage, and masses.  Recommend attention on followup\nimaging.\n\nRECOMMENDATION(S):  Follow-up MRI imaging to resolution."
        },
        {
            "input": "There is no evidence of acute infarction, hemorrhage, edema, mass effect, or\nmidline shift.  There are white matter FLAIR hyperintensities perpendicular to\nthe ependymal surface and surrounding the posterior horn and atria of\nbilateral lateral ventricles, some of which demonstrate hypointensity on T1\nweighted images, likely related to history of known multiple sclerosis.  There\nis no evidence of corresponding enhancement to suggest active demyelinating\nprocess.\n\nThere is prominence of the ventricles and sulci related to involutional\nchanges, greater than would be expected for the patient's age, likely related\nto underlying multiple sclerosis.  The paranasal sinuses and bilateral mastoid\nair cells appear clear.  The orbits and visualized soft tissues appear\nunremarkable.",
            "output": "1. Supratentorial white matter lesions, likely related to known history of\nmultiple sclerosis.  No evidence of enhancement to suggest active\ndemyelinating process.\n2. No evidence of acute infarction, hemorrhage, or edema.  No enhancing mass\nor abnormal enhancement.\n3. Involutional changes, greater than would be expected for the patient's age,\nlikely related to patient's underlying multiple sclerosis."
        },
        {
            "input": "The examination is moderately limited secondary to patient motion.  Within\nthis limitation:\n\nExtensive supraaentorial periventricular, subcortical, and deep white matter\nT2/FLAIR hyperintense lesions compatible with the patient's known underlying\ndemyelinating disease.  These lesions are associated with T1 hypo intensities,\nas would be expected multiple sclerosis.  No evidence for lesion enhancement\nor restricted diffusion to suggest active demyelination.\n\nThere is no evidence of acute infarction.  No intracranial hemorrhage.  No\nmass, mass effect, edema or midline shift.\n\nThe ventricles and sulci are prominent, compatible with age advanced cerebral\natrophic changes.  The basal cisterns are patent.  There is no evidence of\nimpending, downward herniation.  There is gross preservation of the principal\nintracranial vascular flow voids.\n\nFollowing the administration of intravenous contrast material, there is no\nabnormal enhancement.  The dural venous sinuses appear patent on MP-RAGE\nimagine sequences.\n\nMucosal thickening is noted in several left anterior and posterior ethmoid air\ncells.  The remainder of the visualized paranasal sinuses, middle ear\ncavities, and mastoid air cells are well aerated and clear.  The orbits are\nwithin normal limits bilaterally.",
            "output": "1. No acute intracranial process.\n2. Extensive supratentorial T2/FLAIR hyperintense white matter lesions,\ncompatible with the patient's known history of multiple sclerosis.  No\nevidence for lesion enhancement or restricted diffusion to suggest active\ndemyelination.\n3. Moderate severe, age advanced global cerebral atrophic changes, likely\nsecondary to volume loss in the setting chronic demyelination."
        },
        {
            "input": "T1 hypointense signal within the dens (series 3, image 11) could represent a\nprominent bone island, but can't exclude metastatic lesion.  Intermediate T1\nsignal throughout the calvarium, likely represents red marrow, but can't\nexclude a marrow replacing process, including metastatic disease.\n\nThere is no evidence of acute intracranial process or hemorrhage.  Ventricles\nare normal in morphology.  No suspicious intra-axial lesions.\n\nThe orbits are unremarkable.  There is mild mucosal thickening in the\nmaxillary and ethmoid sinuses.  Mastoid air cells are clear.",
            "output": "1. Small area of T1 hypointense signal in the dens, could represent a bone\nisland, but a marrow replacing process, including metastatic disease can't be\nexcluded.  Diffuse intermediate T1 signal throughout the calvarium, likely\nrepresents red marrow reconversion, although this could obscure an underlying\nmetastatic calvarial lesion.  These findings could be further evaluated with a\nCT of the head, extending through the C2 vertebral body if clinically\nindicated.\n2. No intracranial evidence of metastatic disease or abnormal enhancement\nafter contrast administration.\n\nRECOMMENDATION(S):  Diffuse intermediate T1 signal throughout the calvarium,\nlikely represents red marrow reconversion, although this could obscure an\nunderlying metastatic calvarial lesion. These findings could be further\nevaluated with a CT of the head, extending through the C2 vertebral body if\nclinically indicated."
        },
        {
            "input": "The gradient recalled echo images are severely degraded.  The exam is\notherwise mildly degraded due to motion artifact.\n\nThere is a small late acute infarct within the posterior limb of the right\ninternal capsule and a probable small subacute infarct (given the lack of\nclearly low signal on ADC) within the left splenium of the corpus callosum.\n\nNo definite intracranial hemorrhage or mass effect.\n\nThere is a cavum septum pellucidum and variegated, a normal variant.  Small\nareas of hyperintense signal on T2/FLAIR within the periventricular white\nmatter are nonspecific, but likely reflect the sequela of mild chronic small\nvessel disease.\n\nThe major vascular flow voids are preserved.\n\nThere is trace mucosal thickening within a left anterior ethmoid air cell. \nThe orbits are unremarkable.",
            "output": "1. Small late acute infarct within the posterior limb of the right internal\ncapsule.\n2. Small infarct within the left splenium of the corpus callosum, likely\nsubacute.\n3. No intracranial hemorrhage or mass effect.\n4. Probable mild chronic small vessel disease.\n5. Additional findings described above.\n\nNOTIFICATION:  The findings were discussed with ___, M.D. by ___\n___, D.O. on the telephone on ___ at 3:51 pm, 5 minutes after\ndiscovery of the findings."
        },
        {
            "input": "There is no evidence of acute hemorrhage, edema, masses, mass effect, midline\nshift or infarction.  There is prominence of the ventricles and sulci\nsuggestive involutional changes.  There is focal encephalomalacia in the right\nthalamus from a prior lacunar infarction.\n\nNear complete interval resolution of the large right frontal intraparenchymal\nhematoma is seen with encephalomalacia and gliosis at the site of hemorrhage\nand a small amount of residual hemosiderin.  Faint enhancement is seen at this\nsite with no mass like or nodular enhancement identified.  Periventricular and\nsubcortical T2 and FLAIR hyperintensities are noted. The major vascular flow\nvoids are preserved.  The dural venous sinuses are patent.\n\nThere is stable hazy contrast enhancement in the left frontal calvarium which\ndemonstrates trabeculations on the prior CT and likely represents hemangioma.\n\nBilateral cataract extractions are seen.  The mastoid air cells and paranasal\nsinuses are normal.",
            "output": "1. Near complete resolution of the right frontal intraparenchymal hematoma\nwhich is replaced with encephalomalacia and gliosis.  Minimal faint associated\ncontrast enhancement centered in the prior hematoma bed, which likely\nrepresents enhancement of chronic blood products rather than underlying lesion\ngiven the lack of mass like/nodular enhancement or mass effect.\n\n2. Senescent volume loss and white matter is signal abnormality, likely\nsecondary to chronic microvascular ischemic changes."
        },
        {
            "input": "Compared to the ___ MRI, there are multiple new small foci of\nhigh T2 signal in the subcortical, deep, and periventricular white matter of\nthe cerebral hemispheres, without associated mass effect, abnormal diffusion,\ncontrast enhancement, or blood products. No brainstem or cerebellar lesions\nare seen. The corpus callosum remains stable in size. Ventricles, basal\ncisterns, and cerebral sulci remain normal in size.\n\nCranial nerves are not assessed in detail in the absence of high-resolution\nsequences through the skullbase. There is no evidence for abnormal\nleptomeningeal contrast enhancement.\n\nMajor arterial flow voids are grossly preserved.",
            "output": "1. Compared to ___, there are multiple new small T2 hyperintense\nlesions in the supratentorial white matter, which are nonspecific. In a\npatient of this age, diagnostic considerations include demyelinating disease,\nLyme disease, sarcoidosis, vasculitis, and other inflammatory/ post\ninflammatory etiologies. Please correlate clinically.\n2. No evidence for brainstem lesions."
        },
        {
            "input": "Again seen are somewhat prominent level 2 nodes bilaterally. These measure\napproximately 9 mm in short-axis dimension. Although incompletely visualized\non the prior study, the appear unchanged. There is no evidence of necrosis or\nextracapsular spread. Also unchanged is mild prominence of the lingual\ntonsillar tissue.\n\nThere is an enlarged nodular left lobe of the thyroid gland is similar to the\nfindings on the recent thyroid ultrasound The study is otherwise normal. There\nis no evidence of exophytic mucosal mass.  There is no pathologic adenopathy\nby imaging criteria.  Neck vessels are patent.  Normal salivary glands.",
            "output": "Prominent level 2 lymph nodes bilaterally not meeting size or other imaging\ncriteria for malignancy.\nProminent lingual tonsillar tissue.\nEnlarged nodular left thyroid lobe."
        },
        {
            "input": "Postsurgical changes after right frontal craniotomy are again noted.\n\nAgain noted are multiple small subependymal nodules which demonstrate\nhypointensity/susceptibility artifact on the gradient echo sequence,\ncorresponding to calcifications seen on the prior CT.\nSusceptibility artifact in the right cerebellar hemisphere correspond to\ncalcifications on the prior CT, unchanged.\n\nMultiple periventricular and cortical/subcortical FLAIR hyperintensities are\nagain seen and consistent with tubers in the setting of the patient's known\ntuberous sclerosis.\n\nThe right medial temporal lobe is again noted to be smaller when compared to\nthe contralateral left side with associated prominence of the temporal and\noccipital horns of the right lateral ventricle, related to asymmetric atrophy\nin the setting of tuberous sclerosis.  Otherwise, there is unchanged\nprominence of the ventricular system which is unchanged from prior.\n\nThere is opacification of the bilateral mastoid air cells.  Mucosal thickening\nis seen in the bilateral maxillary sinuses and along the ethmoid air cells.\nStable deformity of the right globe.  The left orbit is unremarkable.",
            "output": "1. No change of the multiple intracranial findings consistent with the\npatient's known diagnosis of tuberous sclerosis, as detailed above.  No new\nabnormality is identified.\n2. Stable right temporal lobe atrophy.\n3. Stable asymmetric prominence of the ventricular system.\n4. Paranasal sinus disease and opacification of the bilateral mastoid air\ncells."
        },
        {
            "input": "There is no intra or extra-axial mass, acute hemorrhage or infarct. The sulci,\nventricles and cisterns are within expected limits for the patient's age. \nWithin confines of a nondedicated examination, there is no evidence of\nenhancing lesion along the course of the cranial nerves.  Periventricular and\nsubcortical T2/FLAIR white matter hyperintensities are nonspecific and\nunchanged since ___.  The major intracranial flow voids are preserved.  Mild\nmucosal thickening of the ethmoid air cells is identified.  Otherwise the\nvisualized paranasal sinuses are essentially clear.  Apparent diffuse nasal\npolyposis is identified.  Re-identified is are mucous retention cysts of the\nadenoids.  The orbits are unremarkable.  The mastoid air cells are essentially\nclear.",
            "output": "1. No evidence of intracranial mass.\n2. Apparent diffuse nasal polyposis.  Clinical correlation is recommended."
        },
        {
            "input": "There is significant motion artifact, which limits interpretation of the\nstudy.\n\nThere are multiple stable appearing enhancing lesions within the cerebellum,\nthe largest located in the cerebellar vermis, measuring 1.3 x 1.2 cm. There is\nmild surrounding edema seen around most of these lesions, as before. The edema\naround the lesion in the cerebellar vermis continues results in mass effect on\nthe fourth ventricle, similar to prior.\n\nThere is no intracranial hemorrhage. Diffusion weighting imaging does not\ndemonstrate evidence of acute infarct. The major intracranial vessels exhibit\nthe expected signal void related to vascular flow.  Gray white matter\ndifferentiation is maintained. Ventricles and extra axial CSF spaces are\nunchanged in size and configuration.\n\nThe sella turcica, craniocervical junction, and orbits are unremarkable. The\nparanasal sinuses and mastoid air cells demonstrate normal signal.",
            "output": "Multiple stable appearing enhancing lesions in the cerebellum, the largest of\nwhich is located cerebellar vermis, unchanged from ___. As\nbefore, these lesions are most consistent with metastatic disease."
        },
        {
            "input": "MRI Brain:\nNo intracranial hemorrhage, mass or infarct.\nMild generalized cerebral atrophy with ex vacuo dilatation of the ventricular\nsystem.  A few periventricular and deep white matter T2 and FLAIR\nhyperintensities are nonspecific, most likely related to mild microangiopathy.\nThe intracranial arteries demonstrate normal T2 flow void.  The CP angles\nappear normal.\nModerate mucosal thickening involving the paranasal sinuses.  The orbits\nappear normal.\n\nMRA BRAIN:\nThe intracranial arteries are patent.  Mild irregularity of the cavernous\nsegments of the ICAs bilateral suggesting atherosclerotic disease.  Mild\nnarrowings involving the right M1 segment.  Mild stenosis involving the mid\nleft A1 segment.  Mild narrowings involving the M2 segments bilateral. \nModerate stenosis involving the P2 segments bilateral.  Hypoplastic right A1\nsegment.  No arterial occlusion or aneurysm.\n\nMRA neck: Normal aortic arch branching pattern.  The great vessel origins are\nsuboptimally assessed.  The carotid arteries are patent bilateral.  There is\nsuspected mild stenosis of the carotid bulbs bilaterally.  The vertebral\narteries are patent bilateral appear codominant.",
            "output": "1. No intracranial hemorrhage, mass or infarct.\n2. Mild realized cerebral atrophy with ex vacuo dilatation of the ventricular\nsystem.\n3. Mild white matter microangiopathic changes.\n4. The intracranial arteries are patent and demonstrate multiple\nmild-to-moderate areas of narrowing which is most likely related to\natherosclerotic disease.  No arterial occlusion or aneurysm formation.\n5. Time-of-flight MRA neck demonstrates patent neck vessels.  Suspected mild\nnarrowing of the carotid bulbs bilateral.  MRA neck with contrast or CTA neck\nmay be performed for quantification.\n6. Moderate paranasal sinus disease."
        },
        {
            "input": "There is no intracranial hemorrhage. Diffusion weighting imaging does not\ndemonstrate evidence of acute infarct. The previously seen hyperdense lesion\nin the right cerebellar peduncle on CT is most consistent with an artifact.\nThe major intracranial vessels exhibit the expected signal void related to\nvascular flow. Gray white matter differentiation is otherwise maintained.\nVentricles and extra axial CSF spaces are unchanged.\n\nThe sella turcica, craniocervical junction, and orbits are unremarkable. The\nparanasal sinuses and mastoid air cells demonstrate normal signal.",
            "output": "Unremarkable, unenhanced MRI examination of the brain. The previously seen\nfocal hyperdensity within the right cerebellar peduncle is most consistent\nwith an artifact."
        },
        {
            "input": "There is no acute infarct or intracerebral hemorrhage. Principal intracranial\nvascular flow voids are preserved. No extra-axial blood or fluid collection is\npresent. The ventricles and sulci are prominent suggesting age-related\ninvolutional changes. Multiple foci of T2/FLAIR hyperintensity in the\nperiventricular region and throughout the white matter are compatible with\nchronic small vessel disease.  No diffusion abnormality is detected. There is\nno pathologic parenchymal, leptomeningeal, or dural focus of enhancement after\ncontrast administration. The brainstem, posterior fossa and cervical medullary\njunction are preserved. The orbits, periorbital and paracavernous spaces are\nnormal.\n\nA 3.3 x 2.1 cm extraaxial lesion (4:21) along the inner table of the right\nparietal bone which does not extend through the cortex of the calvarium\n(representative image 3:7) is again seen and unchanged from prior.  The lesion\ndoes not show adjacent edema or significant mass effect.  No other calvaria\nabnormality is seen.",
            "output": "1.  No acute intracranial process.\n\n2.  Unchanged extraaxial lesion along the inner table of the right parietal\ncalvarium.  Differential diagnosis includes ossified meningioma versus\ncalcified old subdural hematoma."
        },
        {
            "input": "The ventricles, sulci, and cisterns appear normal.  There is an 8 mm focus of\nhyperintense signal on FLAIR images within the periventricular white matter\nadjacent to the posterior body of the right lateral ventricle (image 15 series\n7), nonspecific in nature.  The white matter otherwise appears normal in\nsignal intensity.  No abnormal enhancement, acute infarct, intracranial\nhemorrhage, or mass effect.\n\nThere are mucous retention cysts within the bilateral maxillary sinuses.",
            "output": "1.  8 mm nonenhancing focus of white matter signal abnormality adjacent to the\nposterior horn of the right lateral ventricle.  The differential is broad and\nincludes chronic small-vessel disease, demyelination, migraine headaches, the\nsequela of a prior infectious or inflammatory process, low grade neoplasm, and\nmany other less common etiologies.  If clinically warranted follow-up MR head\nwithout contrast is recommended in 12 months to ensure stability.\n2.  Mucous retention cysts within the bilateral maxillary sinuses.\n\nRECOMMENDATION(S):  Point 1.  If clinically warranted follow-up MR head\nwithout contrast is recommended in 12 months to ensure stability."
        },
        {
            "input": "There is a 7 mm (previously 8 mm) focus of hyperintense FLAIR signal within\nthe periventricular white matter adjacent to the posterior body of the right\nlateral ventricle (6:15), grossly unchanged size and appearance since MRI from\n___, allowing for differences in slice selection, and measuring\ntechnique.  There is no associated restricted diffusion.\n\nOtherwise, the white matter is normal in signal intensity.  No evidence of\nacute infarct, intracranial hemorrhage, or mass effect. The ventricles and\nsulci are normal in caliber and configuration.\n\nThere are mucoid retention cysts in the bilateral maxillary sinuses, unchanged\nsince prior MRI.  Otherwise, the remaining paranasal sinuses, mastoid air\ncells and middle ear cavities are clear.  The orbits are unremarkable.  The\nvisualized portion of the principal vascular flow voids are preserved.",
            "output": "1. 7 mm focus of hyperintense FLAIR signal within the periventricular white\nmatter adjacent to the posterior body of the right lateral ventricle, grossly\nunchanged in size and appearance since MRI from ___, allowing for\ndifferences in slice selection and measuring technique.\n2. Again, the differential remains broad and includes chronic small vessel\ndisease, demyelination, migraine headaches, sequela of prior infectious or\ninflammatory process, or low-grade neoplasm.  If clinically warranted,\nconsider routine ___ follow-up brain MRI without contrast to ensure\nstability.\n3. No new sites of abnormal FLAIR signal.\n4. Mucous retention cysts within the bilateral maxillary sinuses are unchanged\nsince prior MRI."
        },
        {
            "input": "Study is mildly degraded by motion.\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.  Periventricular and subcortical T2 and FLAIR hyperintensities\nare noted, which may represent small vessel ischemic changes.\n\nLimited imaging of the cervical spine demonstrate multilevel degenerative\nchanges with at least mild vertebral canal stenosis at C3-4 and C4-5. \nAllowing for differences technique, grossly stable minimal C2 on C3\nanterolisthesis is again seen.",
            "output": "1. Study is mildly degraded by motion.\n2. Partially visualized cervical spine suggests multilevel degenerative\nchanges with least mild vertebral canal stenosis at C3-4 and C4-5.  If\nclinically indicated, consider dedicated cervical spine MRI for further\nevaluation.\n3.  No acute intracranial abnormality, with no evidence of intracranial mass\nor infarct.\n4. Numerous nonenhancing white matter lesions as described.  While findings\nare likely suggestive of microangiopathic changes in this ___ old patient, they\nmay be also seen in the setting of prior trauma or infection, migraine\nheadaches, or inflammatory or demyelinating process."
        },
        {
            "input": "There is no evidence of acute infarction.  No intracranial hemorrhage. No\nmass, mass effect, edema or midline shift. There is no abnormal enhancement. \nThe dural venous sinuses appear patent.\n\nThe ventricles and sulci are mildly prominent.  Periventricular and\nsubcortical white matter FLAIR hyperintensities are noted, a nonspecific\nfinding that most likely represents the sequelae of chronic small vessel\nischemic disease.   There is gross preservation of the principal intracranial\nvascular flow voids.\n\nTrace mucosal thickening is seen in scattered ethmoid air cells.  The\nremainder of the visualized paranasal sinuses, middle ear cavities, and\nmastoid air cells are well aerated and clear.  The orbits are within normal\nlimits bilaterally.",
            "output": "1. No evidence for intracranial metastatic disease.  No acute hemorrhage or\ninfarction.\n2. Mild global parenchymal volume loss and evidence of chronic small vessel\nischemic disease."
        },
        {
            "input": "MRI HEAD:  There is no evidence of acute infarction or hemorrhage.  A tiny\nfocus of susceptibility in the posterior left temporal lobe with corresponding\nenhancement may represent a tiny cavernoma (10:11, 13:12), but a tiny\nhemorrhagic metastasis cannot be excluded. Otherwise, there is no abnormal\nparenchymal, vascular or meningeal enhancement after the administration of\ngadolinium. There is no mass effect, edema, or hydrocephalus. Ventricles and\nsulci are normal in size and configuration. Principal vascular flow voids are\npreserved. Globes and soft tissues are unremarkable. Small left maxillary\nsinus mucous retention cyst is noted.",
            "output": "Tiny focus of enhancement in the posterior left temporal lobe with\nsusceptibility may represent a tiny cavernoma, but a hemorrhagic metastasis\ncannot be excluded. Short-term followup is recommended."
        },
        {
            "input": "There is no evidence of acute intracranial hemorrhage, mass, mass effect or\nshifting of the normally midline structures.  The cisterna magna appears\nslightly prominent (image 12, series 2), likely consistent with anatomical\nvariation, otherwise, the sulci are normal in size and configuration for the\npatient's age.  The lateral ventricles demonstrates minimal asymmetry in the\nright temporal ventricular horn which is slightly more prominent in comparison\nwith the left, probably consistent with anatomical developmental variation\n(image 73, series 14).  After the administration of gadolinium contrast, there\nis evidence of a right subcortical developmental venous anomaly draining in\nthe right subependymal region of the right occipital ventricular horn (image\n103, series 14).  No diffusion abnormality detected.  The major arterial\nvascular flow voids are present and demonstrate normal distribution.  The\norbits are unremarkable, the paranasal sinuses and the mastoid air cells are\nclear",
            "output": "1.  There is minimal asymmetry in the size of the right temporal ventricular\nhorn, probably consistent with an anatomical variation.\n\n2.  The images with gadolinium contrast demonstrates a developmental venous\nanomaly, draining in the subependymal region on the right occipital\nventricular horn."
        },
        {
            "input": "There is an enhancing 4.1 cm TV x 4.3 cm AP x 4.5 cm SI left frontal lobe mass\nwith associated susceptibility artifact corresponding to calcifications seen\non prior CT.  There is surrounding FLAIR hyperintensity.  There is resulting 1\ncm rightward subfalcine herniation. The mass is close to the anterior superior\nsagittal sinus (1018:119) however, no involvement is seen.\n\nThe ventricles are normal in size.  There is no evidence of acute infarction. \nThere is a focus of susceptibility artifact within occipital horn of the right\nlateral ventricle (10:12), possibly representing microhemorrhage or choroid\nplexus calcification.\n\n Otherwise, the remaining dural venous sinuses appears patent.  There is mild\nmucosal thickening of bilateral ethmoid air cells with trace nonspecific fluid\nopacification of bilateral mastoid air cells.  The orbits appear unremarkable.",
            "output": "1. Enhancing calcified left frontal lobe mass, likely representing an\noligodendroglioma, with resulting 1 cm rightward subfalcine herniation.  There\nsuperior sagittal sinus is patent.\n2. No evidence of acute infarction.\n3. Punctate microhemorrhage versus choroid plexus calcification within the\noccipital horn of the right lateral ventricle."
        },
        {
            "input": "Study is mildly degraded by motion.\n\nThe patient is status post bifrontal craniotomy for resection of previously\nseen large anterior parafalcine meningioma.  Bifrontal pneumocephalus has\ndecreased compared to the prior examination.  Small bifrontal postoperative\nextra-axial fluid collections also appear unchanged.  FLAIR hyperintense\nsignal in the brain parenchyma along the posterior and inferior aspect of the\nresection extending to the left lateral ventricle is grossly unchanged\ncompared to the preoperative study of ___.  Mass effect has improved. \nA punctate focus of susceptibility along the atrium of the right lateral\nventricle corresponds to  choroid plexus calcifications on CT.  Foci of\nsusceptibility on gradient echo images in the resection bed likely represent a\ncombination of pneumocephalus and hemorrhagic products.  Hemorrhagic products\nalong the resection margin are better appreciated as areas of intrinsic T1\nhyperintense signal.  Mild enhancement along the craniotomy margin is in\nkeeping with postoperative changes.  Small areas of enhancement which are\nnonspecific are noted within the resection bed.  Areas of slow diffusion along\nthe resection margin are suggestive of postoperative change.  There is no\nevidence of acute vascular territorial infarction.\n\nThere is no significant mass effect or shift of normally midline structures. \nPrincipal intracranial vascular flow voids are preserved.  The dural venous\nsinuses are patent on postcontrast MP-RAGE sequences.  There is mild mucosal\nthickening in the ethmoid air cells and there is fluid signal in some of the\nmastoid air cells, right greater than left.",
            "output": "1. Study is mildly degraded by motion.\n2. Expected recent postoperative changes from anterior parafalcine meningioma\nresection as described above.\n3. Minimal nonspecific enhancement within surgical cavity.  While findings may\nbe postsurgical in nature, small residual tumor is not excluded on the basis\nof this examination.\n4.  Paranasal sinus disease , as described."
        },
        {
            "input": "The patient is status post left frontal craniotomy and resection of a left\nfrontal meningioma, with expected postsurgical changes including underlying\ndural thickening and enhancement and resolution of previously seen\npneumocephalus.  No definite masslike enhancement to suggest residual lesion. \nThe degree of underlying parenchymal FLAIR white matter edema pattern has also\nimproved.  No new enhancing lesions are identified.  Allowing for\npostoperative changes and mild encephalomalacia of the left superior frontal\ngyrus, the sulci, ventricles and cisterns are within expected limits for the\npatient's age.  Punctate microhemorrhage along the trigone of the right\nlateral ventricle is unchanged.  The major intracranial flow voids are\npreserved.  The dural venous sinuses are patent.  There is mild mucosal\nthickening of the visualized paranasal sinuses.  The orbits are unremarkable. \nFluid signal is noted in the bilateral mastoid air cells.",
            "output": "1. Expected postsurgical changes from left frontal craniotomy and meningioma\nresection, including mild dural thickening and residual underlying brain\nparenchyma edema pattern and encephalomalacia.  No convincing evidence to\nsuggest disease recurrence or progression.\n2. No new lesions.\n3. Additional findings described above."
        },
        {
            "input": "Postsurgical changes are again demonstrated consistent with left frontal\ncraniotomy, the patient is status post resection of a left frontal meningioma,\nin comparison with the most recent examination, there is minimal dural\nthickening and mild enhancement throughout the surgical cavity with no frank\nevidence of residual mass or evidence of tumor recurrence, the pattern of\nenhancement at the resection cavity is likely postsurgical, on FLAIR images,\nthere is persistent unchanged mild white matter edema with no evidence of mass\neffect or shifting of the normally midline structures, no diffusion\nabnormalities are detected.  No new lesions or new areas with abnormal\nenhancement are seen.  Unchanged focus of magnetic susceptibility is again\nseen in the  right ventricular trigone, probably consistent with\nmicrohemorrhage versus calcification (image 13, series 6), the major vascular\nflow voids are present and demonstrate normal distribution.  The ventricles\nand sulci otherwise are unremarkable.  The orbits are normal, the paranasal\nsinuses and the mastoid air cells are clear.",
            "output": "1.  Postsurgical changes identified at the left frontal convexity remain\ngrossly unchanged since the prior study, the patient is status post resection\nof a left frontal meningioma, there is minimal dural thickening and mild\nenhancement throughout the surgical cavity, with no evidence of residual mass\nor evidence of tumoral recurrence.\n\n2.  Susceptibility focus along the right ventricular trigone remains\nunchanged, probably consistent with microhemorrhage versus calcification.\n\nRECOMMENDATION(S):  The patient is status post left frontal craniotomy and\nresection of a left frontal meningioma.  Similar pattern of enhancement is\nagain seen throughout the surgical cavity with no evidence of residual mass or\nrecurrent tumor, however long-term follow-up with MRI of the head with and\nwithout contrast is recommended to demonstrate stability or any further\nchanges."
        },
        {
            "input": "Again seen is subdural blood layering along the left convexity measuring\napproximately 7 mm in maximum thickness from the inner table, as well as along\nthe falx and the left tentorium.  There is an associated 3 mm rightward shift\nof the midline structures, unchanged since the prior study.  There is no acute\ninfarct.  There is no edema in the brain parenchyma.  There is no evidence for\nnew blood products.  The age related involutional changes with prominent\nventricles and sulci are again noted.  Scattered T2/FLAIR hyperintensities are\nnoted in the periventricular and subcortical white matters, compatible with\nchronic small vessel ischemic disease.  Major vascular flow voids are\npreserved.  Prior right cataract surgery is again noted.",
            "output": "1. No acute infarct.\n2. Stable subdural hematoma along the left convexity, falx, and tentorium,\nwith stable mild rightward shift of midline structures."
        },
        {
            "input": "6 cm area of slow diffusion is identified in the left occipital region with\ncorresponding hyperintensity on FLAIR images.\nRight occipital and right frontal encephalomalacia is are consistent with\nsequela of old infarct.  Low signal in the areas of encephalomalacia on\ngradient echo images likely reflect blood products from old hemorrhage.\nThere is no evidence of acute hemorrhage, edema, masses, mass effect, or\nmidline shift.  Large ventricles and sulci are consistent with involutional\nchanges.  Several small foci of FLAIR hyperintensity in deep and subcortical\nwhite matter likely reflect chronic small vessel disease.  Mild mucosal\nthickening is noted in the right maxillary sinus.",
            "output": "1. Diffusion abnormality in the left occipital region is consistent with late\nacute to subacute infarct.\n2. Right occipital and frontal encephalomalacia are consistent with sequela of\nold infarcts.\n\nNOTIFICATION:    Impression 1.  was discussed with ___, M.D. by ___\n___, M.D. on the telephone on ___ at 10:23 am, 5 minutes after discovery\nof the findings."
        },
        {
            "input": "There is mild prominence of the the ventricles, sulci, and cisterns,\nreflecting diffuse brain parenchymal volume loss.  The axial FLAIR images\ndemonstrateperiventricular areas of high signal, which are nonspecific and may\nreflect changes due to chronic small vessel disease.  There is no diffusion\nrestriction to suggest acute infarct.  No intracranial hemorrhage or mass is\ndemonstrated.  There is no abnormal enhancement.  The brainstem and the\nposterior fossa are unremarkable.  The pituitary in the suprasellar region are\nunremarkable.  The vascular flow voids are preserved.  The paranasal sinuses\nand the mastoid air cells are clear.\n\nThere is no evidence of intracranial hemorrhage, edema, masses, mass effect,\nmidline shift or infarction.   The ventricles and sulci are normal in caliber\nand configuration.  There is no abnormal enhancement after contrast\nadministration.",
            "output": "1. There is no evidence of acute intracranial process or hemorrhage\n2. Mild brain parenchyma volume loss."
        },
        {
            "input": "MRI of the head without contrast: There is no evidence of intracranial\nhemorrhage, mass, mass effect or shifting of the normally midline structures. \nThe ventricles and sulci are slightly prominent, likely age related and\ninvolutional in nature.  Numerous foci and areas of high signal intensity\ndetected on T2 and FLAIR sequence, distributed in the subcortical and\nperiventricular white matter, which are nonspecific and may reflect changes\ndue to small vessel disease.  No diffusion abnormalities are detected to\nindicate or suggest acute or subacute ischemic changes.  The major vascular\nflow voids are present and demonstrate normal distribution.  The orbits are\nunremarkable, the paranasal sinuses demonstrate hypoplasia of the frontal\nsinus which is consistent with anatomical variation, the ethmoidal air cells,\nthere is moderate mucosal thickening in the ethmoidal air cells and mild\nmucosal thickening in the maxillary sinuses, no air-fluid levels are seen, the\nsphenoid sinus appears normally pneumatized with no evidence of mucosal\nthickening, the mastoid air cells are clear.  Dental hardware obscures the\nanatomical detail in the left maxilla.  The craniocervical junction appears\nunremarkable, mild degenerative changes are visualized at C3/C4 level,\nconsistent with mild posterior spondylosis, partially evaluated in this\nexamination.\n\nMRA Head: There is evidence of vascular flow in both internal carotid arteries\nas well as the vertebrobasilar system, there is minimal segmental narrowing\nthroughout the basilar artery, suggesting mild arteriosclerotic disease with\nno evidence of significant stenosis, the anterior, middle and posterior\ncerebral arteries are patent, no aneurysms are identified.\n\nMRA of the neck:  Both common carotid arteries are patent with no evidence of\nstenosis at the carotid cervical bifurcations.  The right vertebral artery is\nslightly structures, however there is no evidence of flow stenotic lesions,\nand both vertebral arteries are codominant.",
            "output": "1. There is no evidence of acute or subacute intracranial process, no evidence\nof intracranial hemorrhage or diffusion abnormalities to suggest acute or\nsubacute ischemic changes.\n2. T2/FLAIR periventricular and subcortical areas of high signal intensity,\nare nonspecific and suggests changes due to small vessel disease.\n3. Minimal segmental narrowing throughout the basilar artery with no evidence\nof significant stenosis, otherwise, there is no evidence of flow stenotic\nlesions or aneurysms in the circle of ___.\n4. Mild tortuosity of the right vertebral artery with no evidence of flow\nstenotic lesions, there is no evidence of stenosis at the cervical carotid\narteries.\nThe findings were discussed with ___, M.D. by ___, M.D. on\nthe telephone on ___ at 8:58 am, 2 minutes after discovery of the\nfindings."
        },
        {
            "input": "No acute infarct, suspicious focus of intracranial hemorrhage, mass effect,\nshift of normally midline structures or hydrocephalus.\nThere are a few small T2 FLAIR hyperintense foci in the cerebral white matter\nin the frontal lobes, nonspecific in appearance.\nThe ventricles, extra-axial CSF spaces, cerebral sulci and cerebellar folia\nare normal.\nThe major intracranial arterial flow voids are noted.\nSella, pineal gland, craniocervical junction regions are unremarkable.\nThere is moderate mucosal thickening with fluid of the left sphenoid sinus.\nThe imaged orbits are unremarkable.",
            "output": "1. No evidence of acute infarction\n2. Scattered T2 FLAIR hyperintense foci in the cerebral white matter as\ndescribed above, nonspecific in appearance can be seen with small-vessel\nischemic changes, etc. Correlate for risk factors.\n3. Moderate mucosal thickening with fluid of the left sphenoid sinus."
        },
        {
            "input": "Study is moderately degraded by motion.  Within these confines:\n\nThere is slow diffusion with correlate FLAIR hyperintensity within the medial\nright thalamus consistent with acute infarction, without evidence of\nassociated hemorrhage (04:17).  There is a parenchymal hemorrhage at the\nposterior left thalamus extending along the medial subependymal portion of the\nleft lateral ventricular body measuring approximately 6.0 cm AP x 2.6 cm SI x\n2.6 cm TV (12:10; 10:17).  This demonstrates intrinsic T1 hyperintensity, T2\nhyperintensity, and gradient echo blooming.  There are blood products layering\nwithin the bilateral occipital horn lateral ventricles, and marginating the\nsuperior cerebellar vermis.  There is significant susceptibility artifact at a\ncoiled vein ___ fistula which obscures adjacent structures.\n\nThere is a right frontal approach ventriculostomy catheter with tip at the\nanterior horn right lateral ventricle.  There is encephalomalacia chronic\nblood products along the trans mantle frontal course.  There is ventricular\ndilatation which is mildly increased comparison to ___ and\nsignificantly increased in comparison to ___.  There are\nnonspecific scattered periventricular and subcortical white matter FLAIR\nhyperintense foci.  There is no midline shift or downward herniation.  The\nvascular flow voids are preserved.  There is a partially empty sella.\n\nThe orbits, calvarium, and soft tissues are unremarkable.  There is a left\nmastoid air cell effusion.",
            "output": "1.  Study is moderately degraded by motion, and susceptibility artifact at the\ncoiled vein ___ fistula which obscures adjacent structures.\n2. Medial right thalamic acute to subacute infarct, without associated\nhemorrhage.\n3. Large parenchymal hemorrhage extending from posterior left thalamus\nanteriorly along medial  left lateral ventricular body ependymal surface.\n4. Extra-axial hemorrhage layering within the left and right lateral\nventricles occipital horns and at superior vermis.\n5. Right frontal approach ventriculostomy catheter with tip at  right lateral\nventricle anterior horn.\n6. Ventricular dilatation mildly increased compared to ___,\nconcerning for hydrocephalus.\n\nNOTIFICATION:   The findings were discussed with ___, M.D. by ___,\nM.D. on the telephone on ___ at 9 ___, 2 minutes after discovery of the\nfindings."
        },
        {
            "input": "MRI BRAIN:\nThere is no evidence of hemorrhage, edema, mass, mass effect, or acute\ninfarction.  Multiple scattered bilateral periventricular and subcortical foci\nof white matter FLAIR hyperintensities are nonspecific but likely sequelae of\nchronic microangiopathy in a patient of this age.  The ventricles and sulci\nare normal in caliber and configuration for age.  There is no abnormal\nenhancement after contrast administration.  The dural venous sinuses enhance\nappropriately.  There is fluid signal in a few air cells at the mastoid tips\nbilaterally.  The orbits are unremarkable.\n\nMRA brain:  The A1 segment of the right anterior cerebral artery is diminutive\nand both A2 segments are largely supplied by the A1 segment of the left\nanterior cerebral artery, likely a normal variant.  The intracranial vertebral\nand internal carotid arteries and their major branches otherwise appear normal\nwithout evidence of stenosis, occlusion, or aneurysm formation.\nThere is fluid signal in few air cells at the mastoid tips bilaterally.",
            "output": "1. No hemorrhage, edema, mass, mass effect, or acute infarction.\n2. Unremarkable brain MRA."
        },
        {
            "input": "MRI BRAIN:\nThere is a small region of slow diffusion in the posterior aspect of the left\nputamen, leading into the left posterior limb of the internal capsule and\nposterior frontal corona radiata with associated FLAIR hyperintensity\ncompatible with late acute to early subacute infarct corresponding to subtle\nhypodensity seen on CT.\n\nThere is no evidence of hemorrhage, mass, mass effect, midline or midline\nshift.  The ventricles and sulci are normal in caliber and configuration. \nMild areas of periventricular white matter T2/FLAIR hyperintensities in a\nconfiguration most suggestive of chronic small vessel ischemic disease.  The\nprincipal intracranial vascular flow voids are preserved.\n\n The visualized paranasal sinuses are grossly clear.  There are changes from\nbilateral lens replacement surgery.  The orbits are otherwise grossly\nunremarkable.  The mastoid air cells are clear.\n\nMRA BRAIN:\nThe intracranial vertebral and internal carotid arteries and their major\nbranches appear patent without evidence of stenosis, occlusion, or aneurysm\nformation.\n\nMRA NECK:\nThere is a normal variant 4 vessel aortic arch with direct takeoff of the left\nvertebral artery from the aortic arch.  The common, internal and external\ncarotid arteries appear patent.  There is no evidence of internal carotid\nartery stenosis by NASCET criteria.  The origins of the great vessels,\nsubclavian and vertebral arteries appear patent bilaterally.",
            "output": "1. Small late acute to early subacute infarct involving the posterior aspect\nof the left putamen, posterior limb of the left internal capsule and left\nposterior frontal corona radiata.\n2. No hemorrhage.\n3.  Patent intracranial arterial vasculature without significant stenosis,\nocclusion, or aneurysm.\n4.  Patent cervical arterial vasculature without significant stenosis, or\nocclusion.\n\nNOTIFICATION:  The findings were discussed with ___, M.D. by\n___, M.D. on the telephone on ___ at 2:15 pm, 20 minutes after\ndiscovery of the findings."
        },
        {
            "input": "Again seen is tissue loss related to chronic infarction involving a large\nportion of the left deep white matter. However, there are now multiple small\nfoci of slow diffusion in the left posterior frontal and the parietal white\nmatter suggesting superimposed acute or subacute infarction. Again seen is a\nchronic infarction involving the right caudate head extending through the\nanterior limb of the internal capsule and involving the putamen. There are\nseveral small foci of hemorrhage in the same distribution. The ventricles are\nenlarged in an atrophic pattern, as are the sulci. There are no other findings\nto suggest recent infarction. There are no masses are identified and there is\nno evidence of edema.",
            "output": "Acute or subacute left frontal and parietal white matter infarction\nsuperimposed upon chronic infarction in the same distribution. Chronic right\ncaudate head and putaminal infarction."
        },
        {
            "input": "Again seen are multiple small foci of slow diffusion in the left posterior\nfrontal lobe and parietal white matter, with FLAIR hyperintensity, suggesting\nsubacute infarction.  Underlying this process, there is stable tissue loss\nrelated to chronic infarction and involving a large portion of the left deep\nand periventricular white matter.\n\nThere is chronic infarction involving the right caudate head and extending\nthrough the anterior limb of the internal capsule and involving the putamen.\nThere are several small foci of hemorrhage in the same distribution. The\nventricles are enlarged in an atrophic pattern, as are the sulci. There are no\nother findings to suggest recent infarction. There are no masses identified\nand there is no evidence of edema.\n\nThere is dolichoectasia of the left supraclinoid ICA and extending into the\nleft middle cerebral artery M1 segment, unchanged from prior exams.\n\nThere are multiple patchy and confluent areas of T2/FLAIR hyperintensity\nwithin the subcortical, deep and periventricular white matter, most consistent\nwith sequela of severe chronic microvascular ischemic disease.\n\nIntracranial flow voids are maintained. There is mild mucosal thickening of\nthe maxillary sinuses and ethmoid air cells. There is minimal fluid in the\nleft mastoid air cells. Otherwise, paranasal sinuses and mastoid air cells are\nclear.  The orbits demonstrate changes of lens surgery. The soft tissues are\ngrossly unremarkable.",
            "output": "1. Unchanged subacute infarct of the left frontal lobe and parietal white\nmatter, with associated blood products. No other evidence of acute infarct,\nmass effect or extra-axial fluid collection.\n\n2. Chronic right caudate and putaminal infarction.\n\n3. Confluent areas of FLAIR hyperintensity within the white matter are likely\nsequela of severe chronic microvascular ischemic disease ."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.  There are numerous foci of T2/FLAIR hyperintensities in the\nperiventricular and subcortical white matter.  A focus of susceptibility in\nthe left posterior temporal lobe may represent a chronic micro hemorrhage or\ncalcification.\n\nThe paranasal sinuses and mastoid air cells are clear.  The orbits are\nunremarkable.\n\nThe major intracranial flow voids are preserved.",
            "output": "1. No masses or abnormal enhancement.\n2. Scattered foci of nonspecific T2/FLAIR hyperintensities in the\nperiventricular and subcortical white matter, which are more than expected in\na patient of this age.  The differential diagnosis is broad and includes the\nsequela of chronic small vessel ischemic disease (which is most likely in a\npatient with risk factors), prior trauma, infectious, inflammatory, or\ndemyelinating processes, Lyme's disease, vasculitis, or chronic migraines."
        },
        {
            "input": "MRI Brain:\nScattered small acute infarcts in the right inferior cerebellar hemisphere in\nan embolic distribution is identified.  No intracranial hemorrhage.  No\nintracranial mass.  There is high signal within the visualized right vertebral\nartery to the mid V4 segment compatible with known occlusion/thrombosis.  The\nremainder the intracranial flow voids are preserved.  Small mucous retention\ncyst in the left maxillary sinus and mild mucosal thickening of the remainder\nthe visualized paranasal sinuses is noted.  The orbits are unremarkable.  No\nsignificant fluid signal is seen in the mastoid air cells.\n\nThe marrow signal is slightly T1 hypointense, likely secondary to marrow\nreconversion with chronic anemia.\n\nMRA neck:\nThere is intrinsic T1 hyperintense signal of the V3 and V4 segments of the\nright vertebral artery compatible with thrombus, likely secondary to\ndissection.  Slightly decreased flow related signal along the visualized right\nV2 segments is identified,, potentially secondary to the V3/V4 thrombus.  The\nleft vertebral artery is unremarkable.  The bilateral common carotid and\ninternal carotid arteries are unremarkable.",
            "output": "1. Scattered small acute infarcts in the right inferior cerebellar hemisphere\nin an embolic distribution.  No intracranial hemorrhage.\n2. Findings compatible with dissection of the right V3 segment with thrombus\nextending into the right V4 segment.\n3. The bilateral common carotid, internal carotid and left vertebral arteries\nare unremarkable.\n4. The marrow signal is slightly T1 hypointense, likely secondary to marrow\nreconversion with chronic anemia.  Correlation with patient CBC values is\nrecommended.\n5. Additional findings as described above."
        },
        {
            "input": "Dental artifact partially limits evaluation of the anterior, peripheral\nmargins of the oral cavity.\n2 areas of subtle asymmetry along the right lateral tongue, 1 more anteriorly\nseries 11, image 13,  measuring 12 mm x 14 mm, second more posterolaterally in\nthe right tongue measuring 12 x 5 mm in the coronal plane (series 15, image\n15), may represent candidate superficial tongue lesion there is clinically\nevident.\n\nNo extrinsic tongue muscle involvement.  No midline extension.  No involvement\nof the neurovascular bundle and submandibular duct in the floor of mouth.  No\nosseous involvement.\n\nSusceptibility artifact from the dental amalgam slightly obscures the\nperipheral aspect of the tongue.\n\nNo level 1, 2, 3, 4 neck or retropharyngeal adenopathy.\n\nThe submandibular glands appear normal.  Fatty change of the parotid glands. \nNo suspicious parotid masses.  No mass along the aerodigestive tract.  A\ncouple of subcentimeter thyroid nodules the largest measuring 9 mm in the\nsuperior aspect of the left lobe.\n\nMultiple subcentimeter lymph nodes in the right supraclavicular and axillary\narea are abnormal in number.  Largest right supraclavicular lymph node\nmeasures 0.9 cm, at the level of the mid clavicle, right axillary largest\nlymph node measures 1.0 cm.\n\nSmall enhancing lesion in relation to the sphenoid wing on the right only seen\non coronal imaging (series 15, image 16) measuring 9 x 6 mm in the coronal\nplane, indeterminate, may represent meningioma.  In the setting of primary\ncancer dedicated brain imaging should be performed to further assess this\nlesion.\n\nModerate left-sided pleural effusion.  Enhancing opacification in the anterior\nsegment of the left upper lobe and nodular opacification in the right upper\nlobe are nonspecific and reference is made to CT chest done on the same day.\n\nSpondylotic changes of the thoracic spine with grade 1 retrolisthesis of C3 on\nC4, C4 on 5 and C5 on 6 resulting in moderate spinal stenosis.  If clinically\nindicated dedicated imaging of the C-spine can be performed.",
            "output": "Superficial lesion along the right lateral tongue is possibly identified,\nthere are 2 areas which may correspond to clinically evident lesion.  No\nextrinsic tongue muscle, osseous involvement or level ___ adenopathy.\n\nSmall intracranial dural based lesion, may represent meningioma.  Brain MRI\nrecommended.\n\nAirspace opacification as well as right axillary and supraclavicular mild\nlymphadenopathy for which reference to the CT chest done on the same day is\nmade.\n\nRECOMMENDATION(S):  Dedicated brain MRI without and with gadolinium."
        },
        {
            "input": "There is a stable 0.8 x 0.7 x 0.7 cm extra-axial enhancing mass along the\nright sphenoid wing with a dural tail, compatible with a meningioma. No new\nenhancing lesions.  Symmetric susceptibility artifact in the bilateral basal\nganglia may be related to basal ganglia calcifications or chronic hemorrhage. \nNo evidence of acute intracranial hemorrhage or infarct.\n\nThe ventricles and sulci are normal in caliber and configuration.  Subcortical\nand periventricular white matter T2/FLAIR hyperintensities are stable, likely\nrelated to chronic small vessel ischemic disease.\n\nThere is minimal mucosal thickening in the ethmoid air cells and maxillary\nsinuses.  Patient is status post bilateral lens replacement.  The orbits are\notherwise grossly unremarkable.",
            "output": "1. Stable small right sphenoid wing meningioma.  No new enhancing lesions to\nsuggest metastatic disease.\n2. Stable chronic small vessel ischemic changes.\n3. No evidence of acute intracranial hemorrhage or infarct."
        },
        {
            "input": "Re-demonstrated is a 0.3 cm x 0.5 cm enhancing nodule of the left internal\nauditory canal, overall unchanged compared to the most recent prior exam from\n___.  Otherwise, images through the internal auditory canal\ndemonstrates symmetric appearance of the seventh eighth nerve complexes. There\nis no evidence of abnormal enhancement or mass lesion within the right\ninternal auditory canal, bilateral cerebellopontine angles or membranous\nlabyrinth. No other mass lesions are seen within the posterior fossa.\n\nLimited included imaging of the remainder of the brain demonstrates no\nevidence of hemorrhage, edema, masses, mass effect, midline shift or\ninfarction. The ventricles and sulci are normal in caliber and configuration.\nThere is no abnormal enhancement after contrast administration.\n\nNo osseous abnormalities are seen. The paranasal sinuses, mastoid air cells,\nand middle ear cavitiesare clear. The orbits are unremarkable. The visualized\nportion of the principle vascular flow voids are preserved.",
            "output": "1. Stable 0.3 cm x 0.5 cm left internal auditory canal presumed vestibular\nschwannoma compared to the most recent prior exam from ___."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  Nonspecific foci of T2/FLAIR hyperintensity in the right\nfrontal lobe are likely sequela of chronic small vessel ischemic disease.  An\nenhancing focus in the distal left internal auditory canal posteriorly at the\nfundus likely represents a vestibular neuroma.",
            "output": "1. Likely left fundal vestibular neuroma.\n2. There is no acute infarct or intracranial hemorrhage.\n\nRECOMMENDATION(S):  A dedicated MR ___ can be obtained if further evaluation\nis desired."
        },
        {
            "input": "A round, well-circumscribed mass, measuring 3 x 3 x 3 mm, in the posterior\naspect of the left distal internal auditory canal and along the the left\nseventh and eighth nerve complex demonstrates homogeneous enhancement.  The\nmass does not extend to the CPA cistern and does not demonstrate slow\ndiffusion.  The right internal auditory canal and seventh and eighth nerve\ncomplex are normal.  No other mass lesions are seen within the posterior\nfossa.\n\nLimited imaging of the remainder of the brain demonstrates no evidence of\nhemorrhage, edema, mass effect, midline shift or infarction. The ventricles\nand sulci are normal in caliber and configuration.\n\nNo osseous abnormalities are seen. The paranasal sinuses, mastoid air cells,\nand middle ear cavitiesare clear. The orbits are unremarkable. The visualized\nportion of the principle vascular flow voids are preserved.",
            "output": "Three mm enhancing mass in the left posterior and distal internal auditory\ncanal, likely representing a vestibular schwannoma."
        },
        {
            "input": "There is a 3 mm TR x 3 mm AP focus of enhancement in the posterior/distal left\ninternal auditory canal, stable since ___.\n\nImages through the internal auditory canal demonstrates symmetric appearance\nof the seventh eighth nerve complexes.  No other mass lesions are seen within\nthe posterior fossa.\n\nLimited included imaging of the remainder of the brain demonstrates no\nevidence of hemorrhage, edema, masses, mass effect, midline shift or\ninfarction. The ventricles and sulci are normal in caliber and configuration.\nThere is no abnormal enhancement after contrast administration.\n\nNo osseous abnormalities are seen. The paranasal sinuses, mastoid air cells,\nand middle ear cavitiesare clear. The orbits are unremarkable. The visualized\nportion of the principle vascular flow voids are preserved.\n\nDegenerative changes are noted in the upper cervical spine.",
            "output": "1. Stable 3 mm focus of enhancement in the left internal auditory canal,\nrepresenting a vestibular schwannoma."
        },
        {
            "input": "3 mm enhancing nodule of the left internal auditory canal fundus is\nessentially unchanged since examination ___.\n\nImages through the right internal auditory canal demonstrates abnormal\nappearance of the seventh eighth nerve complex.  There is no evidence of\nabnormal enhancement or mass lesion within the right internal auditory canal,\nbilateral cerebellopontine angles or membranous labyrinth. No other mass\nlesions are seen within the posterior fossa.\n\nLimited included imaging of the remainder of the brain demonstrates no\nevidence of hemorrhage, edema, masses, mass effect, midline shift or\ninfarction. The ventricles and sulci are normal in caliber and configuration.\nThere is no abnormal enhancement after contrast administration.\n\nNo osseous abnormalities are seen. The paranasal sinuses, mastoid air cells,\nand middle ear cavitiesare clear. The orbits are unremarkable. The visualized\nportion of the principle vascular flow voids are preserved.",
            "output": "1. Unchanged 3 mm left internal auditory canal presumed vestibular schwannoma."
        },
        {
            "input": "Study is mildly degraded by motion.  No intracranial hemorrhage or acute\ninfarct.  There are innumerable enhancing supra tentorial, infratentorial and\nthe lesions, the largest measuring 8 mm in left frontal lobe.  None of the\nlesions demonstrate associated restricted diffusion or increase\nsusceptibility.  Some of the lesions demonstrate peripheral enhancement.  The\nventricles and sulci are grossly preserved in caliber and configuration.  The\nintracranial arteries demonstrate preserved T2 flow void.  The orbits appear\npreserved.  Minimal mucosal thickening involving the paranasal sinuses.",
            "output": "1. Study is mildly degraded by motion.\n2. Numerous intracranial enhancing lesions as described, some which\ndemonstrate ring enhancing pattern, and the largest measuring 8 mm in the left\nfrontal lobe, concerning for intracranial metastatic disease, with\ndifferential considerations of infectious or inflammatory etiologies less\nlikely.\n3. No evidence of acute intracranial hemorrhage or acute infarct.\n4. Paranasal sinus disease , as described."
        },
        {
            "input": "Study is severely degraded by motion.\n\nWithin limits of study, there is no definite acute infarct or large\nintracranial mass identified.  There is prominence of the ventricles and sulci\nsuggestive involutional changes.  Nonspecific periventricular and subcortical\nT2 hyperintensities are suggested, which may represent chronic small vessel\nischemic changes.  There is suggestion of a chronic right basal ganglia\ninfarct.  Left maxillary sinus mucosal thickening is noted.  Nonspecific right\nmastoid fluid is noted.",
            "output": "1. Study terminated prior to completion due to patient inability to tolerate\nexamination.\n2. Study severely degraded by motion.\n3. Paranasal sinus disease and nonspecific mastoid fluid as described.\n4. Within limits of study, no definite acute infarct or large intracranial\nmass identified.\n5. If clinically indicated, consider repeat examination when patient can\ntolerate exam."
        },
        {
            "input": "Study is moderately degraded by motion, especially on MR angiography.\n\nMR BRAIN:\n\nThere is restricted diffusion with mild enhancement in 2 areas of right corona\nradiata and 1 area in the left corona radiata, concerning for acute to\nsubacute infarct, new since prior exam on ___ and ___.  There\nis also a small punctate increased signal in the left cerebellum, which may be\na subacute infarct.\n\nNumerous punctate nonspecific foci of blood products versus mineralization are\nnoted in bilateral temporal lobes.\n\nThere is no evidence of  masses effect or  midline shift .  There is\nprominence of the ventricles and sulci suggestive involutional changes.  Again\nseen are periventricular and subcortical T2/FLAIR hyperintensities, which are\nnonspecific, but likely due to chronic small vascular ischemic disease.\n\nMucosal thickening of the right maxillary sinus is unchanged from ___.\n\nMRA brain:  Nonocclusive irregularity of left cavernous and supra clinoid\ninternal carotid artery are noted.  The left vertebral artery is not well\nvisualized on current examination.  Otherwise, the intracranial vertebral and\ninternal carotid arteries and their major branches appear grossly patent.",
            "output": "1.  Study is moderately degraded by motion.\n2. Multiple bilateral MCA and single left PCA distribution acute to subacute\ninfarcts without definite evidence of hemorrhagic transformation, as\ndescribed.  Presence of infarcts in bilateral hemispheres and multiple\nvascular territories raises concern for central embolic source.\n3. Poorly visualized left V3 and V4 segments of vertebral artery, which were\nvisualized on ___ prior head and neck CTA, which may be artifactual in\nnature.  If concern for interval occlusion of left vertebral artery, consider\nrepeat head CTA.\n4. Nonocclusive irregularity of left cavernous and supra clinoid internal\ncarotid artery which may represent atherosclerotic changes.\n5. Multiple punctate foci of blood products versus mineralization within\nbilateral temporal lobes.  Differential considerations include amyloid\nangiopathy, prior infection or trauma, and hypertensive microhemorrhages.\n6. Grossly stable paranasal sinus disease as described.\n\nNOTIFICATION:  Impression item number 2 was discussed with ___ ,\nM.D. by ___, M.D. on the telephone on ___ at 5:08 ___, 10 minutes\nafter discovery of the findings."
        },
        {
            "input": "MR BRAIN:\nMotion artifact limits assessment.  There is no evidence of hemorrhage, edema,\nmasses, mass effect, midline shift or infarction.   The ventricles and sulci\nare age-appropriate.  Periventricular and subcortical white matter T2/FLAIR\nhyperintensities are nonspecific but likely sequelae of chronic small vessel\nischemic disease.\n\nLingual tonsils are mildly prominent.  Status post bilateral lens replacement.\nSmall mucous retention cyst in the posterior left ethmoid air cells otherwise\nthe remainder the visualized paranasal sinuses are essentially clear.  The\norbits are unremarkable noting bilateral lens replacements.  Trace fluid\nsignal is seen in the bilateral mastoid tips.\n\nMRA brain:\nThere is a dominant left vertebral artery.  ___ termination of the right\nvertebral artery.  There is a hypoplastic left A1 segment. The intracranial\nvertebral and internal carotid arteries and their major branches otherwise\nappear normal without evidence of stenosis, occlusion, or aneurysm formation.",
            "output": "1. No acute intracranial abnormality on contrast enhanced MRI brain.  No acute\ninfarct or intracranial hemorrhage.  No suspicious parenchymal FLAIR signal\nabnormality.  No intracranial mass or abnormal enhancement.\n2. The dural venous sinuses are patent.\n3. Unremarkable MRA of the head."
        },
        {
            "input": "No acute infarct, suspicious focus of intracranial hemorrhage, mass effect,\nshift of normally midline structures or hydrocephalus.\nThere are a few  small T2 FLAIR hyperintense foci in the cerebral white matter\nin the frontal and parietal lobes predominantly on the left and a few in the\npons, nonspecific in appearance.\nNo focus of abnormal enhancement noted in the brain parenchyma or meninges.\n\nThe ventricles, extra-axial CSF spaces, cerebral sulci and cerebellar folia\nare normal.\nThe major intracranial arterial flow voids are noted.\nSella, pineal gland and craniocervical junction regions are unremarkable.\n\nThe imaged paranasal sinuses and the mastoid air cells are clear.\nThe imaged orbits are unremarkable.\nThe marrow signal intensity is slightly hypointense in the calvarial bones.",
            "output": "No focus of abnormal enhancement in the brain parenchyma or meninges.\nA few small nonspecific cerebral white matter changes, may relate to small\nvessel ischemic changes, postinflammatory sequela etc. Correlate clinically\nfor risk factors.\n\nSlightly hypointense marrow signal, can relate to cellular marrow.\nCorrelate with hematology labs for anemia, systemic disease,\nmyeloproliferative or infiltrative changes.\n\nPlease see the concurrent MR spine study for other important details."
        },
        {
            "input": "There is confluent enhancement within the epidural space of the anterior\nposterior fossa, which is scalloping the pons and medulla, but shows no\nevidence of loculated or rim enhancement fluid collection and is most\nconsistent with a residual phlegmonous process. There is no evidence of slow\ndiffusion associated with this finding. There is no significant mass effect on\nthe brainstem, as shown by no significant FLAIR hyperintensity.\n\nThe right cerebellar hemisphere again demonstrates a focal of abnormal\nenhancement (___), which is decreased in size and less conspicuous compared to\n___. There is no evidence of abnormal diffusion associated with this\nfocus or significant FLAIR abnormality. This focus may represent sequela of\nseptic emboli, versus less likely a subacute infarct.\n\nThere is no hemorrhage, intracranial mass, mass effect, extra-axial fluid\ncollections or midline shift.  There is no slow diffusion to suggest acute\ninfarct. The basilar cisterns are within normal limits.  There are foci of\nT2/FLAIR hyperintensities throughout the deep and periventricular white\nmatter, nonspecific, but most likely sequela of chronic microvascular ischemic\ndisease. There is generalized prominence of the ventricles and sulci,\nconsistent with generalized cerebral volume loss.\n\nIntracranial flow voids are maintained. Visualized paranasal sinuses are\nclear. There is a small amount of fluid in the mastoid air cells. The orbits\nand soft tissues are grossly unremarkable.",
            "output": "1. Confluent enhancement within the epidural space of the posterior cranial\nfossa, scalloping the pons and medulla, but without evidence of loculated or\nrim enhancing fluid collection. Findings are most consistent with phlegmonous\nprocess.  Previously seen loculated fluid within enhancement has resolved. No\nsignificant mass effect on the brainstem. No evidence of hemorrhage.\n2. Focus of enhancement within the right cerebellar hemisphere is stable to\nslightly decreased in size compared to prior study of ___, without\nevidence of abnormal diffusion or other signal abnormality. This may represent\nsequela of septic emboli versus less likely a subacute infarct. Metastatic\nfocus is also a consideration. Attention on followup is recommended.\n3. Cervical spine findings are reported separately on concurrent MRI of the\ncervical spine."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There are no abnormal T2 or FLAIR hyperintensities or areas of\nabnormal postcontrast enhancement.",
            "output": "1. Normal brain MRI.  Specifically, no evidence of intracranial demyelinating\ndisease."
        },
        {
            "input": "In the region of the evacuated cyst in the right cerebellum, there is\nintrinsic T1 hyperintensity representing postoperative hemorrhage.\nAdditionally, there are patchy areas of gadolinium enhancement.\n\nAgain noted, are areas of FLAIR hyperintensity in the bilateral parietal and\nleft occipital lobes and associated susceptibility artifact, representing old\ninfarcts with blood products. Additionally, there are new scattered foci of\nsusceptibility artifact in the frontal and parietal lobes bilaterally, likely\nrepresenting postoperative subarachnoid hemorrhage.\n\nThere is no evidence of acute infarction on diffusion-weighted imaging.\nPostoperative dural enhancement of the internal auditory canal is likely\npostoperative in nature.\n\nThe orbits are unremarkable. Sinus disease, worst in the right maxillary sinus\nis noted.",
            "output": "1. Area of patchy enhancement in area of evacuated right cerebellar cystic\nlesion, may represent subacute infarction or metastasis.\n\n2. Scattered areas of susceptibility artifact in the frontal and parietal\nlobes bilaterally and in the right cerebellum, likely represents postoperative\nsubarachnoid hemorrhage and local hemorrhage at the evacuation site,\nrespectively.\n\n3. Old bilateral parietal and left occipital lobe infarcts with blood\nproducts.\n\n4. Dural enhancement of the internal auditory canal is likely postoperative in\nnature, close attention on followup."
        },
        {
            "input": "Compared to prior MRI, the fluid collection in the right cerebellar surgical\nbed is larger and extends through the right occipital bone defect into the\nscalp, as seen on the CT scan from ___. There there is patchy peripheral\nenhancement around the collection, which may be reactive given the surgery 6\ndays earlier. There is increased effacement of the fourth ventricle and a mild\nincrease in the size of the lateral and third ventricles compared to ___, as\nseen on the ___ CT. There remains effacement of the quadrigeminal plate\ncistern, similar in severity to the CT from ___.\n\nAgain noted are foci of encephalomalacia in the bilateral occipital, right\nparietal and right frontal lobes, with associated gyriform susceptibility\nartifact, representing old infarcts with siderosis. There is no acute\ninfarction.\n\nThere is a mucous retention cyst in the right maxillary sinus.",
            "output": "1. Increased fluid collection in the right cerebellar surgical bed with\nincreased extension through the right occipital bone defect into the scalp\ncompared to ___. A pseudomeningocele is not excluded.\n2. Increased compression of the fourth ventricle by the right cerebellar fluid\ncollection with increased dilatation of the lateral and third ventricles\ncompared to ___.\n3. Patchy rim enhancement along the surgical bed may be reactive on post\npostsurgical day 6, but should be followed to ascertain resolution.\n4. The above findings are similar to the noncontrast head CT from ___\nallowing for differences in modalities."
        },
        {
            "input": "There are postoperative changes from right occipital craniectomy. There are\nhemorrhagic products within the surgical bed. There is unchanged minimal\npatchy peripheral enhancement surrounding the surgical cavity which may\nrepresent postoperative changes, but residual tumor can not be excluded. There\nis decreased mass effect with in the posterior fossa.\n\nBilateral parieto-occipital encephalomalacia with associated gyriform is\nhypointensity on gradient imaging is unchanged.\n\nThere is a right frontal ventriculostomy catheter in place with the tip\nterminating in the right lateral ventricle. The ventricles, sulci and cisterns\nare stable in size and configuration when compared to recent head CT. The\npneumocephalus is grossly unchanged.  There is no acute infarct or new\nhemorrhage. The principal intracranial flow voids are present.\n\nThere is mild ethmoid and bilateral maxillary sinus mucosal thickening. There\nis a right maxillary sinus mucous retention cyst.",
            "output": "There are postoperative changes from right occipital craniectomy and with\nimproved mass effect in the posterior fossa when compared to prior MRI. There\nis unchanged minimal patchy peripheral enhancement surrounding the surgical\ncavity which may represent postoperative changes, but residual tumor cannot be\nexcluded.\n\nRight frontal ventriculostomy catheter is unchanged from recent head CT. The\nventricles are stable in size and configuration."
        },
        {
            "input": "MRI BRAIN:\nThere is no evidence of hemorrhage, edema, masses, mass effect, or midline\nshift.  Multiple small chronic lacunar infarcts are noted: 2 in the right\ncerebellar hemisphere, 1 in the right basal ganglia, 1 in the right thalamus,\npossibly 1 in the left frontal lobe (series 13, image 15) and 1 in the right\nfrontal lobe.  A punctate focus of slow diffusion is seen within the left\nfrontal lobe, series 8, image 23 with associated FLAIR signal abnormality and\npossible low signal on the ADC map.  There is no abnormal enhancement after\ncontrast administration.  Small short linear area of signal void in relation\nto the right central sulcus (series 12, image 20) on the GRE sequence is\nnonspecific and may represent a normal blood vessel.  The pituitary appears\nnormal.  The craniocervical junction appears normal.  The orbits appear\nnormal.  Minimal mucosal thickening in the inferior aspect of the right\nmaxillary sinus.  The intracranial arteries demonstrate normal T2 flow voids.\n\nMRA BRAIN:\nThe intracranial left vertebral and bilateral internal carotid arteries and\ntheir major branches are patent without marked stenosis, occlusion, or\naneurysm formation.  Diminutive right V4 segment.\n\nMRA NECK:\nThe carotid arteries are patent bilateral.  No ICA stenosis by NASCET\ncriteria.  Dominant left vertebral artery appear the vertebral arteries are\npatent bilateral.",
            "output": "1. Punctate focus of embolic infarct is seen in the left frontal lobe likely\nlate acute/early subacute in timing.  No associated enhancement is seen.\n2. Multiple small chronic lacunar infarcts in multiple vascular territories\nsuggest prior embolic infarcts.\n3. No abnormal enhancing lesions.\n4. No intracranial arterial marked narrowing, occlusion or aneurysm. \nDiminutive right V4 segment.\n5. The carotid arteries are patent bilateral.  No proximal ICA stenosis by\nNASCET criteria.\n6. Dominant left vertebral artery.  The vertebral arteries are patent\nbilateral.\n\nNOTIFICATION:  The findings were discussed with ___, M.D. by ___\n___, M.D. on the telephone on ___ at 6:30 pm, 10 minutes after\ndiscovery of the findings."
        },
        {
            "input": "The midline mass centered in the pineal region demonstrates thick, irregular,\nand nodular peripheral enhancement, as seen previously.  The central\nnonenhancing portion of the mass has markedly expanded compared to the\npreoperative MRI from ___.  This causes interval enlargement of\nthe mass with increased anterior extension.  The mass now measures 5.8 cm AP,\n3.7 cm craniocaudad, and 4.8 cm transverse, images 9:125 and 10:13, compared\nto 4.0 x 3.5 x 3.5 cm when measured in the same planes on ___.\nThe central nonenhancing portion of the mass is heterogeneous with\npredominantly high signal on T2 weighted images.  Its signal on precontrast T1\nweighted images is lobe was higher than that of CSF.  It demonstrates only\nsmall foci of low signal intensity on gradient echo images, consistent with\nsmall amount of blood products.  The enhancing rim of the mass demonstrates\nlow signal on gradient echo images, consistent with blood products.\n\nThere is mild contrast enhancement along the right superior cerebellar folia,\nsimilar to the preoperative MRI from ___, suggesting tumor\ninfiltration.\n\nThere is linear T1 hyperintensity, low signal on gradient echo images, and\ncontrast enhancement extending from the right posterior aspect of the pineal\nregion mass to the right parietal burr hole, consistent with blood and\nprobably reactive enhancement along the surgical biopsy track.\n\nA right frontal approach ventriculostomy catheter is again seen in place with\nits tip in the frontal horn of right lateral ventricle.  The ventricles are\nslit-like, unchanged compared to the most recent CT from ___, but\ndecreased compared to the ___ head CT obtained immediately\nfollowing VP shunt placement.  There is persistent slight asymmetry in the\nsize of frontal horns of the lateral ventricles, right smaller than left.\n\nThere is no evidence for acute infarction on diffusion-weighted images.  Major\nflow voids of the circle of ___ appear grossly preserved.\n\n___ cisterna magna is again noted, a normal variant.\n\nThere is mild mucosal thickening in left greater than right maxillary sinuses\nand ethmoid air cells.",
            "output": "1. The ventricles appear slit-like, similar to the most recent CT from ___, but decreased compared to ___.  VP shunt catheter\nposition is stable.\n2. The large peripherally enhancing midline mass centered in the pineal region\ndemonstrates marked enlargement of its central nonenhancing portion compared\nto the preoperative MRI from ___.  The mass is now overall larger,\nextending further anteriorly.  The expanded central nonenhancing portion\nappears heterogeneous, with complex fluid and small amount of blood.  The\nenlargement is most likely secondary to decreased intracranial pressure and\nassociated fluid shifts after relief of hydrocephalus.\n3. Unchanged mild contrast enhancement along the right superior cerebellar\nfolia compared to the preoperative MRI, suggesting tumor infiltration.\n4. Linear blood products and contrast enhancement along the biopsy track\nthrough the right parietal and occipital parenchyma.  The contrast enhancement\nis presumably reactive, but should be reassessed on follow up.\n5. No evidence for an acute infarction."
        },
        {
            "input": "Since the prior MRI from ___, there has been interval decrease in\nsize and a large, peripherally enhancing lobulated mass centered at the pineal\ngland, currently 2.8 x 5.0 x 3.6 cm, previously 3.7 x 5.8 x 4.8 cm (17:95,\n19:60).  Peripheral enhancing ran and posterior enhancing nodularity\ncorrespond to areas of restricted diffusion (6:16, 7:16).\n\nBifrontal ventriculoperitoneal shunt catheters are unchanged in position,\nterminating near the foramen of ___.  There is a small amount of T2/FLAIR\nsignal hyperintensity tracking along the shunt catheter course in the\nbilateral frontal white matter (15:18).  There is no evidence of\nhydrocephalus.  There is no evidence of transependymal CSF migration.  No new\nintracranial mass lesion is identified.  Hemorrhagic rim around the central\ncranial mass is indicated by susceptibility artifact on gradient recalled echo\nimages (14:14), in corresponds to mild increased intrinsic T1 signal\nintensity.\n\nThere is no shift of the normally midline structures.  No acute vascular\nterritorial infarction is identified.  The orbits are unremarkable.  There is\nmild mucosal thickening in the right maxillary sinus (13:6).  Intracranial\nvascular flow voids are preserved.",
            "output": "1. Compared to the prior MRI from ___, there has been interval\ndecrease in size of large peripherally-enhancing lobulated mass centered at\nthe pineal gland.\n2. The previously described enhancement extending along the superior right\ncerebellar folia and along the biopsy tract from the right parietal burr hole\nto the mass lesion are no longer appreciated.\n3.   No new intracranial hemorrhage or focus of pathologic postcontrast\nenhancement is identified.\n4. Slit-like lateral ventricles are slightly smaller in appearance compared to\nthe prior CT from ___, allowing for inter modality differences. \nBifrontal ventriculoperitoneal shunt catheters are unchanged in position."
        },
        {
            "input": "Allowing for differences in patient positioning and technique, the known large\nperipherally enhancing mass centered in the pineal gland is slightly decreased\nin size, currently measuring 2.5 x 5.0 x 3.1 cm, previously 2.8 x 5.0 x 3.6 cm\n(series 17, image 89; series 19, image 63).  As seen on the prior MR\nexamination, the peripheral rim enhancement surrounding the lesion and an area\nof nodularity along the posterior aspect of the lesion corresponds to an area\nof restricted diffusion (series 6, image 15; series 7, image 15). \nAdditionally, hemorrhagic component is again seen around the mass, as\nindicated by susceptibility artifact on gradient recalled echo images (series\n15, image 14).  No new enhancing lesions are identified.\n\nBifrontal approach ventricular drains remain in unchanged position, the right\nterminates proximal to the the foramen of ___, the left in the frontal horn\nof the left lateral ventricle.  T2/FLAIR hyperintensity surrounds the shunt\ncatheter course in the bifrontal white matter.\n\nThere is no evidence of midline shift or infarction.   The ventricles and\nsulci are normal in caliber and configuration.\n\nThere is minimal mucosal thickening of the right maxillary sinus.  Otherwise,\nthe remaining visualized paranasal sinuses and mastoid air cells are clear. \nThe dural venous sinuses are patent.  The intracranial flow voids are\npreserved.  The orbits are unremarkable.",
            "output": "1. Slight interval decrease in size of a large peripherally enhancing mass\ncentered in the pineal gland as compared to the most recent prior MR from ___.\n2. No new enhancing lesions identified.\n3. Bifrontal ventricular drains remain in unchanged position."
        },
        {
            "input": "Metallic artifact from a right frontal ventriculostomy reservoir results in\nsuboptimal evaluation of the adjacent structures.  Bilateral trans frontal\nventriculostomy cysts are unchanged in position.\n\nContinued interval decrease size of a peripherally enhancing 4.1 x 2.9 x 2.3\ncm (AP, TRV, SI) mass centered in the tiny pineal gland, previously measuring\napproximate 5.0 x 3.1 x 2.5 cm.  Again noted is associated peripheral vision\nweighted hyperintense signal and gradient echo susceptibility artifact\ncompatible with posttreatment changes and hemorrhage.  No new lesions.\n\nThere is no ventriculomegaly.  The basilar cisterns are patent.  Major\nintracranial flow voids are preserved.  Mild mucosal thickening of the ethmoid\nair cells and right maxillary sinus is identified.  The orbits are\nunremarkable.  The mastoid air cells are clear.",
            "output": "1. Continued interval decrease size of a 4.1 cm peripherally enhancing mass\ncentered in the pineal gland when compared to prior examination.\n2. No new lesions.\n3. Unchanged position of bilateral transfrontal ventriculostomy catheters.  No\nventriculomegaly."
        },
        {
            "input": "43 x 29 x 24 mm heterogeneously rim enhancing mass with areas of slowed\ndiffusion centered in the pineal gland is unchanged in size since ___\ngiven difference of slice selection.  Surrounding mass effect and effacement\nof the cerebral aqueduct and third ventricle is unchanged.  There is inferior\ndisplacement of the tectal plate.  Re- identified is peripheral susceptibility\nartifact reflecting posttreatment change and hemorrhage.\n\nBilateral frontal approach ventriculoperitoneal shunt catheters are unchanged\nin position and there is no ventriculomegaly.  Susceptibility artifact from a\nVP shunt catheter reservoir on the right, limits evaluation of the immediately\nunderlying right frontal parenchyma.  There is no evidence of acute\nhemorrhage, edema, new masses, midline shift or infarction.  The principal\nintracranial vascular flow voids are preserved.  The dural venous sinuses are\npatent on MP-RAGE images.\n\nThere is mild mucosal wall thickening in the right maxillary sinus.  The\nremainder of the visualized paranasal sinuses are grossly clear.  The orbits\nare grossly unremarkable.",
            "output": "1. Unchanged 43 x 29 x 24 mm heterogeneously rim enhancing mass centered in\nthe pineal gland.\n2. No acute hemorrhage, infarct, or new enhancing mass.\n3. Unchanged position of bilateral frontal approach VP shunt catheters without\nventriculomegaly."
        },
        {
            "input": "Right frontal shunt hardware artifact limits examination.\n\nAllowing for slight differences in image acquisition and measurement\ntechnique, the 4.3 x 2.7 x 2.4 cm rim enhancing heterogeneous mass with areas\nof slowed diffusion centered in the pineal gland is unchanged since ___ (19:73, 17:82).  Surrounding mass effect and effacement of the cerebral\naqueduct and third ventricle is unchanged.  Inferior displacement of the\ntectal plate is also unchanged.  Peripheral susceptibility artifact reflecting\npost treatment change and hemorrhage is again noted.\n\nBifrontal approach ventriculoperitoneal shunt catheters are unchanged in\nposition.  There is no ventriculomegaly.  Susceptibility artifact from the\ncatheter reservoir on the right limits evaluation of the medially underlying\nright frontal parenchyma.  There is no evidence of acute intra hemorrhage,\nedema, new masses, mass effect, midline shift or infarction.\n\nThe principal intracranial flow voids are preserved.  The dural venous sinuses\nare patent at post contrast MPRAGE.\n\nMild mucosal thickening in the right maxillary sinus is unchanged.  The\nremaining paranasal sinuses, mastoid air cells, middle ear cavities are",
            "output": "1. Right frontal shunt hardware artifact limits examination.\n2. Grossly stable 4.3 cm heterogeneously rim enhancing mass in the pineal\ngland compared to ___.\n3.  Within limits of study, no acute hemorrhage, infarction, or new enhancing\nmass.\n4. Grossly stable bilateral frontal approach VP shunt catheters, without\nevidence of ventriculomegaly."
        },
        {
            "input": "There is susceptibility artifact from a right frontal approach VP shunt\ncatheter hardware limiting adjacent evaluation.\n\nRight frontal approach VP shunt catheter tip terminates at the level of the\nforamen ___ and ___ frontal approach VP shunt catheter tip terminates in\nthe left lateral ventricle, unchanged compared to the prior examination. \nThere is near complete collapse of the lateral ventricles, unchanged compared\nthe prior examination.  The ventricles and sulci are otherwise unchanged in\nsize and configuration.\n\nHeterogeneous, rim enhancing mass centered within the pineal gland measures\napproximately 5.3 x 2.1 x 3.0 cm (AP by CC by TV) (13:106, 100a:51) slightly\nincreased in size when utilizing similar technique measuring 4.8 x 2.2 x 2.9\ncm on the ___ examination.  A peripheral rim of slowed diffusion\nand rim of susceptibility artifact indicating blood product is unchanged. \nInferior displacement of the tectal plate and effacement of the cerebral\naqueduct is unchanged.  Surrounding FLAIR hyperintensity involving the\nthalamus and hypothalamus appears slightly increased compared to the prior\nexamination.\n\nThere is no evidence of acute hemorrhage, midline shift or infarction.  No new\nfocus of post contrast enhancement is seen.  The dural venous sinuses are\npatent on MP -RAGE images.  The principal intracranial vascular flow voids are\npreserved.\n\nThere is trace mucosal wall thickening in the right maxillary sinus.  The\nremainder the visualized paranasal sinuses are grossly clear.  The orbits are\ngrossly unremarkable.",
            "output": "1. Slight interval increase in size of a 53 x 21 x 30 mm rim enhancing mass\ncentered in the pineal gland compared to ___, with slight interval\nincrease in surrounding FLAIR signal abnormality along the thalamus and\nhypothalamus.  No definite associated increased nodular enhancement or\ndiffusion-weighted hyperintense signal.\n2. Unchanged positioning of bifrontal approach VP shunt catheters with\nunchanged near complete collapse of the lateral ventricles.\n3. No new enhancing mass."
        },
        {
            "input": "MR BRAIN: Bilateral trans frontal ventriculostomy catheters are unchanged in\nposition from prior examination.  Susceptibility artifact from the right\nfrontal reservoir are results in suboptimal evaluation of adjacent structures.\n\n4.1 x 2.7 by 1.9 cm (AP, TRV, SI) demonstrating T1 peripheral hyperintensity\nand gradient echo hypointensity compatible with posttreatment blood product is\nunchanged in size from prior examination.  There is resolution of previously\ndescribed increased enhancement and FLAIR hyperintense signal along the\nbilateral thalami and hypothalamus.  No discernible enhancement is identified\nassociated with the lesion.  There is increased nonenhancing T1 hyperintense\nnodular focus along the inferior aspect of the lesion, felt to be involutional\nin nature.\n\nThere is mild increased periventricular FLAIR hyperintense signal when\ncompared to prior examination, symmetric, likely representing posttreatment\neffect.  No acute infarct or intracranial hemorrhage is identified.\n\nThe major intracranial flow voids are preserved.  The dural venous sinuses are\npatent on postcontrast MP-RAGE.  There is mild mucosal thickening of the\nbilateral maxillary sinuses and ethmoid air cells.  The orbits are\nunremarkable.  No fluid signal is noted in the mastoid air cells.\n\nMR ___: There is hypoperfusion of the pineal lesion on dynamic\ncontrast susceptibility.\n\nMR Spectroscopy: Single and multi voxel spectroscopy centered over the pineal\nlesion demonstrates a large lactate peak with overall paucity of metabolites\ncompatible with posttreatment change.",
            "output": "1. Unchanged size of 4.1 cm pineal lesion when compared to prior exam, with\nresolution of increased enhancing FLAIR hyperintense signal along the\nbilateral thalami and hypothalami.  The lesion demonstrates no discernible\nenhancement on the current examination.\n2. No new abnormal enhancement is identified.\n3. There is hypoperfusion associated with a pineal lesion.  Single voxel and\nmulti voxel spectroscopy centered over the pineal lesion demonstrates overall\npaucity of metabolites with increased lactate, compatible with posttreatment\nchange.\n4. Mildly increased periventricular FLAIR hyperintense signal, likely\nrepresenting posttreatment effect.\n5. Additional findings as described above."
        },
        {
            "input": "Bilateral frontal approach ventriculostomy catheters are unchanged in position\ncompared to the most recent prior examination and the lateral ventricles\nremain decompressed.  Extensive susceptibility artifact from the right frontal\nreservoir limits assessment of adjacent structures, as before.\n\nRedemonstrated is a an approximately 45 x 22 x 27 mm (AP x SI x TV) lesion in\nthe pineal region demonstrating a thick rim of intrinsically T1 hyperintense\nsignal and low gradient echo signal, consistent with posttreatment hemorrhagic\nproducts.  The mass previously measured 48 x 23 x 27 mm (series 3, image 11;\nseries 5, image 12).  Substantial mass effect on the tectum is unchanged.  The\ncentral portion of the lesion demonstrates hyperintense FLAIR signal, but does\nnot show enhancement.  Confluent bilateral periventricular white matter FLAIR\nhyperintensities are similar compared to the prior examination, likely\nreflecting post treatment changes.  Apparent areas of slow diffusion along the\nperiphery of the lesion are likely related to presence of blood products in\nthese regions.  There is no evidence of acute infarction.  No new enhancing\nlesions identified.  Principal intracranial vascular flow voids are preserved.\nThe dural venous sinuses are patent on postcontrast MP-RAGE sequence.  There\nis mild mucosal thickening in the right maxillary sinus.",
            "output": "1. Grossly unchanged size of pineal lesion with peripheral hemorrhagic\nproducts, likely related to post treatment changes.  There is no definite\ncentral enhancement.\n2. Grossly unchanged confluent periventricular FLAIR hyperintensities may be\nrelated to post treatment effect.\n3. Bilateral ventriculostomy shunts are in place and the ventricles remain\ndecompressed.\n4. No acute intracranial abnormality and no evidence of new enhancing lesions."
        },
        {
            "input": "There is 4.9 cm x 2.4 cm by 2.9 cm peripheral hemorrhagic pineal mass,\ncompared with 4.8 cm x 2.3 cm by 2.9 cm on ___, and 4.8 cm x 2.3 cm\nby 3.0 cm on ___.  No definite new enhancement since prior.  Tumor\nextends anteriorly into the third ventricle, nearly to level of the anterior\ncommissure,, with tiny nodule component draping over superior margin of the\nmamillary bodies.  Anterior, nodular and linear hemorrhagic component of the\ntumor has been increasing, it measured 0.76 mm x 0.41 mm on sagittal image 103\non ___, 0.88 mm by 0.49 mm on sagittal image 126 on ___,\nand it measures 1.2 cm x 0.56 cm today as measured on MP rage images; judging\npre and post spin echo T1 images, this component appears hemorrhagic without\ndefinite enhancement..\n\nMass effect on the posterior midbrain, distinct tectum plate is not\nidentified.  Mass effect on the adjacent superior cerebellum.  Internal\ncerebral veins, vein ___ drape over the mass, appear patent.  Straight\nsinus is patent.\n\nThere are patchy and confluent symmetric nonenhancing T2 signal abnormalities\nin the bilateral centrum semiovale, posterior corona radiata, periatrial white\nmatter extending into the deep white matter of periventricular temporal lobes,\nstable since ___, ___, more prominent compared with ___, consistent with postradiation change.  There is no T2 signal\nabnormality of the adjacent corpus callosum.  Subtle irregularity and\nindistinctness of the adjacent posteromedial margin both thalamus, similar to\nmost recent, mildly improved since ___.  Hypothalamic abnormality\nhas resolved since ___.\nThere are bilateral ventriculostomy shunt in place, with tips in the frontal\nhorns, ventricular system is decompressed, frontal horns are slit-like,\nsimilar to prior.  Areas of T2 signal abnormality surrounding both tracts,\nsimilar compared with ___, likely postoperative.  Generalized\nbrain parenchymal atrophy.  Right parietal burr hole.  Dural venous sinuses\nare patent.  Intracranial vascular flow voids are preserved mild mucosal\nthickening right maxillary sinus.  Mastoid air cells are clear.",
            "output": "1. No new areas of enhancement involving mass centered on the pineal gland,\noverall stable in size.  Slowly increasing hemorrhagic nodular component along\nanterior-most component of the tumor at the level of third ventricle, likely\nposttreatment change.\n2. No hydrocephalus.\n3. Symmetric nonenhancing T2 bright deep white matter hyperintensities, likely\nposttreatment change."
        },
        {
            "input": "There is a 4.7 x 2.9 x 2.4 cm mass centered in the pineal region demonstrating\na central core of T1 hypointensity and T2 hyperintensity, with a peripherally\nT1 hyperintense hemorrhagic rim.  There is minimal peripheral enhancement\nafter contrast administration.  The lesion appears unchanged in size dating\nback to ___.\n\nLocal mass effect on the adjacent midbrain, thalamus, superior cerebellum, and\ntectum appears unchanged.  The adjacent venous structures, including the\nstraight sinus, vein of ___, and bilateral internal cerebral veins appear\npatent on MP rage sequences.\n\nNonenhancing T2/FLAIR signal abnormalities are again noted within the\nposterior bilateral centrum semiovale, periventricular white matter, with\nextension into the bilateral temporal lobe white matter.  These findings are\nunchanged may relate to prior radiation.\n\nThe patient is status post bilateral external ventricular shunt placement,\nwith the  catheters terminating at the level of the foramina of ___,\nunchanged in location from the prior exam.  The lateral and fourth ventricles\nare normal in size.\n\nThe major intracranial flow voids are maintained.\n\nMild mucosal thickening is seen in the right maxillary sinus.  The remainder\nof the visualized paranasal sinuses, middle ear cavities, and mastoid air\ncells are well aerated and clear.  The orbits are within normal limits\nbilaterally.",
            "output": "1. Unchanged appearance of a minimally peripherally enhancing, peripherally\nhemorrhagic mass centered at the level of the pineal gland, reflecting the\nglioblastoma.\n2. Stable bilateral periventricular white matter T2/FLAIR hyperintensities\nwithout associated enhancement, likely due to post radiation changes.\n3. Bilateral lateral ventricular shunts and place with collapse of the lateral\nventricles, unchanged."
        },
        {
            "input": "Again seen is peripheral E T1 hyperintense lesion indicating blood products\nwith mild enhancement in the region of pineal gland which is overall not\nsignificantly changed in size and appearance compared to the prior study. \nBilateral ventricular shunts with collapse lateral ventricles are again noted.\nNo new areas of signal abnormalities or enhancement are identified.  No acute\ninfarcts are seen.",
            "output": "Stable imaging appearance and size of the pineal region lesion compared to the\nprevious MRI of ___."
        },
        {
            "input": "A large area of susceptibility artifact overlying the right frontal lobe\nlimits evaluation of the adjacent structures.  Allowing for this:\n\nCentered within the expected location of the pineal gland, there is again seen\na peripherally enhancing centrally T2/FLAIR heterogeneously hyperintense\nlesion measuring 5.0 x 3.0 cm (AP by TV), overall largely unchanged in size\nmorphology as compared to the previous examination.\n\nAreas of peripheral intrinsic T1 hyperintensity are compatible with blood\nproducts and demonstrate associated gradient echo signal dropout, unchanged\nfrom the examination.\n\nA focus of enhancement, T2 heterogeneity, and gradient echo susceptibility\nseen within the posteromedial right thalamus (17:75, 14:11) appears progressed\nfrom the previous examination, and may represent an area of increased tumor\ninvasion with associated microhemorrhage.\n\nThere is no evidence for acute territorial infarction.  No convincing evidence\nfor acute intracranial hemorrhage.\n\nBilateral external ventricular drains are noted, unchanged in course and\nposition as compared to the previous examination.  The ventricles and sulci\nare unchanged and grossly within normal limits.\n\nThere is no evidence for additional sites of abnormal intracranial enhancement\nor new/additional areas of mass.  No edema, midline shift, or evidence of\nimpending downward herniation at this time.\n\nProminent retro cerebellar CSF spaces are noted, unchanged and most compatible\nwith ___ cisterna magna versus arachnoid cyst.  The principal intravascular\nflow voids are preserved.\n\nMild mucosal thickening is seen in the bilateral maxillary sinuses.  The\nremainder of the paranasal sinuses mastoid air cells are clear bilaterally. \nThe orbits are unremarkable.",
            "output": "1. Large heterogeneous and irregular mass centered within the expected\nlocation of the pineal gland, overall similar in size morphology as compared\nto the previous examination.\n2. Increasingly conspicuous focus of T1/T2 heterogeneity with gradient echo\nsusceptibility seen within the posteromedial right thalamus.  These findings\nmay represent local tumor invasion, potentially with superimposed\nmicrohemorrhage.  Continued attention on follow up is recommended.\n3. Unchanged position of bilateral EVD's, with a stable appearance to the\nventricular size.\n4. No evidence for acute intracranial hemorrhage or infarction."
        },
        {
            "input": "Two new nodular area of enhancements are identified adjacent to the previously\nseen rim enhancing lesion in the  pineal region with extension to the\nposterior third ventricle.  An approximately 1.5 cm enhancing nodular lesion\nis seen in the right posterior temporal lobe (16:12) an as second nodular\nenhancing lesion measuring 13 mm is seen at the medial aspect of the right\nthalamus projected over the right lateral ventricle or could be involving the\nchoroid plexus.  The overall size of the rim enhancement within the pineal\nregion has slightly decreased to 22 x 18 mm compared to 24 x 22 mm previously.\nBilateral frontal shunt catheters extend to both lateral ventricles.  There is\nno hydrocephalus.  There is no leptomeningeal enhancement seen.  No acute\ninfarcts are identified.",
            "output": "1. 2 new nodular areas of enhancement are seen adjacent to previously seen rim\nenhancing lesion in the pineal region as described above.\n2. Previously seen rim enhancing lesion within the pineal region has slightly\ndecreased in size but continues to so enhancement along the posterior aspect\nof the third ventricle.\n3. No hydrocephalus."
        },
        {
            "input": "No significant change in position of the bifrontal ventriculostomies.  There\nis associated susceptibility artifact partially obscuring the right frontal\nlobe.\n\nThere has been a decrease in size of the peripherally enhancing with central\nheterogeneous T2/FLAIR signal, centered in the pineal region, measuring 2.3 cm\nAP x 2.1 cm TV x 1.9 cm SI (previously 2.7 x 2.2 x 1.9 cm).  There has been a\ndecrease in size of the enhancing nodular foci in the posterior right temporal\nlobe and medial right thalamus.  Redemonstrated is possible involvement of the\nchoroid plexus within the right lateral ventricle trigone.  There is a similar\ndegree of associated FLAIR signal abnormality.\n\nThere has been a slight increase in prominence in susceptibility at the\ninferior margin of the mass compatible with old blood products.  Hemosiderin\nstaining continues to a lining the anterior margins of the lesion.\n\nThere is no acute infarction or intracranial hemorrhage.  The ventricles and\nsulci are normal in caliber and configuration.\n\nThe major intracranial vascular flow voids are maintained.  The paranasal\nsinuses, mastoid air cells and orbits are normal.\n\nThere is intermediate/low T1 signal of the visualized cervical vertebral\nbodies.",
            "output": "1. Decrease in size of the peripherally enhancing mass centered in the pineal\nregion is well as decrease in size in previously described surrounding nodular\nenhancement.\n2. Intermediate/low T1 signal of the visualized cervical vertebral bodies.\n3. No acute infarction or intracranial hemorrhage."
        },
        {
            "input": "In comparison with the most recent MRI examination, there is interval\nenlargement and increased pattern of heterogeneous enhancement in the\nposterior aspect of the right thalamus and medial aspect of the right\nventricular trigone, the lesion centered in the area of the pineal gland\nremains hypointense on the sagittal MP RAGE images after contrast\nadministration and measures approximately 19 x 10 mm in sagittal projection,\npreviously 21 x 10 mm (image 29, series 18).  There is increased heterogeneous\npattern of enhancement in the tectal lamina, more significant on the left, and\nextending towards the left superior colliculus (image 38, series 19).  The\npattern of vasogenic edema has increased, extending along the pulvinar regions\nbilaterally, more significant on the right,  (image 14, series 15). \nSusceptibility changes in right colliculus remains unchanged, suggestive of\nresidual blood products/hemosiderin.  On the diffusion-weighted sequence,\nthere is increased DWI signal in the tumoral areas suggesting hypercellularity\nand T2 shine through effect.  There is no significant change in the position\nof the bifrontal ventriculostomies with susceptibility artifact obscuring the\nanatomical details in the right frontal lobe.  The major vascular flow voids\nare present and demonstrate normal distribution.  The orbits are unremarkable,\nthe paranasal sinuses, middle ear cavities and mastoid air cells are clear..",
            "output": "1.  There is interval enlargement and increased pattern of heterogeneous\nenhancement in the posterior aspect of the right thalamus, medial aspect of\nthe right ventricular trigone, suggestive of tumoral progression, please note\nthat there is also increased pattern of enhancement in the tectal lamina\ntowards the left and increased vasogenic edema in the pulvinar region, more\nsignificant on the right.\n\n2.  The tumoral area centered in the pineal gland region remains grossly\nunchanged measuring approximately 21 x 10 mm in sagittal projection.\n\n3.  There is no significant change in the position of the bifrontal\nventriculostomies with susceptibility of the fact in the right frontal lobe\nobscuring the anatomical details.\n\nNOTIFICATION:  The findings were discussed with ___ NP, by ___\n___, M.D. on the telephone on ___ at 1:30 pm, 5 minutes after discovery\nof the findings."
        },
        {
            "input": "Study is degraded by motion.\n\nRight frontal shunt hardware artifact limits examination.\n\nPostoperative changes related to patient's known pineal mass biopsy are again\nseen.\n\nThere has been interval progression of pineal mass with right ventricular\ntrigone, right greater than left thalamic, right hippocampal, right greater\nthan left medial occipital slowed diffusion (see 500,502: ___ on current\nstudy and 7: ___ on ___ prior exam) and T1 hypointense, T2\nhyperintense, which, other than the thalami, demonstrates heterogeneous\nenhancement.  The mass again completely fills the quadrigeminal plate cistern.\nWithin the right hippocampus abnormal tissue, foci of blood products versus\nmineralization not definitely seen on previous exam is noted (06:10 on current\nstudy and 14:10 on ___ prior exam).\n\nThere is no evidence of midline shift or acute infarction.  Bifrontal approach\nventriculostomy catheters are again seen, with the right frontal approach\ncatheter tip again present at approximately the level of the right inferior\nmedial margin of the longitudinal fissure, and with the left catheter tip\nnoted in the region of the left lateral ventricle foramen of ___.  The\nventricles and sulci are grossly stable in caliber and configuration compared\nto ___ prior exam, with no definite evidence of ventriculomegaly. \nMinimal bilateral ethmoid air cell and maxillary sinus mucosal thickening is\npresent.",
            "output": "1. Study is degraded by motion.\n2. Right frontal shunt hardware artifact limits examination.\n3. Interval progression of pineal mass with right greater than left thalamic,\nright ventricular trigone, right hippocampal, right greater than left medial\noccipital expansile abnormal soft tissues compare to ___ prior exam,\nas described, concerning for tumor progression, with differential\nconsideration of pseudoprogression.\n4. Foci of blood products versus mineralization within right hippocampus\nabnormal tissue, not definitely seen on prior exam.  While finding may be\nrelated to differences in technique, interval hemorrhage or mineralization is\nnot excluded.\n5. Grossly stable bifrontal ventriculostomy catheters with grossly stable\nventricular size with no definite evidence of ventriculomegaly."
        },
        {
            "input": "Postoperative changes after pineal mass biopsy and bifrontal approach\nventriculostomy catheter placements with stable position of the bilateral\ncatheter tips.\n\n The pineal mass with right ventricular trigone, right greater than left\nthalamic, right hippocampal, right greater than left medial occipital\nincreased signal on the DTI source images and manually generated ADC images. \nThese areas of high signal correspond to T1 hypointense and T2 hyperintense\nsignal changes which demonstrate heterogeneous enhancement, except for the\nbilateral thalami.  There is stable to minimal increased in nodular\nenhancement involving the periaqueductal region (series 9, image 68) and\nfurther enhancement extending into the splenium of the corpus callosum (series\n9, image 92).\nComplete obliteration of the quadrigeminal plate cistern by the mass is\nunchanged.\n\nThere is no evidence of midline shift or acute intracranial infarction.\n\nThe ventricle sent sulci are grossly stable in caliber and configuration\ncompared to the most recent prior exam.  Unchanged ___ cisterna magna.\nMajor vascular flow voids are preserved.  Major dural venous sinuses are\npatent.\n\nThere is very mild mucosal thickening along the floor of the right maxillary\nsinus.  The remainder of the paranasal sinuses appear clear.  The mastoid air\ncells appear clear.  The orbits are unremarkable.",
            "output": "1. Stable to slight increased size of the pineal mass with  nodular\nenhancement involving the periaqueductal region and splenium of the corpus\ncallosum.  This can be further assessed on close follow-up.\n2. Stable postoperative changes after pineal mass biopsy and bifrontal\napproach ventriculostomy catheter placements with unchanged position of the\nbilateral catheter tips.\n3. Stable ventricular size and sulci without evidence of ventriculomegaly."
        },
        {
            "input": "Postoperative changes again demonstrated related to pineal mass biopsy and\nbifrontal approach ventriculostomy catheter placements, with stable position\nof the bilateral catheter tips.\n\nThere has been further interval increase in size of the mass centered at the\npineal gland, currently measuring 5.6 x 5.8 x 4.9 cm (901:98, 9:70) compared\nto 4.4 x 2.9 x 3.5 cm on prior study (901:103, 9:76).  There is further\ninterval extension of nodular enhancement along the right medial occipital\nlobe, right hippocampus, right ventricular trigone and ependyma, and right\nthalamus.  Nodular enhancement has particularly increased superiorly along the\nmedial right occipital lobe and along the periaqueductal region, with near\ncomplete obliteration of the quadrigeminal plate cistern.  Further nodular\nenhancement along the splenium of the corpus callosum, crossing over midline.\nThere is new nodular enhancement demonstrated along the fornix, predominantly\nright-sided but also crossing over midline on the left (10:11).  Additionally\nnew nodular enhancement is noted within the posterior aspect of the right\nmidbrain and within the right middle cerebellar peduncle.\nAdditionally, there is a new focus of nodular enhancement seen within the\ninferior aspect of the gyrus rectus in the right frontal lobe measuring up to\n7 mm (9:51, 901:45).\nIncreased T1 hyperintense signal and FLAIR signal within the medial aspect of\nthe right occipital lobe, with associated increased signal on DWI images and\nwithout evidence of susceptibility on GRE imaging, findings compatible with\nsubacute blood products.\n\nThe ventricles and sulci are stable in caliber and configuration compared to\nprior study.  No evidence of midline shift.  Similar appearance ___\ncisterna magna.  Major vascular flow voids remain preserved.  Major dural\nvenous sinuses are patent.  Mild mucosal thickening of the right maxillary\nsinus.  The visualized portion of the remaining paranasal sinuses and mastoid\nair cells are clear.  The orbits are unremarkable.",
            "output": "1. New 7 mm focus of nodular enhancement within the right frontal lobe along\nthe inferior aspect of the gyrus rectus.\n2. Redemonstration of the known pineal mass with interval increase in nodular\nenhancement extending along the periaqueductal region, across the midline of\nthe corpus callosum, along the right hippocampus, and within the medial right\noccipital lobe extending more superiorly than on prior study.  New nodular\nenhancement demonstrated along the right ventricular ependyma, along the\nfornix, and within the posterior aspect of the right midbrain and the right\nmiddle cerebellar peduncle, concerning for further disease progression.\n3. New appearance of subacute blood products within the mass, centered\npredominantly within the medial aspect of the right occipital lobe.\n4. Stable postoperative changes related to pineal mass biopsy and bifrontal\napproach ventriculostomy catheter placements, with similar position of\nbilateral catheter tips.\n5. Stable size and appearance of the ventricular system, without evidence of\nventriculomegaly.\n\nNOTIFICATION:  The findings were discussed with ___, N.P. by\n___, M.D. on the telephone on ___ at 4:19 pm, approximately\n___ minutes after discovery of the findings."
        },
        {
            "input": "Study is mildly degraded by motion.  There is no evidence of hemorrhage,\nedema, masses, mass effect, midline shift or infarction.  There is prominence\nof the ventricles and sulci suggestive involutional changes.  Periventricular,\npontine and subcortical T2 and FLAIR hyperintensities are noted which may\nrepresent small vessel ischemic changes. There is no abnormal enhancement\nafter contrast administration.\n\nBilateral maxillary sinus, left sphenoid sinus, and bilateral ethmoid air cell\nmucosal thickening is present.  Nonspecific right mastoid fluid is present.\n\nLimited imaging of cervical spine suggest degenerative changes with at least\nmild vertebral canal narrowing at C4-5 (see 17:86).",
            "output": "1. Study is mildly degraded by motion.\n2. No acute intracranial abnormality.\n3.  Within limits of study, no definite evidence of intracranial mass.\n4.  Paranasal sinus disease and nonspecific right mastoid fluid, as described.\n5. Limited imaging of cervical spine suggest degenerative changes with at\nleast mild vertebral canal narrowing at C4-5.  If clinically indicated,\nconsider cervical spine MRI further evaluation."
        },
        {
            "input": "Study is mildly degraded by motion.  There is no evidence of hemorrhage,\nedema, masses, mass effect, midline shift or infarction.  Subcortical,\nperiventricular, and pontine T2/FLAIR hyperintensities are nonspecific, likely\nthe sequelae of chronic small vessel ischemic disease.  The ventricles and\nsulci are mildly prominent suggestive of involutional changes.  There is no\nabnormal enhancement after contrast administration.\n\nThere is mucosal thickening of the bilateral maxillary sinuses and scattered\nethmoid air cells.  Secretions are seen within the right maxillary and\nbilateral sphenoid sinuses.  Trace fluid is seen within the right mastoid air\ncells, nonspecific, similar to prior.  Left mastoid air cells are clear.  The\npatient is status post right lens replacement.\n\nThe major intracranial vascular flow voids are preserved.  The dural venous\nsinuses are patent.",
            "output": "1.  Study is mildly degraded by motion.\n2.  No acute intracranial abnormality, with no definite evidence of acute\ninfarct.\n3.  Within limits of study, no definite evidence of enhances cranial mass.\n4. Paranasal sinus disease and trace right mastoid fluid, as above."
        },
        {
            "input": "Postsurgical changes are seen related to left suboccipital craniotomy for\nresection of a metastatic lesion described on prior outside imaging.  There is\ndownward descent of the left inferior cerebellum (101a:115, 7:4) demonstrating\nhyperintense FLAIR signal and slow diffusion raising concern for subacute\ninfarction.\n\nInferior to the left occipital craniotomy site is a bilobed fluid collection\n(13:1) measuring 2.4 x 2.4 cm and 2.0 x 3.5 cm with areas of internal slow\ndiffusion and peripheral enhancement suggestive of an abscess.\n\nThere is extensive venous sinus thrombosis involving the left transverse sinus\nextending into the proximal visualized internal jugular vein.  There is\nassociated FLAIR hyperintensity and slow diffusion at the left sigmoid\njunction (07: 10). There is no discrete extra-axial fluid collection to\nsuggest a subdural empyema that was described on the preliminary report; these\nfindings likely reflect changes associated with venous sinus thrombosis.\n\nThere is slow diffusion within the left middle cerebellar peduncle (7:8, 100\na: 26) with associated FLAIR hyperintensity and enhancement, possibly related\nto subacute infarction.   Alternatively, given the history of metastatic lung\ncancer, possibility of an enhancing metastatic lesion is not excluded. There\nis no discrete ring-enhancing lesion to suggest intraparenchymal abscess.\n\nThere is enhancement of the right internal auditory canal, concerning for\nleptomeningeal disease (100 a: 26).  The ventricles are normal in size without\nmidline shift.  There is moderate fluid opacification of bilateral mastoid air\ncells, left greater than right, which may be infectious or inflammatory.",
            "output": "1. Status post left occipital craniotomy with a bilobed fluid collection\nadjacent to the surgical site, concerning for an abscess.\n2. Extensive venous sinus thrombosis involving the left transverse sinus with\nextension into the proximal visualized internal jugular vein.\n3. Enhancing area of slow diffusion in the left middle cerebellar peduncle,\nmay represent subacute infarction, although possibility of metastatic lesion\nis not excluded.\n4. Enhancement of the right internal auditory canal, concerning for\nleptomeningeal disease.\n5. Postoperative changes with downward descent of the left inferior cerebellum\ndemonstrating slow diffusion and FLAIR hyperintensity, which may be\npostoperative although possibility of infarction is not excluded.\n6. Please note, no discrete extra-axial fluid collection to suggest a subdural\nempyema that was described on the preliminary report; these findings likely\nreflect changes associated with venous sinus thrombosis.\n\nNOTIFICATION:  The findings were discussed with ___, M.D. by\n___, M.D. on the telephone on ___ at 10:54 am, 2\nminutes after discovery of the findings."
        },
        {
            "input": "Status post left suboccipital craniotomy for resection of a left cerebellar\nhemisphere metastatic lesion with redemonstrated associated encephalomalacia,\nwith interval decreased dural enhancement on prior examination.  There are new\nnodular foci of enhancement at the posterior left cerebellar hemisphere\n(series 901, images 123 through 126).  A new small focus of enhancement is\npresent within the right cerebellar hemisphere.  There are new small foci of\nenhancement within the right and left occipital lobes (series 900, images 87\nand 76, respectively) as well as two new foci of enhancement within the left\nanterior centrum semiovale.  These new lesions demonstrate associated DWI\nhyperintensity and T2/FLAIR hyperintensity with slight interval increase in\nT2/FLAIR hyperintensity within the left cerebellar hemisphere.\n\nThere is no evidence of acute hemorrhage, midline shift or acute infarction. \nNo significant change in the filling defect within the left sigmoid and\ntransverse sinuses. No change in the small area of enhancement within the\nright internal auditory canal compatible with a vestibular schwannoma.\n\nThe ventricles and sulci are normal in caliber and configuration.  There is a\npersistent effusion within the left mastoid air cells.  The right maxillary\nsinus demonstrates mild mucosal thickening.  The orbits are unremarkable.",
            "output": "1. Evidence of disease recurrence within the left cerebellum and new foci of\nsupratentorial and infratentorial metastatic disease as detailed above.\n2. Unchanged evidence of a right vestibular schwannoma.\n3. Unchanged thrombosis within the left sigmoid and transverse sinuses."
        },
        {
            "input": "There is a new 1 mm right paracentral lobule vertex with enhancing lesion with\nassociated FLAIR hyperintense signal (series 8, image 21; series 700, image\n121; series 10, image 21), concerning for a new metastatic focus.  A single\npunctate focus of postcontrast enhancement of the left medial frontal lobe\n(series 10, image 15) demonstrates equivocal associated FLAIR hyperintense\nsignal (series 8, image 15).\n\nPreviously described enhancing lesion of the left anterior corona\nradiata/centrum semiovale (series 10, image 17; series 700, image 106), now\napproximately 1 mm in size, is much less conspicuous when compared to prior\nexam with decreased surrounding FLAIR hyperintensity.  A posterior enhancing\nnodule in the left centrum semiovale (series 900, image 108 on examination of\n___ is no longer perceptible).\n\nAn enhancing nodule in the right occipital lobe and an enhancing nodule in the\nleft inferior occipital lobe are also no longer appreciated, with resolution\nof associated FLAIR signal abnormality.\n\nA ring-enhancing lesion of the right inferior cerebellar hemisphere is\nsubstantially decreased in size, now measuring approximately 1 mm and almost\nimperceptible (Series 700, image 68) with resolution of surrounding FLAIR\nedema.  Previously described enhancing nodules in the inferior left cerebellar\nhemisphere along the resection margin are also no longer well appreciated.\n\nThe patient is status post left suboccipital craniectomy and left inferior\ncerebellar resection with associated left inferior cerebellar hemisphere\nencephalomalacia, similar in configuration from prior examination.  Mild\nresidual dural thickening is unchanged.  The previously noted extracranial\nsuboccipital soft tissue cysts postoperative fluid collection is slightly\nsmaller when compared to the prior exam with interval decreased surrounding\nenhancement.\n\n6 x 4 mm right internal auditory canal enhancing lesion compatible with a\nschwannoma is unchanged.\n\nRe-identified is left transverse sinus and sigmoid sinus thrombosis extending\ninto the upper internal jugular vein.  The remainder of the dural venous\nsinuses are patent.\n\nThere are mild composed periventricular and subcortical T2/FLAIR white matter\nhyperintensities, which are nonspecific, but compatible with chronic\nmicroangiopathy in a patient of this age.  The sulci, ventricles and cisterns,\nallowing for postoperative findings are within expected limits for the\npatient's age.  The major intracranial flow voids are otherwise preserved. \nThere is mild mucosal thickening of the visualized paranasal sinuses.  The\norbits are unremarkable.  Opacification of the left mastoid air cells is\nunchanged.  Trace fluid signal is noted in the right mastoid tip also\nunchanged.",
            "output": "1. There is a punctate new enhancing lesion of the medial right paracentral\nlobule at the vertex demonstrating associated FLAIR hyperintense signal,\nraising suspicion for new metastatic disease (series 10, image 21) in this\nclinical context.  Close interval follow-up is recommended.\n2. A second punctate left medial frontal lobe white matter enhancing focus\ndemonstrates equivocal FLAIR hyperintense signal, and may be artifactual in\nnature, however close attention on followup is recommended to exclude\nmetastatic disease.\n3. Previously described nodular enhancement of the bilateral cerebellar\nhemispheres, left centrum semiovale and corona radiata have essentially\nresolved as have associated surrounding FLAIR hyperintense signal.  If the\npatient has not received therapy, in retrospect of these could represent\nsequela of subacute infarct rather than metastatic disease.  If the patient\nhas received treatment, this would presumably represent treatment effect. \nClinical correlation is recommended.\n4. Left suboccipital craniectomy and tumor resection appear similar to prior\nexamination, now without evidence of disease recurrence within the resection\nbed.\n5. Left transverse sinus, sigmoid sinus and upper internal jugular vein\nthrombosis is re-identified.\n6. Unchanged right internal auditory canal presumed vestibular schwannoma.\n7. Additional findings as described above.\n\nNOTIFICATION:  The impression and recommendation above was entered by Dr.\n___ on ___ at 09:33 into the Department of Radiology critical\ncommunications system for direct communication to the referring provider."
        },
        {
            "input": "There are ring-enhancing lesions with surrounding edema in the frontal lobes\nbilaterally.  These are new since the study of ___ but allowing for\ndifferences in technique appear similar to the findings on the head CT of ___.  Again seen is an enhancing mass filling the right internal\nauditory canal, presumably a vestibular schwannoma.\nAgain seen are postoperative changes in the posterior fossa after left\nsuboccipital craniectomy.  Extensive opacification of the left mastoid air\ncells and mild opacification of the right mastoid air cells appears unchanged.\nThere is no evidence of hemorrhage, midline shift or infarction.   The\nventricles and sulci are prominent in a mild atrophic pattern.",
            "output": "1. Bilateral frontal lobe ring-enhancing lesions with surrounding edema\nsuggesting necrotic metastases.\n2. Left suboccipital craniectomy with postoperative changes, stable since\n___.\n3. Right internal auditory canal enhancing mass, likely a vestibular\nschwannoma."
        },
        {
            "input": "Postsurgical changes status post left suboccipital craniotomy are again seen,\nwith small foci of susceptibility artifact in the surgical bed, similar to\nprior.  The degree and extent of T2/FLAIR hyperintensity in the left\ncerebellum is essentially unchanged since prior.\n\nApproximately 10 x 8 mm (transverse by AP) medial right frontal lobe lesion\nnear the vertex (___) previously measured approximately 14 x 12 mm when\nmeasured similarly.  The degree of associated surrounding edema has\nsignificantly decreased since prior.\n\nThe previously seen 9 mm ring-enhancing lesion in the anterior left frontal\nlobe is now a 5 mm ovoid enhancing focus.  The previously seen surrounding\nedema has significantly improved and there is now a trace residual associated\nfocus of edema.\n\nAn approximately 13 x 15 mm area of T2/FLAIR hyperintensity in the left\nanterior periventricular white-matter without corresponding enhancement or\nslow diffusion measured approximately 12 x 10 mm on prior.\n\nPunctate focus of T2/FLAIR hyperintensity in the right frontal lobe near the\nvertex (___) is unchanged since prior.\n\nApproximately 10 x 5 mm teardrop shaped and seeing mass in the right internal\nauditory canal measured approximately 11 x 5 mm on prior.\n\nThere is no evidence of acute hemorrhage, mass effect, midline shift or\ninfarction.  Mild prominence of the ventricles and sulci is suggestive of\ninvolutional changes.  The orbits are unremarkable.  There is scattered fluid\nin the left mastoid air cells, slightly improved since prior.  There is mild\nscattered opacification of right mastoid air cells, similar to prior.",
            "output": "1. Interval enlargement of a nonenhancing area of T2/FLAIR hyperintensity,\nconcerning for malignancy.\n2. Interval decrease in size and surrounding edema of multiple ring-enhancing\nlesions seen on prior.\n3. No significant interval change in the right IAC mass, likely a vestibular\nschwannoma."
        },
        {
            "input": "The previously noted medial right frontal lobe lesion as well as punctate\nenhancement in the anterior left frontal lobe have considerably decreased. \nThe previously described FLAIR hyperintensity in the left periventricular\nwhite matter is unchanged signal changes in the left cerebellum are unchanged.\nEnhancement within the right internal auditory canal is also unchanged when\ncompared on the MP rage images.  No definite new areas of enhancement are\nseen.  No mass effect midline shift or hydrocephalus.\n\nPostoperative changes in the left occipital region again noted.  Filling\ndefect within the flow in the left transverse and sigmoid sinus due to a\nchronic thrombosis unchanged.",
            "output": "1. Decrease in size of enhancement in the right medial frontal lobe and\nanterior left frontal lobe.  No new areas of abnormal enhancement.\n2. Unchanged right internal auditory canal enhancement.\n3. Unchanged slow flow in the left transverse sinus with filling defect from a\nchronic thrombus.\n4. Postoperative changes with encephalomalacia in the left cerebellum as\nbefore.\n5. No acute infarcts or hydrocephalus."
        },
        {
            "input": "Study is moderately degraded by motion.  Within these confines:\n\nLeft cerebellar mass resection and abscess debridement postoperative changes\nare again noted, with nonspecific minimal T2 and FLAIR hyperintensity within\nthe left cerebellar lobe and left middle cerebellar peduncle.\n\nMinimal right precentral gyrus curvilinear restricted diffusion (see 500,\n502:24), with grossly stable associated curvilinear T2 and FLAIR\nhyperintensities adjacent to a punctate enhancing lesion is again noted (see\n9:116).\n\nPunctate left frontal enhancing lesion with adjacent minimal T2 and FLAIR\nhyperintensity is grossly unchanged (see 7, 8, 10:16 on current study and\n16:14 on prior exam).\n\n\nFilling defect within left transverse and sigmoid sinuses are grossly\nunchanged, again suggestive of partial thrombosis.\n\nGrossly stable 1 x 0.5 cm right internal auditory canal enhancing lesion is\nagain noted (see 09:37 on current study and 19:40 on prior exam).\n\nThere is no evidence of midline shift or infarction.   The ventricles and\nsulci are stable in caliber and configuration.  Nonspecific bilateral mastoid\nfluid is noted.  Minimal bilateral ethmoid air cell and maxillary sinus\nmucosal thickening is present.",
            "output": "1. Study is moderately degraded by motion.\n2. Grossly stable left cerebellar mass resection and abscess debridement\npostoperative changes.\n3. Grossly stable punctate bifrontal enhancing lesions as described,\ncompatible with patient's known intracranial metastatic lesions.\n4. Grossly stable 1 x 0.5 cm right internal auditory canal probable vestibular\nschwannoma, with differential consideration of metastatic lesion.\n5. Within limits of study, no definite new intracranial enhancing lesions\nidentified.\n6. Grossly stable partial thrombosis of left transverse and sigmoid sinuses.\n7.  Paranasal sinus disease and nonspecific bilateral mastoid fluid, as\ndescribed."
        },
        {
            "input": "Study is moderately degraded by motion.  Within these confines:\n\nNew left anterior corona radiata T2 and FLAIR lesion with associated slow\ndiffusion with minimal enhancement is noted (see 550, 552:20; 4, 7, 8, 09:17;\n10:216).\n\n Right precentral gyrus lesion with T2 and FLAIR hyperintensity and minimal\ncurvilinear restricted diffusion with minimal enhancement is unchanged (see 6,\n9, 11:20).\n\nGrossly stable left cerebellar mass resection and empyema debridement\npostoperative changes are again noted.\n\nNew minimal left corona radiata periventricular new enhancement (see 9, 11:\n___ 10:204-211 on current study and 9:96-102 on ___ prior exam).\n\nGrossly stable approximately 11 x 5 mm right internal auditory canal\nhomogeneously enhancing mass is again seen (see 10:94 on current study and\n09:36 on prior exam).\n\nQuestion re-demonstration left frontal punctate enhancing lesion versus\nartifact (see 09:13 on current study and 10:16 on prior exam).\n\nThere is no evidence of midline shift or infarction.   The ventricles and\nsulci are stable in caliber and configuration.  Grossly stable periventricular\nand subcortical T2 and FLAIR hyperintensities are noted which may represent\ntreatment related effects and/or small vessel ischemic changes.\n\nNonspecific bilateral mastoid fluid is seen.  Bilateral maxillary sinus,\nethmoid air cell, frontal sinus mucosal thickening is noted.\n\nGrossly stable partial filling defects of left transverse and sigmoid sinuses,\nagain suggestive of partial thrombosis are again noted.  Nonspecific adjacent\nenhancement is again seen, unchanged.  (See 1001:56; 10:83 on current study\nand 900:59; 09:33 on prior exam).",
            "output": "1. Study is moderately degraded by motion.\n2. Two new left anterior corona radiata enhancing lesions as described,\nconcerning for new metastatic disease.\n3. Grossly stable enhancing right probable enhancing lesions, as described.\n4. Postsurgical changes related to patient's known left cerebellar mass\nresection empyema debridement.\n5. Grossly stable approximately 11 x 5 mm right internal auditory canal\nprobable vestibular schwannoma.\n6. Grossly stable findings again compatible with left transverse and sigmoid\nsinus partial thrombosis.\n7.  Paranasal sinus disease and nonspecific bilateral mastoid fluid, as\ndescribed.\n\nNOTIFICATION:  The impression and recommendation above was entered by Dr.\n___ on ___ at 21:36 into the Department of Radiology critical\ncommunications system for direct communication to the referring provider."
        },
        {
            "input": "There is interval thickening and enlargement with progressive enhancement of\nthe left anterior corona radiata lesion with associated restricted diffusion\n(image 200-230 of series 10).  Enhancement also extends along the left lateral\nperiventricular region.  There also new punctate foci of enhancement in the\nanterior left frontal lobe periventricular white matter.\n\nPatchy to confluent areas of T2 and FLAIR hyperintense signal abnormalities in\nthe left periventricular white matter are increased compared to prior exam.\n\nThe right precentral gyrus lesion with T2 and FLAIR signal abnormality and\nminimal curvilinear enhancement and restricted diffusion is unchanged (image\n259 of series 10).\n\nStable enhancing mass measuring 11 x 5 mm in the right internal auditory canal\n(image 97 of series 10).\n\nThere are postsurgical changes in the left occipital region.  Irregular\nnodular areas of enhancement in the left cerebellar region appears slightly\nmore prominent and conspicuous compared to prior exam.\n\nThe ventricles and sulci are stable in size and configuration with no mass\neffect or midline shift.\n\nMinimal right mastoid air cell effusion persist, improved compared to prior\nexam.\n\nApparent filling defects in the left transverse and sigmoid sinuses are\ngrossly stable compared to multiple priors.",
            "output": "1. Interval enlargement and enhancement of the left anterior corona radiata\nenhancing lesions concerning for metastatic disease progression.\n2. Postsurgical changes of left cerebellar mass resection with irregular\nnodular foci of enhancement, which appear equivocally increased in size and\nconspicuity compared to prior exam.  Attention on follow-up.\n3. Stable right internal auditory canal probable vestibular schwannoma.\n4. Stable filling defect in the left transverse and sigmoid sinus, which may\nrepresent partial thrombosis."
        },
        {
            "input": "Posttreatment changes.\n\n8 mm ring enhancing focus left centrum semiovale, adjacent subependymal arc of\nenhancement along the left lateral roof and body of the lateral ventricle,\npunctate few foci of enhancement left corona radiata.  Linear component\nabutting ventricular surface is slightly increased since ___,\notherwise stable.  Few punctate foci of microhemorrhage associated with the\nabnormality.  Mildly more prominent surrounding edema.  Configuration favors\npostradiation change.\n\nVolume loss left cerebellum, posttreatment changes, areas of linear and\nnodular enhancement have improved since ___.  Surrounding left\ncerebellar hemisphere edema, volume loss, encephalomalacia is similar. \nPartial thrombosis with slow  flow within left distal transverse, sigmoid\nsinus, is again seen.\n\nSmall area of edema medial margin right precentral gyrus, minimal associated\nenhancement, stable.  2 punctate foci leptomeningeal enhancement overlying\ninferior right parietal lobule is stable since ___..\n\n0.9 cm mass right IAC, stable since ___, likely vestibular\nschwannoma.\n\nNo new masses.  Brain parenchymal atrophy.  Chronic small vessel ischemic\nchanges.  No acute infarct, hydrocephalus or midline shift.  Preserved\nvascular flow voids.",
            "output": "1. Mildly increased enhancement and surrounding edema left vertex,\nconfiguration favors postradiation change over tumor.  Consider follow-up ASL,\nDSC perfusion if indicated.\n2. Improved left cerebellar findings.\n3. No new masses.\n4. Stable nonocclusive left transverse, sigmoid sinus thrombus.\n5. Right IAC mass stable since ___, likely vestibular schwannoma."
        },
        {
            "input": "There are 2 areas of restricted diffusion.\n\n-First area is noted in the right frontal lobe, at the vertex (series 502;\nimage 24), in correlation with base 0.6 x 0.4 cm area of enhancement (series\n9; image 19).  There is mild vasogenic edema without mass effect surrounding\nthis lesion on T2/FLAIR.\n\n-Additional area of slow diffusion (series 502; image 21) appears in a ringed\npattern, which correlates with an area of post-contrast enhancement (series 9;\nimage 17), measuring 1.8 x 1.3 cm, in the deep white matter of the left\nfrontal lobe.  There is mild-to-moderate surrounding, neurogenic edema,\nwithout mass effect or midline shift, which is mildly decreased compared to ___.  Additionally, there is a small amount susceptibility in this areas\nsuggesting underlying hemorrhage, also mildly decreased compared to prior.\n\nPost treatment changes are seen in the left occipital soft tissues as well as\nthe left cerebellum, unchanged compared to multiple priors.  No new lesions\nidentified.\n\nThere are bilateral mastoid effusions, left greater than right.  There is\nmoderate mucosal thickening of the bilateral maxillary sinuses.  Orbits are\nnormal.",
            "output": "1. 1.8 x 1.3 cm enhancing lesion in the deep white matter of the left frontal\nlobe shows restricted diffusion and mild to moderate surrounding neurogenic\nedema.  There is also minimal susceptibility in this area, consistent with\nunderlying hemorrhage.  Susceptibility and neurogenic edema are mildly\ndecreased compared to ___.  There is no mass effect or midline shift.\nLesion is consistent with relatively unchanged metastatic focus.\n2. 0.6 x 0.4 cm area of enhancement and restricted diffusion with mild\nsurrounding neurogenic edema is seen in the right frontal lobe, at the vertex,\nrelatively unchanged compared to prior.  Lesion is consistent with another\nrelatively unchanged metastatic focus.\n3. No new lesions identified.\n4. Unchanged post treatment findings in the left occipital soft tissues as\nwell as the left cerebellum.\n5. Bilateral mastoid effusions, left greater than right, nonspecific."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, significant mass effect or acute\ninfarction.  There is trace prominence of the ventricles and sulci suggestive\nof mild involutional changes.  Minimal periventricular and subcortical T2 and\nFLAIR hyperintensities are noted which are nonspecific but compatible with\nmild chronic small vessel ischemic changes.\n\nWithin the distal right internal auditory canal, there is a 3 x 3 mm nodular\nfocus of enhancement (9:40, 901:98, 900:103).  Findings are most compatible\nwith a small vestibular schwannoma.  Follow-up MRI imaging of the ___ is\nsuggested to confirm stability.  Otherwise, there is no abnormal enhancement\nto suggest metastatic disease.\n\nThere are mild ethmoid and maxillary sinus mucosal inflammatory changes. \nThere is non-specific fluid within the right greater than left mastoid air\ncells.  The orbits and globes appear grossly unremarkable.",
            "output": "1. No hemorrhage, acute infarct, significant mass effect or acute infarct.\n2. No evidence of parenchymal enhancement to suggest metastatic disease.\n3. 3 mm nodular focus of enhancement within the right internal auditory canal\nis most compatible with a small vestibular schwannoma.  In the absence of\navailable prior brain imaging, clinical correlation and if indicated a\nfollow-up MRI of the ___ is suggested to confirm stability.\n4. Mild soft tissue changes and fluid within the right mastoid air cells.\n\nRECOMMENDATION(S):  Follow-up ___ MRI and clinical correlation for small right\ninternal auditory canal enhancing lesion."
        },
        {
            "input": "MR Head: There is no evidence of hemorrhage, edema, mass or  infarctioin.     \nThere is a tiny focus of increased FLAIR signal in the left frontoparietal\ndeep white matter, nonspecific.  Ventricles and extra axial spaces are within\nnormal limits. There is no extra-axial fluid collection.  The major\nintracranial vessels exhibit the expected signal void related to vascular\nflow.\n\nNo enhancing mass is identified. There is no abnormal meningeal enhancement.\nThere is mucosal thickening of the ethmoid sinuses. The paranasal sinuses are\notherwise clear. The mastoid air cells are clear.  The sella turcica,\ncraniocervical junction, and orbits are unremarkable.\n\nMRA head:  Normal flow signal is noted in the petrous, cavernous, and\nsupraclinoid portions of the internal carotid arteries. The anterior and\nmiddle cerebral arteries are normal. The anterior communicating artery region\nis normal.\n\nThe posterior cerebral arteries and basilar artery are unremarkable. The\nsuperior cerebellar arteries are normal. The intradural segments to both\nvertebral arteries are patent; the left vertebral artery is dominant. Normal\nbilateral posterior communicating arteries are identified.\n\nNo arterial stenosis, saccular aneurysm, or AVM is identified. Flow is\nsymmetric.\n\nMRA neck: The origin to the innominate, left common carotid and left\nsubclavian arteries are normal with conventional arch anatomy. The common,\ninternal, and external carotid arteries, as well as the vertebral arteries,\ndemonstrate normal flow signal and enhancement. The vertebral artery origins\nare unremarkable. No stenosis is identified.",
            "output": "1. No evidence of hemorrhage,  infarction, or mass.\n2. Normal MRA of the head and neck."
        },
        {
            "input": "Punctate infarcts within the left thalamus with increased FLAIR signal, early\nsubacute.  Additional larger foci of slow diffusion within the medial right\noccipital lobe, some of which are very dark on ADC with only mild T2\nhyperintensity, others which are only mildly dark on ADC with T2\nhyperintensity, likely representing a combination of acute/early subacute\ninfarcts.  Hyperintensities within the right temporal lobe on the\ndiffusion-weighted images are likely artifactual.\n\nKnown sellar mass measures approximately 2.7 x 1.9 x 2.0 cm on today's\nexamination, which may have slightly increased in size compared to the CT\ndated ___, however this may be due to differences in technique. \nThis mass demonstrates relatively homogeneous enhancement with enlargement of\nthe bony sella, as well as splaying of the cavernous carotid arteries, which\nare patent.\n\nThere is no evidence of hemorrhage, edema, intra-axial masses/mass effect, or\nmidline shift.  The ventricles and sulci are normal in caliber and\nconfiguration.  The vessels of the circle ___ are patent.  The dural venous\nsinuses are also patent.\n\nThe orbits are unremarkable in appearance.  Fluid is seen throughout the\nmastoid this bilaterally, nonspecific..",
            "output": "1. Multiple infarcts within the left thalamus and throughout the medial right\noccipital lobe, a combination of acute/early subacute infarcts.  No evidence\nof hemorrhage.\n2. Known sellar mass/pituitary macroadenoma measures up to 2.7 cm in maximum\n___, slightly increased in size compared to the CT dated ___, however this may be due to differences in technique.\n3. Fluid throughout the mastoid bilaterally, nonspecific."
        },
        {
            "input": "Correlating with hypodensity on prior CT, there is region of restricted\ndiffusion with associated FLAIR hyperintensity compatible with acute infarct\ninvolving the right temporal parietal lobes as well as posterior insula. \nThere is no other acute infarct.  There is no evidence of hemorrhage.\nBilateral chronic cerebellar infarcts are identified.  Diffuse scattered\nperiventricular subcortical white matter T2/FLAIR hyperintensities are likely\nsequela of chronic small vessel disease.\n\nThere is lack of flow related signal in the left vertebral artery, better seen\non prior CTA.\nVisualized paranasal sinuses and mastoid air cells demonstrate no abnormal\nsignal.\n\nThere is T1 hypointensity in posterior aspect of C2 which correlates with the\nwell-circumscribed lucent lesion on recent CTA, presumably degenerative in\nnature.  Anterolisthesis of C4 on C5 is partially visualized, better seen on\nprior CTA.",
            "output": "Acute right MCA territory infarct.\nLack of flow related signal in the left vertebral artery as seen on recent\nCTA."
        },
        {
            "input": "Study is mildly degraded by motion.\n\nMRI Brain:\nThe patient is status post left parietal craniotomy.\nStable left parietal encephalomalacia the region of patient's previously noted\nAVM rupture is again noted with adjacent gliosis.  Adjacent susceptibility\nartifact again may be related to post-surgical changes and/or hemosiderin\nstaining are again seen.  Periventricular and subcortical T2 and FLAIR\nhyperintensities are noted, which may represent small vessel ischemic changes.\nThere is no evidence of edema, masses, mass effect, midline shift or\ninfarction.  There is stable ex vacuo dilatation of the left lateral ventricle\nadjacent to region of probable ruptured AVM.  There is no abnormal enhancement\nafter contrast administration.  Bilateral ethmoid and maxillary sinus mucosal\nthickening is present.\n\nMRA brain: The intracranial vertebral and internal carotid arteries and their\nmajor branches appear normal without evidence of stenosis, occlusion, or\naneurysm formation.\n\nMRA neck:  The common, internal and external carotid arteries appear normal. \nThere is no evidence of internal carotid artery stenosis by NASCET criteria. \nThe origins of the great vessels, subclavian and vertebral arteries appear\nnormal bilaterally.",
            "output": "1. Study is mildly degraded by motion.\n2.  No acute intracranial abnormality.\n3. No evidence of acute infarct.\n4. Stable changes related to patient's left parietal AVM rupture and left\nparietal craniotomy.\n5. No evidence ofaneurysm greater than 3 mm,  dissection, vascular\nmalformation, or significant luminal narrowing."
        },
        {
            "input": "Interval development of cortical nonenhancing FLAIR hyperintense lesion of the\nleft medial temporal cortex (series 5, image 7; series 8, image 49). \nPreviously described dominant right frontal periventricular white matter\nlesion is unchanged in size from prior exam (series 5, image 17).  Additional\nlesions in the subcortical and periventricular left parietal/occipital white\nmatter are also unchanged in appearance.  No new abnormal enhancement.\n\nThere is no acute infarct or intracranial hemorrhage.  Asymmetric prominence\nof the right lateral ventricle is unchanged from the prior exam, presumably\ncongenital.  The major intracranial flow voids are preserved.  The dural\nvenous sinuses are patent.  The paranasal sinuses are clear.  The orbits are\nunremarkable.  The mastoid air cells are clear.",
            "output": "1. A new cortically based nonenhancing FLAIR hyperintense lesion of the left\nmedial temporal cortex.\n2. The remainder of the subcortical and periventricular white matter T2/FLAIR\nnonenhancing FLAIR hyperintensities are unchanged from prior exam, a\ncompatible with demyelinating plaques given the history of multiple sclerosis.\n3. No abnormal enhancement."
        },
        {
            "input": "Nonenhancing periventricular lesions consistent with chronic demyelinating\nplaques are re-demonstrated, unchanged.  1 deep white matter lesion.  There is\napproximately 7 lesions, 6 of these abutting ventricular surface.  No new foci\nare seen.  No infratentorial lesions.  No juxta cortical lesions.  No\nenhancing lesions.  No leptomeningeal enhancement.\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  The paranasal sinuses, mastoid air cells and middle ear\ncavities are clear.  The intraorbital contents are normal.  Preserved vascular\nflow voids, patent dural venous sinus.",
            "output": "1. Findings consistent with chronic demyelination, stable.\n2. No new, no enhancing lesions."
        },
        {
            "input": "Images are mildly motion degraded.\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  Focus of subcortical T2/FLAIR hyperintensity in the right\nfrontal lobe (10:26) and additional small periventricular FLAIR\nhyperintensities are nonspecific may reflect sequela of chronic small vessel\nischemic disease.  Prominence of the ventricles and sulci is consistent with\nage related symptoms.\n\nThere is mild mucosal thickening of the ethmoidal air cells.  There is partial\nopacification of the right mastoid air cells.  A right-sided lens replacement\nis noted.  Orbits are otherwise unremarkable.",
            "output": "1. No evidence of acute infarction.\n2. Nonspecific subcortical and periventricular FLAIR hyperintensities likely\nreflect sequela of chronic small vessel ischemic disease."
        },
        {
            "input": "Examination is severely degraded by artifact from patient's dental hardware.\n\nThe diffusion weighted images and corresponding ADC map are essentially\nnondiagnostic.\n\nWithin the supratentorial brain near the vertex and posterior fossa, no focal\nmasses, areas of abnormal enhancement, or edema are identified.  Within limits\nof study, no definite evidence of ventriculomegaly.",
            "output": "1. Severely artifactually degraded examination as described.\n2. Diffusion images are nondiagnostic for acute infarction.\n3. Within limits of study, no definite evidence of enhancing intracranial mass\nas described."
        },
        {
            "input": "No evidence of acute intracranial hemorrhage.\n\nNo diffusion restriction with corresponding ADC signal to suggest new infarct.\nNo mass or subsequent mass effect.  The ventricle and sulci are unremarkable.\n\nThe intracranial flow voids are preserved.\n\nThe paranasal sinuses, middle ear cavities are unremarkable.",
            "output": "1. No evidence of acute intracranial hemorrhage or large territorial infarct."
        },
        {
            "input": "No evidence of hemorrhage, edema, masses, mass effect, midline shift or\ninfarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  A few, scattered T2/FLAIR focal hyperintensities are\nnon-specific but most likely represent sequelae of chronic small vessel\nischemic disease in this young patient with a history of renal impairment.  No\nMR evidence of PML.  Normal vascular flow voids are present.  The right\nmaxillary sinus is slightly atelectatic.  The right ethmoidal air cells have\nsome minimal opacification.  The remaining paranasal sinuses are clear.  The\nleft mastoid air cells are opacified.  The visualized nasopharynx is within\nexpected limits.",
            "output": "1. No evidence of Progressive Multifocal Leukoencephalopathy (PML).\n2. No acute infarct or intracranial hemorrhage."
        },
        {
            "input": "There is no evidence of acute infarction or intracranial hemorrhage.  There is\ndiffuse parenchymal volume loss with prominence of the ventricles, sulci,\ncisterns without lobar predominance or temporal atrophy.  There is mild\nnonspecific periventricular and subcortical white matter signal abnormality,\nlikely a sequela of chronic small vessel ischemic disease.  The major\nvisualized arterial vascular flow voids are preserved.  There is mild mucosal\nthickening of bilateral ethmoid air cells.  The patient is status post\nbilateral lens replacement.  The visualized soft tissues appear unremarkable.",
            "output": "1. No evidence of acute intracranial process.\n2. Diffuse parenchymal volume loss without lobar predominance, and mild\nprobable chronic small vessel ischemic disease.  No disproportionate mesial\ntemporal volume loss."
        },
        {
            "input": "MRI BRAIN:\nThere is stable right posterior cingulate gyrus FLAIR hyperintensity.  There\nis no evidence of hemorrhage, edema, masses, mass effect, midline shift or\ninfarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.\n\nThere is minimal mucosal thickening in the left maxillary and ethmoid sinuses.\n\nMRA brain:  There is a 0.3 (AP) x 0.2 (TV)  cm focus of T1 hyperintense signal\nat the base of the left PCOM coil pack.  Otherwise, the intracranial vertebral\nand internal carotid arteries and their major branches appear normal without\nevidence of stenosis, occlusion, or aneurysm formation.\n\nDegenerative changes at the C4-C5 levels are partially visualized.",
            "output": "1. Stable findings right posterior cingulate gyrus chronic infarct.\n2. No acute intracranial abnormality.\n3. 0.3 (AP) x 0.2 (TV) cm residual filling at the base of the left PCOM\naneurysm coil pack, seen on angiogram from ___, which has increased since\n___ but grossly stable since ___.\n\nNOTIFICATION:  A message was left with the QA nurse at 10:21 am by Dr.\n___."
        },
        {
            "input": "Moderate motion degradation, limiting assessment. Within these confines:\n\nThere is bilateral grade 3 to grade 4 medial temporal lobe atrophy\nbilaterally, with widening of the choroid fissures and temporal horns of the\nlateral ventricles, and marked hippocampal height loss.  There is suggestion\nof a small focal T2 hyperintense signal within the hippocampal head laterally\non the right (12:39).  No definite signal abnormality within the left\nhippocampus, although evaluation for small areas of signal abnormality is\nlimited due to the degree of motion degradation.\n\nThe mammillary bodies are preserved in signal.  There is no focal lobar\nencephalomalacia. There are no focal cortical dysplasias or gray matter\nheterotopia noted.\n\nThere is no evidence of infarction, hemorrhage, edema, mass, or mass effect. \nThe ventricles and sulci are prominent, compatible with global parenchymal\nvolume loss. Minimal periventricular and a few scattered small deep white\nmatter foci of T2/FLAIR signal hyperintensity are nonspecific but compatible\nwith mild changes of chronic white matter microangiopathy. There is no\nabnormal enhancement after contrast administration.",
            "output": "1. Moderate motion degradation, limiting assessment. Within these confines:\n2. Possible small focus of T2 hyperintense signal in the right hippocampal\nhead, which is nonspecific but could represent a small focus of right\nhippocampal gliosis.  No definite left hippocampal signal abnormality, within\nconfines of motion degradation.\n3. Bilateral grade 3 or 4 medial temporal lobe atrophy, including marked\nhippocampal height loss.\n4. No acute infarct, hemorrhage, or extra-axial collection.\n5. Global parenchymal volume loss.\n6. Mild changes of chronic white matter microangiopathy."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.\n\nThe major intracranial vascular flow voids are maintained.  The ventricles and\nsulci are normal in caliber and configuration.  The paranasal sinuses, mastoid\nair cells and orbits are normal.  The lingual tonsils are mildly prominent\nbilaterally and demonstrate heterogeneous enhancement.",
            "output": "1. No acute intracranial abnormality with no definite evidence of infarct.\n2. No evidence intracranial mass or abscess.\n3. Prominent bilateral lingual tonsils demonstrating heterogeneous enhancement\nmay be reactive.  Consider direct correlation with visualization if clinically\nindicated."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarct.  No dural fluid collections.  Vascular flow voids are preserved. \nTrace mucosal thickening paranasal sinuses, mastoids.  No evidence of diffuse\naxonal injury on gradient images.",
            "output": "1. No acute findings."
        },
        {
            "input": "There is no intracranial mass, mass effect, or midline shift. Ventricles and\nsulci are age-appropriate.  There are few scattered subcortical white matter\nT2/FLAIR hyperintensities which are nonspecific, but had been present on prior\nalthough appear more conspicuous on today's exam, likely technical. There is\nno region of restricted diffusion or abnormal susceptibility artifact. Major\nintravascular flow voids are preserved.\n\nPost contrast images demonstrate no abnormal parenchymal or meningeal\nenhancement.\n\nVisualized paranasal sinuses and mastoid air cells are clear.",
            "output": "Essentially unremarkable MRI of the brain without significant changes since\n___. A few scattered white matter T2/FLAIR hyperintensities which had been\npresent on prior although slightly more conspicuous which may be technical.\nThese are nonspecific but can be seen in setting of chronic small vessel\ndisease."
        },
        {
            "input": "MRA brain: Robust posterior communicating arteries are demonstrated.  The\nintracranial vertebral and internal carotid arteries and their major\nbranchesappear patent without evidence of stenosis, occlusion, or aneurysm\nformation.\n\nThe visualized ventricles and sulci appear normal in size and configuration. \nThere is a small mucous retention cyst in the floor of the left maxillary\nsinus as well as trace mucosal wall thickening in the floor of the right\nmaxillary sinus.\n\nMRA neck: There is a variant 2 vessel aortic arch with common origin of the\nbrachiocephalic and left common carotid arteries.  The common, internal and\nexternal carotid arteries appear patent.  There is no evidence of stenosis by\nNASCET criteria. The origins of the great vessels, subclavian, and vertebral\narteries appear patent bilaterally.  The common carotid bifurcations appear\npatent.",
            "output": "1. Patent intracranial arterial vasculature without significant stenosis,\nocclusion, or aneurysm.\n2. Patent cervical arterial vasculature without significant stenosis or\nocclusion."
        },
        {
            "input": "The cerebellar tonsils are peg-like and protrude 1.2 cm below the foramen\nmagnum.\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  As described on the CT examination, nonspecific flattening of\nthe pituitary, greater than would be expected for a female patient of this\nage.  While this could represent sequela of increased intracranial pressure,\nthis is entirely nonspecific.\n\nThe paranasal sinuses and mastoid air cells are clear.  The orbits are\nunremarkable.\n\nThe major intracranial flow voids are preserved.  The paranasal sinuses are\nclear.  The orbits are unremarkable.  The mastoid air cells are clear.",
            "output": "1. Chiari 1 malformation.\n2. No acute intracranial abnormality.  Unchanged mild flattening of the\npituitary gland, slightly greater than would be expected for a female patient\nof this age.  This can be sometimes seen in the setting of increased\nintracranial pressure such as idiopathic intracranial hypertension, however\nthis finding is entirely nonspecific given the wide range of normal pituitary\nsizes."
        },
        {
            "input": "The internal carotid arteries, vertebral arteries, basilar artery, vessels of\nthe circle ___ and ___ branches are patent, without stenosis.\n\nNo aneurysm is identified.",
            "output": "Normal MRA head.  No aneurysm is identified."
        },
        {
            "input": "MR BRAIN:\nNo evidence of hemorrhage, edema, masses, mass effect, midline shift or\ninfarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  The sella is unremarkable on this non-dedicated exam.  No\nabnormal enhancement on post-contrast images.\n\nThere are small vessels near the trigeminal nerve but no deformity or abnormal\nenhancement or signal abnormality is identified.  Meckel's cave is\nunremarkable.  The cavernous sinus is unremarkable.\n\nThe right frontal sinus is partially opacified with what may be aerosolized\nsecretions, suggesting active sinusitis. Mucosal thickening in the bilateral\nmaxillary sinuses is mild.  The remaining partially imaged paranasal sinuses\nare clear.  The mastoid air cells are clear.  The orbits are unremarkable.\n\nMRA brain: Anterior and posterior circulation flow voids are patent without\nevidence of stenosis or occlusion.  The right A1 segment is attenuated but\npatent.  There is a small 3-mm inferiorly projecting anterior communicating\nartery aneurysm at the junction with the left ACA (series 500, image 18;\nseries 1101, image 54).\n\nMRV brain:  No central venous thrombosis. The major intracranial central\nvenous sinuses appear patent. The left transverse sinus, sigmoid sinus, and\ninternal jugular vein are continuous congenitally hypoplastic as confirmed on\nMPRAGE sequences and slow velocity sequences.  There is a small arachnoid\ngranulation in the left transverse sinus.\n\nThere is a developmental venous anomaly in the right cerebral hemisphere.  No\nevidence to suggest an associated cavernoma.",
            "output": "1. 3-mm anterior communicating artery aneurysm at the ACOM-left ACA junction.\n2. No evidence of cerebral venous thrombosis.\n3. No MRI evidence of trigeminal pathology or increased intracranial pressure.\n4. Incidental right hemisphere developmental venous anomaly.\n5. Active sinusitis.\n\nRECOMMENDATION(S):   The impression and recommendation above was entered by\nDr. ___ on ___ at 12:34 into the Department of Radiology\ncritical communications system for direct communication to the referring\nprovider."
        },
        {
            "input": "There is no intra or extra-axial mass, acute hemorrhage or infarct. The sulci,\nventricles and cisterns are within expected limits for the patient's age. \nThere are periventricular and subcortical nonenhancing T2/FLAIR white matter\nhyperintensities, which are nonspecific, but compatible with chronic\nmicroangiopathy in a patient of this age.  A developmental venous anomaly is\nincidentally noted in the right cerebellar hemisphere (series 19, image 26). \nThe major intracranial flow voids are preserved.  The dural venous sinuses are\npatent on postcontrast MP-RAGE.  There is mild mucosal thickening of the\nethmoid air cells.  The orbits are unremarkable, noting bilateral lens\nreplacements.  Fluid signal is noted in the bilateral mastoid air cells, which\ncan be seen on prior examination of ___.\n\nAlthough the examination is not optimized for such evaluation, a branch of the\nright superior cerebellar artery (series 19, image 32) is closely associated\nwith the root entry zone of the right trigeminal nerve.",
            "output": "1. No evidence for acute intracranial hemorrhage or infarct.  No abnormal\nenhancement.\n2. Periventricular and subcortical T2/FLAIR white matter hyperintensities are\nnonspecific, but compatible with chronic microangiopathy in a patient of this\nage.\n3. Although the examination is not optimized for such evaluation, a branch of\nthe right superior cerebellar artery is closely associated with the root entry\nzone of the right trigeminal nerve.  Correlation with side of trigeminal\nneuralgia described in the patient clinical history.  If clinically indicated,\nthis could be further evaluated with dedicated trigeminal nerve protocol MRI\nwith without contrast."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor acute infarction.  There is no abnormal enhancement after contrast\nadministration.  There are moderate chronic small vessel ischemic changes,\nwith 3 areas of confluence in the bilateral frontal and left parietal lobes,\nsimilar to prior..  Tiny chronic infarct in the right cerebellum, stable since\nprior..\n\nThere is moderate bilateral temporal lobe atrophy.  Prominent sylvian fissures\nbilaterally.  There is moderate right and mild left hippocampal atrophy.  More\nprominent right than left temporal horns.  Moderate atrophy of the left para\nhippocampal gyrus and fusiform gyrus.  There is mild atrophy of the bilateral\ninferolateral parietal lobes, no significant atrophy of the superomedial\nparietal lobes.  There is moderate atrophy of the bilateral frontal lobes.  No\nhydrocephalus.\n\nMild opacification left and trace right mastoid air cells.  Paranasal sinuses\nare clear aside from minimal opacification of left ethmoid air cells.  Benign\nC2 hemangioma, stable.",
            "output": "1. Moderate chronic small vessel ischemic changes.\n2. Moderate brain parenchymal atrophy, including atrophy of the hippocampus\nbilaterally, greater on the right.\n3. Tiny chronic infarct right cerebellum.\n4. No mass, no hydrocephalus."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, mass, or infarction.  Moderate\nprominence of the ventricles and sulci is suggestive of involutional changes.\nThere is no mass effect or midline shift.\n\n Multiple scattered T2 and FLAIR hyperintense foci in the periventricular and\nsubcortical white matter are nonspecific, but likely reflect chronic small\nvessel ischemic changes.\n\nThere is minimal mucosal thickening of the ethmoid sinuses.  Mild left and\ntrace right fluid signal in the mastoid air cells.  Postsurgical changes of\nbilateral lens replacement.",
            "output": "1. No acute infarction or intracranial hemorrhage.\n2. Moderate parenchymal volume loss and chronic small vessel ischemic disease."
        },
        {
            "input": "There is an area of slow diffusion in the posterior splenium of the corpus\ncallosum, with slight corresponding T2 and FLAIR hyperintensity in combination\nwith scattered subcortical T2 and FLAIR hyperintensities is most worrisome for\ndiffuse axonal injury (05:18, 05:28, 05:30).  There are several foci of\nsusceptibility overlying the left superior frontal gyrus (12:18), compatible\nwith foci of hemorrhage.  There is also a small focus of hemorrhage in the\noccipital horn of the right lateral ventricle (12:11).\n\nThe ventricles and sulci are normal in size and caliber.  There is no mass\neffect or midline shift.\n\nA severe mucosal thickening of the left maxillary sinus, and fluid filling the\nleft greater than right anterior ethmoid air cells and sphenoid sinuses. \nThere is partial opacification of the bilateral mastoid air cells.  Extensive\nmaxillofacial fractures are better evaluated on maxillofacial CT from ___.",
            "output": "1. Findings are most compatible with diffuse axonal injury, as evidenced by\nscattered foci of T2 and FLAIR hyperintensity, as well as an area of slow\ndiffusion in the splenium of the corpus callosum.\n2. Several foci of microhemorrhage, as seen over the left frontal lobe, and in\nthe occipital horn of the right lateral ventricle.\n3. Maxillofacial fractures are better evaluated on CT from ___. \nParanasal sinus opacification is probably related to these maxillofacial\ninjuries.\n\nNOTIFICATION:  The findings were discussed with ___, M.D. by ___\n___, M.D. on the telephone on ___ at 3:01 pm, 5 minutes after discovery\nof the findings.\n\nUpdate to the read with the interpretation of diffuse axonal injury paged to\n___ on ___ at 17:15."
        },
        {
            "input": "In comparison with the prior MRI examination dated ___, again\nscattered foci of high signal intensity are again seen in the subcortical\nwhite matter in both centrum semiovale, which are nonspecific and may\nrepresent demyelinating lesions, the pattern and configuration of these\nlesions remains similar with no evidence of new lesions (please compare images\n16 and 17, series 25 with the prior examination images 15 and 16, series 7). \nNone of this lesion demonstrates abnormal enhancement.  No diffusion\nabnormalities are detected.  The ventricles and sulci are normal in size and\nconfiguration, and unchanged since the prior study.  The major vascular flow\nvoids are present.  Slightly prominent pituitary gland is re- demonstrated,\nunchanged since the prior MRI examination.\n\nThere are persistent opacities in the paranasal sinuses, with mild improvement\nin the opacity of the frontal sinus, the ethmoidal air cells remain opacified\nwith mucosal thickening, minimal mucosal thickening is noted in the left\nmaxillary sinus, the mastoid air cells are clear.",
            "output": "1.  Unchanged scattered foci of high signal intensity detected on FLAIR and T2\nweighted images, distributed in the subcortical white matter, more significant\nin both centrum semiovale, these lesions are nonspecific, however in this age\ngroup  may represent demyelinating lesions, similar findings can be seen in\npatients with history of chronic migraines, sequela of viral infections,\nchronic hypertension and vasculitis.\n\n2.  Paranasal sinus disease as described detail above."
        },
        {
            "input": "Study is mildly Degraded by motion.\n\nMRA NECK:  The common, internal and external carotid arteries appear normal. \nThere is no evidence of stenosis by NASCET criteria. The origins of the great\nvessels, subclavian, and vertebral arteries appear normal bilaterally.  The\ncommon carotid bifurcations appear normal.",
            "output": "1.  Study is mildly degraded by motion.\n2. Within limits of study, no evidence of stenosis of bilateral cervical\nvertebral or carotid arteries."
        },
        {
            "input": "MRV: Normal flow signal is demonstrated within the superior sagittal sinus,\nstraight sinus, transverse sinuses, and sigmoid sinuses.  The left transverse\nsinus is hypoplastic.  The jugular bulbs and proximal jugular veins are\npatent. Evaluation of the deep venous systems reveals normal flow signal in\nthe internal cerebral veins. The vein ___ is also unremarkable.\n\nLimited brain:  Study is mildly degraded by motion.  Ventricles and sulci are\ngrossly preserved.",
            "output": "1. No evidence of venous sinus thrombosis."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  There is mild prominence of the ventricles and sulci\nsuggestive involutional changes..  There are mild, nonspecific scattered areas\nof periventricular, subcortical, deep and pontine white matter T2/FLAIR\nhyperintensity, minimally progressed compared to the ___ examination. \nThere is no abnormal enhancement after contrast administration.  There is no\nabnormal focus of slowed diffusion.  The principal intracranial vascular flow\nvoids are preserved.  The dural venous sinuses are patent on the appear age\nimages.\n\nThere is mild mucosal wall thickening in the bilateral anterior ethmoid air\ncells, bilateral frontal sinuses and moderate mucosal wall thickening in the\nright maxillary sinus.  There is a small mucous retention cyst in the left\nmaxillary sinus.\n\nThe orbits are grossly unremarkable.",
            "output": "1. No acute intracranial abnormality including hemorrhage, infarct or\nenhancing mass.\n2. Scattered areas of nonspecific periventricular, subcortical, deep and\npontine white matter signal abnormality, minimally progressed compared to ___.  Differential considerations include sequela of prior trauma or\ninfection, history of migraine headaches, inflammatory or demyelinating\nprocess, and microangiopathic changes.\n3. Paranasal sinus disease, as described."
        },
        {
            "input": "MR BRAIN: Mild approaching moderate periventricular and scattered subcortical\nwhite matter T2/FLAIR hyperintensities have increased over the interval.\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.\n\nThere is a mild left and mild-to-moderate right maxillary sinus signal\nabnormality.  There may be a small air-fluid level within the right maxillary\nsinus.\n\nMRA brain: Moderate narrowing of the distal cavernous to supraclinoid portions\nof the left internal carotid artery appear similar to slightly increased. \nThere may be a component of a pre dilatation within the proximal left\ncavernous internal carotid artery.  There is otherwise normal flow related\nsignal throughout the left internal carotid artery.  The mid right internal\ncarotid artery is normal in appearance.  There is normal flow related signal\nthroughout the basilar, vertebral, anterior, middle and posterior cerebral\narteries.  The intracranial vertebral and internal carotid arteries and their\nmajor branches appear normal without evidence of stenosis, occlusion, or\naneurysm formation.",
            "output": "1. Probable progression in moderate stenosis involving the distal supraclinoid\nportions of the left distal cavernous to supraclinoid internal carotid artery\nwhich may represent atherosclerotic disease.\n2. Mild approaching moderate probable microvascular ischemic change."
        },
        {
            "input": "There is a relatively abrupt narrowing of the left vertebral artery lumen in\nthe distal V1 segment at the level of C5 with crescentic surrounding\nhyperintensity on axial T1 fat saturated images (9:5 with extension of this\nfinding through to the V2 segment, no longer seen by the proximal V3 segment. \nOn the prior CT image, there appears to be a crescentic hypodensity at this\nlevel as well.  The underlying vertebral artery is patent.\n\nThe common, internal and external carotid arteries appear normal.  There is no\nevidence of stenosis by NASCET criteria. The origins of the great vessels,\nsubclavian, and  right vertebral arteries appear normal bilaterally.  The\ncommon carotid bifurcations appear normal.\n\nThere is a small mucous tendon cyst in the right maxillary sinus.",
            "output": "1. Abrupt left vertebral artery caliber change with crescentic T1 hyperintense\nsignal involving the distal V1 through V2 segments concerning for vertebral\nartery dissection, though flow is preserved.\n2. Remainder of the cervical vasculature is patent without occlusion, stenosis\nor other areas of dissection.\n\nNOTIFICATION:  The findings were discussed with ___, M.D. by\n___, M.D. on the telephone on ___ at 2:08 AM, 2 minutes after\ndiscovery of the findings."
        },
        {
            "input": "MRI BRAIN:\n\nPostcontrast MP RAGE images are completely degraded by motion artifact. \nPostcontrast axial T1 weighted images also limited by motion artifact.\n\nThere is an area of encephalomalacia and gliosis in the right superior\nparietal lobe, with high signal on T2 weighted/FLAIR imaging corresponding to\nthe low density on the preceding CT.  There is no associated diffusion\nabnormality to suggest superimposed acute infarction, and no evidence for\nassociated blood products.  Axial T1 weighted images demonstrate no associated\ncontrast enhancement to suggest a superimposed mass lesion.  While no\nenhancing lesions are seen elsewhere in the intracranial compartment,\nevaluation for small lesions is limited by motion artifact on the axial T1\nweighted images.\n\nThere is no acute infarction.  Mild high T2 signal along portions of the\nlateral ventricles is nonspecific but could be secondary to mild chronic small\nvessel ischemic changes.  Ventricles and sulci mildly prominent due to mild\nglobal age-related parenchymal volume loss.  Major intravascular flow voids\nare grossly preserved.\n\nA right anterior ethmoid air cell is opacified.\n\nMRA NECK:\n\nThere is a 3 vessel aortic arch.  Common carotid arteries appear widely\npatent.  There is no evidence for internal carotid stenosis by NASCET\ncriteria, though mild plaque at the right carotid bulb cannot be excluded. \nCervical vertebral arteries appear patent without flow-limiting stenosis.\n\nMRA BRAIN:\n\nImages are limited by motion artifact.  Intracranial vertebral arteries,\nbasilar artery, and intracranial carotid arteries are better assessed on the\ngadolinium enhanced neck MRA.  There is no evidence for occlusion or\nhigh-grade stenosis involving the intracranial internal carotid or vertebral\narteries, or proximal portions of their major branches.  Evaluation of the\ndistal branches, as well as evaluation for mild stenoses, is limited.  No\naneurysm is seen on limited evaluation.",
            "output": "1. Portions of the brain MRI and the brain MRA are motion limited.\n2. Area of encephalomalacia and gliosis in the right superior parietal lobe,\nwithout evidence for superimposed acute infarction or contrast enhancement.\n3. Overall, there is no evidence for intracranial metastatic disease, though\nmotion artifact limits evaluation for small lesions.\n4. No acute infarction.\n5. Unremarkable neck MRA.  Unremarkable motion-limited brain MRA."
        },
        {
            "input": "Study is mildly degraded by motion.\n\nImages through the internal auditory canal demonstrates symmetric appearance\nof the seventh eighth nerve complexes.  There is no evidence of abnormal\nenhancement or mass lesion within the internal auditory canals,\ncerebellopontine angles or membranous labyrinth. No other mass lesions are\nseen within the posterior fossa.\n\nThe left superior cerebellar artery is noted to traverse in close proximity\nto, but not contact, the left trigeminal nerve pre ganglionic segment (see\n100:  117, 13:  42-44).  There is no evidence of hemorrhage, edema, masses,\nmass effect, midline shift or infarction.   The ventricles and sulci are\nnormal in caliber and configuration.\n\nEnhancement of the right maxillary molar is noted (see 101:42, 15:18).",
            "output": "1. Study is mildly degraded by motion.\n2. No evidence of IAC or cerebellopontine angle mass.\n3. Left superior cerebellar artery traverses close to but does not clearly\ncontact left trigeminal nerve pre ganglionic segment.\n4. Probable right maxillary molar periodontal disease as described."
        },
        {
            "input": "The intracranial vertebral and internal carotid arteries and their major\nbranches appear patent without evidence of stenosis, occlusion, or aneurysm\nformation.",
            "output": "Patent intracranial vasculature without significant stenosis, occlusion, or\naneurysm formation."
        },
        {
            "input": "There is thickening and contrast enhancement of the dura along the left\nconvexity, compatible with sequela of prior left subdural hematoma and\nsurgical intervention in ___. There is no pathologic extra-axial\ncollection at this time. There is no evidence of acute infarction, edema,\nintracranial blood products, or intracranial mass. The ventricles and sulci\nare mildly prominent due to age-related parenchymal involutional change.\nMultiple small foci of high T2 signal in the subcortical, deep, and\nperiventricular white matter of the cerebral hemispheres are again seen,\nlikely sequela of chronic small vessel ischemic disease in a patient of this\nage. Major arterial flow voids are preserved. The major dural venous sinuses\nare patent.\n\nThis exam is not technically optimized for evaluation of the pituitary gland,\nand postsurgical changes are not adequately assessed. A small enhancing focus\nin the right aspect of the sella appears grossly stable compared to the MRI\nfrom ___.",
            "output": "1.  Thickening and contrast enhancement of the dura along the left convexity,\ncompatible with sequela of prior left subdural hematoma and surgical\nintervention in ___. No pathologic extra-axial collection and no other\nacute abnormalities are seen at this time.\n2.  Postsurgical changes in the sella are not adequately assessed. A\npreviously noted small enhancing focus in the right aspect of the sella is\ngrossly unchanged, but could be better assessed by dedicated pituitary MRI, if\nclinically warranted."
        },
        {
            "input": "A right frontal approach ventriculostomy shunt is again identified with distal\ntip in the region of the foramen of ___, unchanged in position.  There is a\nsmall amount of FLAIR signal abnormality surrounding the shunt catheter within\nthe right frontal lobe.  Review of gradient echo imaging demonstrates trace\namount of signal dropout in the dependent third ventricle and within the\noccipital horns of the lateral ventricles compatible with intraventricular\nhemorrhage.  Additional foci of signal dropout along the high bilateral\nparietooccipital convexities and in the region of the anterior sylvian\nfissures likely reflects subarachnoid hemorrhage, as previously described.  As\nbefore, there is stable ventriculomegaly.  There is no evidence of masses,\nmass effect, midline shift or acute territorial infarction.\n\nThere is trace fluid within the bilateral mastoid air cells.  The orbits and\nglobes appear within normal limits.  There is mild ethmoid sinus mucosal\nthickening.",
            "output": "1. Grossly stable right frontal approach ventriculostomy catheter with distal\ntip in the region of the foramen ___ and ventriculomegaly.\n2. Trace intraventricular and small volume subarachnoid hemorrhage, as above.\n3. No evidence of mass lesion, midline shift or acute territorial infarction."
        },
        {
            "input": "MRI BRAIN:\nThe patient is status post a right trans parietal ventriculostomy shunt\ncatheter with tip terminating in the left lateral ventricle.  Resolution of\nprevious seen ventriculomegaly.  Gradient echo stool artifact along a right\nfrontal ventriculostomy tract is unchanged.\n\nMetallic artifact from the shunt reservoir results in suboptimal evaluation of\nadjacent structures.  Within this context: There is no evidence of acute\ninfarct or intracranial hemorrhage.  There is no suspicious parenchymal FLAIR\nsignal abnormality or enhancement.  The major intracranial flow voids are\npreserved.  The dural venous sinuses are patent.  Unchanged ___ cisterna\nmagna.\n\nThere is mild mucosal thickening of the ethmoid air cells.  The orbits are\nunremarkable.  Trace fluid signal seen in the mastoid air cells.  No\nsuspicious marrow signal.\n\nMRA BRAIN:\nThe patient is status post coil embolization of a right posterior\ncommunicating artery aneurysm with residual 1 mm flow at its neck (series 4,\nimage 209), centrally unchanged from prior examinations allowing for technical\ndifferences.\n\nThe remainder of the intracranial circulation is unremarkable.  There is\ninterval resolution of previously described vasospasm.  The dural venous\nsinuses are patent on post-contrast imaging.",
            "output": "1. No acute intracranial abnormality a contrast enhanced MRI brain. \nSpecifically no acute infarct or intracranial hemorrhage.  No abnormal\nenhancement.  Resolution of ventriculomegaly.  A right trans parietal\nventriculostomy shunt catheters stable from prior exam.\n2. The patient is status post coil embolization of a right posterior\ncommunicating artery aneurysm.  1 mm residual neck is identified, similar in\nappearance to prior exam.\n3. The remainder of the intracranial circulation is unremarkable with\nresolution of previously described vasospasm.\n4. Additional findings as described above."
        },
        {
            "input": "There is no evidence of acute intracranial hemorrhage or mass effect.  The\nventricles and basal cisterns appear normal.\n\nThere is no evidence of acute ischemia based on diffusion-weighted imaging. \nThere are normal vascular flow voids. There is subcortical and periventricular\nT2/FLAIR white matter hyperintensity which is presumably on the basis of\nsequelae of chronic small vessel ischemic disease.\n\nThe orbits and skull base appear unremarkable.  There is right maxillary sinus\nmucosal thickening with areas of T1 hyperintensity suggesting inspissated\nsecretions or fungal infection.",
            "output": "1. No evidence of acute intracranial hemorrhage, mass effect, or acute\nischemia.\n2. Brain parenchymal volume loss and presumed sequelae of chronic small vessel\nischemic disease.\n3. Paranasal sinus disease, as described."
        },
        {
            "input": "Limited exam due to patient motion.  There is a small 9 mm in length by 2.6 mm\nin transverse dimension  focus of slow diffusion within the posterior limb of\nthe left internal capsule (image 16, series 4), with subtle FLAIR\nhyperintensity compatible with acute/subacute infarct.  Additional area of\nhigh diffusion signal within the anterior left frontal lobe at the cortical\nmargin, without correlate on ADC or other sequences, and is likely\nartifactual.\n\nThere is no evidence of hemorrhage, masses, mass effect, or midline shift. \nThere is prominence of the ventricles and sulci suggesting involutional\nchanges confluent areas of periventricular, subcortical and deep white matter\nT2/FLAIR hyperintensity are in a configuration suggestive of chronic small\nvessel ischemic disease.  The principal intracranial vascular flow voids are\npreserved.\n\nThere is a large mucous retention cyst in the right maxillary sinus with mild\nmucosal wall thickening, as well as mild mucosal wall thickening in the\nbilateral ethmoid air cells.  The remainder the visualized paranasal sinuses\nare grossly clear.  The orbits are grossly unremarkable.",
            "output": "1. Please note that this is an incomplete examination with acquisition of only\nthe axial diffusion, T2, sagittal T1 and half of the interleaved FLAIR\nsequence as patient could not tolerate the examination.\n2. Small acute to subacute infarct of the posterior limb of the left internal\ncapsule.\n3. Prominent global atrophy and chronic small vessel ischemic change.\n\nNOTIFICATION:  The findings were discussed with ___, M.D. by ___\n___, M.D. on the telephone on ___ at 9:33 AM, 5 minutes after\ndiscovery of the findings."
        },
        {
            "input": "There is diffuse increased cortical T2/FLAIR signal hyperintensity in the\nbilateral cerebral hemispheres including the bilateral hippocampal formations\n.There is also increased T2/FLAIR signal in the bilateral basal ganglia. \nThese regions demonstrate slow diffusion on diffusion-weighted images. This\nfinding is likely secondary to severe diffuse hypoxic/ischemic injury.\n\nThere is no intracranial hemorrhage, extracerebral fluid collection, midline\nshift or mass effect.  The cerebral volume is appropriate for the patient's\nstated age.  Flow voids are maintained.  The orbits are unremarkable. There is\nfluid within the ethmoid and sphenoid sinuses and mastoid air cells.\n\nPreviously identified rounded hyperdensity in the right ambient cistern on\nprior CT is not well identified on today's study and therefore cannot be\nfurther characterized.",
            "output": "Increased T2-/FLAIR-hyperintensity with corresponding slow diffusion in the\ncortex of both cerebral hemispheres, as well as within the basal ganglia,\nbilaterallly.\n\nThese finding likely represent severe, diffuse hypoxic-ischemic injury,\nrelated to the given history of cardiac arrest."
        },
        {
            "input": "Limited examination due to patient motion.\n\nThere is susceptibility artifact in the left basal ganglia with associated T1\nisointensity and T2 predominant hypointensity, consistent with acute\nhemorrhage, not significantly changed in extent.  There is mild mass effect on\nthe frontal horn of the left lateral ventricle, stable.  No midline shift. \nThere is no evidence of underlying mass lesion or abnormal enhancement in this\nregion.  Underlying diffusion abnormality is likely due to blood products.\n\nConfluent subcortical, periventricular and brainstem white matter T2/FLAIR\nhyperintensities are nonspecific, however likely represent sequela of chronic\nsmall vessel ischemic disease,  progressed compared with ___.  Scattered\nsmall foci of T2 hyperintensity in the bilateral cerebellar hemispheres are\nnot significantly changed, possibly sequela chronic infarcts.  There is\nsusceptibility artifact in the region of the left cavernous internal carotid\nartery due to an aneurysm coil.  Major intracranial vascular flow voids are\notherwise preserved.  The dural venous sinuses are patent.\n\nThere is mild mucosal thickening in the ethmoid air cells.  Patient is status\npost bilateral lens replacement.  The orbits are otherwise grossly\nunremarkable.",
            "output": "1. Study is mildly degraded by motion.\n2. No significant change in acute intraparenchymal hemorrhage centered in the\nleft basal ganglia with mild mass effect on the adjacent frontal horn of the\nleft lateral ventricle.  No midline shift.\n3. No evidence of underlying mass lesion.\n4. Extensive chronic microvascular ischemic changes.\n5. There is susceptibility artifact in the region of the left cavernous\ninternal carotid artery due to an aneurysm coil."
        },
        {
            "input": "Study is mildly degraded by motion.\n\nRestricted diffusion is seen in the right corona radiata, superior globus\npallidus and putamen, with associated T2 and FLAIR hyperintensity, T1\nhypointensity and no definite associated increase susceptibility.\n\nThere is no evidence of hemorrhage, masses, mass effect or midline shift.  The\nventricles and sulci are prominent, consistent with global cerebral volume\nloss.  Patchy periventricular T2 hyperintensities are most consistent with\nchronic microvascular angiopathy.  Subcentimeter chronic infarcts are seen in\nbilateral basal ganglia and the left corona radiata.\n\nThe mastoid air cells and middle ear cavities are clear.  The patient is\nstatus post bilateral cataract surgery.  Bilateral maxillary sinus, frontal\nsinus, and ethmoid air cell mild mucosal thickening is present.",
            "output": "1.  Study is mildly degraded by motion.\n2. Right MCA distribution acute to subacute infarct as described, without\ndefinite evidence of hemorrhagic transformation.\n3. Global volume loss, probable microangiopathic changes, and bilateral basal\nganglia and left corona radiata chronic infarcts, as described.\n4. Mild paranasal sinus disease , as described.\n\nNOTIFICATION:  The findings were discussed with ___, M.D. by ___\n___, M.D. on the telephone on ___ at 3:23 am, 5 minutes after\ndiscovery of the findings."
        },
        {
            "input": "Study is mildly degraded by motion.  There is no evidence of hemorrhage,\nedema, masses, mass effect, midline shift or infarction.   The ventricles and\nsulci are normal in caliber and configuration.  There is no abnormal\nenhancement after contrast administration.",
            "output": "1. Study is mildly degraded by motion.\n2.  No acute intracranial abnormality.\n3. Within limits of study, no definite evidence of intracranial metastatic\ndisease."
        },
        {
            "input": "MRA brain: The intracranial vertebral and internal carotid arteries and their\nmajor branches appear normal without evidence of stenosis, occlusion, or\naneurysm formation.  The left posterior cerebral artery demonstrates a fetal\norigin.\n\nMRA neck:  The common, internal and external carotid arteries appear normal. \nThere is no evidence of stenosis by NASCET criteria.  The origins of the great\nvessels are not imaged on this current examination.",
            "output": "1. Circle of ___ patent. Left fetal origin posterior cerebral artery.\n2. Bilateral vertebral arteries, common carotid arteries, and carotid\nbifurcations patent.  No evidence of carotid stenosis by NASCET criteria.\nPlease note that the origins of vertebral arteries and common carotid arteries\nwere not included on this examination."
        },
        {
            "input": "MRA brain: Susceptibility artifact in the region of the right para-clinoid to\nsupraclinoid ICA compatible with known flow diverting stent placement is\nunchanged in appearance from examination of ___.  No evidence of\nrecanalization of right ICA aneurysm.  Since the prior examination, interval\nplacement of a left paraclinoid to supraclinoid ICA flow diverting stent, with\nobliteration of a left para ophthalmic artery aneurysm.  No evidence of\nrecanalization.  In-stent stenosis cannot be accurately evaluated due to\ndegree of artifact, however there is unremarkable distal run-off.  The\nremainder of the intracranial ICA, bilateral MCA, ACA and their major branches\nare unremarkable without evidence of high-grade stenosis, occlusion or\naneurysm.  The posterior circulation is also unremarkable.",
            "output": "1. Bilateral paraclinoid ICA flow diverting stents are identified without\nevidence of recanalization of ICA artery aneurysms.\n2. Although in-stent stenosis cannot be accurately evaluated due to\nsusceptibility artifact, there is unremarkable distal run-off.\n3. Otherwise, unremarkable MRA of the head."
        },
        {
            "input": "Incomplete examination secondary to patient's inability to continue. Localizer\nimages were obtained in three planes.\n\nOn markedly limited examination, there is no evidence of large mass or gross\nstructural anomaly.",
            "output": "Incomplete examination (see above).  Please consider repeat study under\nsedation, as warranted."
        },
        {
            "input": "There is no intra or extra-axial mass effect, acute hemorrhage or infarct. \nSulci, ventricles and cisterns are within expected limits given the degree of\nglobal cerebral volume loss, which is also within expected limits for age. \nThere are a few nonspecific T2/FLAIR white matter subcortical and\nperiventricular hyperintensities.  The major intracranial flow voids are\npreserved.  A mucous retention cyst is noted in the right maxillary sinus. \nMild mucosal thickening of the frontal sinuses and ethmoid air cells are\nnoted.  The remainder the paranasal sinuses are clear.  The patient is status\npost bilateral lens replacements otherwise orbits are unremarkable.",
            "output": "1. A few T2/FLAIR white matter subcortical and periventricular\nhyperintensities are nonspecific, but most commonly seen in setting of chronic\nmicroangiopathy in a patient of this age.\n2. No acute intracranial hemorrhage or infarct.  No evidence of mass lesions."
        },
        {
            "input": "There is restricted diffusion with patchy areas of corresponding ADC weighted\nhypointensity involving a large portion of the right cerebral hemisphere and\nright basal ganglia due to infarction of the right MCA. Infarction is now in\nthe subacute phase as ADC signal abnormality is normalizing and the area of\ninfarction demonstrates diffuse cortical enhancement. There is mass effect\nthroughout the right hemisphere with mild mass effect on the right frontal\nhorn. The ventricles are otherwise normal in size. There is no midline shift.\nThe basal cisterns are patent. There is heterogeneity of the flow void of the\nright proximal MCA corresponding to thrombus/stenosis  (within the M1\nsegment), as seen on CTA head from ___.\n\nThere is a 0.8 x 0.7 cm enhancing mass with moderate surrounding edema in the\nleft posterior frontal lobe consistent with a metastasis, unchanged from MRI\non ___.\n\nThe calvarium is intact. The paranasal sinuses are clear. There is scattered\nfluid in the left mastoid air cells. The right mastoid air cells are clear.\nThe orbits are normal.",
            "output": "1. Subacute infarct of the right proximal MCA involving the right cerebral\nhemisphere with hemorrhagic transformation, not significantly changed in\nappearance from CT on ___.  Given the extensive enhancement,\nassociated metastasis or mass difficult to exclude but appears less likely.\n2.  Persistent right M1 thrombus/stenosis.\n3.  Small left frontal lobe possible metastasis with moderate surrounding\nedema, unchanged from MRI on ___."
        },
        {
            "input": "There is unchanged right frontal lobe hemorrhage with mild mass effect. There\nis heterogeneous enhancement in the region of the hemorrhage which could\nreflect an underlying mass. There is a ring-enhancing lesion within the left\ncentrum semiovale.\n\nThere is evolution of a right MCA territory infarct. There are also punctate\nfoci of involving the posterior left frontal lobe (series 6, image 25).\n\nThere is a right frontal subarachnoid hemorrhage that is unchanged. The\nprincipal intracranial flow voids are present. There is mild paranasal sinus\nmucosal thickening. There is small amount of fluid in bilateral mastoid air\ncells.",
            "output": "There is unchanged right frontal lobe hemorrhage with mild mass effect. There\nis heterogeneous enhancement in the region of the hemorrhage which could\nreflect an underlying mass. There is also a ring-enhancing lesion within the\nleft centrum semiovale. Differential considerations would include metastasis\nor septic emboli.  An atypical infection not excluded.\n\nEvolution of right MCA infarct. There is also a punctate focus of infarct in\nthe posterior left frontal lobe."
        },
        {
            "input": "The examination is moderately degraded by patient motion.  Allowing for this:\n\nMRI BRAIN:\nThe previously seen, moderate sized right intraparenchymal hemorrhage centered\nin the right basal ganglia is again noted with extension towards the body\nright lateral ventricle, near ependyma surface, similar the previous\nexamination allowing for difference in modalities.  Mild surrounding T2 signal\nabnormality.  Minimal local mass effect is seen without appreciable midline\nshift.  No evidence of nodular enhancement.  Minimal linear enhancement\nsurrounding hematoma, seen commonly in this setting.\n\nThe dural venous sinuses appear grossly patent.  There is no evidence for\nabnormal intracranial enhancement.\n\nThe ventricles and sulci are prominent enlarged compatible with global\nparenchymal volume loss.  Findings consistent with mild chronic small vessel\nischemic changes.\n\nMild mucosal thickening is seen in scattered ethmoid air cells.  Small volume\nfluid in the sphenoid sinus remainder of the paranasal sinuses and mastoid air\ncells are clear bilaterally.  The patient is status post right lens resection.\nLeft lens dislocation.\n\n\nMRA brain:\nThe 3D time-of-flight MRA images through the intracranial vasculature are\nseverely degraded by patient motion, and are nondiagnostic.  No definite\nvascularity at the level of the hematoma.",
            "output": "1. Moderately motion degraded examination.\n2. Stable known acute right basal ganglia - centered parenchymal hematoma.\n3. No mass.\n4. Brain parenchymal atrophy.  Mild chronic small vessel ischemic changes.\n5. Severely motion degraded nondiagnostic MRA brain.  No definite vascularity\nat the level of the hematoma.\n6. Left lens dislocation, stable.\n\nRECOMMENDATION(S):  Follow-up head CT without contrast within 3 months."
        },
        {
            "input": "Bilateral frontoparietal subdural collections are seen, measuring up to 6 mm\non the right and 8 mm on the left, consistent with subdural hematoma is as\nseen on the prior CT.  Additionally, Re demonstrated are bilateral\nintraventricular blood products within the occipital horns, right greater than\nleft, not significantly changed compared to the prior CT performed on the same\nday.  A small focus of FLAIR hyperintensity is seen in the region of the right\nfrontal intraparenchymal hematoma.  Microhemorrhages adjacent to the anterior\nhorn of the right lateral ventricle (06:17) and a second adjacent to the\nposterior portion of the body of the left lateral ventricle (06:16) may\nsuggest diffuse axonal injury.\n\nMild prominence of ventricles and sulci is likely related to age related\ninvolutional changes.  Periventricular and deep subcortical FLAIR white matter\nhyperintensities are likely sequelae of chronic small vessel ischemic disease.\n\nMild mucosal sinus thickening is seen involving the ethmoid air cells.  The\nvisualized paranasal sinuses, are otherwise unremarkable.  Mild opacification\nis seen involving the mastoid air cells.  The globes are unremarkable.  The\nprincipal vascular flow voids are well preserved.  No concerning enhancing\nlesions are identified.",
            "output": "1. Stable bilateral frontoparietal thin subdural hematomas compared to the\nprior CT performed on the same day.\n2. Stable intraventricular blood products within the occipital horns of the\nbilateral ventricles.  No new evidence of hydrocephalus.\n3. Subtle micro hemorrhages adjacent to the ventricle may suggest diffuse\naxonal injury.\n4. Small right frontoparietal scalp hematoma."
        },
        {
            "input": "There are no focal signal abnormalities identified.  The ventricles and\nextra-axial spaces are normal in size.  No acute infarcts are seen.  Following\ngadolinium there is no abnormal parenchymal, vascular or meningeal enhancement\nseen.  Coronal images through the temporal lobes demonstrate no evidence of\nfocal abnormalities within the medial temporal structures.  The hippocampal\nformations are normal in size.",
            "output": "No significant abnormalities are seen on MRI of the brain with and without\ngadolinium including coronal images through the temporal lobes."
        },
        {
            "input": "There is subtle increased signal noted in the right hippocampus of a\nquestionable nature. There is no evidence of atrophy. There are no migrational\nabnormalities detected.\n\nThere is no acute infarction, intracranial hemorrhage, extracerebral fluid\ncollection, midline shift or mass effect.  No diffusion abnormalities are\ndetected. The cerebral volume is appropriate for the patient's stated age. \nThe major vascular flow voids are maintained, there is no evidence of abnormal\nenhancement. The orbits are unremarkable, the paranasal sinuses and mastoid\nair cells are clear",
            "output": "Subtle increase in signal in the right hippocampus without signs of atrophy.\nGiven the subtlety of this finding, correlation with EEG is recommended to\ndetermine the significance."
        },
        {
            "input": "Study is degraded by motion.  Within these confines:\n\nMR BRAIN:\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline\nshiftorinfarction.  There is prominence of the ventricles and sulci suggestive\nof involutional changes.  Periventricular and subcortical T2 and FLAIR\nhyperintensities are noted which may represent small vessel ischemic changes.\n\nMRA BRAIN:\nThe intracranial vertebral and internal carotid arteries and their major\nbranchesappear grossly preservedwithout evidence of stenosis, occlusion, or\naneurysm formation greater than 3 mm.",
            "output": "1.  Study is degraded by motion.\n2.  No acute intracranial abnormality, with no definite evidence of acute\ninfarct.\n3. Grossly patent circle of ___ without definite evidence of\nstenosis,occlusion,or aneurysm greater than 3 mm."
        },
        {
            "input": "There is no intracranial mass, mass effect, or midline shift. Ventricles and\nsulci are age-appropriate. There is no pathologic intracranial enhancement.\nIntracranial flow voids are maintained. Visualized paranasal sinuses and\nmastoid air cells are clear.  There is no signal abnormality on diffusion\nweighted imaging to suggest acute infarct.  No cerebellar lesion is\nidentified.  Incidental note is made of ___ cisterna magna.",
            "output": "No evidence of acute stroke. No cerebellar lesion identified."
        },
        {
            "input": "There is no intracranial mass, mass effect, or midline shift. Ventricles and\nsulci are enlarged compatible with global volume loss.  T2 hyperintensity\nwithin the central pons likely from prior infarct.   There is no region of\nrestricted diffusion to suggest acute infarct.  A few scattered foci of\nsusceptibility artifact specifically in the left frontal and temporal lobes\nare likely sequela of prior microhemorrhages.  Major intravascular flow voids\nare preserved.\n\nVisualized paranasal sinuses and mastoid air cells are clear.  Bone marrow\nsignal in the upper cervical spine is heterogeneous.  Endotracheal tube is\nvisualized.",
            "output": "No acute infarct.  Global volume loss."
        },
        {
            "input": "The examination is mildly motion degraded, particularly the MP-RAGE\npostcontrast sequences.  Within this confines:\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.\n\nThe major intracranial vascular flow voids are maintained.  The ventricles and\nsulci are normal in caliber and configuration.  The dural venous sinuses are\npatent.  There is no abnormal enhancement after contrast administration. \nThere is mild mucosal thickening of the left sphenoid sinus, extending to the\nlateral recess.  The orbits, mastoid air cells and paranasal sinuses are\notherwise normal.",
            "output": "1. No evidence of intracranial metastatic disease at this time.\n2. Unremarkable MRI of the head without evidence of abnormal enhancement,\nacute infarct or intracranial hemorrhage."
        },
        {
            "input": "There is no evidence of acute intracranial hemorrhage, mass, mass effect or\nshifting of the normally midline structures.  The ventricles and sulci are\nnormal in size and configuration for the patient's age.  No diffusion\nabnormality detected.  The major vascular flow voids are present and\ndemonstrate normal distribution.  The orbits are unremarkable, the paranasal\nsinuses and the mastoid air cells are clear.  The soft tissues are notable for\nsusceptibility changes in the left frontal region (images 14, 15, series 7),\nprobably consistent prior trauma or retained metal foreign body, no underlying\nintracranial changes are identified, if there is clinical concern related with\nthis finding, correlation with CT of the head is advised.",
            "output": "1.  There is no evidence of acute subacute intracranial process, specifically,\nthere is no evidence of hemorrhage or intracranial mass lesion.\n\n2.  Susceptibility changes are visualized in the soft tissues of the left\nfrontal region, probably related with retain metallic foreign body versus\nsequela of prior trauma, if there is concern related with this finding,\ncorrelation with CT of the head is recommended for further characterization.\n\nRECOMMENDATION(S):  Susceptibility changes are visualized in the soft tissues\nof the left frontal region, partially evaluated in this exam, if there is\nclinical concern related with this finding, correlation with CT of the head is\nrecommended."
        },
        {
            "input": "There is no evidence of acute infarction.  No intracranial hemorrhage. No\nmass, mass effect, edema or midline shift.\n\nThe ventricles and sulci are enlarged.  Periventricular and subcortical white\nmatter FLAIR hyperintensities are noted, a nonspecific finding that most\nlikely represents the sequelae of chronic small vessel ischemic disease.  \nThere is gross preservation of the principal intracranial vascular flow voids.\n\nMild mucosal thickening is seen throughout scattered ethmoid air cells and\nwithin the bilateral maxillary sinuses.  The frontal sinuses are\nunderpneumatized.  The remainder of the visualized paranasal sinuses, middle\near cavities, and mastoid air cells are well aerated and clear.  Patient is\nstatus post bilateral lens replacement.",
            "output": "1. No evidence for vascular territorial infarction.  No acute intracranial\nhemorrhage.\n2. Global parenchymal volume loss and evidence of chronic small vessel\nischemic disease."
        },
        {
            "input": "There is an area of restricted diffusion in the medial right precentral gyrus\nwith minimal FLAIR hyperintensity.  Additional small foci of restricted\ndiffusion in the posterior margin left middle frontal gyrus series 6, image\n24, left inferior parietal lobule image 80, right occipital lobe image 15,\nposterior right putamen image 16, 14, right caudate body and probably adjacent\ncorona radiata image 19..  There is no associated enhancement or hemorrhage. \nThere is no or mass.  The flow voids the major intracranial blood vessels are\npreserved.  There is no mass effect.  There is mild partial opacification of\nthe paranasal sinuses, mastoid air cells.  The bilateral orbits are\nunremarkable.",
            "output": "1. There multiple punctate foci of restricted diffusion bilaterally, more\nprominent on the right, consistent with acute/early subacute infarcts.  There\nis no intraparenchymal abscess, hemorrhage or cerebritis.\n\nNOTIFICATION:  The findings were discussed with ___, M.D. by ___\n___, M.D. on the telephone on ___ at 12:55 pm, 5 minutes after\ndiscovery of the findings."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.\n\nA couple scattered T2 and FLAIR hyperintense foci in the periventricular and\nsubcortical white matter are nonspecific, some of which are unchanged in the\nright parietal periventricular white matter compared to ___.\n\nThe major intracranial arterial and venous flow voids are preserved.  The\nright maxillary sinus is hypoplastic.  Mild paranasal sinus mucosal\nthickening.  The mastoid air cells are clear.  The intraorbital contents are\nunremarkable.",
            "output": "1. A couple scattered white matter signal abnormalities are nonspecific.\n2. No acute infarction or intracranial hemorrhage."
        },
        {
            "input": "MRI Brain:\nThere is no infarction or intracranial hemorrhage.  There is prominence of the\nventricles, sulci, and cisterns, which are age-appropriate.  There is no mass\neffect or midline shift.  There is no mass on this unenhanced study.  There\nare nonspecific hyperintense T2/FLAIR signal abnormality within the\nperiventricular and subcortical white matter, which is likely a sequela of\nchronic small vessel microangiopathy.  The major intracranial flow voids are\npreserved.  The paranasal sinuses and bilateral mastoid air cells appear\nclear.\n\nMRA brain:  The bilateral internal carotid arteries and the vertebral arteries\nand branches are patent without significant stenosis, occlusion, or aneurysm\nformation greater than 3 mm.\n\nMRA neck:  There is a 3 vessel aortic arch.  There is mild atherosclerotic\ndisease and minimal  narrowing of the left internal carotid artery at its\norigin with calcified and noncalcified plaque with central defect likely\nartifact(16:44).  The right internal carotid artery demonstrates irregularity\nnear its origin (16:48), without significant stenosis or occlusion per NASCET\ncriteria.  The bilateral common carotid arteries and vertebral arteries are\npatent.",
            "output": "1. No infarction, haemorrhage, or mass on this unenhanced study.\n2. Mild atherosclerotic disease both internal carotid origins  without\nstenosis per NASCET criteria.\n3. Probable chronic small vessel microangiopathy."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  Patchy periventricular T2 hyperintensities are most consistent\nwith chronic microvascular angiopathy.  A focus of encephalomalacia is seen\ninvolving the right parietal lobe.  There is no abnormal enhancement after\ncontrast administration.\n\nA 2 mm hypoenhancing focus is seen in the right aspect of the adenohypophysis\n(series 901, image 67), likely representing a incidental pituitary\nmicroadenoma.",
            "output": "1. No evidence of metastatic disease.\n2. Old infarct involving the right parietal lobe.\n3. 2 mm hypoenhancing focus in the right aspect of the adenohypophysis raises\nthe possibility of an incidental pituitary microadenoma."
        },
        {
            "input": "Examination is moderately degraded by motion.  Within these confines:\n\nExtensive scattered punctate and more confluent periventricular, subcortical,\nand deep white matter foci of T2/FLAIR hyperintense signal without associated\nslow diffusion with a predominantly frontoparietal distribution are\nnonspecific, but most likely sequelae of chronic microangiopathy in a patient\nof this age.\n\nThere is no evidence of hemorrhage, edema, mass, mass effect, midline shift or\nacute infarction.  There is a small chronic lacunar infarction in the left\nbasal ganglia (04:19).  Prominence of the ventricles and sulci is in keeping\nwith global atrophy.\n\nMild mucosal thickening in the left frontal, posterior ethmoid sinuses and\npartial fluid opacification of bilateral mastoid air cells are noted.  The\norbits are unremarkable.",
            "output": "1. Study is moderately degraded by motion.\n2. Chronic small vessel ischemic changes and global atrophy.\n3.  No acute intracranial abnormality, with no evidence of acute infarct.\n4.  Paranasal sinus disease and nonspecific mastoid fluid, as described."
        },
        {
            "input": "Images are mildly limited by motion artifact.\n\nThere is no evidence of an enhancing intracranial mass.  There is no evidence\nfor pathologic leptomeningeal or pachymeningeal contrast enhancement.  There\nis no evidence for an acute infarction, edema, or blood products.  Confluent\nperiventricular high T2 signal, and foci of high T2 signal in the deep and\nsubcortical white matter of the cerebral hemispheres, are nonspecific but\nlikely sequelae of chronic small vessel ischemic disease in this age group.\nThe ventricles and sulci are mildly prominent, compatible with age related\nglobal parenchymal volume loss.There is gross preservation of the principal\nintracranial vascular flow voids. The dural venous sinuses appear patent on\nMP-RAGE imagine sequences.\n\nThere are mucous retention cysts and mild mucosal thickening in the maxillary\nsinuses, as well as mild mucosal thickening in right greater than left ethmoid\nair cells.",
            "output": "No evidence for intracranial metastatic disease or acute intracranial\nabnormalities."
        },
        {
            "input": "1.7 x 1.5 cm expansile mass is noted in the right occipital condyle presents\nT2/FLAIR hyperintensity and T1 hypointensity.  This enhances uniformly after\ncontrast administration.\n\nAreas of chronic lacunar infarction seen in the left putamen and right\ncerebral hemisphere.  Mild periventricular FLAIR hyperintensities are\nnonspecific, but likely secondary to small vessel disease.\nThere is no evidence of hemorrhage, edema, mass effect, midline shift or acute\ninfarction.  The ventricles and sulci are normal in caliber and configuration.\nMild right maxillary sinus disease.",
            "output": "1. 1.7 cm expansile mass in the right occipital condyle, of unclear origin\nbased on this imaging alone.  Given the multiplicity of lesions identified on\nspinal imaging, metastatic disease is a leading possibility.\n2. No evidence of hemorrhage, edema or recent infarction.\n3. Right maxillary sinus disease."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are slightly prominent.  T1\nhyperintensity within the basal ganglia may be related to known underlying\nliver dysfunction.  Single T2/FLAIR hyperintensity in the right frontal\nsubcortical white matter without restricted diffusion is nonspecific.\n\nThe visualized vascular flow voids are grossly preserved.  There is mild\nmucosal thickening of the ethmoid air cells, and right maxillary sinus.  Trace\nof effusion in the bilateral mastoid air cells, greater on the left.  The\nglobes and orbits are unremarkable.  Unremarkable bone marrow.",
            "output": "No evidence of acute infarct, intracranial mass, or hemorrhage.  No evidence\nof anoxic brain injury.  T1 hyperintensity in the basal ganglia likely related\nto patient's known underlying liver dysfunction."
        },
        {
            "input": "There is a right frontal burr hole. There is a catheter seen crossing across\nthe right frontal lobe with tip terminating in the lateral most margin of the\nfrontal horn of the left lateral ventricle. There is minimal increased FLAIR\nsignal surrounding the catheter tract.\n\nThere is no acute infarction, intracranial hemorrhage, extracerebral fluid\ncollection, midline shift or mass effect.  No diffusion abnormalities are\ndetected.  The ventricles and the sulci and extra-axial CSF spaces are normal.\nThe major vascular flow voids are maintained.\nThere is no evidence of abnormal enhancement allowing for the pulsation\nartifacts in the posterior fossa.\n\nThe orbits are unremarkable. There is a mucous retention cyst in the sphenoid\nsinus and minimal mucosal thickening within the right maxillary sinus. The\nmastoid air cells are clear.",
            "output": "Catheter seen crossing the right frontal lobe with tip terminating in the\nlateral most aspect of the left lateral ventricle.\nNo evidence of abnormal enhancement in the brain parenchyma or meninges\nallowing for the pulsation artifacts.\nNo significant change since prior."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  There is a right frontal burr hole from prior ventriculostomy\ncatheter placement with T2 and FLAIR signal hyperintensity along the tract of\nthe prior ventriculostomy catheter.  Periventricular and subcortical white\nmatter hypodensities are nonspecific but likely sequelae of chronic small\nvessel ischemic disease. The ventricles and sulci are normal in caliber and\nconfiguration. There is no abnormal enhancement after contrast administration.\nThere is mild bilateral maxillary sinus mucosal thickening.",
            "output": "1. No abnormal enhancement to suggest intracranial lymphoma recurrence.\n2. Mild chronic microangiopathy.\n3. Interval removal of a right frontal approach ventriculostomy catheter, with\nassociated parenchymal changes."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  Patchy periventricular T2 hyperintensities are most consistent\nwith chronic microvascular ischemic disease. There is no abnormal enhancement\nafter contrast administration.  A right frontal burr hole is seen from a prior\nventriculostomy catheter placement.\n\n The paranasal sinuses, mastoid air cells and middle ear cavities are clear. \nThe intraorbital contents are normal.",
            "output": "1. No metastasis.\n2. No acute intracranial abnormality."
        },
        {
            "input": "Only scout images, sagittal T1 and axial T1 images are available.  The patient\nwas unable to complete the MRI examination.\n\nThere is no evidence of a large intracranial mass.  There is no T1\nhyperintensity to suggest a bleed.  No midline shift, no hydrocephalus.",
            "output": "Limited brain MRI.\nNo abnormality on T1 weighted images."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is a focus of FLAIR hyperintensity in the right frontal\nlobe corresponding to the prior ventricular catheter tract.  Periventricular\nand subcortical white matter T2/FLAIR hyperintensities are nonspecific but\nlikely sequelae of chronic small vessel ischemic disease.  There is no\nabnormal enhancement after contrast administration.  A right frontal burr hole\nis seen from a prior ventriculostomy catheter placement.\n\nParanasal sinuses, mastoid air cells and middle ear cavities are clear.  The\nintraorbital cavities are unremarkable.",
            "output": "No evidence of lymphoma recurrence."
        },
        {
            "input": "There is a region within the left parietal lobe that shows low signal on ADC\nwith corresponding high signal on DWI images, compatible with a recent left\nMCA territory infarct.  This was also seen on yesterday's CTA. No other\ndiffusion abnormalities are detected.  GRE sequence shows hemorrhage within\nthis region. No parenchymal masses are identified.\n\nThe brainstem, posterior fossa and cervical medullary junction are preserved.\nPituitary gland appears normal. Prominent ventricles and sulci are normal for\npatient age. Principal intracranial vascular flow voids are preserved. Basal\ncisterns are patent. The bilateral orbits and periorbital spaces are\nunremarkable. Visualized paranasal sinuses are unremarkable. No abnormalities\nof the skull base or calvarial identified.",
            "output": "1. Evolving left MCA territory infarct, with evidence of local hemorrhage.\n2.  No new ischemia since the prior CT on ___."
        },
        {
            "input": "There is a chronic infarct of the left middle cerebral artery vascular\nterritory, involving the left parietal and left posterior temporal lobes. \nThere is currently no slowed diffusion at this infarct or elsewhere within the\nbrain.  There is hemosiderin throughout the old infarct also present at the\ntime of ___.  There is ex vacuo dilatation of the posterior aspect\nof the left lateral ventricle.\n\nThere are multiple FLAIR hyperintensities in the subcortical, deep, and\nperiventricular white matter consistent with moderate chronic small vessel\ndisease.  Major intravascular flow voids are preserved.\n\nMarrow signal is normal.  The paranasal sinuses and mastoid air cells appear\nclear.  The orbits are normal.",
            "output": "1. Encephalomalacia and hemosiderin deposition in the left parietal and left\nposterior temporal lobes due to a large chronic infarct of the left middle\ncerebral artery territory.  No evidence of acute on chronic infarct.\n2. Underlying moderate chronic small vessel disease."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.\n There are scattered T2/FLAIR hyperintensities in the cerebral hemispheres\nbilaterally, a nonspecific finding and likely related to chronic small vessel\nischemic changes.\n\nThe ventricles and sulci are age appropriate.\nMajor vascular flow voids are preserved.  Incidental note is made of mild\nremodeling of the middle secondary to a large caliber left V4 segment (series\n7, image 4).\n\nThere is mild mucosal thickening along the ethmoid air cells and bilateral\nmaxillary sinuses.  The mastoid air cells appear clear.  The orbits appear\nunremarkable.",
            "output": "1. No significant intracranial abnormality.  No evidence of acute infarction,\nhemorrhage or mass.\n2. Nonspecific white matter changes in the cerebral hemispheres bilaterally,\nlikely sequela of chronic small vessel ischemic changes."
        },
        {
            "input": "MRI Brain:\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  Minimal chronic small vessel ischemic changes, can be seen\nwith chronic migraines, minimally more prominent.  Normal posterior fossa. \nMinimal mucosal thickening bilateral maxillary sinuses, no fluid.  Patent\nmastoid air cells, middle ears.  Normal visualized orbits.\n\nMRA brain: The intracranial vertebral and internal carotid arteries and their\nmajor branches appear normal without evidence of stenosis, dissection,\nocclusion, or aneurysm formation.  Fetal origin right PCA, developmental\nvariant.  Patent A-comm, left PCOM.\n\nMRA neck:  The common, internal and external carotid arteries appear normal. \nThere is no evidence of internal carotid artery stenosis by NASCET criteria. \nThe origins of the great vessels, subclavian and vertebral arteries appear\nnormal bilaterally.  There is moderate narrowing of the right subclavian\nartery as it crosses first rib, 2 cm distal to the origin of the vertebral\nartery.",
            "output": "1. Minimal chronic small vessel ischemic changes, can be seen with chronic\nmigraines.\n2. Normal MRA brain.\n3. Widely patent carotid, vertebral arteries.\n4. Moderate narrowing right subclavian artery"
        },
        {
            "input": "MRI HEAD:  There is no intra or extra-axial mass or hemorrhage. Very subtle\npunctate diffusion weighted hyperintensity along the right aspect of the\nsplenium of the corpus callosum (series 5, image 18) is noted, with suggestion\nof corresponding ADC hypointensity, which may represent a single focus of\nsubacute infarct. Otherwise, no other evidence of acute infarct. There are\nvery few scattered punctate T2/FLAIR nonspecific subcortical and\nperiventricular white matter hyperintensities, which may be seen in the\nsetting of small vessel ischemic disease, predominantly in the left\nhemisphere. Sulci, ventricles and cisterns are within expected limits. The\nmajor flow voids are preserved.\n\nModerate mucosal thickening of the right maxillary sinus with fluid level as\nwell as mucosal thickening of the ethmoid air cells and near-complete\nopacification of the right frontal sinus. The remainder of the paranasal\nsinuses are essentially clear. The mastoid air cells are clear. The orbits are\nunremarkable.\n\nIncidental note is made of a partial empty sella.\n\nHEAD MRA:  Multifocal mild stenosis of the cavernous portions of internal\ncarotid arteries are noted, likely representing atherosclerotic disease. The\nright A1 segment is not well visualized, and is hypoplastic. The left\nvertebral artery is dominant.  Fetal type left PCA and large bilateral\nposterior communicating arteries.  The right vertebral artery ends in a\ndominant ___. Otherwise, the remainder of the anterior cerebral artery, and\nMCAs and posterior circulation are unremarkable. No aneurysm larger than 2 mm\nis identified.\n\nNECK MRA: There is a normal 3 vessel takeoff from the aortic arch.  There is\napproximately 50% stenosis of the right internal carotid artery. The cervical\ncommon carotid, left internal carotid and external carotid arteries are normal\nin course, caliber and contour.  Estimates of the internal carotid artery are\nbased on the NASCET criteria. The left vertebral artery is dominant,\notherwise, the vertebral arteries are normal in course, caliber and contour.\nThey demonstrate normal enhancement without mural irregularity, stenosis or\nevidence of dissection.",
            "output": "1.  Very subtle punctate diffusion-weighted abnormality of the right splenium\nof the corpus callosum, compatible with a subacute infarct; correlate with\nsymptoms.\n\n2.   Otherwise, no other findings to suggest acute ischemia.\n\n3.  Essentially unremarkable MRA of the head and neck, notable only for\nvariant anatomy.  No significant steno-occlusive disease or aneurysm larger\nthan 2 mm.\n\n4.  Acute right-sided sinusitis."
        },
        {
            "input": "Mildly motion degraded exam.\n\n2 separate punctate foci of DWI hyperintensity in the lateral mid right\ncerebellar hemisphere, and superior right cerebellum, without ADC correlate\nbut associated FLAIR hyperintensity and enhancement on the postcontrast images\nis most consistent with a subacute infarcts.\n\nPunctate focus of enhancement left vertex involving very posterior left\nfrontal lobe, consistent with subacute infarct.\n\nAdditional punctate foci of DWI hyperintensity in the right frontal lobe\nposterior middle frontal gyrus and abutting anterior aspect right lateral\nventricle (series 6, image 19, 21 and 24 with ADC correlates but no definitive\nbright signal on the FLAIR sequence or enhancement are most consistent with\nacute infarcts.\n\nThere is no evidence of hemorrhagic transformation.\n\nThere is no evidence of acute intracranial hemorrhage, mass effect, or midline\nshift.\n\nThe ventricles and sulci are normal in caliber and configuration.\nMajor vascular flow voids appear preserved.  Major dural venous sinuses are\npatent.\n\nThe paranasal sinuses and mastoid air cells are clear.  The orbits appear\nunremarkable.\n\nVisualized portion of the cervical spine demonstrates diffuse T1 dark signal\nintensity throughout the vertebral bodies, suggestive of a diffuse bone marrow\nprocess.",
            "output": "1. Findings consistent with small 2 acute and 3 subacute infarcts.\n2. No hemorrhage.\n3. Diffusely decreased T1 marrow signal, commonly seen in this setting, may be\nreactive.  Infiltrative process is possible, less likely."
        },
        {
            "input": "There is a lipoma of the corpus callosum extending from anterior body to the\nsplenium as seen on prior CT (4:11).  There is no abnormality on\ndiffusion-weighted images.  A few scattered punctate foci of high T2/FLAIR\nsignal in the subcortical white matter and right cerebellar hemisphere without\nslow diffusion are nonspecific.  Susceptibility artifact in the globus pallidi\nbilaterally corresponds to calcifications on CT.  There is no intra or\nextra-axial hemorrhage.  No mass or mass effect.  Mild prominence of the\nventricles and sulci is in keeping with age-related involutional change. \nPrincipal intracranial vascular flow voids are preserved.  The orbits are\nunremarkable.",
            "output": "1. No evidence of acute infarct or intracranial hemorrhage.\n2. Lipoma of the corpus callosum."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarct.  Findings consistent with mild chronic small vessel ischemic\nchange.  No chronic cortical infarcts.  Small chronic lacunar infarct left\ncaudate nucleus.  Move moderately prominent prevascular spaces cerebral\nhemispheres..  Preserved vascular flow voids.  Trace mucosal thickening\nparanasal sinuses.  Clear mastoids.\n\n2 punctate superficial distribution parenchymal chronic micro hemorrhages in\nthe right temporal lobe, posterior left frontal lobe, suggestive of amyloid\nangiopathy.  Mild brain parenchymal atrophy at the level of sylvian fissures. \nGrade 2 bilateral hippocampal atrophy, normal for age.  Mild atrophy bilateral\npara hippocampal gyrus, and widening of left collateral sulcus.  No parietal\nlobe atrophy.",
            "output": "1. Mild bilateral temporal lobe atrophy.\n2. Chronic lacunar infarct left basal ganglia.\n3. Mild chronic small vessel ischemic change.\n4. Suggestion of amyloid angiopathy."
        },
        {
            "input": "There is significant artifact on diffusion-weighted images obscuring\nvisualization of the posterior paramedian parietal lobes, large segment of the\nposterior left parietal lobe.\nThere is a small, linear and slightly nodular zone of mildly restricted\ndiffusion in the medial right cerebellum, involving dentate nucleus and\nextending to the ventricular surface, most consistent with early subacute\ninfarct given linear configuration, in the appropriate clinical setting. \nAdjacent area of T2 signal abnormality without restricted diffusion, is\nindeterminate, may be sequela of chronic infarct series 9, image 6.  If there\nis history of malignancy, recommend post gadolinium images of the brain in\nfurther evaluation.  There is indeterminate 1.7 cm exophytic skin nodule at\nthe vertex, likely represents epidermal inclusion cyst, clinically correlate. \nThere is severe generalized brain parenchymal atrophy, with significant white\nmatter loss.  Atrophy of the midbrain, is likely sequela of supratentorial\natrophy.  Progressive supranuclear palsy could have similar appearance.  There\nis moderate to severe bilateral hippocampal atrophy.  There are chronic\nlacunar infarcts at the level of bilateral corona radiata 1 on the right\nextends into the right putamen.  Mild-to-moderate chronic small vessel\nischemic changes.\nThere is no evidence of hemorrhage, edema, midline shift.  There is 2.4 cm x\n0.9 cm T2 signal abnormality with broad-based dural attachment overlying left\nfrontal operculum and adjacent triangular, near expected Broca's area, with\ndark signal on gradient images, differential considerations include partially\ncalcified meningioma or subdural bleed.  Meningioma is probably more likely. \nSmall volume fluid in the sphenoid sinus, trace mucosal thickening paranasal\nsinuses.  Trace fluid bilateral mastoid air cells.",
            "output": "1. Findings consistent with small subacute medial right cerebellar infarct.\n2. Probable 2.4 cm x 0.9 cm left frontal meningioma, adjacent to expected\nBroca's area.  Small subdural bleed is less likely.  Noncontrast head CT or\npost gadolinium brain MRI recommended.\n3. Severe brain parenchymal atrophy, including moderate to severe bilateral\nhippocampal atrophy.  Prominent ventricular system, likely on the basis of\natrophy.  Atrophic midbrain, likely on the basis of supratentorial atrophy.\n4. Chronic lacunar infarcts bilateral corona radiata.\n\nRECOMMENDATION(S):  Noncontrast head CT or post gadolinium only brain MRI."
        },
        {
            "input": "There is a lobulated right parietal mass, measuring 4.7 cm AP x 3.6 cm in\nmaximal axial cross-section, wit irregular peripheral contrast enhancement,\nareas of central necrosis, evidence of blood products well as prominent\ninternal blood vessels on gradient echo images, and surrounding vasogenic\nedema within the right parietal and right temporal lobes. There is slow\ndiffusion within the central portions of the mass indicating hypercellularity.\nThe mass abuts the right lateral ventricle with subependymal contrast\nenhancement.  The mass extends into the right aspect of the splenium of the\ncorpus callosum but does not cross the midline. There is mild associated\nleftward midline shift which measures approximately 5 mm. There is enlargement\nof the temporal horn of the right lateral ventricle suggesting obstruction at\nthis level. The findings are most concerning for GBM, less likely lymphoma.\n\nThere are preserved major vascular flow voids. There is minimal subcortical\nand periventricular T2/FLAIR signal hyperintensity with additional involvement\nof the brainstem, a nonspecific finding though presumably on the basis of\nchronic small vessel ischemic disease. There is no evidence of acute infarct\nbased on diffusion-weighted imaging.\n\nThere is a partially empty sella, likely age-related.",
            "output": "1. Peripherally enhancing right parietal mass extending to the right splenium\nof the corpus callosum, with central necrosis, blood products, and\nsubependymal spread along the right lateral ventricle, most likely GBM, and\nless likely lymphoma if the patient is immunocompromised.\n2. Mild leftward shift of midline structures.\n3. Entrapment of the temporal horn of the right lateral ventricle."
        },
        {
            "input": "There has been no significant interval change in peripherally enhancing\nirregular right parietal mass. The mass is again noted to extend into the\nright aspect of the splenium of the corpus callosum. Subependymal contrast\nenhancement is also again noted and unchanged. Surrounding T1 hypointensity\nlikely reflecting vasogenic edema, local mass effect, and mild leftward shift\nof midline are also unchanged. Enlargement of the temporal horn of the right\nlateral ventricle suggesting obstruction is also unchanged. No new enhancing\nlesions are identified.",
            "output": "No significant interval change in peripherally enhancing right parietal mass.\nNo new enhancing lesions identified."
        },
        {
            "input": "Please note the study is mildlydegraded by motion. Again are noted\npostsurgical changes related to the patient's recent right parietal craniotomy\nand right parietal mass resection. Nonspecific postcontrast image enhancement\nis seen along the margins of the surgical cavity and of the dura. Some portion\nof surgical bed contain nonenhancing material with thick irregular enhancement\nalong margin, that is similar in appearance to pre-surgical imaging for\npatient's right parietal mass (series 900, image ___-67) .  Question minimal\nrestricted diffusion along the surgical margins. Grossly stable edema is noted\nthroughout the right parietal, occipital and temporal lobes. There is\ncontinued mass effect on the with right lateral ventricle, with continued\ndilatation of the temporal horn of the right lateral ventricle, and stable\napproximately 5 mm right to left midline shift.\n\nAdditional punctate scattered periventricular and subcortical white matter\nhyperintensities are noted, which may represent small vessel ischemic changes\nor treatment effects.\n\nThe paranasal sinuses are preserved.  Small nonspecific fluid is noted in the\nright mastoid air cells.",
            "output": "1.  Study is mildly degraded by motion.\n2. Evolving postsurgical changes related to patient's recent right parietal\nlobe mass resection as described.\n3. Stable 5 mm right to left midline shift with continued mass effect on right\nlateral ventricle and entrapment of temple horn of right lateral ventricle.\n4. Grossly stable right temporal, parietal, and occipital regions of edema.\n5. Nonspecific enhancement and restricted diffusion along margins of surgical\nbed. Residual tumor is not excluded on the basis of this examination.\nRecommend attention on followup imaging."
        },
        {
            "input": "Previously seen postsurgical pneumocephalus has been resorbed and is now\nfluid-filled cavity.  A right parietal inhomogeneously-enhancing tumor is now\nmuch larger in size compared to prior study from 5 weeks ago with more\nextension into the corpus callosum.  There is significant surrounding\nvasogenic edema involving the right parietal, temporal, and occipital lobes,\nwhich together with tumor, contributes to the near effacement of the posterior\nhorn of the right lateral ventricle.  4 mm leftward shift of midline\nstructures is largely unchanged.  No new mass is detected. There is no\nhemorrhage.\n\nThe paranasal sinuses and mastoid air cells demonstrate normal signal.",
            "output": "Rapid right parietal tumor progression since ___.  No new lesions\ndetected."
        },
        {
            "input": "MR BRAIN:\n\nThere is no evidence an intracranial mass or pathologic meningeal contrast\nenhancement.  There is no evidence for edema, acute infarction, or blood\nproducts.  There is diffuse parenchymal volume loss with commensurate\nprominence of the ventricles, sulci, and cisterns, as seen previously.  There\nis mild confluent T2 hyperintensity within the periventricular subcortical\nwhite matter, which is nonspecific but likely sequela of chronic small vessel\nmicroangiopathy in a patient of this age.  There are several prominent\nperivascular spaces in the region of bilateral basal ganglia.  Linear\nhyperintensity on FLAIR images along the margin of a fluid signal intensity\nstructure in the right putamen may represent sequela of a chronic infarction,\nimage 9:14.  The major intracranial vascular flow voids are preserved.  Major\ndural venous sinuses appear patent on postcontrast MP RAGE images.\n\nThere is minimal mucosal thickening in the ethmoid air cells.\n\nNo suspicious bone marrow lesion is identified.  Sagittal T1 weighted images\ndemonstrate ossification of either the anterior longitudinal ligament or of\nthe longus ___ inferior to the anterior arch of C1.\n\nMRA BRAIN:\n\nDistal basilar artery appears moderately narrowed and slightly irregular. \nThere is fetal configuration of the right posterior cerebral artery.  The left\nposterior cerebral artery appears to receive slightly greater contribution\nfrom the basilar artery than from the left posterior communicating artery.  P1\nsegment of the left posterior cerebral artery is mildly irregular.  Proximal\nP2 segment of the left posterior cerebral artery is smaller than the right. \nDistal P2 segment of the contralateral right posterior cerebral artery\ndemonstrates diminished caliber with some irregularity.  While evaluation of\ndistal posterior cerebral arteries by MRA is limited, the above described\nasymmetry and changes in caliber suggest atherosclerotic disease.\n\nThere is no evidence for flow-limiting stenosis in the anterior circulation. \nThere is no evidence for an aneurysm.",
            "output": "1. No evidence for intracranial metastatic disease.\n2. No acute infarction.\n3. Irregular, moderately narrowed distal basilar artery.  Mildly irregular P1\nsegment of the left posterior cerebral artery.  Diminished caliber of the\nproximal P2 segment of the left posterior cerebral artery compared to the\nright.  Diminished caliber of the distal P2 segment of the right posterior\ncerebral artery compared to its proximal portion.  These findings are most\nlikely related to atherosclerosis in this age group.\n4. No evidence for an intracranial aneurysm.\n\nRECOMMENDATION(S):  If there is a clinical concern for arterial dissection,\nthen neck MRA with axial fat suppressed T1 weighted images through the\nskullbase and through the basilar artery should be obtained.  Please note that\nextension of the axial fat suppressed T1 weighted images through the basilar\nartery should specifically be included in the requisition.\n\nNOTIFICATION:  The impression and recommendation above were entered by Dr.\n___ on ___ at 15:14 into the Department of Radiology critical\ncommunications system for direct communication to the referring provider."
        },
        {
            "input": "MRV: Normal flow signal is demonstrated within the superior sagittal sinus,\nstraight sinus, transverse sinuses, and sigmoid sinuses. The jugular bulbs and\nproximal jugular veins are patent. The vein ___ is also unremarkable.\n\nNoncontrast brain imaging: There is no midline shift, abnormal extra-axial\nfluid collection, or mass. The ventricles and sulci are normal in caliber and\nconfiguration.",
            "output": "1. No evidence of acute infarction or hemorrhage.\n2. No evidence of venous sinus thrombosis."
        },
        {
            "input": "Study is severely degraded by motion.  Within these confines:\n\nThere is a dominant area of acute infarction involving the right frontal lobe,\nalso with involvement of the right postcentral gyrus (6:26).  Large amount of\nassociated FLAIR hyperintensity.  Focus of susceptibility within the posterior\nright frontal lobe is compatible with hemorrhagic transformation.  Multiple\nadditional scattered side of acute infarctions are noted in the right frontal,\ntemporal, parietal, and occipital lobes, compatible with embolic infarction. \nNo infarctions are noted on the left.  Within limits of study, no definite\nareas of elevated mean transit time, decreased rCBV, or decreased rCBF are\ndefinitely noted.\n\nThere is an extra-axial left parafalcine lesion measuring approximately 1.0 x\n0.8 cm which demonstrates at least mild homogeneous enhancement, and\nsuggestive of a meningioma (700:113).  Right paraclinoid additional enhancing\nlesion superior to the sphenoid sinus is noted, measuring 1.2 x 1.1 cm, with\nassociated FLAIR hyperintensity (series 700, image 72).  No associated slow\ndiffusion within this lesion to suggest infarction.  On the prior CTA\nperformed ___, this structure was clearly separate from the\nadjacent ICA and anterior cerebral arteries, and therefore not an aneurysm. \nAdjacent pituitary gland is grossly preserved and separate from this mass.\n\nDural venous sinuses are patent.  Known MCA trifurcation aneurysm measures\napproximately 9 x 6 mm (700:68).\n\nThere is no evidence of masses or midline shift.  Ventricles and sulci are\ncompatible with age related involutional changes.  Mild scattered bilateral\nperiventricular and subcortical T2/FLAIR white matter hyperintensities are\nnonspecific, but likely reflect chronic small vessel ischemic changes. \nBilateral maxillary sinus mucous retention cysts are noted.  Bilateral\nsphenoid sinus air-fluid levels are noted.  Bilateral sphenoid, ethmoid, and\nmaxillary sinus mucosal thickening is present.",
            "output": "1.  Study is severely degraded by motion.\n2. Right MCA territory infarction with evidence of hemorrhagic transformation.\n3. Multiple additional infarcts in the right MCA and PCA territories.\n4. Known 9 x 6 mm right MCA trifurcation aneurysm.\n5. Probable left parafalcine meningioma measuring 1.0 x 0.8 cm.\n6. Limited imaging of 1.2 x 1.1 cm enhancing midline lesion posterior to the\ngyrus rectus and superior to the sphenoid sinus, noted to be separate from\ncircle of ___ on recent CTA.  Findings suggestive meningioma, with\ndifferential consideration of metastatic disease.  If clinically indicated,\nconsider follow-up contrast brain MRI for stability evaluation.\n7. Paranasal sinus disease, as described.\n\nNOTIFICATION:   The findings were discussed with ___, M.D. by\n___, M.D. on the telephone on ___ at 11:27 am, 2 minutes after\ndiscovery of the findings."
        },
        {
            "input": "Study is moderately degraded by motion.  Within this confines:\n\nThere is no evidence of infarction, hemorrhage, edema, or midline shift. \nThere is no definite abnormal enhancement within the limitations of the study.\nThere is right parietal, left basal ganglia, and left cerebellar T2 and FLAIR\nsignal abnormality related to prior infarctions.\n\nThere is diffuse parenchymal volume loss with prominence of ventricles, sulci,\nand cisterns.  There is minimal nonspecific T2 and FLAIR hyperintensity within\nthe periventricular and subcortical white matter, including pons, likely a\nsequela of chronic small vessel microangiopathy.  The major visualized\narterial vascular flow voids are preserved.\n\nThere is mild bilateral ethmoid mucosal thickening.  There is mild bilateral\nmastoid air cell opacification.  The orbits and visualized soft tissues appear\nunremarkable.",
            "output": "1. Study is moderately degraded by motion.  Within this confines:\n2. No evidence of acute infarction.\n3.  Within limits of study, no definite evidence of enhancing intracranial\nmass.\n4. Chronic infarctions within the right parietal lobe, left basal ganglia, and\nleft cerebellum.\n5.  Paranasal sinus disease and nonspecific mastoid opacification, as\ndescribed."
        },
        {
            "input": "There is no evidence of intracranial hemorrhage, mass, mass effect or shifting\nof the normally midline structures.  Unchanged chronic ischemic changes are\nagain seen in both cerebellar hemispheres.  The ventricles and sulci are\nslightly prominent, suggesting mild cortical volume loss, likely age related\nand involutional in nature, grossly unchanged since the prior exam.  Again\nfoci of T2/FLAIR high signal intensity are demonstrated in the periventricular\nand subcortical white matter which including the region of the right central\ngyrus (series 10, image 20), which are nonspecific and may reflect changes due\nto chronic small vessel disease.  Small lacunar ischemic change appears\nunchanged in the left basal ganglia.  No diffusion abnormalities are detected\nto indicate acute or subacute ischemic changes.  The major vascular flow voids\nare present and demonstrate normal distribution.\n\nThe paranasal sinuses demonstrate minimal mucosal thickening in the left\nethmoidal air cells, and unchanged mucous retention cysts in the floor of the\nmaxillary sinuses, no air-fluid levels are seen, the orbits are unremarkable,\nthe middle ear cavities and mastoid air cells are clear.",
            "output": "1.  There is no evidence of acute intracranial process or hemorrhage.\n\n2.  Unchanged chronic ischemic changes are visualized in both cerebellar\nhemispheres.\n\n3.  T2/FLAIR high-signal intensity foci identified in the subcortical white\nmatter are nonspecific and may reflect changes due to chronic small vessel\ndisease.\n\n4.  Lacunar ischemic changes in the left basal ganglia remain unchanged."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.\n There are patchy T2/FLAIR hyperintensities in the cerebral hemispheres\nbilaterally and in the pons, a nonspecific finding and likely related to\nchronic small vessel ischemic changes.\nThere is no abnormal enhancement after contrast administration.\n\nThere is mild generalized parenchymal volume loss, most likely age related. \nProminence of the ventricular system and extra-axial CSF spaces consistent\nwith the previously mentioned parenchymal volume loss.\nMajor vascular flow voids are preserved.  Major dural venous sinuses are\npatent.\n\nThe paranasal sinuses and mastoid air cells appear centrally clear.  The\norbits appear grossly unremarkable.",
            "output": "1. No evidence of infarction, hemorrhage or mass.\n2. Nonspecific white matter changes in the cerebral hemispheres bilaterally\nand in the pons, likely sequela of chronic microangiopathy."
        },
        {
            "input": "Multiple enhancing masses are seen throughout the brain.\n\n- large right frontal lobe mass, measures 3.7 cm x 3.2 cm, series 1600, image\n134.  Increased precontrast T1 signal and susceptibility artifact associated\nwith this mass, suggests a hemorrhagic component.  Extensive vasogenic edema\nis seen associated with this mass extending to the right parietal and inferior\nfrontal lobes.  Midline shift to the left of approximately 1.6 cm, is\nunchanged compared to the prior CT.  Surrounding restricted diffusion\nassociated this mass, is likely secondary to mass effect.\n\n- right frontal lobe mass, series 1600, image 112 measures approximately 0.8\ncm x 1.3 cm also demonstrating extensive surrounding vasogenic edema.  Minimal\nsusceptibility artifact is seen associated this mass.\n\n- enhancing mass centered within the tail of the right caudate nucleus\nmeasures 1.8 cm x 1.6 cm causing significant mass effect on the posterior horn\nand body of the right lateral ventricle, series 1600, image 108 again\nextensive surrounding vasogenic edema is seen associated with this mass.  A\nsmall amount of susceptibility artifact is also suggests a hemorrhagic\ncomponent.\n\n- small right temporal lobe enhancing lesion measures 0.6 cm x 0.8 cm, series\n1600, image 93.\n\n- small right cerebellar lesion, measures 0.9 cm x 0.8 cm, series 1600, image\n76.\n\n- faintly enhancing small left cerebellar lesion measures 0.6 cm x 0.5 cm,\nseries 1600, image 67.\n\n- faint 4 mm left cerebellar lesion, series 1600, image 64 is seen with\nassociated FLAIR signal abnormality.\n\n- small focus of enhancement in the left temporal lobe (13;10, 14;19)\n\nThe visualized paranasal sinuses are clear aside from mild mucosal sinus\nthickening.  The globes are unremarkable.  No marrow signal abnormalities are\nidentified.  The principal vascular flow voids appear to be well preserved.",
            "output": "1. Multiple enhancing bilateral lesions are identified within the brain, with\nthe largest in the right frontal lobe measuring up to 3.7 cm with associated\nan hemorrhagic component and extensive vasogenic edema.  Findings are\nconcerning for metastatic disease.\n\n2. Stable midline shift to the left of approximately 1.6 cm compared to the\nmost recent prior CT."
        },
        {
            "input": "The patient's previously noted right frontal lobe enhancing mass measuring 3.4\n(AP) x 3.1 (TV) x 3.3 (SI) cm  (series 3, image 77) appears stable.  A second\nfrontal lobe enhancing lesion measures 1.2 cm AP by 1 cm TV, and is stable\n(series 3, image 60).  The right thalamic enhancing lesion measures 1.7 cm AP\nby 1.8 cm TV, and is stable (series 3, image 60).  The right temporal lobe\nenhancing lesion is stable in size and measures 0.7 cm AP by 0.8 cm transverse\n(series 3, image 48).  The right lower hemispheric enhancing lesion is stable\nmeasures 0.7 cm AP by 0.8 cm transverse.\n\nLeft periventricular enhancing lesion measures 0.5 cm AP x 0.4 cm transverse\n(series 3, image 59).  A left cerebellar hemispheric enhancing lesion measures\n0.5 cm (series 3, image 31), and is stable from prior study.  A second left\ncerebellar hemispheric enhancing lesion measures 0.4 cm is stable (series 3,\nimage 28).\n\nNo new lesions are identified.\n\nThere is 1.2 cm of leftward midline shift, which is stable compared to prior\nMRI.",
            "output": "1. No significant change in the size of multiple primarily right cerebral and\ncerebellar hemispheric enhancing lesions, presumably a metastases.\n2. There continues to be approximately 1 cm of leftward midline shift."
        },
        {
            "input": "Compare to ___, the patient is status post resection of a large right\nfrontal lobe mass.  There is minimal enhancement along the superior lateral\naspects of the resection cavity.  There is persistent right hollow hemispheric\nsulcal effacement and right to left midline shift, measuring approximately 10\nmm (___), previously 12 mm.  As before, there is narrowing of the right\nlateral and third ventricles.  There are expected postoperative changes,\nincluding blood products, pneumocephalus and surrounding edema.  Again seen\nare multiple unchanged enhancing lesions, likely representing other\nmetastases, as described on ___.\n\nThere is no evidence of acute infarction.  There is a mucous retention cyst in\na left anterior ethmoidal air cell.  There is minimal bilateral, left greater\nthan right, maxillary sinus mucosal thickening.  Other paranasal sinuses are\nclear.  Mastoid air cells are clear.  Orbits are normal.",
            "output": "1. Compared to ___, the patient is status post resection of a large\nright frontal lobe mass.  There is minimal enhancement along the superior\nlateral aspects of the resection cavity, which may represent postoperative\nchanges with residual tumor not excluded.\n2. There is persistent right hollow hemispheric sulcal effacement and 10 mm of\nright to left midline shift.  There are other postoperative changes, as\ndescribed above.\n3. No significant change in multiple other enhancing lesions, likely\nrepresenting additional metastases.  Please see report from ___ for\nspecific details of these lesions."
        },
        {
            "input": "An enhancing lesion with associated susceptibility artifact adjacent to the\nlateral wall of the right ventricle is increased in size, now measuring 2.0 x\n1.8 cm and previously measuring 1.6 x 1.1 cm.  There is persistent adjacent\nsubependymal enhancement, possibly a contiguous subependymal vein or\nsubependymal spread of tumor.  An enhancing lesion with susceptibility\nartifact in the right frontal lobe is essentially unchanged in size, measuring\n1.4 x 1.1 cm.  An enhancing right temporal lobe lesion has increased in size,\nnow measuring 1.0 x 0.9 cm and previously measuring 0.8 x 0.8 cm.\n\nPunctate foci of enhancement in the cerebellum correspond to previously seen\nenhancing lesions on prior MRI, decreased or unchanged since ___.  A\n4 mm enhancing lesion in the lateral left cerebellar hemisphere demonstrates\nsusceptibility artifact (series 16, image 17; series 18, image 97). \nAdditional enhancing lesions measure 2 mm (series 16, image 21; series 18,\nimage 101), 2 mm (series 16, image 27; series 18, image 108), and 3 mm (series\n16, image 27; series 18, image 99).\n\nThere is a new focus of detectable enhancement in the lateral aspect of the\nleft superior frontal gyrus(series 16, image 68; series 18, image 64; series\n17, image 39).\n\nThe patient otherwise appears status-post right frontal craniotomy and right\nfrontal lobe mass resection with no evidence of focal enhancement.  A punctate\nfocus of apparent restricted diffusion is unchanged.\n\nThe major intracranial arteries and dural venous sinuses appear patent on\npost-contrast MPRAGE sequences.",
            "output": "Two dominant intracranial metastatic lesions have increased in size since ___.  Additional known lesions in the right frontal lobe and cerebellum\nare unchanged.  A punctate focus of enhancement in the lateral left superior\nfrontal gyrus cortex likely corresponds with a new metastatic lesion."
        },
        {
            "input": "No acute infarction, hemorrhage, edema, mass, or mass effect.\n\nThe ventricles and sulci are prominent, compatible with global parenchymal\nvolume loss.\n\nBilateral periventricular and deep white matter foci of T2/FLAIR signal\nhyperintensity are nonspecific but compatible with moderate changes of chronic\nwhite matter microangiopathy.  Small chronic lacunar infarct right corona\nradiata.  Mild paranasal sinus disease.  Clear mastoids.\nThe globes and orbits are unremarkable.  Major intracranial vascular flow\nvoids are preserved.",
            "output": "1. No acute infarct.\n2. Small chronic infarct right corona radiata.\n3. Moderate chronic small vessel ischemic changes, brain parenchymal atrophy."
        },
        {
            "input": "There is no intracranial mass, mass , or midline shift.  Chronic right\ncerebellar infarct is again noted.  Scattered periventricular and subcortical\nwhite matter T2/FLAIR hyperintensities are noted.  There is no additional\nfocal parenchymal signal abnormality. Ventricles and sulci are\nage-appropriate.  There is no restricted diffusion to suggest acute infarct.\nNo abnormal susceptibility artifact identified. Major intravascular flow voids\nare preserved including within the major dural venous sinuses.\n\nFluid signal is noted within left mastoid air cells.  Other visualized\nparanasal sinuses and mastoid air cells demonstrate no abnormal signal.",
            "output": "No acute infarct.  Chronic right cerebellar infarct.  Scattered\nperiventricular and subcortical white matter T2/FLAIR hyperintensities, likely\nsequela of chronic small vessel disease."
        },
        {
            "input": "The ventricles and extra-axial spaces are normal in size. There is no evidence\nof midline shift, mass effect or hydrocephalus. There are no acute infarcts.\nThere is no evidence of focal abnormalities.  The vascular flow voids are\nmaintained. The visualized paranasal sinuses are clear. Following gadolinium\nadministration there is no evidence of abnormal parenchymal, vascular and\nmeningeal enhancement seen.\n\nCoronal images of the temporal lobes demonstrate no evidence of atrophy or\nincreased signal within the hippocampal region or other medial temporal lobe\nstructures.",
            "output": "No significant abnormalities are seen on MRI of the brain with and without\ngadolinium.  No evidence of hippocampal sclerosis."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  Few punctate subcortical T2 signal abnormalities, can be seen\nwith chronic migraines, early chronic small vessel ischemic changes, similar\ncompared with ___.  Preserved vascular flow voids.  Clear paranasal\nsinuses, mastoids.",
            "output": "1. No acute findings.  No mass."
        },
        {
            "input": "Postcontrast sequences are severely degraded by motion.  The GRE an initial\nFLAIR sequence are moderately degraded by motion.  Additional sequences are\nmildly degraded by motion.\n\nThere is severe encephalomalacia in posterior, inferior, medial left temporal\nlobe.  There is mild FLAIR signal hyperintensity in the adjacent parenchyma,\nunchanged since ___.  No areas of slow diffusion.  No evidence of\nintracranial hemorrhage.  Unchanged periventricular and subcortical white\nmatter T2/FLAIR hyperintensities are nonspecific but likely sequelae of\nchronic small vessel ischemic disease.  The ventricles and sulci are\nprominent, consistent with involutional change.  The major intracranial flow\nvoids are preserved.  A left cerebellar hemisphere developmental venous\nanomaly is better assessed on outside hospital head and neck CTA.\n\nThere is mild sphenoid sinus mucosal thickening and bilateral maxillary sinus\nmucous retention cysts.",
            "output": "1. Motion limited examination.  Postcontrast images are uninterpretable.\n2. No evidence of intracranial hemorrhage or acute or subacute infarction.\n3. Severe encephalomalacia of the posterior, inferior, medial left temporal\nlobe.  Adjacent FLAIR signal hyperintensity may reflect gliosis or trace\npostictal edema.\n4. Left cerebellar hemisphere developmental venous anomaly."
        },
        {
            "input": "There are diffuse bilateral supra and infratentorial late acute to early\nsubacute embolic infarcts.  Several of the infarcts demonstrate associated\nsusceptibility on gradient echo imaging compatible with hemorrhagic infarcts. \nThere is mild increased leptomeningeal enhancement associated with some of the\nregions of infarct and subarachnoid hemorrhage, likely representing luxury\nperfusion.\n\nNo change in the bifrontal subarachnoid hemorrhage.\n\nThere is no evidence of mass effect or midline shift.  The ventricles and\nsulci are within expected limits in caliber and configuration.  There is no\nabnormal enhancement after contrast administration.\n\n The major intracranial vascular flow voids are maintained.  The dural venous\nsinuses are patent.  The paranasal sinuses, mastoid air cells and orbits are\nnormal.",
            "output": "1. Diffuse bilateral supra and infratentorial acute to early subacute embolic\ninfarcts some of which are hemorrhagic.\n2. Unchanged bifrontal subarachnoid hemorrhage.\n3. Additional findings as described above."
        },
        {
            "input": "There is no intracranial mass, mass effect, or midline shift. Ventricles and\nsulci are age-appropriate.  Mild T2 and FLAIR hyperintensity in the\nsubcortical white matter bilaterally are indicative of chronic small vessel\nischemia, present on the prior study, with differences which are likely due to\nscanning the current study on a 3T magnet.\n\nThere is no pathologic intracranial enhancement. Intracranial flow voids are\nmaintained.  There is enlargement of the left cavernous sinus, likely from the\nknown underlying aneurysm.\n\n1.4 cm intermediate T1, T2 hypointense lesion in the left parietal scalp\nlikely represents a sebaceous cyst, essentially unchanged since ___. \nVisualized paranasal sinuses and mastoid air cells are clear.",
            "output": "Enlargement of the left cavernous sinus likely secondary to the underlying\nleft ICA aneurysm status post pipeline embolization.  Exam was not tailored\nfor evaluation of residual/recurrent flow within aneurysm.  In the setting of\nnew cranial neuropathy attributable to the left cavernous sinus, further\nevaluation for possible remnant or recurrent flow within the aneurysm should\nbe considered."
        },
        {
            "input": "There is loss of signal along the cavernous segment of the left internal\ncarotid artery consistent with the presence of the flow diverting stent. \nThere is questionably a less than 2 mm focus of flow related enhancement seen\nlateral to the paraclinoid segment of the distal end of the stent.  However,\nthis is less conspicuous than on the previous MRA.  The aberrant course of the\nleft vertebral artery V3 segment is again demonstrated, as seen previously.\n\n\nThe intracranial vertebraland internal carotid arteries and their major\nbranches otherwise appear normal without evidence of stenosis,occlusion,ornew\naneurysm formation.",
            "output": "1. Pipeline stent in the cavernous and paraclinoid left internal carotid\nartery appears patent.\n2. Less conspicuous focus of curvilinear flow related enhancement just lateral\nto the distal end of the flow diverting stent as compared to the previous\nexamination.\n3. No new aneurysm is demonstrated."
        },
        {
            "input": "MR Head: Diffusion weighting imaging does not demonstrate evidence of acute\ninfarct. There are multiple small scattered T2/FLAIR high signal foci\nthroughout the brain, nonspecific. These may be the sequela of chronic\nmicrovascular changes. Gray white matter differentiation is maintained.  The\nlateral and third ventricles are enlarged, can relate to parenchymal volume\nloss. The fourth ventricle is normal in size. There is prominence of the\nextra-axial spaces.  The major intracranial vessels exhibit the expected\nsignal void related to vascular flow.\n\nThere is mucosal thickening of the left maxillary sinus. The paranasal sinuses\nare otherwise clear. The mastoid air cells are clear.  The sella turcica,\ncraniocervical junction, and orbits are unremarkable.\n\nMRA head:  Normal flow signal is noted in the petrous, cavernous, and\nsupraclinoid portions of the internal carotid arteries. The anterior and\nmiddle cerebral arteries are normal. The anterior communicating artery region\nis normal.\n\nThe posterior cerebral arteries and basilar artery are unremarkable.  The\nsuperior cerebellar arteries are normal. The intradural segments to both\nvertebral arteries are patent; the right vertebral artery is dominant. Normal\nbilateral posterior communicating arteries are identified.\n\nNo arterial stenosis, saccular aneurysm, or AVM is identified. Flow is\nsymmetric.\n\nMRA neck: The origin to the innominate, left common carotid and left\nsubclavian arteries are normal with conventional arch anatomy. The common,\ninternal, and external carotid arteries, as well as the vertebral arteries,\ndemonstrate normal flow signal and enhancement. The vertebral artery origins\nare unremarkable. No stenosis is identified.\n\nDegenerative changes in cervical spine, inadequately assessed",
            "output": "1. No acute infarct.\n2.  Scattered foci of FLAIR signal throughout the white matter, nonspecific\nbut consistent with chronic small vessel ischemic disease.\n3.  Patent major intra and extra cranial arteries"
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  Multifocal areas of periventricular, subcortical and deep\nwhite matter T2/FLAIR hyperintensities are in a configuration most suggestive\nof chronic small vessel ischemic disease.  There is moderate prominence of the\nventricles and sulci suggestive of involutional change.  There is no abnormal\nfocus of slowed diffusion.  The principal intracranial vascular flow voids are\npreserved.\n\nThere is a moderate mucous retention cyst in the floor of the right maxillary\nsinus along with background mild mucosal thickening in the bilateral maxillary\nand ethmoid sinuses.  The remainder of the visualized paranasal sinuses are\notherwise clear.  There are changes from bilateral lens replacement surgery. \nThe orbits are otherwise grossly unremarkable.  The mastoid air cells are\nclear.",
            "output": "1. No acute infarct, hemorrhage, or suggestion of mass.\n2. Generalized moderate global atrophy without focal lobar or hippocampal\npredominance and multifocal areas of white matter signal abnormality in a\nconfiguration most suggestive of chronic small vessel ischemic disease."
        },
        {
            "input": "Examination is severely degraded by motion.  Within these confines:\n\nThere are multiple predominantly rim enhancing lesions throughout the\nbilateral cerebral hemispheres concerning for metastases with representative\nexamples as follows:\n\n-Dominant 5.2 x 3.1 x 5.9 cm (SI by TRV by AP; series 15, image 12 and series\n14, image 19) mass centered within the left parieto-occipital lobe result in\nmass effect on the occipital horn of the left lateral ventricle.  This mass\ndemonstrates central T2 hyperintense and T1 hypointense signal characteristics\nwith the peripheral rim demonstrating slow diffusion and postcontrast\nenhancement.  There is moderate adjacent sulcal effacement and mass effect.\n-1.5 x 1.4 x 1.2 cm (AP by TRV by SI; series 15, image 17 and series 14, image\n15) predominantly T1 hypointense, T2/FLAIR hyperintense, enhancing mass with\nslowed diffusion in the left precentral gyrus is also concerning for\nmetastasis and demonstrates mild adjacent sulcal effacement.\n-There is a 1.0 x 1.2 x 1.0 cm (AP by TRV by SI; series 15, image 13 and\nseries 14, image 7) T1 hypointense, T2 hyperintense, peripherally enhancing\nmass in the right frontal lobe abutting the anterior horn of the right lateral\nventricle.  This is associated with mild predominantly peripheral slowed\ndiffusion.\n-11 mm right parietal lesion (15:13) measuring 11 mm.\nExtensive T2/FLAIR hyperintensity predominately seen in the right MCA\ndistribution with associated volume loss and ex vacuo dilatation of the right\noccipital and temporal horns of the right lateral ventricle is without\nassociated slowed diffusion or appreciable postcontrast enhancement.  Findings\nlikely reflect sequelae of remote infarction.\n\nThere is no evidence of recent infarction or hemorrhage.  No midline shift.\n\nThe visualized orbits are unremarkable.",
            "output": "1. Severely motion degraded examination which may limit evaluation for subtle\nmetastatic lesions..\n2. Several supratentorial enhancing masses are concerning for metastases and\nmeasure up to 5.9 cm in maximal AP dimension in the left parieto-occipital\nlobe, as detailed above.  Other prominent lesions are seen in the right\nfrontal lobe and both parietal lobes.\n3. Volume loss with ex vacuo dilatation of the right lateral ventricle in the\nright MCA distribution is likely compatible with sequelae of prior infarction.\n4. No evidence of intracranial hemorrhage or recent infarction."
        },
        {
            "input": "There is no acute infarction, intracranial hemorrhage, extracerebral fluid\ncollection, midline shift or mass effect.  Ventricles and extra-axial spaces\nare normal in size.  Flow voids are maintained. Suprasellar and craniocervical\nregions are unremarkable.",
            "output": "No significant abnormalities are seen on MRI of the brain without gadolinium."
        },
        {
            "input": "The patient is status post resection of bilateral occipital lobe enhancing\nlesions.  There is hemorrhage at the surgical site, greater on the right than\nleft.  The left postoperative site demonstrates a thin rim of enhancement. \nThis is similar to the appearance of the lesion margin on the preoperative\nstudy.  However, it it may represent postsurgical change with no evidence of\nresidual pathology.  The right sided lesion was partially resected and the\nlateral enhancing component of it appears unchanged.  Also unchanged is the\nenhancing lesion in the left cerebellar hemisphere.  Extensive vasogenic edema\nin the occipital and parietal lobes appears similar to the prior examination.\nThere is a small amount of subdural hemorrhage in the left hemisphere and a\nfar smaller right-sided subdural hematoma.",
            "output": "Status post resection of bilateral occipital lobe enhancing lesions with\ndefinite residual enhancing tissue in the right occipital lobe and in the left\ncerebellar hemisphere.  The left occipital lesion may have been completely\nresected."
        },
        {
            "input": "There are postoperative changes of prior bilateral resection of occipital\nlesions.  There is increased size of peripherally enhancing mass centered\nwithin the right occipital lobe which measures 4.4 cm AP by 2.8 cm transverse\nwith increased non-enhancing component as well as part of the enhancing\nnodular component.  There is increased size of a more punctate focus of\nenhancement just superior this lesion which now measures 0.5 cm, previously 2\nmm.\nAdditionally, the is mildly increased enhancement within the left occipital\nlobe, specifically a more nodular focus medially (series 3, image 12) with\ninterval necrosis in the lateral aspect.  This lesion is decreased\nsignificantly compared to the initial study of ___.  There is\ndecrease in the previously noted extra-axial fluid collection adjacent to this\nlesion.\nThere is surrounding T1 hypointensity indicating edema and seen on prior\nexams.\nThere is increased nodular enhancement within the left cerebellar hemisphere,\nthe dominant lesion of which now measures 1.7 cm transverse by 1.4 cm AP,\npreviously 1.5 cm transverse by 1 cm AP.  There are additional new areas of\nenhancement adjacent to this lesion, more medially in a total region measuring\n1.3 cm AP x 0.6 cm transverse.  There are tiny new punctate foci of nodular\nenhancement within the right precentral gyrus and left posterior parietal lobe\nand in left occipital lobe.  Assessment for subtle lesions is somewhat limited\ngiven the lack of precontrast sequence.\nThere is mild diffuse brain parenchymal volume loss.\n\nSmall focus of fenestration noted in the basilar artery.\nThere is increased size of heterogenous, nodular enhancing lesions within the\nscalp, most prominently involving a lesion just over the vertex which measures\n2.4 cm superior inferior by 2.2 cm transverse, previously 1 cm superior\ninferior by 1.5 cm transverse.\nThere are multiple additional increased size of heterogenous lesions within\nthe left aspect of the scalp.",
            "output": "1. Interval increase in size of heterogenously enhancing bilateral occipital\nlesions with increased surrounding edema.  There are also multiple new and\nincreased in size satellite lesions surrounding the bilateral occipital\nlesions.\n2. Increased size of left cerebellar metastatic lesions with new punctate\nareas of surrounding enhancement.\n3. New punctate foci of enhancement within the right precentral gyrus an left\nparietal and occipital lobes, likely representing new metastatic lesions.\n4. Marked increase in size of several lesions within the scalp, most\nprominently involving lesions near the vertex, compatible with increased\nmetastatic disease."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor recent infarction.  There are foci of fluid in the posterior limb of the\nleft internal capsule with involvement of the globus pallidus and putamen that\nmay represent chronic lacunar infarctions or dilated perivascular spaces.\nThe ventricles and sulci are normal in caliber and configuration.  There are\nscattered white matter hyperintensities on FLAIR, more predominantly\nperiventricular.  These are nonspecific but often attributed to chronic small\nvessel ischemia in a patient of this age.",
            "output": "1. Possible left posterior limb of internal capsule, globus pallidus and\nputaminal chronic lacunar infarctions.  No evidence of recent infarction.\n2. No evidence of mass or hemorrhage.\n3. Scattered periventricular and deep white matter hyperintensities on FLAIR\nsuggest chronic small vessel ischemia."
        },
        {
            "input": "The aortic arch appears normal. The origins of the vertebral arteries are not\nwell visualized which is felt to be most likely on an artifactual basis\nalthough stenosis cannot be entirely excluded. The origins of the great\nvessels including the bilateral common carotid arteries and bilateral\nvertebral arteries appear patent. There is no evidence of pathologic large\nvessel occlusion or hemodynamically significant stenosis within the\nvasculature of the neck.\n\nLimited imaging of intracranial contents and soft tissues within the neck\nappear unremarkable.",
            "output": "1. No pathologic large vessel occlusion or clear evidence of hemodynamically\nsignificant stenosis within the neck."
        },
        {
            "input": "Carotid and vertebral arteries demonstrate normal flow signal. There is no\nevidence of vascular, stenosis or dissection. The. The thoracic aorta and its\nmajor branches also demonstrate normal appearances. The vertebral artery\nartery origins are patent.",
            "output": "No significant abnormalities are seen on MRA of the neck."
        },
        {
            "input": "The ventricles and sulci are slightly prominent, suggesting cortical volume\nloss, likely age related and involutional nature.  There is mild increased\nmidbrain to pons ratio, there is no imaging signs to suggest iron deposition\nat basal ganglia, red nuclei or substantia nigra.\n\nThere is no evidence of acute intracranial hemorrhage, edema, masses, mass\neffect, midline shift or acute infarction, no diffusion abnormalities are\ndetected.\nThere is no abnormal enhancement after contrast administration.  The major\nvascular flow voids are present and demonstrate normal distribution.\n\nThe orbits are notable for lens replacement on the left.  Paranasal sinuses\nand mastoid air cells are unremarkable.",
            "output": "1. There is a mild brain atrophy, with with mild reduced midbrain to pons\nratio, although this findings are nonspecific will be seen in patients with\n___ syndrome.\n2. No imaging signs to suggest iron deposition at basal ganglia.\n3. There is no evidence of acute intracranial process or hemorrhage."
        },
        {
            "input": "Study is mildly degraded by motion.\n\nMRI BRAIN:\n\nThere is interval evolution of bilateral cerebellar infarcts with\nre-demonstration of inferior left cerebellar petechial micro hemorrhages. \nQuestion minimal interval inferior displacement of cerebellar tonsils, with\ngrossly patent fourth ventricle serrated (see 11:13).\n\nMultiple punctate periventricular and deep white matter hyperintensities most\nlikely represent microangiopathy are again noted.  The ventricles and sulci\nare stable in caliber and configuration.  Partially empty sella is again\nnoted.  There is no abnormal enhancement after contrast administration.  The\norbits appear normal.  Mild mucosal thickening present in the anterior\nethmoidal air cells.\n\nMRA BRAIN:\nThe internal carotid arteries and their major branches appear normal without\nevidence of stenosis, occlusion, or aneurysm formation. The basilar artery is\npatent.  There is narrowing of the proximal and distal left V4 segments which\nappear similar compared to prior.\n\nMRA NECK:\nThe common, internal and external carotid arteries appear normal.  There is\nmild narrowing of the left internal carotid artery at the level of the bulb,\nbut no significant stenosis by NASCET criteria.  The left vertebral artery\nappears normal.  There is poor flow seen in the proximal and mid right\nvertebral artery (V1 and V2 segments).  Poor right vertebral artery flow seen\nin the V3 and proximal V4 segments.  There is a single foci of hyperintense\nsignal on the T1 fat-sat imaging at the distal aspect of the right v\n2/proximal V3 segment which is most likely artifactual in nature.",
            "output": "1. Study is mildly degraded by motion.\n2. Interval evolution of bilateral cerebellar subacute infarcts with edema and\nmass effect and left inferior cerebellar petechial hemorrhage.  Question\nminimal interval down a progression of cerebellar tonsils with grossly\npreserved fourth ventricle.\n3.  Within limits of study, no definite new infarct.\n4. Nonvisualization of right V1 and V2 vertebral artery segments grossly\nsimilar to ___ prior exam, again concerning for occlusion.\n5. Left V4 segment narrowing versus right V4 segment dominance is again noted,\ngrossly similar to ___ prior exam.\n6. There is limited visualization of bilateral V3 and proximal V4 segments\ngrossly similar to prior exam.  Finding may represent artifact,\nsteno-occlusive disease is not excluded on the basis of this examination.  If\nclinically indicated, consider neck CTA for further evaluation.\n7. No ICA stenosis by NASCET criteria.\n\nNOTIFICATION:  The impression and recommendation above was entered by Dr.\n___ on ___ at 15:38 into the Department of Radiology critical\ncommunications system for direct communication to the referring provider."
        },
        {
            "input": "MRI BRAIN:\nThere are acute to early subacute infarctions involving a large portion of the\nleft cerebellar hemisphere (with inferior and superior involvement), a\nmoderate portion of right inferior cerebellar hemisphere, bilateral cerebellar\ntonsils, and a small lateral portion of the left superior cerebellar vermis. \nThe brainstem does not appear involved.  Gradient echo images demonstrate\nhemorrhagic transformation of the infarction bilaterally.  There is minimal\neffacement of the fourth ventricle and mild rightward displacement of the\nfourth ventricle, new since the prior CT.  There is no effacement of CSF in\nthe foramen magnum.  There is no supratentorial hydrocephalus.\n\nIn the supratentorial compartment, minimal periventricular T2 hyperintensity,\nand multiple small foci of high T2 signal in the subcortical, deep, and\nperiventricular white matter of the cerebral hemispheres, are nonspecific but\nlikely sequela of chronic small vessel ischemic disease in this age group. \nThere is mild age-related parenchymal volume loss in the supratentorial\ncompartment.\n\nThere is mild mucosal thickening in right greater than left maxillary sinuses\nwith trace fluid on the right.  There is mild mucosal thickening in the\nethmoid air cells.\n\nMRA NECK: There is a 3 vessel aortic arch.  Left subclavian artery origin is\nnot included on the images.  Bilateral common carotid arteries appear widely\npatent.  There are small filling defects in bilateral proximal internal\ncarotid arteries, presumably atherosclerotic, without evidence for stenosis by\nNASCET criteria on the right, and with 20% or less stenosis by NASCET criteria\non the left.\n\nEvaluation of the left vertebral artery origin and proximal V1 segment is\nlimited by artifacts.  V2 segment appears patent.  V3 segment is not fully\nincluded on the field of view of the dynamic contrast enhanced MRA due to\ntechnical error.\n\nNo signal is seen in the proximal V1 segment of the right vertebral artery on\nthe gadolinium enhanced dynamic MRA.  V2 segment appears smaller in caliber\nthan the partially visualized V3 segment. V3 segment is not fully included on\nthe field of view of the dynamic contrast enhanced MRA due to technical error.\nFlow in the right vertebral artery is not well seen on the 2D   time-of-flight\nimages.\n\nFat-suppressed T1 weighted images of the neck were obtained after intravenous\ngadolinium administration, with physiologic enhancement in the Phoenix plaques\na along the vertebral arteries limiting evaluation.  However, flow void of the\nleft vertebral artery remains visible, while flow void of the right vertebral\nartery is obliterated by high signal.  In combination with the findings of the\ngadolinium enhanced MRA, this is concerning for right vertebral dissection.\n\nMRA BRAIN:\nFlow is better seen in the distal V4 segments of the bilateral vertebral\narteries than in the proximal V4 segments, likely due to technical factors. \nThe intracranial right vertebral artery is dominant.  Bilateral proximal PICAs\nare visualized.  Flow is seen in the basilar artery.  Left AICA is also\nvisualized with infundibular origin.  Bilateral superior cerebellar arteries\nare visualized.  There is fetal type configuration of bilateral posterior\ncerebral arteries.  There is no evidence for flow-limiting stenosis in the\nanterior circulation.  There is no evidence for an aneurysm allowing for\nbulbous appearance of the basilar tip due to infundibular origins of the\nbilateral superior cerebellar arteries.",
            "output": "1. Acute to early subacute infarctions with hemorrhagic transformation, large\nin the left cerebellar hemisphere with superior and inferior involvement,\nmoderate in the inferior right cerebellar hemisphere, and also involving\nbilateral cerebellar tonsils and a small portion of the left superior vermis.\n2. Minimal effacement of the fourth ventricle and mild rightward displacement\nof the fourth ventricle, new since the ___ CTs.  No supratentorial\nhydrocephalus.\n3. Findings concerning for right vertebral dissection from its origin through\nthe V2 segment with questionable involvement of the V3 segment, with occlusion\nof the proximal V1 segment.  Please note that evaluation for dissection is\nlimited because the axial T1 weighted fat-suppressed images were obtained\nafter, rather than before intravenous contrast administration.\n4. Flow is seen within bilateral proximal PICAs, basilar artery, in the left\nAICA with infundibular origin, in bilateral superior cerebellar arteries with\ninfundibular origins, and within bilateral posterior cerebral arteries with\nfetal type configuration.\n\nNOTIFICATION:  The findings were discussed with ___, M.D. by ___\n___, M.D. on the telephone on ___ at 5:24 pm, 20 minutes after\ndiscovery of the findings when Dr. ___ Dr. ___.  Dr.\n___ was already aware of the extent of cerebellar infarctions and\nhemorrhagic transformation."
        },
        {
            "input": "The ventricles and extra-axial spaces are normal in size. There is no evidence\nof midline shift, mass effect or hydrocephalus. There are no acute infarcts.\nThere is no evidence of focal abnormalities.  The vascular flow voids are\nmaintained. The visualized paranasal sinuses are clear. Following gadolinium\nadministration there is no evidence of abnormal parenchymal, vascular and\nmeningeal enhancement seen.  The dural venous sinuses are patent and there is\nno evidence of venous sinus thrombosis or stenosis.  There is incidental note\nof prominent nasopharyngeal soft tissues likely related to presence of\nadenoidal tissue, a normal appearance for patient's age.",
            "output": "No significant abnormalities are seen on MRI of the brain with and without\ngadolinium."
        },
        {
            "input": "There is no evidence of acute hemorrhage or mass effect. The ventricles and\nbasal cisterns appear normal.  There is a punctate focus of gradient signal\nhypointensity at the level of the posterior pons corresponding to a vessel\nseen on the post-contrast imaging which may represent an occult cavernoma with\nassociated developmental venous anomaly although comparison with prior exams\nis recommended.\n\nThere are otherwise normal vascular flow voids. There is no evidence of acute\ninfarct based on diffusion-weighted imaging. The brain parenchymal volume is\nwithin normal limits.\n\nThere is no abnormal brain parenchymal or leptomeningeal enhancement.\n\nThere is a left maxillary sinus mucosal retention cyst. The orbits and mastoid\nair cells are unremarkable.",
            "output": "1. No acute hemorrhage, mass effect, or acute infarct.\n2. Punctate focus of gradient signal hypointensity at the level of the\nposterior pons corresponding to a vessel seen on the post-contrast imaging\nwhich may represent an occult cavernoma with associated developmental venous\nanomaly although comparison with prior exams is recommended."
        },
        {
            "input": "In comparison with the prior examinations, again there is a punctate focus of\nsusceptibility identified in the right frontal lobe (6:15), with no evidence\nof associated edema mass effect, measuring approximately 2 x 2 mm in\ntransverse dimension, likely consistent with calcification.\nNo new lesions or new areas of magnetic susceptibility are identified.\nBilateral hippocampal formations and mammillary bodies are normal in signal\nand configuration. There is no disproportionate medial temporal atrophy. There\nare no focal cortical dysplasias or gray matter heterotopia noted.\n\nThere are new scattered foci of FLAIR high-signal intensity, distributed the\nsubcortical white matter bilaterally, which are nonspecific and may reflect\nchanges due to chronic small vessel disease.  No diffusion abnormalities are\ndetected.  There is no evidence of abnormal enhancement after contrast\nadministration.  The major vascular flow voids are present and demonstrate\nnormal distribution.\n\nThe orbits are unremarkable, the middle ear cavities and mastoid air cells are\nclear.",
            "output": "1.  Unchanged focus of magnetic susceptibility identified in the right frontal\nlobe consistent calcification, previously demonstrated, probably related with\nprior infection or underlying granulomatous process, there is no evidence of\nmass effect or edema surrounding this lesion.\n\n2.  New scattered foci of FLAIR high-signal intensity identified in the\nsubcortical white matter, which are nonspecific and may reflect changes due to\nchronic small vessel disease.\n\n3.  The high-resolution images throughout the temporal lobes are normal with\nno evidence of mesial temporal sclerosis.\n\n4.  There is no evidence of acute intracranial process or hemorrhage.\n\n5.  There is no evidence of abnormal enhancement after contrast\nadministration."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.\nThere is no abnormal enhancement after contrast administration.\n\n There are scattered T2/FLAIR hyperintensities in the cerebral hemispheres\nbilaterally, a nonspecific finding and likely related to chronic small vessel\nischemic changes.\n\nThere is mild generalized parenchymal volume loss, most likely age related. \nMild prominence of the ventricular system and extra-axial CSF spaces is again\nidentified and consistent with the previously mentioned parenchymal volume\nloss.\n\nMajor vascular flow voids are preserved.  Major dural venous sinuses are\npatent.\n\nThere is partial opacification of the right mastoid air cells.  The paranasal\nsinuses and left mastoid air cells appear otherwise clear.  Note is made of\nbilateral lens replacement surgery.  The orbits appear otherwise unremarkable.",
            "output": "1. No evidence of acute infarction, hemorrhage or intracranial mass.\n2. Nonspecific white matter changes in the cerebral hemispheres bilaterally,\nlikely sequela of minimal chronic small vessel ischemic changes."
        },
        {
            "input": "There is narrowing at the left carotid bulb resulting in approximately 50%\nshort segment stenosis of the left ICA origin.\nOtherwise, the common, internal and external carotid arteries appear\nunremarkable.\n\nThe origins of the great vessels, subclavian, and vertebral arteries appear\nnormal bilaterally.\n\nThere is mild focal narrowing of the left V2 segment which may be due to\natherosclerotic disease or hypertrophic degenerative changes of the cervical\nspine (series 104, image 12).\nOtherwise, the vertebral arteries appear normal in course and caliber.",
            "output": "1. No evidence of vessel dissection, high-grade stenosis or occlusion.\n2. Short segment stenosis of the left ICA origin measuring up to 50% by NASCET\ncriteria.\n3. Mild focal narrowing of the left V 2 segment may be due to atherosclerotic\ndisease or external compression from hypertrophic degenerative changes of the\ncervical spine."
        },
        {
            "input": "Multiple sequences are limited secondary to motion artifact.\n\nThere is no evidence of acute intracranial hemorrhage or mass effect. The\nventricles and basal cisterns appear normal. There is no evidence of acute\nischemia based on diffusion-weighted imaging. There is mild brain parenchymal\nvolume loss.  There is scattered subcortical and periventricular white matter\nT2/FLAIR signal hyperintensity which is nonspecific though is presumably on\nthe basis of chronic small vessel ischemic disease. There are normal vascular\nflow voids.\n\nThe orbits and paranasal sinuses are unremarkable.\n\nThere is no evidence of focal vessel cut off, aneurysm, or hemodynamically\nsignificant stenosis within the intracranial vasculature. The anterior\ncommunicating artery is seen. The posteriorly can arteries are small or\nabsent.\n\nThere is no evidence of focal vessel cut off, dissection, or hemodynamically\nsignificant stenosis within the vasculature of the neck. The vertebral\narteries are codominant.",
            "output": "1. No evidence of acute intracranial hemorrhage, mass effect, or acute\nischemia.\n2. Brain parenchymal volume loss and presumed sequelae of chronic small vessel\nischemic disease.\n3. No evidence of hemodynamically significant stenosis, pathologic large\nvessel occlusion, or aneurysm within the vasculature of the head or neck."
        },
        {
            "input": "There are periventricular and subcortical T2/FLAIR white matter\nhyperintensities in a distribution compatible with demyelinating plaques given\nthe history of multiple sclerosis.  When compared to MRI head of ___, there\nare a few new nonenhancing T2/FLAIR white matter hyperintense lesions, most\nnotably in the left frontal lobe (series 5, image 19) and right peritrigonal\nwhite matter (series 5, image 14).  A 7 mm right subependymal enhancing FLAIR\nhyperintense lesion (series 8, image 16) along the posterior body of the right\nlateral ventricle demonstrates associated diffusion-weighted hyperintense\nsignal.\n\nThere is no acute infarct or intracranial hemorrhage.  The sulci, ventricles\nand cisterns are overall similar to prior examination, within expected limits\nfor the patient's age.  The major intracranial flow voids are preserved.  The\ndural venous sinuses are patent on postcontrast MP-RAGE.  There is mild\nmucosal thickening of the paranasal sinuses.  The orbits are unremarkable.  No\nfluid signal is seen in the mastoid tips.",
            "output": "1. Enhancing 7 mm right subependymal enhancing FLAIR and diffusion-weighted\nhyperintense lesion along the posterior body of the right lateral ventricle,\nlikely representing an active demyelinating plaque given the patient's\nclinical history of multiple sclerosis.\n2. There are additional nonenhancing T2/FLAIR white matter hyperintensities,\nincreased in number from prior examination of ___, most notably in the left\nfrontal lobe and right peritrigonal white matter, also likely representing\ndemyelinating plaques.\n3. No acute infarct or intracranial hemorrhage.  Additional findings described\nabove."
        },
        {
            "input": "There is no abnormal parenchymal or meningeal enhancement to suggest\nmetastatic disease. There is no suspicious osseous lesion.\n\nAgain noted are postsurgical changes of left occipital craniotomy with volume\nloss of the left cerebellar hemisphere, as seen on remote MRI from ___. There are areas of parenchymal volume loss within the peripheral right\nfrontal lobe with associated increased FLAIR signal, suggesting posttraumatic\nchanges of prior contusion (series 7, image 18). There are old blood products\nand associated FLAIR signal abnormality within the left frontal lobe along the\nprobable prior tract of a ventriculostomy catheter.\n\nThere is no acute infarct. Ventricles are normal in position and age\nappropriate in size.\n\nThere is a small retention cyst in the right maxillary sinus. The paranasal\nsinuses and mastoid air cells are otherwise clear. The orbits are normal.",
            "output": "1.  No evidence of metastatic disease.\n2.  Postsurgical changes of remote left occipital craniotomy with left\ncerebellum parenchymal volume loss, unchanged from remote MRI on ___.\n3.  Somewhat linear areas of increased FLAIR signal in the right peripheral\nfrontal lobe associated with enlarged sulci, consistent with the sequelae of\nremote contusion-related injury."
        },
        {
            "input": "Ventricles, sulci, and cisterns appear normal.  No parenchymal signal\nabnormality or abnormal intracranial enhancement.  There is no acute infarct,\nintracranial hemorrhage, or mass effect.  The major vascular flow voids are\npreserved.  Overall mild low marrow signal is noted.\n\nThere is diffuse paranasal sinus mucosal thickening.",
            "output": "1. No evidence of intracranial mass or lesion.\n2.  Paranasal sinus disease, as described.\n3. Nonspecific overall mild low marrow signal is noted.  While finding may be\nwithin normal limits for patient of this age,, similar findings may be seen in\nthe setting of anemia.  If clinically indicated, consider correlation with\nCBC.\n\nNOTIFICATION:  The impression and recommendation above was entered by Dr.\n___ on ___ at 14:51 into the Department of Radiology critical\ncommunications system for direct communication to the referring provider."
        },
        {
            "input": "No evidence of intraparenchymal hemorrhage, edema, masses, mass effect,\nmidline shift or infarction.  No abnormal post-contrast enhancement. \nVentricles and sulci are normal in size and configuration for the patient's\nage.  Trace periventricular T2/FLAIR signal hyperintensities are nonspecific\nbut likely reflect the sequela of chronic small vessel ischemic disease.\n\nThere is a 11 mm T2/FLAIR hyperintense, homogeneously enhancing lesion within\nthe greater wing of the left sphenoid bone, close to the foramina ovale\n(10:5).  No other osseous lesions are identified.  Punctate mucous retention\ncyst in the right maxillary sinus.  Otherwise, the mastoid air cells and\nparanasal sinuses are clear.",
            "output": "11 mm homogeneously enhancing lesion within the greater wing of the left\nsphenoid bone. In conjunction with the findings on the prior PET-CT, this\nfinding is consistent with the provided diagnosis of multiple myeloma."
        },
        {
            "input": "MRI Brain:\nThere is no evidence of acute intracranial hemorrhage, edema, masses, mass\neffect, midline shift or slowed diffusion to suggest acute infarction. \nChronic right MCA infarction involving the right frontal lobe, insula, and\nbasal ganglia, with associated volume loss.  There also chronic infarctions in\nthe bilateral cerebellum.  Wallerian degeneration right brainstem.\n\nConfluent periventricular, deep, and subcortical white matter T2/FLAIR\nhyperintensities are likely sequelae of severe chronic small vessel ischemic\ndisease.\n\nMRA brain: There is moderate severe right and moderate left cavernous segment\nICA narrowing.  Moderate right and mild left M1 segment narrowing.  Right A1\nsegment is hypoplastic or occluded..  Widely patent left A1, A-comm supplying\nboth PCAs.  Moderate narrowing distal left V4 segment.  Diminished flow\nrelated enhancement in the right V4 segment.  Moderate to severe narrowing\nleft P2 segment.  Mild-to-moderate narrowing left P3 segment moderate to\nsevere narrowing right P3 segment.\n\nThe intracranial vertebral and internal carotid arteries and their major\nbranches appear patent without evidence of occlusion, or aneurysm formation. \nIncidentally, the distal cervical left internal carotid artery is tortuous\n(7:21).\n\nMRA neck: Motion artifact and aliasing limit evaluation of the proximal common\ncarotid and vertebral arteries.  The distal common carotid and vertebral\narteries appear patent, without evidence of stenosis or occlusion..  Widely\npatent left proximal ICA without narrowing by NASCET criteria.  Motion\nartifact limits evaluation of the proximal right ICA.\nOrigins of the great vessels, subclavian and vertebral arteries are not well\nevaluated, due to motion.  Small left pleural effusion partially seen.",
            "output": "1.  No evidence of acute intracranial hemorrhage or infarction.\n\n2.  Extensive intracranial atherosclerotic disease involving anterior,\nposterior circulation.  No occlusion.  No aneurysm..\n\n3.  Motion artifact limits evaluation of the neck vessels."
        },
        {
            "input": "The study is very limited due to motion.\n\nAllowing for this, there is no gross evidence of hemorrhage, edema, masses,\nmass effect, midline shift or acute infarction.  There is right MCA territory\nvolume loss as seen on the preceding CT study as well as diffuse areas white\nmatter FLAIR signal abnormality likely representing a combination of old\ninfarction and small vessel disease.  There is associated ex vacuo dilatation\nof the right lateral ventricle.  There is an old left cerebellar infarct with\nmild volume loss and gliosis.  Prominence of the ventricles and cerebral sulci\nare compatible with age related involutional changes.\n\nExtensive subcortical and periventricular white matter FLAIR hyperintensity\ncompatible with small vessel disease.\n\nThe major intracranial vascular flow voids are maintained.  The paranasal\nsinuses, mastoid air cells and orbits are normal.",
            "output": "1. Severely degraded study due to motion artifact.\n2. While the study is essentially nondiagnostic for small infarcts, there is\nno gross evidence of large acute infarction.\n3. Likely old right MCA territory infarct where there is associated volume\nloss and ex vacuo dilatation of the right lateral ventricle.\n4. Old left cerebellar infarct where there is associated mild volume\nloss/gliosis.\n5. Extensive white matter small vessel disease.\n6.  Generalized parenchymal volume loss, likely age related."
        },
        {
            "input": "There is a small focus of slow diffusion involving the cortex and subcortical\nwhite matter of the left frontal operculum, images 4:20 and 3:20, with high\nsignal on FLAIR images new compared to ___, consistent with an\nacute to early subacute infarction.\n\nThere is also a small focus of high signal on diffusion tracer images in the\nleft frontal corona radiata, image 4:19, without a correlate on the ADC map,\nand with an unchanged small focus of high signal on FLAIR images.  It is not\nclear whether this represents another small focus of subacute infarction.\n\nThere is no edema or mass effect.  There are numerous foci of high T2 signal\nin the subcortical, deep, and periventricular white matter of the cerebral\nhemispheres, as before, likely sequela of chronic small vessel ischemic\ndisease in this age group.  There is age-related cerebral atrophy with\nprominent ventricles and sulci.  There is an asymmetric extra-axial space\nlateral to the left paracentral lobule with slight displacement of the\nadjacent sulci and scalloping of the inner table, unchanged, likely an\narachnoid cyst.\n\nMajor arterial flow voids grossly preserved, but the intracranial vasculature\nwas better assessed on the recent CTA.\n\nThere is mild mucosal thickening in the ethmoid air cells.\n\nSagittal images demonstrates multilevel degenerative disease in the included\ncervical spine with significant spinal stenosis and mass effect on the spinal\ncord at C5-6.  Bone marrow signal is heterogeneous.",
            "output": "Small acute to early subacute infarction involving the cortex and subcortical\nwhite matter of the left frontal operculum.  Possible additional focus of\nsubacute infarction in the left frontal coronal radiata.  These are both in\nthe left middle cerebral artery territory but likely embolic."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration given the degree of mild age related global cerebral volume\nloss.  There is no abnormal enhancement after contrast administration.  The\nmajor intracranial flow voids are preserved.  The dural venous sinuses are\npatent on postcontrast MPRAGE.  Mild mucosal thickening of the ethmoid air\ncells is identified.  The remainder the paranasal sinuses are essentially\nclear.  The orbits are unremarkable.  The mastoid air cells are clear.",
            "output": "Unremarkable brain MRI.  No evidence of intracranial mass."
        },
        {
            "input": "Hardware artifact limits examination.  Bilateral brain stimulator leads are in\nplace with tips terminating in the subthalamic regions.  Postoperative changes\nincluding pneumocephalus is noted.\n\nThere is no evidence of no evidence of infarction, hemorrhage, edema, or mass.\nThe ventricles and sulci are normal in size and configuration for age. \nChoroid plexus xanthogranulomas are noted bilaterally.  There is no abnormal\nfocus of slowed diffusion.  Mild mucosal wall thickening is noted in the\nbilateral ethmoid air cells.\n\nThere is no evidence of osseous abnormality. The paranasal sinuses, mastoid\nair cells, and middle ear cavities are clear. The orbits are unremarkable.",
            "output": "1. Postoperative changes from deep brain stimulator placement including\npneumocephalus.  DBS leads tips terminate in the bilateral subthalamic region.\n2. No acute intracranial abnormality."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.\n\nThe major intracranial vascular flow voids are maintained.  There is a 1.0 cm\nmucous retention cyst within the right maxillary sinus.  Mild mucosal\nthickening of the left maxillary sinus, ethmoid air cells and right frontal\nsinus.  The mastoid air cells and orbits are normal.",
            "output": "1. No acute intracranial abnormality.\n2. No evidence of a dural venous sinus thrombosis.\n3. Paranasal sinus inflammatory changes as described above."
        },
        {
            "input": "There is mild volume loss with prominence of the ventricles and sulci,\nsuggestive of involution changes.  There is hyperintense T2/FLAIR signal\nwithin the periventricular and subcortical white matter and the pons, which is\nnonspecific, but likely related to chronic small vessel microangiopathy.\n\nThere is no evidence of slow diffusion to suggest acute ischemia.  The\nprincipal intracranial vascular flow voids are patent.  There is no evidence\nof hemorrhage, edema, space-occupying lesion, mass effect, or midline shift.\n\nThe paranasal sinuses and mastoid air cells appear clear.  The orbits and the\nvisualized soft tissues appear unremarkable.",
            "output": "1. No evidence of acute ischemia, hemorrhage, mass lesion, or mass effect.\n2. Mild volume loss with periventricular and subcortical white matter changes,\nlikely a sequela of chronic small vessel microangiopathy."
        },
        {
            "input": "There has been a right parietal craniotomy. The right parietal lobe operative\nbed is stable in appearance with unchanged FLAIR signal compared MRI from ___. An enhancing dural-based nodule in the right parietal parasagittal\nregion inferior to the resection bed is also unchanged (series 16, image 17).\nThere no new enhancing lesions. There has also been a right occipitotemporal\ncraniotomy with unchanged FLAIR signal in the right occipital lobe operative\nbed. There is no pathologic enhancement at the operative site. Nonenhancing,\nFLAIR hyperintense lesions in the bilateral frontal white matter are\nunchanged. Cerebellar volume loss is unchanged.\n\nThe paranasal sinuses and mastoid air cells appear clear. The orbits are\nnormal.",
            "output": "No evidence of recurrent tumor. The right parietal dural-based enhancing\nnodule and postsurgical changes are stable."
        },
        {
            "input": "There are stable post craniotomy changes with associated mild dural thickening\nand enhancement at the high right parietal calvarium.  Subcortical white\nmatter FLAIR signal hyperintensity within the parafalcine right parietal\nprecentral gyrus, stable in comparison to prior study, consistent with\nencephalomalacia.  Encephalomalacia within the right occipital cortex\nconsistent with remote infarction.  There is periventricular FLAIR signal\nhyperintense foci most likely representing chronic microangiopathy.\n\n 1.2 (AP) x 1.3 (TV) x 1.4 (SI) cm posterior right parafalcine dural based\nmass with homogeneous postcontrast enhancement and internal cystic change\nwhich marginates but does not occlude vein traversing the superior sagittal\nsinus.\n\nThere is no acute infarct, hemorrhage, mass, or mass effect.  The ventricular\nsize is normal for degree of cortical sulcation.  The orbits and soft tissues\nare normal.  The paranasal sinuses and mastoid air cells are clear.  There is\nno abnormal postcontrast enhancement.",
            "output": "1. No evidence of recurrent tumor.  Stable post surgical changes.\n2. Right parietal dural-based enhancing mass, likely representing a\nmeningioma, is relatively stable in comparison to ___."
        },
        {
            "input": "Motion artifact limits evaluation.  Periventricular and subcortical white\nmatter T2/FLAIR hyperintensities are nonspecific but likely sequelae of\nchronic small vessel ischemic disease.  The focal areas of hypodensity in the\nright temporal lobe and right inferior frontal lobe on CT correspond to areas\nof gliosis.  There is low signal on the GRE sequences along the right frontal\nparietal temporal cortex and the left posterior subependymal region,\nconsistent with hemosiderin staining likely from prior hemorrhage.  There is\nno evidence of an acute infarction, hemorrhage, or midline shift.  The\nventricles and sulci are prominent, consistent with involutional changes.  The\nvenous sinuses are patent.\n\nA tube is seen in the left nasal cavity, entering the nasopharynx.  The\nvisualized portions of the orbits and paranasal sinuses are unremarkable.",
            "output": "1. Hypodensities seen on CT in the right temporal and inferior right frontal\nlobes correspond to areas of gliosis from prior chronic infarction.\n2. No acute infarction or hemorrhage.  Extensive periventricular and\nsubcortical white matter T2/FLAIR hyperintensities suggestive of chronic\nmicroangiopathy."
        },
        {
            "input": "MRI BRAIN:\nThere is no evidence of hemorrhage,edema,masses, mass effect, midline shift or\nacute infarction.  There is prominence of the ventricle, cortical sulci, most\nlikely representing age-related involutional changes.  There is\nencephalomalacia in the right temporal parietal region with associated ex\nvacuo dilatation of the right occipital horn, likely related to prior infarct\nin the left MCA distribution.  There are foci T2/FLAIR hyperintensity in the\nbilateral centrum semiovale, likely related to chronic small vessel ischemic\nchanges.  The paranasal sinuses bilateral mastoid air cells are clear.  The\nglobes and orbits are normal.  The partially visualized upper cervical spine\ndemonstrate low T1 signal intensity at the inferior endplate of T2, most\nlikely related to degenerative changes.\n\nMRA BRAIN:\nThe distal bilateral ICAs are widely patent.  The bilateral ACA, MCA, and PCA\nor unremarkable.  The basilar artery is patent.\n\nThe right vertebral artery is dominant, and the left vertebral artery is\ndiminutive.  There is no evidence of eccentric T1 hyperintensity to suggest\ndissection of the vertebral artery bilaterally.\n\nThere is no evidence of high-grade stenosis, occlusion, or aneurysm.\n\nMRA NECK:\n\nThere is approximately 70% stenosis of the right cervical internal carotid\nartery by NASCET criteria, presumably secondary to atherosclerotic narrowing\nof the right carotid bifurcation.  There is approximately 40% stenosis of the\nleft cervical internal carotid artery by NASCET criteria, presumably secondary\nto atherosclerotic narrowing of the left carotid bifurcation.\n\nThere is short-segment severe stenosis with near occlusion of the left\nsubclavian artery distal to the takeoff of the left vertebral artery, with\nreconstitution distally.  There is near complete occlusion of the proximal\nleft vertebral artery to the level of the thyroid, where it reconstitutes\ndemonstrating contrast opacification.  Of note, on 2D   time-of-flight\nlocalizers, no flow related signal is noted in the left vertebral artery and\nthus, opacification on contrast enhanced MRA of the neck is secondary to grade\nflow.\n\nThe right brachiocephalic, bilateral common carotid, right subclavian and\nright vertebral arteries are patent.\n\nThere is no T1 hyperintense signal of the vertebral arteries to suggest mural\nthrombus.",
            "output": "1. No acute intracranial abnormality.  Specifically, no evidence of acute\ninfarct, hemorrhage or intracranial mass.\n2. Right temporal lobe encephalomalacia, presumably sequela of prior infarct\nis identified.\n3. There is severe short-segment stenosis, with near occlusion of the left\nsubclavian artery just prior to the takeoff of the left vertebral artery and\nof the proximal left vertebral artery.  There is distal reconstitution of the\nleft subclavian artery.  There is retrograde flow through the remainder of the\nleft vertebral artery from the mid V1 segments to the V4 segment.\n4. No T1 hyperintense signal of the left vertebral artery to suggest mural\nthrombus and acute dissection.\n5. There is approximately 40% stenosis of the left cervical internal carotid\nartery by NASCET criteria and 70% stenosis of the right cervical internal\ncarotid artery by NASCET criteria.  The remainder of the MRA neck is\nunremarkable.\n6. Unremarkable MRA of the head.\n7. Additional findings described above."
        },
        {
            "input": "Study is moderately degraded by motion.\n\nCompared to the prior exam from ___, there has been no\nsignificant interval change in the extent of the multiple confluent and\ndiscrete T2/FLAIR hyperintense lesions in the periventricular, deep and\nsubcortical white matter of the cerebral hemispheres in a ___ fingers\npattern consist palpable with patient's known multiple sclerosis.  Additional\nT2/FLAIR hyperintense lesions within the left pons and midbrain, measuring up\nto 1.4 cm, is also unchanged compared to the prior exam.\n\nThere is no evidence of acute intracranial infarction or hemorrhage.  Re\ndemonstrated is thinning of the corpus callosum as well as mild global\nparenchymal volume loss with mildly prominent ventricles and sulci.\n\nMild mucosal sinus thickening is seen involving the ethmoid air cells.  The\nremainder of the visualized paranasal sinuses, mastoid air cells, and middle\near cavities are clear.  The principal vascular flow voids appear to be well\npreserved.",
            "output": "1.  Study is moderately degraded by motion.\n2. Grossly stable nonenhancing white matter lesions as described, compatible\nwith patient's provided history of multiple sclerosis.\n3.  Within limits of study, no definite new white matter lesions identified.\n4. Stable thinning of the corpus callosum and mild global volume loss.\n5. Mild paranasal sinus disease."
        },
        {
            "input": "Multiple confluent and discrete T2/ FLAIR hyperintense lesions are seen in the\nperiventricular, deep, and subcortical white matter of the cerebral\nhemispheres, including callosal and pericallosal lesions in a ___\nFingers\"  pattern, consistent with patient's known multiple sclerosis.  A 1.1\nx 0.7 cm T2/ FLAIR hyperintense lesion is seen in the left hemi pons (4;7). \nSmaller T2/FLAIR hyperintense lesions are seen in the right pons and right\nmidbrain, images ___.  There are no enhancing lesions and no lesions with\nslow diffusion.  There are multiple black holes on precontrast T1 weighted\nimages.  There is severe thinning of the corpus callosum, as well as mild\nglobal parenchymal volume loss with mildly prominent ventricles and sulci.\n\nThere is no evidence for an intracranial mass, acute infarction, or\nintracranial blood products.  Major intravascular flow voids are grossly\npreserved.  Major dural venous sinuses are patent on postcontrast MP RAGE\nimages\n\nThere is opacification of several anterior ethmoid air cells, right greater\nthan left, extending into the frontoethmoidal recesses, with mild mucosal\nthickening in the frontal sinuses and in other anterior ethmoid air cells\nbilaterally.  There is mucosal thickening and probably also dependent\nsecretions in the left sphenoid sinus.",
            "output": "1. Extensive supratentorial white matter signal abnormalities, as well as\nsignal abnormalities in the midbrain and pons, compatible with demyelinating\ndisease.  No enhancing lesions.\n2. Severe thinning of the corpus callosum and mild global volume loss\nelsewhere in the brain parenchyma.\n3. Paranasal sinus disease, as detailed above."
        },
        {
            "input": "The examination is motion degraded.  Within these confines:\n\nPatient is status post left craniotomy with stable underlying pachymeningeal\nthickening and enhancement, consistent with postsurgical changes. \nEncephalomalacia involving the left posterior frontal and parietal lobes are\nunchanged.  There is no abnormal diffusion identified.  Ventricles and sulci\nare stable in size and configuration.  There is no shift of normally midline\nstructures.  Degree of cerebellar atrophy thought related to chronic anti\nseizure medications is not significantly changed.  No enhancing lesion is\nidentified.  Scattered T2 hyperintense foci within the subcortical white\nmatter bilaterally appear unchanged relative to prior study and remain\nnonspecific.  There is no evidence of acute hemorrhage.\n\nMajor intracranial flow voids are preserved.  Major dural sinuses are grossly\npatent.  The orbits are unremarkable.  Imaged paranasal sinuses and bilateral\nmastoid air cells are clear.",
            "output": "1. The examination is motion degraded.  Within these confines:\n2. Stable postoperative changes involve a left craniotomy with resultant\nencephalomalacia within the posterior left frontal/parietal lobe.  Atrophy of\nthe cerebellum is similar in degree relative to prior examinations, likely\nsequela of chronic antiepileptic medications.\n3. Periventricular and subcortical FLAIR white matter hyperintensities are\nsimilar in appearance to prior exam allowing for technical differences.\n4. No acute intracranial abnormality."
        },
        {
            "input": "There is no evidence of infarction, hemorrhage, mass, mass effect, edema or\nmidline shift. There is no abnormal enhancement.  The dural venous sinuses\nappear patent.\n\nThe ventricles and sulci are normal, without evidence of hydrocephalus. There\nis gross preservation of the principal intracranial vascular flow voids.\n\nMild mucosal thickening is seen throughout scattered ethmoid air cells\nbilaterally.  The remainder of the visualized paranasal sinuses, middle ear\ncavities, and mastoid air cells are well aerated and clear.  The orbits are\nwithin normal limits bilaterally.",
            "output": "1. Unremarkable brain MRI without evidence of infarction or hemorrhage. \nSpecifically, no abnormal enhancement or mass is identified."
        },
        {
            "input": "There are multiple areas of slowed diffusion with associated FLAIR\nhyperintensity affecting multiple vascular territories.  There is a large\nregion of medial right occipital and posterior temporal slowed diffusion in\nthe PCA territory.  This area corresponds to subtle hypodensity is seen on the\nearlier same day CT examination.  There are additional small cortical based\nareas of slow diffusion in the left parietal lobe with additional subcortical\nwhite matter focus (302:21, 23, 25, 26).  There is additional punctate\ninvolvement of the left thalamus, left caudate, additional punctate areas in\nthe right anterior frontal white matter, as well as a slightly larger area in\nthe left frontal corona radiata (302:18).  There is additional punctate\ncortical focus in the left posterior temporal lobe (302:16).  There also tiny\nbilateral foci in the cerebellar hemispheres.\n\nThere is no evidence of hemorrhage, masses, mass effect, or midline shift. \nThe ventricles and sulci are normal in caliber and configuration.  The\nvisualized major intracranial flow voids are preserved.  There is mild mucosal\nthickening of the ethmoid air cells.  The orbits are unremarkable.  A\nnonspecific T2 hyperintense T1 hypointense 4 mm focus adjacent to the right\nmandibular condyle (series 5, image 3) is incompletely characterized, but\npotentially representing synovial fluid, corresponding to nonenhancing fluid\nattenuating focus seen on prior CTA.",
            "output": "1. Numerous late acute to early subacute supra and infratentorial infarcts in\nmultiple vascular territories bilaterally, as described, with most prominent\narea affecting the medial right occipital and posterior temporal lobes in the\nPCA distribution, corresponding to subtle hypodensity on prior CT.\n2. No hemorrhage.\n3. Additional findings described above.\n\nNOTIFICATION:  Neurology service was aware of these findings at time of\ndictation, per OMR note."
        },
        {
            "input": "The right superior ophthalmic vein is dilated and demonstrates a large filling\ndefect on the post-contrast images (series 12 images ___ series 13, image\n15).  There is a questionable filling defect within the left superior\nophthalmic vein (series 13, image 15) which is not dilated.  There is\ndiminished enhancement of the lateral margins of the cavernous sinus, with a\npossible filling defect lateral and superior to the cavernous portion of the\nright internal carotid artery (series 12, image 9).  There is no evidence of\nhemorrhage, edema, masses, mass effect, midline shift or infarction.   The\nventricles and sulci are normal in caliber and configuration.  There are\nmoderate FLAIR signal hyperintensities in the periventricular and subcortical\nwhite matter as well as the pons.\n\nThere is mucosal thickening within the inferior frontal sinuses and several\nethmoid air cells.  The remaining paranasal sinuses, mastoid air cells and\nmiddle ear cavities are patent.",
            "output": "1. Dilated right superior ophthalmic vein with a large filling defect\ncompatible with thrombosis.\n2. Diminished enhancement of the right cavernous sinus lateral to the\ncavernous portions of the internal carotid arteries with a questionable\nfilling defect lateral and superior to the right ICA, possibly representing\nextension of thrombosis into the right cavernous sinus.\n3. Questionable central filling defect in the left superior ophthalmic vein. \nSmall thrombus is not excluded.\n4. Paranasal sinus disease as detailed above."
        },
        {
            "input": "Study is mildly degraded by motion.\n\nThere is no imaging signs to suggest right superior ophthalmic vein\nthrombosis.  Bilateral cavernous sinuses show symmetrical appearance with\nnormal convex border appearance.  There is no imaging signs to suggest\ncavernous sinus thrombosis. Status post lens removal surgery of both globes. \nBoth orbits otherwise are unremarkable.\n\nThere is a focal enhancing intraosseous abnormality with corresponding slow\ndiffusivity at left parietal bone (series 8, image 102); stable since previous\nexamination dated ___.  Interval stability suggests benign etiology.\nThere is no other abnormal enhancement after contrast administration.\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor acute infarction.  There are bilateral periventricular and deep white\nmatter multifocal T2 FLAIR hyperintensities; nonspecific in appearance and\ncould be related to chronic small vessel disease.  Background of involutional\nchanges is noted evidenced by ex vacuo dilatation of lateral ventricles and\nenlargement of extra-axial CSF spaces.  The ventricles and sulci are age\nappropriate and stable\nMajor intracranial vascular flow voids are unremarkable.  No sinus venous\nthrombosis.\n\nMild mucosal thickening involving ethmoid air cells.  Paranasal sinuses and\nmastoid air cells otherwise are essentially clear.",
            "output": "1. Resolution of previous right ophthalmic vein thrombosis seen in ___.  No\nevidence of ophthalmic vein or cavernous sinus thrombosis on the current exam\n2. Normal shape and appearance of both cavernous sinuses.\n3. Background of involutional changes with white matter chronic\nmicroangiopathy.\n4. No acute intracranial abnormality.\n5. Focal enhancing intraosseous abnormality with corresponding slow\ndiffusivity at left parietal bone (series 8, image 102); stable since previous\nexamination dated ___. Interval stability suggests benign etiology; for\nfollow-up if clinically indicated."
        },
        {
            "input": "MRI BRAIN:\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.  There is no abnormal focus of slowed diffusion.  A few,\npunctate scattered areas of bifrontal subcortical white matter T2/FLAIR\nhyperintensity are nonspecific.  The principal intracranial vascular flow\nvoids are preserved.  The dural venous sinuses are patent on MP rage images.\n\nThe paranasal sinuses are grossly clear.  The orbits are grossly unremarkable.\n\nMRA NECK:\nThe common, internal and external carotid arteries appear normal.  There is no\nevidence of internal carotid artery stenosis by NASCET criteria.  The origins\nof the great vessels, subclavian and vertebral arteries appear normal\nbilaterally.  There is no evidence of dissection.",
            "output": "1. No acute intracranial abnormality including infarct, hemorrhage, or\nenhancing mass.\n2. Scattered punctate areas of bifrontal nonspecific white matter signal\nabnormality given appearance most likely represent prominent perivascular\nspaces.  The differential is broad, and includes migraine headache.\n3. Patent cervical vasculature without significant stenosis, occlusion, or\ndissection.\n\nNOTIFICATION:  The findings were discussed by Dr. ___ with Dr. ___\n___ on the telephoneon ___ at 5:02 ___, 5 minutes after discovery of\nthe findings."
        },
        {
            "input": "There is no evidence of intracranial hemorrhage, mass, mass effect or shifting\nof the normally midline structures.  The ventricles and sulci are normal in\nsize and configuration for the patient's age.  No diffusion abnormalities are\ndetected.  Small subependymal hyperintense areas are noted adjacent to the\nleft ventricular horns (for example image 14, series 10), which are\nnonspecific and may represent some gliotic areas and of doubtful clinical\nsignificance.  The major vascular flow voids are present and demonstrate\nnormal distribution.  The orbits are unremarkable, the paranasal sinuses are\nnotable for mucosal thickening in the maxillary sinuses, more significant on\nthe right, frontoethmoidal recesses, frontal sinus, sphenoid sinus.  Bilateral\nmucosal thickening is present mastoid air cells, more significant on the left.",
            "output": "1.  There is no evidence acute or subacute intracranial process, there is no\nevidence of intracranial hemorrhage.\n\n2.  Paranasal sinus disease as described above."
        },
        {
            "input": "There is no evidence of intracranial hemorrhage, edema, masses, mass effect,\nmidline shift or infarction.   The ventricles and sulci are prominent,\nconsistent with global cerebral volume loss.  Subcentimeter T2 hyperintense\nlesions in the left basal ganglia likely represent prominent perivascular\nspaces.  Patchy periventricular T2 hyperintensities are most consistent with\nchronic small vessel ischemic disease.  There is mild mucosal thickening of\nthe left maxillary sinus.  A linear enhancing focus is seen in the right\nperitrigonal area (image 100 series 900), consistent with a developmental\nvenous anomaly.  There is no abnormal enhancement after contrast\nadministration.",
            "output": "1. No enhancing lesions.\n2. Small developmental venous anomaly.\n3. Chronic small vessel ischemic disease changes.\n4. Global cerebral volume loss."
        },
        {
            "input": "MRI Brain:\nGlobal atrophy of the gray and white matters are seen, unchanged from prior. \nAgain seen are multiple FLAIR/T2 white matter plaques and associated T1 black\nholes, unchanged from prior.  There are no new areas of inflammation or new\nlesions.\nThere is no evidence of acute hemorrhage, edema, masses, mass effect, midline\nshift or infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.\n\nMRA brain: The intracranial vertebral and internal carotid arteries and their\nmajor branches appear normal without evidence of stenosis, occlusion, or\naneurysm formation.\n\nMRA neck:  The common, internal and external carotid arteries appear normal. \nThere is no evidence of internal carotid artery stenosis by NASCET criteria. \nThe origins of the great vessels, subclavian and vertebral arteries appear\nnormal bilaterally.  Proximal right vertebral artery appears stenosed on\nsubtracted images, but appears patent on source images.",
            "output": "1. Numerous white plaques and associated T1 black holes, unchanged from prior.\n2. No acute infarct or intracranial hemorrhage."
        },
        {
            "input": "There are 2 FLAIR/T2 white matter lesions located in the left frontal lobe\n(series 5, image 18, series 5, image 15).  In addition, there is interval\nincreased size of a right frontal periventricular white matter FLAIR\nhyperintense lesion (series 5, image 15).  There is associated enhancement of\nthe new left frontal lobe lesions located in the superior frontal gyrus\n(series 5, image 18; series 1102 B, image 75).  There is no associated slow\ndiffusion.\n\nAdditional previously seen in nonenhancing FLAIR hyperintense supra and\ninfratentorial white matter lesions are essentially unchanged since\nexamination of ___.\n\nThe majority of these lesions are associated with T1 \"Black holes\".\n\nThe sulci, ventricles and are unchanged in configuration from prior exam.  The\ndural venous sinuses are patent.  The major intracranial flow voids are\npreserved.  Mucosal thickening of the ethmoid air cells and left frontal sinus\nas well as sphenoid sinus is noted.  Fluid signal is seen in the left mastoid\ntip.  The orbits are unremarkable.",
            "output": "1. Two new left frontal lobe lesions with associated enhancement of a lesion\nlocated at the vertex.  Interval increased size of a previously seen right\nfrontal periventricular lesion.  Additional supra and infratentorial white\nmatter FLAIR signal abnormalities are noted.  These are in a configuration\ncompatible with demyelinating plaques given the history of multiple sclerosis.\n\n2. No acute infarct or intracranial hemorrhage."
        },
        {
            "input": "MRI BRAIN:\n\nThere is no evidence of acute infarction, hemorrhage, edema, mass effect or\nother signal abnormalities in the brain parenchyma.  Ventricles and sulci are\nnormal in size for age. There is minimal mucosal thickening within the ethmoid\nair cells.\n\nMRA BRAIN:\n\nThere is an apparent linear filling defect seen in the distal basilar artery\non 3D time-of-flight MRA images, where there is pulsation artifact. No\nabnormality of the basilar artery is seen on post-contrast MRA of the neck,\nand the basilar artery flow-void is normal on T2 weighted images of the brain\nMRI.  Therefore, the finding on the 3D time-of-flight images is artifactual. \nA hypoplastic A1 segment of the left anterior cerebral artery artery is again\nnoted.  Otherwise, the intracranial vertebral and internal carotid arteries\nand their major branches appear patent without evidence of stenosis or\naneurysm formation.\n\nMRA NECK:\n\nThe common, internal and external carotid arteries appear normal.  There is no\nevidence of stenosis by NASCET criteria.  The origins of the great vessels,\nsubclavian and vertebral arteries appear normal bilaterally.",
            "output": "1.  No acute infarction.\n\n2.  Normal intracranial MRA, allowing for pulsation artifact through the\ndistal basilar artery.\n\n3.  ___ MRA of the neck."
        },
        {
            "input": "There is encephalomalacia in the right frontal lobe.  There is no acute\ninfarct identified.  In the region of encephalomalacia there is no abnormal\nenhancement is seen.  There is mild to moderate brain atrophy identified. \nFollowing gadolinium there is no abnormal parenchymal vascular and meningeal\nenhancement seen.  Mild changes of small vessel disease seen.  Fluid is seen\nin both maxillary sinuses.\n\nMRA of the head shows normal signal in the arteries of the anterior and\nposterior circulation. No evidence of vascular occlusion stenosis or an\naneurysm greater than 3 mm in size seen.\n\nMRA of the neck shows normal flow in the carotid and vertebral arteries. No\nevidence of stenosis or occlusion or dissection seen.  The left external\ncarotid artery is not well visualized likely secondary to atherosclerotic\ndisease.  Mild atherosclerotic disease is also seen at the origin of left\ninternal carotid artery.",
            "output": "Frontal encephalomalacia is seen.  No acute infarcts or enhancing brain\nlesions are identified.  No mass effect is seen.  No significant abnormalities\non MRA of the head and neck."
        },
        {
            "input": "There is no intracranial mass, mass effect, or midline shift. Ventricles and\nsulci are age-appropriate. There is no focal parenchymal signal abnormality.\nThere is no region of restricted diffusion or abnormal susceptibility\nartifact. Major intravascular flow voids are preserved.\n\nMedial temporal lobes are symmetric in size and signal. There is no evidence\nof heterotopia or cortical dysplasia.\n\nVisualized paranasal sinuses and mastoid air cells are clear.  Susceptibility\nartifact in the bilateral frontal scalp is presumably from prior surgical\nprocedure.",
            "output": "No findings to explain patient's symptoms, no focal parenchymal signal\nabnormality."
        },
        {
            "input": "The study is somewhat limited by motion.\n\nThere is no evidence of hemorrhage, infarction, edema, or mass effect. \nPrincipal intracranial vascular flow voids are preserved. No extra-axial blood\nor fluid collection is present. The ventricles and sulci are age appropriate.\n\nThere is a 4 mm focus of enhancement seen within the posterior limb of the\nleft internal capsule/putamen seen on both post-contrast T1 (20:71) and\npost-contrast MPRAGE (17:12) sequences with FLAIR (16:12) and possible\nsusceptibility signal abnormality (15:12). There is no associated mass effect.\nNo other foci of abnormal enhancement are seen.  There is a single 3 mm focus\nof FLAIR signal abnormality in the right temporal lobe (16:10) which, though\nlimited by motion, shows no enhancement. There is also no correlation seen on\nsubsequent sequences.  There is no pathologic pachymeningeal or enhancement.\n\nIncidental note is made of a 9 mm pineal gland cyst (11:12). The brainstem,\nposterior fossa and cervico-medullary junction are preserved. The orbits are\nwithin normal limits.  The paranasal sinuses are clear.  No abnormality of the\nskull base or calvaria is identified.",
            "output": "1. 4 mm focus of enhancement near the posterior limb of the left internal\ncapsule, nonspecific, but may reflect metastatic disease. Short-term followup\nis recommended.  No other abnormal enhancement identified.\n2. 3 mm focus of FLAIR signal abnormality in the right temporal lobe has no\ncorrelation on subsequent sequences and may represent artifact. Attention on\nfollowup is recommended."
        },
        {
            "input": "Previously demonstrated small 4 mm enhancing focus in the posterior limb of\nthe left internal capsule is again noted with associated FLAIR lesion, similar\nin appearance to prior exam on both T1 postcontrast and MP-RAGE sequences\n(series 10, image 13 and series 901b, image 62, and series ).\n\nPreviously described a FLAIR hyperintense the right temporal lobe focus,\nadjacent to a sulcus (series 11, image 12) is noted, although there is\npostcontrast enhancement (series 901B, image 62 and series 10, image 11),\nwhich was not demonstrated on prior exam.\n\nNo other new enhancing lesions are noted. Unchanged appearance of a 9 mm\npineal cyst. There are additional superimposed very few subcortical and\nperiventricular white matter hyperintensities, which likely represent sequela\nsmall vessel ischemic disease in a patient of this age. There is no evidence\nof acute infarct or hemorrhage.\n\nThe major intracranial flow voids preserved. Mild mucosal thickening of the\nmaxillary, frontal and sphenoid sinuses with partial opacification of the\nethmoid air is noted. Paranasal sinus mucosal thickening has increased from\nprior exam. Fluid signal in the left mastoid air cells are noted, slightly\nincreased from prior exam. Interval improvement in fluid signal within the\nright mastoid air cells.\n\nThe A1 segment is not seen, likely hypoplastic. There is apparent fetal type\norigins of the bilateral posterior cerebral arteries on postcontrast MPRAGE\nsequences. This is unchanged from prior examination.",
            "output": "1. Stable nonspecific 4 mm enhancing left internal capsule posterior limb\nstructure  and .  Differential considerations continue to include metastatic\nlesion or treatment related effects.  Recommend clinical correlation and\nattention on followup is recommended.\n2. Redemonstration of previously noted 3mm right temporal lobe lesion, now\ndemonstrating new enhancement.  Differential considerations continue to\ninclude metastatic lesion or treatment related effects. Recommend clinical\ncorrelation and attention on followup is recommended.\n3. No new lesions are identified.\n4. Interval worsening of pan sinus disease. Interval increase fluid within the\nleft mastoid air cell."
        },
        {
            "input": "There is no evidence for an intracranial mass, abnormal pachymeningeal or\nleptomeningeal contrast enhancement, or abnormal vascular enhancement.  There\nis no evidence for edema, mass effect, abnormal diffusion, blood products, or\nother signal abnormalities in the brain parenchyma. Ventricles, basal\ncisterns, and cerebral sulci are normal in size. The cerebellar tonsils are\nnormally positioned. Major arterial flow voids are grossly preserved. Major\nintracranial arteries and major dural venous sinuses appear unremarkable on\npostcontrast MP RAGE images.",
            "output": "Normal brain MRI with and without contrast."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.\n\n The major intracranial vascular flow voids are maintained.  The paranasal\nsinuses, mastoid air cells and orbits are normal.",
            "output": "1. No acute intracranial abnormality.\n2. Otherwise normal MRI head."
        },
        {
            "input": "Numerous sequences are limited by patient motion to varying degrees,\nmoderate-severe, particularly affecting the axial T2 and postcontrast\nsequences.\n\nMRI BRAIN:\n Allowing for this, there is no evidence of acute infarction.  No intracranial\nhemorrhage. No mass, mass effect, edema or midline shift. There is no abnormal\nenhancement.  The dural venous sinuses appear patent.\n\nThe ventricles and sulci are normal, without evidence of hydrocephalus. There\nis gross preservation of the principal intracranial vascular flow voids.\n\nThe visualized paranasal sinuses, middle ear cavities, and mastoid air cells\nare well aerated and clear.  The orbits are within normal limits bilaterally.\n\nMRA BRAIN:\nThe intracranial vertebral and internal carotid arteries and their major\nbranches appear grossly patent without evidence of stenosis, occlusion, or\naneurysm formation.\n\nMRV BRAIN:\nThe superior sagittal sinus, transverse sinuses, sigmoid sinuses, straight\nsinus, vein of ___, and internal cerebral veins appear grossly patent\nbilaterally.\n\nMRA NECK:\nA normal, three-vessel aortic arch is identified.  Although evaluation of the\ncervical vasculature is limited by patient motion, the vertebral, common\ncarotid, and in the internal carotid arteries all appear grossly patent\nbilaterally.",
            "output": "1. Moderately limited examination secondary to patient motion, particularly\naffecting the axial T2, post contrast, and MRA neck sequences.\n2.  Within limits of study, no definite evidence of vascular territorial\ninfarction,  acute intracranial hemorrhage or abnormal enhancement.\n3. Grossly patent intracranial and cervical vasculature without high-grade\nstenosis, occlusion, or aneurysm.\n4. Patent dural venous sinuses without evidence of thrombosis.\n5.  Paranasal sinus disease , as described."
        },
        {
            "input": "There are confluent areas of slow diffusion involving the left frontoparietal\ncortex as well as the insula with a punctate focus of slow diffusion in the\nleft posterior limb of the internal capsule in the left middle cerebral artery\ndistribution in keeping with acute infarct.  There are also small foci of\nrestricted diffusion in the right cerebellar hemisphere (4:5, and 7). \nAdditional focus within the ventral pons on the right (4:7) is seen without\ndefinite correlate on the ADC map but is associated with T2 hyperintensity.\n\nThere is an encephalomalacia involving the left occipital lobe with ex vacuo\ndilatation of the body and occipital horn of left lateral ventricle, likely\nsecondary to old infarct.\n\nThere is  a focus of microhemorrhage in the left basal ganglia.\n\nThere is no evidence of acute hemorrhage, edema, masses, mass effect or\nmidline shift.   The ventricles and sulci are patent and prominent in keeping\nwith age-related volume loss.\n\nThere are scattered foci and more confluent areas of T2/FLAIR hyperintensity\nin the subcortical, periventricular and deep white matter, nonspecific, likely\nsecondary to small vessel ischemic disease.\n\nThe orbits are unremarkable noting prior bilateral cataract surgeries.  The\nvisualized paranasal sinuses and mastoid air cells are clear.",
            "output": "1. Acute infarct in the left middle cerebral artery distribution as described\nabove.\n2. Additional small acute infarcts in the right cerebellar hemisphere.  In\ncombination with above, there is possibility of a central embolic source.\n3. Age-related volume loss with prominence of ventricles and sulci.\n4. Old infarct in the left occipital lobe with ex vacuo dilatation of the left\nlateral ventricle."
        },
        {
            "input": "There is a 3 x 2.5 cm partially cystic and partially solid mass identified in\nthe left cerebellopontine angle with mild indentation on the adjacent brain\nstem.  Mass extends into the internal auditory canals to the region of fundus.\nFoci of susceptibility indicate calcification within the mass.  The mass\nextends to the left trigeminal nerve region.  Findings are consistent with a\nvestibular schwannoma.  There is no hydrocephalus seen.  The right auditory\ncanal appears normal without abnormal enhancement.  No other abnormal areas of\nenhancement seen in the posterior fossa.  There is no evidence of abnormal\nparenchymal vascular or meningeal enhancement seen.  Mild to moderate changes\nof small vessel disease and brain atrophy are seen.  Vascular flow voids are\nmaintained.",
            "output": "Approximately 3 x 2.5 cm partially cystic and solid mass in the left\ncerebellopontine angle extending to the internal auditory canal consistent\nwith a vestibular schwannoma.  There are no prior studies for direct\ncomparison assessment of interval change.  No acute infarcts are seen"
        },
        {
            "input": "No evidence of acute infarction, hemorrhage or mass-effect.  Periventricular\nand subcortical white matter T2/FLAIR hyperintensities are nonspecific but\nlikely sequelae of chronic small vessel ischemic disease.  The ventricles and\nsulci are prominent, consistent with involutional changes.",
            "output": "1.  No evidence of acute infarction or hemorrhage.\n2.  Chronic ischemic small vessel disease."
        },
        {
            "input": "Study is mildly degraded by motion.  There is right precentral gyrus and right\nmiddle frontal gyrus restricted diffusion with associated FLAIR\nhyperintensity.  There are additional small foci of restricted diffusion\nwithin right middle frontal gyrus (302-22), and right inferior temporal gyrus\n(302-18).\n\nThere is no definite evidence of acute hemorrhage.  A punctate focus of blood\nproducts versus mineralization is noted in the right occipital lobe (see\n07:13).\n\nThe ventricles, sulci, and cisterns are age appropriate without mass effect or\nmidline shift.  There are nonspecific periventricular and subcortical FLAIR\nhyperintense foci, likely a sequela of chronic small vessel microangiopathy\nthe major visualized arterial vascular flow voids are preserved\n\nThere is mild mucosal thickening of bilateral maxillary and anterior ethmoid\nair cells.  There is mild bilateral mastoid air cell opacification.  The\norbits and visualized soft tissues appear unremarkable.",
            "output": "1.  Study is mildly degraded by motion.\n2. Acute to early subacute infarction within the right MCA distribution\nfrontal lobe with additional scattered foci within right middle frontal gyrus\nand right inferior temporal gyrus.  These findings raise concern for embolic\nsource at right carotid or central location.\n3. Punctate right occipital focus of blood products versus mineralization, not\ndefinitely associated with focus of acute infarct.\n4. Probable chronic small vessel microangiopathy and mild paranasal sinus\ndisease, as above.\n\nNOTIFICATION:  The findings were discussed with ___, M.D. by ___\n___, M.D. on the telephone on ___ at 10:05 am, 1 minute after\ndiscovery of the findings."
        },
        {
            "input": "Compared with ___, again seen are areas of slow diffusion in the\nright precentral and middle frontal gyrus, as well as right inferior temporal\ngyrus, with associated FLAIR signal hyperintensity.  Again seen is a punctate\nfocus of blood products versus mineralization in the right occipital lobe. \nThere is no new evidence of new infarct.  The ventricles and sulci are age\nappropriate.  Subcortical and periventricular FLAIR/T2 hyperintensities are\nnonspecific, however likely represent sequela of chronic small vessel ischemic\ndisease.  The major intracranial flow voids are preserved.\n\nThere is mucosal thickening in the bilateral maxillary sinuses and ethmoid air\ncells.  There the visualized paranasal sinuses and mastoid air cells are\nclear.  The orbits are grossly unremarkable.",
            "output": "Interval evolution of previously seen right-sided infarcts.  No new infarcts."
        },
        {
            "input": "There is no intra or extra-axial mass, acute hemorrhage or infarct. There is a\npunctate focus of gradient echo susceptibility within the pons compatible with\nsequela of micro hemorrhage. In addition, there is a 5 mm pineal cyst\ndemonstrating gradient echo susceptibility, likely representing\ncalcifications. There is no abnormal enhancement. Nonspecific periventricular\nand subcortical T2/FLAIR white matter hyperintensities are noted, which may be\nseen in the setting of small vessel ischemic disease in a patient of this age.\nSulci, ventricles cisterns are within expected limits given the degree of age\nappropriate global cerebral volume loss. The major intracranial flow voids are\npreserved. The dural venous sinuses are patent. The patient is status post\nbilateral lens replacements otherwise the orbits are unremarkable. There is\nmild mucosal thickening of the paranasal sinuses. The mastoid air cells appear\nclear.",
            "output": "1. No evidence of metastatic disease to the head.\n2. White matter changes as described above compatible small vessel ischemic\ndisease.\n3. Gradient echo susceptibility in the pons, presumably representing sequela\nof prior microhemorrhage, likely hypertensive in nature.\n4. Presumed calcified pineal cyst is incidentally noted."
        },
        {
            "input": "The intracranial arteries in the anterior and posterior circulation are\ntortuous without evidence of stenosis or occlusion or an aneurysm greater than\n3 mm in size.  There is marked tortuosity of the left distal survey internal\ncarotid artery visualized.  There is a linear defect seen within the flow\nsignal of distal left internal carotid artery (8:79) which is also seen on the\nmaximum intensity projections (8 02:11).  Similar findings are also visualized\non the neck MRA.  These findings are suggestive of chronic dissection.  This\nfindings were not clearly visualized on the previous neck CT or brain MRI as\nthis area was not fully evaluated.\n\nMRA of the neck shows no evidence of vascular occlusion or stenosis.  Linear\ndefect in the distal left cervical internal carotid artery.  (5 00:14) is\nvisualized as seen on the brain MRA and is suspicious for chronic dissection\nwith intimal flap.  Distal right internal carotid artery is also tortuous but\nno distinct defect is visualized.",
            "output": "Question of chronic dissection in the distal left internal carotid artery near\nthe skullbase.  Further evaluation can be obtained with CT angiography, as\nclinically indicated.\n\nNOTIFICATION:   The impression and recommendation above was entered by Dr.\n___ on ___ at 11:34 into the Department of Radiology\ncritical communications system for direct communication to the referring\nprovider."
        },
        {
            "input": "MRI BRAIN:\nThere is no intra or extra-axial mass, acute hemorrhage or infarct.   Right\nfrontal, right parietal and left occipital lobe encephalomalacia is\nre-identified.  Prior infarcts of the bilateral cerebellar hemispheres are\nalso noted.  Periventricular, pontine and subcortical T2/FLAIR white matter\nhyperintensities superimposed hyperintensities are nonspecific, but compatible\nwith chronic microangiopathy in a patient of this age.  The sulci, ventricles\nand cisterns are within expected limits for the patient's age.  Etat crible\nappearance of the bilateral basal ganglia secondary to prominent perivascular\nspaces.\n\nScattered punctate gradient echo susceptibility foci in the left frontal\nparietal lobe, basal ganglia and, right thalamus, pons and right cerebellar\nhemispheres are unchanged from prior examination, compatible with sequela of\nprior micro hemorrhages.   The major intracranial flow voids are preserved. \nThe dural venous sinuses are patent postcontrast MP-RAGE.  There is mild\nmucosal thickening of the paranasal sinuses as well as dependent fluid in the\nbilateral maxillary sinuses. The orbits are unremarkable noting bilateral lens\nreplacements. Trace fluid signal is seen in the mastoid tips.\n\nT2 hyperintense focus in the right parotid tail measuring approximately 1.3 cm\nand may be slightly increased in size since examination of ___.\n\nMRA BRAIN:\nThe intracranial vertebral and internal carotid arteries and their major\nbranches appear normal without evidence of stenosis, occlusion, or aneurysm\nformation.\n\nMRA NECK:\nRe-identified is chronic dissection of the distal left internal carotid\nartery, unchanged in appearance from prior examination.\n\nThere is a 3 vessel arch.  The common carotid, bilateral subclavian, bilateral\nvertebral and right internal carotid artery are unremarkable.  There is no\nevidence of T1 hyperintense signal on axial T1 fat saturated sequences to\nsuggest recent dissection.  There is linear signal of the bilateral V3\nsegments, particularly seen on axial time-of-flight images of the head, most\ncompatible with laminar flow.  There is no stenosis of the cervical internal\ncarotid arteries by NASCET criteria.",
            "output": "1. There is no acute infarct or intracranial hemorrhage.  No abnormal\nenhancement or intracranial mass at this time.\n2. Unchanged appearance of chronic left distal cervical ICA dissection.  No\nnew dissections identified.\n3. There is a T2 hyperintense right parotid tail lesion, which slightly\nincreased in size since ___.  This could represent a parotid node however,\nfurther evaluation with ultrasound is recommended.\n4. Essentially unremarkable MRA of the head.\n5. Additional findings as described above."
        },
        {
            "input": "There is a large enhancing extraaxial mass in the left frontal lobe measuring\napproximately 7.3 cm AP x 6.7 cm SI by 6.0 cm TV. This mass has a dural\nattachment and is arising from the greater wing of the sphenoid bone. There is\nsevere mass effect with 16 mm shift of midline to the right, displacement of\nthe anterior cerebral arteries to the right, effacement of the\nperimesencephalic cisterns with resulting deformity of the mid brain, and\nlow-lying cerebellar tonsils likely acquired secondary to mass effect. There\nis increased T2/FLAIR signal in the surrounding brain parenchyma likely\nreflecting vasogenic edema. There is effacement of the left lateral ventricle\nwith dilatation of the right ventricular system and transependymal flow of\nCSF. There is prominent vascularity noted within the mass.\nThere is no evidence of acute hemorrhage or infarction. Vascular flow voids\nare preserved. The orbits are unremarkable. The paranasal sinuses and mastoid\nair cells are clear.",
            "output": "7.3 cm AP x 6.7 cm SI by 6.0 cm TV enhancing extra-axial mass in the left\nfrontal lobe which most likely represents a large meningioma. This mass is\nresulting in significant mass effect as detailed above. As this mass\ndemonstrates prominent vascularity, a CTA could be obtained for pre-surgical\nplanning."
        },
        {
            "input": "The cystic encephalomalacia seen in the left frontal region. Small area of\nenhancement is seen in the inferior left frontal lobe. Best visualized on\nseries 42, image 98.  There is no midline shift or mass effect seen. Mild ex\nvacuo dilatation left lateral ventricle seen. No acute infarcts identified.",
            "output": "MRI performed for cyber knife radiosurgery demonstrated small area of\nenhancement in the inferior left frontal lobe adjacent to the postsurgical\nencephalomalacia."
        },
        {
            "input": "Left inferior frontal surgical cavity is again seen.  Thin linear contrast\nenhancement along the inferior margin of the cavity, along the gyrus rectum,\nappears unchanged on axial postcontrast T1 weighted images, and decreased on\npostcontrast coronal MP RAGE images compared to ___.  No new masslike\ncontrast enhancement is seen.  There is minimal high T2 signal along the\nsurgical cavity margins without mass effect.  There is persistent dural\nthickening and contrast enhancement along the left frontal convexity, left\nanterior temporal lobe, and left anterior falx.  There is ex vacuo dilatation\nof the frontal horn and anterior body of the left lateral ventricle.  The\nremainder the ventricular system is normal in size.\n\nThere is no acute infarction.  Major arterial flow voids appear grossly\npreserved.  Major dural venous sinuses appear patent on postcontrast MP RAGE\nimages.\n\nThere is a fluid level, as well as moderate mucosal thickening in the right\nsphenoid sinus.  There is mild mucosal thickening in the ethmoid air cells.",
            "output": "Thin linear contrast enhancement along the inferior margin of the left\ninferior frontal surgical cavity appear stable on axial postcontrast T1\nweighted images and slightly decreased on coronal postcontrast MP RAGE images.\nNo masslike enhancement is seen.  No new lesions are seen."
        },
        {
            "input": "Study is mildly degraded by motion.    There is no evidence of hemorrhage,\nedema, masses, mass effect, midline shift or infarction.   The ventricles and\nsulci are normal in caliber and configuration.  Partially empty sella.  The\ncraniocervical junction appears normal.  The intracranial arteries demonstrate\nnormal T2 flow voids.  Minimal bilateral ethmoid air cell mucosal thickening\nis present.",
            "output": "1.  Study is mildly degraded by motion.\n2.  Within limits of study, no intracranial mass, hemorrhage or infarct.\n3. Minimal paranasal sinus disease, as described."
        },
        {
            "input": "There is no intra or extra-axial mass, acute hemorrhage or infarct. The sulci,\nventricles and cisterns are within expected limits for the patient's age.  No\nsuspicious parenchymal FLAIR signal abnormality.  The major intracranial flow\nvoids are preserved.  There is minimal mucosal thickening of the ethmoid air\ncells.  The orbits are unremarkable.  Trace fluid signal is seen in the\nmastoid tips, unchanged from prior exam.  There is no suspicious marrow\nsignal.",
            "output": "1. Unremarkable noncontrast MRI brain.  Specifically, no evidence of abnormal\nmass, acute infarct or intracranial hemorrhage.  No suspicious parenchymal\nFLAIR signal abnormality.\n2. Additional findings described above.."
        },
        {
            "input": "MRI Brain:\nThere is an area of slow diffusion with associated FLAIR signal abnormality\ninvolving the right front to parietal lobe centered around the central sulcus\ninvolving the precentral, post central gyrus and paracentral lobule in keeping\nwith a subacute infarct.  There is no evidence of associated hemorrhage.\n\nThere is no evidence of masses, mass effect or midline shift.   The ventricles\nand sulci are patent and prominent in keeping with age-related volume loss.\n\nThere is a punctate focus of micro hemorrhage in the left basal ganglia.\n\nThere are extensive scattered foci and more confluent areas of T2/FLAIR\nhyperintensity in the subcortical and periventricular white matter,\nnonspecific, likely secondary to small vessel ischemic disease.\n\nThe orbits are unremarkable.  Mild mucosal thickening in bilateral ethmoid air\ncells and right maxillary sinus with a mucous retention cyst in the right\nfrontal sinus.  The remaining visualized paranasal sinuses are clear.\n\nMRA brain:  There is decreased arborization of the distal cortical branches of\nthe inferior branch of right middle cerebral artery.  Also seen is irregular\nluminal narrowing of anterior and posterior circulation bilaterally, most\nlikely secondary to atheromatous disease.  The intracranial vertebral and\ninternal carotid arteries and their major branches appear otherwise\nunremarkable without evidence of occlusion, or aneurysm formation.\n\nMRA neck:  The common, internal and external carotid arteries appear normal. \nThere is no evidence of internal carotid artery stenosis by NASCET criteria. \nThe origins of the great vessels, subclavian and vertebral arteries appear\nnormal bilaterally.",
            "output": "1. Acute/subacute infarct in the right frontal and parietal lobe centered\naround the central sulcus.\n2. Decreased arborization of the distal cortical branches of right inferior\nMCA division as described above.\n3. Luminal irregularity involving bilateral anterior and posterior\ncirculation, likely secondary to atheromatous disease.\n4. Unremarkable MRA of the neck without stenosis by NASCET criteria."
        },
        {
            "input": "There is a 2.2 x 1.7 cm dural-based mass in the right frontal convexity region\nadjacent to the superior sagittal sinus. There is no significant surrounding\ndural enhancement seen.  The mass demonstrates much less homogeneous\nenhancement and expected from meningioma. There is extensive surrounding edema\nseen with mass effect on the right lateral ventricle. No other areas of\nabnormal enhancement seen. There is no significant midline shift or\nhydrocephalus. No blood products are identified. There is no meningeal\nenhancement. No acute infarcts are seen. The mass does not demonstrate\nrestricted diffusion.",
            "output": "Right frontal convexity mass with extensive surrounding edema. Although the\nmass is dural-based, the appearances are not typical for a meningioma and\ncould represent a dural-based metastatic lesion.  Clinical correlation\nrecommended."
        },
        {
            "input": "MR BRAIN:\nThere is a large late acute infarct within the frontal lobe and insular\ncortex.  Multiple punctate satellite infarcts within the left frontal lobe\nsuperiorly.  Additional small punctate infarcts are seen within the left\noccipital cortex (series 4, image 18), left corona radiata, and left\nperiatrial white matter.  On the right, there are punctate infarcts within the\nright frontal lobe near the vertex (series 4, image 26), and within the right\ncerebellum (series 4, image 8).  Curvilinear T1 hyperintense signal of the\nleft parietal lobe is likely sequela of cortical laminar necrosis or\nmineralization from prior infarct.\n\nThere is no evidence of hemorrhage, edema, masses, mass effect,or midline\nshift.  Severe confluent white matter T2/FLAIR hyperintensities are\nnonspecific, but likely represent the sequela of chronic microvascular\nischemia.  Prominence of the ventricles and sulci, suggesting involutional\nchanges.\n\nComplete opacification of the left maxillary sinus with dehiscence of the\ninferior maxillary wall and extension into the left buccal space and\npterygopalatine fossa (series 8, image 7), as described on the CT head with\nthe same date.  Mucosal thickening the left frontal sinuses and ethmoid air\ncells.  Patient is status post bilateral lens resections.  Otherwise, orbits\nare unremarkable in appearance.\n\nMRA brain: No evidence of large vessel occlusion.  The previously described\nmid to distal M1 occlusion has recanalized however, there remains occlusion of\nthe right M2 superior segment just distal to its take-off.  There is also\nmultifocal mild-to-moderate intracranial arterial stenosis.  Mild narrowing\nand irregularity of the cavernous carotid arteries bilaterally.  Narrowing of\nthe M1 segments bilaterally, mild on right, moderate on the left.  Mild to\nmoderate narrowing of the bilateral A1 segments.  No evidence of aneurysm\nformation.",
            "output": "1. Large late acute infarct within the right frontal lobe and insular cortex\nwith multiple punctate satellite infarcts.\n2. Additional punctate infarcts within the left corona radiata, left\nperiatrial white matter, left occipital cortex, right frontal lobe, and right\ncerebellum.\n3. There is recanalization of the mid to distal left M1 segment occlusion seen\non prior CT head.  There remains occlusion of the left M2 superior segment\njust distal to its take-off.  Additional multifocal mild to moderate arterial\nstenosis.\n4. Complete opacification of the maxillary sinus with dehiscence of the\ninferior wall with extension into the left buccal space and pterygopalatine\nfossa, as described on the prior CT.\n5. Additional findings described above."
        },
        {
            "input": "There are innumerable enhancing lesions with extensive surrounding edema again\nnoted both supra and infratentorially.  Compared to prior study, there has\nbeen decrease in the size of several of these lesions and in the degree of\nsurrounding vasogenic edema.  Gradient echo images again demonstrate\ninnumerable hemorrhages with and many of the lesions.  No definite new\nenhancing lesions are identified.  There is no evidence of infarction or\nextra-axial collection.  Previously identified midline shift has improved\n\nThe ventricles and sulci are normal in caliber and configuration.  The orbits\nare unremarkable.  The paranasal sinuses and mastoid air cells are clear. \nMajor vascular flow voids are preserved.",
            "output": "Innumerable enhancing lesions again identified post super and\ninfratentorially.  The size of these lesions in surrounding vasogenic edema\nhas significantly improved compared to prior study.  No definite new enhancing\nlesions are identified."
        },
        {
            "input": "There are innumerable supratentorial and infratentorial, enhancing lesions,\nseveral of which have decreased in size and several of which have remained\nstable in comparison to the prior examination.  None of these lesions have\nincreased in size.  The enhancing lesion in the right frontal lobe on image\n96, series 19 has decreased in size, measuring 1.5 x 0.8 cm, previously\nmeasuring 1.9 x 1.0 cm.  The dominant enhancing mass with susceptibility in\nthe left occipital lobe is unchanged in size, measuring 3.0 x 2.5 cm.  The\ndegree of surrounding vasogenic edema is again seen, with perhaps mild\nincrease surrounding several lesions.  Several of these lesions demonstrate\nsusceptibility, consistent with hemorrhage.  No new enhancing lesions are\nidentified.\n\nThere is no midline shift or infarction.  The ventricles are unchanged in\nsize.",
            "output": "Innumerable supratentorial and infratentorial metastases, several of which\nhave decreased in size and several of which have remained stable.  No new\nlesions."
        },
        {
            "input": "There are numerous contrast enhancing lesions throughout the supra and\ninfratentorium, all of which are either stable in size or have decrease in\nsize.  The largest lesion is in the posterior left temporal lobe measures 1.7\ncm x 1.6 cm.  Decreased FLAIR hyperintense signal is seen surrounding the\nlarger lesions, particularly the posterior left temporal lesion.  Many of\nthese lesions including the dominant mass contained susceptibility on gradient\necho imaging.  No new contrast enhancing lesion is identified.  No midline\nshift is seen.\n\nThere is new patchy confluent FLAIR hyperintense signal in the subcortical,\ndeep and periventricular white matter.\n\nThere is no acute infarction.  The ventricles and sulci are normal in caliber\nand configuration.  The major vascular flow voids are preserved.\n\nThere is a 0.9 cm x 0.9 cm exophytic lesion arising from the posterior left\nnasopharynx which is mildly T2 hyperintense and does not demonstrate contrast\nenhancement, medial to the fossa of ___, series 4, image 5, likely\nrepresenting a retention cyst.  Mild fluid is seen in the left mastoid air\ncells.  The orbits are normal.  Minimal fluid is seen and and ethmoid sinuses.\n\nThere is a 0.6 cm exophytic contrast enhancing left temporal scalp skin\nlesion, series 4, image 13.",
            "output": "1. Numerous intracranial metastatic lesions throughout the supra and\ninfratentorium, all of which have demonstrated stability or decrease in size. \nNo new or enlarging intracranial metastatic lesion identified.  Interval\ndecreased edema surrounding the dominant masses.\n2. New posttreatment changes in the white matter.\n3. A 0.6 cm skin lesion in the left temporal scalp.  Correlate with physical\nexam."
        },
        {
            "input": "Numerous enhancing supra and infratentorial lesions are predominately smaller\nin size when compared to prior examination of ___.  The degree of\nsurrounding FLAIR hyperintense white matter signal as also significantly\ndecreased.  For example, a dominant right anterior insular 6 mm lesion (series\n1001b, image 86) previously measured 9 mm.  Many of these lesions demonstrate\nassociated gradient echo susceptibility compatible with hemorrhage,\nessentially unchanged from prior exam.  No definitive new enhancing lesions.\n\nConfluent periventricular white matter T2/FLAIR hyperintensity is similar from\nexamination of ___, likely posttreatment in nature.  Sulci,\nventricles cisterns are unchanged.  There is no ventriculomegaly.  There is no\nacute infarct.  The major intracranial flow voids are preserved.  The dural\nvenous sinuses are patent.  The paranasal sinuses are essentially clear.  The\norbits are unremarkable.  The mastoid air cells again demonstrates fluid\nsignal.  A small exophytic lesion along the left fossa Rosenmueller is stable,\nlikely representing a mucous retention cyst.  Interval decrease size of an\nexophytic left temporal scalp lesion (series 6, image 12).",
            "output": "1. Diffuse supra and infratentorial intracranial metastatic lesions are\ndecreased in size from prior exam with associated decreased surrounding white\nmatter FLAIR hyperintense edema pattern.\n2. No new lesions.\n3. Previously described 6 mm left temporal scalp skin lesion has decreased in\nsize."
        },
        {
            "input": "The study is somewhat limited secondary to patient motion, within these\nlimitation, widespread supra and infratentorial intracranial metastatic\nlesions with internal hemorrhagic products and minimal surrounding edema\neither not visualized or smaller compared to the prior study from ___.  Examples include:  A punctate left cerebellar lesion (100:27),\npreviously 5 mm in size.  Adjacent satellite lesions near this nodule are no\nlonger seen.  A posterior right cerebellar lesion is similar, again measuring\n3 mm (100:29).  A more superior right cerebellar lesion is now 4 mm,\npreviously 6 mm (100:40).  Tiny foci of enhancement in the left aspect of the\nsuperior cerebellar vermis are barely perceptible (100:36), degraded by motion\nartifact.  Tiny foci along the right tentorium is currently 3 mm, previously 7\nmm (100:45).  A right temporal lobe lesion is barely perceptible on the\ncurrent examination, previously 3 mm (100:44).  A peripheral left parietal\nlobe lesion is also barely perceptible on the current study, previously 5 mm\nin size (100:47).  A right frontal cortex lesion is approximately 1 mm in size\ncurrently, previously 5 mm (100:69).  Curvilinear enhancing lesion along the\nright frontal cortex near the vertex on the prior study are barely perceptible\non the current exam (100:97).\n\nNo new lesions are identified.  There is no acute vascular territorial\ninfarction.  No shift of the normally midline structures is identified.  The\nventricles and sulci are normal in size and configuration.  Intracranial\nvascular flow voids are preserved.  The orbits are unremarkable.  A left\ntemporal scan lesion is similar in size allowing for plane of scanning and\nmeasurement technique (100a: 56), approximately 7 mm.",
            "output": "1. Widespread supra and infratentorial intracranial metastatic lesions are\ndecreased in size or resolved compared to the prior examination from ___.\n2. No new lesions are identified."
        },
        {
            "input": "The most inferior left cerebellar hemispheric enhancing lesion is no longer\nseen.  More superiorly, a posterior right cerebellar hemispheric 3 mm lesion\nis unchanged (series 900 image 70).  More superiorly there is a 4 mm enhancing\nfocus in the right cerebellar hemisphere which is stable (series 900, image\n78).  The previously demonstrated right temporal lobe enhancing focus is no\nlonger seen.  The 3 mm medial right temporal lobe lesion is stable (series 900\nimage 81).  A peripheral left temporal lobe lesion is no longer seen.  A\nperipheral right frontal previously 1-2 mm focus of enhancement is not seen. \nThe punctate enhancing focus in the right frontal lobe near the vertex is\nunchanged (series 900, image 132).  Many of these lesions demonstrate foci of\nsusceptibility artifact on gradient echo images compatible with internal\nhemorrhage, as on prior exams.  A\n\nDiffuse hyperintensities in the white matter likely related to therapy are\nunchanged.  A chronic left occipital lobe encephalomalacia are with chronic\nblood products is unchanged.\n\nThe 8 mm scalp enhancing lesion is not appreciably changed (series 900 image\n81).  There is mild right maxillary sinus mucosal thickening; otherwise, the\nimaged paranasal sinuses and mastoid air cells are well aerated.  The globes\nand intraorbital structures are normal.",
            "output": "1. Interval stability or resolution of multiple supra and infratentorial\nenhancing, hemorrhagic metastases.  No new lesions seen.  No new mass, mass\neffect, large hemorrhage, or evidence of acute infarction.\n2. Unchanged 8 mm enhancing left frontal scalp lesion."
        },
        {
            "input": "MR BRAIN:\nThere is expected evolution of the large intraparenchymal hematoma in the left\nfrontal lobe with stable surrounding edema.  There is stable effacement of the\nleft frontal horn without herniation or midline shift.\n\nThere is redistribution of the previously seen subdural hematomas, now\noverlying the left temporal, left frontal and, to a lesser extent, the left\nparieto-occipital lobes.  A tiny subdural hematoma is seen overlying the right\nparietal lobe.\n\nStable foci of subarachnoid hemorrhage are seen along the left parietal and\ntemporal lobes, the sylvian fissures and the frontal lobes.\n\nAreas of slow diffusion are seen the bilateral frontal lobes and left\noccipital lobe.\n\nAreas of hemorrhage are seen along the tract of the right frontoparietal shunt\ncatheter, which has since been removed.  A small subgaleal and scalp hematoma\nis seen in the region of the catheter placement.\n\nThere is worsening enlargement of the bilateral lateral and third ventricles. \nThe fourth ventricle is normal in size. There is significant improvement in\nthe degree of intraventricular blood products, now with minimal layering seen\nwithin the occipital lobes, left greater than right.\n\nThere is moderate mucosal thickening of the sphenoid sinuses.\n\nMRA brain:\nThe internal carotid arteries are patent.\n\nThe patient is post coiling of an anterior communicating artery aneurysm.  No\nresidual aneurysm is seen.  There is patency of the anterior cerebral arteries\nat the A2 segments and distally.  A hypoplastic right A1 segment is seen. \nThere is stable mild narrowing of the left pericallosal and callosomarginal\narteries.\n\nThere is mild narrowing of the left M2 and M3 segments.  The right middle\ncerebral artery is patent.\n\nThere is multifocal narrowing of the bilateral posterior cerebral arteries,\npresumably due to atherosclerotic disease.  The vertebrobasilar system is\npatent, with a dominant right vertebral artery.",
            "output": "1. Status post removal of the right ventricular shunt catheter.  Worsening\nenlargement of the bilateral lateral and third ventricles.  Normal-sized\nfourth ventricle.\n2. Improvement in degree of intraventricular hemorrhage.\n3. Expected evolution of the large intraparenchymal hematoma in the left\nfrontal lobe with stable surrounding edema, causing effacement of the left\nfrontal horn without herniation or midline shift\n4. Redistribution of the previously seen subdural hematomas, now overlying the\nentire left cerebral hemisphere.  Tiny subdural hematoma over the right\nparietal lobe.\n5. Subacute infarct involving the bilateral frontal and left occipital lobes.\n6. Stable foci of subarachnoid hemorrhage in the left parietal and temporal\nlobes, the sylvian fissures and frontal lobes.\n7. Stable mild narrowing of the left pericallosal and callosomarginal\narteries, likely due to vasospasm.\n8. Mild narrowing of the left M2 and M3 segments.\n9. Multifocal narrowing of the PCAs, presumably due to atherosclerotic\ndisease.\n10. Status post coiling of an A-comm aneurysm with no residual aneurysm seen."
        },
        {
            "input": "MRI Brain:\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  FLAIR hyperintense signal is noted in the suprasellar cistern\nand sulcus of the bilateral gyrus rectus.  No abnormal signal is seen on the\nremainder of the sequences and this is likely artifactual in nature.  The\nventricles and sulci are normal in caliber and configuration.  The previously\nidentified pituitary lesion is not well visualized on this study.\n\nThere is minimal mucosal thickening in the ethmoid sinuses.\n\nMRA brain: The intracranial vertebral and internal carotid arteries and their\nmajor branches appear normal without evidence of stenosis, occlusion, or\naneurysm formation.\n\nMRV brain:  There is normal opacification of the superior sagittal sinus,\nstraight, transverse and sigmoid sinuses.  No filling defect or occlusion is\nidentified.\n\nMRA neck:  The common, internal and external carotid arteries appear normal. \nThere is no evidence of internal carotid artery stenosis by NASCET criteria. \nThe origins of the great vessels, subclavian and vertebral arteries appear\nnormal bilaterally.",
            "output": "1. No acute intracranial abnormality.  No acute infarct.\n2. Normal MRA and MRV of the brain.  Normal MRA of the neck."
        },
        {
            "input": "The examination is motion degraded.  Within these confines:\n\nSlow diffusion of the right insula, posterior putaminal extending into the\ncentrum semiovale and subependymal right lateral ventricle body is compatible\nwith a right lateral lenticulostriate distribution infarct.  Additional\nequivocal foci of equivocal diffusion-weighted hyperintense signal of the\nperipheral right precentral gyrus (series 4, image 19 and 18) may also\nrepresent additional regions of infarct.  Left frontal and right inferior\ncerebellar encephalomalacia is unchanged since ___.  Right occipital lobe\nencephalomalacia is new since examination of ___.  There is no evidence of\nacute intracranial hemorrhage.  The major intracranial flow voids are\npreserved.  The paranasal sinuses are essentially clear.  The orbits are\nunremarkable.  Mastoid air cells are clear.",
            "output": "1. Findings compatible with a right lateral lenticulostriate distribution\ninfarct as well as additional foci of peripheral diffusion-weighted\nhyperintense signal without clear ADC hypointense correlate of the peripheral\nright prefrontal gyrus.\n2. Left frontal, right inferior cerebellar and right occipital lobe\nencephalomalacia.  The right occipital lobe encephalomalacia is new since a\n___.\n3. Allowing for motion degraded sequences, no evidence of large acute\nintracranial hemorrhage."
        },
        {
            "input": "Examination is moderately limited by motion artifact.  Within these\nlimitations:\n\nPatient is intubated and there is an upper enteric tube in place.  There is\nassociated partial fluid opacification of the posterior nasopharynx.  No gross\nexophytic mass is seen.  There is no lymphadenopathy by imaging criteria.  The\nsalivary glands are grossly unremarkable for is the visualized paranasal\nsinuses are grossly clear.  The imaged portion of the brain is grossly\nunremarkable.  Nonspecific bilateral mastoid fluid is noted, which may be\nrelated to intubation status.\n\nMultiple right lobe T2 hyperintense thyroid nodules measuring up to 10 mm are\nnoted.",
            "output": "1. Examination is highly limited by motion, lack of contrast and intubation\nstatus, which causes fluid layering within posterior nasopharynx and\nsupraglottic neck, rendering the examination nondiagnostic for the evaluation\nof oropharyngeal masses.\n2. No cervical lymphadenopathy.\n3. Multiple right lobe thyroid nodules measuring up to 10 mm.  The ___\nCollege of Radiology guidelines suggest that in the absence of risk factors\nfor thyroid cancer, no further evaluation is recommended.\n\nRECOMMENDATION(S):  If clinically indicated, consider contrast neck CT for\nfurther evaluation, preferably after extubation."
        },
        {
            "input": "The examination is moderately to severely motion degraded.  Within this\nconfine:\n\nThere is an apparent 4.0 x 2.7 cm left frontal parietal lobe mass\ndemonstrating peripheral rim of gradient echo susceptibility\ndiffusion-weighted hypointense signal, suggestive of trace hemorrhage product.\nProminent left hemispheric edema pattern is identified, resulting in\neffacement of the left lateral ventricle and approximately 1 cm rightward\nmidline shift.  There is minimal mass-effect on the left aspect of the\nmidbrain.  The basilar cisterns are patent.  There is no acute infarct.  No\ndefinitive hydrocephalus.  The major intracranial flow voids are preserved. \nThere is mild mucosal thickening of the ethmoid air cells and partial\nopacification of the sphenoid sinuses.  The orbits are unremarkable.",
            "output": "1. Moderately to severely motion degraded examination without FLAIR or\npostcontrast images performed secondary to patient intolerance.  Within this\nconfines:\n2. Apparent heterogeneous 4 cm mass in the left frontal parietal lobe with\nsuggestion of scattered pleural gradient echo susceptibility, which may\nrepresent hemorrhage product.  Prominent left hemispheric white matter edema\npattern results in 1 cm rightward midline shift and effacement of left lateral\nventricle.  The basilar cisterns remain patent.\n3. Recommend repeat examination when clinically feasible with contrast."
        },
        {
            "input": "Re-identified is a heterogeneously rim enhancing left parieto-occipital mass\nmeasuring up to 45 x 39 x 41 mm (___: ___ a: 107), with areas of\nslowed diffusion and susceptibility artifact denoting hemorrhage.  There is\nprominent surrounding vasogenic edema extending throughout the left cerebellar\nhemisphere.  There is prominent associated mass effect with effacement of the\nadjacent sulci and up to 8 mm rightward midline shift.  There is associated\neffacement of the left lateral ventricle.  There is associated mass effect and\nrightward shift of the mid brain.  The basal cisterns remain patent.  There is\nno uncal herniation.\n\nBackground areas of periventricular, subcortical and deep white matter\nT2/FLAIR hyperintensity likely represents the sequela of chronic small vessel\nischemic disease.  Punctate foci of chronic microhemorrhage are noted in the\nleft occipital lobe and left temporal lobe.  There is no evidence of acute\nterritorial infarct.  The background ventricular system appears mildly\nprominent, likely representing age-related involutional change.  There is no\ndefinite hydrocephalus.  The principal intracranial vascular flow voids are\npreserved.\n\nThere is fluid layering in the posterior nasopharynx, likely secondary to\nintubation.  There is moderate right and mild left polypoid mucosal wall\nthickening in the sphenoid air cells.  There is minimal mucosal wall\nthickening of the posterior ethmoid air cells.  The remainder the visualized\nparanasal sinuses are clear.  The orbits are grossly unremarkable.  There is\nminimal has occasion of a few right-sided mastoid air cells.  The left-sided\nmastoid air cells are clear.",
            "output": "1. 45 x 39 x 41 mm hemorrhagic heterogeneous rim enhancing left\nparieto-occipital mass with prominent surrounding vasogenic edema, mass effect\nand up to 8 mm of rightward midline shift.  This appearance is most suspicious\nfor high-grade glial neoplasm.\n2. This examination was performed for pre-surgical planning."
        },
        {
            "input": "There are postsurgical changes from left parietal craniotomy and mass\nresection with underlying dural thickening and enhancement, fluid within the\nresection cavity with associated postoperative blood product and expected\nsmall to moderate pneumocephalus.  Within the inferomedial aspect of the\nresection bed, there remains at least 34 x 17 mm area of enhancement,\nextending towards the ependymal surface of the left lateral ventricle.  Some\nenhancing portion is seen extending slightly superior and laterally.  There\nappears to be no residual enhancing component within the superior aspect of\nthe resection bed.  Prominent surrounding FLAIR hyperintensity in the left\ncerebral hemisphere appears largely unchanged, though with slight reduction of\nassociated mass effect due to the resection.  There continues to be effacement\nof the localized sulci, effacement of the left lateral ventricle, and up to 8\nmm of rightward midline shift.\n\nNo new enhancing masses identified.\n\nThere is an ovoid area of slow diffusion in the right parietal corona radiata\n(06:21), with subtle associated FLAIR signal abnormality (11:16) compatible\nwith acute to early subacute infarct.  The principal intracranial vascular\nflow voids are preserved.  The dural venous sinuses are patent on MP-RAGE\nimages.  Scattered background areas of periventricular, subcortical and deep\nnonspecific white matter T2/FLAIR hyperintensities are unchanged.  Punctate\nareas of chronic microhemorrhage in the left occipital lobe and left temporal\nlobe are unchanged.\n\nThere is nonspecific layering fluid within the bilateral sphenoid sinuses. \nThe remainder the visualized paranasal sinuses are grossly clear.  The orbits\nare grossly unremarkable.  There is opacification of a few inferior right\nmastoid air cells.  The left mastoid air cells are clear.",
            "output": "1. Postsurgical changes from left parietal craniotomy and mass resection, with\nresidual areas of enhancement within the inferomedial aspect of the resection\nbed, as described.  Prominent surrounding FLAIR signal abnormality throughout\nthe left hemisphere is overall unchanged compared the prior examination,\nthough with some reduction of mass effect given resection, with persistent 8\nmm of rightward midline shift.\n2. Small acute to late acute infarct in the right parietal corona radiata.\n3. No new enhancing mass.\n\nNOTIFICATION:  The findings were discussed with ___, M.D. by\n___, M.D. on the telephone on ___ at 1:22 pm, 5 minutes after\ndiscovery of the findings."
        },
        {
            "input": "The patient remains status post a left parietal craniotomy with tumor\nresection.  Expected postoperative changes are again seen, including dural\nthickening and linear enhancement, with multiple small punctate foci of\nadjacent chronic hemorrhagic products..  There is 0.6 cm chronic subdural\nhematoma overlying anterior left frontal lobe, extending posteriorly to the\ncraniotomy flap.\n\nPersistent ring enhancement is noted surrounding the resection cavity in the\nleft parietal lobe, extending towards the ependyma surface of the left lateral\nventricle, without reaching ependyma surface..  Most notably, an area of\nclustered peripheral linear and nodular enhancement surrounding surgical\ncavity along the inferomedial aspect of the resection bed measures 1.9 x 1.2\ncm (1100:104), previously measuring 3.5 x 1.5 cm on the prior examination. \nLargest nodular component measures 0.6 cm today.  The overall extent of\nsurrounding T2/FLAIR hyperintensity has significantly decreased as compared to\nthe prior examination.  There is no significant local mass effect, sulcal\neffacement, or residual left ventricular effacement.  Diffusion-weighted\nimages are difficult to interpret given blood products marginating surgical\ncavity.\n\nThere is no evidence of acute infarction.  A previously noted acute/subacute\ninfarction within the right parietal corona radiata no longer demonstrates\nrestricted diffusion, and now appears chronic.  There is no acute intracranial\nhemorrhage identified.  Several punctate micro hemorrhages within the left\noccipital lobe are chronic and unchanged.\n\nThe ventricles and sulci are mildly prominent, suggestive of cerebral atrophy.\nPeriventricular and subcortical white matter T2 hyperintensities are likely\nsecondary to chronic small vessel ischemic disease.  There few small chronic\nlacunar infarcts.  The basal cisterns are patent.  Left V4 segment of\nvertebral artery has diminished flow void, is significantly narrowed, stable\ncompared to prior, likely atherosclerotic.  The principal intracranial\nvascular flow voids are preserved.  The dural venous sinuses appear patent on\nthe MP-RAGE sequences.\n\nThe visualized paranasal sinuses and middle ear cavities cells are well\naerated and clear.  Several bilateral mastoid air cells are partially\nopacified.  The orbits are within normal limits bilaterally.",
            "output": "1.  Persistent contrast enhancement surrounding surgical resection margins,\nsome nodular, overall decreased since prior.  Continued follow-up recommended.\n2.  Status post left parietal approach craniotomy and tumor resection, with\n0.6 cm thick chronic subdural hematoma.\n3.  Severe narrowing left vertebral artery V4 segment.\n4.  Remainder as above"
        },
        {
            "input": "Stable postoperative changes status post left parietal craniotomy relating to\nglioblastoma tumor resection.  No change to slight decrease in dural\nthickening/enhancement adjacent to the resection bed as well as the multiple\npunctate foci of adjacent chronic blood products.\n\nNo significant change in peripheral enhancement surrounding the resection\ncavity in the left parietal lobe that extends toward but not reaching the\nependymal surface of the left lateral ventricle.  The enhancement is more\nnodular in appearance inferiorly, which is also unchanged with the largest\nnodular component measuring 1.9 x 0.8 cm (series 101, image 80).  There is no\nnew enhancing lesion.\n\nModerate scattered and confluent subcortical and deep white matter T2/FLAIR\nhyperintensities are similar to slightly increased and may represent a\ncombination of post radiation treatment changes and/or chronic small vessel\ndisease.\n\nThe previously described chronic left subdural hematoma has essentially\nresolved.\n\nThere is no evidence of acute hemorrhage or acute infarction.  There is\ndiffuse prominence of the ventricles and sulci compatible with age related\ninvolutional changes.  The orbits, paranasal sinuses and mastoid air cells are\nunremarkable.  The major intracranial flow voids are preserved.  The dural\nvenous sinuses are patent.",
            "output": "1. Stable postoperative changes of a left parietal craniotomy relating to\nglioblastoma tumor resection.\n2. Unchanged appearance of the left parietal resection bed, which demonstrates\nnodular periphery enhancement inferiorly.\n3. Resolution of the previously described chronic small left subdural\nhematoma.\n4. No change to slight increase in the scattered and confluent subcortical and\ndeep white matter T2/FLAIR hyperintensities that may represent a combination\nof post radiation treatment changes and/or chronic small vessel disease."
        },
        {
            "input": "Postsurgical changes are again seen consistent with left parietal craniotomy,\nthe patient is status post glioblastoma resection, in comparison with the most\nrecent exam grossly no significant changes are demonstrated in the surgical\nbed, with persistent nodular enhancement measuring approximately 8 x 20 mm in\ntransverse dimension, no new areas with abnormal enhancement are demonstrated.\nT2 shine through changes are demonstrated on the diffusion-weighted images\nwith no evidence of slow diffusion to indicate acute or subacute ischemic\nchanges.  Similar FLAIR hyperintensity signal is seen in both centrum\nsemiovale and surgical area consistent with a combination of underlying\nchronic microvascular disease and posttreatment changes.  No new lesions or\nnew areas with abnormal enhancement are seen.  The major vascular flow voids\nare present and demonstrate normal distribution.  The orbits are unremarkable,\nthe paranasal sinuses are notable for mucosal thickening in the sphenoid\nsinus,, right ethmoidal air cells, there is patchy mucosal thickening of both\nmastoid air cells.",
            "output": "1.  Postsurgical changes consistent with left parietal craniotomy remain\ngrossly unchanged.\n\n2.  Similar pattern of nodular enhancement in the surgical bed is consistent\nwith posttreatment changes, however residual mass cannot be completely\nexcluded and long-term follow-up is recommended to demonstrate stability or\nany further changes.  No new areas with abnormal enhancement are seen.\n\n3.  Similar pattern of high-signal intensity is noted in the centrum semiovale\nand subcortical white matter, likely consistent with a combination of chronic\nmicrovascular ischemic disease and posttreatment changes.\n\n4.  Mucosal thickening is noted in the sphenoid sinus, right ethmoidal air\ncells, and patchy mucosal thickening is noted in mastoid air cells\nbilaterally."
        },
        {
            "input": "Left parietal craniotomy is identified.  Area of FLAIR hyperintensities and\nenhancement are seen in the left parietal region.  Since the previous study\nthere has been interval change in the appearance of the surgical cavity but\noverall the degree and size of the enhancement has not significantly changed. \nThe surrounding hyperintensities are also unchanged on the FLAIR images.  Mild\ndiffuse hyperintensities in the white matter indicate posttreatment changes. \nAt the site of resection a small area of restricted diffusion is seen\ndecreased in size from the previous study.  Overall the enhancement has\ndecreased compared to the examination of ___.  There is no midline shift\nor hydrocephalus.  No new areas of enhancement are seen..",
            "output": "Overall the size of enhancement and surrounding FLAIR hyperintensities are\nunchanged although the configuration of enhancement has changed since the\nprevious study.  The surrounding restricted diffusion has decreased.  No new\nsignal abnormalities or enhancement seen."
        },
        {
            "input": "Postoperative changes in the left parietal region identified with enhancement\nat the surgical site and also enhancing deeper to the surgical margin towards\nthe ventricular surface (11:17) are unchanged in size and configuration.  The\nsurrounding FLAIR hyperintensities are also unchanged.\n\nHowever, new since the prior studies a small focus of FLAIR abnormality\n(08:17), diffusion abnormality (602:21) and enhancement (11:17).  It is\nunclear whether this is due to a satellite site of tumor enhancement or due to\na subacute infarct which demonstrate enhancement.  This area should be\nassessed on the follow-up examination.\n\nThere are extensive white matter hyperintensities and prominence of sulci\nunchanged from the prior study.  A small left-sided subdural collection is\nalso unchanged.",
            "output": "1. Small punctate focus of new signal abnormality and enhancement in the left\nside of the body of the corpus callosum could be due to satellite focus of\ntumor enhancement or subacute infarct with enhancement.  This area should be\nclosely followed.\n2. Size and degree of enhancement and surrounding FLAIR hyperintensities in\nthe left parietal lobe are unchanged."
        },
        {
            "input": "Study is mildly degraded by motion.\n\nStatus post left parietal craniotomy for mass resection with a grossly stable\nenhancement at the medial margin of the surgical site.  Grossly stable minimal\nrestricted diffusion along medial resection cavity margin without definite\nassociated enhancement, and again demonstrating grossly stable T2 and FLAIR\nhyperintensities again seen (see 500:23 on current study and 6; 23 on prior\nexam).  Associated surrounding FLAIR signal abnormality is grossly stable. \nRedemonstrated is confluent white matter FLAIR signal abnormality involving\nthe left greater than right cerebral hemispheres, which may be related to\ntreatment related effects and/or microangiopathic changes.  A few foci of\nsusceptibility on gradient echo images within the resection cavity is\ncompatible with old blood products, unchanged.\n\nThere is trace extra-axial fluid over the medial left frontal convexity,\nunchanged.\n\nThere has been a slight increase in size of a 0.6 cm focus of enhancement at\nthe left body of the corpus callosum (9:104).  As before, this lesion\ndemonstrates corresponding FLAIR signal and diffusion abnormality.\n\nThere is no evidence of intracranial hemorrhage or acute infarction. \nProminence of the ventricles and cerebral sulci are compatible with age\nrelated involutional changes, unchanged.\n\nGrossly stable right parietal calvarium probable hemangioma is again noted\n(see 9:141 on current study and 10:153 on prior exam).\n\nThe major intracranial vascular flow voids are maintained.  There is a mild\namount of nonspecific fluid within the right mastoid air cells.  Mild mucosal\nthickening of the ethmoid air cells.  Status post bilateral lens replacements.",
            "output": "1.  Study is mildly degraded by motion.\n2. Slight increase in prominence of a 0.6 cm focus of enhancement of the left\nbody of the corpus callosum raises concern for a satellite tumor focus\ncompared to ___ prior exam.\n3. Status post left parietal craniotomy for mass resection with grossly stable\nenhancement and nonenhancing restricted diffusion at medial margin of the\nresection site.  While finding may be related to postoperative changes,\nrecurrent or residual tumor is not excluded on the basis of this examination.\n4. Unchanged associated FLAIR signal abnormality surrounding resection site.\n5. Stable confluent white matter FLAIR signal abnormality involving the left\ngreater than right cerebral hemispheres likely represents combination of post\ntreatment change in small-vessel disease.\n6. Grossly stable nonspecific left hemisphere small subdural collection.\n7. Paranasal sinus disease and nonspecific right mastoid fluid, as described."
        },
        {
            "input": "MR BRAIN: Enhancement in the left side of the corpus callosum is more\nprominent than on the study of ___.  Enhancement adjacent to the\nsurgical site appears unchanged.  Extensive white matter FLAIR hyperintensity\nthat may represent tumor infiltration, treatment effect, or both appears\nunchanged.  No new lesions are identified.\n.\nDynamic susceptibility contrast Perfusion: There is no evidence of elevated\nrelative blood flow or blood volume in the enhancing regions..\n\nASL Perfusion: There is no evidence of increased blood flow in the enhancing\nregions..\n\nDiffusion imaging: There is slow diffusion in the corpus callosum lesion and\nin areas corresponding to enhancement at the depth of the surgical site.\n\nMR Spectroscopy: There is marked choline elevation in a voxel overlying the\ndepth of the surgical site, including the region of enhancement.  Spectroscopy\nwas not performed over the corpus callosum lesion..",
            "output": "1. Enlargement of an enhancing focus in the left side of the corpus callosum\nsince ___.  This area demonstrates slow diffusion.  Spectroscopy was\nnot\n2. This finding presumably represents a region of tumor progression.\n3. Enhancement at the surgical site appears unchanged."
        },
        {
            "input": "Re-demonstrated is a 0.8 x 0.5 x 0.8 cm focus of enhancement along the left\nbody of the corpus callosum (4:67), similar in size and appearance to the\nprior study from ___.\n\nPersistent enhancement along the surgical site in the left parietal lobe\nappears unchanged.\n\nNo new enhancing lesions are identified.",
            "output": "1. 8 mm focus of enhancement along the left body of the corpus callosum is\nre-demonstrated.  Attention on follow-up is recommended.\n2. Persistent enhancement of the left parietal lobe surgical site.  No new\nenhancing lesions."
        },
        {
            "input": "Slight interval increase in size of the enhancing lesion along the left body\nof the corpus callosum (series 17, image 114) now measuring 0.9 x 0.8 x 0.8 cm\n(AP X TR X SI) from previously 0.8 x 0.5 x 0.8 cm.  There is unchanged DWI\nhyperintensity within this lesion and also within an area of enhancing soft\ntissue nodules in the initial resection site (series 17, image 119).\nThere is no new focus of abnormal enhancement.\n\nThere is stable FLAIR hyperintensity about the resection site.  Unchanged\nFLAIR hyperintensity about both lateral ventricles as well as unchanged\nT2/FLAIR hyperintensities in the cerebral hemispheres bilaterally, a\nnonspecific finding and likely related with posttreatment changes and chronic\nsmall vessel ischemic changes.\n\nThere is no evidence of acute intracranial hemorrhage, midline shift or acute\nterritorial infarction.\n\nThere is mild generalized parenchymal volume loss, most likely age related. \nMild prominence of the ventricular system and extra-axial CSF spaces is\nconsistent with the previously mentioned parenchymal volume loss.\n\nThe paranasal sinuses and mastoid air cells are essentially clear.  Note is\nmade of a bilateral insert replacement surgeries.  The orbits appear otherwise\nunremarkable.",
            "output": "1. Slight interval increase in size of the enhancing lesion along the left\nbody of the corpus callosum measuring 0.8 x 0.8 x 0.8 cm (AP X TR X SI) from\npreviously 0.8 x 0.5 x 0.8 cm.\n2. Persistent area of nodular soft tissue enhancement in the left parietal\nlobe resection site, unchanged.\n3. No new focus of abnormal enhancement."
        },
        {
            "input": "In comparison with the most recent exam dated ___, again there\nis interval increase in size of the previously described enhancing lesion\ncentered along the left body of the corpus callosum measuring approximately 15\nx 7.6 mm in transverse dimension, and previously 8 x 6 mm, and approximately\n15 x 6.6 mm in coronal projection and previously 9 x 5 mm.  There is unchanged\nDWI high-signal intensity within this lesion, and also within the area of\nenhancing in the  nodules in the initial resection cavity, which appears\nslightly more conspicuous, however with no evidence of new enhancing areas. \nThere is persistent pachymeningeal thickening, likely reactive and\npostsurgical in nature.\n\nUnchanged T2/FLAIR high-signal intensity around the resection site, and along\nthe subcortical and periventricular white matter, likely consistent with a\ncombination of posttreatment changes, underlying chronic microvascular and\nlacunar ischemic disease.  Prominent ventricles and sulci remain unchanged,\nsuggesting cortical volume loss.\n\nNo diffusion abnormalities are detected to indicate or suggest acute ischemic\nchanges.  There is no evidence of acute intracranial hemorrhage.  The major\nvascular flow voids are present and demonstrate normal distribution.  The\norbits are unremarkable, the paranasal sinuses, middle ear cavities and\nmastoid air cells are clear.",
            "output": "1.  In comparison with the most recent examination, again there is mild\ninterval increase in size of the previously noted enhancing lesion along the\nleft body of the corpus callosum as described detail above, in this area there\nis persistent slow diffusion suggesting tumoral activity.\n\n2.  Persistent area of nodular soft tissue enhancement in the left parietal\nregion and resection area, consistent with postsurgical changes.  Allowing for\nthe slice selection and technique, the pattern of enhancement at the surgical\nsite is slightly more conspicuous, however no new areas of abnormal\nenhancement in the surgical cavity are seen.\n\n3.  Unchanged T2/FLAIR high-signal intensity around the resection site, and\nalong the subcortical periventricular white matter, likely consistent with a\ncombination of posttreatment changes and underlying chronic microvascular\nischemic disease."
        },
        {
            "input": "Patient is status post resection left parietal glioblastoma with persistent\npostoperative changes noted in the surgical bed.  Curvilinear and nodular\nenhancement within the surgical bed has increased compared to ___.  There are areas of slow diffusion within the area of enhancement in the\nsurgical bed as on prior studies.  No new lesion within the surgical bed.  The\nT1 and T2 hypointense 1.3 x 0.7 x 0.9 cm (TV by AP by CC) lesion with\nperipheral enhancement in the body of the left corpus callosum has decreased\nenhancement compared to ___, although it is larger in size. The\nlesion again demonstrates slowed diffusion.  T2/FLAIR hyperintensity in the\nbilateral periventricular and subcortical region and adjacent to the surgical\nsite could represent a combination of posttreatment changes and chronic small\nvessel ischemic changes.  Asymmetric left pachymeningeal thickening is similar\nto ___ which is post treatment in nature.\n\nNo evidence new mass, hemorrhage, or infarction.  Enlargement of the lateral\nventricles are unchanged.  Major intracranial flow voids are preserved.  The\ndural venous sinuses are patent.\n\nThere is mild mucosal thickening of the ethmoid air cells.  Otherwise the\nparanasal sinuses and bilateral mastoid air cells are unremarkable.  Patient\nis status post bilateral lens replacements.  Otherwise the orbits are\nunremarkable.  Post left parietal craniotomy changes are noted.  No abnormal\nbone signal abnormalities.",
            "output": "1. Interval increase curvilinear and nodular enhancement within the left\nparietal surgical bed.\n2. Interval decrease enhancement but larger size of a 1.3 x 0.7 x 0.9 cm\nlesion in the body of the left corpus callosum.\n3. No new enhancing lesions."
        },
        {
            "input": "Study is mildly degraded by motion.\n\nPostsurgical changes related to patient's left parietal mass resection are\nagain noted.\n\nQuestion minimal interval progression in size of left corpus callosum mass\nwith restricted diffusion, demonstrating faint peripheral enhancement 6 (see\n6, 07:22; 12, 16:17 on current study and 500, 502:20; 4, 10:16 on ___ prior exam).  Additional nonspecific curvilinear enhancement overlying\nthe surgical bed is again seen (see 18:14 on current study 900:57 on ___ prior exam).\n\nMass with grossly stable restricted diffusion along medial resection cavity\nmargin, demonstrate interval progression of heterogeneous enhancement (see 6,\n07:23; 12, 16:16 on current study and 500, 502:22; 10:16 on ___\nprior exam).\n\nExtensive supratentorial T2 and FLAIR white matter hyperintensities are again\nseen.\n\nThere is no evidence of midline shift or infarction.   The ventricles and\nsulci are stable in caliber and configuration.  Minimal nonspecific right\nmastoid fluid is seen.  Bilateral ethmoid air cell and maxillary sinus mucosal\nthickening is present.  Bilateral lens replacement postoperative changes are\nnoted.",
            "output": "1. Study is mildly degraded by motion.\n2. Postsurgical changes related to known left parietal mass resection with\nnonspecific overlying enhancement.\n3. Question interval minimal progression in size of faintly enhancing left\ncorpus callosum mass as described, concerning for tumor progression.\n4. Left parietal resection cavity medial margin mass with interval progression\nof heterogeneous enhancement and grossly stable restricted diffusion as\ndescribed.\n5. Grossly stable size supratentorial diffuse white matter parenchymal signal\nintensity abnormality as described.  While findings may represent treatment\neffects, edema is not excluded on the basis examination.\n6. Within limits of study, no definite evidence of new enhancing intracranial\nmass."
        },
        {
            "input": "Again seen are postoperative changes after left parietal craniotomy for tumor\nresection.  There has been a marked increase in enhancement at the surgical\nsite.  There has been an increase in FLAIR hyperintensity surrounding the\nenhancing lesion since the study of ___.  Again seen and largely\nunchanged is a minimally enhancing area of FLAIR hyperintensity and slow\ndiffusion in the left side of the corpus callosum extending into the adjacent\nwhite matter.  In spite of the enlargement of the enhancing compon\nEnt of the tumor, the extent of slow diffusion within the enhancing tumor has\ndecreased since the prior study.\nOverall, the increase in contrast-enhancement is worrisome for tumor\nprogression, as is the increase in FLAIR abnormality, potentially a\ncombination of edema and tumor infiltration.  However, if there has been a\nreduction in avastin, this may be responsible for both the increase in\nenhancement and increase in FLAIR abnormality.\nNo other lesions are detected.  The remaining bilateral white matter\nhyperintensity on FLAIR appears unchanged and is likely treatment related. \nThere are small foci of chronic hemorrhage at the surgical site.  There is no\nevidence of new hemorrhage.",
            "output": "1. Persistent area of FLAIR hyperintensity, faint enhancement and slow\ndiffusion in the left corpus callosum extending into the adjacent white\nmatter.\n2. Increased volume of tumor enhancement at the left parietal surgical site\nwith increase in surrounding FLAIR white matter abnormality.\n3. This latter finding may reflect tumor progression or, with the appropriate\nhistory, a reduction in anti angiogenesis medication."
        },
        {
            "input": "Postoperative changes from left parietal craniotomy are again demonstrated. \nSince the previous examination, there has been interval increase in size and\nenhancement of the underlying lesion in the parietal lobe, with further\nextension into the superior body of the corpus callosum and new involvement of\nthe septum pellucidum.  There are multiple areas of associated slowed\ndiffusion in the parietal lobe tumor site as well as in the corpus callosum\nextending into the septum pellucidum all associated with enhancing lesions. \nThere is extensive surrounding T2 prolongation, which has increased from the\nprevious examination particularly with respect to involvement of the frontal\nparietal operculum as well as portions of the lateral parietal lobe with\nincreased mass-effect on the posterior body and atrium of the left lateral\nventricle compared to the previous exams.\n\nAreas of T1 shortening and susceptibility in the tumor correspond to\nhemorrhage in calcifications as seen on CT.\n\nThere are no other lesions.  Other areas of confluent T2 prolongation in the\nwhite matter appear similar to the previous exams.  Chronic lacunar infarcts\nin the thalami are noted.\n\nThe major intracranial vascular flow voids are preserved.  Bilateral lens\nreplacements are noted.  There is minimal patchy fluid signal in the inferior\nmastoid air cells.   Small mucous retention cyst in the inferior maxillary\nsinus.  There is mild mucosal thickening scattered in the ethmoid air cells.",
            "output": "1. Increase in extent of enhancing tumor involving the left parietal surgical\nsite, corpus callosum, and now extending into the septum pellucidum. \nIncreased surrounding FLAIR signal changes, with increased mass-effect on the\nleft lateral ventricle but no shift of the midline structures."
        },
        {
            "input": "Study is moderately degraded by motion.  Within these confines:\n\nThere are small acute infarctions in the posterior inferior right cerebellar\nhemisphere.\n\nThere is no evidence of hemorrhage, masses, mass effect, or midline shift. \nThere is prominence of the ventricles and sulci suggestive involutional\nchanges.  Periventricular and subcortical T2 and FLAIR hyperintensities are\nnoted. There is an empty sella.  The major vascular flow voids are preserved.\n\nBilateral cataract extractions are seen.  There is opacification of the right\nmastoid air cells.  Mucosal thickening and retention cysts are noted in the\nleft maxillary sinus.  Mucosal thickening is also seen in the ethmoid sinus.\n\nDegenerative changes are noted in the visualized upper cervical spine.",
            "output": "1.  Study is moderately degraded by motion.\n2. Small right ___ distribution cerebellar acute infarcts as described, with\nno evidence of hemorrhagic transformation.\n3. Chronic changes as described.\n4.  Paranasal sinus disease as described."
        },
        {
            "input": "There is no evidence of intracranial hemorrhage, edema, masses, mass effect,\nmidline shift or infarction.  No diffusion abnormalities are detected.  Small\nfocus of blooming artifact in the right frontal lobe white matter near the\nvertex could reflect a chronic microhemorrhage or mineralization (12:23).  The\nventricles and sulci are normal in caliber and configuration.\n\nThere is mild mucosal thickening of the anterior ethmoid air cells.  The\norbits are unremarkable.",
            "output": "1. No evidence of acute intracranial hemorrhage, infarction, or mass. The\ncerebellum is unremarkable.\n2. Punctate focus of blooming in the right frontal lobe near the vertex could\nreflect a chronic microhemorrhage versus mineralization."
        },
        {
            "input": "There is no evidence for a mass or leptomeningeal contrast enhancement along\nthe trigeminal nerves.  Bilateral superior cerebellar arteries common close\nproximity with the bilateral trigeminal nerve root entry zones.  Meckel caves\nand cavernous sinuses appear symmetric and unremarkable.\n\nElsewhere in the intracranial compartment, there is no evidence for an\nenhancing mass or acute infarction.  There is a small developmental venous\nanomaly in the right middle frontal gyrus, images 18: 116-120.  There is no\nevidence for an associated cavernous malformation or other intracranial blood\nproducts.  Several small foci of high signal on T2 weighted and FLAIR images\nwithin bifrontal periventricular and deep white matter are nonspecific.  Major\nvascular flow voids are grossly preserved.  Dural venous sinuses are patent on\npostcontrast MP RAGE images.\n\nThere is mild mucosal thickening in the ethmoid air cells and maxillary\nsinuses.",
            "output": "1. No evidence for a mass or leptomeningeal enhancement along the trigeminal\nnerves. Bilateral superior cerebellar arteries common close proximity with the\nbilateral trigeminal nerve root entry zones, but any clinical significance of\nthis finding cannot be determined based on imaging.\n2. Small developmental venous anomaly in the right middle frontal gyrus.  No\nevidence for associated cavernous malformation.\n3. Several small T2 hyperintense foci within bifrontal white matter are\nnonspecific and may sometimes be seen in asymptomatic patients.  Diagnostic\nconsiderations also include migraine related lesions and sequela of\ninflammation."
        },
        {
            "input": "MR BRAIN:\nMillimetric focus of high signal on diffusion-weighted images located in the\nparamedian left frontal (302:21) is likely an artifact, please correlate.  No\nconvincing evidence of acute territorial infarct is identified.\nThere is no evidence of intracranial hemorrhage,edema,masses,mass\neffect,midline shift orinfarction.  Extensive confluent periventricular white\nmatter T2/FLAIR hyperintensity is likely secondary to chronic small vessel\ndisease.  Prominent ventricles and sulci likely reflect involutional changes. \nThe patient is status post bilateral lens replacement, otherwise the orbits\nare unremarkable, the paranasal sinuses and mastoid air cells are clear.\n\nMRA brain: The intracranial vertebral and internal carotid arteries and their\nmajor branches appear normal without evidence of stenosis, occlusion, or\naneurysm formation.\n\nOther findings: Multilevel degenerative changes are visualized in the upper\ncervical spine, partially evaluated in this exam.",
            "output": "1. No acute territorial infarct is identified.\n2. Millimetric focus of high signal on diffusion-weighted images located in\nthe paramedian left frontal (302:21) is likely an artifact, please correlate.\n3. Extensive confluent periventricular white matter T2/FLAIR high-signal\nintensity, which is a nonspecific finding and may reflect chronic\nmicrovascular ischemic disease.\n4. Major intracranial arteries are patent without dissection."
        },
        {
            "input": "There are numerous periventricular oblong T2/FLAIR hyperintensities, oriented\nperpendicular to the corpus callosum, compatible with the patient's history of\nmultiple sclerosis.  There is a left pericallosal T1 hypointensity (series 9,\nimage 16) on the spin echo images, and multiple similar-appearing\nhypointensities on the MPRAGE images, representing at least one black hole. \nAlthough there are no priors for comparison, there are no enhancing lesions to\nsuggest active demyelination.\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  There is no evidence of atrophy and the ventricles and sulci\nare normal in caliber and configuration.\n\nThe major intracranial flow voids are preserved.  The orbits, paranasal\nsinuses, and mastoids are within normal limits.",
            "output": "1. Numerous periventricular oblong T2/FLAIR hyperintensities oriented\nperpendicular to the corpus callosum, compatible with the patient's history of\nmultiple sclerosis.\n2. No evidence of atrophy or enhancing lesions to suggest active\ndemyelination.\n3. A single T1 hypointensity on the spin echo images, and multiple\nsimilar-appearing hypointensities on the MPRAGE images, representing at least\none black hole."
        },
        {
            "input": "Multiple oblong periventricular T2/FLAIR hyperintensities, oriented\nperpendicular to the corpus callosum are stable since prior MRI from ___ and compatible with provided history of multiple sclerosis.  Punctate\nleft pericallosal T1 hypointensity (5:23), as well as additional\nhypointensities on MPRAGE images, are similar to prior MRI from ___\nand likely reflect at least one black hole.  No enhancing lesions to suggest\nactive process.  No parenchymal or vascular enhancement on MPRAGE images.\n\nThere is no evidence of infarction, hemorrhage, edema, mass, mass effect or\nsignificant midline shift.  Ventricles and sulci are normal in size and\nconfiguration and there is no evidence of cerebral atrophy.  Dural venous\nsinuses are patent on postcontrast MPRAGE images.  Principal intracranial\nvascular flow voids are preserved.\n\nParanasal sinuses, mastoid air cells and middle ear cavities are.  The orbits\nare unremarkable.",
            "output": "1. Stable numerous oblong periventricular T2/FLAIR hyperintensities, oriented\nperpendicular to the corpus callosum, consistent with provided history of\nmultiple sclerosis.  There is no evidence of enhancing lesions.\n2. Re-demonstrated T1 hypointensity on spin echo images, as well as multiple\nhypointensity on MPRAGE images, are suggestive of at least one black hole."
        },
        {
            "input": "Study is moderately degraded by motion.  Within these confines:\n\n Grossly stable numerous supratentorial nonenhancing T2 and FLAIR white matter\nlesions are again noted, several which demonstrate associated T1\nhypointensities.  No lesions demonstrate restricted diffusion or increase\nsusceptibility.\n\nThere is no evidence of hemorrhage, masses,mass effect,midline shift or\ninfarction.   The ventricles and sulci are preserved in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.  Minimal bilateral maxillary sinus and ethmoid air cell\nmucosal thickening is present.",
            "output": "1. Study is moderately degraded by motion.\n2. Grossly stable supratentorial nonenhancing white matter lesions as\ndescribed, compatible with patient's provided history of multiple sclerosis.\n3. Within limits of study, no definite evidence of new enhancing or white\nmatter lesions.\n4.  Paranasal sinus disease , as described."
        },
        {
            "input": "MR BRAIN:\nThere is no intra or extra-axial mass, acute hemorrhage or infarct.  The\nsulci, ventricles and cisterns are within expected limits for the patient's\nage.  A very few punctate subcortical right frontal (series 32, image 18, 19\nand left frontal operculum (series 32, image 15 and 16) are nonspecific.  Very\nhazy posterior periventricular white matter hyperintensity (series 32, image\n16) and to a lesser extent along the left periventricular white matter is\nnoted.\n\nThe major intracranial flow voids are preserved.  There is mild mucosal\nthickening of the paranasal sinuses.  The orbits are unremarkable.  No fluid\nsignal is seen in the mastoid air cells.\n\n\nMRA BRAIN: Fetal left PCA noted.  Left V4 segment is diminutive but patent. \nThe intracranial vertebral and internal carotid arteries and their major\nbranches otherwise appear normal without evidence of stenosis, occlusion, or\naneurysm formation.\n\nMRV BRAIN: The inferior sagittal sinus is not well visualized and likely\ncongenitally diminutive given absence of abnormal signal on additional\nsequences.  Normal flow signal is demonstrated within the superior sagittal\nsinus, straight sinus, transverse sinuses, and sigmoid sinuses. The jugular\nbulbs and proximal jugular veins are patent. Evaluation of the deep venous\nsystems reveals normal flow signal in the internal cerebral veins. The vein of\n___ is also unremarkable.",
            "output": "1. Nonspecific very few punctate subcortical right frontal and left frontal\noperculum a white matter hyperintensities.  This could represent sequela of\nchronic headache, infectious/inflammatory etiology or prior trauma.  These are\nnot in a distribution typical for demyelinating disease.  Very hazy and subtle\nposterior periventricular white matter hyperintensities also noted.\n2. No acute infarct or intracranial hemorrhage.  No intracranial mass.\n3. Unremarkable MRV and MRA brain."
        },
        {
            "input": "There is a punctate focus of DWI hyperintensity along the subependymal lining\nof the right occipital horn (series 4, image 11), which possibly demonstrates\nan ADC correlate (series 3, image 11), but there is no definitive FLAIR\nabnormality.  This focus could represent a tiny infarct.  There is no evidence\nof associated hemorrhage.\n\nThere is no evidence of acute hemorrhage, edema, masses, mass effect or\nmidline shift.\nThere are old lacunar infarcts in the right corona radiata and anterior limb\nof the right internal capsule.\nThere are patchy T2/FLAIR hyperintensities in the cerebral hemispheres\nbilaterally and in the pons, a nonspecific finding and likely related to\nchronic small vessel ischemic changes.\n\nThere is generalized parenchymal volume loss, most likely age related.  Mild\nprominence of the ventricular system and extra-axial CSF spaces is consistent\nwith the previously mentioned parenchymal volume loss.\nMajor vascular flow voids appear preserved.\n\nThere is mucosal thickening throughout the ethmoid air cells, bilateral\nsphenoid sinuses and right maxillary sinus.  There is a small amount of\nlayering fluid in the right sphenoid sinus.  The bilateral mastoid air cells\nare opacified.  Note is made of bilateral lens replacement surgery.  The\norbits appear otherwise grossly unremarkable.",
            "output": "1. Punctate focus of DWI hyperintensity along the subependymal lining of the\nright occipital horn with possible ADC correlate could reflect a tiny\ninfarction.\n2. Old lacunar infarcts in the right corona radiata and anterior limb of the\nright internal capsule.  Patchy periventricular white matter changes in the\ncerebral hemispheres bilaterally and in the pons, likely a sequela of chronic\nmicroangiopathy.\n3. Diffuse paranasal sinus disease with small amount of layering fluid in the\nright sphenoid sinus which can be seen with acute sinusitis in the appropriate\nclinical setting.  Complete opacification of the bilateral mastoid air cells."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is 0.3 cm focus of faint enhancement in the ventral\npons, with associated decreased signal on gradient images, and very subtle T2\nsignal abnormality on coronal series 10, image 39, findings most consistent\nwith benign capillary telangiectasia.  There is moderate to severe\nopacification of the paranasal sinuses, with mucosal thickening and\nsecretions, most prominent at the ethmoid and sphenoid acute paranasal\nsinusitis, consistent with acute sinusitis.  0.2 cm focus of enhancement is\nsuggested at the posterior right cingulate gyrus series 12, image 18, without\nassociated edema.\n\nLeft hippocampus is atrophic compared to the right.  Hippocampal signal\nintensities are symmetric.  There is asymmetric atrophy of the left para\nhippocampal gyrus, with preserved signal intensity.  There is no associated\nmass.  Bilateral mammillary bodies are preserved in configuration.  There is\nno focal lobar encephalomalacia. There are no focal cortical dysplasias or\ngray matter heterotopia noted.",
            "output": "1. Atrophy of the left hippocampus, with symmetric hippocampal signal\nintensities bilaterally.\n2. There is no temporal lobe mass.\n3. Suggestion of tiny focus of enhancement posterior right cingulate gyrus.\n4. Paranasal sinus disease, with suggestion of acute paranasal sinusitis."
        },
        {
            "input": "There is no evidence of acute intracranial hemorrhage or mass effect. The\nventricles and basal cisterns appear normal.\n\nThere is no evidence of acute ischemia based on diffusion-weighted imaging.\nThere is moderate brain parenchymal volume loss. There is subcortical,\nperiventricular, and brainstem T2/FLAIR signal hyperintensity which is\npresumably on the basis of chronic small vessel ischemic disease. There is a\nmore focal area of T2/FLAIR hyperintensity within the left pons which likely\nrepresents a prior infarct.  There are normal vascular flow voids.  There is a\npunctate focus of gradient blooming within the left parietal lobe which likely\nrepresents chronic microhemorrhage.\n\nThere is no abnormal brain parenchymal or leptomeningeal enhancement.\n\nThe orbits, skull base, and paranasal sinuses are unremarkable.\n\nMRA head/neck:  There is no hemodynamically significant stenosis, aneurysm, or\nfocal vessel cut off within the intracranial vasculature.\n\nThe origins of the great vessels are patent. There is no evidence of\ndissection or pathologic large vessel occlusion within the vasculature of the\nneck.",
            "output": "1. No evidence of acute intracranial hemorrhage, mass effect, or acute\nischemia.\n2. Presumed sequelae of chronic small vessel ischemic disease and prior\ninfarcts, as described.\n3. No evidence of hemodynamically significant stenosis or pathologic large\nvessel occlusion within the vasculature of the head and neck."
        },
        {
            "input": "The left vertebral artery is not seen.  The left ___ appears to arise from a\nrobust right vertebral artery.  This may be due ___ hypoplastic left vertebral\nartery, or occlusion of the left vertebral artery.\n\nRobust bilateral posterior communicating arteries are noted.  The intracranial\nright vertebraland internal carotid arteries and their major branches \notherwise appear patent without evidence of stenosis, occlusion, or aneurysm\nformation.",
            "output": "1. Non visualization of the left vertebral artery.  Given that the left ___\narises from a robust right vertebral artery this likely represents non\nvisualization due to a hypoplastic left vertebral artery, though left\nvertebral artery occlusion is a differential possibility.\n2. Otherwise patent intracranial vasculature without significant stenosis,\nocclusion, or aneurysm formation."
        },
        {
            "input": "There is no intra or extra-axial mass, acute hemorrhage or infarct. The sulci,\nventricles and cisterns are within expected limits for the patient's mild\nsenescent related global cerebral volume loss.  There are moderate\nperiventricular and subcortical T2/FLAIR white matter hyperintensities, which\nare nonspecific, but compatible with chronic microangiopathy in a patient of\nthis age.  Sequela of right more prominent than left small lacunar infarcts\n(series 5, image 7) in the bilateral cerebellar hemispheres is noted.  The\nmajor intracranial flow voids are preserved. There is mild mucosal thickening\nof the paranasal sinuses.  The orbits are unremarkable.  No fluid signal is\nseen in the mastoid tips.",
            "output": "1. Sequela of right more prominent than left small lacunar infarcts of the\nbilateral cerebellar hemispheres.\n2. No acute infarct or intracranial hemorrhage.\n3. Moderate periventricular and subcortical T2/FLAIR white matter\nhyperintensities, nonspecific, but compatible with chronic microangiopathy in\na patient of this age."
        },
        {
            "input": "There is no evidence of an intracranial mass or pathologic meningeal contrast\nenhancement. There is no evidence for edema, abnormal diffusion, blood\nproducts, or other parenchymal signal abnormalities. The ventricles and basal\ncisterns appear normal.  Cerebellar tonsils are normally positioned. There are\npreserved major arterial flow voids and patent major dural venous sinuses.",
            "output": "Normal MRI of the brain."
        },
        {
            "input": "The pituitary stalk is mildly deviated to the left, unchanged from prior\nexamination..  A 5 x 6 x 2 mm ovoid hypoenhancing lesion in the anterior\npituitary to the right of midline may represent a pituitary macroadenoma\n(series 9, image 129; series 901, image 75).  There is no evidence of\nextension into the suprasellar cistern or cavernous sinus.  The optic chiasm\nand optic nerves are unremarkable.\n\nImaging of the brain do not demonstrate evidence of hemorrhage, edema, mass,\nmass effect, infarction, or abnormal enhancement.  The ventricles and sulci\nare age-appropriate.  Principal intracranial vascular flow voids are\npreserved.  The dural venous sinuses are patent on postcontrast MP-RAGE\nsequences.\n\nThere is a mucous retention cyst in the right maxillary sinus there is mild\nmucosal thickening in the ethmoid air cells.  The orbits are grossly\nunremarkable.",
            "output": "5 x 6 x 2 mm ovoid hypoenhancing lesion in the anterior pituitary to the right\nof midline with mild leftward deviation of the pituitary stalk may represent a\npituitary macroadenoma.  This was not definitively seen on prior examination\nof ___."
        },
        {
            "input": "MRI Brain:\nThere is a 1.1 x 0.7 cm area of heterogeneous of T1 and T2 hypointense and\nhyperintense signal in the right parietal periventricular white matter.  This\narea demonstrates susceptibility.  There are also numerous other punctate foci\nof susceptibility within the right frontal, right parietal, right occipital\nlobes, right basal ganglia, right cerebral peduncle, right midbrain, and\nbilateral cerebellar hemispheres.\n\nThere are multiple foci a of her T2/FLAIR hyperintensities in the\nperiventricular, subcortical, and deep white matter.  There is no evidence\nofedema, masses, mass effect, midline shift or infarction.   The ventricles\nand sulci are normal in caliber and configuration.\n\nThere is an empty sella.  The optic nerves are slightly tortuous as partially\nevaluated.\n\nThe right maxillary sinus is completely opacified.  There is mild mucosal\nthickening in the left sphenoid sinus and moderate mucosal thickening in the\nbilateral ethmoid sinuses.  The mastoid air cells are clear.\n\nMRA brain: The intracranial vertebral and internal carotid arteries and their\nmajor branches appear normal without evidence of stenosis, occlusion, or\naneurysm formation.\n\nMRA neck:  The common, internal and external carotid arteries appear normal. \nThere is no evidence of internal carotid artery stenosis by NASCET criteria. \nThe origins of the great vessels, subclavian and vertebral arteries appear\nnormal bilaterally.",
            "output": "1. Late subacute/chronic hemorrhage in the right parietal periventricular\nwhite matter with numerous other punctate foci of chronic microhemorrhages in\nthe right frontal, parietal, occipital lobes, right basal ganglia, right\nmidbrain, and bilateral cerebellar hemispheres, likely hypertensive in\netiology or due to cavernous malformations.\n2. Extensive, nonspecific white matter lesions, most likely representing the\nsequela of chronic small vessel ischemic changes given the patient's provided\nhistory of preeclampsia and hypertension.  No signs of reversible\nencephalopathy syndrome\n3. Normal MRA of the head and neck.\n4. Empty sella intra which slightly tortuous optic nerves are nonspecific\nfinding which could be seen in patients with pseudotumor cerebri."
        },
        {
            "input": "Study is mildly degraded by motion.  There is no evidence of hemorrhage,\nedema, masses, mass effect, midline shift or infarction.   The ventricles and\nsulci are normal in caliber and configuration.  There is minimal left\nmaxillary sinus and mild ethmoid air cell mucosal thickening.",
            "output": "1.  Study is mildly degraded by motion.\n2.  No acute intracranial abnormality.\n3.  Paranasal sinus disease as described."
        },
        {
            "input": "The common, internal and external carotid arteries appear normal.  There is no\nevidence of stenosis by NASCET criteria. The origins of the great vessels,\nsubclavian, and vertebral arteries appear normal bilaterally.  The common\ncarotid bifurcations appear normal.  There is no evidence for dissection.",
            "output": "1. Normal MRA neck."
        },
        {
            "input": "There is no acute infarction, intracranial hemorrhage, extracerebral fluid\ncollection, midline shift or mass effect.  Ventricles and extra-axial spaces\nare normal in size.  Flow voids are maintained. Suprasellar and craniocervical\nregions are unremarkable.\n\nNo focal abnormalities are seen of blood products noted in the occipital\nregion.  Visualized paranasal sinuses are clear.",
            "output": "No significant abnormalities are seen on MRI of the brain without gadolinium."
        },
        {
            "input": "MRI HEAD:  Encephalomalacia caring in the right parietal lobe is unchanged.\nThere are chronic small vessel ischemic changes in the white matter.  No\nevidence for acute ischemia or hydrocephalus . Chronic blood products are\nnoted in the bilateral parietal lobes .  There is no evidence of acute\ninfarction or hemorrhage. There is no mass effect, edema, or hydrocephalus. \nPrincipal vascular flow voids are preserved. There is no abnormal parenchymal,\nvascular or meningeal enhancement after the administration of gadolinium.\nGlobes and soft tissues are unremarkable. Visualized paranasal sinuses and\nmastoid air cells are well aerated.\n\nHEAD MRA:  Images are technically limited, only the proximal flow voids are\nwell seen . A partially thrombosed left vertebral artery aneurysm is\nunchanged.  There is no additional aneurysm or high-grade stenosis in the\ncarotid or vertebral arteries.\n\nNECK MRA:  There is no high-grade stenosis in the carotid and vertebral\narteries.",
            "output": "No acute abnormality on the brain MRI. Chronic encephalomalacic changes in the\nright parietal lobe. No significant stenosis in the intracranial or neck\nvasculature."
        },
        {
            "input": "MRI HEAD: T1 sagittal images of the head brain is limited secondary to motion.\nThere is no intra or extra-axial mass, acute hemorrhage or infarct. There are\ndiffuse periventricular and subcortical confluent nonspecific T2/FLAIR white\nmatter hyperintensities, several which are confluent, which may be seen in the\nsetting of small vessel ischemic disease in a patient of this age.  There is\nage-appropriate global cerebral volume loss. Sulci, ventricles and cisterns\nare within expected limits for age. There are prominent perivascular spaces\nextending along the  centrum semiovale . In addition, previously described\nlacunar along the left anterior limb of the internal capsule appears to be\nsecondary to perivascular spaces.  The major intracranial flow voids are\npreserved.  The paranasal sinuses are essentially clear. There are bilateral\nlens replacements otherwise the orbits are unremarkable. The mastoid air cells\nare essentially clear. The major dural sinuses are patent.\nHEAD MRA: There cavernous ICAs are slightly torturous. Otherwise, normal flow\nrelated signal is seen in the intracranial internal carotid, middle cerebral\nand anterior cerebral arteries without significant mural irregularity or\nstenosis. There is normal symmetric arborization of the MCA branches. There is\nno aneurysm greater than 3 mm. Normal flow related signal is seen in the\nintracranial vertebral arteries (the left vertebral artery is dominant), the\nbasilar artery, and the bilateral superior cerebellar and posterior cerebral\narteries.\nNECK MRA: There is a normal 3 vessel takeoff from the aortic arch. The\ncervical common carotid, internal carotid and external carotid arteries are\nnormal in course, caliber and contour. They demonstrate normal enhancement\nwithout mural irregularity, stenosis or evidence of dissection. There is no\nsignificant stenosis of the extracranial internal carotid arteries by NASCET\ncriteria. The left vertebral artery is dominant. Otherwise, the vertebral\narteries are normal in course, caliber and contour. They demonstrate normal\nenhancement without mural irregularity, stenosis or evidence of dissection.",
            "output": "1. Nonspecific white matter changes as described above, which may be seen in\nsetting of small vessel ischemic disease.\n2. No evidence of acute infarct.\n3. Of note, previously described hypodensity of the left anterior limb of the\ninternal capsule appears to be secondary to prominent perivascular spaces.\n4. Unremarkable MRA of the head and neck."
        },
        {
            "input": "The ventricles, sulci, and cisterns are age appropriate. There is no mass\neffect, midline shift, hemorrhage or extra axial fluid collection. No\ndiffusion abnormalities are detected. The corpus callosum is normally formed.\nThere is a normal pattern of myelination. There is no evidence of structural\nabnormality, malformation of cortical development or heterotopia.  The\nhigh-resolution images throughout the temporal lobes demonstrates normal\nsignal in both temporal lobes, there is no evidence of mesial temporal\nsclerosis, the mamillary bodies are symmetric as well as the fornices.  The\nmajor vascular flow voids are present and demonstrate normal distribution.\n\nThe orbits are unremarkable, the paranasal sinuses and the mastoid air cells\nare clear.",
            "output": "Essentially normal MRI of the brain, there is no evidence of acute or subacute\nintracranial process."
        },
        {
            "input": "The left inferior frontal and temporal lobe contain blood products and mild\nenhancement representing evolving contusions.  There are no new areas of\nhemorrhage.  There is no hydrocephalus.  There is no evidence of infarction. \nThere is no enhancing mass.\n\nThere is an area of increased susceptibility over the left frontal/ parietal\nlobe (06:23) likely representing residual superficial siderosis from prior\nsubarachnoid hemorrhage. There is a small focus of likely extra- axial high T1\nsignal at the tip of the clivus (4:13), likely representing residual blood\nproducts.\n\nScattered T2/FLAIR periventricular hyper intensities, are non specific but may\nrepresent the sequelae of chronic small vessel disease.  The imaged orbits,\nmaxillary sinuses and mastoid air cells are clear.",
            "output": "1. Evolving left inferior frontal and left temporal lobe contusions without\nmass effect.\n2. There is no new hemorrhage.  No acute infarcts."
        },
        {
            "input": "Multiple subcortical and periventricular T2/FLAIR nonenhancing white matter\nhyperintensities, most prominent along the bilateral frontal centrum semiovale\nand along the right posterior lateral ventricle.  There is no intra or\nextra-axial mass, acute hemorrhage or infarct.  There is no abnormal\npostcontrast enhancement.  The major intracranial flow voids are preserved. \nThe dural venous sinuses are patent postcontrast MP-RAGE.  The sulci,\nventricles and cisterns are within expected limits for the patient's age. \nMild mucosal thickening of the ethmoid air cells is noted.  The remainder the\nparanasal sinuses are clear.  The orbits are unremarkable.  The mastoid air\ncells are essentially clear.",
            "output": "1. Multiple scattered subcortical deep white matter and periventricular T2\nFLAIR hyperintense lesions are nonspecific in a patient of this age with a\nwide differential diagnosis, including but not limited to sequelae of chronic\nmigraine headaches, demyelinating disease, sequela of prior\ninflammatory/infectious etiology or vasculitides.\n2. No evidence of restricted diffusion or enhancement to suggest active\nprocess."
        },
        {
            "input": "There are foci of slow diffusion involving the right insular cortex and\nadjacent frontotemporoparietal cortex.  A couple additional punctate foci of\nslow diffusion are present within the frontal and parietal lobes(series 7,\nimage 22, 23 and 25).  There is corresponding T2/FLAIR signal abnormality.\n\nThere is a focus of right occipital gyriform enhancement, without evidence of\nassociated signal abnormality on other sequences including diffusion-weighted,\nGRE, T2/FLAIR.  Trace hazy enhancement in the left frontal parietal lobe\n(series 102, image 66) in the region of infarct, may represent luxury\nperfusion.\n\nRedemonstrated is superimposed subcortical and deep white matter T2/FLAIR\nhyperintensities that are nonspecific.  There is no evidence of infarction,\nmass, mass effect or midline shift.\n\nThe major intracranial vascular flow voids are maintained.  The dural venous\nsinuses are patent.  The ventricles and sulci are normal in caliber and\nconfiguration.  There is mild mucosal thickening of the ethmoid air cells. \nOtherwise, the orbits, paranasal sinuses and mastoid air cells are normal.",
            "output": "1. Acute infarcts involving the right insular cortex and adjacent\nfrontotemporoparietal cortex.  A few additional scattered punctate acute\ninfarcts involve the right frontal and parietal lobes.  Trace hazy enhancement\nin the left frontoparietal lobe associated with the infarct is thought to\nrepresent luxury perfusion.  Otherwise, there is no associated enhancement\nwith the infarct.\n2. Focal cortical gyriform enhancement in the right occipital lobe, without\nevidence of associated signal abnormality on other sequences.\n3. Redemonstrated subcortical and deep white matter T2/FLAIR hyperintensities\nare nonspecific.  However, in the patient's age range the differential\nincludes but is not limited to sequela of chronic migraine headaches,\ndemyelinating or other infectious/inflammatory process.\n4. Given the patient's clinical history of migraine headache, the\nconstellation of findings could represent migrainous infarct.  Cortical\ngyriform enhancement of the right occipital lobe may represent sequela of\nmigraine headache, which has been previously described.  Differential\nconsideration for the enhancement includes subacute infarct, although this is\nconsidered unlikely given lack of associated diffusion-weighted or T2/FLAIR\nsignal abnormality or encephalomalacia.  Infectious or neoplastic etiologies\nare considerations, although also consider less likely.\n\nRECOMMENDATION(S):  Recommend repeat examination following resolution of\nheadache, to document stability or resolution of abnormal right occipital lobe\nenhancement.\n\nNOTIFICATION:   *** ED URGENT ATTENTION ***"
        },
        {
            "input": "No intra or extra axial mass, acute infarct or hemorrhage. There is\ndisproportionate to mild atrophy of the cerebellum relative to the cerebrum,\nwhich is unchanged from prior CT examination. This may be seen in the setting\nof anti seizure medication. Otherwise, sulci, ventricles and cisterns are\nwithin expected limits. The major intracranial flow voids are preserved. The\nmesial temporal cortex are symmetric and unremarkable.  No evidence of\ncortical dysplasia or heterotopia. The paranasal sinuses are essentially\nclear. The orbits are unremarkable. The mastoid air cells are clear.",
            "output": "1. Stable atrophy of the cerebellum, which may be seen in the setting of anti\nseizure medication. Clinical correlation is recommended.\n2. The mesial temporal cortex and hippocampal formations are unremarkable.\n3. No evidence of cortical dysplasia or heterotopia."
        },
        {
            "input": "Examination is moderately degraded by motion.\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  Again, there is disproportionate diffuse moderate atrophy of\nthe cerebellum relative to the remainder the brain.  The ventricles and sulci\nare otherwise normal in caliber and configuration.  There is no abnormal\nenhancement after contrast administration.  There is no abnormal focus of\nslowed diffusion.\n\nBilateral hippocampal formations and mammillary bodies are grossly preserved\nin signal and configuration. There is no disproportionate medial temporal\natrophy. There is no focal lobar encephalomalacia. There are no focal cortical\ndysplasias or gray matter heterotopia noted on motion degraded examination.\n\nThe principal intracranial vascular flow voids are preserved.  The visualized\nparanasal sinuses are grossly clear.  The orbits are grossly unremarkable.  No\nsuperficial soft tissue abnormality is noted on the current examination,\nthough on the prior CT head examination from ___, there is a roughly 6\nx 2 mm well-circumscribed bony excrescence from the outer table of the midline\nfrontal calvarium, the contour of which can be subtly visualized on the axial\nMP rage images (902b:65) (02:26 on the ___ CT examination).",
            "output": "1. Unchanged cerebellar atrophy which can be seen in the setting of chronic\nanticonvulsant therapy.\n2. No definite epileptogenic focus.\n3. No hemorrhage, infarct or enhancing mass.\n4. 6 x 2 mm midline frontal calvarial osteoma better seen on the prior CT\nexamination, which likely accounts for the palpable midline forehead scalp\nnodule.  No soft tissue abnormality in this area."
        },
        {
            "input": "Study is mildly degraded by motion.  There is no evidence of hemorrhage,\nedema, masses, mass effect, midline shift or infarction.   The ventricles and\nsulci are normal in caliber and configuration.  A partially empty sella is\nnoted. There is no abnormal enhancement after contrast administration.  Mucous\nretention cysts are present in the left maxillary and right sphenoid sinuses,\nunchanged.",
            "output": "1. Study is mildly degraded by motion.\n2. No acute intracranial abnormality.\n3. No evidence of demyelinating disease.\n4. Paranasal sinus disease as described."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.\n\nThe maxillary sinuses are partially opacified bilaterally.  There is mild\nmucosal thickening of the anterior ethmoid air cells.  There is nearly\ncomplete opacification of the right mastoid air cells.",
            "output": "1. No evidence of acute infarct.\n2. Paranasal sinus disease.\n3. Nonspecific opacification of the right mastoid air cells."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.\n\nThe ventricles and sulci are normal in caliber and configuration.\nMajor vascular flow voids are preserved.\n\nMinimal mucosal thickening along the ethmoid air cells.  The remainder of the\nparanasal sinuses and mastoid air cells is clear.  The orbits appear\nunremarkable.",
            "output": "Unremarkable brain MRI."
        },
        {
            "input": "Please note the study is moderately degraded by motion.\n\nThere is a 2.7 (AP) x 3.6 (TV) x 3.3  (SI) cm lobulated mass in the intra\nsellar and suprasellar region extending into the floor of the third ventricle.\nThis lesion is separate from the pituitary gland.  A normal optic chiasm is\nnot seen, likely secondary to displacement.  The mass demonstrates\nheterogeneous signal with multiple T2 hyperintense cysts seen throughout\nlesion.  Small fluid fluid levels are seen in the larger superior lobulations,\nleft greater than right, which are hyperdense on CT.  The left lobulation\ndemonstrates intrinsic T1 hyperintense signal, however no corresponding fat\ndensity is noted on CT or nulling of signal on fat saturation imaging to\nsuggest fat.  The left lobulation also contains calcifications on the prior CT\nwhich demonstrates susceptibility on MRI.  Thin peripheral contrast\nenhancement of the dominant right T2 hyperintense cyst is seen with thicker\nnodular enhancement along the inferior aspect of the lesion.\n\nThere is no evidence of hemorrhage, edema, midline shift or infarction.   The\nventricles and sulci are normal in caliber and configuration.  Periventricular\nand subcortical T2 and FLAIR hyperintensities are noted. There is no abnormal\nenhancement after contrast administration.\n\nThe orbits are normal.  Retention cysts are noted in the bilateral maxillary\nsinuses with mucosal thickening of the ethmoid sinus.  The mastoid air cells\nand visualized soft tissues are normal.  Evaluation of the posterior vascular\nflow voids is limited given mass-effect of the suprasellar lesion.",
            "output": "1. Please note the study is moderately degraded by motion.\n2. A 2.6 cm intra sellar and suprasellar mass, which is separate from the\npituitary gland, extending into the third ventricle and displacing the optic\nchiasm, containing internal calcification, enhancement, proteinaceous debris\nand small amount of internal hemorrhage favored to represent a\ncraniopharyngioma.\n3. No acute infarct."
        },
        {
            "input": "Limited examination due to patient motion.  In comparison with the prior MRI\nexamination without contrast dated ___,  there are no significant\nchanges on the previously seen sellar and suprasellar heterogeneous enhancing\nlesion, measuring approximately 26 x 32 mm in transverse dimension and\napproximately 33 mm in coronal projection this lesion is causing obliteration\nof the suprasellar cistern and the optic chiasm is not clearly seen due to\ndisplacement.  Again there is a persistent area of low signal on the right\nside of this mass, measuring approximately 20 x 30 mm in transverse dimension,\nsuggestive of cystic change, apparently there is no extension into the\ncavernous sinuses.  The course of the anterior cerebral arteries is anterior\ndisc mass.  There is no evidence of intracranial hemorrhage, midline shifting\nor hydrocephalus.  The orbits are unremarkable, mucous retention cyst is again\nseen in the left maxillary sinus.",
            "output": "Limited examination due to patient motion.  No significant changes are\ndemonstrated in the previously noted sellar and suprasellar heterogeneous\nenhancing lesion, producing obliteration of the suprasellar cistern and\ndisplacement of the optic chiasm as described above.  Proteinaceous debris and\ncystic changes appear unchanged and favors the possibility of\ncraniopharyngioma."
        },
        {
            "input": "Study is mildly degraded by motion.  The patient's previously noted inter\nsellar mass with suprasellar extension into the floor the third ventricle is\nagain seen.  There is no midline shift and stable mass effect optic chiasm and\nbilateral basal ganglia.  An approximately 2 x 2.3 x 1.8 cm cystic\nnonenhancing mass component is again noted.  The ventricles and sulci are\nstable in size and configuration.  Bilateral maxillary sinus mucous retention\ncysts versus polyps are again noted.",
            "output": "1. Study is mildly degraded by motion.\n2. Redemonstration of patient's previously noted solid and cystic sellar mass\nwith suprasellar extension into third ventricle with stable mass effect on\nbilateral basal ganglia and optic chiasm, again suggestive of\ncraniopharyngioma.\n3. Ventricles stable in size."
        },
        {
            "input": "Patient is status post resection of a parasellar tumor with expected\npostoperative changes related to right frontal craniotomy including a right\nfrontal subdural hematoma, pneumocephalus, and a right subgaleal hematoma. \nRestricted diffusivity within the right anterior temporal lobe with associated\nFLAIR and T2 hyperintensity is consistent with an acute to subacute area of\ninfarction (5:12, 6:12, 12:10).  Mild residual peripheral enhancement in the\nsurgical bed likely represents postsurgical change rather than residual tumor\n(100b:48), attention on followup imaging is recommended.  Multiple bilateral\nmucous retention cysts are noted.",
            "output": "1. Status post recent resection of a parasellar tumor with postoperative\nchanges including a right frontal subdural hematoma, pneumocephalus, and a\nright subgaleal hematoma.\n2. Right anterior temporal lobe decreased diffusivity consistent with an acute\nto subacute infarction.\n3. Peripheral enhancement of the surgical bed without definite evidence of\nresidual mass, attention on follow-up imaging is recommended.\n\nNOTIFICATION:  The findings related with the ischemic changes on the right\nanterior temporal lobe were discussed with ___ pager ___ by\n___, M.D. on the telephone on ___ at 5:31 ___, 5 minutes after\ndiscovery of the findings."
        },
        {
            "input": "Comparison with the postoperative MRI is difficult as it was performed as a\nbrain MRI at other than of focused sellar MRI.  However, within this\nlimitation, there appears to be new cystic suprasellar lesion measuring\napproximately 15 mm with enhancement near the hypothalamus measuring\napproximately 11 mm.  Right frontal craniotomy is identified with\npachymeningeal enhancement which appears postoperative in nature.  In\naddition, there is also abnormal FLAIR signal and enhancement in the right\nanterior temporal lobe which is at the site of previously seen infarct on MRI\nof ___.  There are no other areas of abnormal brain enhancement seen.\nVentricular size has slightly increased with mild periventricular\nhyperintensities which are new since the MRI of ___ and could be due\nto evolving communicating hydrocephalus.",
            "output": "1. Recurrent suprasellar cystic lesion with recurrent area of enhancement as\ndescribed above.\n2. Slight increase in size of the ventricles with surrounding hyperintensities\non FLAIR images may suggest evolving communicating hydrocephalus.\n3. Evolving right anterior temporal lobe infarct.\n\nNOTIFICATION:  The impression and recommendation above was entered by Dr.\n___ on ___ at 15:21 into the Department of Radiology\ncritical communications system for direct communication to the referring\nprovider."
        },
        {
            "input": "The patient is status post right frontal craniotomy with unchanged\npostsurgical right frontal dural thickening and enhancement, unchanged from\nprior examination.  Abnormal nodular 1 cm enhancement along the anterior right\ntemporal lobe corresponding to region of prior infarct is unchanged from prior\nexam.  Re-identified is a multi cystic peripherally enhancing lesion of the\nsuprasellar cistern measuring a conglomerate 2.0 x 1.4 x 1.7 cm (SI, TRV, AP)\noverall with minimally increased in size to prior examination.  There is mild\nmass effect on the anterior communicating artery complex (series 5, image 47).\n\nThere is no acute infarct.  The dural venous sinuses are patent on\npostcontrast MP-RAGE.  With the size the ventricles are unchanged since\nexamination of ___.\n\n3 mucous retention cysts are noted in the bilateral maxillary sinuses.  The\norbits are unremarkable.",
            "output": "1. Multi cystic peripherally enhancing lesion of the suprasellar cistern\nappears minimally increased in size when compared to examination of ___ allowing for technical differences, measuring approximately 2.0 cm in\ngreatest dimension.\n2. Additional findings described above."
        },
        {
            "input": "Study is moderately degraded by motion, especially on postcontrast imaging.\n\nThere are stable postoperative changes from right frontal craniotomy and\nsuprasellar mass resection with associated chronic blood products and\nunderlying dural thickening and enhancement.  Associated periventricular white\nmatter FLAIR hyperintensity adjacent to the frontal horn of the right lateral\nventricle is unchanged, and may be postsurgical in nature.  Again identified\nis a multilobulated peripherally enhancing cystic lesion based within the\nsuprasellar cistern measuring approximately 2.2 x 1.6 x 2.0 cm (10:9, 901:66),\nincreased in size compared the prior examination where it measured\napproximately 1.7 x 1.5 x 1.9 cm.   There is unchanged mass effect upon the\nanterior communicating artery.\n\nAgain identified is right anterior temporal encephalomalacia from prior\ninfarct with unchanged 1.0 x 0.9 cm area of enhancement within the area of\ninfarct (10:8).  There is associated ex vacuo dilatation of the temporal horn\nof the right lateral ventricle.\n\nThere is no evidence of acute hemorrhage, increasing edema, midline shift or\nacute infarction.  Mildly prominent ventricular size and configuration is\noverall unchanged compared to the prior examination.  Areas of periventricular\nand subcortical white matter T2/FLAIR hyperintensity are nonspecific, most\nlikely representing the sequela of chronic small vessel ischemic disease. \nThere is no new abnormal enhancement after contrast administration.  There is\nno abnormal focus of slowed diffusion.  The principal intracranial vascular\nflow voids are preserved.\n\nThere are small mucous retention cysts in the bilateral maxillary sinuses. \nThe orbits are grossly unremarkable.",
            "output": "1.  Study is moderately degraded by motion.\n2. Interval increase in size of a 2.2 x 1.6 x 2.0 cm cystic peripherally\nenhancing suprasellar lesion, consistent with residual/recurrent\ncraniopharyngioma.\n3. No significant interval change of mildly prominent ventricular size and\nconfiguration.  Communicating hydrocephalus cannot be excluded.\n4. Chronic right anterior temporal infarct, with stable enhancement.  Findings\nmay again be related to evolving postoperative or therapy related effects. \nPlease note that underlying mass is not excluded on the basis examination. \nRecommend attention on followup imaging.\n5. No acute hemorrhage or acute infarct.\n6. Paranasal sinus disease, as described.\n\nNOTIFICATION:  Impression #2 was discussed with ___, M.D. by ___\n___, M.D. on the telephone on ___ at 1:14 AM, 5 minutes after\ndiscovery of the findings.  Please note the change in the final interpretation\nis that the ventricular size and configuration is largely unchanged compared\nto prior examinations."
        },
        {
            "input": "This study is moderate to severely degraded by motion.\n\nThere are postsurgical changes related to prior right frontotemporal\ncraniotomy for resection of a suprasellar craniopharyngioma.  Peripherally\nenhancing cystic suprasellar mass measures 1.6 x 2.0 x 1.7 cm TV x AP x CC\n(900:80, 901:68), similar to ___ accounting for differences in\nmeasurement technique.  There is mass effect upon the anterior communicating\nartery.  Right anterior temporal lobe encephalomalacia with associated\nex-vacuo dilation of the right temporal horn is consistent with a sequela of\nprior infarction.  Known area of enhancement in the right temporal lobe is not\nwell appreciated due to patient motion.  No evidence of acute infarction. \nThere is no midline shift.\n\nThere is prominence of the ventricles and sulci, suggestive of atrophy.  There\nis asymmetrical periventricular and subcortical white matter T2/FLAIR\nhyperintensity, which is most pronounced around the frontal horn of the right\nlateral ventricle.  This has increased compared to the most recent study\nperformed on ___, and suggests sequela of post-treatment change.\nThis is likely superimposed upon a background of chronic microangiopathic\nchanges.\n\nThere are mucous retention cysts in the maxillary sinuses bilaterally. \nMastoid air cells are clear.  The orbits are unremarkable.",
            "output": "1. Moderate to severely motion degraded study.\n2. Interval increase in pronounced T2/FLAIR white matter hyperintensities\nsurrounding the frontal horn of the right lateral ventricle, suggestive of\npost-treatment change.\n3. No significant interval change in size of the cystic suprasellar mass\nmeasuring 1.6 x 2.0 x 1.7 cm, consistent with known residual/recurrent\ncraniopharyngioma.\n4. Right temporal lobe encephalomalacia."
        },
        {
            "input": "Please note, study is moderate to severely degraded by motion.  No MPRAGE\nimages were obtained.\nWithin the confines of the study, findings are as follows:\n\nThere are postsurgical changes related to prior right frontotemporal\ncraniotomy for resection of a suprasellar craniopharyngioma with mild chronic\nblood products and dural thickening and enhancement.\nPlease note, measurements were made on the T1 postcontrast images as the\nMPRAGE images are not available on this study for direct comparison.\n\nWithin the limitations, there is no significant interval change in a\nperipherally enhancing cystic suprasellar mass, which measures approximately\n1.6 cm TV x 1.5 cm AP x 1.7 cm SI (12:10, 11:12), when remeasured at the same\nplane.  Again seen is mild mass effect on the anterior communicating artery. \nThere is continued interval increase in hyperintense T2/FLAIR signal\nintensity, most pronounced within the frontal horn of the right lateral\nventricle, dating back to ___.\n\nThere is stable right anterior temporal lobe encephalomalacia with ex vacuo\ndilatation of the right temporal horn, likely a sequela of prior infarction. \nOtherwise, there is no evidence of acute infarction or new hemorrhage.  There\nis no midline shift.  There is diffuse parenchymal volume loss with prominence\nof the ventricles and sulci.  Mucosal retention cysts are again seen within\nbilateral maxillary sinuses.  The remaining paranasal sinuses and bilateral\nmastoid air cells are clear.  The orbits and soft tissues appear unremarkable.",
            "output": "1. Please note, study is moderate to severely degraded by patient motion.  No\nMPRAGE were obtained.  Within the confines, findings are as follows:\n2. Continued interval increase in hyperintense T2/FLAIR signal intensity\nsurrounding the frontal horn of the right lateral ventricle.  Finding is\nnonspecific, and may be related to post treatment change.  Continued attention\non follow-up is recommended.\n3. No significant change in size of a cystic suprasellar mass, consistent with\nknown residual/recurrent craniopharyngioma.\n4. Right temporal lobe encephalomalacia again seen."
        },
        {
            "input": "There is large zone of chronic infarct involving left temporal lobe, extending\ninto the lateral left occipital lobe.  Foci of mildly restricted diffusion\nalong the posterior periphery of the infarct, with normalized to mildly\ndecreased ADC values, consistent with late subacute component of the infarct. \nThere are areas of cortical laminar necrosis and cortical mineralization seen\non T1 and gradient weighted images.  No parenchymal hemorrhage.\n\nSuggestion of small focus of mildly restricted diffusion posterior left\nthalamus, suggestive of late subacute infarct.\n\nThere is large chronic right PCA distribution infarct involving posteromedial\nright temporal, right occipital lobes.\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift.\nFindings consistent with severe chronic small vessel ischemic changes.  Small\nleft, tiny right chronic cerebellar infarcts.  Intracranial vascular flow\nvoids are preserved.  There is extensive opacification of the paranasal\nsinuses, with periostitis and air-fluid levels, consistent with acute on\nchronic paranasal sinusitis.  Mastoids are clear.",
            "output": "1. Late subacute on chronic infarct centered on left temporal lobe, with areas\nof cortical laminar necrosis and mineralization.  No parenchymal hematoma.\n2. Suggestion of late subacute infarct posterior left thalamus.\n3. Chronic infarcts right PCA distribution, bilateral cerebellum.\n4. Severe chronic small vessel ischemic changes.\n5. Extensive paranasal sinus opacification, consistent with acute on chronic\nsinusitis"
        },
        {
            "input": "MRI BRAIN:\nThere is no evidence of hemorrhage,edema,masses, mass effect, midline shift or\ninfarction.\n\nThere are scattered T2/FLAIR hyperintensities in the cerebral hemispheres\nbilaterally, a nonspecific finding but likely related to chronic small vessel\nischemic changes.  There is a small focus of encephalomalacia in the posterior\nright cerebellar hemisphere, which most likely represents a chronic border\nzone infarct.\n\nThere is a small focus of enhancement in the right basal ganglia region which\nis most likely vascular in etiology and could reflect a small developmental\nvenous anomaly (series 26, image 101).  Otherwise, there is no abnormal\nenhancement after contrast administration.\n\nThe ventricles and sulci are normal in caliber and configuration.\n\nMajor vascular flow voids are preserved.  Major dural venous sinuses are\npatent.\n\nParanasal sinuses and mastoid air cells appear clear.  Note is made of\nbilateral lens replacement surgery.  The orbits appear otherwise unremarkable.\n\nMRA BRAIN:\nThe intracranial vertebral and internal carotid arteries and their major\nbranches appear normal without evidence of stenosis,occlusion,or aneurysm\nformation.\n\nMRA NECK:\nNormal three vessel aortic arch.  The origins of the great vessels, subclavian\nand vertebral arteries appear normal bilaterally.  The common, internal and\nexternal carotid arteries appear normal.  There is no evidence of internal\ncarotid artery stenosis by NASCET criteria.",
            "output": "1. No significant intracranial abnormality.  No evidence of acute infarction,\nhemorrhage or intracranial mass.\n2. Small chronic border zone infarct in the posterior right cerebellar\nhemisphere.  Nonspecific white matter changes in the cerebral hemispheres\nbilaterally likely reflect sequela of chronic microangiopathic changes.\n3. Patent intracranial and cervical vasculature without evidence of\ndissection, stenosis, vessel occlusion or aneurysm formation."
        },
        {
            "input": "The left centrum semiovale demonstrates a round and ill-defined area of T2 and\nFLAIR hyperintensity (___), measuring approximately 1.5 x 1.4 cm. The\nappearance is atypical for white matter related microvascular ischemic disease\nand further evaluation with contrast-enhanced MRI of the head is recommended.\nThe right centrum semiovale also demonstrates a smaller focus of T2/FLAIR\nhyperintensity, which is nonspecific but most likely related to chronic\nmicroangiopathic changes.\n\nOtherwise, no evidence of intracranial mass, mass effect, or midline shift.\nVentricles and sulci are age-appropriate. There is no evidence of slow\ndiffusion to suggest acute infarct. There is no evidence of hemorrhage or\nextra-axial fluid collections.\n\nThere is an extra-axial 16 mm AP x 5 mm TR focus of FLAIR hyperintensity along\nthe left cerebellopontine angle. This focus is most likely related to flow\nrelated artifacts, however, further evaluation with contrast-enhanced MRI may\nbe performed to exclude an extra-axial mass.\n\nThe inner tables frontal bones along the convexities demonstrate regions of T2\nhyperintensity which may represent hemangioma versus epidermoids.\n\nIntracranial flow voids are maintained. There is moderate to severe mucosal\nthickening within the left maxillary sinus with an apparent air-fluid level.\nMild mucosal thickening is also seen at the right maxillary sinus with a\nretention cyst. Otherwise, paranasal sinuses and mastoid air cells are clear. \nThe orbits and soft tissues are grossly unremarkable.",
            "output": "1.  No evidence of acute intracranial process extra-axial fluid collection.\n\n2. Focus of T2 and FLAIR hyperintensity within the left centrum semiovale\nshows no definite mass effect but is atypical in appearance for white matter\nrelated microvascular ischemic disease and further evaluation with\ncontrast-enhanced MRI of the head is recommended.\n\n3. Focus of FLAIR hyperintensity at the left cerebellopontine angle is most\nlikely related to flow artifacts although further evaluation with\npost-contrast MRI of the head is recommended to exclude an extra-axial mass.\n\n4. Regions of T2 hyperintensity along the inner tables of the frontal bones\nlikely represent hemangioma versus epidermoid. Further evaluation can also be\nperformed with MRI head with and without contrast.\n\n5. Moderate to severe mucosal thickening of the left maxillary sinus with an\napparent air-fluid level, concerning for acute sinusitis."
        },
        {
            "input": "The previously described ill-defined white matter foci of T2/FLAIR\nhyperintensity within the left (___) and right (___) centrum semiovale, are\nagain visualized and demonstrates no evidence of abnormal enhancement or slow\ndiffusion. These are most likely related to chronic microvascular ischemic\nchange.\n\nPreviously described focus of extra-axial FLAIR hyperintensity along the left\ncerebellopontine angle is most likely related to flow artifact, given absence\nof enhancement or signal abnormality in the current exam.\n\nThe bilateral inner tables of the frontal bones demonstrate well-marginated T1\nhypointense regions which demonstrate avid enhancement on postcontrast images\nsuspicious for metastasis or myeloma.\n\nOtherwise exam is unchanged. There is no hemorrhage, intracranial mass, mass\neffect, extra-axial fluid collections or midline shift.  There is no slow\ndiffusion to suggest acute infarct.  The ventricles are stable. The basilar\ncisterns are within normal limits. There is no pathologic intracranial\nenhancement.  There\n\nIntracranial flow voids are maintained.  Again seen is moderate to severe\nmucosal thickening of the left maxillary sinus, which has worsened compared to\n___, with near complete opacification of the left maxillary sinus.\nThere is mild mucosal thickening of the right maxillary sinus with an\nunchanged retention cyst. Mastoid air cells are clear. The orbits and soft\ntissues are grossly unremarkable.",
            "output": "1. No evidence of abnormal enhancement, mass effect or acute intracranial\nprocess.\n2. Previously described white matter foci of FLAIR hyperintensity in the\nbilateral centrum semiovale show no evidence of enhancement or slow diffusion\nand are most likely related to chronic microvascular ischemic change.\n3. Previously described focus of extra-axial FLAIR hyperintensity along the\nleft cerebellopontine angle is most likely related to flow artifact.\n4. Regions of T1 hypointensity with avid enhancement along the bilateral\nfrontal bones are suspicious for bony metastasis.  Bone scan can help for\nfurther assessment.\n5. Ior study of ___.\n\nNOTIFICATION:  Findings compared to critical communication dashboard."
        },
        {
            "input": "When compared to previous exam, there has been no significant interval change\nagain seen is hyperintense presumably enhancing bilateral calvarial lesions. \nThe right calvarial lesion measures 2.3 cm x 0.5 cm. The left frontal\ncalvarial lesion measures 1.5 x1.0 cm, both essentially unchanged from prior.\nThere is no new region of abnormal enhancement. There is no midline shift or\nmass effect.",
            "output": "Essentially unchanged bifrontal calvarial lesions."
        },
        {
            "input": "The patient is status post right cranioplasty and surgical removal of a\nintraosseous hemangioma complicated by wound dehiscence. Postsurgical changes\nin the right temporal bone at the site of prior cranioplasty are expected. \nEnlargement of the subdural space beneath the surgical bed is expended.  There\nis no discrete fluid collection or acute hemorrhage in the surgical bed. There\nis no abnormal enhancement of the underlying meninges. There are no soft\ntissue fluid collections.\n\nA 15 x 10 mm homogeneously enhancing mass in the left frontal bone is\nunchanged compared to the prior examination. Focal areas of high signal\nintensity seen on T2 and FLAIR in the periventricular white matter are\nunchanged compared to the prior MR examination and most likely represent\nchronic small vessel ischemic disease. There is no evidence of infarct.  The\nmajor intracranial vessels have expected flow voids. The ventricles are normal\nin size for the patient's age. There is mucosal thickening in the left\nmaxillary sinus. The remainder the paranasal sinuses and mastoid air cells are\nclear.\n\nThere is no evidence of acute hemorrhage, edema, intra-axial masses, mass\neffect, or infarction. There is no abnormal intracranial enhancement after\ncontrast administration.",
            "output": "Status post right cranioplasty and surgical removal of a intraosseous\nhemangioma with expected post operative appearance.  There are no intra-axial,\nextra-axial or soft tissue fluid collections.  No abnromal adjacent\npachymeningeal or leptomeningeal enhancement."
        },
        {
            "input": "Patient is status post right frontal craniectomy with cranioplasty changes. \nThere is herniation of underlying right frontal lobe into the craniectomy bed.\nThin overlying pachymeningeal enhancement in this region is postoperative.\n\nThere is no acute infarct.  T2/FLAIR white matter hyperintensities are seen in\nthe subcortical white matter on the right and in the left centrum semiovale\nwhich are unchanged, potentially from prior ischemia.  Major intravascular\nflow voids are preserved.  Fusiform dilation of the left intradural vertebral\narteries again noted.\n\nNo unexpected parenchymal or meningeal enhancement identified.\n\nMucosal thickening seen within the left maxillary sinus which is also\nfluid-filled.  Mild mucosal thickening also seen in the right maxillary sinus.\nRemaining paranasal sinuses and mastoids demonstrate no abnormal signal.  The\nT2 hyperintense enhancing left frontal calvarial lesion is unchanged dating\nback to ___ and is most compatible with an intraosseous meningioma.",
            "output": "Expected postoperative changes of right sided craniectomy with cranioplasty\nchanges.\nNo significant interval change of the left frontal calvarial lesion compatible\nwith a hemangioma since ___.\nSinus disease as above."
        },
        {
            "input": "Continued evolution of right frontal craniectomy and cranioplasty changes for\na intraosseous hemangioma, with very minimal herniation of the adjacent brain\nparenchyma into the defect.  There remains an enhancing left frontal lobulated\n1.1 x 0.7 cm (AP, TRV) intraosseous lesion, stable since MRI examination of ___, presumably representing a second hemangioma.  No new lesions are\nidentified.\n\nThere is no intra or extra-axial mass effect, acute hemorrhage or infarct. \nThe sulci, ventricles and cisterns are within expected limits for the\npatient's age related global cerebral volume loss.  The major intracranial\nflow voids are preserved.  The dural venous sinuses are patent.\n\nIncompletely evaluated is an apparent fusiform dilatation of the left V4\nsegment on both MPRAGE and T2 sequences (series 13, image 4; series 19, image\n24), unchanged from prior exam.\n\nPolypoid mucosal thickening and near complete opacification of the left\nmaxillary sinus and mild mucosal thickening of the right maxillary sinus is\nunchanged from prior exams.  The remainder the paranasal sinuses are clear. \nThe orbits are unremarkable.  The mastoid air cells are clear.",
            "output": "1. Enhancing lobulated left frontal intraosseous 1.1 cm lesion is unchanged\nsince examination of ___.  This likely represents an intraosseous\nhemangioma.\n2. Continued evolution of a prior right frontal craniectomy and cranioplasty\nfor resection of an intraosseous hemangioma with mild herniation of the right\nfrontal lobe into the cranioplasty bed.\n3. No new lesions.\n4. An apparent fusiform dilatation of the left V4 segment, unchanged from\nprior exams.  This may be further evaluated with MRA as clinically indicated.\n\nRECOMMENDATION(S):  Point 4:  An apparent fusiform dilatation of the left V4\nsegment, unchanged from prior exams. This may be further evaluated with MRA as\nclinically indicated."
        },
        {
            "input": "Again signal abnormality in the periventricular and subcortical white matter\nidentified indicating diagnosis of multiple sclerosis. There are no new focal\nabnormalities are identified. No evidence of new subcortical abnormalities are\nseen. No evidence of restricted diffusion identified. There is no midline\nshift or hydrocephalus.",
            "output": "No significant interval change since the previous MRI of ___. \nThere are no new signal abnormalities identified suspicious for progressive\nmultifocal leukoencephalopathy."
        },
        {
            "input": "This exam is somewhat limited due to the presence of EEG leads, particularly\nat the vertex.  There is no evidence of hemorrhage, masses, mass effect,\nmidline shift or infarction.   The ventricles and sulci are normal in caliber\nand configuration.  There is mild FLAIR hyperintense signal along the sulci at\nthe vertex, which may represent a combination of increased oxygenation from\nintubation as well as postcontrast venous enhancement.  There is equivocal\nFLAIR hyperintense signal with associated diffusion-weighted per intensity\nwithout correlative ADC hypointensity (series 8, image 13; series 602, image\n17).  There is no abnormal enhancement after contrast administration. \nIntracranial flow voids are preserved.\n\nAir-fluid level is seen within the left maxillary as well as the bilateral\nsphenoid sinuses.  There is extensive mucosal thickening in the ethmoid air\ncells.  These are likely related to prolonged intubation.  The orbits are\nunremarkable.",
            "output": "The equivocal FLAIR and diffusion-weighted hyperintense signal of the\nbilateral pulvinar, without associated ADC hypointensity.  While this could be\nartifactual, the thalamus is particularly sensitive for ischemia.  Close\nattention on followup is recommended.\nThe remainder the exam is grossly unremarkable."
        },
        {
            "input": "There are multiple areas of deep white matter hyperintensity on the\ndiffusion-weighted images bilaterally.  Most of these demonstrate normal\ndiffusion coefficients on the ADC map.  A number of these areas are bright on\nthe FLAIR images while others are not visible on FLAIR.  There is no evidence\nof hemorrhage.  Altogether, these findings suggest acute and subacute\nwatershed infarction.  There is no evidence of edema, masses, mass effect or\nmidline shift.   The ventricles and sulci are normal in caliber and\nconfiguration.",
            "output": "1. Multiple bilateral white matter acute and subacute infarctions, likely\nwatershed."
        },
        {
            "input": "MRA brain: The intracranial vertebral and internal carotid arteries and their\nmajor branches appear normal without evidence of stenosis, occlusion, or\naneurysm formation.\n\nMRA neck: The common, internal and external carotid arteries appear normal. \nThere is no evidence of stenosis by NASCET criteria. The origins of the great\nvessels, subclavian, and vertebral arteries appear normal bilaterally.  The\ncommon carotid bifurcations appear normal.",
            "output": "1. No evidence of stenosis, occlusion or aneurysmal dilatation of the large\narterial vessels of the head and neck."
        },
        {
            "input": "MRA brain: The intracranial vertebral and internal carotid arteries and their\nmajor branches appear normal without evidence of stenosis, occlusion, or\naneurysm formation.  The right vertebral artery is dominant.\n\nMRA neck:  Evaluation of the carotid arteries is sigmoid mildly limited due to\ncontrast bolus timing. The left common, internal, and external carotid\narteries appear normal.\n\nThe right carotid bifurcation is not optimally seen due to contrast bolus\ntiming but there is no high-grade stenosis or occlusion. The right common,\ninternal, and external carotid arteries otherwise appear normal.\n\nThe cervical vertebral arteries are normal.\n\nThe origins of the great vessels, subclavian and vertebral arteries appear\nnormal bilaterally.",
            "output": "1.  Normal MRA head.\n2.  Normal left common, cervical internal, and external carotid artery.\n3.  Suboptimal visualization of the right carotid bifurcation due to contrast\nbolus timing but no high-grade stenosis or occlusion.\n4.  Normal cervical vertebral arteries."
        },
        {
            "input": "There is an incompletely evaluated T1 hypointense, T2 hyperintense lesion\nwhich demonstrates restricted diffusion with its epicenter in the left\nparietal bone with an exophytic component extending inferiorly into the left\nfrontoparietal subarachnoid space.  The lesion measures 22 x 16 mm on sagittal\nT1 imaging.  There is no adjacent edema in the left perirolandic cortex.\nNo limbic system signal abnormality to suggest a paraneoplastic/limbic\nencephalitis.  No acute intracranial infarct or hemorrhage.\nMild generalized cerebral atrophy with ex vacuo dilatation of the ventricular\nsystem.  Mild periventricular and deep white matter T2 and FLAIR hyperintense\nchanges are most likely sequela of microangiopathy.  Punctate focus of high\nsignal on the diffusion weighted images (7;19) demonstrates no correlate on\nthe other sequences - and may be artifactual in etiology.  No territorial\ninfarction.\nThe craniocervical junction appears normal.  Partially empty sella.  The\nintracranial arteries demonstrate normal T2 flow voids.  The orbits appear\nnormal.  The paranasal sinuses are essentially clear.",
            "output": "There is an incompletely evaluated T1 hyperintense, T2 hyperintense lesion\nwhich demonstrates restricted diffusion with its epicenter in the left\nparietal bone with an exophytic component extending inferiorly into the left\nfrontoparietal subarachnoid space.  The lesion measures 22 x 16 mm on sagittal\nT1 imaging.  There is no adjacent edema in the left perirolandic cortex.\nPostcontrast MP rage imaging is advised to better assess this lesion.\n\nThis lesion was present on prior CT brain done ___, but is increased\ncompared to prior CT done ___ and was not clearly seen on prior\nCT done ___.\n\nNo acute intracranial infarct or hemorrhage. No limbic system signal\nabnormality to suggest a paraneoplastic/limbic encephalitis.\n\nRECOMMENDATION(S):  MRI head with contrast is recommended for further\nevaluation."
        },
        {
            "input": "There is no evidence of acute infarction.  A chronic lacunar infarction versus\nprominent perivascular spaces noted within the right putamen.  No intracranial\nhemorrhage.  No mass, mass effect, edema or midline shift.\n\nThe ventricles and sulci are normal, without evidence of hydrocephalus. \nProminent perivascular spaces are noted in the bilateral basal ganglia.  The\nbasal cisterns are patent.  There is gross preservation of the principal\nintracranial vascular flow voids.\n\nFollowing the administration of intravenous contrast material, there is no\nabnormal enhancement.  The dural venous sinuses appear patent on MP-RAGE\nimagine sequences.\n\nMild mucosal thickening is seen in scattered ethmoid air cells.  The remainder\nof the visualized paranasal sinuses, middle ear cavities, and mastoid air\ncells are well aerated and clear.  The orbits are within normal limits\nbilaterally.",
            "output": "1. No evidence for acute intracranial hemorrhage, ischemia, infarction, or\nabnormal enhancement."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor acute infarction.  The chronic lacunar infarction in the right basal\nganglia is unchanged.  Scattered foci of T2/FLAIR hyperintensities in the\nsupratentorial white matter are nonspecific, but may represent the sequela of\nmild chronic small vessel ischemic disease.  The ventricles and sulci are\nprominent, likely related to diffuse cerebral volume loss.  The hippocampi and\nmamillary bodies are symmetric and normal in size and signal.\n\nThere is mild mucosal thickening in the bilateral ethmoid air cells.  The\npatient is status post bilateral cataract surgery.\n\nThe major intracranial flow voids are preserved.",
            "output": "1. Normal size and signal of the hippocampi.\n2. Brain atrophy.\n3. No acute intracranial abnormality."
        },
        {
            "input": "MRI:  There is no intracranial hemorrhage, mass, mass effect, or acute\ninfarction. Ventricles and sulci are age-appropriate. Scattered white matter\nFLAIR hyperintensities are nonspecific but likely sequelae of chronic small\nvessel ischemic disease.\n\nThere is no region of restricted diffusion or abnormal susceptibility\nartifact. Major vascular flow voids are preserved.\n\nPost contrast images demonstrate no abnormal parenchymal or meningeal\nenhancement.\n\nVisualized paranasal sinuses are notable for mild mucosal thickening in the\nmaxillary sinuses and opacification of few ethmoid air cells.  Mastoid air\ncells are clear.\n\nMRV: There is no evidence of dural venous sinus thrombosis.",
            "output": "No evidence of acute infarction or dural venous sinus thrombosis."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, or infarction.\nThe ventricles and sulci are normal in caliber and configuration. A partially\nempty sella is again noted. There is stable scattered foci of T2/FLAIR signal\nhyperintensity in the periventricular, subcortical, and deep white matter.\nThere is similar T2 hyperintensity also noted within the central pons. These\nfindings are most likely secondary to chronic small vessel ischemic disease.\nThere is no abnormal enhancement after contrast administration.  Major\nvascular flow voids are preserved. The orbits are unremarkable. There is\nminimal mucosal thickening within the ethmoid air cells and a mucous retention\ncyst in left maxillary sinus. The remaining paranasal sinuses and mastoid air\ncells are clear.",
            "output": "No evidence of acute infarction or enhancing mass lesion\n\nStable T2/FLAIR signal hyperintensity in the periventricular, subcortical, and\ndeep white matter and central pons which is nonspecific but likely reflective\nof early chronic small vessel ischemic disease."
        },
        {
            "input": "Image quality is degraded by motion artifact.\n\nA thin right parafalcine subdural hematoma is again noted.  This is not\nsignificantly changed compared to prior study. No new acute hemorrhage is\nidentified.\n\nThere is no acute infarction, midline shift or mass effect.  No diffusion\nabnormalities are detected. The cerebral volume is appropriate for the\npatient's stated age.  A partially empty sella is again visualized. The major\nvascular flow voids are maintained.\n\nThere is no evidence of abnormal enhancement.\n\nThe orbits are unremarkable, the paranasal sinuses and mastoid air cells are\nclear\n.\nBone marrow signal in the included limited cervical spine, calvaria, and\nclivus appear diffusely and uniformly T1 hypointense. There is no evidence of\na destructive focal lesion. There is no abnormal enhancement.\n\nLimited cervical soft tissues reveal no lymphadenopathy.",
            "output": "1.  Trace right parafalcine subdural hematoma, unchanged compared to prior\nstudy.\n2.  No new hemorrhage.\n2.  Diffusely and uniformly T1-hypointense regional bone marrow signal. This\nfinding may represent red marrow reconversion secondary to patient's\nunderlying disease versus treatment effect versus underlying osteopenia.\nClinical correlation is recommended."
        },
        {
            "input": "There is no evidence of acute intracranial hemorrhage, mass, mass effect or\nshifting of the normally midline structures. The ventricles and sulci are\nprominent, likely age related and involutional in nature. Multiple scattered\nfoci of high signal intensity are detected in the subcortical and\nperiventricular white matter, which are nonspecific and may reflect changes\ndue to small vessel disease.  No diffusion abnormalities are detected to\nindicate acute or subacute ischemic changes.  The major vascular flow voids\nare present.  The orbits are unremarkable. There is mucosal thickening in the\nethmoid air cells and maxillary sinuses; otherwise, the paranasal sinuses and\nthe mastoid air cells are clear.",
            "output": "There is no restricted diffusion concerning for infarction. No other acute\nintracranial processes identified.\n\nMultiple scattered foci of high signal intensity identified in the subcortical\nand periventricular white matter, are nonspecific and may reflect changes due\nto small vessel disease.\n\nIf there is clinical concern for metastatic disease, MRI with contrast is more\nsensitive for metastatic lesions."
        },
        {
            "input": "There is a superficial lesion at the junction of left occipital and parietal\nlobes with peripheral contrast enhancement and at least one enhancing internal\nseptation, which measures 1.3 x 1.3 x 1.3 cm.  The lesion abuts the dura,\ncompatible with either extra-axial or superficial cortical location.  There is\nmild to moderate edema in the adjacent occipital and inferior parietal\nparenchyma.  There is no shift of midline structures.  The occipital horn of\nthe left lateral ventricle is smaller than the right, but the frontal horn of\nthe left lateral ventricle is also slightly smaller than the right, suggesting\nthat the ventricular asymmetry could be congenital or developmental, rather\nthan related to mass effect, as the parenchymal edema does not extend along\nthe occipital horn.\n\nThere is a developmental venous anomaly in the right precentral gyrus. \nOtherwise, comprehensive evaluation of the brain parenchyma is not performed\nwith this limited postcontrast exam which is targeted for surgical planning.\n\nMajor dural venous sinuses are patent.  Major intracranial arteries are not\noptimally evaluated.",
            "output": "1. Peripherally enhancing septated 1.3 cm lesion at the junction of the left\noccipital and parietal lobes, which may be extra-axial or superficial\ncortical.  Given the presence of mild to moderate edema despite the small size\nof the lesion, diagnostic considerations include metastatic disease and a\nprimary glial/neuroglial neoplasm.\n2. Developmental venous anomaly in the right precentral gyrus."
        },
        {
            "input": "Patient is status post left occipital biopsy. Left occipital burr hole is\nnoted. There is expected postoperative pneumocephalus projecting over the\nsurgical site.  There is similar pattern of edema around the surgical site,\nwith persistent effacement of the adjacent sulci.  No diffusion abnormality is\ndetected. There are no new lesions.\nDevelopmental venous anomaly is unchanged in the right frontal lobe.\nThe paranasal sinuses and mastoid air cells demonstrate normal signal.",
            "output": "Expected postoperative changes related to the recent left occipital biopsy."
        },
        {
            "input": "Left occipital craniotomy and left occipital lobe mass resection is a\nre-identified.  There is decreased amount of gradient echo susceptibility\nwithin the resection cavity.  However, there is now more confluent nodular\nenhancement and thickening along the periphery of the resection margin\nparticularly along its inferior aspects (series 1001b, image 90) the\nenhancement at the inferior aspect of the resection margins measures\napproximately 1.5 x 1.2 x 0.7 cm (TRV, AP, SI) with increased confluence and\nconspicuity of surrounding FLAIR hyperintense edema pattern.  There is local\nsulcal and occipital horn of the left lateral ventricle effacement secondary\nto the mass effect\n\nNo other enhancing foci are identified.  There is no acute intracranial\nhemorrhage or infarct.  And incidentally noted right frontal supplemental\nmotor area developmental venous anomaly (series 1001 B, image 105) is stable. \nSulci, ventricles and cisterns are within expected limits for the patient's\nage.  The paranasal sinuses are essentially clear.  The orbits are\nunremarkable.  The mastoid air cells demonstrate mild fluid signal at the\ntips.  Incidental note is made of a metopic suture.",
            "output": "1. The patient is status post left occipital craniotomy with resection of a\nleft occipital lobe mass.\n\n2. When compared to the prior exam there is increase enhancement and nodular\nthickening along the periphery of the resection margin particularly along the\ninferior aspects.  There is increased surrounding FLAIR hyperintense edema\npattern with local sulcal effacement and mild effacement of the occipital horn\nof the left lateral ventricle.  While this may represent posttreatment\nchanges, disease progression and residual tumor is not excluded.\n\n3. No additional lesions are identified.\n\nRECOMMENDATION(S):  Point 2:  Close attention on followup imaging is\nrecommended.  This could be further evaluated with perfusion and STIR tracts\ncould be as indicated on follow-up."
        },
        {
            "input": "MR BRAIN:  Left occipital craniotomy with left occipital mass resection is\nre-identified.  When compared to the previous examination of ___,\nthere is increased size T2/FLAIR white matter hyperintensity of the left\nparieto-occipital lobe with new extension the corpus callosum and posterior\nleft temporal lobe.  There is increased effacement of the track on and\noccipital horn of the left lateral ventricle and local sulcal effacement.  In\nparticular, the superior FLAIR hyperintense signal of the left parietal lobe\nappears fairly well defined and masslike (series 10, image 20).\n\nFLAIR hyperintense signal of the resection margin is substantially more\nconfluent am prominent, now measuring 3.5 x 2.7 cm (AP, TRV ; series 10, image\n16) and demonstrates postcontrast enhancement (series 11, image 17),\nsignificantly increased in size.\n\nThere is a new 3 mm enhancing nodule within the posterior horn of the left\nlateral ventricle (series 1201b, image 51 and series 11, image 11), concerning\nfor ventricular extension.  The lesion demonstrates possible restricted\ndiffusion (series 502, image 11, series 500, image 11).\n\nLinear enhancement of the right precentral gyrus is compatible with a\ndevelopmental venous anomaly, unchanged from prior exam.  Trace linear FLAIR\nhyperintense signal of the left cerebellar hemisphere corresponds to vessels.\n\nThe remainder of the sulci, ventricles cisterns are within expected limits for\nthe patient's age.  The dural venous sinuses are patent.  The paranasal\nsinuses are clear.  The orbits are unremarkable.  The mastoid air cells\ndemonstrate trace fluid signal in the tips.\n\nIncidental note is made of a metopic suture per\n\nMR ___: There is no increased blood flow or volume on dynamic\nsusceptibility contrast perfusion images relative to the contralateral\nnormal-appearing white matter.\n\nASL Perfusion: There is suggestion of minimally increased perfusion on ASL in\nthe region of the resection cavity.\n\nMR Spectroscopy: Single voxel spectroscopy centered in the resection margin at\nthe region of avid enhancement demonstrates increased choline to NAA ratio of\n2.8.\n\nMulti voxel spectroscopy centered in the resection cavity and the\ncontralateral normal appearing parieto-occipital demonstrates increased\ncholine to NAA ratio in voxels 4 (1.9) and 5 (2.10) at the periphery of the\nresection margin.  The voxel located within the resection cavity itself\ndemonstrate increased lactate and overall decreased metabolites, compatible\nposttreatment changes and with minimally increased choline to NAA ratio\nmeasuring approximately 1.5 in voxels 8 and 9 and < 2 in voxels 14 and 15.",
            "output": "1. Significant interval size and distribution of increased FLAIR hyperintense\nsignal involving the left parietal occipital and temporal lobes with extension\nto the corpus callosum when compared to examination of ___.\n2. The resection margin now demonstrates a thick rind of nodular enhancement\nmeasuring 3.5 x 2.7 cm (AP, TRV).\n3. There is a new punctate focus of left lateral posterior horn enhancement.\n4. Increased choline to NAA ratio in single and multi voxel spectroscopy.\n5. The constellation of findings are concerning for disease progression rather\nthan pseudo progression, particularly given the new focus of enhancement with\nin the occipital horn of the left lateral ventricle."
        },
        {
            "input": "The patient is status post left occipital parietal craniotomy and left\nparieto-occipital mass resection, expected postsurgical changes are present\nconsistent with surgical cavity, filling with CSF and residual pneumocephalus,\nthe T1 weighted images without contrast, demonstrate high-signal intensity in\nthe surgical bed, consistent with blood products, after the administration of\nintravenous contrast material, there is no evidence of significant enhancement\nsurrounding the surgical bed, there is no evidence of residual mass, however\nlong-term followup is advised to demonstrate stability or any further tumoral\nrecurrence.  The diffusion-weighted images are notable for slow diffusion in\nthis left occipital lobe and in the inferior aspect of the surgical cavity\n(images 14 through 16, suggesting acute ischemic changes, probably venous in\nnature.  There is persistent vasogenic edema surrounding the left occipital\nventricular region.  No new lesions are identified there is a small\ndevelopmental venous anomaly on the right frontal lobe.  The orbits, the\nparanasal sinuses and mastoid air cells are unremarkable.",
            "output": "1.  Status post left parieto-occipital craniotomy and left parietal occipital\nmass resection, postsurgical and expected changes are seen, with no evidence\nof residual mass lesion, long-term followup is advised to demonstrate\nstability or any further tumoral recurrence.\n\n2.  Small area of slow diffusion is identified in the lower aspect of the\nsurgical bed, involving the medial aspect of the left occipital lobe,\nconsistent with acute ischemia, probably venous in nature.\n\nNOTIFICATION:  The findings were discussed by Dr. ___ with Dr. ___\non the telephone on ___ at 11:34 AM, 5 minutes after discovery of the\nfindings.\n\nRECOMMENDATION(S):  Long-term followup with MRI of the brain with and without\ncontrast, is recommended to demonstrate stability or possible tumoral\nrecurrence."
        },
        {
            "input": "The patient's previously noted left occipital resection cavity is again seen. \nThere is nodular slow diffusion at the anterior margin with corresponding\npostcontrast hyperintensity consistent with evolving, subacute ischemic change\ngiven the acute ischemia seen on prior study.\n\nThere is punctate hyperintensity at the left lateral ventricular occipital\nhorn that is not clearly identified on the most recent prior exam (see9:34). \nThere is hypointense adjacent edema or infiltrative tumor.  There is no\nsignificant mass or midline shift.  The vasculature is patent.  A stable right\nfrontal precentral gyrus DVA is again seen.  The remainder of the visualized\nstructures are unremarkable.",
            "output": "1. Grossly stable left occipital resection cavity with adjacent subacute\nischemic change as described.\n2. Limited evaluation of a punctate left lateral ventricle occipital horn\nstructure.  Within limits of this postcontrast only study, differential\nconsiderations include subacute blood products or new ependymal enhancement. \nRecommend clinical correlation and attention on followup imaging.\n\nRECOMMENDATION(S):  Limited evaluation of a punctate left lateral ventricle\noccipital horn structure.  Within limits of this postcontrast only study,\ndifferential considerations include subacute blood products or new ependymal\nenhancement. Recommend clinical correlation and attention on followup imaging."
        },
        {
            "input": "The patient's pre-existing metastatic lesions have increased in size since MRI\n___:\n\n1. Right parietal lobe, 16 mm in greatest dimension (previously 6 mm),\nheterogeneously enhancing with diffusion restriction, peripheral areas of\nsusceptibility artifact, as well as disproportionate perilesional T2 FLAIR\nhyperintensity.\n2. Left thalamus, 9 mm in greatest dimension (previously 4 mm),\nheterogeneously enhancing with diffusion restriction.\n\nThere are several new lesions on today's examination:\n\n1. Anterior right corona radiata, 12 mm in greatest dimension, heterogeneously\nenhancing with peripheral diffusion restriction, susceptibility artifact, and\ndisproportionate perilesional T2 FLAIR hyperintensity.\n2. Parafalcine left parietal lobe, 12 mm in greatest dimension, ring-enhancing\nwith susceptibility artifact, peripheral diffusion restriction, as well as\ndisproportionate perilesional T2 FLAIR hyperintensity.\n3. Left middle frontal gyrus, 5 mm in greatest dimension, nonenhancing but\nwith peripheral T2 FLAIR hyperintensity and susceptibility artifact.  This\nlesion is new since comparison examinations and is also suspicious for\nmetastasis.\n\nThere is no leptomeningeal or pachymeningeal enhancement.  On the remainder of\nthe examination, there is no hemorrhage, infarct, edema, mass effect or\nhydrocephalus.  There are scattered T2 FLAIR hyperintense foci in the\nsubcortical and periventricular white matter of the cerebral hemispheres\nfavored to represent chronic microangiopathic ischemic disease.\n\nThere is no thrombus within the major intracranial arteries and dural venous\nsinuses.\n\nThere is no abnormal enhancement within the orbits.  The frontal sinuses are\natrophic.  The remaining paranasal sinuses and mastoid air cells appear\nwell-aerated.  No aggressive osseous lesion is identified in the calvarium or\nskull base.",
            "output": "1. Interval progression of the pre-existing metastatic lesions in the right\nparietal lobe and left thalamus since MRI ___.  The right parietal\nlobe lesion now measures 16 mm (previously 6 mm), while the left thalamic\nlesion now measures 9 mm (previously 4 mm).\n2. There are 2 additional lesions in the anterior right corona radiata\nmeasuring 12 mm and in the parafalcine left parietal lobe measuring 12 mm.\n3. There is a new 5 mm lesion in the left middle frontal gyrus without\npostgadolinium enhancement, but with peripheral T2 FLAIR hyperintensity and\nsusceptibility artifact which is nonetheless suspicious for a hemorrhagic\nmetastasis."
        },
        {
            "input": "There are multifocal supratentorial metastatic lesions (about 9 lesions), some\nof them newly developed, and some increased in size compared to prior\nexaminations as follows:\n\n-Two new left middle frontal gyrus enhancing hemorrhagic metastases measuring\n5 mm and 6 mm.  (10:206 and 212).\n-New left medial frontal metastatic lesion measuring 3 mm (10:142).\n-New left occipital temporal hemorrhagic small metastatic lesion measuring 2-3\nmm (10:137).\n-Interval enlargement of left parietal hemorrhagic metastatic lesion measuring\nnow 18 mm compared to 12 mm.  (10:241).\n-Interval enlargement of right frontoparietal hemorrhagic metastatic lesion\nmeasuring now 19 mm compared to 16 mm.  (10:214)\n-Interval enlargement of right anterior frontal lobe parenchymal hemorrhage\nmetastatic lesion measuring now 17 mm compared to 12 mm.  (10:167)\n-Interval enlargement of left thalamic hemorrhagic metastatic lesion measuring\n13 mm compared to 9 mm.  (10:63).\n-Interval enlargement of left orbital gyrus hemorrhagic metastatic lesion\nmeasuring now 9 mm compared to 7 mm.  (10:105).\n\nThe associated surrounding T2 FLAIR hyperintensity is increased in all lesions\nas well as extent of associated increased susceptibility related to blood\nproducts.\n\nThere is no acute infarct, midline shift, brain herniation or hydrocephalus. \nThere are scattered T2 FLAIR hyperintense foci in the subcortical and\nperiventricular white matter of the cerebral hemispheres favored to represent\nchronic microangiopathic ischemic disease.  Unremarkable major intracranial\nvascular flow voids.  Patent dural venous sinuses.\n\nBoth orbits are unremarkable.  Small bilateral maxillary sinuses retention\ncysts.  Is trace fluid signal intensity at both mastoid air cells.  No\naggressive osseous lesions.",
            "output": "1. Multifocal supratentorial hemorrhagic metastatic lesions (about 9), either\nnew (4 lesions) or show interval increase in size compared to prior\nexamination.\n2. Interval increased extent of associated T2 FLAIR hyperintensity as well as\nhemorrhagic component.\n3. No midline shift, brain herniation or acute hydrocephalus.  No acute\ninfarction."
        },
        {
            "input": "MR BRAIN:\n\nThere are scattered acute to subacute infarcts within the left frontal lobe,\nparacentral lobule, and left superior parietal lobule, without evidence of\nhemorrhagic transformation.  The largest approximately 18 mm infarct involves\nthe left frontal subcortical white matter, and an adjacent smaller infarct\ninvolves the left frontal centrum semiovale.  Other small infarcts are\ncortical.  These infarcts are of varying ages within the acute to subacute\ntime frame.\n\nThe largest recent infarct is adjacent to a prior chronic infarct in the left\nfrontal lobe. There is an additional small old lacunar infarct within the head\nof the right caudate nucleus.There are confluent small areas of hyperintense\nsignal on T2 weighted images within the bilateral cerebral hemispheres and\npons, nonspecific although likely the sequela of mild chronic small vessel\ndisease.\n\nThere is minimal hyperintense signal on FLAIR images within the left central\nsulcus and overlying the medial surface of the left superior frontal gyrus,\nconsistent with the mild subarachnoid blood products seen on recent CT.\n\nThere is a small focus of low signal intensity on GRE within the left lateral\noccipital temporal gyrus, consistent with a chronic microhemorrhage, image\n13:9.\n\nThe major vascular flow voids are preserved.\n\nMRA BRAIN:\n\nThe MRA images are mildly degraded due to motion artifact.  There is no\nevidence for flow-limiting stenosis or aneurysm.  There is fetal configuration\nof the right posterior cerebral artery with an infundibulum at the origin of\nthe aplastic right P1 segment, as seen on the subsequent CTA.",
            "output": "1. Acute to subacute infarcts of varying ages within the left frontal and\nsuperior parietal lobes as detailed above, without evidence of hemorrhagic\ntransformation.  These are likely embolic in nature.\n2. Trace subarachnoid hemorrhage overlying the left superior frontal gyrus and\nwithin the left central sulcus, as seen on the preceding CT.  The relationship\nof this trace subarachnoid hemorrhage to the acute to subacute infarcts is\nuncertain.\n3. Small old lacunar infarct within the head of the right caudate nucleus and\nan old infarct within the left middle frontal gyrus in the left ACA-MCA border\nzone.\n4. Punctate chronic microhemorrhage in the left lateral occipital temporal\ngyrus.\n5. Mildly degraded MRA head due to motion artifact.  No evidence for\nflow-limiting stenosis or aneurysm.  Infundibulum at the origin of the\naplastic right P1 segment.\n\nNOTIFICATION:  The acute/subacute infarctions and subarachnoid hemorrhage were\ndiscussed with ___, M.D. by ___, M.D. on the\ntelephone on ___ at 4:58 pm"
        },
        {
            "input": "There is incompletely characterized calvarial defect of the right parietal\nskull (series 17, image 144), with gradient echo susceptibility blooming\nartifact overlying the right parietal lobe (series 14, image 20).  This could\nrepresent sequela of prior instrumentation or trauma.\n\nThere is no evidence of hemorrhage, edema, midline shift or infarction.   The\nventricles and sulci are prominent, within appropriate limits for patient's\nage.  Few periventricular and subcortical white matter hypodensities are\nnonspecific but likely sequelae of chronic small vessel ischemic disease. \nThere is no abnormal enhancement after contrast administration.\n\nThe dural venous sinuses are patent.  The major intracranial flow voids are\npreserved.\n\nThe orbits are unremarkable.  Mild mucosal thickening and mucous retention\ncyst noted in the left maxillary sinus.  The mastoid air cells, middle ear\ncavities are unremarkable.  Major intracranial vascular flow voids are\npreserved.",
            "output": "1. There is a right parietal defect overlying the right parietal lobe with\nsubjacent chronic blood products.  This may represent sequela prior trauma or\ninstrumentation.  Correlation with patient clinical history is recommended. \nGiven the patient's clinical history, this could be further evaluated with CT\nhead.\n2. No evidence of intracranial metastatic disease at this time.\n3. No acute infarct or suspicious parenchymal FLAIR signal abnormality.  No\nabnormal enhancement.\n4. Additional findings described above."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  No abnormal postcontrast enhancement.  The sulci, ventricles\nand cisterns are within expected limits for the patient's mild senescent\nrelated global cerebral volume loss.  Minimal punctate periventricular and\nsubcortical T2/FLAIR white matter hyperintensities are nonspecific, but\ncompatible with chronic microangiopathy in a patient this age and within\nexpected limits for age, unchanged.  The major intracranial flow voids are\npreserved.  The dural venous sinuses are patent.  There is mild mucosal\nthickening of the paranasal sinuses.  The orbits are unremarkable.  No\nsignificant fluid signal in the mastoid air cells.  Right parietal defect is\nunchanged from prior exam.",
            "output": "1. No evidence of intracranial metastatic disease at this time.  No suspicious\nparenchymal FLAIR signal abnormality or abnormal enhancement.\n2. No acute intracranial abnormality on contrast enhanced MRI brain.\n3. Unchanged appearance of right parietal calvarial defect."
        },
        {
            "input": "There are nonenhancing and nonspecific periventricular and subcortical\nT2/FLAIR white matter hyperintensities.  There is no acute infarct or\nintracranial hemorrhage.  There are no intracranial masses.  Sulci, ventricles\nand cisterns are within expected limits for the patient's age.  The dural\nvenous sinuses are patent.  The major intracranial flow voids are preserved. \nThe paranasal sinuses are clear.  The orbits are unremarkable.  The mastoid\nair cells are clear.",
            "output": "1. Nonspecific periventricular and subcortical T2/FLAIR white matter\nhyperintensities.  \n2. No acute infarct or intracranial hemorrhage.\n\nRECOMMENDATION(S):  Comparison to prior examinations is recommended when\navailable."
        },
        {
            "input": "There is no intra or extra-axial mass or hemorrhage.  A few punctate\ndiffusion-weighted hyperintense foci of the left occipital lobe (series 4,\nimage 9 and 10) does not demonstrate definitive associated ADC hypo intensity\nor FLAIR hyperintensity.  Otherwise, no definitive acute infarct.  The sulci,\nventricles and cisterns are within expected limits for the degree of moderate\nsenescent related global cerebral volume loss.  There is no evidence of\ncortical thickening or signal abnormality.  There are subcortical and\nperiventricular T2/FLAIR white matter hyperintensities, which are nonspecific,\nbut compatible with chronic microangiopathy in a patient of this age.  The\nmajor intracranial flow voids are preserved.  There is mild mucosal thickening\nof the ethmoid air cells.  The orbits are unremarkable.  No fluid signal is\nnoted in the mastoid tip.",
            "output": "1. No evidence of intracranial mass or hemorrhage.\n2. No definitive acute infarct.  A few punctate diffusion-weighted\nhyperintense foci of the left occipital lobe does not demonstrate definitive\nADC hypointensity or associated FLAIR abnormality.  These are felt to be\nlikely artifact, although tiny embolic infarcts are not entirely excluded\ngiven patient's recent vascular procedure.\n3. No evidence of suspicious parenchymal signal abnormality or cortical\nthickening.\n4. White matter changes, nonspecific, but commonly seen in setting of chronic\nmicroangiopathy in a patient of this age."
        },
        {
            "input": "Study is moderately degraded by motion.  Within these confines:\n\nMR BRAIN:\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are preserved in caliber and\nconfiguration.  Right sphenoid sinus near complete opacification is again\nnoted.  There is re-demonstration of low-lying cerebellar tonsils, extending\nat least 4 mm inferior to foramina magnum (see 11:104).  An approximately 3 mm\npineal cyst is noted.  A right frontal developmental venous anomaly is noted\n\nMRA BRAIN: The intracranial vertebral and internal carotid arteries and their\nmajor branchesappear grossly preserved,without definite evidence of stenosis,\nocclusion, or aneurysm formation.",
            "output": "1. Study is moderately degraded by motion.\n2.  No acute intracranial abnormality.\n3.  Within limits of study, no definite evidence of intracranial mass or\nlesion.\n4. Grossly patent circle of ___ without definite evidence of aneurysm,\nstenosis, or occlusion.\n5.  Paranasal sinus disease , grossly similar to ___ prior exam\nwhere findings were concerning for chronic and/or fungal sinusitis, as\ndescribed.\n6. Grossly stable low-lying cerebellar tonsils as described, again which may\nbe seen in the setting of Chiari 1 malformation.\n7. Right frontal probable developmental venous anomaly, which is a normal\nvariant."
        },
        {
            "input": "The ventricles and extra-axial spaces are normal in size. There is no evidence\nof midline shift, mass effect or hydrocephalus. There are no acute infarcts.\nThere is no evidence of focal abnormalities.  The vascular flow voids are\nmaintained. The visualized paranasal sinuses are clear. Following gadolinium\nadministration there is no evidence of abnormal parenchymal, vascular and\nmeningeal enhancement seen.  The cerebellopontine angles are unremarkable.",
            "output": "Normal MRI of the brain"
        },
        {
            "input": "There has been interval resection of the previously demonstrated mass at the\nleft cerebellopontine angle, with expected postsurgical changes at the left\nsuboccipital craniotomy site.  Small volume blood products layering within the\nresection cavity are consistent with postsurgical change.  Mild nodular\nthickening and enhancement is demonstrated along the periphery of the\nresection cavity, predominantly along the anterior aspect with similar\nextension into the medial IAC.\n\nLimited included imaging of the remainder of the brain demonstrates no\nevidence of hemorrhage, edema, masses, mass effect, or midline shift.  There\nis a tiny focus of increased signal on diffusion-weighted images within the\nleft central aspect of the pons, with associated increased signal on FLAIR\nimaging (7:9, 4:9) findings which could represent a small focus of subacute\ninfarct.  The ventricles and sulci are normal in caliber and configuration.\n\nMild mucosal thickening of the bilateral ethmoid air cells.  The visualized\nportion of the remaining paranasal sinuses,mastoid air cells, and middle ear\ncavitiesare clear. The orbits are unremarkable. The visualized portion of the\nprinciple vascular flow voids are preserved.",
            "output": "1. Status post resection of the previously demonstrated mass at the left\ncerebellopontine angle, with mild nodular thickening and enhancement\ndemonstrated along the periphery of the resection cavity predominantly along\nthe anterior aspect with similar extension into the medial IAC, findings which\nmay be related to postsurgical change or residual tumor.  Continued close\nattention on follow-up imaging is recommended.\n2. Tiny focus of increased signal within the left central aspect of the pons\non both DWI and FLAIR imaging, findings which could represent a small focus of\nsubacute infarct.\n\nNOTIFICATION:  The findings were discussed with ___. by ___.\n___, M.D. on the telephone on ___ at approximately 2pm, 90 minutes\nafter discovery of the findings."
        },
        {
            "input": "This report covers two exams performed concurrently including MRI of the\ninternal auditory canals (IAC's), as well as MRV of the head, please note that\nthe study is slightly limited due to patient motion.\n\nImages through the internal auditory canals.  Again demonstrate left posterior\nfossa postsurgical changes. Approximately 8 CC x 11 AP x 9 TRV mm triangular\nenhancement within the left cerebellopontine angle that extends into the\ninternal auditory canal appears similar to the ___ study.  Previously\nseen peripherally enhancing fluid collection adjacent to the left mastoid\nsinus has significantly decreased over the interval, suggestive of evolving\npostoperative change.  Enhancement of the left transverse and sigmoid sinus is\nagain noted, consistent with recanalization of the previously thrombosed\nsinuses.\n\nNo convincing abnormality involving in the right seventh made cranial nerve\ncomplex is evident.\n\nLimited imaging of the remainder of the brain demonstrates no evidence of\nacute infarction or hemorrhage.  The ventricles and sulci are normal in\ncaliber and configuration.\n\nThere is mild mucosal thickening of the right maxillary sinus.  In bilateral\nmaxillary sinus air fluid levels have resolved.  The orbits are unremarkable.\nThe visualized portion of the principle vascular flow voids are preserved.\n\nMRV of the head: There has been interval recanalization of the left transverse\nand sigmoid sinuses.  Irregularity and incomplete flow related signal are\nnoted in the left transverse sinus adjacent to the superior sagittal sinus. \nCorrelation with the brain MRI scan demonstrates fairly homogeneous\nenhancement with these regions which may indicate areas of stenosis with\ncorresponding diminished flow.  There is also diminished flow related signal\nseen in the mid right transverse sinus which is similar to the prior study and\ncould represent a focal stenosis.  There is normal flow related signal\nthroughout the superior sagittal sinus, straight sinus and right sigmoid\nsinus.  Normal flow related signal is seen within the internal cerebral veins,\nvein ___ and internal jugular veins.",
            "output": "1.  Status post resection of left cerebellopontine angle mass with similar\nresidual enhancement within the resection bed that may represent a combination\nof residual/recurrent tumor and postoperative change.\n\n2.  Interval improvement in probable postoperative collection of the left\nposterior fossa.\n\nBrain MRV:\n1.  Interval recanalization of the previously seen thrombosed left transverse\nand sigmoid sinuses.  Areas of persistent diminished in the left transverse\nsinus flow could reflect stenosis, scarring or chronic residual thrombus.\n\n2.  Diminished flow within the right transverse sinus could represent\nstenosis."
        },
        {
            "input": "There is redemonstration of left suboccipital craniotomy postsurgical changes.\nThere has been interval decrease in amount of fluid along the left\ncerebellopontine angle and area of resection site with decreased associated\nmass effect and re-expansion of the fourth ventricle to now a more normal\nconfiguration.  There has also been decrease in size of a fluid collection\nimmediately subjacent to the left craniotomy site.  There is residual nodular\nenhancement at the left cerebellopontine angle with extension into the porous\nacoustics, fairly similar to prior and may reflect residual tumor and/or a\ncombination of postsurgical changes.  There is a small amount of new rim\nenhancement surrounding the decreased fluid collection subjacent to the left\nsuboccipital craniotomy site which could reflect an abscess formation.  There\nis slightly increased T2 hyperintense signal in the mastoid air cells\nanteriorly which given the new rim enhancement is suggestive of associated\ninflammatory changes.\n\nThere has been resolution of the previously seen left transverse and sigmoid\nsinus thrombosis.\n\nThere is no evidence of acute infarction, hemorrhage or new intracranial mass.\nThe supratentorial ventricular system is normal in size and configuration.\n\nThere is fluid layering in both maxillary sinuses and there is near complete\nopacification of the ethmoid air cells.  The right mastoid air cells appear\nclear.  The orbits appear grossly unremarkable.",
            "output": "1. Redemonstration of postoperative changes after left occipital craniotomy\nfor resection of a left cerebellopontine angle mass.  Reduction in fluid along\nthe resection cavity with decreased cerebellopontine angle mass effect.\n2. Residual nodular enhancement along the left cerebellopontine angle with\nextension into the porous acusticus, similar to prior and may residual\ntumor/and or a combination of postsurgical changes.\n3. New rim enhancement along a decreased fluid collection subjacent to the\nleft suboccipital craniotomy site could reflect inflammatory changes. \nAssociated increase in mild fluid within the anterior left mastoid air cells\ncould represent additional inflammatory changes.  However, there is no\nrestricted diffusion seen within the collection to indicate an abscess.\n4. Resolution of the previously seen left transverse and sigmoid sinus\nthrombosis.\n5. Paranasal sinus disease with fluid in both maxillary sinuses, can be seen\nwith active sinusitis in the appropriate clinical setting."
        },
        {
            "input": "MRI HEAD:  There is no evidence of acute infarction or hemorrhage. There is no\nmass effect, edema, or hydrocephalus. Ventricles and sulci are normal in size\nand configuration. Principal vascular flow voids are preserved. There is no\nabnormal parenchymal, vascular or meningeal enhancement after the\nadministration of gadolinium. Globes and soft tissues are unremarkable.\nVisualized paranasal sinuses and mastoid air cells are well aerated.\n\nHEAD MRA:  Normal flow related signal is seen in the intracranial internal\ncarotid, middle cerebral and anterior cerebral arteries without significant\nmural irregularity or stenosis. There is normal symmetric arborization of the\nMCA branches. There is no aneurysm greater than 3 mm. Normal flow related\nsignal is seen in the codominant intracranial vertebral arteries, the basilar\nartery, and the bilateral superior cerebellar and posterior cerebral arteries.\n\nNECK MRA: There is a normal 3 vessel takeoff from the aortic arch. The\ncervical common carotid, internal carotid and external carotid arteries are\nnormal in course, caliber and contour. They demonstrate normal enhancement\nwithout mural irregularity, stenosis or evidence of dissection. The roughly\ncodominant vertebral arteries are normal in course, caliber and contour. They\ndemonstrate normal enhancement without mural irregularity, stenosis or\nevidence of dissection.",
            "output": "1. Normal MRI of the head; no evidence for demyelinating process.\n2. Normal MRA of the head and neck."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, or infarction.\nThe ventricles and sulci are normal in caliber and configuration. There is no\nabnormal enhancement after contrast administration.  A\n\nMRA of the head shows fall low signal along the right middle cerebral artery\nand distal right internal carotid carotid artery suggestive of a stent. \nApproximately 3 mm area of flow related enhancement is seen anterior to the\nstent (6:72) suggestive of a small area of residual flow within the aneurysm. \nNo other aneurysms or vascular occlusion is identified.  An infundibulum is\nidentified at the origin of right posterior communicating artery.",
            "output": "1. No acute infarcts mass effect hydrocephalus or abnormal enhancement seen. \nNo MRI signs of acute or chronic hemorrhage identified.\n2. MRI demonstrates a stent within the right distal intracranial internal\ncarotid artery and extending to the right middle cerebral artery.  Subtle 3 mm\narea of flow related enhancement is identified in the region of previously\nseen aneurysm."
        },
        {
            "input": "The ventricles and extra-axial spaces are normal in size. There is no evidence\nof midline shift, mass effect or hydrocephalus. There are no acute infarcts. \nA few scattered FLAIR hyperintensities are identified in the white matter\nnonspecific nature and could indicate early changes of small vessel disease. \nNo acute infarcts are seen.  The vascular flow voids are maintained. The\nvisualized paranasal sinuses are clear. Following gadolinium administration\nthere is no evidence of abnormal parenchymal, vascular and meningeal\nenhancement seen.  Incidentally noted is a developmental venous anomaly in the\nright medial parietal lobe (101: 87-93).\n\nCoronal T2 weighted images demonstrate no evidence of abnormal signal or\natrophy of the medial temporal lobe structures.",
            "output": "No significant abnormalities are seen on MRI of the brain with and without\ngadolinium except for early changes of small vessel disease.  No focal\nabnormalities are seen within the medial temporal lobe structures."
        },
        {
            "input": "There are multiple punctate foci of slow diffusion involving the left frontal,\nparietal and occipital lobes.  Most of these lesions demonstrate corresponding\nFLAIR signal abnormality.\n\nThere is a 3.5 x 4.1 x 2.8 cm right anterior cranial fossa extra-axial\nenhancing mass arising from the planum sphenoidal, demonstrating surrounding\nvasogenic edema, partially crossing midline extending into the left side.  No\ndefinite extension into the nasal cavity. The mass demonstrates slightly low\nsignal on the ADC map.  There is central T2 hyperintensity likely representing\nnecrosis.  Resulting mass effect on the frontal horn of the right lateral\nventricle as well as 7 mm midline shift to the left at the level of the\nanterior cranial fossa and frontal horns.  There is no uncal or tonsillar\nherniation..  There is no evidence of intracranial hemorrhage.\n\nThere are a few old small infarcts involving the bilateral cerebellar\nhemispheres, right thalamus and probably posterior limb of the left internal\ncapsule.  Area of encephalomalacia involving splenium corpus callosum, likely\nrelated to prior infarct, or possibly sequela of distant demyelinating\nprocess, with encephalomalacia.\nModerate subcortical and periventricular white matter T2/FLAIR\nhyperintensities are nonspecific but compatible with small vessel disease.\n\nThe major intracranial vascular flow voids are maintained.  The paranasal\nsinuses, mastoid air cells and orbits are normal.  Calcifications involving\nleft globe, decreased size of the globe is again seen.",
            "output": "1. Multiple punctate acute to subacute infarcts involving the left frontal,\nparietal occipital lobes in a watershed type distribution.\n2. Enhancing right frontal extra-axial mass arising from the planum sphenoidal\nis most compatible with a meningioma.  Extent surrounding right frontal lobe\nedema , Can be seen with atypical meningioma.  Local mass effect.\n3. A few small chronic infarcts.\n4. Evidence of moderate white matter small vessel disease.\n\nNOTIFICATION:  The findings were discussed with ___, M.D. by ___\n___, M.D. on the telephone on ___ at 9:47 am, 10 minutes after\ndiscovery of the findings."
        },
        {
            "input": "Multiple foci of restricted diffusion is identified in the left basal ganglia\nand left cerebral hemisphere, most of them are in the watershed distribution. \nSome of these areas are were present in ___, however some of them\nare new, especially in the left frontal lobe and in the left hippocampus,\nextending into the posterior limb of the left internal capsule.  Pre-existing\nareas of slow diffusion demonstrate corresponding FLAIR hyperintensities.\nSmall foci of chronic infarcts are noted in bilateral cerebellar hemispheres\nand basal ganglia.\n\nEnhancing right frontal extra-axial mass arising from the planum sphenoidale\nmeasures 4.3 x 4.4 x 2.7 cm (AP by TV by SI), unchanged.  Surrounding\nconfluent FLAIR hyperintensity is slightly smaller compared to before.\nThere is no evidence of hemorrhage.  Prominent ventricles and sulci likely\nreflect involutional changes.  Periventricular and subcortical white matter\nFLAIR hyperintensities are consistent with chronic small vessel disease.",
            "output": "1. Multiple foci of acute and subacute infarcts are identified in the left\nbasal ganglia and cerebral hemisphere, mostly in watershed distribution.  Some\nof these were present in ___.  Some of them are new, especially in\nthe left frontal lobe and in the left hippocampus extending to the left\ninternal capsule posterior limb.\n2. Vasogenic edema surrounding the right large right frontal mass is slightly\nimproved compared to ___.  The mass is otherwise unchanged and\ncompatible with meningioma."
        },
        {
            "input": "Previously seen multiple infarctions in the left MCA territory have increased\nin extent and become more confluent compared to ___.  Progression\nis most evident in the left temporal, inferior parietal, and insular cortex,\nwhere new gyriform infarctions are present.  There has also been progression\nin the left lentiform nucleus and adjacent deep white matter. Multiple\npre-existing subacute infarcts are again seen in the left frontal cortex, with\nprogression in the left frontal centrum semiovale.  Left frontal and parietal\ndeep white matter infarcts are both acute and subacute.  There is no evidence\nfor associated blood products in the left cerebral hemisphere.  No significant\nmass effect at this time.\n\nChronic small bilateral cerebellar infarcts are against.\n\nNo significant change in the enhancing right frontal extra-axial mass arising\nfrom the planum sphenoidale measuring approximately 4.3 x 4.4 x 2.7 cm (AP by\nTV by SI).  Stable extensive associated right frontal vasogenic edema.  No\nchange in the associated 0.7 cm leftward shift of the anterior falx.  Stable\nmild distortion of the frontal horn of the right lateral ventricle.\n\nProminence of the ventricles and cerebral sulci are compatible with age\nrelated involutional changes.  Periventricular, deep, and subcortical white\nmatter, and pontine, T2/FLAIR hyperintensities without associated acute\ndiffusion abnormality are compatible with small vessel disease given the\npatient's age.\n\nThere is loss of the normal left intracranial ICA flow void and a diminished\nleft MCA M1 flow void, compatible with the near complete occlusion seen on the\n___ CTA head/neck.\n\nThere is mild mucosal thickening in the ethmoid air cells, sphenoid sinuses,\nfrontal sinuses, and left maxillary sinus.  There is left pthisis bulbi and\nevidence of right cataract surgery.",
            "output": "1. Compared to ___, multiple acute and subacute infarctions\nwithin the left MCA territory have increased in extent become more confluent,\nas detailed above.  No evidence for associated blood products.  No significant\nmass effect at this time.\n2. Loss of normal left intracranial ICA flow void and a diminished left MCA M1\nflow void, corresponding to the near complete occlusion identified on the ___ CTA.\n3. Unchanged 4.4 cm right planum sphenoidale extra-axial mass, likely\nmeningioma, with stable mass effect, including approximately 7 mm leftward\nshift of midline structures.\n4. Small chronic bilateral cerebellar infarcts, as well as supratentorial\nwhite matter and pontine signal abnormalities which are likely sequela of\nchronic small vessel ischemic disease, are again demonstrated."
        },
        {
            "input": "There is re- demonstration of slow diffusion within the posterior left centrum\nsemiovale, posterior left insula, and posterior left temporal cortices, which\nis unchanged in its extent, consistent with subacute infarction within the\nleft middle cerebral artery territory.  There is no evidence of hemorrhagic\nconversion.\n\nThere is new restricted diffusion within the mid to lateral right precentral\ngyrus, posterior right insula, lateral right postcentral gyrus, and within the\nposterior right middle temporal gyrus consistent with acute infarction within\nthe right middle cerebral artery territory.  There is no evidence of\nhemorrhagic conversion.\n\nThere is extensive confluent bilateral periventricular and subcortical white\nmatter and central pontine FLAIR hyperintensity consistent with chronic\nmicrovascular changes.  There is a punctate focus of gradient echo blooming\nwithin the right subinsular white matter which is unchanged consistent with a\nchronic microhemorrhage.  There is prominence of the ventricles and cortical\nsulci consistent with moderate atrophy without lobar predominance.  There is\nbilateral symmetric convexity sulcal FLAIR signal hyperintensity, which is new\nin comparison to prior study.  The vascular flow voids are preserved.\n\nThe left lens is absent.  The paranasal sinuses and mastoid air cells are\nclear.  The calvarium and soft tissues are unremarkable.",
            "output": "1. New geographic areas of slow diffusion within the right middle cerebral\nartery territory, as described, consistent with interval acute infarction.  No\nevidence of hemorrhagic conversion.\n2. Unchanged geographic areas of slow diffusion within the left middle\ncerebral artery territory consistent with evolving infarction.  No evidence of\nhemorrhagic conversion.\n3. New bilateral convexity sulcal FLAIR hyperintensity which is a nonspecific\nfinding which may be seen with retained gadolinium from previous injection on\n___.  Other possibilities such as infection or hemorrhage appears\nless likely.\n4. Unchanged extensive chronic microvascular disease."
        },
        {
            "input": "There are mild chronic small vessel ischemic changes.  There is no evidence of\nhemorrhage, edema, masses, mass effect, midline shift or infarction.   The\nventricles and sulci are normal in caliber and configuration.  There is small\nfocus of faint subcortical enhancement involving inferior left frontal lobe,\ninvolving either motor or pre motor gyrus, well lateral to the expected\nposition of the hand motor homunculus, series 100 a image 71, without\nassociated T2 signal abnormality, most consistent with small developmental\nvenous anomaly ; small area of nonenhancing T2 signal abnormality medial to\nthis may represent gliosis associated with it.  There is no abnormal\nenhancement after contrast administration.  There are mild mucosal thickening\nof the paranasal sinuses, most prominent in the maxillary sinuses.  Mastoid\nair cells, middle ear cavities are clear.  Intracranial vascular flow voids\nare preserved.",
            "output": "1. There is no evidence of mass or infarct.\n2. There are mild chronic small vessel ischemic changes."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There are mild chronic small vessel ischemic changes.  Small\nchronic lacunar infarcts seen in the posterior right putamen and probably in\nthe left thalamus.  There is trace opacification of the ethmoid air cells,\nright mastoid air cells.  Otherwise, paranasal sinuses, left mastoid air\ncells, middle ear cavities are clear.  Intracranial vascular flow voids are\npreserved",
            "output": "1. There are no acute changes.\n2. Chronic lacunar infarct in the right putamen, and probably left thalamus."
        },
        {
            "input": "The study is mildly limited by motion artifact.  Redemonstration of mild\nthickening and enhancement of the mid to posterior aspect of the falx, (series\n701, image 110), unchanged when compared to prior.  No new extra-axial or\nextra-axial lesions.  There is no evidence of hemorrhage, edema, midline shift\nor infarction.  Incidental note is made of a partially empty sella.  The major\nvascular flow voids are preserved.  The dural venous sinuses are patent.\n\nMild to moderate mucosal thickening of ethmoid air cells, worse on the left. \nMild mucosal thickening of both maxillary sinuses.  The remaining paranasal\nsinuses, middle ear cavities and mastoid air cells are well pneumatized.  The\norbits are unremarkable.",
            "output": "1. Unchanged mild thickening and enhancement of the mid to posterior aspect of\nthe falx likely secondary to a small meningioma.  No adjacent mass effect on\nthe brain or brain edema.\n2. No new extra-axial or intra axial lesions.\n3. No evidence of infarction or intracranial hemorrhage.\n4. Mild paranasal sinus disease."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.\nIncidental note is made of a partially empty sella.\nThere is mild thickening and enhancement of the mid to posterior aspect of the\nfalx (series 1001, image 102 and series 10, image 116)\n\nThe ventricles and sulci are age appropriate.  There is mild generalized\nparenchymal volume loss, most likely age related.\nMajor vascular flow voids are preserved.  Major dural venous sinuses are\npatent.\n\nThere is mild mucosal thickening in the ethmoid air cells and bilateral\nmaxillary sinuses.  The mastoid air cells are clear.  The orbits appear\nunremarkable.",
            "output": "1. Mild thickening and enhancement of the mid to posterior aspect of the falx\ncould represent an en plaque meningioma versus leptomeningeal thickening and\nenhancement possibly in an infectious or neoplastic context.\n2. No evidence of acute infarction or hemorrhage.\n3. Mild paranasal sinus disease.\n\nNOTIFICATION:  Findings discussed with Dr. ___ by Dr. ___.  ___\n(neuroradiology fellow) via telephone on ___ at 11:06 am."
        },
        {
            "input": "There is a punctate focus of slow diffusion abutting the occipital horn of the\nright lateral ventricle (5, 06:15).  There is extensive subcortical and\nperiventricular white matter FLAIR hyperintensities compatible with small\nvessel disease.  Curvilinear diffusion abnormality (06:12) appears to be\nartifactual.\n\nThere is no evidence of intracranial hemorrhage, masses or mass effect. \nProminence of the ventricles and cerebral sulci are compatible with age\nrelated involutional changes.  There is no abnormal enhancement after contrast\nadministration.\n\n The major intracranial vascular flow voids are maintained.  There is mild\nmucosal thickening of the left anterior ethmoid air cells and left frontal\nsinus.  The mastoid air cells are clear.  The orbits are normal.",
            "output": "1. Evidence of a late acute to early subacute punctate infarct abutting the\noccipital horn of the right lateral ventricle.\n2. Extensive white matter small vessel disease.\n3.  Generalized parenchymal volume loss, likely age related.\n4. Mild inflammatory changes of the left anterior ethmoid air cells and left\nfrontal sinus.\n\nNOTIFICATION:  The findings were discussed with ___, M.D. by\n___, M.D. on the telephone on ___ at 1:22 pm, 10 minutes\nafter discovery of the findings."
        },
        {
            "input": "Evaluation is limited due to only one sequence obtained and motion artifact. \nWithin these confines:\n\nT2 hyperintensity is seen in the region of the previously seen right\nmandibular abscess, involving the subcutaneous tissues, the right buccal space\nwith involvement of the right medial and lateral pterygoids and right mastoid\nare muscle and the right parotid space.  There is obliteration of the right\nparapharyngeal fat space.  Question infiltration into the right sublingual\nspace.  However this is difficult due to motion artifact.  Question multiple\ncortical breaks in the right mandible including the body and ramus.  There is\nsuggestion of a surgical drain in place.\n\nThere are bilateral mastoid effusions.  There is mucosal thickening of the\nleft sphenoid sinus and bilateral ethmoid air cells.",
            "output": "1. Limited exam due to incomplete study and severe motion artifact.\n2. Edema secondary to the patient's known right mandibular abscess involves\nthe subcutaneous tissues, right buccal space and right parotid space with\nobliteration of the right parapharyngeal fat space.  Question infiltration of\nthe right sublingual space.\n3. Question right mandibular cortical breaks involving the body and ramus.\n4. Bilateral mastoid effusions.\n5.  Paranasal sinus disease and nonspecific mastoid fluid, as described."
        },
        {
            "input": "MR Head: There is no intracranial hemorrhage, mass, mass effect or shifting of\nthe normally midline structures. Diffusion weighting imaging does not\ndemonstrate evidence of acute infarct. Gray white matter differentiation is\nmaintained. Ventricles and extra axial spaces are normal in size and\nconfiguration for patient's age.\n\nScattered foci of high signal intensity are detected on FLAIR and T2 weighted\nimages, distributed the subcortical and periventricular white matter, which\nare nonspecific and may reflect changes due to small vessel disease.\n\nMRA Head: In comparison with the prior CTA of the head and neck dated ___, no significant changes are identified, there is an infundibular\ndilatation at the origin of the left posterior communicating artery with no\naneurysms larger than 3 mm in size (image 70, series 11), normal flow signal\nis noted in the petrous, cavernous, and supraclinoid portions of the internal\ncarotid arteries. The anterior and middle cerebral arteries are normal. The\nanterior communicating artery region is normal.\n\nThe posterior cerebral arteries and basilar artery are unremarkable.  The\nsuperior cerebellar arteries are normal. The intradural segments to both\nvertebral arteries are patent; the vertebral arteries are codominant.  The\nright posterior communicating artery is patent and appears normal, no arterial\nstenosis, saccular aneurysm, or AVM is identified. .\n\nMRA of the neck: The origin of the supraaortic vessels appears normal with 3\nbranching pattern. Both common carotid arteries are patent with no evidence of\nstenosis at the carotid cervical bifurcations. The vertebral arteries are\nslightly tortuous, however there is no evidence of flow stenotic lesions, and\nboth vertebral arteries are codominant.  The fat saturation images throughout\nthe neck are normal with no evidence of dissection.",
            "output": "1. There is no evidence of acute or subacute intracranial process, no\ndiffusion abnormalities are detected to indicate acute or subacute ischemic\nchanges.\n2. Few scattered foci of high signal intensity detected on FLAIR and T2\nweighted images, which are nonspecific and may reflect changes due to small\nvessel disease.\n3. Normal MRA of the head with no evidence of flow stenotic lesions or\naneurysms larger than 3 mm size.\n4. Axial fat saturation images throughout the neck are normal with no evidence\nof dissection."
        },
        {
            "input": "Patient is post suboccipital craniotomy, with expected postsurgical changes in\nthe cerebellum.  A right-sided VP shunt terminates in the region of the\nforamen of ___, unchanged in position since the most recent CT.\n\nMultiple enhancing metastatic lesions are again identified and appear slightly\nlarger when compared with the MR from ___.  For example, of round\nenhancing lesion in the left parietal lobe measures from 8 mm, previously 6 mm\n(10:15).  The lesion in the right brainstem measures 7 mm, previously 6 mm\n(10:9).  Another lesion in the right frontal lobe measures 6 mm, previously 3\nmm (10:14).  No definite new lesions identified.\n\nThere is no evidence of acute infarction or new hemorrhage.",
            "output": "1. Motion degrades image quality and limits evaluation for new lesions.\n2. Compared with ___ prior brain MRI, multiple known enhancing\nmetastatic lesions have slightly increased in size, as described above.\n3. Within limits of study, no definite new lesions identified.\n4. No acute intracranial abnormality.\n5. Post suboccipital craniotomy with expected, evolving postsurgical changes\nin the cerebellum."
        },
        {
            "input": "Patient is post suboccipital craniotomy, with expected postsurgical changes in\nthe cerebellum.  A right-sided VP shunt terminates in the region of the\nforamen of ___, unchanged in position.\n\nPreviously noted enhancing lesions are barely detectable or no longer\nvisualized.  No new enhancing lesions are seen.\n\nThere is no evidence of \\infarction or new hemorrhage.  The ventricles and\nsulci are stable.  The major vascular flow voids are preserved.  The orbits\nare unremarkable.  There is mild mucosal thickening within the ethmoid air\ncells.  There is trace fluid noted in the left mastoid air cells.",
            "output": "Patient is status post suboccipital craniotomy with stable postoperative\nchanges.  There has been dramatic decrease in enhancement and visualization of\nthe previously noted enhancing lesions.  No new lesions are identified."
        },
        {
            "input": "The patient is status post suboccipital craniectomy and resection of 2\nenhancing cerebellar hemisphere lesions with progressive decrease in the\ncurvilinear enhancement within the postsurgical bed.  A ventriculoperitoneal\nshunt via a right frontal approach terminates in the right foramen of ___,\nunchanged in position from the prior examination.  The 4 mm faintly enhancing\nlesion in the left parietal lobe on 16:15 with corresponding T2/FLAIR\nhyperintensity is unchanged in size and appearance from the MRI head ___, but decreased in size and enhancement from the MRI head ___ and\nprior.  The punctate, 1 mm enhancing lesion in the right frontal lobe on 19:64\nis also unchanged in size and appearance from the MRI head ___, but\ndecreased in size and enhancement from the MRI head ___.  No new\nenhancing lesions are identified.\n\nThere is no evidence of hemorrhage, midline shift or infarction.   The\nventricles and sulci are normal in caliber and configuration.  Scattered foci\nof T2/FLAIR hyperintensities in the supratentorial subcortical white matter\nare unchanged and nonspecific, but may represent the sequela of chronic small\nvessel ischemic disease.\n\nThe paranasal sinuses and mastoid air cells are clear.  The orbits are\nunremarkable.\n\nThe major intracranial flow voids are preserved.",
            "output": "1. Unchanged, small enhancing lesions in the left parietal and right frontal\nlobes from the MRI ___, but decreased in size and enhancement from\nthe MRI ___ and prior.\n2. Status post suboccipital craniectomy with progressive decrease in the\ncurvilinear enhancement within the resection cavities, likely representing\npostsurgical changes.\n3. No new enhancing lesions."
        },
        {
            "input": "Since the prior study, there has been no significant interval change in mildly\nenhancing 3 mm lesion in the left parietal lobe (10:15), with corresponding\nT2/FLAIR signal hyperintensity (07:14).  The previously described 1 mm\npunctate enhancing focus in the right frontal lobe on prior exams is not\nappreciated currently.  No new enhancing lesions are identified.\n\nPostsurgical changes related to suboccipital craniectomy and for resection of\nenhancing cerebellar lesions is unchanged, with persistent FLAIR signal\nhyperintensity in the right greater than left cerebellar hemispheres (7:4).  A\nright frontal approach ventriculostomy catheter is unchanged in position, with\nstable size and configuration of the ventricles.  There is no intracranial\nhemorrhage, midline shift, or acute infarction.  Scattered foci of\nperiventricular and subcortical white matter T2/FLAIR signal hyperintensities\nare stable and remain nonspecific, although likely represent the sequelae of\nchronic small vessel ischemic disease.  The orbits are unremarkable.  The\nvisualized paranasal sinuses and mastoid air cells are grossly clear. \nIntracranial vascular flow voids are preserved.",
            "output": "1. Mildly enhancing 3 mm left parietal lesion is not significantly changed\nsince the prior study.\n2. Previously described punctate right frontal enhancing lesion is not\ncurrently visualized.\n3. No new enhancing lesions are identified.\n4. Stable postsurgical changes, as described above."
        },
        {
            "input": "There are stable postsurgical changes related to suboccipital craniectomy and\nresection of enhancing cerebellar lesions with persistent FLAIR signal\nabnormality, right greater than left.  No abnormal enhancement in the\nresection cavity to suggest recurrent or residual disease.  There remains mild\ndural thickening with FLAIR intensity and enhancement, less prominent when\ncompared to examination of ___.\n\nThe previously seen minimally enhancing left parietal lobe lesion does not\ndemonstrate any enhancement on postcontrast images on today's study.  There is\nhowever, stable associated FLAIR signal abnormality (15:14).\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.\n\nAre right frontal approach ventriculoperitoneal shunt catheter terminating in\nthe foramen ___ is seen in place with stable the surrounding FLAIR signal\nabnormality along the catheter tract.\n\nThere are few scattered foci of T2/FLAIR hyperintensity in the subcortical and\nperiventricular white matter, nonspecific.\n\nThe orbits are unremarkable.  The visualized paranasal sinuses are clear. \nMinimal nonspecific fluid opacification of the left mastoid air cells.  The\nright mastoid air cells are clear.  Intracranial flow voids are maintained.",
            "output": "1. Stable postsurgical changes related to suboccipital craniotomy and\nresection of previously seen cerebellar lesions without associated enhancement\nto suggest residual or recurrent disease.\n2. Previously seen left parietal lobe enhancing lesion does not demonstrate\nany enhancement on today's study.  Stable associated FLAIR signal abnormality.\nStable enhancing mild dural thickening and FLAIR hyperintensity.\n3. No new lesions are seen."
        },
        {
            "input": "Study is moderately degraded by motion, especially on postcontrast imaging.\n\nPostsurgical changes are seen related to prior suboccipital craniectomy and\nresection of cerebellar lesions.  Persistent T2/FLAIR signal abnormalities\nseen within the right cerebellar hemisphere appear similar to prior, and\nappear slightly more conspicuous within the left cerebellar hemisphere, which\nmay be in part due to technique.  A punctate 3 mm focus of increased signal\nalong the resection margin on T1 post-contrast sequences (10:5, 902:31)\nappears similar in appearance to ___, and likely represents a\ntraversing vessel.  No abnormal enhancement in the resection cavity to suggest\nrecurrent or residual disease.  The previously-described dural thickening with\nFLAIR signal hyperintensity is less conspicuous on this study.  The previously\ndescribed 3 mm left parietal lobe lesion does not demonstrate enhancement, but\nhas persistent associated T2/FLAIR signal abnormality (8:15, 7:15).  No new\nfoci of enhancement are seen.\n\nA right frontal approach ventriculostomy catheter terminates in the foramen of\n___, unchanged.  Stable surrounding T2/FLAIR signal abnormality is seen\nalong the catheter tract.\n\nSeveral scattered foci of T2/FLAIR hyperintensity in the subcortical and\nperiventricular white matter are nonspecific, and appear similar to prior.\n\nThere is no evidence of hemorrhage, edema, mass, mass effect, shift of the\nnormally midline structures, or acute large territorial infarction.  The\nventricles and sulci are normal in caliber and configuration.  The major\nintracranial flow voids are maintained.\n\nThe paranasal sinuses are clear.  The orbits are unremarkable.",
            "output": "1. Study is moderately degraded by motion.\n2. Stable postsurgical changes related to suboccipital craniotomy and\nresection of previously seen cerebellar lesions.\n3. Stable nonenhancing parenchymal signal intensity abnormality associated\nwith previously described left parietal lobe lesion.\n4. Within limits of study, no new lesions identified.\n5. Stable right frontal approach ventriculostomy catheter, with stable\nventricular size."
        },
        {
            "input": "Stable postsurgical changes after suboccipital craniotomy for resection of\ncerebellar lesions with stable T2/FLAIR hyperintensities about the resection\nsite and evidence of old blood products.  There is no new abnormal enhancement\nabout the resection site.\n\nUnchanged findings related to postsurgical right frontal approach\nventriculostomy catheter placement with the tip at the level of foramina of\n___.  There unchanged T2/FLAIR hyperintense foci the catheter tract.  The\nventricles and sulci are stable in size and configuration.\n\nThere is unchanged dural thickening and enhancement.\nA previously described nonenhancing 3 mm left parietal lobe lesion is again\nidentified and unchanged (series 7, image 15).\nAdditional nonenhancing scattered T2/FLAIR hyperintensities in the cerebral\nhemispheres bilaterally appear similar to prior.\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.\nMajor intracranial flow voids are preserved.  Major dural venous sinuses are\npatent.\n\nThe paranasal sinuses and mastoid air cells are clear.  The orbits appear\nunremarkable.",
            "output": "1. Stable postsurgical changes after suboccipital craniotomy and right frontal\napproach ventriculostomy catheter with stable position of its tip and\nunchanged configuration of the ventricular system.\n2. No evidence of acute infarction, sinus venous thrombosis, hemorrhage or\nprogression of intracranial metastatic disease.\n3. Stable nonenhancing white matter lesions in the cerebral hemispheres\nbilaterally as well as unchanged dural thickening and enhancement.  No new\nlesions or abnormal contrast enhancement identified."
        },
        {
            "input": "There are six enhancing mass lesions identified:  a 2 mm punctate focus of\nenhancement in the right frontal lobe, a 2 x 4 mm homogeneously enhancing\nlesion in the right frontal lobe, an 8 x 7 mm homogeneously enhancing mass in\nthe left parietal occipital lobe, a 6 x 6 mm homogeneously enhancing mass in\nthe pons, a 2.5 x 2.6 cm heterogeneously enhancing mass in the inferior right\ncerebellum, and a 2.6 x 1.9 cm heterogeneously enhancing mass with some\ncentral necrosis in the inferior left cerebellum. Each of these masses is\nassociated with surrounding vasogenic edema. Mass effect from the bilateral\ncerebellar mass lesions results in low lying cerebellar tonsils, crowding of\nthe foramen magnum, effacement of the adjacent sulci, as well as a cisterna\nmagna/prepontine cistern and fourth ventricle, and narrowing of the cerebellar\npontine angle. There is no resultant hydrocephalus.\n\nA 6 x 5 mm T1, T2, and FLAIR hyperintense lesion is noted along the inner\ntable of the right parietal bone (image 20, series 7), which may represent\nfat, however it osseous metastatic focus could also be considered.\n\nThere is no intracranial hemorrhage. Diffusion weighting imaging does not\ndemonstrate evidence of acute infarct. The major intracranial vessels exhibit\nthe expected signal void related to vascular flow.  Gray white matter\ndifferentiation is maintained. Ventricles are within normal limits.  Multiple\nfoci of slow diffusion in the bilateral parotid glands likely represents intra\nparotid lymph nodes.\n\nThe sella turcica, craniocervical junction, and orbits are unremarkable. The\nparanasal sinuses and mastoid air cells demonstrate normal signal.",
            "output": "1.    Multiple intracranial mass lesions, as described above, consistent with\nmetastatic disease.\n\n2.  Mass effect from the bilateral cerebellar mass lesions results in low\nlying cerebellar tonsils, crowding of the foramen magnum, effacement of the\ncisterna magna/prepontine cistern, fourth ventricle, and narrowing of the\ncerebellar pontine angle. No evidence of hydrocephalus.\n\n3.  A T1, T2, and FLAIR hyperintense lesion in the inner table of the right\nparietal bone may represent a focus of fat, however an osseous metastatic\nlesion could also be considered, close attention in the followup examinations\nin this area is advised."
        },
        {
            "input": "External fiducial markers are noted.\n\n6 x 6 mm (TRV, AP) left parietal lobe (___), 1 mm right frontal lobe (___),\n3 mm right temporal operculum (___), 6 x 5 mm pontine (___), left cerebellar\nhemisphere 2.0 x 2.5 x 2.7 cm and right cerebellar hemisphere 2.4 x 2.6 x 2.5\ncm enhancing lesions are unchanged from prior exam of ___. The left\ncerebellar hemispheric lesion exerts mass effect on the brainstem and the\ninferior aspect of the fourth ventricle and obex.\n\nThere is a very subtle rounded apparent left post central gyrus 3 mm enhancing\nfocus (___), not seen on T1 postcontrast turbo spin echo sequences were on\nthe prior exam. This may be artifactual in nature although a subtle additional\nmetastatic focus is not entirely excluded.\n\nThe dural venous sinuses are patent. The paranasal sinuses are clear. The\norbits are unremarkable. The mastoid air cells appear clear.",
            "output": "1. Multiple bilateral supratentorial, cerebellar and pontine enhancing lesions\nare stable from prior exam.\n2. Previously noted left cerebellar hemispheric lesion again exerts mass\neffect on the brainstem and inferior aspect of the fourth ventricle.\n3. New subtle rounded apparent left post central gyral 3 mm enhancing focus,\nwhich may represent artifact, although subtle new lesion is not entirely\nexcluded. Close attention to this region on followup examination is\nrecommended.\n\nRECOMMENDATION(S):   RE 3:  Recommend clinical correlation and close attention\non followup imaging.."
        },
        {
            "input": "The patient has undergone posterior fossa craniectomy. The previously seen\nenhancing lesions in both cerebral hemispheres have been results have been\nresected. There is mild meningeal enhancement seen in this region without\ndefinite intraparenchymal enhancement identified. Previously seen enhancing\nlesion in the brainstem as well as in the supratentorial region are again\nidentified. There is no hydrocephalus. There remains mass effect on the\nposterior aspect of the fourth ventricle and the narrowing of the\nquadrigeminal cistern. Restricted diffusion in the region of resection likely\nis related to surgery but no territorial acute infarcts are seen.",
            "output": "Postoperative changes are identified with resection of cerebellar metastatic\nlesions. No definite residual parenchymal enhancement seen with some mild\nmeningeal enhancement noted. Persistent mass effect on the fourth ventricle\nand quadrigeminal cistern. No hydrocephalus. No change in previously seen\nenhancing supratentorial and brainstem lesions."
        },
        {
            "input": "Patient is status post right parietal craniotomy for mass resection.  Within\nthe right parietal lobe surgical bed, there is increased peripheral\nenhancement compared to the MR brain from ___ concerning for\ndisease progression.  The size of enhancement is not significantly changed,\nspanning a region measuring 3.0 x 3.8 cm however there is increased edema\nwhich extends into the temporal lobe.  There is no midline shift.  Also new\nfrom the prior study is increased signal along the sulci in the right temporal\noccipital lobe on FLAIR images (7:9) with corresponding enhancement on T1\npostcontrast images (10:9).  There is also enhancement along the right sylvian\nfissure which is new since the previous study (10:14) and along the medial\nright temporal lobe along the choroidal fissure (10:9).  This findings are\nsuspicious for leptomeningeal disease new since the previous study.\n\nThe previously demonstrated focus of FLAIR hyperintensity within the left\nparietal lobe is more conspicuous than prior and demonstrates increased\nenhancement measuring approximately 6 mm.  Additional enhancing lesions along\nthe inner table of the left parietal bone measuring 7 mm and in the left\ntemporalis muscle measuring 9 mm are unchanged from prior.\n\nThere is no evidence of intracranial hemorrhage or infarct.  No evidence of\nmidline shift.  Ventricles are stable from prior.\n\nThe orbits are unremarkable.  The paranasal and mastoid air cells are patent.",
            "output": "1. Status post right parietal craniotomy for mass resection.  Increased\nperipheral enhancement along the right parietal lobe surgical bed is\nsuspicious for disease progression.  The region of enhancement remains stable\nin size however there is increased surrounding edema.  No evidence of midline\nshift.\n2. Findings suggestive of new leptomeningeal disease along the right temporal\nlobe sulci and sylvian fissure suspicious for leptomeningeal disease.\n3. Increased prominence of 6 mm enhancing lesion in the white matter of the\nleft parietal lobe concerning for a metastatic lesion.\n4. Stable appearance of enhancing lesions along inner table of the left\nparietal bone and the left temporalis muscle.\n5. No evidence of intracranial hemorrhage."
        },
        {
            "input": "Again seen are postoperative changes after resection of a right parietal mass.\nAdjacent edema appears unchanged since the ___ study.  The degree of\nenhancement surrounding the surgical site has decreased since the prior\nexamination.  No new lesions are identified.  There are small amounts of\nunchanged hemorrhage at the surgical site with no evidence of hemorrhage\nelsewhere.",
            "output": "1. Evolving changes at the right temporal lobe resection site with unchanged\nsurrounding edema and a decrease in the extent of enhancement.\n2. No evidence of tumor progression."
        },
        {
            "input": "Please note the study is degraded by motion. There is a left frontal lobe\ndiploic space expansile mass measuring up to approximately 12 x 9 x23 mm (see\nseries 4, image 14, 700 image 60 and 701 image 72).\n\nThere is no acute intracranial hemorrhage, abnormal extra-axial fluid\ncollection, midline shift, or acute territorial infarction. The ventricles and\nsulci are preserved. The mastoid air cells are preserved. There is no abnormal\nenhancement on post-contrast imaging.   There is minimal mucosal thickening of\nthe left frontal, right sphenoid, bilateral ethmoid and bilateral maxillary\nsinuses.",
            "output": "1. Study degraded by motion.\n2. Approximate 12 x 9 x 23 mm left frontal calvarial diploic space enhancing\nmass concerning for metastatic disease.\n3. Within limits of motion degraded study, no definite intracranial metastatic\ndisease identified.\n4.  Paranasal sinus disease as described.\n\nNOTIFICATION:  RE 2:  Recommend clinical correlation."
        },
        {
            "input": "There are postsurgical changes from right parietal craniectomy and tumor\nresection.  There is dural thickening and enhancement subjacent to the\nsurgical site which is likely postsurgical.  There is a cavity in the\nunderlying right inferior parietal lobule which contains T1 hyperintense\nmaterial most consistent with blood products, also associated with\nsusceptibility artifact.  No definite enhancement at the surgical site to\nsuggest residual/recurrent tumor.\n\nInferior to the surgical site, in the adjacent temporal lobe, is of FLAIR\nhyperintense focus with a rim of intrinsic T1 shortening (image 13 series 4,\nmeasuring approximately 1.0 x 0.7 cm.  This is new from ___.\n\nNew from ___ is a punctate enhancing lesion in the left parietal lobe (image\n121 series 9).\n\nThere is an irregularly enhancing mass in the left temporalis muscle likely\nreflecting metastatic disease, measuring approximately 15 x 9 mm on image 15\nof series 10, decreased in size from ___, on which it was felt to be in the\ndiploic space but on further review appears to be in the musculature of rather\nthan bone).  Best seen on the MPRAGE images is a small enhancing lesion in the\nleft posterior temporal calvarium measuring approximately 4 mm, new from\n___..  A focus of enhancement along the superior aspect of the left frontal\nsinus appears to have a more mucosal type enhancement pattern on the MPRAGE\nimages and may reflect underlying sinus disease.\n\nThere is no evidence of acute or subacute infarction.\n\nThe ventricles and sulci are normal in size and configuration.  No evidence of\nhydrocephalus.  No mass effect, shift of the midline structures, or basal\ncistern effacement.\n\nThe major intracranial vascular flow voids are preserved.  Orbits are\nunremarkable.  There is scattered mucosal thickening in the paranasal sinuses.",
            "output": "1. Postsurgical changes following right posterior parietal craniectomy.  There\nis prominent dural thickening and enhancement at the surgical site which can\nbe reactive/postoperative.  Please correlate for any evidence of ongoing\ninfection at this site in the context of the previous surgical site infection\nin this region.\n2. Underlying surgical cavity in the right inferior parietal lobe contains\nblood products without convincing additional enhancement to suggest\nrecurrent/residual tumor.\n3. Inferior to the surgical site in the right temporal lobe is a focus of\nFLAIR hyperintensity with rim of T1 shortening.  It does not show definite\nassociated enhancement.  This may reflect an additional (possibly treated)\nmetastatic lesion, but should be correlated with outside imaging and history\nrelated to the underlying diagnosis of metastatic renal cell carcinoma.  This\nis new from ___.\n4. Additional punctate enhancing lesion in the left parietal lobe suspicious\nfor metastasis, new from ___.\n5. Irregularly enhancing mass in the left temporalis muscle likely represents\nmetastatic disease, as does a 4 mm enhancing focus in the left posterior\ntemporal calvarium.  The former is decreased in size from ___ (previously\nreported as diploic space osseous lesion but appearing intramuscular on this\nexam and on correlation with CT).  The latter appears new from ___\n6. Focus of enhancement at the superior margin of the left frontal sinus\nappears to demonstrate mucosal enhancement pattern on the MPRAGE images,\ntherefore probably related to sinus disease."
        },
        {
            "input": "Postsurgical changes from right parietal craniectomy and tumor resection are\nagain seen with dural thickening and enhancement, unchanged from MRI ___.  Resection cavity in the right parietal lobe containing blood\nproducts is unchanged.  There is no evidence of abnormal enhancement in the\nresection cavity. There is a tiny punctate focus of enhancement in the left\nparietal lobe (see 5:124) which is unchanged MRI ___.  The\nremaining parenchyma is unremarkable. The ventricles and sulci are normal in\nsize and configuration.\n\nEnhancing left temporalis lesion measures 1.5 x 0.8 cm, previously 1.5 x 0.9\ncm.  A second enhancing lesion in the left posterior temporal calvarium\nmeasures 5 mm, previously 4 mm, likely unchanged accounting for differences in\ntechnique and measurement.\n\nParanasal sinus disease with enhancing mucosal thickening in the frontal\nsinuses is stable.",
            "output": "1. Postsurgical changes following right posterior parietal craniectomy with\ndural thickening and enhancement are unchanged and underlying resection cavity\nin the right parietal lobe is unchanged.\n2. A punctate focus of enhancement in the left parietal lobe as unchanged\ncompared to the previous MRI dated ___.\n3. The irregularly enhancing masses in the left temporal muscle lesion in the\nleft posterior temporal calvarium are unchanged."
        },
        {
            "input": "The patient is status post right parietal craniotomy and tumor resection, in\ncomparison with the most recent brain MRI examination, there is a new scalp\nfluid collection overlying the craniotomy site and apparently abutting the\ndura and causing mild effacement of the sulci, with no evidence of shifting of\nthe normally midline structures, this fluid collection measures approximately\n9 mm from the skin to the outer table and approximately 5 mm from the inner\ntable through the dura (13:20, 19:20).  There is mild and unchanged dural\nthickening at the surgical site (19:16), and a grossly unchanged surgical\ncavity in the right inferior parietal lobe, with unchanged T1 hyperintense and\nmagnetic susceptibility areas, consistent with residual blood products.  After\ncontrast administration, there is mild and grossly unchanged minimal\nenhancement surrounding the surgical cavity (16: 99-121), likely postsurgical,\nwith no frank evidence of enhancement to indicate or suggest residual mass,\nclose follow-up is recommended.\nThere is a grossly unchanged 2 x 3 mm focus of enhancement in the left\nparietal lobe (16: 132), with mild a new underlying vasogenic edema\ndemonstrated on the axial FLAIR (15:19).  No other intracranial areas with\nabnormal enhancement are seen.\n\nThe previously described left temporalis muscle lesion appears slightly\nsmaller measuring approximately 14 x 5 mm and previously 15 x 9 mm.  A\nheterogeneous pattern of enhancement in the frontal bone towards the left\nappears slightly diffusely larger (16: 94, 95).\n\nFocal area of enhancement in the left parietooccipital bone appears slightly\nlarger measuring approximately 7 mm and previously 5 mm (16:71).\n\nThere is no evidence of acute intracranial hemorrhage, the ventricles\ndemonstrate persistent asymmetry of the right ventricular atrium, likely\npostsurgical, there is no evidence of hydrocephalus.  No diffusion\nabnormalities are detected to indicate acute or subacute ischemic changes.\n\nThe major vascular flow voids are present and demonstrate normal distribution.\nThe orbits are unremarkable, the paranasal sinuses demonstrate mild mucosal\nthickening in the ethmoidal air cells, no air-fluid levels are seen, the\nmiddle ear cavities and mastoid air cells are clear.  7.6 x 6.0 mm focus of\nT2/FLAIR high-signal intensity area is demonstrated posterior to the masseter\nmuscle and anterior to the right parotid gland, also visible on DWI sequence\n(8:4, 15:4), probably consistent with slightly prominent lymph node, attention\nin this area in follow-up exams is advised.",
            "output": "1. The patient is status post right parietal craniotomy, in comparison with\nthe most recent brain MRI examination, there is a new scalp fluid collection\noverlying the craniotomy site, causing mild effacement of the sulci with no\nevidence of shifting of the normally midline structures, apparently abutting\nthe dura, this fluid collection measures approximately 9 mm from the skin to\nthe outer table and approximately 5 mm from the inner table through the dura\n(13:20, 19:20).\n\n2.  There is mild and unchanged dural thickening at the surgical site (19:16),\nand a grossly unchanged surgical cavity in the right inferior parietal lobe,\nwith unchanged T1 hyperintense and magnetic susceptibility areas, consistent\nwith residual blood products.\n\n3.  After contrast administration, there is mild and grossly unchanged minimal"
        },
        {
            "input": "The patient is status post right parietal craniotomy and tumor resection with\npostoperative changes evidenced by pachymeningeal thickening and dural\nenhancement and residuala minimal extra-axial fluid collection.  There is\nalmost complete resolution of previously identified extra-axial and\nextracranial collections/pseudomeningeocele.\n\nAnd a grossly unchanged surgical cavity in the right inferior parietal lobe,\nwith unchanged T1 hyperintense and magnetic susceptibility areas, consistent\nwith residual blood products.  After contrast administration, there is\nunchanged minimal enhancement surrounding the surgical cavity likely\npostsurgical, with no frank evidence of enhancement to indicate or suggest\nresidual disease or tumoral progression.\n\nThere is a unchanged less than 3 mm mm focus of enhancement in the left\nparietal lobe (8:123), with unchanged surrounding T2 FLAIR abnormality with\nnewly developed focus of slow diffusivity (402: 22).\n\nThere is unchanged left superior cerebellar tiny less than 2 mm abnormal\nenhancement (8:53).\n\nThere is no newly developed intracranial areas with abnormal enhancement.\n\nThe previously described left temporalis muscle lesion appears slightly larger\nmeasuring approximately 13 x 8 mm and previously 11 x 6 mm (8:89).  A\nheterogeneous pattern of enhancement in the frontal bone towards the left\nappears unchanged (8: 93).  Focal area of enhancement in the left\nparietooccipital bone appears unchanged measuring 8.5 x 7 mm (8:62).  Within\nthe left parietal lobe, faint areas of enhancement appears slightly more\nconspicuous, likely representing a small developmental venous anomaly (9:18). \nThere is no other definite suspicious newly developed abnormal extracranial\nenhancement or masses.\n\nThere is no evidence of acute intracranial hemorrhage, the ventricles\ndemonstrate persistent asymmetry of the right ventricular atrium, likely\npostsurgical, there is no evidence of hydrocephalus.  No other diffusion\nabnormalities are detected to indicate acute or subacute ischemic changes.\n\nThe major vascular flow voids are present and demonstrate normal distribution.\nThe orbits are unremarkable, the paranasal sinuses demonstrate mild mucosal\nthickening in the ethmoidal air cells, no air-fluid levels are seen, the\nmiddle ear cavities and mastoid air cells are clear.\n\nInterval stability of partially included T2/FLAIR high-signal intensity areas\nposterior to the masseter muscle and anterior to the right parotid gland, also\nvisible on DWI sequence (402:3 and 8:27), probably consistent with slightly\nprominent lymph node.",
            "output": "1. Status post right parietal craniotomy with postoperative changes and\ninterval resolution of previously identified extra-axial and extracranial\ncollections.\n2. Unchanged small with mild enhancement along surgical cavity with no newly\ndeveloped nodular or new enhancement; appearance likely related to\npostsurgical changes.\n3. Unchanged intraparenchymal left parietal and left superior cerebellar\nhemisphere less than 3 mm foci of abnormal enhancement; suggestive of\nmetastatic disease.\n4. Within the left parietal lobe, faint areas of enhancement appear slightly\nmore conspicuous, likely consistent with small developmental venous anomaly\n(9:19), close attention this area is advised.\n5. No newly developed intra-axial brain parenchyma abnormal enhancement or\nmasses.\n6. Mild interval increase i"
        },
        {
            "input": "Again seen are postoperative changes after right parietal craniotomy for tumor\nresection.  There is an increased in enhancement surrounding the surgical\nsite, along with increased edema surrounding the resection site.  Although\nthis may represent treatment changes, the finding is worrisome for tumor\nprogression.\nThere is a hyperintense focus on the FLAIR images in the left parietal white\nmatter, best seen on image 18 of series 15.  This appears somewhat more\nprominent than on the ___ study, but similar to the ___ study.  These\ndifferences may be related to differences in slice position.  The small amount\nof enhancement noted in ___ decreased as ___ and is barely detectable on\nthe current study.\nThere is an unchanged enhancing lesion in the left temporalis muscle.  There\nis an unchanged enhancing lesion in the left parietal bone, best seen on\nseries 17, image 64.\nNo new lesions are identified.  There is no evidence of infarction.  There is\na small amount of hemorrhage at the margins of the surgical cavity with no\nevidence of other hemorrhage.",
            "output": "1. Increased enhancement and edema at the surgical site, worrisome for tumor\nprogression although this may be treatment effect.\n2. Left parietal lobe enhancing focus is less prominent than on prior studies.\n3. Left temporalis muscle and parietal bone lesions appear unchanged."
        },
        {
            "input": "Motion artifact limits evaluation on postcontrast MP RAGE images.  Right\nparietal craniotomy is again noted with subjacent dural enhancement.  The rim\nof contrast enhancement along the right parietal surgical cavity is thickest\nmedially, up to 10 mm on coronal image 1001:111, which is unchanged compared\nto ___.  The overall surgical cavity and peripheral enhancement\nmeasure 3.7 x 3.0 cm on image 10:100, also unchanged compared to ___.  The extent of edema surrounding the surgical cavity has slightly\ndecreased since ___.\n\nCompared to ___, previously seen FLAIR hyperintensity in the\nright temporal sulci is no longer conspicuous.  There is gyriform\nhyperintensity in the right temporal lobe on precontrast and postcontrast T1\nweighted images, compatible with mineralization.  Assessment for superimposed\nleptomeningeal contrast is limited.\n\nLeft parietal subcortical FLAIR hyperintense lesion now demonstrates a 3 mm\nhyperintensity on precontrast T1 weighted images, which may represent\nmineralization, without clear evidence for superimposed contrast enhancement,\nimages 4:19, 10:117, 11:19, compared to 6 mm contrast enhanced superimposed\nupon 3 mm T1 hyperintensity on the MRI from ___.  This lesion\ndemonstrates slow diffusion on the ADC map on ___, and now with pseudonormalization on the ADC map and\npersistent high signal on the diffusion tracer.  This lesion was present on ___, without slow diffusion.  A metastatic rather than ischemic lesion\nis suspected.\n\nNo new enhancing intracranial lesions are identified.  No evidence for new\nunexplained blood products or acute infarction.  Ex vacuo enlargement of the\natrium and temporal horn of the right lateral ventricle are again noted.  Of\nventricles are stable in size.  Basal cisterns are preserved.\n\n7 mm T1 hyperintense lesion in the left parietal bone on images 4:10, 11:9,\n10:53 is stable.\n\n10 mm T1 hypointense, contrast enhancing lesion in the left temporalis muscle\non image 10:73 stable when measured in the same fashion.\n\nThere is mild mucosal thickening in the ethmoid and maxillary sinuses.  There\nis partial left mastoid air cell opacification.",
            "output": "1. Stable size and configuration of peripheral enhancement along the right\nparietal surgical cavity compared to ___.\n2. Previously seen FLAIR hyperintensity in the right temporal sulci, which was\nsuspicious for leptomeningeal carcinomatosis, is no longer conspicuous. \nGyriform hyperintensity in the right temporal lobe on precontrast and\npostcontrast T1 weighted images is compatible with mineralization.  Assessment\nfor superimposed leptomeningeal contrast enhancement is limited.  Correlation\nwith CSF cytology would be helpful regarding the possibility of leptomeningeal\ncarcinomatosis.\n3. Left parietal subcortical lesion demonstrates 3 mm intrinsic T1\nhyperintensity, which may represent mineralization, without clear evidence for\nsuperimposed contrast enhancement, compared to 6 mm contrast enhancement on ___.\n4. No evidence for new enhancing intracranial lesions.\n5. Stable T1 hyperintense left parietal bone lesion.\n6. Stable enhancing left temporalis muscle lesion."
        },
        {
            "input": "There are multiple subcentimeter foci of increased signal intensity on\nT2/FLAIR in a periventricular and subcortical white matter distribution (2:42,\n49, 52, 54, 58, 75, 77, 86), in a pattern consistent with multiple sclerosis. \nThere is associated abnormal enhancement with an 8 mm lesion in the left\nmiddle frontal gyrus (14:121), consistent with active demyelination.\n\nThere is also an 8 mm focus of increased signal intensity on T2/FLAIR in the\nleft dorsal lateral cervical spinal cord at the craniocervical junction\n(3:12).  There is no associated abnormal enhancement.\n\nThere is no evidence of hemorrhage, edema, mass effect, midline shift or\ninfarction.   The ventricles and sulci are normal in caliber and\nconfiguration.\n\nThere is a small mucous retention cyst mucosal thickening in the left\nmaxillary sinus.  There is mild mucosal thickening in the left frontal sinus\nand ethmoid air cells.\n\nThe imaged orbits are unremarkable.",
            "output": "1. Multiple subcentimeter foci of T2/FLAIR signal abnormality in the\nperiventricular and subcortical white matter demonstrates a pattern compatible\nwith multiple sclerosis.\n2. Abnormal enhancement of one of these lesions measuring 8 mm in the left\nmiddle frontal gyrus is consistent with active demyelination.\n3. 8 mm area of T2/FLAIR signal abnormality in the left dorsolateral spinal\ncord at the craniocervical junction is consistent with cord involvement."
        },
        {
            "input": "There are small, symmetric, bilateral subdural fluid collections along the\ncerebral hemispheres, falx, and tentorium with pronounced diffuse\npachymeningeal contrast enhancement, T1 isointensity, and T2/FLAIR\nhyperintensity.  There is no evidence for blood products within these\ncollections on gradient echo images.  There is no pachymeningeal nodularity. \nThere is 3 mm displacement of the cerebellar tonsils into the foramen magnum. \nVentricles, sulci, and basal cisterns are small.  These findings are highly\nsuggestive of intracranial hypotension.\n\nThere is no evidence for pathologic leptomeningeal contrast enhancement or\nother leptomeningeal signal abnormality.  There is no evidence for parenchymal\nmass, edema, blood products, acute infarction, or other signal abnormality. \nMajor vascular flow voids are preserved.  Dural venous sinuses are patent on\npostcontrast MP RAGE images.\n\nThere is minimal mucosal thickening in the ethmoid air cells.",
            "output": "Thin diffuse bilateral subdural collections along the convexities, falx, and\ntentorium with diffuse pachymeningeal contrast enhancement, 3 mm downward\ndisplacement of the cerebellar tonsils, and effacement of the sulci,\nventricles, and basal cisterns, highly suggestive of intracranial hypotension."
        },
        {
            "input": "There is a 4.3 x 4.3 cm left parietal lesion, which is hyperintense on\nT2/FLAIR sequence images, and demonstrates small internal foci of low signal\non T1 images, which may represent areas of necrosis (11:16).  The lesion abuts\nthe left ventricular atria, and extends to the level of the cortex, were there\nis a obscuration of the normal gray-white matter differentiation, and abnormal\nsulcation.  The lesion has increased in size since the prior MRI, when it span\napproximately 3.8 x 4.0 cm.  There is minimal postcontrast enhancement. There\nis no significant mass effect upon the adjacent lateral ventricle, although\nthere is no longer any intervening plane of normal brain parenchyma between\nthe lesion and the left lateral ventricle itself. A small focus of increased\nFLAIR signal abnormality along the falx in the contralateral hemisphere was\npresent previously.\n\nNo new areas of abnormal signal intensity or pathologic postcontrast\nenhancement are identified.  There is no intracranial hemorrhage or areas of\nischemia.  In the orbits are unremarkable.  Vascular flow voids are preserved,\nand there is contrast filled vessels coursing through the anterior portion of\nthe lesion, with no evidence of stenosis or occlusion.",
            "output": "1. Interval growth of known left parietal lesion with signal characteristics\ncompatible with internal necrosis, compatible with malignant glioma.\n2. Contralateral parafalcine signal abnormality is stable since ___, but\nremains suspicious for invasion.\n3. No evidence of intracranial hemorrhage or new lesions since the prior study\nfrom ___."
        },
        {
            "input": "Left parietal signal abnormality involving the cortical and subcortical region\nwithout definite enhancement is again identified and is not significantly\nchanged from the previous MRI examination.  The small area of FLAIR signal\nabnormality in the right parafalcine region is unchanged.  There is no\nsignificant mass effect on the ventricles or midline shift.  There is no\nhydrocephalus.  No other areas of abnormal enhancement seen.",
            "output": "Unchanged appearance of the left parietal and right parafalcine parietal\nsignal abnormalities without definite enhancement compared with the previous\nMRI examination.  The examination is performed for surgical planning."
        },
        {
            "input": "The patient is status post left parietal craniotomy and biopsy of a left\nparietal lobe lesion.  The T2/FLAIR hyperintense lesion in the left parietal\nlobe, which slightly expands the gyri and effaces the left parietal sulci,\nextending to the left ventricular atria, is unchanged in size and extent from\n___, but increased in size in comparison to ___.  Small\nareas of T1 hypointensity within this lesion likely represent areas of\nnecrosis as well as scattered calcifications as seen on prior CT.  A tubular,\n7 x 6 mm area of enhancement extending from the dura in the left parietal lobe\nis new from the prior examination and does not demonstrate restricted\ndiffusion.\n\nThe small area of T2/FLAIR hyperintense, nonenhancing signal in the right\nparasagittal parietal lobe is unchanged.\n\nScattered foci of T2/FLAIR hyperintensities in the periventricular and\nsubcortical white matter are unchanged and nonspecific.\n\nThere is no evidence of acute hemorrhage, midline shift or infarction.   The\nventricles and sulci are normal in caliber and configuration.  There is no\nabnormal enhancement after contrast administration.\n\nThe left maxillary sinus contains a tiny mucous retention cyst.  The mastoid\nair cells are clear.  The orbits are unremarkable.\n\nThe major intracranial flow voids are preserved.",
            "output": "1. Unchanged, slightly expansile, T2/FLAIR hyperintense lesion in the left\nparietal lobe, with internal calcifications and necrosis, consistent with the\npatient's known oligodendroglioma.\n2. New, tubular area of enhancement, extending from the dura in the left\nparietal lobe without restricted diffusion, which may reflect changes related\nto prior biopsy.  Close attention on follow-up is recommended.\n3. Unchanged area of T2/FLAIR hyperintense signal in the right parasagittal\nparietal lobe, suspicious for an additional focus of oligodendroglioma."
        },
        {
            "input": "Again seen is FLAIR/T2 hyperintensity centered in the left parietal lobe with\nexpansion of the gyri and mild sulcal effacement.  Overall the appearance has\nnot significantly changed in size or appearance since recent ___. \nThere is no extension of abnormal signal or new mass effect.  There is minimal\nintrinsic T1 hyperintensity without parenchymal enhancement.  Foci of T1\nhypointensity are also noted.\n\nLeft parietal craniotomy is again noted with associated pachymeningeal\nenhancement.  A nodular component of enhancement (21:111) has decreased in\nsize now measuring 6 x 4 mm, previously 9 x 6 mm.  There is no new abnormal\nenhancement.\n\nSmall area of FLAIR hyperintensity in the parasagittal right parietal lobe\n(17:18) has not changed.  There is no associated abnormal enhancement or\nrestricted diffusion in this region.  There is no new parenchymal signal\nabnormality or restricted diffusion.  Susceptibility artifact seen in the post\nbiopsy bed, not unexpected.  No new abnormal susceptibility artifact.  Major\nintravascular flow voids including within the major dural venous sinuses are\npreserved.\n\nNo abnormal signal seen the paranasal sinuses or mastoids.",
            "output": "1.  Interval decrease in size of the nodular enhancing extra-axial lesion\noverlying the left parietal mass, potentially post biopsy related.\n2. Otherwise, no significant interval change in the appearance of the left\nparietal lesion compatible with known oligodendroglioma.\n3. No significant interval change of the right parietal parasagittal signal\nabnormality since ___.  Continued attention on follow-up suggested."
        },
        {
            "input": "There are stable postsurgical changes from left parietal craniotomy and biopsy\nwith adjacent mild dural thickening and enhancement.  A focus of nodular\nextra-axial enhancement underlying the craniotomy site is less apparent than\non prior examination, and is likely postoperative in nature.\n\nMasslike expansile left parietal T2/FLAIR hyperintensity with gyral expansion\nand adjacent sulcal effacement is overall unchanged compared to the prior\nexamination, mildly increased in size compared to the earliest study from ___.  Punctate areas of intrinsic T1 hyperintensity are again noted.  There\nis no definite associated post gadolinium enhancement.\n\nSubtle right parietal parasagittal FLAIR hyperintensity is unchanged since\n___ (11:20).\n\nThere is no evidence of hemorrhage, midline shift or infarction.  There is\nprominence of the ventricles and sulci suggestive involutional changes.  There\nis no abnormal enhancement after contrast administration.  The principal\nintracranial vascular flow voids are preserved.  The dural venous sinuses are\npatent on a.  Images.\n\nThe visualized paranasal sinuses are grossly clear.  The orbits are grossly\nunremarkable.",
            "output": "1. No significant interval change of a nonenhancing left parietal mass\ncompatible with known oligodendroglioma, though there has been mild stepwise\nincrease since ___.\n2. Interval decrease of a focus of nodular extra-axial enhancement underlying\nthe left parietal craniotomy site, likely postoperative in nature.\n3. Small area of right parietal parasagittal signal abnormality is unchanged\nsince ___.\n4. No new enhancing mass."
        },
        {
            "input": "There is no evidence of intracranial hemorrhage, mass, mass effect or shifting\nof the normally midline structures.  The ventricles and sulci are normal in\nsize and configuration for the patient's age.  No diffusion abnormalities are\ndetected.  There is no evidence of abnormal enhancement to indicate\nleptomeningeal or metastatic disease.  Few scattered foci of high signal\nintensity are seen in the periventricular white matter, more significant in\nthe ventricular atria, which are nonspecific and may reflect changes due to\nsmall vessel disease.  The major vascular flow voids are present and\ndemonstrate normal distribution.  The orbits are unremarkable, the paranasal\nsinuses are notable for mucosal thickening in the sphenoid sinus on the left,\nwhich apparently is new since the prior study, there is a slightly larger\nmucosal thickening on the left maxillary sinus.",
            "output": "1.  There is no evidence of acute or subacute intracranial process.  There is\nno evidence of abnormal enhancement to indicate leptomeningeal or metastatic\ndisease.\n\n2.  Scatter foci of high signal intensity identified in the subcortical white\nmatter are nonspecific and may reflect changes due to small vessel disease.\n\n3.  Mucosal thickening in the sphenoid sinus on the left is new since the\nprior study.  A slightly larger mucous retention cyst is noted on the left\nmaxillary sinus."
        },
        {
            "input": "There is no evidence of mass, mass effect, intracranial hemorrhage, edema, or\nacute/subacute territorial infarct, no diffusion abnormalities are detected,\nthere is no evidence of abnormal enhancement after contrast administration to\nindicate or suggest metastatic disease, few scattered foci of high signal\nintensity in the posterior periventricular region remain unchanged, which are\nnonspecific and may reflect changes due to small vessel disease.  The major\nvascular flow voids are present and demonstrate normal distribution.  The\norbits are unremarkable, the paranasal sinuses again demonstrates a mucous\nretention cyst on the left maxillary sinus, grossly unchanged, no air-fluid\nlevels are identified.  The mastoid air cells are clear.",
            "output": "1.  There is no evidence of abnormal enhancement to indicate or suggest\nleptomeningeal or metastatic disease.\n\n2.  There is no evidence of acute or subacute intracranial process or\nhemorrhage.\n\n3.  Unchanged scattered foci of high signal intensity detected on T2 and FLAIR\nsequences, surrounding the periventricular atria, which are nonspecific and\nmay reflect changes due to small vessel disease.\n\n4.  Unchanged left maxillary mucous retention cyst."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, or infarction.\nThe ventricles and sulci are normal in caliber and configuration. There is no\nabnormal enhancement after contrast administration.\n\nHigh-resolution images of the cisternal segment of the fifth cranial nerve and\nof the Meckel's cave region reveal no abnormalities.",
            "output": "Normal study."
        },
        {
            "input": "Redemonstrated is a 3.1 cm x 3.6 cm left cerebellar anterior venous\nmalformation status post partial embolization.  There are prominent draining\nveins draining into the straight sinus.  Inferior to the AVM is a T1/T2\nhyperintense ovoid focus (8.3 AP x 2.7 cm TV) compatible with subacute\nhematoma.  Peripheral T1 hypointensity likely represents hemosiderin\nformation.  There is no new hemorrhage.\n\nThere is no evidence of infarction or midline shift.  The ventricles and sulci\nare normal in caliber and configuration.  The major intracranial vascular flow\nvoids are maintained.  The paranasal sinuses, mastoid air cells and orbits are\nnormal.",
            "output": "1. Left cerebellar 3.6 cm AVM status post partial embolization.  Allowing for\nlack of a comparison MRI study it is difficult to determine change in AVM\nsize.\n2. Evolving subacute bleed inferior to the AVM."
        },
        {
            "input": "Previously seen arteriovenous malformation in the left cerebellum with nidus\nin the left cerebellum again identified.  Flow voids due to dilated arterial\nand venous structures are identified projected over the left cerebellum left\ntentorial margin as before.  However previously these areas where previously\nseen as enhancement.  This could be due to technical differences.  Previously\nseen blood products have evolved and hyperintensities in the left cerebellum\nare no longer visible.  Diffusion images demonstrate no evidence of acute\ninfarct except for some signal changes adjacent to the arteriovenous\nmalformation likely secondary to blood products and T2 shine through..",
            "output": "Left cerebellar arteriovenous malformation with arterial and venous\nstructures.  Evolution of blood products seen in the left cerebellum compared\nwith previous MRI.  Examination performed for surgical planning."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor acute territorial infarction.  Unchanged chronic encephalomalacia within\nthe left parietal and temporal lobes.  Ex-vacuo dilatation involving the\noccipital horn of the left lateral ventricle with adjacent susceptibility\nartifact on the GRE images, compatible with chronic microhemorrhage.  Chronic\ninfarct within the left cerebellum, unchanged since ___ (series 300,\nimage 7).  Moderate subcortical, deep, and periventricular white matter\nT2/FLAIR hyperintensities are nonspecific, but likely represents the sequela\nof chronic microvascular ischemia.  Prominence of the ventricles and sulci,\nsuggesting age-related involutional changes.  There is no abnormal enhancement\nafter contrast administration.\n\nMajor intracranial vessels are patent.  Patient is status post bilateral lens\nresections.  Otherwise, orbits are unremarkable in appearance.  Mucosal\nthickening within the anterior right ethmoid air cells (series 7, image 9).",
            "output": "1. No acute intracranial abnormalities.\n2. Unchanged chronic encephalomalacia within the left parietal and temporal\nlobes with ex vacuo dilatation of the occipital horn.  Adjacent chronic\nmicrohemorrhage in the left occipital lobe.\n3. Chronic left cerebellar infarct, unchanged.\n4. Moderate chronic microvascular ischemic and age-related involutional\nchanges."
        },
        {
            "input": "There is a 5 x 12 mm focus of abnormal slow diffusion in the posterior limb of\nthe left internal capsule that is bright on T2 and FLAIR sequences and new\ncompared to the prior study, consistent with a subacute infarct. The left\ntemporoparietal encephalomalacia is unchanged. Additional scattered\nperiventricular and subcortical foci of white matter FLAIR hyperintensity are\noverall unchanged and although nonspecific likely represent chronic small\nvessel ischemic disease. Enlargement of the lateral and third ventricles\nincluding ex vacuo dilatation of the atrium of the left lateral ventricle is\nunchanged compared to the prior study of ___. Principal intracranial\nvascular flow voids including dose of the dural venous sinuses are preserved.\nThere is no evidence of hemorrhage, edema, mass, or mass effect.\n\nThere is diffuse sinus disease including complete opacification of the left\nmaxillary sinus, mucosal thickening and an air-fluid level in the right\nmaxillary sinus, and near total opacification of bilateral ethmoid and\nsphenoid sinuses. The mastoid air cells and middle ear cavities are clear.",
            "output": "1. A new focus of slow diffusion measuring 5 x 12 mm with corresponding high\nsignal on T2 and FLAIR in the posterior limb of the left internal capsule is\nconsistent with a subacute infarct.\n\n2. Diffuse extensive opacification of the paranasal sinuses including an\nair-fluid level in the right maxillary sinus is new compared to the prior\nstudy of ___ and is likely inflammatory.\n\n3.  Stable appearance of chronic infarcts and ventriculomegaly."
        },
        {
            "input": "The left temporoparietal encephalomalacia, associated with ex vacuo dilatation\nof the occipital horn and atrium of the left lateral ventricle, is unchanged. \nThere is a chronic infarction in the left posterior limb of the internal\ncapsule.  The mild enlargement of the lateral and third ventricles and\nprominence of the sulci, likely related to central parenchymal volume loss, is\nunchanged.  There is no evidence of hemorrhage, edema, masses, mass effect,\nmidline shift or acute infarction.  T2/FLAIR hyperintensities in the\nperiventricular, subcortical, and deep white matter are unchanged and\nnonspecific, but may represent the sequela of chronic small vessel ischemic\ndisease.  No enhancing lesions are identified.  There is no pachymeningeal or\nleptomeningeal enhancement.  There is no abnormal enhancement in the upper\ncervical spine.\n\nThe paranasal sinuses and mastoid air cells are clear.  The patient is status\npost bilateral cataract surgery.\n\nThe major intracranial flow voids are preserved.\n\nThe bone marrow signal in the calvarium is slightly, diffusely heterogeneous,\nunchanged from the prior examinations.",
            "output": "1. No evidence of metastatic disease.\n2. No acute intracranial abnormality.\n3. Chronic infarctions in the left temporoparietal lobe and posterior limb of\nthe left internal capsule."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor acute infarction.  Stable zone of chronic encephalomalacia posterior left\ntemporal, parietal lobe, with few areas of decreased signal on gradient images\nconsistent with mineralization, with ex vacuo dilatation of the atrium,\noccipital horn left lateral ventricle.  Findings consistent with moderate to\nsevere chronic small vessel ischemic changes, similar to prior.  Advanced\nbrain parenchymal atrophy, with severe atrophy of both temporal lobes, at\nsylvian fissures, bilateral hippocampal formations, stable.  Tiny chronic left\ncerebellar infarct, new since ___.  Intracranial vascular flow voids are\npreserved.  Preserved intracranial vascular flow voids.  No abnormal\nenhancement.  Normal visualized orbits.",
            "output": "1. No acute findings.\n2. Chronic encephalomalacia left temporal, parietal lobes.\n3. Advanced parenchymal atrophy at temporal lobes, sylvian fissures."
        },
        {
            "input": "MRI Brain:\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There are multiple subcortical and deep white matter T2/FLAIR\nhyperintensities, predominantly in the frontal lobes.  There is no abnormal\nenhancement after contrast administration.\n\nThe orbits, mastoid air cells and visualized soft tissues are normal.  Minimal\nmucosal thickening in the ethmoid sinus is seen.\n\nMRA brain:  There is a 2 mm anteriorly oriented outpouching off of the right\ninferior M2 branch, series 10, image 91.  There appears to be a small vessel\narising from it, and this is likely an infundibulum.  The possibility of an\naneurysm cannot be entirely excluded.  The intracranial vertebral and internal\ncarotid arteries and their major branches appear normal without evidence of\nstenosis, occlusion, or aneurysm formation.\n\nMRA neck:  The common, internal and external carotid arteries appear normal. \nThere is no evidence of internal carotid artery stenosis by NASCET criteria. \nThe origins of the great vessels, subclavian and vertebral arteries appear\nnormal bilaterally.",
            "output": "1. Multiple small white matter lesions, predominantly in the frontal lobes,\nlikely secondary to patient's known lupus.  No acute infarct.\n2. A 2 mm anteriorly oriented outpouching off of the right inferior M2 branch,\nwhich is likely an infundibulum.  The possibility of a small aneurysm cannot\nbe excluded.  .  Otherwise, normal MRA of the brain.\n3. Normal MRA of the neck."
        },
        {
            "input": "Mild motion artifact limits evaluation.\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, or infarction.\nThe previously described diffusion-weighted hyperintensities in the left\nparietal white matter are not seen on the current study. Nonspecific punctate\nareas of increased FLAIR intensity in the bilateral frontal white matter are\nnot changed. The ventricles and sulci are normal in caliber and configuration.\n\nThe paranasal sinuses and mastoid air cells are clear. The orbits are\nunremarkable.",
            "output": "1. Mild motion artifact limits evaluation.\n2. No evidence of posterior fossa infarct.\n3. Previously described left parietal white matter lesions not seen on current\nstudy."
        },
        {
            "input": "Large areas of slowed diffusion predominantly involving left MCA territory\nincluding left frontal and temporal lobes, and to a lesser extent left\noccipital total lobe. There is associated T2/FLAIR hyperintensity within the\ncorresponding regions. Overall appearance is compatible with a subacute\ninfarction, likely distal embolic in origin given its distribution and\nunilateral involvement.  There are small areas of hemorrhage in the largest\ninfarction in territory of the superior division of the left MCA.\n\nThere is no evidence of midline shift. The ventricles and basilar cisterns\nappear stable in size.\n\nThere is additional periventricular and subcortical white matter T2/FLAIR\nsignal abnormality is most often attributed to chronic small vessel ischemic\ndisease.\n\nThe orbits and mastoid air cells appear normal. There is paranasal sinus\nmucosal thickening, most prominently involving bilateral maxillary sinuses,\nleft greater than right.",
            "output": "1. Slow diffusion with corresponding T2/FLAIR signal abnormality within left\nfrontotemporal and left occipital regions indicating subacute infarction,\nlikely distal embolic in etiology given distribution and unilateral\ninvolvement.\n2. Small areas of hemorrhagic conversion.\n3. Additional T2/FLAIR subcortical white matter hyperintensity which is most\noften attributed to sequela of chronic small vessel ischemic disease.\n4. Paranasal sinus disease."
        },
        {
            "input": "Study is moderately degraded by motion.  Within these confines:\n\nMRI BRAIN:\nThere are scattered punctate T2/FLAIR hyperintensities in the periphery of the\nwhite matter in no recognizable pattern.  These lesions do not enhance after\ncontrast administration.  There are no T2/FLAIR hyperintense lesions in the\npericallosal region.\n\nOtherwise, there is no evidence of hemorrhage, edema, masses, mass effect,\nmidline shift or infarction.   The ventricles and sulci are normal in caliber\nand configuration.\n\nThere is no abnormal enhancement after contrast administration.\n\nThe paranasal sinuses are clear.  There is partial opacification of the\nmastoid air cells bilaterally.  The middle ears are clear.\n\nMRA BRAIN:\nThe intracranial vertebral and internal carotid arteries and their major\nbranches appear normal without evidence of stenosis, occlusion, or aneurysm\nformation.\n\nMRA NECK:\nThe common, internal and external carotid arteries appear normal.  There is no\nevidence of internal carotid artery stenosis by NASCET criteria.  The origins\nof the great vessels, subclavian and vertebral arteries appear normal\nbilaterally.  Evaluation of the origin of the carotid artery and vertebral\nartery is somewhat limited due to artifacts.  However, there is no clear\nevidence of vertebral or carotid artery dissection.",
            "output": "1.  Study is moderately degraded by motion.\n2. Nonspecific nonenhancing white matter lesions as described.  Differential\nconsiderations include sequela of prior trauma or infection, history of\nmigraine headaches, inflammatory or demyelinating process, and\nmicroangiopathic changes.\n3. No evidence of carotid or vertebral artery dissection, though evaluation at\nthe origin is somewhat limited due to artifacts.\n4. Patent circle of ___, without definite evidence of aneurysm no stenosis.\n5. Nonspecific bilateral mastoid described."
        },
        {
            "input": "Unchanged left 1.4 x 1.3 cm left para hippocampal cyst is unchanged from\nexamination dating back to ___.  In addition, there is a midline nonenhancing\n4 mm cystic lesion in the pituitary, also unchanged since ___, most likely a\nRathke's cleft cyst.  Otherwise, there is no evidence of hemorrhage, edema,\nmasses, mass effect, midline shift or infarction.   The ventricles and sulci\nare within expected limits in caliber and configuration.  There is no abnormal\nenhancement after contrast administration.  The major intracranial flow voids\nare preserved.  The dural venous sinuses are patent.  There is mild mucosal\nthickening of the ethmoid air cells.  The orbits are unremarkable.  No\nsignificant fluid signal is seen the mastoid air cells.",
            "output": "1. No acute intracranial abnormalities on contrast enhanced MRI brain. \nSpecifically no abnormal enhancement, acute infarct or intracranial\nhemorrhage.  No suspicious intracranial mass.\n2. Unchanged 4 mm nonenhancing cystic lesion in the midline pituitary since\nexamination of ___, felt to be most likely a Rathke's cleft cyst\n3. A 1.4 cm left para hippocampal cyst, also unchanged since ___.\n4. Additional findings as described above."
        },
        {
            "input": "Study is degraded by motion.   There is no evidence of infarction, hemorrhage,\nedema, mass, or mass effect.\n\nThe ventricles and sulci are prominent, compatible with global parenchymal\nvolume loss.\n\nBilateral periventricular and numerous deep and a few subcortical white matter\nfoci of T2/FLAIR signal hyperintensity are nonspecific but compatible with at\nleast moderate changes of chronic white matter microangiopathy.\n\nThere is moderate sphenoid sinus and mild ethmoid air cell and maxillary sinus\nmucosal thickening.  There are trace bilateral mastoid effusions.\n\n The globes and orbits are preserved.  The visualized portion of the major\nintracranial vascular flow voids are preserved.",
            "output": "1.  Study is degraded by motion.\n2. No acute intracranial abnormality.  No infarction.\n3. Global volume loss and probable microangiopathic changes as described.\n4.  Paranasal sinus disease and nonspecific bilateral mastoid fluid, as\ndescribed."
        },
        {
            "input": "MRI HEAD: There is slow diffusion in the posterior right thalamus, splenium of\nthe corpus callosum and the occipital lobe with associated FLAIR hyperintense\nsignal, compatible with a infarct of the right PCA distribution, likely late\nacute with associated hemorrhagic transformation within the right occipital\nlobe. There is associated sulcal effacement of the right occipital lobe,\nresulting in mild effacement of the trigone and posterior horn of the right\nlateral ventricle. Mild asymmetry of the bilateral temporal horns, with the\nright slightly larger is stable from exam of ___. Nonspecific subcortical\nFLAIR white matter hyperintensities of the right coronal radiata are unchanged\nsince exam of ___. The major intracranial flow voids are preserved.  A large\nmucous retention cyst in the right maxillary sinus as well as mucosal\nthickening of ethmoid air cells are noted. The orbits are unremarkable. The\nmastoid air cells are clear.\n\nHEAD MRA: Irregularity and mild stenosis of the carotid siphons are noted\nbilaterally secondary to atherosclerotic calcifications seen on prior CT\nexamination. Otherwise, there is normal flow related signal seen within the\nmiddle cerebral and anterior cerebral arteries without significant mural\nirregularity or stenosis. There is normal symmetric arborization of the MCA\nbranches. There is no aneurysm greater than 3 mm. Normal flow related\nenhancement is seen in the codominant intracranial vertebral arteries, the\nbasilar artery, and the bilateral superior cerebellar and posterior cerebral\narteries. The right ___ is not seen a finding unchanged from prior\nexamination.\n\nNECK MRA: There is a normal 3 vessel takeoff from the aortic arch. The\ncervical common carotid, internal carotid and external carotid arteries are\nnormal in course, caliber and contour. They demonstrate normal enhancement\nwithout mural irregularity, stenosis or evidence of dissection. There is no\nsignificant extracranial internal carotid artery stenosis by NASCET criteria.\nThe vertebral arteries are roughly codominant. There is apparent narrowing of\nthe origins of bilateral vertebral arteries, slightly greater on the left,\nalthough this may be secondary to motion artifact. The remainder of the\nvertebral arteries are normal in course, caliber and contour to the skullbase.\nThey demonstrate normal enhancement without mural irregularity, stenosis or\nevidence of dissection.",
            "output": "1. Large infarct of the right posterior cerebral artery distribution involving\nthe posterior right thalamus, splenium of the corpus callosum and occipital\nlobe with hemorrhagic transformation within the right occipital lobe. There is\nassociated sulcal effacement, as well as effacement of the tried on and\nposterior horn of the right lateral ventricle.\n2. No significant flow-limiting stenosis is seen in the MRA of the head and\nneck, although there may be mild narrowing at the origins of the cervical\nvertebral arteries, potentially secondary to motion artifact."
        },
        {
            "input": "There is no evidence of acute infarction.  No intracranial hemorrhage.  No\nmass, mass effect, edema or midline shift.\n\nThe ventricles and sulci are normal, without evidence of hydronephrosis.  The\nbasal cisterns are patent.  There is no evidence of impending, downward\nherniation.  There is apparent preservation of the principal intracranial\nvascular flow voids.\n\nFollowing the administration of intravenous contrast material, there is no\nabnormal enhancement.  The dural venous sinuses appear patent on MP-RAGE\nimagine sequences.\n\nThe visualized paranasal sinuses, middle ear cavities, and mastoid air cells\nare well aerated and clear.  There is no abnormal inner ear or mastoid\nenhancement.  The orbits are within normal limits bilaterally.",
            "output": "Unremarkable MRI examination of the brain."
        },
        {
            "input": "MRI BRAIN:\nThere is hyperintense diffusion-weighted signal in the left periventricular\nwhite matter adjacent to the left lateral ventricle (series 302, image 20),\nwithout low ADC values.  This area is T2/Flair hyperintense (series 7, image\n16).  There is no evidence of intracranial hemorrhage, mass, mass effect, or\nmidline shift.  Chronic infarcts in the bilateral frontal subcortical white\nmatter are noted (series 7, image 14 and 15).  Mild prominence of the\nventricles and sulci suggests volume loss.  Periventricular and subcortical\nT2/FLAIR hyperintensities are nonspecific, but likely represent sequela of\nchronic small vessel ischemic disease. There is increased T1 signal in the\nleft basal ganglia more than the right side, possibly due to mineralization.\n\nMucous retention cysts are noted in the left maxillary sinus.  Otherwise, the\nparanasal sinuses and mastoid air cells are clear.  The orbits are\nunremarkable.  Note is made of an empty sella.\n\nMRA BRAIN:\nBilateral anterior cerebral arteries are again noted to arise from the left\nmiddle cerebral artery, unchanged.  The right A1 segment is hypoplastic,\nunchanged.  Otherwise, the intracranial vertebraland internal carotid arteries\nand their major branches appear normal without evidence of high-grade\nstenosis,occlusion,oraneurysm formation.",
            "output": "1. Subacute infarct involving the left periventricular white matter (series\n302, image 20).  No hemorrhagic conversion or other intracranial hemorrhage.\n2. Redemonstration of hypoplastic A1 segment of the right anterior cerebral\nartery.  Otherwise, no evidence of high-grade stenosis, occlusion, or aneurysm\nformation in the major intracranial vessels."
        },
        {
            "input": "MRI BRAIN:\nThere is no intra or extra-axial mass, acute hemorrhage or acute infarct.  The\nsulci, ventricles and cisterns are within expected limits for the patient's\nage.  There is no abnormal enhancement or parenchymal FLAIR signal\nabnormality.  The major intracranial flow voids are preserved.  The dural\nvenous sinuses are patent on postcontrast MP-RAGE.  There is mild mucosal\nthickening of the paranasal sinuses.  The orbits are unremarkable.  The\nmastoid air cells middle years demonstrate no fluid signal.\n\nMRA brain: The intracranial vertebral and internal carotid arteries and their\nmajor branches appear normal without evidence of stenosis, occlusion, or\naneurysm formation.",
            "output": "1. There is no acute infarct, intracranial hemorrhage or mass.  No parenchymal\nsignal abnormality or abnormal enhancement.\n2. Unremarkable MRA of the head."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  Incidental note is made of a 5 mm CSF intensity nonenhancing\nfocus along the left aspect of the sella, which appears to have mild mass\neffect on the anterior pituitary, potentially an arachnoid cyst (series 1201,\nimage 69).\n\nThere are bilateral occipital xanthogranulomas incidentally noted.\n\nThere are scattered T2/FLAIR hyperintensities in the cerebral hemispheres\nbilaterally, a nonspecific finding and likely related to chronic small vessel\nischemic changes.\nThere is no abnormal enhancement after contrast administration.\n\nThe ventricles and sulci are unremarkable in caliber and configuration.\nMajor vascular flow voids are preserved.  Major dural venous sinuses are\npatent.\n\nThere is mild mucosal thickening along the ethmoid air cells.  The remainder\nof the paranasal sinuses appear clear.  There is partial bilateral mastoid air\ncell effusions, left more than right.",
            "output": "1. No evidence of acute infarction, hemorrhage or intracranial mass on\ncontrast enhanced MRI brain.  No abnormal enhancement.\n2. Nonspecific scattered white matter changes in the cerebral hemispheres\nbilaterally, likely sequela of chronic microangiopathy.\n3. Additional findings described above"
        },
        {
            "input": "Limited examination secondary to premature termination of the study.  Within\nthese confines:\n\nThere is no evidence of infarction, masses, mass effect, or midline shift. \nThe ventricles and sulci are normal in caliber and configuration for patient\nage.\n\nProbable opacification of the bilateral mastoid air cells, right greater than\nleft.  The visualized orbits are unremarkable.",
            "output": "1. Limited examination due to premature termination.  No evidence of\ninfarction.\n2. Probable opacification of the bilateral mastoid air cells, right greater\nthan left."
        },
        {
            "input": "No evidence for an enhancing intracranial mass.  No evidence for pathologic\nleptomeningeal or pachymeningeal contrast enhancement.  No evidence for edema,\nacute infarction, or blood products.  No extra-axial collection.  Unchanged\nmoderately numerous T2/FLAIR hyperintense foci in the periventricular, deep,\nand subcortical white matter are nonspecific, with diagnostic considerations\nincluding sequela of chronic small vessel ischemic disease, plus/minus sequela\nof prior inflammation, plus/minus sequela images suppressive medications. \nVentricles and sulci are age-appropriate.\n\nMajor vascular flow voids appear grossly preserved.  Dural venous sinuses are\npatent on postcontrast MP RAGE images.\n\nThere is opacification of both mastoid air cells right greater than left. \nThere is an unchanged small focus polypoid mucosal thickening in the left\nposterior ethmoid.",
            "output": "1. No acute infarction.  No imaging manifestations of intracranial infection. \nNo evidence for other acute abnormalities.\n2. Right greater than left mastoid air cell opacification may be secondary to\nprolonged supine positioning in the inpatient setting.  However, please\ncorrelate with any associated infectious symptoms."
        },
        {
            "input": "MR BRAIN:\nThere is patchy slow diffusion in the ventromedial aspect of the left thalamus\nextending to involve the medial aspect of the left cerebral peduncle, with\nearly high signal on the FLAIR images in keeping with a subacute infarction. \nThere is a small amount of central hemorrhage.  There are also multiple\nbilateral supratentorial and infratentorial microbleeds within the white\nmatter, with only a few small foci within the basal ganglia, which are\nrelatively spared. There are multiple foci of T2/FLAIR hyperintensity in both\ncerebellar hemispheres, in the left thalamus, right lentiform nucleus, left\nhead of caudate nucleus, left corona radiata anteriorly, right medial frontal\nlobe, anterosuperior to the frontal horn of the right lateral ventricle and\nleft side of the pons, which likely represent a combination of old lacunar\ninfarcts and dilated perivascular spaces.  There are nonspecific T2/FLAIR\nhyperintensities within the pons, which may represent the sequelae of\nmicroangiopathy.  There is no evidence of masses, mass effect,or midline\nshift.  The ventricles and sulci are normal in caliber and configuration.\n\nThere is a small left mastoid effusion.\n\nMRA brain: There is apparent severe atherosclerotic narrowing of the internal\ncarotid arteries bilaterally within the carotid canals and cavernous sinuses,\nwhich appears more severe than the CTA head and neck performed ___, where there is moderate atherosclerotic narrowing.  The apparent\ndifference in severity is likely artifactual in nature.  The intracranial\nvertebral and internal carotid arteries and their major branchesappear\notherwise normalwithout evidence of stenosis, occlusion, or aneurysm\nformation.  The left vertebral artery is diminutive.",
            "output": "-Acute infarction in the ventromedial aspect of the left thalamus, extending\ninto the medial aspect of the left cerebral peduncle.  There is a small focus\nof hemorrhage within the infarct.\n-Multiple supratentorial and infratentorial microbleeds.  Although there is\nrelatively little central involvement, the evidence of extensive\natherosclerotic change and the multiple chronic lacune favor hypertension as\nan overall etiology.  Amyloid angiopathy would be more typical for the micro\nbleed distribution but would not explain the remainder of the vascular\nfindings."
        },
        {
            "input": "There are new areas of slow diffusion involving the right ventromedial\nthalamus and medial aspect of the right cerebral peduncle.\n\nGrossly unchanged areas of diffusion restriction involving the left ventral\nmedial thalamus and medial aspect of the left cerebral peduncle.",
            "output": "1. New areas of slow diffusion indicating acute infarcts, involving the right\nventromedial thalamus and the medial aspect of the right cerebral peduncle.\n2. Grossly stable areas of infarct in the left ventromedial thalamus and\nmedial aspect of the left cerebral peduncle."
        },
        {
            "input": "There is a 2 vessel aortic arch with the left common carotid artery arising\nfrom the common trunk of the right brachiocephalic artery.  There is similar\nsevere irregular narrowing of the origin and proximal left subclavian artery\nthere appears more severe than on the prior CTA.  There is narrowing of the\nproximal left common carotid artery that appears more pronounced than on the\nCTA.  There is irregular narrowing of the bilateral common carotid\nbifurcations and proximal internal carotid arteries with approximately ___\nstenosis of the proximal right internal carotid artery by NASCET criteria\nrelated to mixed atheromatous plaque.  There is no left internal carotid\nartery stenosis by NASCET criteria.  Irregular narrowing of the bilateral\nexternal carotid arteries is again visualized.  The left vertebral artery is\ndiffusely small in caliber with stenosis of the origin.  There is multifocal\nirregular narrowing of the right vertebral artery, most pronounced at the\norigin.  The common, internal and external carotid arteries otherwise appear\npatent.  The origins of the great vessels, subclavian, and vertebral arteries\nappear patent bilaterally.  The common carotid bifurcations appear patent.",
            "output": "1. Multiple sites of narrowing of the left common carotid, left subclavian,\nleft vertebral, right vertebral origin, bilateral external carotid and\nbilateral internal carotid arteries.\n2. Some of these stenoses appear more severe than on the CTA of ___. \nThe rapid change in caliber would not be consistent with entirely atheromatous\ndisease.\n3. Diffusely small caliber of the left vertebral artery without\natherosclerotic plaque.\n4. No evidence of occlusion, dissection or aneurysm."
        },
        {
            "input": "2 foci of diffusion-weighted hyperintense signal of the right cerebral\npeduncle is overall similar to examination of ___, however with\npotential slight increased prominence along the medial aspects, although this\nis felt to be likely secondary to differences in technique (series 4, image\n12).\n\nAcute infarct of the right parasagittal mid brain is slightly decreased in\nprominence compared to prior exam.\n\nDiffusion-weighted hyperintense signal of the left greater than right thalami\nis also less conspicuous.\n\nUnchanged areas of T2/FLAIR hyperintensity in the bilateral cerebellar\nhemispheres, left corona radiata anteriorly, right frontal lobe, \nanterosuperior to the frontal horn of the right lateral ventricle, likely\nsequela lacunar infarcts.  T2/FLAIR hyperintensities of the bilateral basal\nganglia chronic lacunar infarcts and/or perivascular spaces.\n\nMultiple scattered foci of susceptibility, predominantly in the occipital\nlobes and cerebellum, are unchanged, compatible with chronic micro\nhemorrhages.\n\nThe sulci, ventricles and cisterns are within expected limits for the\npatient's age.  The major intracranial flow voids are preserved.  No\nintracranial mass effect.  There is mild mucosal thickening of the ethmoid air\ncells.  The orbits are unremarkable.  Left greater than right mastoid\neffusions are identified, slightly worsened on the right from prior exam.",
            "output": "1. Re-demonstrated multiple subacute infarcts in the right midbrain and\nthalami.  No new infarcts.\n2. Unchanged multiple supra and infratentorial microhemorrhages.\n3. No acute intracranial findings."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, or infarction.\nThe ventricles and sulci are normal in caliber and configuration. There is no\nabnormal enhancement after contrast administration.\n\nCoronal T2 weighted images as well as MP rage images demonstrate\nwell-maintained gray-white matter differentiation.  There is no evidence of\nthickening of the cortex seen.  No evidence of migration abnormality is\nidentified.  There is no abnormal signal or atrophy seen within the\nhippocampal formations.",
            "output": "No significant abnormalities are seen on MRI of the brain with and without\ngadolinium including coronal images through the temporal lobes."
        },
        {
            "input": "Motion artifact mildly limits evaluation.\n\nThere is no evidence for an enhancing mass, edema, blood products, or acute\ninfarction.  There is no pathologic leptomeningeal or pachymeningeal contrast\nenhancement.  Scattered small foci of high T2/FLAIR signal in the subcortical,\ndeep, and supratentorial white matter of the cerebral hemispheres have\nminimally progressed compared to ___, with at least 1 new lesion in\nthe right superior frontal gyrus subcortical white matter on image 7:19. \nVentricles, sulci, and basal cisterns are normal in size for age.  Cerebellar\ntonsils are normally positioned.\n\nMajor arterial flow voids are grossly preserved.  Dural venous sinuses are\npatent on postcontrast MP RAGE images.\n\nThere is mild mucosal thickening in the ethmoid air cells.  There is moderate\nright and mild left mastoid air cell opacification.",
            "output": "1. No evidence for an intracranial mass or acute intracranial abnormalities.\n2. Scattered T2/FLAIR signal abnormalities in the supratentorial white matter,\nslightly progressed since ___. Since these were present when the\npatient was ___, a number of etiologies may be considered, including sequela of\nchronic small vessel ischemic disease if the patient has longstanding\ncardiovascular risk factors, migraine related lesions, sequela of\ndemyelination or inflammation, and sequela of vasculitis."
        },
        {
            "input": "MRI Brain:\nThere is no intra or extra-axial mass, acute hemorrhage or infarct.  Sulci,\nventricles cisterns are within expected limits for the degree of global\ncerebral volume loss which is slightly greater than would be expected for the\npatient's age.  The major intracranial flow voids are preserved.  The dural\nvenous sinuses are patent.  The paranasal sinuses are clear.  The orbits are\nunremarkable.  The mastoid air cells are clear.  There is no abnormal\nenhancement.\n\nMRI pituitary:  The pituitary gland measures approximately 10 mm, with mild\nconvex bulging at the dorsum sella.  This is top-normal in size for a female\nof reproductive age.  There is an equivocal 2 mm slightly hypo enhancing\nnodule along the left aspect of the sella (series 35, image 9) most compatible\nwith volume averaging through a vessel, however a small microadenoma is not\nentirely excluded.\n\nThe cavernous sinuses demonstrate no filling defects with expected\npostcontrast enhancement.\n\nMRV brain:  The left transverse sinus is dominant with congenitally\nhypoplastic right transverse sinus and sigmoid sinus.  There is no evidence\nfor venous sinus thrombosis.\n\nMRA brain:  MRA brain is slightly motion degraded.  Within these confines: \nThe intracranial vertebral and internal carotid arteries and their major\nbranches appear normal without evidence of stenosis, occlusion, or aneurysm\nformation.\n\nMRA neck:  The common, internal and external carotid arteries appear normal. \nThere is no evidence of internal carotid artery stenosis by NASCET criteria. \nThe origins of the great vessels, subclavian and vertebral arteries appear\nnormal bilaterally.  There is no evidence for dissection.",
            "output": "1. No acute hemorrhage or infarct.  There is no abnormal FLAIR hyperintense\nsignal or enhancement.\n2. The dural venous sinuses are patent:  No evidence for dural venous sinus\nthrombosis.  The cavernous sinuses appear unremarkable.\n3. Unremarkable MRA of the head and neck, allowing for motion artifact.  No\nevidence for dissection.\n4. The pituitary gland is top-normal in size measuring approximately 10 mm in\ncranial caudal dimension, which may be seen with physiologic hyperplasia in a\nwoman of reproductive age.  There is an equivocal 2 mm slightly hypo enhancing\nnodule in the left aspect of the pituitary, most likely representing volume\naveraging through a vessel.  A small microadenoma is not entirely excluded.\n5. There is no evidence for pituitary apoplexy.\n\nRECOMMENDATION(S):  Point 4:  Close attention on followup.  Correlation with\nlaboratory values is recommended."
        },
        {
            "input": "Hyperintense signal in layering dependently in the occipital horns of the\nright and left lateral ventricles on diffusion images does not demonstrate low\nsignal on the GRE images (series 10, image 16).  This could represent early\nblood products related to recent spine surgery, less likely infection given\nthe absence of enahncement or other findings in the brain to suggest\nmeningitis.  There is also no enhancement to suggest ependymoma.\n\nBilateral white matter T2 FLAIR hyperintensities without abnormal diffusion\nare nonspecific and likely reflect sequelae of chronic small vessel ischemic\ndisease.  No evidence of intraparenchymal hemorrhage, mass, or infarct.  No\nshift of normally midline structures.  The basal cisterns are patent. \nVentricle size is normal.\n\nMajor intracranial vascular flow voids are present.\n\nA 4-mm left frontal scalp lesion the does not appear to enhance could reflect\na sebaceous cyst or granuloma (series 3, image 14).  There is partial\nopacification of the left posterior ethmoidal air cells and sphenoid sinus as\nwell as right maxillary sinus.  Otherwise, the remaining paranasal sinuses are\nclear.  The visualized orbits are within normal limits.  The mastoid air cells\nare clear.\n\nNo abnormal enhancement after contrast administration.",
            "output": "1.  Hyperintense signal layering dependently in the bilateral occipital\nventricular horns could represent early blood products related to recent spine\nsurgery, less likely infection given the absence of infection or other signs\nto suggest meningitis.  Recommend interval follow-up with MR to assess for\nevolution.\n\n2.  No enhancing lesions to suggest tumor such as ependymoma.\n\n3.  Non-specific FLAIR hyperintense white matter lesions likely sequelae of\nchronic small vessel ischemic disease.\n\n4.  Paranasal sinus disease.\n\nRECOMMENDATION(S):  Follow-up MR to further assess evolution of presumed blood\nproducts in the lateral ventricles.\n\nNOTIFICATION:   The findings were discussed with ___, M.D. by\n___, M.D. on the telephone on ___ at 5:29 ___, 15 minutes after\ndiscovery of the findings."
        },
        {
            "input": "MR Head:  There is an unchanged left temporal hemorrhagic contusion/hematoma\nassociated with subdural collections along the left temporal frontal and\nparietal regions, a thin subdural hematoma is also identified on the right\nfrontal temporal parietal regions, better depicted in the FLAIR sequence\n(images 7 through 18, series 19), stable mild mass effect, causing\napproximately 3.8 mm of shifting of the midline structures towards the right.\nThere are unchanged areas of encephalomalacia in the frontal lobes with\nsusceptibility changes, indicating chronic hemorrhage, there is also evidence\nof a chronic hemorrhage in the head of the caudate nucleus on the left,\nextending partially into the left basal ganglia (image 13, series 18).  Small\nfluid level is identified in the right occipital ventricular horn, indicating\nresidual intraventricular hemorrhage. No diffusion abnormalities are detected\nto indicate acute or subacute ischemic changes. The major vascular flow voids\nare present and demonstrate normal distribution. The orbits are unremarkable,\nthe paranasal sinuses are notable for bilateral mucosal thickening in the\nethmoidal air cells and both maxillary sinuses, the mastoid air cells are\nclear.\n\nMRA Head:  There is evidence of vascular flow in both internal carotid\narteries as well as the vertebrobasilar system, anatomical variant consistent\nwith hypoplasia of the A1 segment on the right is seen, both anterior cerebral\narteries are filling from the left, no aneurysms or areas of stenosis are\nidentified.\n\nMRV of the head: The major dural venous sinuses are present with no evidence\nof venous sinus thrombosis, the preferential drainage is via the right\ntransverse sinus.",
            "output": "1. Unchanged left temporal lobe intraparenchymal hematoma as described in\ndetail above. Unchanged areas of encephalomalacia on the frontal lobes and\nleft basal ganglia.\n2. Bilateral subdural collections are seen with no significant mass effect,\nmore evident on the left side causing mild midline shifting of the normally\nmidline structures towards the right. Small trace of intraventricular blood is\nidentified in the right occipital ventricular horn.\n3. Unremarkable MRA of the head with no evidence of flow stenotic lesions or\naneurysms. Unremarkable MRV of the head with no evidence of dural venous sinus\nthrombosis."
        },
        {
            "input": "There are multiple foci of slowed diffusion with corresponding ADC weighted\nhypointensity consistent with acute infarcts in the left frontal lobe along\nthe motor strip (series 402, image 24) and left parasagittal frontoparietal\nregion(series 402, image 23), and left parietal subcortical white matter\n(series 402, image 20). These acute infarcts are within the distribution of\nthe left middle cerebral and left anterior cerebral arteries.  There is a\nsmall focus of slowed diffusion with corresponding ADC weighted hypointensity\nwithin the right occipital lobe within the distribution of the right posterior\ncerebral artery (series 402, image 15).  Infarcts are new from MRI on ___.\n\nThere are chronic infarcts of the left frontal lobe and left caudate head,\nalso chronic on prior MRI from ___.\n\nThere is an evolving left temporal lobe hematoma with surrounding edema. Blood\nproducts of the hematoma on are predominantly T1 hyperintense and T2\nhyperintense, consistent with the late subacute phase. There is mass effect on\nthe involved sulci and right lateral ventricle. The left convexity subdural\nhematoma is not significantly changed in size from recent CT on ___, measuring approximately 7 mm in thickness. There is also a small right\ntemporoparietal subdural hematoma that measure up to 3 mm in thickness. There\nare scattered blood products in the bilateral frontal lobes and right tectum,\nunchanged from prior MRI on ___.  There is encephalomalacia of\nthe right frontal lobe.\n\nThere is hypoplasia of the A1 segment of the right anterior cerebral artery,\nas seen on MRI from ___.  There is absence of the normal flow\nvoid within the left transverse and left sigmoid sinuses, although this is\nlikely due to slow flow rather than thrombus as these structures were\ndemonstrated to be normally patent on recent CTA from ___. Major\nintravascular flow voids are otherwise preserved.\n\nThere have been prior maxillary antrostomies. There is fluid and mucosal\nthickening in the ethmoid and maxillary sinuses. There is a polypoid lesion in\nthe right posterior nasal cavity, not significantly changed from CT on ___. The mastoid air cells appear clear. There is been prior right\nlens surgery. The orbits are otherwise normal.",
            "output": "1. Scattered infarcts in the left middle cerebral, left anterior cerebral, and\nright posterior cerebral territories, new from MRI on ___. The\nlargest infarcts involve the left motor strip and left parasagittal\nfrontoparietal region and punctate infarct in the right occipital lobe. No\nassociated mass effect.\n2. Evolving multicompartmental hemorrhages, detailed above. The left temporal\nlobe hematoma is now in the late subacute phase."
        },
        {
            "input": "The examination is mildly motion degraded.  Within these confines:\n\nThere is no evidence of intracranial hemorrhage, edema , midline shift or\ninfarction.   The ventricles and sulci are normal in caliber and\nconfiguration.\n\nA homogeneously T1 isointense, T2 hyperintense, enhancing, round, extra-axial,\nmidline falcine mass in the superior parietal convexity measures 1.2 x 1.2 x\n1.1 cm.  No other enhancing lesions are identified.\n\nThere is mild mucosal thickening in the bilateral ethmoid sinuses.  The\nmastoid air cells are clear.  The orbits are unremarkable.\n\nThe moderate, lacerated, right frontal subgaleal scalp hematoma is unchanged\nin size.\n\nThe major intracranial flow voids are preserved.",
            "output": "1. No acute intracranial abnormality.\n2. Homogeneously enhancing 1.2 cm extra-axial, midline falcine mass in the\nsuperior parietal convexity, most likely representing a meningioma.\n3. Unchanged, moderate, lacerated right frontal subgaleal scalp hematoma."
        },
        {
            "input": "Please note the study is mildly degraded by motion.\n\nThere is an approximately 5 x 7 x 5 mm extra-axial left frontal enhancing mass\nthat is suggest to be dural-based and demonstrates associated susceptibility\n(see 13:41, 10:18, 100:75, 14:18).  There is no definite edema in the adjacent\nleft frontal lobe.  This structure was not clearly seen on the prior\nnoncontrast brain MRI from ___\n\nThere is no evidence of hemorrhage, edema, or infarction. The ventricles and\nsulci are normal in caliber and configuration. Major intravascular flow voids\nare preserved.\n\nMarrow signal is normal.  The paranasal sinuses and mastoid air cells appear\nclear.  The orbits are normal.",
            "output": "1.  Please note the study is mildly degraded by motion.\n2. Approximately 5 x 7 x 5 mm left frontal extra-axial enhancing mass\ncontaining blood products versus mineralization, which may be dural based, and\nnot definitely seen on prior examinations.  Differential considerations\ninclude meningioma and dural metastatic disease.  Recommend clinical\ncorrelation.  If clinically indicated, noncontrast head CT may be obtained for\nfurther evaluation.\n3. Within limits of study, no acute intracranial abnormality.\n\nRECOMMENDATION(S):\n1. Approximately 5 x 7 x 5 mm left frontal extra-axial enhancing mass\ncontaining blood products versus mineralization, which may be dural based, and\nnot definitely seen on prior examinations.  Differential considerations\ninclude meningioma and dural metastatic disease. Recommend clinical\ncorrelation.  If clinically indicated, noncontrast head CT may be obtained for\nfurther evaluation."
        },
        {
            "input": "The previously seen 6 mm left frontal extra-axial mass lesion is again seen on\nimage 800b:71.  The lesion demonstrates intrinsic T2 hypointensity with\nenhancement on postcontrast images and is most likely in keeping with a\nmeningioma with some internal mineralization.  However, a superficial aneurysm\nor a venous varix is another possibility and further evaluation with CTA of\nthe head is recommended.\n\nThere is no evidence of hemorrhage, edema,  mass effect, midline shift or\ninfarction.   The ventricles and sulci are normal in caliber and\nconfiguration.\n\nThere are few (less than 5) scattered foci of T2/FLAIR hyperintensity in the\nsubcortical and periventricular white matter, nonspecific, likely secondary to\nsmall vessel ischemic disease.\n\nThe orbits are unremarkable.  Visualized paranasal sinuses and mastoid air\ncells are clear.  Intracranial flow voids are maintained.",
            "output": "1. Stable 6 mm left frontal extra-axial enhancing lesion, most likely in\nkeeping with a meningioma with some mineralization.  However, a superficial\naneurysm or a venous varix  is another possibility and further evaluation with\nCTA of head is recommended.\n2. Otherwise, unremarkable head MRI.\n\nRECOMMENDATION(S):   further evaluation with CTA of head is recommended.\n\nNOTIFICATION:  The impression and recommendation above was entered by Dr.\n___ on ___ at 09:23 into the Department of Radiology\ncritical communications system for direct communication to the referring\nprovider."
        },
        {
            "input": "6 x 5 mm left posterior frontal extra-axial enhancing lesion with broad-based\ndural attachment has not significantly changed in size since ___,\ncompatible with meningioma.\n\nThere is no evidence of hemorrhage, edema, new masses, significant mass\neffect, midline shift or infarction.   The ventricles and sulci are normal in\ncaliber and configuration for age.  A single nonspecific punctate focus of\nleft frontal subcortical white matter T2/FLAIR hyperintensity is unchanged and\nis of doubtful clinical significance (16:18).  There is no new abnormal\nenhancement after contrast administration.  There is no abnormal focus of\nslowed diffusion.  The principal intracranial vascular flow voids are\npreserved.\n\nThere is mild mucosal thickening in a few left anterior ethmoid air cells. \nThe remainder the paranasal sinuses are grossly clear.  The orbits are grossly\nunremarkable.",
            "output": "1. 6 x 5 mm extra-axial left frontal enhancing mass has not significantly\nchanged since ___, compatible with meningioma.\n2. No hemorrhage, infarct or new enhancing mass."
        },
        {
            "input": "The ventricles and extra-axial spaces are normal in size. There is no evidence\nof midline shift, mass effect or hydrocephalus. There are no acute infarcts.\nThere is no evidence of focal abnormalities.  The vascular flow voids are\nmaintained. The visualized paranasal sinuses are clear. Following gadolinium\nadministration there is no evidence of abnormal parenchymal, vascular and\nmeningeal enhancement seen.\n\nThere is a focal area of low T1 signal and high in FLAIR signal demonstrate\nmild enhancement in the left parietal bone (3:20, 14:20 and 11:20).  This area\ncould represent an atypical hemangioma but a sclerotic metastasis could have\nsimilar appearance.  As this area was not visualized on the ___ PET study of\n___, a bone scan would help for further assessment.",
            "output": "1. No enhancing brain lesions mass effect or hydrocephalus.\n2. Area of signal abnormality in the left parietal bone could be due to\natypical hemangioma but a sclerotic metastasis could not be excluded.  Further\nevaluation with bone scanning is recommended.\n\nRECOMMENDATION  Bone scan to further evaluate left parietal bony lesion."
        },
        {
            "input": "There is no acute infarction, edema, mass effect, or evidence for blood\nproducts.  There is mild confluent periventricular white matter hypodensity\nalong the lateral ventricles.  There also small discrete foci of high T2\nsignal in the deep and subcortical white matter of the cerebral hemispheres,\nmild-to-moderate in extent, progressed since the ___ MRI.  These are\nnonspecific but likely sequela of chronic small vessel ischemic disease in\nthis age group.\n\nThere is disproportionate cortical volume loss in the medial temporal lobes. \nElsewhere, global parenchymal volume is essentially normal for age, with only\nminimal enlargement of the ventricles and sulci compared to the ___ MRI from\n___ years ago.\n\nMajor vascular flow voids are grossly preserved.\n\nThe patient is status post bilateral cataract surgery.  There is mild mucosal\nthickening in the ethmoid air cells.  There are dependent secretions and/or a\nmucous retention cyst in the medial aspect of the left sphenoid sinus,\npartially marginated by a septation.  There also secretions or fluid in the\nnasopharynx.\n\nSagittal images demonstrate bilat uncovertebral osteophytes in the upper\ncervical spine at C3-C4, as seen on the prior ___ cervical spine CT. \nAssociated neural foraminal narrowing is not assessed on this exam.",
            "output": "1. Mildly to moderately extensive T2 hyperintensities in the supratentorial\nwhite matter, slightly progressed since ___, are nonspecific but likely\nsequela of chronic small vessel ischemic disease in this age group.\n2. Disproportionate cortical volume loss in the medial temporal lobes. \nElsewhere, global parenchymal volume is essentially normal for age, with only\nminimal enlargement of the ventricles and sulci compared to the ___ MRI from\n___ years ago.\n3. Dependent secretions and/or mucous retention cyst in the left sphenoid\nsinus.  Please correlate whether there are any symptoms of active\ninflammation."
        },
        {
            "input": "There is no evidence of acute intracranial hemorrhage, mass, mass effect or\nshifting of the normally midline structures.  No diffusion abnormalities are\ndetected to indicate acute or subacute territorial infarction.  Scattered foci\nof high signal intensity detected in the subcortical periventricular white\nmatter on FLAIR and T2 weighted images, which are nonspecific and may reflect\nchanges due to small vessel disease, additionally gyriform pattern of\nhigh-signal intensity is noted on FLAIR images within the right occipital,\nright parietal, left occipital parietal and left temporal regions, more\nconspicuous or evident on the right side (images ___, series 13), there is\nno evidence of hemorrhage in this areas, or evidence of abnormal enhancement\nafter contrast administration.  The ventricles and sulci are slightly\nprominent for the patient's age suggesting mild cortical volume loss.  The\nmajor vascular flow voids are present and were better depicted in the prior\nCTA of the head.  The orbits are unremarkable.  The paranasal sinuses\ndemonstrate mild mucosal thickening in the ethmoidal air cells, there is\npatchy mucosal thickening in the mastoid air cells bilaterally.",
            "output": "1. Gyriform pattern of FLAIR high-signal intensity identified in the right\noccipital, right parietal, left occipital parietal and left temporal regions\nas described detail above, which is nonspecific, this type of findings can be\nseen in patients with posterior reversal encephalopathy (PRES), however post\nictal changes may have similar appearance, if clinically warranted, MRI could\nbe repeated in few days to demonstrate resolution of this findings.\n\n2.  There is no evidence of diffusion abnormalities to indicate acute or\nsubacute ischemic changes\n\n3.  Numerous scattered foci of high signal intensity identified in the\nsubcortical and periventricular white matter are nonspecific and may reflect\nchanges due to small vessel disease, however unusual for the patient's age,\ntherefore demyelinating changes cannot be completely rule out.\n\n4.  There is minimal mucosal thickening in the ethmoidal air cells bilaterally\nand patchy mucosal thickening the mastoid air cells.\n\nNOTIFICATION:  The findings were discussed with the ___ team including\n___, M.D. by ___, M.D. on the telephone on ___ at 10:01\nam, 5 minutes after discovery of the findings."
        },
        {
            "input": "Compared with the prior MRI of ___, posterior parietooccipital\ngyral and subcortical FLAIR signal hyperintense signal has resolved.  No\nresidual infarcts.\n\nUnchanged are bilateral, left more numerous than right periventricular and\ndeep white matter T2/FLAIR hyperintense foci (see series 8 images ___,\nnonspecific, may be sequela of chronic small vessel ischemic changes, chronic\ndemyelination could have similar appearance..\n\nThere is no evidence of acute infarction, hemorrhage, or mass effect.  The\nventricles and sulci are prominent, compatible with global parenchymal volume\nloss, which appears slightly advanced for this patient's age.  The visualized\nparanasal sinuses and mastoids appear clear.  The globes are unremarkable. \nMajor intracranial vascular flow voids are preserved.",
            "output": "1. Interval resolution of cortical and subcortical T2 signal abnormality.\n2. Unchanged deep white matter T2 signal abnormalities, may represent chronic\nsmall vessel ischemic changes, chronic demyelination could have similar\nappearance.\n3. Moderate parenchymal atrophy."
        },
        {
            "input": "Craniotomy, postsurgical, posttreatment changes.  Stable nonenhancing T2\nsignal abnormality marginating surgical cavity.  Confluent T2 signal\nabnormality at the centrum semiovale, corona radiata, right greater than left\nvertex subcortical white matter, stable, likely postradiation change, stable. \nNo new enhancement or restricted diffusion in the treatment bed.\n\nNo acute infarcts.  No midline shift, hydrocephalus or herniation.  Probable\nchronic lacunar infarcts right basal ganglia, stable.  Vascular flow voids are\npreserved.  Mild opacification right mastoids, similar.  Clear paranasal\nsinuses, left mastoids.  Faint focus of enhancement lateral right IAC, likely\npostradiation change.",
            "output": "1. Stable exam.  No evidence of tumor progression."
        },
        {
            "input": "There are postsurgical changes of right temporoparietal craniotomy for\nresection of an underlying right temporal lobe mass.  Confluent FLAIR and T2\nhyperintense signal abnormalities in the right corona radiata and centrum\nsemiovale extending into the right subcortical frontal and parietal white\nmatter are unchanged, likely postradiation changes.  A small area of\nenhancement along the anterolateral margin of the dilated atrium of the right\nlateral ventricle appears unchanged compared to prior studies.  There is no\nevidence increasing enhancement surrounding the resection cavity to suggest\ntumor progression.\n\nThe ventricles and sulci are unchanged in size and configuration with ex vacuo\ndilatation of the right lateral ventricle.\n\nThere is no evidence of infarction.  There is no evidence of new hemorrhage.\n\nThere is a partially empty sella.\n\nMild mucosal thickening of the paranasal sinuses.  Fluid signal in the right\nmastoid air cells persists.  Unremarkable intraorbital contents.",
            "output": "Unchanged MRI appearance of the brain.\nPersistent enhancement at the surgical margin with no findings to suggest\ntumor progression."
        },
        {
            "input": "Patient is status post right temporoparietal craniotomy for resection of\nanaplastic astrocytoma. The previous area of enhancement along the\nanterolateral margin of the right atrium is unchanged on today's study (series\n9, image 24).  Re-demonstrated is persistent unchanged T2 FLAIR hyperintensity\nalong the right hemisphere including regions of cortex along the right\nparietal lobe and extends anteriorly along the centrum semiovale.  Ex vacuole\ndilation of the right ventricle which appears unchanged compared to prior\nstudies.    No evidence of new areas of enhancement.  The sella turcica is\nunchanged in appearance.\n\nNo evidence of acute infarct or intracranial blood products.  Major\nintracranial flow voids are preserved.  The orbits are unremarkable.  The\nparanasal and mastoid sinuses are patent.",
            "output": "1. Stable postsurgical appearance of right temporoparietal lobe mass\nresection.\n2. No interval change of previously noted area of enhancement in the\nanterolateral right atrium."
        },
        {
            "input": "Re-identified is 6-7 mm inferior displacement of the cerebellar tonsils,\ncompatible with Chiari 1 malformation, unchanged from prior examination. \nThere is no intra or extra-axial mass, acute hemorrhage or infarct.  The\nsulci, ventricles cisterns are within expected limits for the patient's age. \nThere is no parenchymal signal abnormality or abnormal enhancement.  The major\nintracranial flow voids are preserved.  The dural venous sinuses are patent.\nThere is mild mucosal thickening of the paranasal sinuses.  The orbits are\nunremarkable.  No fluid signal is seen in the mastoid air cells.\n\nCSF phase contrast images demonstrate normal biphasic CSF flow in the\nprepontine cistern as well as the pontomedullary cistern and\ncerebellomedullary cisterns.",
            "output": "1. Re-identified is 6-7 mm inferior displacement of the cerebellar tonsils\ncompatible with Chiari 1 malformation.\n2. Unremarkable CSF flow study demonstrating biphasic CSF flow in the\nprepontine, pontomedullary and cerebellomedullary cisterns.\n3. Additional findings as described above."
        },
        {
            "input": "The ventricles and extra-axial spaces are normal in size. There is no evidence\nof midline shift, mass effect or hydrocephalus. There are no acute infarcts.\nThere is no evidence of focal abnormalities.  The vascular flow voids are\nmaintained. The visualized paranasal sinuses are clear. Following gadolinium\nadministration there is no evidence of abnormal parenchymal, vascular and\nmeningeal enhancement seen.\n\nThe cerebellar tonsils are approximately 4 mm below the level of foramen\nmagnum which is at the upper limit of normal.  The CSF spaces at the foramen\nmagnum are maintained and both anterior and posterior pathways are well seen. \nThere is no deformity of the tonsils identified.\n\nThe phase contrast images demonstrate normal bidirectional flow at the\ncervicomedullary junction.  There is no evidence of CSF flow obstruction at\nthe foramen magnum.",
            "output": "1. No significant abnormalities are seen on MRI of the brain with and without\ngadolinium.\n2. Minimal tonsillar herniation which does not meet the criteria for Chiari 1\nmalformation.\n3. Well maintained CSF flow at the foramen magnum without CSF flow\nobstruction."
        },
        {
            "input": "Two foci of slow diffusion are visualized in the right occipital region\n(images number 14 and 16, series 6), measuring approximately 3 x 3 mm in size\nwith no evidence of mass effect or hemorrhagic transformation, suggestive of\nsubacute ischemic changes. The ventricles and sulci are prominent and\nunchanged, suggesting cortical volume loss. Multiple scattered foci of high\nsignal intensity are re- demonstrated on T2 and FLAIR sequences, distributed\nin the subcortical and periventricular white matter and both cerebellar\nhemispheres, which are nonspecific and may reflect changes due to small vessel\ndisease. There is no evidence of abnormal enhancement to suggest\nleptomeningeal disease. The major vascular flow voids are present and\ndemonstrate normal distribution. The orbits are unremarkable, the paranasal\nsinuses are clear, mucosal thickening is noted in the mastoid air cells\nbilaterally, new since the prior examination.",
            "output": "1. Two small foci of slow diffusion identified in the right occipital region\nas described above, suggesting acute/subacute ischemic changes, postictal\nareas of slow diffusion is also a consideration, there is no evidence of mass\neffect or hemorrhagic transformation.\n\n2. No enhancing lesions are identified. Scattered foci of high signal\nintensity on T2 and FLAIR sequences history in the subcortical white matter\nare nonspecific and may reflect changes due to small vessel disease\n\n3. Mild mucosal thickening is identified in the mastoid air cells bilaterally,\nnew since the prior examination.\n\nNOTIFICATION:  These findings were discovered and communicated via phone call\nto Dr. ___ by Dr. ___ on ___ at 12:40 ___."
        },
        {
            "input": "There is no acute infarct. There is no intracranial hemorrhage. There is\ngyriform T1 hyperintensity within the right occipital lobe consistent with\nlaminar necrosis, as seen on prior MRIs from ___ and ___. There is atrophy of the bilateral hippocampi, as seen on prior MRI from\n___. There is no positive mass effect. There is no midline\nshift.  There is no pathologic intracranial enhancement.\n\nVentricles and sulci are age-appropriate. Intracranial flow voids are\nmaintained. There is mucosal thickening of the ethmoid sinuses and left\nmaxillary sinus. The paranasal sinuses and mastoid air cells otherwise appear\nclear.",
            "output": "1. No evidence of infarction.\n2. Laminar necrosis of the right occipital lobe due to prior infarct,\nunchanged from prior MRIs.\n3. Bilateral hippocampal atrophy, unchanged from prior MRI."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor acute infarction.  Chronic bilateral occipital lobe infarcts appear similar\ncompared to prior.  Mild periventricular T2 and FLAIR hyperintense changes\nappear similar compared to prior.  Moderate generalized cerebral atrophy with\nex vacuo dilatation of the ventricular system.  There is no abnormal\nenhancement after contrast administration.  Bilateral nonenhanced parotid\ndilated ductules or cysts are nonspecific and was also noted on prior MR\nstudy, but slightly more prominent.  The intracranial arteries demonstrate\nnormal T2 flow voids.  Mild mucosal thickening involving the paranasal\nsinuses.  The orbits appear normal.  The craniocervical junction appears\nnormal.",
            "output": "No significant interval change compared to prior MR imaging.\n\nNo acute intracranial infarct, mass or hemorrhage. No abnormal enhancing\nlesions.\n\nChronic small bilateral occipital lobe infarcts appear similar compared to\nprior imaging.\n\nMild white matter microangiopathic changes are fairly stable.  Generalized\ncerebral atrophy with ex vacuo dilatation of ventricular system."
        },
        {
            "input": "There has been expected interim evolution of the left occipital and inferior\nparietal infarct seen on the ___, with progression of volume loss,\ndecreased high signal on diffusion tracer sequence, and interim development of\nhyperintensity on the ADC map.  There is also interim development of\npseudolaminar necrosis, which limits reassessment of the gyriform contrast\nenhancement previously seen within this infarct.  As visualized, the gyriform\ncontrast enhancement appears to persist with decreased thickness.\n\nA chronic right occipital infarct is also again noted.  A small chronic\ninfarct is also again seen in the superior left frontal lobe at the gray/white\nmatter junction, image 7:16.  T2/FLAIR hyperintense foci in the\nperiventricular, deep, and subcortical white matter of the cerebral\nhemispheres, and in the bilateral pons, are also again noted, nonspecific but\nlikely sequela of chronic small vessel ischemic disease in this age group.\n\nAllowing for susceptibility artifact at the posterior vertex, which is most\npronounced on diffusion weighted and gradient echo images, and which appears\nto be related to the external object, there is no evidence for an acute\ninfarction or intracranial blood products.  No evidence for new enhancing\nlesions.\n\nMild-to-moderate global parenchymal volume loss is again seen with prominent\nventricles and sulci.  Basal cisterns are preserved.\n\nMajor vascular flow voids are grossly preserved.\n\nThere is mild mucosal thickening in the ethmoid air cells.  There is trace\nopacification of the dependent left mastoid air cells.  The patient is status\npost bilateral cataract surgery.",
            "output": "1. Expected interim evolution of the left occipital and inferior parietal\ninfarct seen on ___, with progression of volume loss.  Interim\ndevelopment of pseudolaminar necrosis limits reassessment of the previously\nseen gyriform contrast enhancement within this infarct.  As visualized, the\ngyriform contrast enhancement appears to persist with decreased thickness.\n2. Chronic right occipital infarct and a small chronic infarct in the superior\nleft frontal lobe at the gray/white matter junction are again demonstrated.\n3. Allowing for susceptibility artifact at the posterior vertex, there is no\nevidence for an acute infarction.\n4. No evidence for new enhancing intracranial lesions."
        },
        {
            "input": "No intra or extra-axial mass, acute hemorrhage or infarct. Sulci, ventricles\nand cisterns are within expected limits for the patient's age. The major\nintracranial flow voids are preserved. No abnormal enhancement. The dural\nvenous sinuses are patent. Mild mucosal thickening of ethmoid air cells and\nmucous retention cysts in the right maxillary sinus are identified. The orbits\nare unremarkable. The mastoid air cells are clear.",
            "output": "Unremarkable contrast-enhanced examination of the brain. No evidence of mass\nlesion or abnormal enhancement. No acute infarcts."
        },
        {
            "input": "No acute infarct, mass effect, shift of normally midline structures or\nsuspicious focus of negative susceptibility to suggest hemorrhage.\nThere is moderate to marked dilation of the lateral and the third ventricles\nincluding the temporal horns along with prominent Sylvian fissures and\ncerebral sulci and extra-axial CSF spaces.\nThe ventricular dilation is more than the sulcal prominence.  There is\nindentation and thinning of the corpus callosum by the dilated lateral\nventricles.\nNo significant change however is noted compared to the prior MRI of ___\nA few multiple small scattered T2 FLAIR hyperintense foci are noted in the\ncerebral white matter.   Minimal smoked periventricular hyperintense signal is\nalso noted.\n\nThe major intracranial arterial flow voids are noted.\nThe cavernous carotid segments are slightly tortuous in course.\nThe venous sinuses are unremarkable on the routine study.\nDegenerative changes in the cervical spine with disc osteophyte complex\ncausing indentation on the cord with moderate canal narrowing and deformity.",
            "output": "1. No acute infarct or mass effect.\n2. Moderate to marked dilation of the lateral and the third ventricles more\nthan the sulcal prominence, correlate for communicating hydrocephalus such as\nNPH, superimposed on parenchymal volume loss.  No significant change compared\nto the prior study of ___ mild progression compared to ___."
        },
        {
            "input": "MRI HEAD: There is a poorly visualized 3 mm nodule centered in the foramen of\n___ (series 16, image 14), corresponding to a hyperdense lesion seen on\nprior CT, compatible with a colloid cyst. Otherwise, no intra or extra-axial\nmass is identified. Acute intracranial hemorrhages or infarct. The sulci,\nventricles and cisterns are within expected limits. The major flow voids are\npreserved. There are very mild scattered periventricular and subcortical\nnonspecific T2/FLAIR hyperintensities, which may be seen in setting of small\nvessel ischemic disease. The paranasal sinuses are clear. The orbits are\nunremarkable. The mastoid air cells are clear. .\n\nHEAD MRA: There is a 2 mm inferior lateral projecting outpouching along the\nleft aspect of the basilar artery (series 10, image 67), likely representing\nan infundibulum at the left AICA origin. Otherwise, the intracranial ICA, ACA,\nMCA and the remainder the posterior circulation is unremarkable without\nevidence of stenosis or dissection.\n\nNECK MRA: Incidental note is made of retropharyngeal course of the right\nextracranial ICA. Otherwise the common carotid, extracranial ICA have and\nvertebral arteries are normal in contour and caliber. The vertebral arteries\nare codominant. No significant stenosis of the extracranial internal carotid\narteries based on NASCET criteria. No evidence of stenosis or dissection.",
            "output": "1. No acute intracranial process. White matter changes, which are nonspecific,\nbut compatible with small-vessel ischemic disease as described above.\n\n2. Likely 2 mm infundibulum of the basilar artery at the AICA origin.\nOtherwise, no evidence of intracranial aneurysm larger than 3 mm."
        },
        {
            "input": "There is a poorly visualized but likely stable colloid cyst better seen on\nprior CT scan dated ___. There is no hydrocephalus. There is no\nevidence of acute hemorrhage or acute infarct. There is no midline shift.\nVentricles and sulci are age-appropriate.  There are unchanged T2/FLAIR\nhyperintense lesions in the periventricular and subcortical white matter.\nThere is no abnormal intracranial enhancement. Intracranial flow voids are\nmaintained.  The orbits are unremarkable. There is minimal mucosal thickening\nwithin the ethmoid and sphenoid air cells. The remainder of the paranasal\nsinuses and mastoid air cells are clear.",
            "output": "No evidence of acute hemorrhage or infarction.\n\nPoorly visualized subcentimeter colloid cyst, better seen on prior CT scan\ndated ___.\nNo evidence of hydrocephalus.\n\nStable T2/FLAIR hyperintense lesions in the bilateral periventricular and\nsubcortical white matter."
        },
        {
            "input": "Previously seen presumed tiny colloid cyst is again identified.  No\nhydrocephalus is seen.  Minimal changes of small vessel disease identified\nwhich are stable.  There is no evidence of significant brain atrophy.  No\nacute infarcts mass effect or midline shift seen.  There is no micro\nhemorrhages.  Vascular flow voids are maintained.  Visualized paranasal\nsinuses are clear.",
            "output": "Stable appearance of the brain without acute abnormalities since ___.  No acute infarcts are seen.  No focal abnormalities within the brain\nstem."
        },
        {
            "input": "There is 0.6 cm x 0.4 cm: Cyst along the anterosuperior third ventricle,\nstable compared with ___, compared with 0.5 cm\nx 0.3 cm on ___.\n\nThere is no evidence of hemorrhage, edema, parenchymal masses, mass effect,\nmidline shift or infarction.  Advanced degenerative changes in the visualized\nupper cervical spine, with mild anterolisthesis of C2 on C3, C3 on C4, likely\ndegenerative.  There are mild chronic small vessel ischemic changes.  There is\ngeneralized brain parenchyma atrophy, with biparietal predominance.  Paranasal\nsinuses, mastoid air cells are clear.\n0.4 cm x 0.2 cm extra-axial dural-based enhancing lesion overlying\ninferolateral left frontal lobe is most consistent with meningioma, it is\nsimilar compared with ___, there is adjacent benign-appearing\nosseous thickening, without associated marrow infiltration or enhancement to\nsuggest intraosseous involvement.  Dural venous sinuses are patent.  Patent\nintracranial vascular flow voids.  Significant synovial enhancement of the\nright temporomandibular joint is likely degenerative, consider inflammatory\narthritis if appropriate.",
            "output": "There are no infarcts.\nStable colloid cyst in the anterosuperior third ventricle, no hydrocephalus.\nStable tiny left frontal meningioma.\nBrain parenchymal atrophy."
        },
        {
            "input": "Please note the study is mildly degraded by motion.\n\nThere is restricted diffusion in the right insular cortex, frontal lobe,\nparietal lobe, medial right temporal lobe, posterior limb of the internal\ncapsule, right basal ganglia and ventral, medial right thalamus.  Infarct is\npredominantly in the subcortical region.  Periventricular and subcortical T2\nand FLAIR hyperintensities are noted.  The normal flow void of the right\npetrous, cavernous and communicating ICA are not well visualized with\nreconstitution at the level of the right MCA, as seen on the prior CTA.\n\nMinimal mucosal thickening of the ethmoid and left maxillary sinuses is seen. \nThe orbits and mastoid air cells are normal.\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, or midline\nshift.   The ventricles and sulci are normal in caliber and configuration.",
            "output": "1. Right basal ganglia and deep watershed infarction with no evidence of mass\neffect or hemorrhage.\n2. Re- demonstration of the thrombus in the right petrous, cavernous and\ncommunicating ICA, reconstituting at the level of the MCA, better visualized\non prior CTA."
        },
        {
            "input": "There is DWI/FLAIR hyperintense signal in the region of the right insula and\nadjacent frontal operculum and the right parieto-occipital border zone with\nassociated low signal on the ADC map, consistent with late acute/early\nsubacute infarcts (series 10, image 14).  There is also a punctate focus of\nslow diffusion in the left occipital lobe (series 4, image 13).  Multiple\nscattered supra and infratentorial chronic micro hemorrhages are unchanged.\n\nEncephalomalacia in the left occipital lobe is noted.  Additional small\nscattered white matter FLAIR hyperintense foci in the periventricular and\nsubcortical white matter that are present on the prior examination likely\nrepresent sequelae of chronic small vessel ischemic disease.\n\nThere is no evidence of recent hemorrhage, edema, mass, or mass effect.  The\nventricles and sulci are age-appropriate.  Principal intracranial vascular\nflow voids are preserved.  There is mild mucosal thickening in the ethmoid and\nmaxillary sinuses.  The orbits are unremarkable.",
            "output": "1. Late acute/early subacute infarcts involving the right insula, frontal\noperculum, and inferior parietal lobe, corresponding to the right MCA\ndistribution.\n2. Single punctate focus of slow diffusion in the left occipital cortex, in\nproximity to a chronic infarct in this region.\n3. Multiple scattered chronic supra and infratentorial micro hemorrhages are\ngrossly unchanged.  There is no new hemorrhage."
        },
        {
            "input": "There are new small foci of slow diffusion, one anterior to the right\nprecentral sulcus, the other(s) along the left parietotemporal operculum\n(Series 402, images 21 and ___, with corresponding subtle FLAIR\nhyperintense signal, consistent with late acute infarct.  Evolving subacute\ninfarcts in the region of the right insula/frontal operculum and right\nparieto-occipital border zone are more conspicuous on FLAIR (Series 10, image\n14).  Encephalomalacia in left occipital lobe related to chronic infarct, is\nunchanged.  Additional small scattered white matter FLAIR hyperintense foci in\nthe periventricular subcortical white matter are grossly unchanged but likely\nsequelae of chronic small vessel ischemic disease.  A few scattered punctate\nmicro hemorrhages are unchanged.\n\nThere is no evidence of recent hemorrhage, edema, mass, or mass effect.  The\nventricles and sulci are age-appropriate.  Principal intracranial vascular\nflow voids are preserved.  There is mild mucosal thickening in the ethmoid air\ncells.  The orbits are grossly unremarkable.  A partially empty sella is\nnoted.",
            "output": "1.  New small foci of late acute infarction at the gray-white junction of the\nright posterior frontal and left parietotemporal operculum, likely embolic in\netiology.\n\n2.  Evolving subacute infarcts as described.  Chronic left occipital infarct.\n\n3.  Scattered punctate micro hemorrhages are unchanged.  There is no recent\nhemorrhage."
        },
        {
            "input": "MR BRAIN:\nThere is linear gyriform cortical restricted diffusion involving primarily the\nposterior aspect of the precentral gyrus but also likely a small area of the\nanterior aspect of the postcentral gyrus (see series 7 images 24, 25, 26 as\nwell as series 6, images 24, 25, 26).  There is no definite corresponding\nFLAIR signal abnormality in these areas.  There is no evidence of additional\ninfarction elsewhere.  A few foci of brainstem and basal ganglia, as well as a\nright temporal lobe, focus of susceptibility likely relates to small foci of\nchronic microhemorrhage, possibly related to hypertension given distribution\n(series 13 images 14 and 10).  Elsewhere, there is no evidence of intracranial\nhemorrhage, edema, mass or mass effect.  The ventricles and sulci are\nprominent consistent with moderate global involutional changes. \nPeriventricular and scattered bilateral deep and subcortical white matter foci\nof T2/FLAIR signal hyperintensity are nonspecific but compatible with moderate\nchanges of chronic white matter microangiopathy. The visualized paranasal\nsinuses and mastoid air cells appear clear.  The globes and orbits are\nunremarkable.\n\nMRA BRAIN:\nThe circle of ___ vasculature and principal intracranial branches\ndemonstrate normal flow related enhancement without evidence of significant\nstenosis, occlusion, or aneurysm.",
            "output": "1. Cortically-based gyriform restricted diffusion along the posterior aspect\nof the left precentral gyrus, with a small similar area along the anterior\naspect of the postcentral gyrus, consistent with acute infarct.\n2. A few small foci of left basal ganglia, right temporal lobe, and right\nbrainstem microhemorrhage likely relate to chronic hypertension.  Otherwise,\nno intracranial hemorrhage.\n3. Unremarkable MRA brain.  Patent circle of ___ vasculature.\n4. Chronic findings include moderate global involutional changes and moderate\nchanges of chronic white matter microangiopathy.\n\nNOTIFICATION:  The findings above including modification to preliminary\ninterpretation were discussed with ___, M.D. by ___\n___, M.D. on the telephone on ___ at 12:42 pm, 15 minutes after\ndiscovery of the findings."
        },
        {
            "input": "MRI BRAIN:\nThere is a small amount of residual blood in the body of the left lateral\nventricle and occipital horn of the right lateral ventricle, with associated\nlow signal on gradient echo images, and high signal on diffusion tracer and\nFLAIR images.  There is also mild residual nonacute subarachnoid hemorrhage,\nno longer dense on the CT from ___, demonstrating high signal on\nFLAIR and diffusion tracer images and left greater than right sulci.\n\nThe ventricles are normal in size, similar to ___.  Track from\nprior right frontal approach ventriculostomy catheter is noted with mild\nassociated linear T2 hyperintensity.\n\nThere is linear hyperintensity on the diffusion tracer, FLAIR, precontrast T1\nweighted, and postcontrast T1 weighted images in the medial left thalamus,\nimage 14 of series 6, 14, 15, and 17, and images ___ of series 17, most\nlikely related to a prominent vein.  While this may represent a small\ndevelopmental venous anomaly, there is no evidence for an associated cavernous\nmalformation.\n\nThere is no evidence for an acute infarction.  There is no evidence for an\nenhancing mass. Dural venous sinuses are patent on postcontrast MP RAGE\nimages.\n\nMRA NECK: There is a 3 vessel aortic arch.  There is no right carotid stenosis\nby NASCET criteria.  Irregular plaque is again seen in the proximal left\ninternal carotid artery, without evidence for stenosis by NASCET criteria on\nthe preceding CTA which provides better quantification.  Bilateral vertebral\narteries appear patent without evidence for flow-limiting stenosis.",
            "output": "1. Mild residual non acute subarachnoid hemorrhage in left greater than right\nsulci.\n2. Small amount of residual blood in the body of the left lateral ventricle\nand occipital horn of the right lateral ventricle.  No hydrocephalus with\nstable size of the ventricles compared to ___.\n3. Small vein in the medial left thalamus, possibly developmental venous\nanomaly.  No evidence for an associated cavernous malformation.\n4. No evidence for a mass.\n5. Irregular plaque is again demonstrated in the proximal left internal\ncarotid artery, with ulceration better demonstrated on the ___\nCTA.  No evidence for carotid stenosis by NASCET criteria."
        },
        {
            "input": "There are punctate areas of diffusion abnormalities in the right posterior\ncerebellum, left superior cerebellar and left  posterior frontal cortical\nregion and right posterior temporal regions without corresponding ADC\nabnormality suggestive of subacute infarcts.  There are extensive\nhyperintensities in the periventricular and subcortical white matter\nhypodensity which suggest changes of small vessel disease. There is no midline\nshift, mass effect or hydrocephalus.  There is mild to moderate brain atrophy.\nFollowing gadolinium administration, there is no evidence of abnormal\nparenchymal, vascular and meningeal enhancement.  There are no obvious bony\nabnormalities or abnormal enhancement seen within",
            "output": "Bilateral cerebellum, right posterior temporal and left posterior frontal\nsubacute infarcts which are likely embolic in nature.  Severe changes of small\nvessel disease. No enhancing brain lesions.\n\nNOTIFICATION:  Critical  communication dashboard."
        },
        {
            "input": "There are new scattered foci of restricted diffusion in the bilateral frontal\nlobes and left parietal and occipital lobes concerning for new thromboembolic\ninfarcts. There continues to be periventricular and subcortical\nhyperintensities which are likely secondary to chronic small vessel ischemic\ndisease. There are small stable areas of microhemorrhage (15:11,16). Areas of\nsusceptibility along the left parietooccipital convexity may be due amyloid\ndeposition or subarachnoid blood.  No enhancing mass is seen. The orbits are\nunremarkable, and the paranasal sinuses and mastoid air cells are clear.",
            "output": "1. New scattered foci of restricted diffusion as described above are\nconcerning for infarcts from a thromboembolic etiology.\n2. Chronic bilateral microhemorrhages.\n3. Susceptibility along the left parietoccipital convexity may reflect\nsubarachnoid blood or amyloid deposition.\n4. Severe chronic small ischemic changes.\n\nNOTIFICATION:  The findings were discussed by Dr. ___ with Dr. ___ on\nthe telephone on ___ at 11:25 AM, at the time of discovery of the\nfindings."
        },
        {
            "input": "There is no evidence of a mucosal mass.  There is no pathologic adenopathy by\nimaging criteria.  Neck vessels are patent.  Normal salivary glands.\nNormal thyroid.\n\nThe hypopharynx she will soft tissue fullness present on the ___\nexamination is no longer present.",
            "output": "1. Normal study.  The hypo pharyngeal fullness noted on ___ is no\nlonger present."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift.\nThere are no acute infarcts.  There are severe chronic small vessel ischemic\nchanges.  There is no hydrocephalus.  No volume loss.  There is chronic\ninfarct in the right vertex, with small focus of associated calcification and\nchronic blood products, involving probably both precentral and postcentral\ngyrus, similar compared with head CT ___, head CT ___. \nThere is tiny chronic cortical infarct involving left medial parietal lobe. \nModerate opacification of right mastoid air cells, similar compared with CT ___.  Left mastoids are clear, clear paranasal sinuses.  Intracranial\nvascular flow voids are preserved.",
            "output": "1. There are no acute infarcts.\n2. Chronic infarcts, stable.\n3. Severe chronic small vessel ischemic changes.\n4. Moderate opacification right mastoids."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There are scattered nonspecific T2/FLAIR hyperintensities in\nthe subcortical and periventricular white matter without enhancement. \nPrevious cochlear enhancement is not evident on the current examination. \nThere is no abnormal enhancement after contrast administration.\n\nThe major intracranial vascular flow voids are preserved.  Orbits and\nvisualized E extracranial soft tissues are unremarkable.",
            "output": "1. No acute intracranial abnormality.\n2. No evidence of intracranial metastatic disease.\n3. Nonspecific white matter signal changes appear slightly increased compared\nto ___.  These can reflect chronic microangiopathy, but could also reflect\nsequela of previous inflammatory processes or vasculitis in the context of a\nhistory of lupus noted on the previous exam."
        },
        {
            "input": "There is a 0.3 cm focus of hypo enhancement in the anterior pituitary gland,\nseries 9, image 125 dens 116 to.\n\nThere is no evidence of hemorrhage, edema, mass effect, midline shift or\ninfarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There are few stable scattered subcortical and periventricular\nwhite matter signal abnormalities.  There is no abnormal enhancement after\ncontrast administration.  A left cerebellar developmental venous anomaly is\nseen.  The major vascular flow voids are preserved.\n\nA large retention cyst is seen in the left maxillary sinus.  The orbits and\nmastoid air cells are normal.  There is a nonenhancing, FLAIR hyperintense 0.8\ncm lesion in the posterior nasopharynx, likely representing a retention cyst\nor Tornwaldt cyst.",
            "output": "1. A 0.3 cm focus of hypo enhancement in the anterior pituitary gland which\nmay represent a small microadenoma versus a coursing vessel.  Recommend\ncorrelation with dedicated MRI of the pituitary gland for further evaluation.\n2. No evidence of abnormal enhancement.\n3. Few scattered white matter signal abnormalities which is a nonspecific\nfinding and may be secondary to migraines, infection, inflammation,\ndemyelination or vasculitis.\n\nRECOMMENDATION(S):  A 0.3 cm focus of hypo enhancement in the anterior\npituitary gland which may represent a small microadenoma versus a coursing\nvessel.  Recommend correlation with dedicated MRI of the pituitary gland for\nfurther evaluation."
        },
        {
            "input": "There is a parenchymal hemorrhage at the posterior inferior left thalamus\nmeasuring 1.1 x 1.3 cm containing subacute and chronic blood products (12:14).\nThere are foci of slow diffusion within this hemorrhage likely representing\nartifact.  There is a punctate focus of slow diffusion at the mid superior\nleft thalamus (502:18) without corresponding blood products which may\nrepresent true infarct.  There are foci of slow diffusion at the superior\naspect of the fourth ventricle corresponding to foci of blood.\n\nThere is a right convexity chronic subdural hematoma/hygroma measuring up to 6\nmm in depth.  There is a small amount of blood layering within the occipital\nhorns there is mild thickening enhancement of the dural falx, which is likely\nreactive.  Mild FLAIR hyperintensity and thickening of the right cerebral\nhemisphere dura is also identified, presumably reactive in nature.  Left\nfrontal and right temporal lobe subarachnoid hemorrhage is also identified. \nThere periventricular and subcortical white matter FLAIR hyperintense foci in\naddition to central pontine FLAIR hyperintensity which are nonspecific but\nlikely secondary to sequela of chronic microangiopathy.  There are small\nchronic parenchymal micro bleeds at the right frontal cortex.  There are\nprominent perivascular spaces. There is mild prominence of the ventricles and\ncortical sulci consistent with volume loss.  Known left supra-clinoid\ncalcified ICA aneurysm is not well evaluated on the current exam.  There is no\nabnormal postcontrast enhancement.\n\nThe bilateral lenses are absent.  There is a right scalp hematoma.  There is\nmild mucosal thickening of the paranasal sinuses and bilateral mastoid air\ncell effusions.  There is layering blood within the bilateral sphenoid and\nmaxillary sinuses.  Known facial fractures are not well seen on MRI are better\ncharacterized on prior CT.",
            "output": "1. Parenchymal hemorrhage at the posterior inferior left thalamus without\nevidence of underlying enhancing mass.  Small amount of blood layering in the\nbilateral occipital horns and within the fourth ventricle.  Trace left frontal\nand right temporal lobe subarachnoid hemorrhages identified.  There is right\nconvexity chronic subdural hematoma/hygroma.  These findings are relatively\nunchanged.\n2. Punctate focus of slow diffusion at the mid superior left thalamus without\ncorresponding blood products which may represent an acute infarct.\n3. Background sequela chronic microangiopathy and small right frontal remote\nmicrobleeds.\n4. Facial fractures are not well seen on MRI and are better characterized on\nprior dedicated CT.\n\nNOTIFICATION:  The findings were discussed by Dr. ___ with Dr.\n___ on the telephoneon ___ at 2:00 ___, 5 minutes after\ndiscovery of the findings."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, intracranial masses, mass effect,\nor infarction.  Again seen is a small right frontal scalp lipoma. The\nventricles and sulci are normal in caliber and configuration.  The C2 and C3\nvertebral bodies are congenitally fused.  There is no abnormal enhancement\nafter contrast administration.\n\nImages of the pontine cistern, cavernous sinuses, Meckel's cave, and included\nportion of the course of the fifth cranial nerves appear normal.",
            "output": "No evidence of cavernous sinus or other lesion along the course of the fifth\nnerve.  Incidentally noted right frontal scalp lipoma and congenital fusion of\nthe C2 and C3 vertebral bodies."
        },
        {
            "input": "There is no evidence of infarction or hemorrhage.  There is no enhancing mass\nor abnormal enhancement.  There is diffuse parenchymal volume loss with mild\nnonspecific periventricular and subcortical FLAIR hyperintensities, likely a\nsequela of chronic small vessel ischemic disease.  There is a 7 x 5 mm\nprominent and ectatic vascular flow void of the right carotid terminus at the\norigin of the right ophthalmic artery (08:10), 900:75), which may represent\nvascular ectasia, however, aneurysm or infundibulum cannot be completely rule\nout.  The dural venous sinuses appear patent on the postcontrast images. \nThere is mild mucosal thickening of bilateral ethmoid air cells.",
            "output": "1. No evidence of infarction, hemorrhage, mass, or abnormal enhancement.\n2. Mild diffuse parenchymal volume loss with mild probable chronic small\nvessel ischemic disease.\n3. Question of vascular ectasia versus aneurysm or vascular infundibulum of\nthe right carotid terminus, as described above.  Recommend CTA or MRA to\nfurther assess.\n\nRECOMMENDATION(S):  Recommend CTA or MRA to further assess question of\nvascular ectasia, aneurysm versus infundibulum, as above."
        },
        {
            "input": "Corresponding to the abnormal flow void on the recent MRI is a focal\noutpouching arising from the clinoid segment of the right internal carotid\nartery (2:112), likely representing a blister aneurysm measuring 4 x 3 mm.\n\nThere is a question of 2 mm outpouching arising from the clinoid segment of\nthe left internal carotid artery (2:106), possibly representing an additional\naneurysm versus infundibulum.\n\nOtherwise, the bilateral internal carotid arteries and vertebral arteries\nappear patent without stenosis, occlusion, or other aneurysm.  There is\nhypoplastic A1 segment of the left anterior cerebral artery, likely a\ncongenital variant.",
            "output": "1. Blister aneurysm arising from the clinoid segment of the right internal\ncarotid artery, corresponding to abnormal flow void seen on the recent MRI\nmeasuring 4 x 3 mm.\n2. Question of 2 mm outpouching arising from the clinoid segment of the left\ninternal carotid artery, possibly an additional aneurysm versus infundibulum."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, or infarction.\nThe ventricles and sulci are normal in caliber and configuration. There is no\nabnormal enhancement after contrast administration.\n\nMajor intravascular flow voids are preserved. There is normal enhancement of\nthe major intracranial arteries and dural venous sinuses following contrast\nadministration.\n\nMarrow signal is within normal limits. There is mild scattered mucosal\nthickening of the ethmoid sinuses and fluid in the left maxillary sinus. The\nparanasal sinuses are otherwise appear clear. The mastoid air cells appear\nclear. The orbits are normal.",
            "output": "1. No MRI evidence of an intracranial infectious process.\n2. Fluid in the left maxillary sinus."
        },
        {
            "input": "There is no evidence of edema, masses, mass effect, midline shift or\ninfarction.  There is prominence of the ventricles and sulci suggestive\ninvolutional changes.  Periventricular and subcortical T2 and FLAIR\nhyperintensities are noted.  There are numerous foci of micro hemorrhages\nthroughout the thalami, basal ganglia, pons medial left cerebellum and medial\nright temporal lobe.  These findings with the mild white matter hyperintensity\non the FLAIR images suggest amyloid angiopathy.  The major vascular flow voids\nare preserved.\n\nBilateral cataract extractions are seen.  There is thick mucosal thickening in\nthe sphenoid sinus.  The mastoid air cells are clear.\n\nDegenerative changes are visualized to of the upper cervical spine.",
            "output": "1. No acute infarct or mass effect.\n2. Multiple micro hemorrhages throughout predominantly the basal ganglia,\nbrainstem and cerebellum, likely due to amyloid angiopathy.  Hypertensive is a\nless likely alternative.\n3. Senescent volume changes and white matter signal abnormality, likely\nsecondary to chronic microvascular ischemic changes."
        },
        {
            "input": "There is no acute infarction, intracranial hemorrhage, extracerebral fluid\ncollection, midline shift or mass effect. There are postsurgical changes seen\nin the posterior fossa and encephalomalacia in the posteromedial right\ncerebellar hemisphere consistent with the patient's surgical history.  There\nis a tiny focus of enhancement on the lateral border of surgical bed in the\nright posteromedial right cerebellar hemisphere which most likely represents a\nvascular structure.\n\nThe cerebral volume is appropriate for the patient's stated age. The major\nvascular flow voids are maintained, there is no evidence of abnormal\nenhancement.\n\nThe orbits are unremarkable, the paranasal sinuses and mastoid air cells are\nclear",
            "output": "1. No evidence of acute hemorrhage or infarction. An area of enhancement on\nthe lateral border of the surgical bed in the right cerebellar hemisphere most\nlikely represents a vascular structure, however attention should be paid on\nfollowup examination or comparison made to prior exams."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are within expected limits in\ncaliber and configuration.  There is no abnormal enhancement after contrast\nadministration.  There is linear sulcal FLAIR hyperintense signal in the right\nparietal vertex (series 7, image 19), compatible with slow flow within a\ncortical vein corresponding to an enhancing tubular structure on MP-RAGE\n(series 900, image 131) without evidence of abnormality on other sequences. \nThe major intracranial flow voids are preserved.  The dural venous sinuses are\npatent.\n\nHeterogeneity of the clivus with T1 hypointensity is similar in appearance to\nMR from ___.  No definite osseous lesion is seen.\n\nThe visualized paranasal sinuses, mastoid air cells and middle ear cavities\nare essentially clear.  The orbits are unremarkable.",
            "output": "1. No evidence of intracranial metastatic disease.  No abnormal enhancement. \nNo acute infarct or intracranial hemorrhage.\n2. The dural venous sinuses are patent.\n3. A linear sulcal FLAIR hyperintense focus in the right parietal vertex is\nassociated with tubular MP-RAGE postcontrast enhancement and no other signal\nabnormality on other sequences, likely representing slow flow through a\ncortical vein (series 7, image 19).\n4. Heterogeneity of the clivus is similar in appearance to MR from ___. \nGiven stability and lack of FDG avidity on recent PET-CT, this is unlikely to\nrepresent metastatic disease.  However, close attention on follow-up imaging\nis recommended."
        },
        {
            "input": "There is no FLAIR abnormality to correspond to findings on ___.\nNormal clivus.\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  Clear paranasal sinuses, mastoids.  Intracranial vascular flow\nvoids are preserved.\nWell-circumscribed 5 mm x 3 mm cystic abnormality right lateral fossa rising\n___,, similar compared with ___, did not show enhancement on\npriors, there was no mucosal thickening on priors, findings most consistent\nwith benign submucosal cyst.",
            "output": "Normal intracranial findings.  No osseous abnormality."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.  Evaluation of the trigeminal nerves show no evidence of mass,\nlesions or abnormal enhancement.  No evidence of vascular compression of the\ntrigeminal root entry zones.\n\nThere is mucosal thickening of the left ethmoidal air cells.  The remaining\nvisualized paranasal sinuses and mastoid air cells are clear.  The orbits are\nunremarkable.\n\nThe dural venous sinuses are patent.  Intracranial flow voids are preserved.",
            "output": "1. Unremarkable brain MRI.  No evidence of mass, lesions or abnormal\nenhancement involving the trigeminal nerves.  No evidence of vascular\ncompression of the trigeminal root entry zones."
        },
        {
            "input": "Please note the study is mildly degraded by motion.  MRI Brain:  There is a 7\nmm left insula area of restricted diffusion (702,700:9) with some associated\nFLAIR signal abnormality (9:13).  An additional curvilinear region of\nrestricted diffusion is seen within the left temporal lobe (700, 702:10).\n\n\nThere is no evidence of hemorrhage, edema, masses.  Ventricles and sulci are\nnormal in caliber and configuration.\n\nMRA brain: The intracranial vertebral and internal carotid arteries and their\nmajor branches appear normal without evidence of stenosis, occlusion, or\naneurysm formation.\n\nMRA neck:  There is limited evaluation of the origins of bilateral common\ncarotid and vertebral arteries.  Within the limits of this examination, The\ncommon, internal and external carotid arteries appear normal.  There is no\nevidence of internal carotid artery stenosis by NASCET criteria.  The origins\nof the great vessels, subclavian and vertebral arteries appear normal\nbilaterally.",
            "output": "1.  Study is mildly degraded by motion, and examination of bilateral common\ncarotid and vertebral artery origins limited secondary to motion artifact.\n2. Within limits of examination, no definite dissection or significant\nocclusion of head or neck MRA.\n3. 7 mm left insula subacute infarct.\n4. Additional curvilinear region of restricted diffusion in left temporal lobe\nmay represent acute infarct, or may be artifactual in nature.  Recommend\nclinical correlation and attention on followup imaging."
        },
        {
            "input": "There are 2 punctate areas of restricted diffusion with mild FLAIR\nhyperintensity within the right posterior putamen and internal capsule,\nconsistent with acute infarct.  Punctate areas of increased susceptibility and\nT1 hypodensity are seen within the anterior pons and left periatrial white\nmatter, new compared to prior MR from ___.  There is no evidence of edema,\nmasses, mass effect, or midline shift.  The ventricles and sulci are normal in\ncaliber and configuration.  There is no abnormal enhancement after contrast\nadministration.",
            "output": "1. Punctate areas of acute infarct in the right posterior putamen and internal\ncapsule.\n2. Punctate chronic hemorrhage in the anterior pons and left periatrial white\nmatter.\n3. No acute hemorrhage, ring-enhancing mass, mass effect or hydrocephalus is\nseen."
        },
        {
            "input": "There is no evidence of acute intracranial hemorrhage or mass effect. The\nventricles and basal cisterns appear normal.\n\nThere is no evidence of acute ischemia based on diffusion-weighted imaging. \nThere are normal vascular flow voids.\n\nThere is no abnormal brain parenchymal or leptomeningeal enhancement.\n\nThe orbits, skull base, and paranasal sinuses are unremarkable.",
            "output": "Normal MRI of the head."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, or infarction.\nThere are multiple foci of T2/FLAIR hyperintensity in the subcortical, deep,\nand periventricular white matter. These are nonspecific but commonly due to\nchronic small vessel ischemic disease. No lesions are identified within the\nbrainstem. There is an empty sella. There is prominence of the ventricles and\nsulci suggesting mild generalized parenchymal volume loss. There is no\nabnormal enhancement after contrast administration.",
            "output": "1. No hemorrhage, infarct, or mass.\n2. Multiple foci of T2/FLAIR hyperintensity in the cerebral white matter,\nnonspecific but consistent with moderate chronic small vessel ischemic\ndisease.\n3. Mild generalized parenchymal volume loss."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  Periventricular and subcortical T2 and FLAIR hyperintensities\nare noted.  There is a questionable 0.3 cm of hypo enhancement in the\nposterior pituitary gland, seen best on series 10, image 83.  There is no\nabnormal enhancement after contrast administration.  The major vascular flow\nvoids are preserved.\n\nThe orbits and mastoid air cells are normal.  Retention cysts are seen in the\nright maxillary sinus.  There is minimal mucosal thickening of the ethmoid\nsinuses.\n\nMild degenerative changes are visualized in the upper cervical spine.",
            "output": "1. White matter signal abnormality which can be seen in the setting of chronic\nsmall vessel disease in a patient with appropriate history/risk factors. \nThese findings however remain nonspecific and differential considerations\nwould also include demyelination, inflammation, infection, or vasculitis.  No\nabnormal contrast enhancement to suggest an underlying mass.  No acute\ninfarct.\n2. A 0.3 cm focus of hypo enhancement in the pituitary gland which may\nrepresent a coursing vessel, Rathke's cleft cyst or microadenoma.  Recommend a\ndedicated pituitary MRI for further evaluation.\n\nRECOMMENDATION(S):  A 0.3 cm focus of hypo enhancement in the pituitary gland\nwhich may represent a coursing vessel, Rathke's cleft cyst or microadenoma. \nRecommend a dedicated pituitary MRI for further evaluation."
        },
        {
            "input": "There is a 2.3 x 1.7 cm intra-axial nonenhancing T1 hypointense, T2\nintermediate lesion in the left frontal lobe which demonstrates slow diffusion\nand signal dropout on the gradient echo sequences, most likely representing\noccult vascular malformation with hemorrhage.  Less likely considerations\ninclude oligodendroglioma, low grade, or anaplastic glioma.  There is no\nevidence of midline shift or infarction.  The ventricles and sulci are normal\nin caliber and configuration.  The major flow voids are preserved.  Note is\nmade of a small posterior fossa.  However, there is no definite tonsillar\nherniation.\n\nThere is moderate mucosal thickening seen in the bilateral ethmoid sinuses. \nMild mucosal thickening is seen in the sphenoid sinuses and maxillary sinuses,\nleft greater than right.  The mastoid air cells appear grossly patent.\n\nMultiple subcutaneous lesions are seen scattered throughout the scalp, which\nis nonspecific.",
            "output": "1. 2.3 x 1.7 cm intra-axial nonenhancing lesion in the left frontal lobe\nlikely represents occult vascular malformation.  Less likely considerations\ninclude oligodendroglioma, low grade, or aplastic glioma.\n2. Multiple subcutaneous lesions are seen scattered throughout the scalp,\nwhich is nonspecific.  Consider the possibility of neurofibromatosis. \nRecommend correlation with clinical exam.\n3. Moderate paranasal sinus disease, as above.\n\nNOTIFICATION:  The findings were discussed with Dr.  ___  by ___,\nM.D. on the telephone on ___ at 5:28 pm, 1 minutes after discovery of\nthe findings."
        },
        {
            "input": "The T1 hyperintense and T2 heterogenously Iso and hypointense lesion in the\nleft frontal lobe measuring approximately 22 x 16 mm in the axial plane is\nunchanged compared to prior imaging.  However, the surrounding rim of FLAIR\nhyperintense signal/edema (series 11, image 15) appears slightly more\nconspicuous when compared to the prior examination, although this may be due\nto differences in slice selection.  The lesion demonstrates marked blooming on\nthe gradient echo.  No restricted diffusion or avid enhancement.  It is\ndifficult to place this lesion intra or extra-axial as on postcontrast imaging\nthere is vessel seen running external to the mass suggesting an intra-axial\nposition, but on T2 imaging there is T2 high-signal immediately deep to the\nlesion which may suggest a T2 cleft sign (extra-axial), but this may also\nsuggest edema.\n\nNo new lesions.  No intracranial infarct.  The pituitary gland appears normal.\nThe craniocervical junction appears normal.  The intracranial arteries\ndemonstrate normal T2 flow voids.  The orbits appear normal.  Mild mucosal\nthickening involving the paranasal sinuses.\n\nPlease note that the previously suspected multiple subcutaneous lesions are\nthought to more likely represent ECG leads.\n\nCurrently there is multiple fiducial markings overlying the calvarium.",
            "output": "1. Indeterminate left frontal lesion is stable in size, although surrounding\nrim of FLAIR hyperintense signal may be slightly more prominent, potentially\nartifactual secondary to differences in slice selection.  It is difficult to\naccurately place this lesion intra or extra-axial as described above.  In the\ndifferential diagnosis consider: If intra-axial an occult vascular\nmalformation or a low-grade glioma.  If extra-axial consider meningioma,\nalthough the lesion does not demonstrate avid enhancement.  Extra-axial a call\nmalformations are also possible.\n2. No additional lesions.  No new lesions.\n3. Please note that the previously suspected multiple subcutaneous lesions are\nthought to more likely represent ECG leads.   Currently there is multiple\nfiducial markings overlying the calvarium.\n4. Additional findings described above."
        },
        {
            "input": "A left frontal lesion, felt to appear more likely extra-axial on today's\nexamination, measuring approximately 2.1 x 0.9 cm (TRV, AP) appears slightly\nsmaller when compared to examination of ___.  In addition, the lesion\nnow demonstrates fairly homogeneous enhancement.  Surrounding parenchymal\nFLAIR edema pattern is identified, slightly less conspicuous compared to prior\nexam.  Surrounding dural thickening and enhancement is identified.  Gradient\necho susceptibility artifact within the lesion appears less conspicuous when\ncompared to prior examination, compatible with calcium and/or blood product. \nThe sulci, ventricles and cisterns are within expected limits for the\npatient's age.\n\nNo new abnormal enhancement.  No additional lesions are identified.  Very few\npunctate periventricular and subcortical T2/FLAIR white matter\nhyperintensities are identified, nonspecific in a patient of this age.  The\nmajor intracranial flow voids are preserved.  The dural venous sinuses are\npatent.  Mild mucosal thickening of the paranasal sinuses.  The orbits are\nunremarkable.  Trace fluid signal is seen the mastoid air cells.",
            "output": "1. A left frontal lesion is again noted, felt to be more likely extra-axial on\ntoday's examination.  The lesion measures approximately 2.1 x 0.8 cm, slightly\nsmaller in size when compared to the prior examination.  In addition, the\ndegree of surrounding parenchymal FLAIR edema pattern has also decreased.  The\nlesion demonstrates gradient echo susceptibility artifact, which may represent\na combination of calcifications and/or hemorrhage product, decreased in\nconspicuity.\n2. No additional new lesions are identified.\n3. No acute infarct or new intracranial hemorrhage.\n4. Additional findings as described above."
        },
        {
            "input": "Again seen in the anterior left frontal lobe is a lobulated, oval, enhancing\n12 x 7 x 8 mm (TV by AP by SI) (400:68 and 4:93) masslike focus which\ncontinues to decrease in size, previously measuring 14 x 9 x 8 mm when\nmeasured in a similar fashion on the prior study of ___.  The mass\ndoes not demonstrate restricted diffusion.  Dural thickening and enhancement\nanterior to the lesion is similar to prior exams.\n\nThere is no acute intracranial infarction, additional area of abnormal\nenhancement, additional mass, or mass effect.  The ventricles sulci are normal\nin caliber and configuration.  Major dural venous sinuses are grossly patent. \nThere is likely mild ethmoid air cell and bilateral maxillary sinus mucosal\nthickening.",
            "output": "Continued interval decrease in size of a now 12 x 7 x 8 mm anterior left\nfrontal lobe enhancing lesion.  Given progression on prior studies including\nCT and MRI from ___ and ___, and interval evolution in appearance and\ndecrease in size, neoplasm is considered less likely and benign etiology such\nas evolving/resolving hemorrhagic contusion/parenchymal hematoma is suggested;\nin particular, it is possible that this represents a contrecoup lesion in the\nsetting of a coup lesion in the suboccipital region, especially given history\nof prior trauma.  Recommend follow-up imaging to confirm continued involution.\n\nRECOMMENDATION(S):  Follow brain imaging in ___ weeks for further evaluation."
        },
        {
            "input": "Again seen along the left frontal convexity is previously identified 1.4 x 0.8\ncm lesion.  As on prior studies, it is difficult to ascertain whether the\nlesion is intraparenchymal or extra-axial.  Compared with the prior study of\n___, previously homogeneous enhancement is no longer seen, and\nthere is only heterogeneous, serpiginous enhancement within the lesion, more\nsimilar in appearance to the prior studies ___.\n\nThe hyperintense FLAIR signal abnormality seen just deep to lesion within the\nleft frontal lobe is again decreased compared with the most recent prior study\nof ___ (at that time, decreased from the study of ___ (see\nseries 7, image 14).  Foci of either trace chronic blood products or\nmineralization are again seen within the lesion, unchanged (06:14).\n\nElsewhere, there is no evidence of infarction, hemorrhage, edema, mass, or\nmass effect.  The ventricles and sulci are normal in caliber and\nconfiguration.  A few scattered white matter FLAIR hyperintense foci are\nunchanged, nonspecific in a patient of this age group.\n\nThere is mild maxillary sinus and ethmoid air cell mucosal thickening. \nRemaining visualized paranasal sinuses and mastoids appear clear.  Major\nintracranial vascular flow voids are preserved.  Globes and orbits are\nunremarkable.  Diminutive left transverse sinus, unchanged.  Otherwise,\ngrossly patent major dural venous sinuses.",
            "output": "1.4 x 0.8 cm left frontal lesion is unchanged in size but now demonstrates\ndecreased enhancement, now heterogeneous/serpiginous (previously homogeneous).\nThere is continued stepwise decrease in the now minimal FLAIR signal\nabnormality in the adjacent left frontal lobe white matter.  As previously,\nthe lesion is difficult to characterize with respect to intraparenchymal or\nextra-axial location, as well as ultimately etiology.  As previously,\ndifferential includes extra-axial lesion such as meningioma, as well as\nevolving hemorrhagic contusion/parenchymal hematoma in the setting of prior\ntrauma."
        },
        {
            "input": "1.5 cm x 0.9 cm abnormality anterior left frontal lobe, similar size since ___, previous surrounding mild edema has resolved.  Findings have\nsignificantly improved since ___.  Findings most likely\nrepresent sequela of hemorrhagic contusion.  Trace enhancement on today's\nscan, continually decreasing since ___.  Residual chronic blood\nproducts, decreased since priors.  No evidence of AVM, dural venous fistula or\nasymmetry in the arteries, veins\nMild flattening of the ventral pons, similar.  No sagging of the midbrain,\nnormal pituitary, normal foramina magnum, no subdural hygroma or hematoma. \nModerate mucosal thickening paranasal sinuses.  Clear mastoids.  Suggestion of\nsmall arachnoid cyst left cerebellopontine, cerebellar medullary angle.  Small\nnodule left face, similar.  Preserved vascular flow voids",
            "output": "1. Findings most consistent with chronic hemorrhagic contusion anterior left\nfrontal lobe."
        },
        {
            "input": "There is no evidence of intracranial hemorrhage, mass, mass effect or shifting\nof the normally midline structures.  The ventricles and sulci are normal in\nsize and configuration for the patient's age, there is no evidence of abnormal\nenhancement after contrast administration to suggest leptomeningeal or\nmetastatic disease.  No diffusion abnormalities are detected.  Few scattered\nfoci of high signal intensity are demonstrated on T2 and FLAIR sequences,\ndistributed the subcortical white matter and pons, which are nonspecific and\nmay reflect changes due to small vessel disease.  The major vascular flow\nvoids are present and demonstrate normal distribution.  The orbits are\nunremarkable, the previous described Rathke's cleft cyst in the sella turcica\nis not seen in the current exam.  The paranasal sinuses, middle ear cavities\nand mastoid air cells are clear.  The visualized osseous structures are\nunremarkable.",
            "output": "1.  There is no evidence of acute intracranial process or hemorrhage.\n\n2.  There is no evidence of abnormal enhancement to indicate or suggest\nmetastatic or leptomeningeal disease.\n\n3.  Few scattered foci of T2/FLAIR high-signal intensity distributed the pons,\nand subcortical white matter are nonspecific and may reflect changes due to\nchronic small vessel disease."
        },
        {
            "input": "No evidence for an enhancing intracranial mass.  No pathologic leptomeningeal\nor pachymeningeal contrast enhancement.  No acute infarction, edema, or\nevidence for blood products.\n\nBilateral T2/FLAIR hyperintensity in the pons, as well as scattered small foci\nof T2/FLAIR hyperintensity in the subcortical, deep, and periventricular white\nmatter of the cerebral hemispheres, are unchanged in number.  A left frontal\ncorona radiata lesion on image 7:15 appears slightly larger compared to the\nFLAIR images from ___, which may be secondary to motion artifact\non ___ as well as slice selection, given 5 mm slice thickness. \nThis lesion demonstrates no associated diffusion abnormality contrast\nenhancement on the prior or present studies.\n\nVentricles and sulci are normal in size for age.\n\nMajor vascular flow voids are preserved.  Dural venous sinuses are patent on\npostcontrast MP RAGE images.\n\nThere is trace fluid within left greater than right mastoid air cells.  There\nis minimal mucosal thickening in the ethmoid air cells.",
            "output": "1. No evidence for intracranial metastatic disease.\n2. Unchanged T2/FLAIR signal abnormality in the bilateral pons.  Essentially\nunchanged mild T2/FLAIR signal abnormalities in the supratentorial white\nmatter.  These findings are nonspecific but likely sequela of chronic small\nvessel ischemic disease in this age group."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, or midline\nshift.  Scattered periventricular and subcortical T2 and FLAIR\nhyperintensities are nonspecific and similar to prior, and are likely sequela\nof chronic ischemic small vessel disease.  The ventricles and sulci are\nprominent, suggestive of involutional changes.\n\nThe paranasal sinuses and mastoid air cells are clear.  The bilateral orbits\nare unremarkable.",
            "output": "1. No masses, hemorrhage, or mass effect.\n2. Unchanged scattered periventricular and subcortical T2 and FLAIR\nhyperintensities, which are nonspecific, but likely sequela of chronic\nischemic small vessel disease."
        },
        {
            "input": "MRI BRAIN:\nFoci of slow diffusion are seen in the left frontal and right parietal lobes,\nconcerning for small embolic infarcts.  A tiny punctate focus of small\ndiffusion is seen within the posterior limb of the right internal capsule\nadjacent to a micro hemorrhage.  Multiple tiny foci of susceptibility artifact\non the gradient echo sequences, is likely secondary to chronic micro\nhemorrhages.  There is complete opacification of the right maxillary sinus, as\nwell as mild opacification of the left maxillary sinus.  The mastoid air\ncells, and middle ear cavities are clear.  Subcortical and deep white matter\nFLAIR and T2 hyperintensities, likely sequelae of chronic small vessel\nischemic disease.  Area of increased FLAIR signal, encephalomalacia within the\nleft cerebellum, with a small region of susceptibility artifact, is sequelae\nof a prior chronic infarct.  Increased subtle T2/FLAIR signal within the ___,\n___ also be secondary to a chronic infarct.\n\nNo concerning enhancing lesions identified.\n\nMRA BRAIN:\nThere is attenuation of signal within the left V3 and V4 segments of the\nvertebral artery as well as irregularity along the distal basilar and P1\nsegments of the bilateral PCAs, which may be secondary to intracranial\natherosclerotic disease.\n\nMRA NECK:\nThe common, internal and external carotid arteries appear normal.  There is no\nevidence of internal carotid artery stenosis by NASCET criteria.  The origins\nof the great vessels, subclavian and vertebral arteries appear normal\nbilaterally.",
            "output": "1. Foci of slow diffusion in the left frontal, right parietal lobe, and\npossibly within the posterior limb of the right internal capsule concerning\nfor small embolic acute/subacute infarcts.\n2. Small area of encephalomalacia, FLAIR signal abnormality and susceptibility\nartifact within the left cerebellum and ___, are likely secondary to chronic\ninfarcts.\n3. Multiple micro hemorrhages in the basal ganglia cerebellum temporal lobes\ncould be due to hypertension or less likely a amyloid angiopathy (given\npatient's age).\n4. Severe sinus disease, with complete opacification of the right maxillary\nsinus.\n5. Attenuation of the left V3/ V4 segment of the vertebral artery maybe likely\nsecondary to intracranial atherosclerotic disease.  Otherwise, unremarkable\nMRA of the brain and neck."
        },
        {
            "input": "There is crescentic T1 hypo intense, noncontrast enhancing signal in the left\nfacial subcutaneous soft tissues, anterior to the left masseter muscle, best\nseen on series 3, image 4, at the site of the prior soft tissue nodule, seen\non MRI from ___.  A second 0.4 cm, T1 hypo intense, noncontrast\nenhancing lesion is noted medial to the first lesion, best seen on series 3\nimage 4 and 5.  There is continued asymmetric enlargement of the left\ninfraorbital nerve, much less prominent than on the prior studies.\n\nThere is no evidence of hemorrhage, edema, mass effect, midline shift or\ninfarction.  There is prominence of the ventricles and sulci suggestive\ninvolutional changes.   Periventricular and subcortical T2 and FLAIR\nhyperintensities are noted. There is no abnormal enhancement after contrast\nadministration.  The major vascular flow voids are preserved.\n\nAir-fluid levels are noted in the bilateral maxillary sinuses.  Bilateral\ncataract extractions are seen.  There is partial opacification of the mastoid\nair cells.",
            "output": "1. Minimal residual abnormal signal in the left facial subcutaneous soft\ntissues, at the site of the 2 previously seen soft tissue nodules, likely\nrepresenting residua of previous lesions.\n2. Continued asymmetric enlargement of the left infraorbital nerve, largely\nresolved since the prior studies.\n3. White matter signal abnormality, likely representing sequelae of chronic\nmicrovascular ischemic changes.\n4. No acute intracranial abnormality.\n5. Stable air-fluid levels in bilateral maxillary sinuses."
        },
        {
            "input": "There is no abnormal focus of slow diffusion.  There is no evidence of\nhemorrhage on gradient echo images.  Multiple scattered punctate\nperiventricular and subcortical white matter foci of FLAIR hyperintense\nsignal, overall unchanged compared to the prior examination, are nonspecific\nbut likely sequelae of chronic small vessel ischemic disease.  There is no\nparenchymal signal abnormality otherwise.  There is no mass or mass effect. \nThe ventricles and sulci are age-appropriate.  Principal intracranial vascular\nflow voids are preserved.  Dural venous sinuses are patent on postcontrast\nMP-RAGE sequences.  There is fluid signal in a few mastoid air cells\nbilaterally.\n\nAsymmetric enlargement of V3 division of the left trigeminal nerve extending\nproximally to the Meckel's cave and distally into the muscle of mastication\nwithout involvement of the cisternal portion of the left trigeminal nerve is\nunchanged.  Diffuse enlargement of the left infraorbital nerve also appears\ngrossly unchanged.  Known perineural spread along the left facial nerve within\nthe left parotid is better evaluated on prior examination.",
            "output": "1. Enlargement of the V3 division of the left trigeminal nerve and the left\ninfraorbital nerve extending to the Meckel's cave is unchanged.  The cisternal\nportion of the left trigeminal nerve is not affected.  Perineural spread along\nthe left facial nerve in the left parotid gland is better evaluated on prior\nexamination.\n2. Aside from nonspecific chronic white matter changes, the brain parenchyma\nis within normal limits without evidence of mass, mass effect, hemorrhage or\ninfarction.\n3. No evidence of cerebral abscess or septic emboli."
        },
        {
            "input": "Of note, postcontrast imaging is moderately motion degraded..\n\nThe extent of thickening of the left trigeminal nerve V3 branch from Meckel's\ncave to the pterygoid muscles is similar to the prior study.  Previously\ndescribed lesion in the left parotid gland is not well evaluated on the\ncurrent examination.  New punctate foci of restricted diffusivity in a sulcal\npattern is without definitive abnormal enhancement or T2 or FLAIR abnormality\n(802: 18, 21, 25).  However, does appear to be scattered associated foci of\nsubtle postcontrast enhancement in the right temporal operculum (series 25,\nimage 14), left occipital lobe (series 25, image 13) and left superior\ntemporal lobe (series 25, image 13) near Heschle's gyrus.\n\nThere is no abnormal diffusion within the brain parenchyma.\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor acute infarction.  The ventricles and sulci are prominent consistent with\nage related involutional changes.  Periventricular and subcortical white\nmatter T2 and FLAIR hyperintensities are nonspecific but likely represent the\nsequelae of chronic small vessel ischemic disease, similar to prior studies. \nThere is partial opacification of the mastoid air cells, left greater than\nright.  Principal intracranial flow voids are preserved.  The dural venous\nsinuses are patent.  The orbits are unremarkable, noting bilateral lens\nreplacements.",
            "output": "1. Postcontrast imaging is severely limited by motion, however thickening and\nenhancement of the left trigeminal nerve appears unchanged.  Previously\ndescribed lesion in the left parotid gland is not well evaluated on the\ncurrent examination.\n2. There are new foci of diffusion-weighted hyperintense signal, some which\ndemonstrates restricted diffusion, in a sulcal pattern is identified. \nAlthough there is no definitive associated T2/FLAIR hyperintense signal, a few\nof these lesions do appear to demonstrate subtle postcontrast enhancement in\nthe right temporal operculum, left occipital lobe and left temporal lobe. \nGiven the patient's known leptomeningeal disease in the lumbar spine, this\ncould represent new regions of disease.  It is notable however, the patient\ndoes receive intrathecal cytarabine, which could demonstrate restricted\ndiffusion assuming recent treatment although this would not be expected to\nenhance.  Recommend close interval follow-up to confirm/exclude worsening\ndisease.\n3. Aside from nonspecific T2/FLAIR hyperintensities likely representing the\nsequelae of mild to moderate small vessel ischemic disease and moderate age\nrelated involutional changes, the brain parenchyma is unremarkable.\n\nNOTIFICATION:  The findings were discussed with ___, M.D. by\n___, M.D. on the telephone on ___ at 4:14 pm, 15 minutes\nafter discovery of the findings.\n\n The slightly amended findings described in impression 2 of possible\nenhancement associated with sulcal diffusion-weighted signal described in the\npreliminary report, raising increased concern for new disease were discussed\nwith Dr. ___, M.D. by ___, M.D. on the telephone on\n___ at 6:42 pm, 10 minutes after discovery of the findings."
        },
        {
            "input": "There is mild brain atrophy and minimal changes of small vessel disease. \nThere is no mass effect midline shift or hydrocephalus.  Post gadolinium\nimages demonstrate no evidence of abnormal parenchymal vascular or meningeal\nenhancement.\n\nImages through the orbits demonstrate soft tissue thickening of the left\ninferior orbital nerve.  There is enhancement seen in this region.  Both\ncavernous sinuses are symmetric.  The extraocular muscles are symmetric. \nAxial images demonstrates slight thickening of the soft tissues along the\nmedial aspect of the anterior wall of the right maxillary sinus (4:3).",
            "output": "1. New thickening enlargement of the left anterior orbital nerve indicate\ninfiltrative process.  This may represent perineural involvement of the nerve.\nSlight thickening on the medial aspect of the anterior wall of the left\nmaxillary sinus could be due to thickening of the nerve or soft tissue lesion.\nClinical correlation recommended.\n2. Mild brain atrophy.  No enhancing brain lesions.\n\nRECOMMENDATION  CLINICAL CORRELATION RECOMMENDED TO EXCLUDE SOFT TISSUE LESION\nAT THE MEDIAL ASPECT OF THE LEFT INFERIOR ORBITAL MARGIN"
        },
        {
            "input": "Thickening of the left inferior orbital nerve is unchanged compared to ___ and ___ MRIs.  There also small soft tissue nodules\noverlying the left maxillary alveolar ridge and the left masseter, in the\nlocation of the branches of the left facial nerve, images 10:4, 10:7, which\nappears similar to the noncontrast CT portion of the ___ FDG\ntumor imaging.\n\nThere is no evidence for an intracranial mass.  There is no pathologic\nleptomeningeal or pachymeningeal contrast enhancement.  There is no acute\ninfarction, edema, or evidence for intracranial blood products.  Confluent\nperiventricular high T2 signal, as well as discrete small foci of high T2\nsignal in the deep and subcortical white matter of the cerebral hemispheres,\nsimilar to ___, are nonspecific but likely sequela of chronic\nsmall vessel ischemic disease in this age group.  Ventricles and sulci are\nage-appropriate.  Major intracranial arterial flow voids are grossly\npreserved.  Major dural venous sinuses appear patent on postcontrast MP RAGE\nimages.\n\nEvidence of bilateral cataract surgery is again seen.  There is trace mucosal\nthickening in the ethmoid air cells and left maxillary sinus, as well as trace\nopacification of bilateral dependent mastoid air cells.\n\nThere is susceptibility artifact in the left mandible.  Otherwise, no gross\nbone marrow signal abnormalities detected.",
            "output": "1. Unchanged thickening of the left inferior orbital nerve compared to ___ and ___ MRIs.  Unchanged soft tissue nodules\noverlying the left maxillary alveolar ridge and the left masseter, in the\nlocation of the branches of the left facial nerve, compared to the noncontrast\nCT portion of the ___ PET-CT allowing for differences in\nmodalities.  These findings remain compatible with perineural spread of\nmalignancy.\n2. No evidence for intracranial malignancy or acute intracranial\nabnormalities."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  Periventricular and subcortical T2 and FLAIR hyperintensities\nare noted.  There is no abnormal enhancement after contrast administration. \nThe major vascular flow voids are preserved.\n\nThe two previously seen soft tissue nodules in the left face, anterior and\nlateral to the left masseter muscle are not definitively visualized on this\nstudy.  There is stable asymmetric enlargement of the left infraorbital nerve.\n\nNew air-fluid levels are noted in the bilateral maxillary sinuses.  Minimal\nopacification of the mastoid air cells is seen.  Bilateral cataract\nextractions are seen.",
            "output": "1. Stable asymmetric enlargement of the left infraorbital nerve.\n2. Two previously seen soft tissue nodules in the left face, anterior and\nlateral to the left masseter muscle, are no longer definitively seen.  Given\nthat they were previously palpable, recommend correlation with physical exam.\n3. New paranasal sinus disease.\n4. Stable nonspecific white matter signal abnormality, likely secondary to\nchronic microvascular ischemic changes."
        },
        {
            "input": "MRI BRAIN: There are multiple small foci of diffusion restriction with\nassociated FLAIR hyperintensity scattered throughout bilateral cerebral\nhemisphere, such as in the bilateral frontal corona radiata, right precentral\ngyrus, right posterior cingulate gyrus, and right paramedian occipital lobe. \nAnother small foci of diffusion restriction is present in the right posterior\ncerebellum.  The apparent diffusion-weighted hyperintensity in ___ the\nmidbrain is artifactual.\n\nThere is no evidence of hemorrhage,edema,masses, mass effect, midline shift or\nlarge vascular infarction.  The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.\n\nThere are scattered T2/FLAIR hyperintensities in the white matter likely\nrepresenting chronic microangiopathy.  The visualized vascular flow voids are\ngrossly preserved.  There is mild mucosal thickening of the ethmoid air cells,\notherwise the paranasal sinuses are clear.  The mastoid air cells are clear. \nNo abnormal marrow signal.\n\nMRA BRAIN:\nThe intracranial vertebral and internal carotid arteries and their major\nbranches appear normal without evidence of stenosis,occlusion,or aneurysm\nformation.  There is fetal configuration of the right PCA.  The right A1\nsegment is hypoplastic, normal variant.\n\nMRA NECK:\nThere is a common origin of the innominate artery and the left common carotid,\nnormal variant.  Otherwise, the origins of the great vessels, subclavian and\nvertebral arteries appear normal bilaterally.  There is mild focal narrowing\nof the left proximal ICA near the bifurcation causing approximately 35%\nstenosis, with normal flow distally.  Another at least moderate focal\nnarrowing is present at the origin of the right external carotid artery, with\nnormal runoff distally.  The common, right internal and left external carotid\narteries appear normal.  There is no evidence of internal carotid artery\nhigh-grade stenosis by NASCET criteria.",
            "output": "1. Several foci of diffusion restriction in the bilateral cerebral hemisphere\nand right posterior cerebellum, compatible with acute infarct, most likely\nembolic in etiology.\n2. Patent circle of ___ without evidence of high-grade\nstenosis,occlusion,or aneurysm.\n3. Mild focal narrowing involving the left proximal ICA near the carotid\nbifurcation and at least moderate narrowing at the origin of the right\nEXTERNAL carotid artery.  Otherwise MRI of the neck demonstrates patent\nbilateral cervical carotid and vertebral arteries without evidence of\nflow-limiting stenosis of the internal carotid arteries or vertebral arteries,\nocclusion,or dissection."
        },
        {
            "input": "MRI BRAIN:\nSusceptibility artifact is seen AFTER anterior communicating artery aneurysm\ncoiling.\n\nThere is no evidence of hemorrhage,edema,masses, mass effect, midline\nshiftorinfarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  An enlarged pituitary is seen with convexity of the\ndiaphragmatic sella, abutting the optic chiasm.\n\n\nMRA BRAIN:\nThe patient is status post coiling of a ruptured anterior communicating artery\naneurysm without residual flow within the aneurysm coil pack.  A patent\nanterior communicating artery is seen.\n\nOtherwise, the intracranial vertebraland internal carotid arteries and their\nmajor branches appear normal without evidence of stenosis,occlusion,ornew\naneurysm formation.",
            "output": "1. Status post coiling of a ruptured anterior communicating artery aneurysm\nwithout residual flow within the aneurysm coil pack.  Patent anterior\ncommunicating artery.  No new aneurysm.\n2. Enlarged pituitary with convexity of the diaphragmatic sella, abutting the\noptic chiasm.  No definite lesion is seen.\n3. No evidence of hemorrhage or infarction.\n\nRECOMMENDATION(S):  MRI pituitary with and without contrast."
        },
        {
            "input": "Punctate foci of diffusion-weighted hyperintense signal involving the\nsubependymal posterior body of the left lateral ventricle (series 6, image 20,\nwith associated subtle ADC hypointensity), cortical left parietal lobe (series\n6, image 26, without definitive ADC hypointense correlate) and right frontal\ncortex (series 6, image 26, without definitive ADC hypointense correlate),\nwhich may represent embolic infarcts of mixed ages ranging from acute to\nsubacute.  These lesions do not demonstrate associated enhancement.\n\nThe marrow signal is heterogeneous compatible with given history multiple\nadenoma without evidence of expansile osseous lesion within the calvarium. \nThere is no evidence of intra or extra-axial enhancing mass.  Punctate focus\nof microhemorrhage of the left frontal lobe is noted (series 10, image 17). \nThe visualized intracranial flow voids are preserved.  The dural venous\nsinuses are patent.  The orbits are unremarkable.  The mastoid air cells are\nclear.  The visualized paranasal sinuses are clear.",
            "output": "1. 3 foci of diffusion-weighted hyperintense signal concerning for embolic\ninfarcts of mixed ages ranging from acute to subacute as described above.\n2. A single gradient echo susceptibility hypointensity of the left frontal\nlobe, compatible with prior micro hemorrhage.\n3. The marrow signal is T1 heterogeneous compatible with given history of\nmultiple myeloma.  No expansile osseous lesion is identified.\n4. No definitive evidence for intracranial metastatic disease at this time.\n\nNOTIFICATION:  The findings were discussed with ___, NP by ___\n___, M.D. on the telephone on ___ at 9:36 AM, 10 minutes after\ndiscovery of the findings."
        },
        {
            "input": "Severe motion degradation, most notable involving post-contrast images,\nmarkedly limiting assessment, particularly with respect to evaluation for\nintracranial metastatic disease.  Within these confines:\n\nSmall area of encephalomalacia in the high left frontal lobe involving the\nprecentral gyrus, likely sequelae of chronic infarct (15:22).\n\nThere is no evidence of acute infarct, extra-axial collection, edema, mass, or\nmass effect.  No definite abnormal enhancement is identified, although\nevaluation for small metastases is very limited on this study.\n\n The ventricles and sulci are prominent, compatible with global parenchymal\nvolume loss.\n\n Bilateral periventricular, deep, and subcortical white matter foci of\nT2/FLAIR signal hyperintensity are nonspecific but compatible with severe\nchanges of chronic white matter microangiopathy.\n\nThe globes and orbits are intact.  The visualized paranasal sinuses and\nmastoids appear clear.  Major intracranial vascular flow voids are preserved. \nMajor dural venous sinuses are patent.",
            "output": "1. Severely motion degraded examination, limiting assessment, particularly\nwith respect to evaluation for intracranial metastatic disease.  Within these\nconfines, no definite evidence of enhancing intracranial mass and no definite\nevidence of acute infarct.\n2. Small chronic infarct, high left frontal lobe.\n3. Severe changes of chronic white matter microangiopathy.\n4. Global parenchymal volume loss."
        },
        {
            "input": "MR BRAIN:\nThere are new right parietal and right occipital FLAIR hyperintensity with\nsuggestion of subtle hyperintense DWI signal, and apparent normalization on\nADC, suggestive of subacute infarction.  1 of these lesions is hemorrhagic\n(12:18).\n\nThere is interval increase in size of a left cavernous internal carotid artery\naneurysm, with new intrinsic hyperintense T1 signal posteriorly (8:9).  There\nis diffuse parenchymal volume loss with commensurate prominence of the\nventricles, sulci, and cisterns.  There are nonspecific periventricular and\nsubcortical white matter FLAIR hyperintensity, likely a sequela of chronic\nsmall vessel microangiopathy.\n\nMRA brain:\nPatient is status post pipeline embolization of left ICA aneurysm.  There is\ninterval increase in size of a left cavernous ICA aneurysm, measuring 2.2 x\n2.4 cm, previously 2.0 x 2.0 cm (9:99).  This exerts greater mass effect on\nthe adjacent cavernous ICA, and narrowing of the distal petrous ICA.  The\nright ophthalmic aneurysm is not identified.\n\nThere is no evidence of a new aneurysm.  Otherwise, the circle of ___ and\nthe visualized principal intracranial branches appear patent without stenosis\nor occlusion.",
            "output": "1. Right parietal and occipital lobe subacute infarction, with a small right\nparietal lobe hemorrhage.\n2. Left ICA aneurysm status post pipeline embolization, with interval increase\nin size of the aneurysm, with new layering acute to subacute hemorrhage\nposteriorly.\n3. The right ophthalmic aneurysm is no longer seen"
        },
        {
            "input": "Examination is mildly motion degraded.\n\nThere is diffusion-weighted hyperintense signal, predominantly cortical\ninvolving the left parietooccipital lobe extending into the posterior left\ntemporal lobe without corresponding FLAIR/T2 signal abnormality or involvement\nof the adjacent white matter.  No definite ADC hypointensity is noted. \nSimilar signal is subtly noted along the contralateral right parietooccipital\nlobe.  Overall the findings appear likely artifactual given lack of\ncorresponding signal on T2 and FLAIR.  There is no mass effect or midline\nshift.  The ventricles and sulci are within expected limits in caliber and\nconfiguration.  No definite infarct.  No suspicious parenchymal FLAIR signal\nabnormality.  The major intracranial flow voids are preserved.\n\nThere is mild mucosal thickening within the paranasal sinuses.  Small amount\nof fluid signal is seen in the right mastoid air cells.  There are\npostsurgical changes related to bilateral lens replacement.",
            "output": "1. Examination is mildly motion degraded.  Within this confines:\n2. Thin cortical diffusion-weighted hyperintense signal along the left\nparietooccipital lobe and to a much milder extent potentially along the right\nparietooccipital lobe.  This is felt to be artifactual given lack of\ncorresponding signal abnormality on FLAIR or T2 sequences.  However, if there\nremains high clinical suspicion, recommend repeat examination as artifact\nwould be expected to resolve.\n3. No convincing evidence for acute infarct or intracranial hemorrhage.  No\nsuspicious parenchymal FLAIR signal abnormality.\n4. Additional findings described above."
        },
        {
            "input": "MR BRAIN: There is redemonstration of diffusion weighted hyperintense signal\ninvolving the cortex of the the left parietooccipital region, without\ncorresponding FLAIR or T2 abnormality.\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nthe ventricles and sulci are normal in caliber and configuration.  There is no\nabnormal enhancement after contrast administration.\n.\nMR ___: Not available at the time of the dictation.\n\nASL Perfusion: There is area of hypoperfusion involving the left occipital\nlobe, and extended to the occipital pole, seen from image ___ to ___..\n\n\nMR Spectroscopy: Unremarkable.  There is no evidence of lactate peak to\nsuggest acute infarct.",
            "output": "1. Redemonstration of area of cortical diffusion restriction along the left\nparietooccipital lobe without evidence of corresponding spectroscopic\nabnormality.  In addition, there is hypoperfusion on ASL in the left occipital\nregion.\n2. Evaluation of the previous CT angiography demonstrates decreased vascular\ninjury in the left occipital region with decreased caliber of the left distal\nposterior cerebral artery.\n3. The described changes could be post seizure in nature or could be due to\nischemia.\n4. Consider a follow up examination with diffusion and ASL in 1 week for\nfurther assessment\n\nRECOMMENDATION(S):   Follow-up examination with diffusion and ASL in 1 week.\n\nNOTIFICATION:  Findings as discussed with ___ (pager ___ by\n___, MD at 15:30 on ___ via phone."
        },
        {
            "input": "Again seen is diffusion-weighted hyperintense signal involving the left\nparietooccipital cortex with associated decreased ASL perfusion in the left\noccipital lobe, similar to ___.  There is subtle cortical\nthickening and FLAIR hyperintensity involving the median occipital lobe\n(series 6, image 12 to 14), new compared to prior MRIs.\n\nNo new foci of restricted diffusion.  No hemorrhage, edema, mass, or mass\neffect.  The ventricles and sulci are within normal limits for patient's age. \nThe major intracranial flow voids preserved.\n\nThere is trace right mastoid air cells.  There is mild mucosal thickening of\nthe paranasal sinuses.  Patient is status post bilateral lens replacement.",
            "output": "1. Redemonstration of diffusion-weighted hyperintense signal involving the\nleft parietooccipital cortex, with associated decreased ASL perfusion in the\nleft occipital lobe with similar distribution and extent.  Interval\ndevelopment of subtle cortical thickening and FLAIR hyperintensity involving\nthe median occipital lobe most likely represents manifestation of the\nperfusion abnormality.\n2. No additional new intracranial abnormalities."
        },
        {
            "input": "There is no evidence of recent infarction or intracranial hemorrhage.  No\ndiffusion abnormalities are detected.  There are chronic (lacunar) infarcts\ninvolving the right thalamus (series 6, image 12), right frontal lobe (series\n6, image 14), and left centrum semiovale (series 6, image 17). There is mild\nprominence of the ventricles and sulci most consistent with age-related\nparenchymal atrophy. Scattered periventricular and subcortical white matter\nT2/FLAIR signal hyperintensities are nonspecific but may reflect sequelae of\nchronic small vessel ischemic disease. There are three lobe punctate foci of\nGRE susceptibility within left frontoparietal lobes consistent with sequelae\nof remote microhemorrhage (series 7, image 18). The principal intracranial T2\nflow voids are maintained. There are trace mucosal inflammatory changes within\nthe paranasal sinuses. There is trace right greater than left opacification of\nthe mastoid air cells. The orbits are unremarkable in appearance. Incidental\nnote is made of a partially empty sella. There is a probable tiny left\nnasopharyngeal mucous retention cyst (series 5, image 5).",
            "output": "1. No acute intracranial process. No evidence of recent infarction or\nintracranial hemorrhage.\n2. Chronic infarcts involving the right thalamus, right frontal lobe and left\ncentrum semiovale as described above.\n3. Three lobe punctate foci of GRE susceptibility within the left\nfrontoparietal lobes consistent with sequelae of remote microhemorrhage\n(7:18).\n4. Chronic small vessel ischemic disease and mild age-related parenchymal\natrophy.\n5. Paranasal sinus disease as described above."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  There is a nonspecific punctate FLAIR white matter\nhyperintensity adjacent to the frontal horn of the right lateral ventricle.\nThe ventricles and sulci are within expected limits in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.  The major intracranial flow voids are preserved.  The dural\nvenous sinuses are patent.\n\nThere is minimal mucosal thickening of the anterior ethmoid air cells.  The\norbits are unremarkable.",
            "output": "1. A nonspecific punctate FLAIR white matter hyperintensity adjacent to the\nfrontal horn of the right lateral ventricle.  In a patient of this age this\ncould represent sequela of chronic headache such as migraine, with\ninfectious/inflammatory etiology, prior trauma or small vessel ischemic\ndisease differential considerations.  This is not in a distribution typical of\ndemyelinating process.\n2. There is no acute infarct or intracranial hemorrhage.  No abnormal\npostcontrast enhancement.\n3. The dural venous sinuses appear patent."
        },
        {
            "input": "Incomplete study of the head as only scout images and T1 weighted sagittal\nimages were obtained.  Allowing for this, there is redemonstrated early\nsubacute blood within the lateral, third, fourth ventricles.  There is\nhemorrhage within left thalamus.\n\nThere is a right frontal approach ventriculostomy in place. Again seen is the\nleft lateral ventricle being relatively prominent compared to the right and\nthere is slightly improved expansion of the right lateral ventricle from\nprior.",
            "output": "1. Incomplete study.\n2. Intraventricular, left thalamus hemorrhage is again seen."
        },
        {
            "input": "Left basal ganglia hemorrhage (in relation to the cardiothymic groove)\nmeasuring 15 x 21 mm in the axial plane with associated blood products seen in\nthe frontal horn of the left lateral ventricle appears fairly similar compared\nto most recent CT, and improved compared to initial CT done ___. \nRight frontal approach external ventricular drain in situ in the frontal horn\nof the right lateral ventricle.  The ventricular system is mildly dilated,\nappearing fairly similar compared to most recent imaging, but improved\ncompared to initial imaging with no evidence of impending herniation.\n12 x 7 mm area of moderate restricted diffusion in the right thalamus (series\n6, image 19) with associated T2 and FLAIR hyperintensity and no blooming on\nthe gradient echo suggest a subacute infarct.  This area also demonstrates\nlinear postcontrast enhancement typical for subacute infarct.\nPunctate area of enhancement in the right putamen (series 101, image 64) with\nno signal abnormality on the diffusion weighted, T2 or FLAIR sequences also\nmost likely representing a subacute infarct.\nThere is a punctate foci of slow diffusion in the right corona radiata (series\n6, image 20) with associated T2 and FLAIR hyperintensity most likely\nrepresenting a subacute punctate infarct.\nThere is extensive cortical T2 and FLAIR hyperintensity demonstrating\nserpentine cortical enhancement in bilateral occipital areas and posterior\nparietal convexities (right more than left) with some areas demonstrating mild\nrestricted diffusion and others not (possibly pseudonormalization) in keeping\nwith subacute infarcts.\nMinor cortical enhancement also noted in the posterior aspect of the left\nfrontal lobe in relation to the left superior frontal and middle gyri (series\n101, image 91) also most likely representing subacute infarcts.\nNonspecific bilateral midbrain hypodensities most likely representing old\nlacunar infarcts (left larger than right) was noted on initial CT, but less\nwell characterized.\nThe craniocervical junction is normal.  The pituitary appears normal.  The\nintracranial arteries demonstrate normal T2 flow void.  The CP angles appear\nnormal.  Edema in the right frontal scalp soft tissues most likely secondary\nto EVD insert.  Mild mucosal thickening in the posterior aspect of the right\nmaxillary sinus.  Partial opacification of the right mastoid air cells.",
            "output": "Left basal ganglia hemorrhage with intraventricular extension appear similar\ncompared to most recent prior CT done, but appears improved compared to\ninitial CT as described above.  No underlying mass or vascular malformation. \nImaging follow-up after complete resolution is advised to exclude an\nunderlying mass or vascular malformation with certainty.\n\nThe ventricular profile is stable and improved compared to initial CT.  Right\nfrontal approach external ventricular drain in situ.\n\nThere are multiple most subacute infarcts in the right basal ganglia and\nthalamus as well as bilateral occipital and to a lesser degree the posterior\nparietal and left frontal cortical gray matter as described above.  Infarcts\nin various vascular territories suggest an embolic etiology.\nSuspected chronic lacunar infarcts also noted in the midbrain bilateral.\nHemorrhagic transformation of a left basal ganglia infarct and subsequent\nhemorrhage should be considered as a possible explanation of all of the above\nfindings.\n\nNOTIFICATION:  The findings were discussed by Dr. ___ with\nDr. ___ on the ___ ___ at 12:24 pm, 20 minutes after\ndiscovery of the findings."
        },
        {
            "input": "Thick spin echo postcontrast images demonstrate leptomeningeal areas of\nenhancement involving the cerebellum and vermis which correspond to areas of\nFLAIR hyperintense signal abnormalities (images ___ of series 11).  There may\nalso be asymmetric nodular FLAIR hyperintense signal along the left occipital\nlobe sulcus and bilateral sylvian fissures and enhancement in the bilateral\ninternal auditory canals.  The findings are favored to reflect leptomeningeal\ndisease.  There is also suggestion of mild FLAIR hyperintense dural thickening\nalong the right temporal convexity, this however may be secondary to\nsuperimposition of venous structures.\n\nThere is no evidence of hemorrhage, edema, or infarction.  The ventricles and\nsulci are age-appropriate.  There is no mass effect or midline shift.\n\n The major intracranial arterial flow voids are preserved.  The dural venous\nsinuses are patent.\n\nThere is mild mucosal thickening of the ethmoid sinuses.  The mastoid air\ncells appear clear.  The intraorbital contents are unremarkable.",
            "output": "1. Subtle leptomeningeal enhancement and FLAIR hyperintense signal\nabnormalities as described above are more consistent with leptomeningeal\ncarcinomatosis given the clinical history.\n2. No acute infarction, intracranial hemorrhage, or hydrocephalus."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There are scattered periventricular and subcortical white\nmatter FLAIR and T2 hyperintensities which are nonspecific but suggest chronic\nsmall vessel ischemic changes in a patient of this age.  The major\nintracranial flow voids are preserved.\n\nSmall right maxillary mucous retention cyst noted.  Otherwise the paranasal\nsinuses are clear.  Mastoid air cells are clear.  Bilateral orbits are\nunremarkable.",
            "output": "1. No evidence of masses, infarction, or hemorrhage.\n2. Scattered nonspecific white matter FLAIR hyperintensities suggest chronic\nsmall vessel ischemic changes."
        },
        {
            "input": "There is no evidence of intracranial hemorrhage, mass, mass effect or shifting\nof the normally midline structures, the ventricles and sulci are normal in\nsize and configuration for the patient's age, no diffusion abnormalities are\ndetected, the major vascular flow voids are present and demonstrate normal\ndistribution.  The orbits are unremarkable, the paranasal sinuses, middle ear\ncavities and mastoid air cells are clear.  The visualized aspect of the\ncraniocervical junction is normal.",
            "output": "Essentially normal MRI of the head, there is no evidence of acute or subacute\nintracranial process or hemorrhage."
        },
        {
            "input": "There is no hemorrhage, intracranial mass, mass effect, extra-axial fluid\ncollections or midline shift. There is no slow diffusion to suggest acute\ninfarct. Ventricles and sulci are age-appropriate. The basilar cisterns are\nwithin normal limits. There is no pathologic intracranial enhancement. There\nare multiple foci of T2/FLAIR hyperintensity in the deep and periventricular\nwhite matter, most likely sequela of mild chronic microvascular ischemic\ndisease.\n\nIntracranial flow voids are maintained. Visualized paranasal sinuses and\nmastoid air cells are clear.  The orbits and soft tissues are grossly\nunremarkable.  The left parietal bone demonstrates a well-defined T1\nhypointense focus, which may represent a calvarial hemangioma.",
            "output": "No evidence of acute intracranial process, abnormal enhancement or mass\neffect."
        },
        {
            "input": "MRI BRAIN:\n\nThere is no diffusion abnormality to suggest acute infarction.  Prominence of\nthe ventricles and sulci is consistent with a least moderate globe atrophy. \nPeriventricular and bilateral scattered subcortical and deep white matter\nFLAIR hyperintensities are nonspecific but likely sequelae of chronic\nmicroangiopathy.  There is no enhancing mass or mass effect.  There is no\nintra or extra-axial hemorrhage.  Major intracranial vascular flow voids are\npreserved.  The dural venous sinuses are patent.  There is mild mucosal\nthickening along the left maxillary sinus.\n\nMRA BRAIN:\nThe intracranial vertebral and internal carotid arteries and their major\nbranches appear normal without evidence of stenosis, occlusion, or aneurysm\nformation.\n\nMRA NECK:\nThe common, internal and external carotid arteries appear normal.  There is no\nevidence of internal carotid artery stenosis by NASCET criteria.  The origins\nof the great vessels, subclavian and vertebral arteries appear normal\nbilaterally.",
            "output": "1.  Extensive chronic white matter ischemic change and at least moderate\nglobal atrophy.  No intracranial hemorrhage or acute infarction.\n\n2.  Normal head and neck MRA."
        },
        {
            "input": "Majority of the sequences are mildly motion degraded with moderate motion\ndegradation of the MPRAGE sequences.  Within this confines:\n\nThere is no intra or extra-axial mass, acute hemorrhage or infarct.  The\nsulci, ventricles and cisterns are within expected limits for the patient's\nage.  There are very minimal periventricular and subcortical FLAIR white\nmatter hyperintensities, nonspecific, but commonly seen in the setting of\nchronic microangiopathy.\n\nNo evidence for focal cortical dysplasia or gray matter heterotopia.  The\nhippocampal formations are symmetric bilaterally and demonstrates unremarkable\ncontour and signal.  The visualized intracranial flow voids are preserved. \nThere is mild mucosal thickening of the left maxillary sinus and mild mucosal\nthickening of the ethmoid air cells.  The orbits are unremarkable.",
            "output": "1. No evidence for focal cortical dysplasia, gray matter heterotopia, focal\nlobar encephalomalacia or mesial temporal sclerosis on motion degraded\nexamination.\n2. No acute intracranial abnormality.  No acute infarct or intracranial\nhemorrhage.\n3. Mild periventricular T2/FLAIR hyperintensity.  Differential consideration\nis broad, but commonly seen in the setting of chronic microangiopathy in a\npatient of this age."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  There is mild prominence of the ventricles and sulci well\nwithin the range of normal for age.  Periventricular and subcortical T2 and\nFLAIR hyperintensities are noted.  Although nonspecific, these are often\nattributed to chronic small vessel ischemia.  The major vascular flow voids\nare preserved.\n\nThe orbits and paranasal sinuses are normal.  Minimal fluid is seen in the\nbilateral mastoid air cells.",
            "output": "1. No evidence of infarction.\n2. Mild white matter hyperintensity on FLAIR, likely secondary to chronic\nmicrovascular ischemic changes."
        },
        {
            "input": "There is an area of restricted diffusion involving the splenium of the corpus\ncallosum on the left as well as on the right, without definite hypointensity\non the ADC, which is new compared to the prior exam, representing\nacute/subacute infarct (series 4, image 17).  There is an additional new\npunctate focus of restricted diffusion within the left parietal lobe, also\nrepresenting acute/subacute infarct (series 4, image 19).  The multiple\nperiventricular and subcortical T2/FLAIR hyperintensities likely represent\nchronic microvascular ischemic disease.\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, or midline\nshift.  There is mild prominence of the ventricles and sulci suggesting\nage-related atrophy.  The major vascular flow voids are preserved.",
            "output": "New foci of restricted diffusion involving the splenium of the corpus callosum\n, and left parietal lobe, which are new compared to the prior examination, and\nrepresent acute/subacute infarcts.\n\nRECOMMENDATION(S):  The findings were discussed by Dr. ___\nwith Dr. ___ on the ___ ___ at 2:34 ___, 5 minutes after discovery\nof the findings."
        },
        {
            "input": "Study is mildly degraded by motion.\n\nThere is unchanged geographic FLAIR hyperintensity at the left splenium corpus\ncallosum with mild expansion.  There is correlate pseudo normalization on the\nADC map and T2 shine through on the isotropic sequence, which suggest subacute\ninfarct.  There is unchanged diffusion isotropic hyperintensity at the left\nparieto-occipital subcortical white matter (302:19), with pseudo normalized\nADC suggesting subacute infarct.\n\nThere is new punctate diffusion isotropic mild hyperintensity at the posterior\nleft centrum semiovale (302:22), without definitive ADC hypointensity, likely\nartifact.\n\nThere is background nonspecific periventricular and subcortical white matter\nFLAIR hyperintensity, likely representing sequela of chronic microangiopathy. \nThere is no evidence of hemorrhage, mass, or mass effect.  There is mild\nprominence of the ventricles and cortical sulci consistent with volume loss. \nThe extra-axial spaces are unremarkable.  The vascular flow voids are\npreserved.\n\nThe orbits, calvarium, and soft tissues are unremarkable.  The paranasal\nsinuses and mastoid air cells are clear.",
            "output": "1.  Study is mildly degraded by motion.\n2. Stable left splenium of corpus callosum subacute infarct .\n3. Stable punctate left parietal occipital subcortical white matter subacute\ninfarct."
        },
        {
            "input": "There is region of bright signal on DWI sequence in the left splenium of the\ncorpus callosum and 2 punctate foci the left parietal white matter, which\ndemonstrate mild dark signal on the ADC sequences.  There is a questionable\nfocus of restricted diffusion in the anterior superior left thalamus.\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, or midline\nshift.  There is prominence of the ventricles and sulci suggestive\ninvolutional changes.  Periventricular and subcortical T2 and FLAIR\nhyperintensities are noted.  The major vascular flow voids are preserved.\n\nThe orbits, paranasal sinuses, mastoid air cells and visualized soft tissues\nare normal.",
            "output": "1. Evolving subacute infarcts in the splenium of the corpus callosum and\nparietal lobe.\n2. Punctate focus of questionable restricted diffusion in the superior medial\nleft thalamus, which may represent an acute infarction versus artifact. \nOtherwise, no new large acute infarct or mass effect."
        },
        {
            "input": "There is small susceptibility along the right superior frontal gyrus\nconvexity, most compatible with dural calcification with corresponding finding\non CTA head and neck of ___ (series 2, image 23; series 3, image 313\non CT examination).  There is unchanged large right frontal subgaleal\nhematoma, when compared to prior CT, taking into account the difference in\ntechnique.\n\nThere is no evidence of intra-axial hemorrhage, edema, masses, mass effect,\nmidline shift or infarction.  No definite intracranial hemorrhage.  The\nventricles and sulci are within normal limits in caliber and configuration. \nThe visualized major vascular flow voids are grossly preserved.  The paranasal\nsinuses are clear.  There is small effusion in the right mastoid tip.  There\nis no abnormal marrow signal.",
            "output": "1. No acute intracranial abnormality.  No evidence of an acute infarct,\nintracranial mass, intracranial hemorrhage.\n2. A focus of extra-axial right frontal gradient echo susceptibility blooming\nartifact corresponds to a dural ossification/calcification on CTA exam of the\nsame day.\n3. Stable large right frontal subgaleal hematoma.  Additional findings\ndescribed above."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  A few scattered punctate subcortical T2/FLAIR hyperintensities\nare nonspecific.  The ventricles and sulci are normal in caliber and\nconfiguration.\n\nThe paranasal sinuses and mastoid air cells are clear.  The orbits are grossly\nunremarkable.  The major intracranial vascular flow voids are preserved.",
            "output": "1. No acute intracranial abnormality on noncontrast MRI head.  Specifically no\nevidence of intracranial mass, acute infarct or intracranial hemorrhage.\n2. There are very few periventricular and subcortical T2/FLAIR white matter\nhyperintensities, which are nonspecific in a patient of this age, but may be\nseen in setting of chronic headache such as migraine.  Additional differential\nconsiderations include sequela of prior trauma, infectious/inflammatory\nallergy.  These are not in a distribution typical for demyelinating process."
        },
        {
            "input": "There is asymmetric subcortical white matter T2 and FLAIR signal\nhyperintensity extending to the subcortical U fibers, most dominant in the\nleft frontal lobe and bilateral parieto-occipital lobes.  There is poorly\ndefined subcortical white matter enhancement involving regions of the\nbilateral frontal, parietal, and temporal lobes.  Scattered foci of\nsusceptibility artifact correspond to parenchymal calcifications identified on\nrecent outside hospital noncontrast head CT.  Around the largest known\ncalcification in the right mid brain, there is peripheral, rim enhancement. No\nevidence of hemorrhage, infarction, or mass effect.  The ventricles and sulci\nare normal in caliber and configuration.\n\nThe major vascular flow voids appear patent.  On post-contrast MPRAGE\nsequences, there is a probable developmental venous anomaly draining the right\nbasal ganglia.  The dural venous sinuses are patent.  There is mild mucosal\nthickening of the ethmoid air cells.",
            "output": "1. Overall distribution of T2/FLAIR signal hyperintensity extending to the\nsubcortical U fibers is most consistent with PML rather than HIV encephalitis.\n2. Relatively subtle subcortical white matter enhancement involving regions of\nthe bilateral frontal, parietal, and temporal lobes has an appearance most\nconsistent with immune reconstitution inflammatory syndrome.  However, the\ndocumented clinical picture may be more consistent with progressive\nimmunocompromise rather than immune reconstitution.  In this setting, it is\nconceivable that the subtle enhancement is related to PML, though PML does not\nusually enhance.\n3. Peripheral enhancement around a prominent right midbrain calcification\nsuggests reactivated toxoplasmosis.  However, calcifications as demonstrated\non prior outside hospital CT suggests there is likely a superimposed component\nof neurocysticercosis.\n\nNOTIFICATION:  The findings were discussed with ___, M.D. by\n___, M.D. on the telephone on ___ at 4:44 pm, approximately\n10 minutes after discovery of the findings."
        },
        {
            "input": "There has been interval progression of disease notable for confluent regions\nof subcortical white matter T2/FLAIR hyperintensity.  There is now more\nextensive involvement the bilateral frontal lobes and left temporal lobe with\nassociated mild sulcal effacement which is essentially new. Additional areas\nof FLAIR hyperintensity noted within the cerebellum involving the middle\ncerebellar peduncles extending posteriorly, left greater than right.\n\nPreviously seen subcortical white matter T2/FLAIR hyperintensity in the\nbilateral parietal lobes is again noted noting that the white matter changes\nin the right parietal lobe are less confluent and the degree of mass effect\nhas also decreased.  There is also now normal signal in the splenium of the\ncorpus callosum which had been T2 hyperintense and expanded on the prior exam.\n\nPatchy areas of enhancement in the subcortical white matter in the parietal\nlobes and left temporal lobe on prior have regressed however there is now\nsimilar enhancement extending more anteriorly into the frontal lobes, left\ngreater than right.  Of note, these areas of enhancement demonstrate slightly\nincreased FLAIR signal but are discrete from the more confluent areas of white\nmatter signal abnormality described above.\n\nCalcified density seen on prior CT in the midbrain on the right is again seen\nand demonstrates persistent mild peripheral enhancement..  Thin rim of\nassociated FLAIR hyperintensity is also unchanged.  No significant mass\neffect..\n\nThere is no restricted diffusion.  Major intravascular flow voids including\nwithin the major dural venous sinuses are patent.\n\nMild mucosal thickening seen in the maxillary sinuses.",
            "output": "Interval change in the appearance of the brain with overall similar findings\ncompared to prior though the distribution has changed.  Specifically more\nconfluent white matter T2 FLAIR hyperintensity involving the bilateral frontal\nlobes and left temporal lobe.  Improvement in the signal abnormality\npreviously seen in the splenium of the corpus callosum and right parietal\nlobe.  Shifting pattern of enhancement which has somewhat improved where seen\non prior though now extending more anteriorly in the bilateral frontal lobes\nthough in discrete regions from new signal abnormality described above.\n\nOverall, findings may represent similar pathology compared to prior which may\nrepresent PML in the nonenhancing confluent regions and/or ___ given\ncomponent of regression and possible mild volume loss in the right parietal\nlobe and corpus callosum.\n\nRing-enhancing lesion in the midbrain on the right similar to prior without\nsurrounding edema likely sequela of prior toxoplasmosis."
        },
        {
            "input": "MRI head:\nThere is an approximately 8 mm focus of ill-defined FLAIR hyperintensity in\nthe left medial temporal lobe (series 17, image 9). This lesion is centered in\nthe white matter with its edges extending into the gray matter. This foci\ndemonstrate slowed diffusion (series 6, image 11) and enhancement (series 19,\nimage 9). No additional parenchymal brain lesions are identified. This small\nlesion was not apparent on the noncontrast CT head from ___.\nThere is no intracranial hemorrhage. The ventricles and sulci are normal in\ncaliber and configuration.\n\nMajor intravascular flow voids are maintained.\n\nThe paranasal sinuses and mastoid air cells appear clear.\n\nMRI orbits:\nThe globes and optic nerves are normal. The extra-ocular muscles and\nintraorbital fat are normal. The superior ophthalmic veins demonstrate normal\nenhancement following contrast administration.\n\nThe left medial temporal lobe enhancing lesion is again seen (series 14 images\n___.\n\nMRA head:\nThere is irregularity of the anterior cerebral arteries just proximal to the\nbranch points of the pericallosal and callosal marginal arteries (series 102\nimage 16). There is irregularity and narrowing of the M2 segment of the right\nmiddle cerebral artery (series 102, image 11).\n\nThe major intracranial arteries otherwise appear normal with no evidence of\nstenosis, occlusion, or aneurysm formation.",
            "output": "1. Approximately 8 mm focus of FLAIR hyperintensity with slowed diffusion and\nenhancement in the left medial temporal lobe (series 17, image 9). Also, there\nis multifocal narrowing of the A2 segments of the bilateral anterior cerebral\narteries and the M2 segment of the right middle cerebral artery. The overall\nappearance is suggestive of vasculitis with the left medial temporal lobe\nlesion being either sequela of an inflammatory process that may also be\ncausing the vasculitis or a subacute infarct due to vasculitis itself.\nDemyelinating disease is considered much less likely as no other parenchymal\nlesions are present.\n2. Normal MRI of the orbits."
        },
        {
            "input": "Stable nonenhancing 0.7 x 0.3 cm ovoid focus within the left medial temporal\nlobe (07:10) only seen on FLAIR imaging.  No enhancing lesion identified.\n\nNo meningeal enhancement. There is no evidence of hemorrhage, edema,  mass\neffect, or infarction. The ventricles and sulci are normal in caliber and\nconfiguration.  The globes, extraocular muscles, intraorbital fat, and optic\nnerves are unremarkable.",
            "output": "Stable 0.7 cm nonenhancing focus in left medial temporal lobe.  No new\nenhancing lesion.  The possibility of sequela of an inflammatory process is a\nconsideration, long-term followup with MRI with and without contrast is\nadvised."
        },
        {
            "input": "There is continued interval normalization of the left mesial temporal cortex\nsignal with questionable punctate residual FLAIR signal hyperintensity seen on\nseries 7, image 10 which may represent residual FLAIR signal hyperintensity\nversus background noise.  No evidence of acute infarct, hemorrhage, mass, or\nmass effect.  There is no abnormal postcontrast enhancement.\n\nThe ventricles and extra-axial spaces are unremarkable.  The vasculature is\npatent.  The orbits, calvarium, and soft tissues are unremarkable.  The\nparanasal sinuses and mastoid air cells are clear.",
            "output": "Continued interval signal normalization of the left mesial temporal cortex\nlesion with questionable punctate FLAIR signal hyperintensity at the lesion\nsite which may represent mild residual FLAIR signal hyperintensity versus\nbackground noise.  No evidence of new or progressive lesions."
        },
        {
            "input": "There is a solitary subcortical white matter FLAIR signal hyperintense focus\nat the right frontal cortex (___) which is unchanged comparison to prior\nstudy.  The remainder of the gray-white matter signal is normal without\nevidence of infarct, hemorrhage, mass, or mass effect.  There is no signal\nabnormality at the left mesial temporal cortex as described on prior studies. \nThe ventricles and extra-axial spaces are unremarkable.  The vasculature is\npatent.  The orbits, calvarium, and soft tissues are unremarkable.",
            "output": "1. Unremarkable MRI of the brain without evidence of acute intracranial\nabnormality.  No evidence of multiple sclerosis.\n2. Normal appearance of the left mesial temporal cortex with resolution of\npreviously described signal abnormality."
        },
        {
            "input": "Again in comparison with the most recent study, a punctate solitary focus of\nhigh signal intensity is detected in the subcortical white matter the right\nfrontal lobe on the FLAIR 3D sequence (image 50, series 2 and image 59, series\n100b) with no significant change, no new lesions are identified.  The\npreviously area of high signal intensity identified in the left temporal\nmesial cortex is not longer present or identified, there is no evidence of\nabnormal enhancement.  The ventricles and sulci are normal in size and\nconfiguration for the patient's age.  No diffusion abnormalities are detected.\nThe major vascular flow voids are present and demonstrate normal distribution.\nThe orbits are unremarkable, the paranasal sinuses and the mastoid air cells\nare clear.",
            "output": "1.  An unchanged punctate focus of high signal is again identified on FLAIR\nsequence on the right frontal lobe as described above, this finding is\nnonspecific and may represent gliotic focus and of doubtful clinical\nsignificance.\n\n2.  No new lesions are identified.  Specifically normal appearance of the left\ntemporal mesial temporal cortex, with apparent resolution of the previously\ndescribed signal abnormality.  There is no evidence of abnormal enhancement."
        },
        {
            "input": "The T2/FLAIR hyperintense focus in the right frontal subcortical white matter\non 06:17 is unchanged.  No new T2/FLAIR hyperintense or enhancing lesions are\nidentified.  There is no evidence of hemorrhage, edema, masses, mass effect,\nmidline shift or infarction.   The ventricles and sulci are normal in caliber\nand configuration.  There is no abnormal enhancement after contrast\nadministration.\n\nThe paranasal sinuses and mastoid air cells are clear.  The orbits are\nunremarkable.\n\nThe major intracranial flow voids are preserved.",
            "output": "1. Unchanged, single focus of T2/FLAIR hyper intensity in the right frontal\nsubcortical white matter, which is nonspecific.\n2. No new T2/FLAIR hyperintense or enhancing lesions."
        },
        {
            "input": "Study is mildly degraded by motion.  Chronic right temporoparietal infarct\nwith hemosiderin staining is noted.  Additional chronic right corona radiata\nchronic infarct is noted.\n\nThere is no evidence of edema, masses, mass effect, midline shift or acute\ninfarction.  There is prominence of the ventricles and sulci suggestive\ninvolutional changes.  Periventricular, pontine and subcortical T2 and FLAIR\nhyperintensities are noted, which may represent small vessel ischemic changes.\nA 5 mm pineal cyst is noted.",
            "output": "1. Study is mildly degraded by motion.\n2. Chronic right temporoparietal hemorrhagic infarct.\n3. Chronic right corona radiata infarct.\n4. No acute intracranial abnormality.\n5. Atrophy and probable small vessel ischemic changes."
        },
        {
            "input": "The study is partially degraded due to motion artifact.  Neuroradiology\n\nThere is an acute right ACA territory infarction involving the posterosuperior\nright frontal gyrus.  A few scattered additional punctate acute infarcts\ninvolve the right frontal, left parietal, left occipital lobes and right\ncerebellum.  There is associated FLAIR signal abnormality at the sites of\ninfarct.  There is a large old right parietal lobe infarct with associated\nvolume loss.  Extensive subcortical and periventricular and pontine white\nmatter FLAIR hyperintensities are compatible with small vessel disease given\nthe patient's age.\n\nThere is no evidence of hemorrhage, mass effect or midline shift. Prominence\nof the ventricles and cerebral sulci are compatible with age related\ninvolutional changes.\n\n The major intracranial vascular flow voids are maintained.  The paranasal\nsinuses, mastoid air cells and orbits are normal.",
            "output": "1. Acute right ACA territory infarct involving the posterosuperior right\nfrontal gyrus.\n2. A few scattered punctate acute infarcts involving the right frontal, left\nparietal, left occipital lobes and right cerebellum are likely of involve\netiology.\n3. Large old right parietal lobe infarct with associated volume loss.\n4. Extensive white matter small vessel disease.\n\nNOTIFICATION:  The findings were discussed with ___, M.D. by ___\n___, M.D. on the telephone on ___ at 2:00 pm, 10 minutes after\ndiscovery of the findings."
        },
        {
            "input": "MRA HEAD:  The intracranial internal carotid, anterior cerebral and middle\ncerebral arteries are unremarkable. There is a fetal type left PCA. The\nposterior circulation is otherwise unremarkable. There is no evidence of\nsignificant stenosis, aneurysm greater than 3 mm, or other vascular\nabnormality.\n\nMRV HEAD:  There are hypoplastic left transverse and sigmoid sinuses. The\ndural sinuses, cortical veins, and deep cerebral veins are widely patent.",
            "output": "There is no significant stenosis, aneurysm greater than 3 mm or other vascular\nabnormality on the head MRA.\n\nThere is no of dural sinus thrombosis on the head MRV."
        },
        {
            "input": "There are nonspecific scattered periventricular and subcortical white matter\nFLAIR hyperintensities. There is no infarct, hemorrhage, or mass effect. The\nventricles and sulci are appropriate for age.\n\nThe principal intracranial flow voids are present. The orbits, paranasal\nsinuses and visualized soft tissues are unremarkable. There is fluid within\nthe right mastoid air cells.",
            "output": "Scattered nonspecific white matter abnormalities, atypical in appearance for\ndemyelinating disease.\n\nThere is no infarct, hemorrhage or mass effect."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.\n\nThere is a left frontal patchy subcortical T2 FLAIR hyperintensity associated\nwith volume loss likely representing changes related to remote infarction or\ncontusion.  There are bilateral periventricular and deep white matter\nmultifocal T2 FLAIR hyperintensities; nonspecific in appearance and could be\nrelated to moderate form of chronic microangiopathy.\n\nVentricular system appears normal in size and configuration.  Major intra\ncranial vascular flow voids are preserved.\n\nStatus post lens removal surgery of both globes.  Otherwise both orbits are\nnormal.  Mild mucosal thickening involving left posterior ethmoid air cells. \nBilateral mastoid air cells are aerated.",
            "output": "1. No acute intracranial abnormality.\n2. Left frontal cortical tissue loss likely due to prior infarction or\ncontusion."
        },
        {
            "input": "T1 hypointense, T2 hyperintense irregularly enhancing lesion in the superior\naspect of the right cerebellar hemisphere abutting the tentorium measuring 9 x\n11 x 13 mm (TV by SI by AP).  2 smaller enhancing lesion in the inferomedial\naspect of the right cerebellar hemisphere (series 7, image 19) as well as in\nthe left cerebellar hemisphere (series 17, image 43) measuring 5 and 6 mm in\ndiameter respectively.  The ventricles and sulci are normal in caliber and\nconfiguration.  The intracranial arteries demonstrate normal T2 flow void. \nThe orbits appear normal.  The paranasal sinuses are clear.  The pituitary\nappears normal.  The craniocervical junction appears normal.  Bilateral globus\npallidus T1 hyperintensity is nonspecific.  Numerous T1 hyperintense, T2\nhyperintense enhancing calvarial metastatic lesions the largest measuring 12 x\n9 mm in the coronal plane in the right occipital bone.",
            "output": "3 cerebellar metastatic lesions the largest in the superior aspect of the\nright cerebellar hemisphere measuring 9 x 11 x 13 mm.\n\nMultiple calvarial metastatic lesions.\n\nBilateral globus pallidus T1 hyperintensity is nonspecific, but is most\ncommonly seen in hepatic failure, hyperalimentation and prolonged parenteral\nnutrition."
        },
        {
            "input": "There has been no significant interval change. Again bithalamic T2 and FLAIR\nhyperintensities are seen with subtle hyperintensity on T1 weighted images.\nThere is no significant enhancement seen in this region. There is no evidence\nof restricted diffusion. Compared to the prior study the right thalamic as\nwell as the periventricular signal abnormalities are stable. No new signal\nabnormalities or evidence of enhancement seen. There is no mass effect,\nmidline shift or hydrocephalus. No evidence of blood products seen.",
            "output": "Stable appearance ofthalamic and periventricular signal abnormalities without\nenhancement compared with the previous MRI examinations. No new abnormalities\nare seen."
        },
        {
            "input": "Compared with ___ and ___ there has been no significant\ninterval change in a bithalamic, left greater than right, region of T2 and\nFLAIR hyperintensity with subtle high signal on T1 weighted images but no\nsignificant enhancement. The lesion measures 27 x 16 mm in its most discrete\nregion (series 7, image 14), and although unchanged compared with the 3 most\nrecent MR's dating back to ___, it is slightly decreased in size\nfrom MR performed on ___ when it measured 29 x 19 mm at\napproximately the same level allowing for differences in slice selection. The\nlesion is also substantially decreased in size compared with pre-treatment MR\nfrom ___ when it measured 33 x 24 mm.\n\n No new signal abnormalities or evidence of enhancement seen. There is no mass\neffect, midline shift or hydrocephalus. No evidence of blood products or focal\nslow diffusion. Principal intracranial vascular flow voids are preserved.\nConfluent periventricular and scattered subcortical white matter changes are\nnon-specific but could represent a combination of small vessel disease and\nposttreatment changes.\n\nThe orbits are within normal limits.  The paranasal sinuses are clear.  No\nabnormality of the skull base or calvaria is identified.",
            "output": "Stable appearance of bi-thalamic and periventricular signal abnormalities\nwithout enhancement compared with the previous MRI examinations dating back to\n___ although the bi-thalamic lesion is decreased in size compared\nwith ___ and significantly decreased in size compared with\npretreatment MRI from ___. No new abnormalities identified."
        },
        {
            "input": "The previously noted bilateral thalamic signal abnormality is again seen\nwithout enhancement . From ___ this lesions appear less apparent and\nsmaller. There is periventricular hyperintensity seen as before which could be\nrelated to posttreatment changes. There are no new focal abnormalities or\nacute infarct identified. There is no mass effect midline shift or\nhydrocephalus. Following gadolinium administration no evidence of abnormal\nparenchymal vascular injury enhancement seen.",
            "output": "Unchanged signal abnormality in bilateral thalamic regions and periventricular\nwhite matter compared to the previous MRI examination.  No abnormal\nenhancement seen. No new signal abnormalities or acute infarct."
        },
        {
            "input": "There are stable T2/FLAIR hyperintensities within the bilateral thalami, left\ngreater than right (16:13; 14:13). There is no associated enhancement, and no\nnew enhancing lesions are seen. There is mild periventricular and scattered\ndeep white matter T2/FLAIR hyperintensities, which are nonspecific and may be\nsecondary to chronic small vessel ischemic disease or post-treatment changes.\nThe ventricles and sulci are stable in size and configuration, and there is no\nacute hemorrhage or infarction. The principal intracranial vascular flow voids\nare patent. The paranasal sinuses are clear, and orbits are within normal\nlimits. The bone marrow signal is normal.",
            "output": "Stable bilateral thalamic and periventricular signal abnormalities without\nassociated enhancement. No new enhancing lesions or focal abnormalities."
        },
        {
            "input": "Again seen is a FLAIR hyperintense lesion, in the thalami , left more than\nright, with indentation on the left lateral ventricle, measuring approximately\n1.8x2.5 cm, with slight decrease FLAIR signal compared to the recent study of\n___.\nThere is mild to moderate decrease compared to the study of ___.\nNo abnormal enhancement is noted, allowing for the slightly increased\nenhancement in the  choroid plexus of the left lateral ventricle.\n\nMild to moderate dilation of the lateral and the third ventricles,  with\nbifrontal diameter of the lateral ventricles measuring approximately 4.0 cm\nand 6.6 mm of the third ventricle, without significant change compared to the\nmost recent study allowing for the technical differences.\n\nConfluent and discrete FLAIR hyperintense foci, in the cerebral white matter\nin the frontal and the parietal lobes on both sides nonspecific in appearance\nand similar to the prior study.  Some of these areas are prominent compared to\nthe study of ___ and may relate to treatment related changes.\n\nNo acute infarct, suspicious focus of intracranial hemorrhage, mass effect or\nshift of normally midline structures.\nNo abnormal enhancement is noted in the brain parenchyma or leptomeninges.\nThe major intracranial arterial flow voids are noted .\nThe enhancement in the venous sinuses is unremarkable.\nSella, pineal gland and the craniocervical junction regions are unremarkable.\n\nMinimal ethmoidal mucosal thickening.\nThe mastoid air cells and the rest of the paranasal sinuses are clear.",
            "output": "MRI of the brain without and with IV contrast:\nLesion in the bilateral thalami  as described above, with slightly decreased\nsignal compared to the recent study of ___ without significant\nchange; mild to moderate decrease in size compared to the study of ___.\nOther details as above.\n\nRECOMMENDATION(S):  Continued followup as needed"
        },
        {
            "input": "When compared to priors, there has been no significant interval change.  Again\nseen is bithalamic T2/FLAIR hyperintensity more extensive on the left than on\nthe right.  There is mild intrinsic T1 hyperintensity without enhancement. \nPredominately periventricular white matter T2/FLAIR hyperintensity is\nunchanged.  More focal T2 hyperintensity within the dorsal aspect of the pons\nis stable.  Ventricles and sulci are stable in configuration noting some\ndistortion of the third ventricle due to the thalamic lesion.  There is no\ninfarct.\n\nPost-contrast images demonstrate no abnormal parenchymal or meningeal\nenhancement.  Major intravascular flow voids are preserved.\n\nPost contrast images demonstrate no abnormal parenchymal or meningeal\nenhancement.\n\nVisualized paranasal sinuses and mastoid air cells are clear.  Enhancing left\nparietal scalp lesion measuring 11 mm is unchanged, to be correlated\nclinically.   Left frontal burr hole from prior biopsy is again noted.",
            "output": "No significant interval change in the bithalamic, left greater than right\nsignal abnormality with mild mass effect without evidence of progression or\nnew lesion."
        },
        {
            "input": "MR BRAIN:  Again seen is faint hyperintensity of the medial thalamus a on the\nFLAIR images.  This appears somewhat less prominent than on the prior images,\nalthough the current study is compromised by motion artifact.  Periventricular\nwhite matter hyperintensity appears unchanged over this period of time.  There\nis no abnormal enhancement after contrast administration.  There is no\nevidence of hemorrhage.  A focal hyperintensity in the posterior pons on the\nT2 weighted images appears unchanged.  This may represent an old lacune or\ninfarction.  There is no abnormal enhancement after contrast administration.\n\nASL Perfusion: There is no evidence of abnormal blood flow in that thalami, or\nelsewhere..\n\nMR Spectroscopy: There is mild choline elevation in several voxels overlying\nthe medial thalamus a, compatible with the clinical diagnosis of malignant\nglioma..",
            "output": "1. No evidence of tumor progression.  Mild choline elevation in the medial\nthalami."
        },
        {
            "input": "MR BRAIN:  There is new 1.3 x 0.4 cm (AP, TRV) left lateral ventricle\nependymal enhancing FLAIR hyperintense signal (series 10, image 22; series 11,\nimage 22) with apparent subtle associated slow diffusion.\n\nLeft frontal burr hole is unchanged.  Confluent periventricular and left\ngreater than right medial thalamic FLAIR hyperintensities are unchanged from\nprior examination.  Punctate the T2 hyperintensity of the posterior pons is\nunchanged from prior exam, presumably representing prior lacunar infarct.  The\nsulci, ventricles and cisterns are within expected limits for the patient's\nmild age related global cerebral volume loss.  There is no acute infarct or\nintracranial hemorrhage.  The major intracranial flow voids are preserved.\n\nThe paranasal sinuses are essentially clear.  The orbits are unremarkable. \nThe mastoid air cells are clear.\n\n1.1 cm subcutaneous left parietal and 7 mm right parietal subcutaneous T2\nhyperintense lesions are unchanged from prior exam likely representing\nsebaceous cysts.\n.\nMR ___: There is increased blood flow and blood volume of the\nnew left ventricular enhancing lesion.\n\nASL Perfusion: No definitive increase perfusion is identified on ASL.\n\nMR Spectroscopy: Single voxel spectroscopy centered over the left thalamus\ndemonstrates mildly increased choline to NAA ratio, unchanged from prior\nexamination.  Multi voxel spectroscopy demonstrates similar findings.",
            "output": "1. New left lateral ventricle up abnormal enhancing 1.3 cm FLAIR hyperintense\nsignal with apparent associated subtle slow diffusion.  The lesion\ndemonstrates increased perfusion on dynamic contrast susceptibility.  The\nfindings are concerning for disease progression.\n2. Unchanged FLAIR hyperintense signal of the left greater than right medial\nthalami, mild elevated choline to NAA ratio, unchanged from prior examination.\n\nNOTIFICATION:  The impression and recommendation above was entered by Dr.\n___ on ___ at 12:57 into the Department of Radiology critical\ncommunications system for direct communication to the referring provider."
        },
        {
            "input": "Examination is mildly degraded by motion.\n\nMR BRAIN:\nThere are stable postoperative changes from left frontal burr hole.  There has\nbeen interval increase in size of a heterogeneously rim enhancing 1.3 x 3.4 x\n1.7 cm left lateral ventricle ependymal lesion, previously measuring 1.3 x 0.6\nx 0.9 cm (1200b:92, 1201b:70).  There is associated slowed diffusion and new\nareas of susceptibility suggestive of blood products versus mineralization. \nThere has been prominent interval increase of surrounding white matter\nT2/FLAIR hyperintensity, with associated mildly increased mass effect.\n\nNodular enhancement along the right parietal dura is again seen, unchanged\ncompared to ___ prior exam, again suggestive of venous Lake (see\n1201b:115 on current study, 1401b:115 on ___ prior exam, 1001:112\non ___ prior exam, and 10:115 on ___ prior exam).\n\nPunctate area of FLAIR hyperintensity in the right thalamus and minimal FLAIR\nhyperintensity centered in the left thalamus appears unchanged compared the\nprior examination.  The punctate area on the right demonstrates associated\nenhancement, unchanged and there is subtle wispy enhancement within the left\nthalamus, unchanged.\n\nThere is no evidence of  midline shift or infarction.  There is prominence of\nthe ventricles and sulci suggestive of involutional changes.  Background\nperiventricular, subcortical and deep white matter T2/FLAIR hyperintensity is\nnonspecific, likely representing chronic microangiopathy.  The principal\nintracranial vascular flow voids are preserved.\n\nThe visualized paranasal sinuses are grossly clear.  The orbits are grossly\nunremarkable.  Several T1 intermediate, T2 hyperintense enhancing scalp\nlesions measuring up to 12 mm in the left parietal scalp are unchanged, and\nlikely represent sebaceous cysts (6:  25, 26, 28, 29).\n\nMR ___:\nThere is suggestion of increased perfusion of the enhancing left ependymal\nlesion.  There is no definite increased perfusion thalami.\n\nASL Perfusion:\nThere is suggestion of increased perfusion of the enhancing left ependymal\nlesion. There is no definite increased perfusion thalami.\n\nMR Spectroscopy:\nSingle voxel spectroscopy performed in the region of the enhancing left the\nependymal lesion demonstrates increased choline and decreased NAA peak with\nprominently elevated lipid/ lactate peak.  Multi voxel spectroscopy centered\nin the bilateral thalami demonstrate mildly elevated choline and decreased NAA\npeaks in regions of interest 7 and 9.",
            "output": "1. Examination is mildly degraded by motion.\n2. Interval increase in size and surrounding white matter signal abnormality\nof a heterogeneously enhancing 1.3 x 3.4 x 1.7 cm left lateral ventricle\nependymal lesion demonstrating increased perfusion and metabolite profile. \nFinding concerning for tumor progression, with differential consideration of\ntreatment related effects.  Recommend attention on follow-up imaging.\n3. Subtle areas of signal abnormality and equivocal enhancement in the\nbilateral thalami, unchanged compared to the prior examination, with\nmetabolite profile concerning for residual tumor.\n4. No new enhancing mass identified.\n5. Grossly stable mild global atrophy and background white matter parenchymal\nabnormalities.\n6. Stable scattered scalp lesions, again likely representing sebaceous cysts.\n\nRECOMMENDATION(S):  Interval increase in size and surrounding white matter\nsignal abnormality of a heterogeneously enhancing 1.3 x 3.4 x 1.7 cm left\nlateral ventricle ependymal lesion demonstrating increased perfusion and\nmetabolite profile.  Finding concerning for tumor progression, with\ndifferential consideration of treatment related effects.  Recommend attention\non follow-up imaging."
        },
        {
            "input": "MR BRAIN:  The study is extremely limited due to lack of postcontrast imaging.\nThe patient is status post left frontal burr hole, with interval increase in\nareas of slow diffusion along the left centrum semiovale extending to the left\ncorona radiata, compared to the prior exam from ___.  The\nassociated FLAIR signal abnormality appears overall unchanged compared to the\nprior exam.  Extent of associated blood products appears slightly improved\ncompared to the prior exam.\n\nAdditional foci of FLAIR hyperintensity in the right thalamus and FLAIR\nhyperintensity in the left thalamus are unchanged compared the prior exam.\n\nThere is no evidence of midline shift or acute intracranial hemorrhage. \nAdditional periventricular and deep subcortical white matter FLAIR\nhyperintensities are likely secondary to chronic microangiopathy.  The\nprincipal vascular flow voids are well preserved.\n\nMild mucosal sinus thickening is seen involving the ethmoid air cells.  The\nremainder the visualized paranasal sinuses, mastoid air cells, and middle ear\ncavities are clear.  The globes are unremarkable.\n\nMR ___: Subtle increased mean transit time and perfusion is\nseen involving the region of the left ependymal lesion.\n\nASL Perfusion: Subtle increased perfusion is seen involving the areas of slow\ndiffusion within the left ependymal lesion with extension to the left corona\nradiata and centrum semiovale.",
            "output": "1. Extremely limited study as no postcontrast imaging or spectroscopy was\nperformed, as patient could not tolerate completion of the exam.\n2. Interval increase in slow diffusion involving the left ependymal lesion\nwith extension to the left centrum semiovale and corona radiata, and subtle\nincrease in profusion is concerning for progression of disease.\n3. Re demonstrated is mild blood products within the left tumor bed.\n\nRECOMMENDATION(S):  Recommend re-scheduling the patient for completion of the\nstudy.\n\nNOTIFICATION:  MRI senior technologists were emailed by Dr. ___ on\n___ to re-schedule the patient."
        },
        {
            "input": "MR BRAIN:  The study is extremely limited secondary to extensive motion\ndegradation.  Compared to the prior exam from ___, there has\nbeen interval improvement in the rim enhancing, left lateral ventricle up in\nthe mole lesion, now demonstrating minimal residual enhancement and areas of\nintrinsic T1 hyperintensity consistent with blood products.  The extent of\nsurrounding FLAIR signal abnormality, has not significantly changed compared\nto the prior exam, given differences in acquisition technique.  The extent of\nslow diffusion associated with this lesion appears slightly more prominent\ncompared to the prior exam.  Prominence of ventricles and sulci is likely\nrelated to age related involutional changes. Periventricular deep subcortical\nFLAIR white matter hyperintensities are sequelae of chronic microangiopathy.\nMild mucosal sinus thickening is seen involving the ethmoid air cells. The\nremainder of the visualized paranasal sinuses, mastoid air cells, and middle\near cavities are clear.  The globes are unremarkable. The principal vascular\nflow voids are well preserved.\n\nMR ___: There is no evidence of asymmetrically increased\nperfusion.\n\nASL Perfusion: There is no evidence of asymmetrically increased perfusion.",
            "output": "1. Study is moderately degraded by motion artifact.\n2. Overall, interval improvement in the previously seen heterogeneously\nenhancing left lateral ventricle ependymal lesion compared to the prior exam\nfrom ___, now with minimal residual enhancement, areas of\nintrinsic T1 hyperintensity consistent with blood products, and stable FLAIR\nsignal abnormality.\n3. Slight interval increase in the prominence of the extent of slow diffusion\ninvolving the left ependymal lesion with extension to the left centrum\nsemiovale and corona radiata, which could be related to posttreatment effects\nhowever interval progression of disease cannot be excluded given the lack of\nIV contrast on the prior most recent exam from ___.  Continued\nclose monitoring is recommended."
        },
        {
            "input": "The exam is moderately degraded due to motion artifact.\n\nThere is a small focus of high signal on the diffusion weighted images with a\ncombination of slow and fast diffusion on the ADC maps within the left\nparacentral lobule (series 4, image 24) with associated hyperintense signal on\nT2/FLAIR (series 11, image 23).  This is consistent with a subacute\ninfarction.  No hemorrhage is identified.\n\nThere are remote infarcts within the right frontal and parietal lobes in the\nexpected location of the right ACA-MCA and right MCA-PCA vascular watershed\nterritories.  Additionally, there is a remote lacunar infarct within the left\nthalamus.  Loss of the right ICA flow void is consistent with the known right\nICA occlusion.  The major vascular flow voids are otherwise preserved.",
            "output": "1. Small subacute infarct within the left paracentral lobule, without\nhemorrhagic transformation.\n2. Remote right ACA-MCA and MCA-PCA border zone infarcts and underlying right\ninternal carotid artery occlusion as previously identified on the ___\nCTA.\n3. Remote lacunar infarct within the left thalamus."
        },
        {
            "input": "Right frontal, right parietal, and to a lesser extent right occipital\nencephalomalacia from old infarcts are again noted.  Multiple chronic lacunar\ninfarcts are also noted in the left thalamus, left corona radiata, and within\nthe pons.  Additional scattered periventricular, subcortical, and deep white\nmatter foci of hyperintense signal on FLAIR are nonspecific, but likely\nsequelae of small vessel ischemic disease.  There is no evidence of recent\ninfarction or of hemorrhage.  Ex vacuo dilatation of the right lateral\nventricle is unchanged.  There is no evidence of hydrocephalus.\n\nLoss of flow void in the petrous and cavernous segments of the right internal\ncarotid artery with redemonstration of flow voids in the supraclinoid ICA and\nits branches is consistent with known occlusion.  There is no abnormal\nparenchymal or meningeal enhancement.  The dural venous sinuses are patent.\n\nThere is mild mucosal thickening in an atelectatic left maxillary sinus. \nMucosal thickening in the left sphenoid sinus and the ethmoid air cells is\nalso noted.",
            "output": "1. Multiple chronic infarcts as described above without evidence of acute\ninfarction.  No hemorrhage.\n2. Known occlusion of the right internal carotid artery with reconstitution of\nflow in the supraclinoid segment and more distal branches.\n3. Paranasal sinus inflammatory changes."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.\n\nBilateral hippocampal formations and mammillary bodies are preserved in signal\nand configuration. There is no disproportionate medial temporal atrophy. There\nis no focal lobar encephalomalacia. There are no focal cortical dysplasias or\ngray matter heterotopia noted.",
            "output": "1. Normal brain MRI."
        },
        {
            "input": "In the right PCA territory centered in the right medial occipital lobe, there\nis an approximately 4.9 x 2.8 x 4.6 cm hemorrhagic infarction.  There is\nintense heterogeneous enhancement throughout the infarcted region.  There is\nmild surrounding edema and mass effect with near complete effacement of the\noccipital horn of the right lateral ventricle.\nSubarachnoid hemorrhage is noted along the vertex of the left parietal lobe\n(10:20).  There is no significant midline shift.  Prominence of the ventricles\nand sulci suggest involutional changes.\nThere are scattered periventricular white matter hyperintensities on FLAIR. \nAlthough nonspecific, these are often attributed to chronic small vessel\nischemia.",
            "output": "1. Right PCA territory hemorrhagic infarction.\n2. There is mild edema surrounding the lesion causing mass effect and\neffacement of the occipital horn of the right lateral ventricle.\n3. Small focus of subarachnoid hemorrhage at the vertex of the left parietal\nlobe."
        },
        {
            "input": "MRI BRAIN:\nThe chronic infarction in the right parietal lobe is unchanged.  The scattered\nfoci of T2/FLAIR hyperintensities in the periventricular and subcortical white\nmatter are unchanged and nonspecific.  The chronic hemosiderin staining within\nthe right parietal lobe is unchanged.  There is no evidence of acute\nhemorrhage, edema, masses, mass effect, midline shift or acute infarction.  \nThe ventricles and sulci are normal in caliber and configuration.  There is no\nabnormal enhancement after contrast administration.\n\nThe paranasal sinuses and mastoid air cells are clear.  The patient is status\npost bilateral cataract surgery.\n\nMRA brain:  The patient is status post coil embolization coiling of a right\nposterior communicating artery aneurysm with associated susceptibility\nartifact related to the coils.  There is no evidence of recanalization.  No\nnew aneurysms are identified.  The intracranial internal carotid arteries,\nbilateral anterior, middle, and posterior cerebral arteries as well as the\nintradural vertebral and basilar arteries are patent without evidence of\nstenosis or occlusion.",
            "output": "1. Status post coil embolization of a right posterior communicating artery\naneurysm with no evidence of recanalization.\n2. No new aneurysms.\n3. No acute infarctions.\n4. Unchanged chronic infarction in the right parietal lobe."
        },
        {
            "input": "Study is degraded by motion.\n\nThere is no evidence of infarction, hemorrhage, edema, or mass effect.\n\nQuestion areas of bilateral parietal calvarium slow diffusion (see 500,\n502:26).  Question punctate focus of enhancement within this area (see\n901:135; 03:12; 04:17).  Evaluation for associated T2 or FLAIR\nhyperintensities limited secondary to motion degradation.\n\nThere is diffuse pachymeningeal thickening and enhancement.  There is\nprominence of the dural venous sinuses.  The mammillary body-pontine distance\nis grossly preserved.  There is upward convexity of the pituitary gland,\nwithin range for age.\n\nThe ventricles and sulci are grossly stable in caliber and configuration,\nwithout definite evidence of ventriculomegaly.\n\nBilateral maxillary sinus mucosal thickening and probable mucous retention\ncysts are noted.  Minimal bilateral ethmoid air cell mucosal thickening is\npresent.  The globes and orbits are preserved.  Major intracranial vascular\nflow voids are preserved.  Major dural venous sinuses are patent.  Limited\nimaging of the parotid gland suggests subcentimeter nonspecific bilateral\nprobable lymph nodes.",
            "output": "1. Study is degraded by motion.\n2. Diffuse pachymeningeal thickening and enhancement and prominent dural\nvenous sinuses without definite evidence of leptomeningeal or intraparenchymal\nabnormal enhancement. Findings are nonspecific but can be related to recent\nlumbar puncture, with differential consideration of intracranial lymphoma less\nlikely.\n3. Bilateral parietal calvarial nonspecific nonenhancing diffusion signal\nfindings as described, with single punctate focus of enhancement versus\nartifact.  Findings may be artifactual, differential consideration of osseous\nlymphoma involvement.  If concern for parietal calvarial lymphoma involvement,\nconsider head FDG PET-CT for further evaluation.\n4. Paranasal sinus disease , as described.\n\nNOTIFICATION:  The impression and recommendation above was entered by Dr.\n___ on ___ at 12:55 into the Department of Radiology critical\ncommunications system for direct communication to the referring provider."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, or infarction.\nThe ventricles and sulci are normal in caliber and configuration. There is no\nabnormal enhancement after contrast administration. FLAIR images demonstrate\nno focal abnormalities within the supra or infratentorial brain.\n\nCoronal high-resolution images demonstrate normal appearance of the medial\ntemporal lobe structures. There is no evidence of atrophy or increased signal\nwithin the hippocampal regions.  There is no evidence of migration abnormality\nidentified.",
            "output": "Normal MRI of the brain without gadolinium using seizure protocol. ."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  There is mild prominence of the ventricles and sulci\nsuggestive of involutional change.  Confluent scattered areas of\nperiventricular, subcortical and deep white matter T2/FLAIR hyperintensities\nare in a configuration most suggestive of chronic small vessel ischemic\ndisease.  There is no abnormal focus of slowed diffusion.  The principal\nintracranial vascular flow voids are preserved.\n\nThe paranasal sinuses are grossly clear.  The orbits are unremarkable.  There\nis partial right greater than left mastoid air cell opacification,\nnonspecific.",
            "output": "1. No acute intracranial abnormality including hemorrhage, infarct, or\nsuggestion of mass.\n2. Mild global atrophy and areas of white matter signal abnormality in a\nconfiguration most suggestive of chronic small vessel ischemic disease.\n3. Nonspecific right greater than left mastoid air cell opacification which\ncan be seen in the setting of mastoiditis."
        },
        {
            "input": "Study is mildly degraded by motion.\n\nMRI BRAIN:\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  There is mild prominence of the ventricles and sulci\nsuggestive involutional changes, unchanged.  Periventricular and subcortical\nT2 and FLAIR hyperintensities are noted which may represent small vessel\nischemic changes, stable.  Again is noted right-sided near complete and left\nminimal mastoid air cell opacification.\n\nMRA BRAIN:\nThe left supraclinoid internal carotid artery demonstrates left posterior\ncommunicating artery and left ophthalmic branch probable infundibula (see\n103:5).  The intracranial vertebral and internal carotid arteries and their\nmajor branches appear normal without evidence of stenosis, occlusion, or\naneurysm formation.\n\nMRA NECK:\nThe common, internal and external carotid arteries appear normal.  There is no\nevidence of internal carotid artery stenosis by NASCET criteria.  The origins\nof the great vessels, subclavian and vertebral arteries appear normal\nbilaterally.",
            "output": "1. Study is mildly degraded by motion.\n2. No evidence of acute infarct.\n3. Patent circle of ___.\n4. Patent bilateral cervical carotid or vertebral arteries.\n5. Grossly stable mild global volume loss and extensive probable\nmicroangiopathic changes.\n6. Grossly stable nonspecific near complete right and partial left mastoid air\ncell opacification."
        },
        {
            "input": "MRI BRAIN:\nThere is no evidence of hemorrhage,edema,masses, mass effect, midline shift or\ninfarction.   The ventricles and sulci are mildly prominent in caliber and\nconfiguration consistent with involutional changes.  There is redemonstration\nof stable periventricular and subcortical T2 and FLAIR hyperintensities, which\nare nonspecific but may reflect small vessel ischemic changes.  There is no\nabnormal enhancement after contrast administration.\n\nThere is stable chronic opacification of the right mastoid air cells.  The\nparanasal sinuses appear clear.  The visualized bilateral orbits appear\nunremarkable.\n\nMRA BRAIN:\nThe intracranial vertebral and internal carotid arteries and their major\nbranches appear normal without evidence of stenosis,occlusion,or aneurysm\nformation.\n\nMRA NECK:\nThe origins of the great vessels, subclavian and vertebral arteries appear\nnormal bilaterally.  The common, internal and external carotid arteries appear\nnormal.  There is no evidence of internal carotid artery stenosis by NASCET\ncriteria.The right V2 segment is poorly visualized, better seen on the CTA\nhead and neck from 1 day prior.\n\nThere is a common origin of the left common carotid artery and the right\nbrachiocephalic artery.",
            "output": "1. No acute intracranial abnormality.\n2. Stable T2/FLAIR periventricular and subcortical signal abnormalities, again\nnonspecific, but may reflect small vessel ischemic changes.\n3. Patent circle of ___ without evidence of stenosis,occlusion,or aneurysm.\n4. Patent bilateral cervical carotid and vertebral arteries without evidence\nof stenosis, occlusion, or dissection."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor acute infarction.  There is mild parenchyma atrophy.  Prominent parenchymal\nperivascular spaces.  Possible small chronic infarct anterior right corona\nradiata versus focally ectatic prevascular space.  Partially empty sella. \nPreserved vascular flow voids.  Trace mucosal thickening paranasal sinuses,\nclear mastoids.  Small right nasopharyngeal retention cyst,.",
            "output": "1. No acute infarct.\n2. Mild brain parenchymal atrophy."
        },
        {
            "input": "Study is mildly degraded by motion.\n\nAxial 3 mm T1 post imaging through the internal artery canal suggests minimal\nleft internal artery canal faint enhancement measuring up to approximately 1\nmm (see 6, 8:9; 7:8), in the approximate corresponding region of curvilinear\nenhancement on axial MPRAGE postcontrast imaging (see 9: 09: 33-34).  There is\nno definite associated restricted diffusion.\n\nOtherwise, images through the internal auditory canal demonstrates symmetric\nappearance of the seventh eighth nerve complexes.  There is no evidence of\nabnormal enhancement or mass lesion within the internal auditory canals,\ncerebellopontine angles or membranous labyrinth. No other mass lesions are\nseen within the posterior fossa.\n\nLimited included imaging of the remainder of the brain demonstrates no\nevidence of hemorrhage, edema, masses, mass effect, midline shift\norinfarction.  Left frontal probable hemangioma is again seen (see 9:85 on\ncurrent study and 08:18 on prior brain MRI).  There is prominence of the\nventricles and sulci suggestive of involutional changes.  Periventricular and\nsubcortical T2 and FLAIR hyperintensities are noted which may represent small\nvessel ischemic changes.  There is no abnormal enhancement after contrast\nadministration.\n\nMinimal nonspecific right mastoid fluid is noted, grossly unchanged compared\nto ___ brain MRI (see 5:92; 6, 8:14; 09:15 on current study and\n9:3 on prior exam).  The paranasal sinuses, andmiddle ear cavitiesare clear.\nThe orbits are preserved.  The visualized portion of the principle vascular\nflow voids are preserved.  Partially empty sella is again noted.",
            "output": "1.  Study is mildly degraded by motion.\n2. Question minimal left internal auditory canal enhancement in pattern\nsuggestive of vessel, with differential consideration of small enhancing mass\nor artifact.\n3. Otherwise, no definite evidence of IAC or cerebellopontine angle mass.\n4. Minimal nonspecific right mastoid fluid."
        },
        {
            "input": "The 2 mm apparent focus of enhancement within the left internal auditory canal\n(10:30, 1001:87) is unchanged, as seen on prior exam, possibly a small vessel.\n\nElsewhere, there is no evidence of acute infarction, hemorrhage, edema, mass,\nextra-axial collection, or mass effect.  No other abnormal enhancement. \nProbable chronic lacunar infarcts bilateral anterior corona radiata, stable. \nModerately prominent prevascular spaces.  Mild generalized brain parenchymal\natrophy.  Partially empty sella.\n\n The visualized paranasal sinuses and mastoids appear clear.  The globes and\norbits are unremarkable.  Major intracranial vascular flow voids are\npreserved.  Major dural venous sinuses are patent.",
            "output": "1. No evidence of recent infarct.\n2. Two small chronic supratentorial lacunar infarcts.\n3. 2 mm enhancement left ICA, may represent vessel or vestibular schwannoma. \nMalignancy, inflammatory or infectious process is unlikely in the absence of\nclinical concern for these entities"
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.",
            "output": "Brain atrophy.  No acute infarcts mass effect or hydrocephalus.  No etiology\nidentified for persistent lower extremity weakness ."
        },
        {
            "input": "There is extensive encephalomalacia involving the right MCA territory,\npredominately involving the right parietal lobe and insula with regional\nT2/FLAIR signal hyperintensity compatible with gliosis.  There is superimposed\nperiventricular and subcortical white matter foci of T2/FLAIR signal\nhyperintensity, likely sequelae of chronic microangiopathy.  There is no\nevidence of hemorrhage, edema, masses, mass effect, midline shift or acute\ninfarction.  There is prominence of the ventricles and sulci suggestive of\ninvolutional changes.  There is no abnormal enhancement after contrast\nadministration.\n\nThe orbits are unremarkable, the paranasal sinuses demonstrate mucous\nretention cyst on the left maxillary sinus and mucosal thickening on the right\nmaxillary sinus, the middle ear cavities and mastoid air cells are clear.",
            "output": "1. No acute infarction, acute intracranial hemorrhage, masses, mass effect or\nmidline shift.\n2. Sequelae of remote/chronic right MCA territory infarct, with gliosis and\nencephalomalacia in the right parietal lobe and insula, progressed since ___.\n3. Periventricular and subcortical white matter signal changes, likely\nsequelae of chronic microvascular ischemic disease."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction findings consistent with minimal chronic small vessel ischemic\nchanges.  Mild brain parenchymal atrophy, most prominent at the sylvian\nfissures.  Intracranial vascular flow voids are preserved.  Clear paranasal\nsinuses.  Trace opacification bilateral mastoids.",
            "output": "1. No acute findings put"
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   Prominence of the ventricles and cerebral sulci are\ncompatible with age related involutional changes.  There is no abnormal\nenhancement after contrast administration.\n\n The major intracranial vascular flow voids are maintained.  There is a 1.5 cm\nmucous retention cyst within the right maxillary sinus.  Trace nonspecific\nfluid is present within the bilateral mastoid air cells.  The orbits are\nnormal.",
            "output": "1. No acute intracranial abnormality.\n2. Generalized parenchymal volume loss, likely age related.\n3. No enhancing brain lesions."
        },
        {
            "input": "There is no acute infarction, intracranial hemorrhage, extracerebral fluid\ncollection, midline shift or mass effect. The cerebral volume is appropriate\nfor the patient's stated age. There is nonspecific T2/FLAIR signal\nhyperintensity in the periventricular and deep white matter. There is a single\npunctate focus of signal loss along     the right tentorium which may\nrepresent a tiny calcification versus a vessel. Flow voids are maintained. \nThe orbits are unremarkable. There is minimal mucosal thickening within the\nethmoid sinuses. The remainder of the visualized paranasal sinuses and mastoid\nair cells are clear.",
            "output": "Periventricular white matter hyperintensities that may reflect chronic small\nvessel ischemia. Otherwise normal study     ."
        },
        {
            "input": "There is a 1.7 x 1.4 x 1.6 cm (TRV, AP, SI ; series 901b, image 37)\nhomogeneously enhancing extra-axial lesion in the right paramedian posterior\nfossa, abutting the inferior aspect of the tentorium, torcula and right\ntransverse sinus exerting minimal mass effect on the right transverse sinus. \nThere is no clear evidence for invasion.  No other enhancing masses are noted.\n\nThere is no acute infarct or intracranial hemorrhage.  The sulci, ventricles\nand cisterns are within expected limits for the patient's age.  The major\nintracranial flow voids are preserved.  The dural venous sinuses are patent. \nMild mucosal thickening of the paranasal sinuses are noted.  The orbits are\nunremarkable. The mastoid air cells are clear.  Incidental note is made of a\nmetopic suture.",
            "output": "1. 1.7 cm homogeneously enhancing extra-axial lesion of the right paramedian\nposterior fossa abutting the tentorium, torcula and right transverse sinus\nwithout clear evidence of invasion.  Findings are most compatible with an\nmeningioma.\n2. No other lesions are noted.  No infarct or intracranial hemorrhage."
        },
        {
            "input": "There is no significant interval change in the appearance and size of\nright-sided posterior fossa meningioma near the torcula.  There are no new new\nenhancing lesions identified.  There are no acute infarcts seen.  There is no\nmass effect midline shift or hydrocephalus.",
            "output": "Stable appearance of the posterior fossa meningioma compared with the previous\nMRI."
        },
        {
            "input": "There is a stable homogeneously enhancing extra-axial mass within the\nposterior right cerebellar hemisphere adjacent to the confluence of the\nsinuses (100:41) measuring 1.8 cm TV x 1.5 cm AP x 1.9 cm SI, unchanged in\nsize when dating back to ___.  The transverse sinuses appear\npatent.  There is no evidence of additional mass or abnormal enhancement. \nThere is no evidence of infarction or hemorrhage.  The ventricles are normal\nin size.  There is mild diffuse parenchymal volume loss.  The major arterial\nvascular flow voids are preserved.  The dural venous sinuses appear patent on\nthe postcontrast images.  There is near complete opacification of the left\nfrontal sinus with mild mucosal thickening of the bilateral ethmoid air cells.\nThe bilateral mastoid air cells appear clear.  The orbits appear unremarkable.",
            "output": "1. Stable size of a right cerebellar meningioma.\n2. No evidence of new mass or abnormal enhancement.\n3. No evidence of infarction or hemorrhage."
        },
        {
            "input": "The ventricles and extra-axial spaces are normal in size. There is no evidence\nof midline shift, mass effect or hydrocephalus. There are no acute infarcts.\nThere is no evidence of focal abnormalities.  The vascular flow voids are\nmaintained. The visualized paranasal sinuses are clear. Following gadolinium\nadministration there is no evidence of abnormal parenchymal, vascular and\nmeningeal enhancement seen.",
            "output": "No significant abnormalities are seen on MRI of the brain with and without\ngadolinium.  There is no significant change from the previous study."
        },
        {
            "input": "There is no evidence of intracranial hemorrhage, edema, masses, mass effect,\nmidline shift or territorial infarction.  No diffusion abnormalities are\ndetected.  Ventricles and sulci are normal in caliber and configuration for\nthe patient's age. There is no abnormal enhancement after contrast\nadministration.  Punctate foci of slow diffusion in the left frontal sinus,\nlikely represents inspissated mucus secretion (series 6, image 22).  The\norbits are unremarkable, the paranasal sinuses and the mastoid air cells are\nclear.",
            "output": "1. There is no evidence of acute intracranial process or hemorrhage.\n2. No evidence of diffusion abnormalities or abnormal enhancement after\ncontrast administration."
        },
        {
            "input": "Study is moderately degraded by motion, especially on axial T1 fat-suppressed\nimages.  Within these confines:\n\nMRI BRAIN:\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.  Moderate mucosal thickening affects the paranasal sinuses and\nethmoidal air cells.\n\nMRA BRAIN:\nThe intracranial vertebral and internal carotid arteries and their major\nbranches appear normal without evidence of stenosis, occlusion, or aneurysm\nformation.\n\nMRA NECK:\nThe common, internal and external carotid arteries appear normal.  There is no\nevidence of internal carotid artery stenosis by NASCET criteria.  The origins\nof the great vessels and subclavian arteries appear normal bilaterally.\n\n There is loss of the normal flow void within the right vertebral artery from\nits origin through the V2 segment, with question faint distal V3 segment\nreconstitution and opacification of right V4 segment.  On T1 fat saturated\nimaging question minimal increased signal corresponding to the right vertebral\nartery in these nonvisualized segments, versus artifact (see series 19 and\n20).  Left vertebral artery is patent.",
            "output": "1. Study is moderately degraded by motion.\n2. Nonvisualization of right vertebral artery V1 through V3 segments with\nquestioned faint distal V3 segment reconstitution, and noted V4 segment\nopacification as described.  While findings may represent right vertebral\nartery dissection or thrombosis, depiction of diminutive right vertebral\nartery V1 and V2 segments on outside CTA suggest differential consideration of\ndominant left and hypoplastic right vertebral arteries.  If clinically\nindicated, consider repeat neck CTA or fat-suppressed T1 axial cervical\nimaging when patient can tolerate exam.\n3. Left vertebral artery is patent.\n4. No evidence of acute infarct.\n5. Paranasal sinus disease , as described."
        },
        {
            "input": "There are postsurgical changes from suboccipital craniotomy and left\ncerebellar mass resection with prominent left cerebellar volume loss in the\nresection bed.  There is additionally significant right cerebellar and diffuse\nmedullary atrophy.  The bilateral inferior olivary nuclei appear large with\nincreased T2 signal (15:6). There is no evidence of local recurrence.\n\nA left frontal approach ventriculoperitoneal shunt catheter is in place with\nthe tip crossing midline, terminating in the frontal horn of the right lateral\nventricle, pressing against the right caudate head.  There is a tract from a\nold right frontal approach ventriculostomy catheter.\n\nA 10 mm focus of FLAIR hyperintensity in the right subinsular white matter\nadjacent to the putamen may represent a chronic infarct.\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor acute infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.",
            "output": "1. Postsurgical changes from suboccipital craniotomy and left cerebellar mass\nresection without evidence of recurrence.  No enhancing intracranial mass.\n2. Left frontal approach VP shunt catheter terminates in the frontal horn of\nthe right lateral ventricle adjacent to the caudate head, without\nventriculomegaly.\n3. Probable right subinsular chronic infarct.\n4. Prominent right cerebellar and bilateral medullary atrophy with\ndisproportionately large appearance of the bilateral inferior olivary nuclei\nwhich represents either hypertrophic olivary degeneration versus relative\nsparing of atrophy compared to the remainder of the medulla."
        },
        {
            "input": "Please note the study is moderately degraded by motion.   Slow diffusion with\ncorrelate FLAIR signal intensity within the right striatum, anterior right\ncentrum semiovale, anterior right frontal operculum, anterior right temporal,\nand posterior lateral right parietal cortices consistent with acute\ninfarction.  No evidence of hemorrhagic conversion.  Scattered periventricular\nsubcortical white matter FLAIR signal hyperintensity consistent with chronic\nmicrovascular white matter changes.\nNormal ventricular system for age.\nDiminished T2 flow void within the right M1 middle cerebral artery (see\n10:11). The visualized orbits are normal.The paranasal sinuses appear normal\nwhere visible",
            "output": "1.  Study is moderately degraded by motion.\n2. Acute infarction without hemorrhagic conversion within the right middle\ncerebral artery distribution involving the right frontal, temporal, and\nparietal cortices in addition to the striatum.\n3. Diminished T2 flow void within the right M1 segment middle cerebral artery\nwhich may represent slow flow versus occlusion.  This could be further\ncharacterized with a dedicated CTA or MRA of the head, if clinically\nindicated.\n\nRECOMMENDATION(S):  Diminished T2 flow void within the right M1 segment middle\ncerebral artery which may represent slow flow versus occlusion.  This could be\nfurther characterized with a dedicated CTA or MRA of the head, if clinically\nindicated."
        },
        {
            "input": "There is no evidence of infarction, acute hemorrhage,mass, or edema.  There\nare microbleeds in the right frontal and parietal lobes.  The focus of\nsusceptibility artifact in the right globus pallidus may represent\nmineralization or another microhemorrhage.  Ventricles and sulci are\nprominent, consistent with age-related global parenchymal loss.\nPeriventricular, subcortical, and deep white matter T2/FLAIR hyperintensities\nare nonspecific, but may represent small vessel ischemic changes.\n\nSevere paranasal sinus inflammatory disease is again seen with complete\nopacification of the right frontal sinus, right ethmoid air cells, right\nmaxillary sinus, and right sphenoid sinus and subtotal opacification of the\nleft frontal sinus, left ethmoid air cells, and left sphenoid sinus.  There is\nmoderate mucosal thickening in the left maxillary sinus.  There is partial\nopacification of the bilateral mastoid air cells.  The middle ear cavities are\nclear.  The orbits are unremarkable.",
            "output": "1. No evidence of infarction or recent hemorrhage.\n2. Right frontal and parietal chronic micro bleeds\n3. Severe paranasal sinus disease, unchanged from ___."
        },
        {
            "input": "MRI head:  There is no acute infarct or intracranial hemorrhage. No mass, mass\neffect or midline shift is present. The ventricles, cerebral sulci and\ncisterns are age appropriate. A few scattered foci of T2 and FLAIR\nprolongation are present within the subcortical white matter, a nonspecific\nfinding, but may be related to the sequela of chronic small vessel ischemic\ndisease. No other regions of abnormal signal intensity are seen within the\nbrain parenchyma.\n\nMild ethmoid sinus mucosal thickening and a delay the visualized soft tissues\nand orbits are unremarkable.\n\nMRA head:  MR angiogram images are suboptimal secondary to patient motion.\nWithin these confines, the major intracranial vessels are patent. No large\naneurysm or arterial venous malformation is detected. There are prominent\nbilateral posterior communicating arteries with the basilar and intracranial\nvertebral arteries Bean consequently small in caliber.\n\nMRA neck:  The aortic arch demonstrates a normal branching pattern.  Both\nvertebral arteries are patent. The bilateral common carotid, internal carotid\nand external carotid arteries are patent. There is no evidence for significant\nstenosis by NASCET criteria.",
            "output": "1. No acute infarct, intracranial hemorrhage or space-occupying lesion.\n2. Normal MR angiogram of the neck without evidence of significant stenosis or\nocclusion.\n3. Suboptimal MR angiogram of the head secondary to patient motion, but no\nobvious abnormality is detected."
        },
        {
            "input": "There is a 10 x 14 x 11 mm focus of slow diffusion and T2/FLAIR hyperintensity\nin the paramedian left cerebellar hemisphere with smaller foci slightly more\nlaterally and a similar smaller focus involving the cortex and subcortical\nwhite matter of the left inferior occipital lobe, consistent with likely\nembolic late acute infarcts.  There is no parenchymal signal abnormality\notherwise.  There is no hemorrhage.  The ventricles and sulci are\nage-appropriate.  Principal intracranial vascular flow voids including those\nof the dural venous sinuses are preserved.  The orbits are grossly\nunremarkable.  There is mild mucosal thickening in the ethmoid air cells.\nBilateral maxillary sinus mucous retention cyst, right greater than left are\nnoted.",
            "output": "1.  Left cerebellar and occipital, likely embolic, late acute infarcts as\ndescribed.\n\n2.  Sinus disease.\n\nNOTIFICATION:  The findings were discussed with ___, M.D. by ___\n___, M.D. on the telephone on ___ at 9:25 am, 30 minutes after\ndiscovery of the findings."
        },
        {
            "input": "MRI BRAIN:\nThere is evolution of previously seen infarctions in the left occipital lobe\nand left cerebellar hemisphere when compared with the prior study dated ___.  There is no evidence of acute infarction or of hemorrhage. The\nventricles are normal in size without mass effect or midline shift. The major\nvisualized arterial vascular flow voids are preserved. The mucosal retention\ncysts within bilateral maxillary sinuses with mild mucosal thickening of\nbilateral ethmoid air cells.  There is trace T2 hyperintensity within the left\nmastoid air cells.  The orbits appear unremarkable.\n\nMRA BRAIN:\nThe intracranial vertebral and bilateral internal carotid arteries and the\nmajor branches appear patent without stenosis, occlusion, or aneurysm.  There\nis no evidence of dissection.\n\nMRA NECK:\nThe previously seen dissections involving the V3 segment of the left vertebral\nartery and V1/V 2 segments of the right vertebral artery as seen on the prior\nCTAs dated ___ and ___ on the current study demonstrate no\ncorresponding intrinsic T1 hyperintensity.  There is expected enhancement of\nbilateral vertebral arteries without stenosis or occlusion.  Constellation of\nfindings suggest interval resolution of previously seen dissections.  The\nbilateral common carotid arteries appear patent.  There is no internal carotid\nartery stenosis by NASCET criteria.",
            "output": "1. No evidence of acute infarction or of  hemorrhage.\n2. Evolution of left cerebellar and left occipital lobe infarctions.\n3. Interval resolution of previously seen bilateral vertebral artery\ndissections when compared with the prior CTAs dated ___ and ___, and corresponding to most recent outside CTA dated ___. \nOtherwise, unremarkable MRA neck.\n4. Unremarkable MRA head without intracranial stenosis, occlusion, or\naneurysm.\n5. Mild paranasal sinus disease, as above."
        },
        {
            "input": "MR BRAIN:\nThere is a late acute to early subacute infarct in the right cerebellar\nhemisphere in the right ___ distribution also with involvement of the right\ncentral vermis.  There is no evidence of intracranial hemorrhage, masses,mass\neffect, or midline shift.  The ventricles and sulci are normal in caliber and\nconfiguration.  Two areas of chronic infarct in the left cerebellar hemisphere\nare noted (series 7, image 4).\n\nThe visualized portion of the orbits are unremarkable.  There is mucosal\nthickening in the ethmoidal air cells, moderate amount of fluid in the right\nparanasal sinus, and mucosal thickening and fluid with near complete\nopacification in the left paranasal sinus.\n\nMRA brain:\nThere is asymmetric intrinsic T1 hyperintensity in the right vertebral artery\nV3-V4 junction corresponding to the region of dissection on prior CTA,\nconsistent with patient's known vertebral artery dissection.  The diminutive\nremaining right V4 segment is unchanged from prior exam.  No evidence of\nocclusion or aneurysm.  The intracranial left vertebraland internal carotid\narteries and their major branches appear normal without evidence of stenosis,\nocclusion, or aneurysm formation.",
            "output": "1. Moderate-sized late acute to early subacute infarct of the right cerebellar\nhemisphere and right central vermis.\n2. Right vertebral artery dissection involving the segment V3-V4 junction.\n3. Evidence of active sinus disease as described above.\n\nNOTIFICATION:   The findings were discussed with ___, M.D. by\n___, M.D. on the telephone on ___ at 4:06 pm, 5 minutes after\ndiscovery of the findings."
        },
        {
            "input": "The ventricles and sulci are prominent suggesting global cortical volume loss\nand cerebral atrophy, please correlate.  There is no evidence of acute\nterritorial infarction, intracranial hemorrhage, extracerebral fluid\ncollection, midline shift or mass effect.  No diffusion abnormalities are\ndetected.  the major vascular flow voids are maintained. The orbits are\nunremarkable, the paranasal sinuses, middle ear cavities and mastoid air cells\nare clear",
            "output": "1.  Prominent ventricles and sulci for the patient's age suggesting global\ncortical volume loss please correlate.\n\n2.  There is no evidence of acute intracranial process or hemorrhage, no\ndiffusion abnormalities are detected to indicate acute or subacute ischemic\nchanges."
        },
        {
            "input": "There is a small area of slowed diffusion with associated FLAIR hyperintensity\nin the posterior limb of the right internal capsule, corresponding to an area\nof subtle hypodensity on prior CT examination, compatible with subacute\ninfarct.\n\nRoughly 27 x 17 X 19 mm hemorrhage centered in the left thalamus, with\nextension into the left lateral ventricle appears grossly unchanged compared\nthe prior CT examination given difference of technique.  There is no definite\nunderlying enhancing mass.  There is unchanged small amount of hemorrhage\nlayering within the occipital horns of the lateral ventricles.\n\nA left frontal approach ventriculostomy catheter is unchanged in position,\nterminating in the frontal horn of the left lateral ventricle.  The ventricles\nand sulci are unchanged in size and configuration.  A tract from prior right\nfrontal approach ventriculostomy catheter is noted, with small area of\nsurrounding FLAIR hyperintensity and blood product.\n\nAn area of volume loss and susceptibility artifact is noted in the left\nexternal capsule, in area of prior hemorrhage.  Numerous areas of\nsusceptibility artifact are noted in the bilateral corona radiata, right\nhippocampus, brainstem, and particularly the cerebellum, denoting chronic\nmicrohemorrhage.  There is no evidence of new hemorrhage, edema, masses, or\nmidline shift.  The principal intracranial vascular flow voids are preserved. \nThere is otherwise no abnormal focus of enhancement.\n\nThere is mild mucosal wall thickening in the right maxillary sinus, right\nethmoid air cells, right sphenoid sinus and right frontal sinus.  The\nremainder of the paranasal sinuses are grossly clear.  There is opacification\nof the bilateral mastoid air cells.  The orbits are grossly unremarkable.",
            "output": "1. Grossly unchanged intraparenchymal hemorrhage centered in the left\nthalamus, likely hypertensive, with intraventricular extension into the left\nlateral ventricle with small amount of hemorrhage layering within the\noccipital horns of the lateral ventricles.  No new hemorrhage.\n2. Small subacute infarct in the posterior limb of the right internal capsule.\n3. No enhancing mass, ventriculitis or encephalitis.\n4. Unchanged position of a left frontal approach ventriculostomy catheter with\nstable size and configuration of the ventricular system.\n5. Scattered chronic micro hemorrhages with cerebellar predominance, in a\ndistribution suggestive of hypertensive microangiopathy."
        },
        {
            "input": "Some of the images are limited by motion.\n\nThere is a large area of T2 hyperintensity in the right upper pons, a small\narea of T2 hyperintensity in the left lower pons, bilateral multifocal T2\nhyperintensity throughout the middle of, and large areas of T2 hyperintensity\nin bilateral cerebellar peduncles, larger on the left than right, which have\nall markedly progressed compared to ___. There is faint wispy linear contrast\nenhancement in the left pons and anterior aspect of the left cerebellar\npeduncle, along the margins of the T2 hyperintense lesions, which may indicate\nacute demyelination. There is no associated slow diffusion.\n\nPreviously noted extensive confluent demyelinating disease in the\nsupratentorial white matter has slightly increased in extent and now\ndemonstrates low signal on precontrast T1 weighted and FLAIR images,\nconsistent with parenchymal volume loss and black hole formation. There is\ninterim enlargement of the ventricles, also indicating progressive cerebral\nvolume loss, as well as persistent unchanged enlargement of the sulci. A\nlinear focus of contrast enhancement along the medial margin of the occipital\nhorn of the left lateral ventricle, images 14:88 and 102:41, may indicate\nanother focus of acute demyelination.\n\nThere is no evidence for intracranial blood products. Major arterial flow\nvoids are grossly preserved.",
            "output": "1. Compared to ___, there is progression of demyelinating disease in\nbilateral pons, bilateral medulla, and bilateral cerebellar peduncle\nsemilunaris. Faint wispy linear contrast enhancement along the anterior margin\nof left pontine and left cerebellar peduncle lesions suggests acute\ndemyelination.\n2. Progression of extensive confluent demyelinating disease in the\nsupratentorial white matter with diffuse black hole formation and increased\ndiffuse parenchymal volume loss. Linear contrast enhancement along the medial\nmargin of the occipital horn of the left lateral ventricle may indicate\nanother focus of acute demyelination."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  The ventricles and sulci are normal in caliber and\nconfiguration. There is no abnormal enhancement after contrast administration.\n\nMajor intracranial vascular flow voids are preserved.\n\nThere is minimal mucosal thickening within the ethmoid air cells bilaterally.\nRemainder of the visualized paranasal sinuses, right air cells and middle ear\ncavities are clear. The orbits are unremarkable.",
            "output": "1. Normal brain MRI."
        },
        {
            "input": "1.6 cm x 1.2 cm intraparenchymal subacute hematoma is re-demonstrated in the\nright cerebellar hemisphere, similar in size.  Mildly more prominent\nsurrounding edema, expected finding.  Mild linear peripheral enhancement\nsurrounding hematoma, typical of subacute stage.  No nodular enhancement.\n\nLinear focus of leptomeningeal enhancement left paracentral lobule seen on\nFLAIR images series 11, image 19, not seen on prior, indeterminate, may be\nnormal vessel, or inflammatory, infectious or neoplastic etiology, follow-up\nrecommended.\n\nOther punctate microhemorrhages are seen in the left frontal lobe, left\nthalamus.\n\nThere is no evidence of midline shift.  Brain parenchymal atrophy.  Findings\nconsistent with moderate chronic small vessel ischemic changes..  There is no\nabnormal enhancement after contrast administration..  Mild opacification left\nmastoids.  Preserved vascular flow voids.  Patent dural venous sinuses.",
            "output": "1. Subacute hematoma right medial cerebellum.  Follow-up to resolution\nrecommended..\n2. Subtle leptomeningeal enhancement left vertex, may be normal vessel,\nconsider inflammatory, infectious or neoplastic etiology, follow-up\nrecommended."
        },
        {
            "input": "Motion artifact limits evaluation.  Postcontrast MP RAGE images are\nparticularly degraded.  The postcontrast evaluation is based on the contrast\nenhanced axial T1 weighted images.\n\nThere is expected evolution of the right cerebellar hemisphere\nintraparenchymal hematoma, with resolution of T1 hyperintense blood products,\nas well as resolution of edema and mass effect.  There is small residual\nhypointensity on all sequences at the site of the prior hematoma, decreased in\nsize.  There is no evidence for contrast enhancement on the postcontrast axial\nT1 weighted images.  Motion-degraded postcontrast MP RAGE images suggest\nfaint, thin marginal contrast enhancement without evidence for nodular\ncomponents.\n\nChronic microhemorrhages are again seen in the frontal lobe at the gray/white\nmatter junction and left thalamus, unchanged (11:21, 11:13).\n\nA small focus of curvilinear leptomeningeal enhancement and FLAIR\nhyperintensity are again demonstrated along the parasagittal posterior left\nfrontal lobe (13:19).\n\nThere is no evidence of new blood products, acute infarction, new enhancing\nmass, or edema.  Moderately numerous T2/FLAIR hyperintensities in the\nperiventricular, deep, and subcortical white matter of the cerebral\nhemispheres are grossly unchanged, nonspecific but likely sequela of chronic\nsmall vessel ischemic disease in this age group.  There is unchanged mild\nglobal parenchymal volume loss with mild prominence of the ventricles and\nsulci.\n\nMajor arterial flow voids are grossly preserved.  Dural venous sinuses appear\npatent on postcontrast MP RAGE images.\n\nThere is mild mucosal thickening along the floors of the maxillary sinuses\nwith a small mucous retention cyst in the inferior left maxillary sinus,\nunchanged.  There is a small amount of fluid in the left mastoid air cells,\nunchanged.  Status post bilateral lens replacement.",
            "output": "1. Motion limited exam.\n2. Expected evolution of the right cerebellar hemisphere hematoma with\nresolution of mass effect.  No evidence for underlying mass lesion.  Faint\nthin marginal contrast enhancement on motion degraded MP RAGE images likely\nrepresents residual reactive enhancement.  No enhancement seen on less motion\nlimited postcontrast axial T1 weighted images.\n3. Unchanged chronic microhemorrhages at the gray/white matter junction of the\nleft frontal lobe and in the left thalamus.  Unchanged small focus of\nleptomeningeal enhancement at the left parasagittal posterior frontal vertex. \nThese findings are compatible with amyloid angiopathy.\n4. No acute infarct.  No evidence for new intracranial blood products."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  The ventricles and sulci are mildly prominent, consistent with\nmild global cerebral volume loss.  Patchy periventricular T2 hyperintensities\nare most nonspecific but most likely represent changes of chronic\nmicrovascular angiopathy.  There is no abnormal enhancement after contrast\nadministration.\n\n The paranasal sinuses, mastoid air cells and middle ear cavities are clear. \nThe patient is status post bilateral cataract surgery.",
            "output": "1. Scattered white matter hyperintensities on FLAIR, perhaps related to\nchronic small vessel ischemia.\n2. Otherwise normal study."
        },
        {
            "input": "In comparison with the prior examination, there is an unchanged 19 x 29 mm\narachnoid cysts formation in the anterior aspect of the right temporal fossa,\ncausing similar mass effect and remodeling of the adjacent temporal lobe,\nthere is no evidence of vasogenic edema, please note that this examination is\npartially limited due to susceptibility/metal artifact from dental hardware\nobscuring the anatomical detail in the maxilla and inferior aspect of the\nethmoidal air cells and nose.\nWithin the limits of this exam, there is no evidence of acute intracranial\nhemorrhage, mass, mass effect or shifting of the normally midline structures. \nThe lateral ventricles are normal in size and configuration.  No diffusion\nabnormalities are detected.  The middle ear cavities and mastoid air cells are\nclear.",
            "output": "1.  Limited examination due to significant susceptibility/metal artifact from\ndental hardware, obscuring the anatomical details as described detail above,\nwithin this limitation grossly there is an unchanged right temporal fossa\narachnoid cyst, measuring approximately 19 x 29 mm in transverse dimension,\nproducing similar pattern of mass effect and remodeling of the right temporal\nlobe.\n\n2.  No new lesions are demonstrated, there is no evidence of acute\nintracranial process.\n\nNOTIFICATION:  The findings were discussed with Dr. ___. by ___, M.D.\non the telephone on ___ at 6:36 pm, 5 minutes after discovery of the\nfindings."
        },
        {
            "input": "The study is slightly degraded by motion artifact.  Within these confines:\n\nThere is large area slow diffusion in the right frontal, parietal, and\ntemporal lobes as well as the head and the body of the caudate nucleus with\ncorresponding low ADC and T2/FLAIR hyperintense signal.  Findings are\ncompatible subacute infarction.  There are multiple areas of hemorrhagic\ntransformation within the infarcted tissue.\n\nOtherwise, there is no evidence of mass effect or midline shift. The\nventricles and sulci are normal in caliber and configuration.\n\nThe principal intracranial flow voids are preserved.  The mastoid air cells\nand the paranasal sinuses are clear.  The imaged orbits are unremarkable.",
            "output": "Subacute infarction with multiple areas of hemorrhagic transformation in the\nright frontal, parietal and temporal lobes as well as the caudate nucleus.\n\nNOTIFICATION:   The findings were discussed with ___, m.D. by\n___, M.D. on the telephone on ___ at 8:49 am."
        },
        {
            "input": "Again noted is a large area of subacute infarction in the right frontal,\nparietal, and the temporal lobes as well as the caudate nucleus.  There is\nredemonstration of scattered areas of intrinsic T1 hyperintense signal with\ncorresponding blooming artifact, correlating to known areas of hemorrhagic\ntransformation.  There is patchy multifocal enhancement, in keeping with\nsubacute infarction.\n\nThere is no new infarction.  There is no mass effect or midline shift.  The\nventricles and sulci are normal in caliber and configuration.\n\nThe intracranial flow voids are preserved.  There are trace bilateral mastoid\neffusions.  The paranasal sinuses are clear.  The imaged orbits are\nunremarkable.",
            "output": "1. Redemonstration of subacute infarction with hemorrhagic transformation in\nthe right frontal, parietal and temporal lobes as well as the caudate nucleus.\n2. Patchy multifocal enhancement in the infarcted tissue, in keeping with\nsubacute infarction.\n3. The diffusion abnormality has somewhat decreased in some areas of the\ninfarcts secondary to evolution."
        },
        {
            "input": "Evaluation is limited by motion artifact.  Within these confines:\n\nAero digestive tract:\nThere is no mass.\n\nNeck lymph nodes:\nThere is mildly enlarged right cervical lymphadenopathy.  The largest node\nmeasures 1.6 x 0.8 cm at level IIa station ( 8,25).  In addition, there is a\nshotty supraclavicular lymphadenopathy.\n\nThere is no retropharyngeal adenopathy.\n\nExtra nodal tumor spread:\nThere are no findings suggestive of extra nodal extension.\n\nDeep neck muscles, masticator space:\nThere is no muscle invasion.\n\nBones, skull base:\nThere is C6-C7 T1 hypointense and T2 hyperintense signal abnormality with\nenhancement after contrast administration.  This involves the endplates and\nthe intervertebral disc.  There is no associated paraspinal soft tissue\nabnormality.  This and findings at this level on the CTA suggest discitis and\nosteomyelitis.\nNo definite suspicious focal osseous lesions are seen.\nThere are no findings suggestive of perineural tumor extension.\n\nVessels:\nThere is heterogeneously enhancing T2 hyperintense signal abnormality in the\nposterior aspect of the right distal common carotid artery and proximal\ninternal carotid artery (10, 29; 4, 29), correlating to recently noted\nnonocclusive thrombus on prior CT.  There is surrounding shoddy\nlymphadenopathy as well as fascial fluid tracking in the carotid space.\n\nBrachial Plexus:\nThere is no brachial plexus contact or invasion.\n\nThyroid, salivary glands:\nThere is no mass.\n\nOther findings:\nThere is partial visualization of right MCA territory subacute infarction with\nareas of hemorrhagic transformation.",
            "output": "1. Nonocclusive thrombus of the right distal common carotid and proximal\ninternal carotid artery.  Adjacent reactive lymphadenopathy and fascial edema.\n2. No organized abscess or phlegmon in the neck.\n3. Changes at C6-7 suggesting discitis and osteomyelitis.  Degenerative disc\ndisease is an alternate possibility.  However in this patient with recently\nnoted septic emboli, underlying infection appears more likely.  Please note\nthe current exam is optimized for cervical spine imaging."
        },
        {
            "input": "The study is mildly motion degraded.  Allowing for this limitation:\n\nPatient is status post left suboccipital craniectomy with cranioplasty for\nresection of a left cerebellar mass.  There is progressive thin rim of\nenhancement around the margin of the resection cavity since ___. \nThe degree of FLAIR hyperintense signal around the resection cavity is\nunchanged.  This may reflect post surgical change but continued attention on\nfollow-up is recommended.  No new enhancing lesion is seen.\n\nThere is no evidence of acute hemorrhage, infarct edema, mass, mass effect, or\nshift of normally midline structures.  Scattered T2/FLAIR hyperintensities are\nagain noted in the periventricular and subcortical white matter, which are\nnonspecific but likely reflect sequelae of chronic small vessel ischemic\ndisease.  The ventricles and sulci are stable in caliber and configuration. \nThere is a focal T2 hyperintense area in the right cerebellum compatible with\nan old infarct.\n\nMajor intracranial flow voids are preserved.  The dural venous sinuses are\npatent.  Patient is status post bilateral lens replacements.  The orbits are\notherwise unremarkable.  There is mild mucosal thickening in the bilateral\nmaxillary sinuses as well as the ethmoid air cells and left frontal sinus. \nPartial opacification of the left mastoid air cells are also noted.",
            "output": "1. Status post left suboccipital cranioplasty for resection of prior\nmetastasis.  Progressive thin rim of enhancement around the margin of the\nresection cavity since ___.  While this may reflect post surgical\nchange, continued attention to this area on follow-up is recommended.\n2. No new enhancing lesions identified.\n3. Paranasal sinus disease as described above."
        },
        {
            "input": "Patient is status post left sub occipital craniectomy with cranioplasty for\nresection of a left cerebellar mass.  A nodular rim of enhancement around the\nmargin of the resection cavity, appears slightly progressed compared to the\nprior exam from ___.  The degree of associated FLAIR signal\nabnormality is unchanged compared to the prior exam.\n\nNo new enhancing lesion is seen.  There is no evidence of acute intracranial\nhemorrhage or infarction.  Ventricles and sulci are age appropriate. \nPeriventricular and deep subcortical FLAIR white matter hyperintensities are\nlikely sequelae of chronic microangiopathy.\n\nMild mucosal sinus thickening is seen involving the ethmoid air cells.  The\nremainder the visualized paranasal sinuses are clear.  Moderate fluid\nopacification is seen within the left mastoid air cells and mild fluid\nopacification within the right mastoid air cells.  The principal vascular flow\nvoids appear to be grossly preserved.  The globes are unremarkable.",
            "output": "1. Status post left sub occipital cranioplasty for resection of prior\nmetastases, with mild interval progression of thin rim of enhancement around\nthe margin of the resection cavity compared to the most recent prior exam from\n___. Continued attention on follow-up is recommended.\n2. No acute intracranial abnormalities identified.  Chronic microangiopathy.\n3. Paranasal sinus disease."
        },
        {
            "input": "Prior left suboccipital craniectomy and left cerebellar tumor resection\nsequela are unchanged from prior exam.  There is progressive peripheral\nenhancement and thickening of the left cerebellar resection margin when\ncompared to prior exams (series 11, image 7).  Associated surrounding FLAIR\nhyperintense signal appears to have increased in conspicuity along the\ninferior aspect of the resection margins (series 8, image 6) when compared to\nexamination of ___.  No new enhancing lesions are identified.\n\nThere is no acute infarct or intracranial hemorrhage.  Superimposed moderate\nperiventricular and subcortical T2/FLAIR nonenhancing white matter\nhyperintensities are nonspecific and unchanged in configuration from prior\nexamination, likely representing sequela of chronic microangiopathy in a\npatient of this age.  Right cerebellar chronic lacunar infarct is unchanged.\n\nThe major intracranial flow voids are preserved.  The dural venous sinuses are\npatent.  There is mild mucosal thickening of the paranasal sinuses.  The\norbits are unremarkable, noting lens replacements.  Fluid opacification of the\nleft-greater-than-right mastoid air cells is noted.",
            "output": "1. Continued progressive peripheral enhancement and thickening of the left\ncerebellar resection margin when compared to prior exams.  Associated\nsurrounding FLAIR hyperintense signal appears to have increased in conspicuity\nalong the inferior margins of the resection cavity.  While the findings may\nrepresent evolving postsurgical sequela, interval change and progressive\nenhancement does raise suspicion for disease progression.  Recommend further\nevaluation with MRI perfusion and spectroscopy.\n2. No new enhancing lesions.\n3. Additional chronic findings as described above.\n\nRECOMMENDATION(S):  Further evaluation of impression 1 with MRI brain\nspectroscopy and perfusion."
        },
        {
            "input": "The study is mildly degraded area limited by patient motion.  Within this\nconfines:\n\nThere a new hemorrhagic lesion with peripheral rim enhancement in the left\ncerebellar hemisphere, measuring 1.5 x 1.9 x 1.7 cm in transverse dimension,\nwith surrounding FLAIR hyperintensity in keeping with vasogenic edema.  The\nlesion is exerting mass effect causing partial effacement of the left aspect\nof the fourth ventricle: No other areas with abnormal enhancement are seen.\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  In comparison with the prior MRI dated ___, the\nventricles and sulci are slightly more prominent, suggesting mild cortical\nvolume loss, probably age related and involutional in nature.\n\nThere are scattered foci of T2/FLAIR hyperintensity in the subcortical and\nperiventricular white matter, nonspecific, likely secondary to small vessel\nischemic disease.\n\nThe orbits are unremarkable noting prior bilateral cataract surgeries.  There\nis mild mucosal thickening involving bilateral ethmoid air cells, bilateral\nmaxillary sinuses an bilateral frontal sinuses.  Also seen is nonspecific\nfluid opacification of bilateral mastoid air cells, left greater than right. \nIntracranial flow voids are maintained.",
            "output": "1. New hemorrhagic lesion in the left cerebellar hemisphere with surrounding\nedema and mass effect as described above, likely metastasis from patient's\nknown renal cancer.\n2. Paranasal sinus disease and nonspecific fluid opacification of bilateral\nmastoid air cells.\n\nRECOMMENDATION(S):  The findings were discussed by Dr. ___ with\nDr. ___ on the ___ ___ at 3:37 ___, immediately after\ndiscovery of the findings."
        },
        {
            "input": "Since the previous MRI examination patient has undergone resection of left\ncerebellar rim enhancing lesion.  Blood products as well as a air are seen\nwithin the surgical cavity.  There is no evidence of an acute infarct.  There\nis no evidence of hydrocephalus.  Mild surrounding edema to the surgical bed\nis seen as before.  There is subtle residual enhancement identified at the\ninferior lateral portion of the surgical cavity.  Mild changes of small vessel\ndisease are seen.",
            "output": "Expected postsurgical changes are identified in the left cerebellum.  Subtle\nresidual enhancement is seen at the inferior portion of the surgical cavity. \nNo hydrocephalus or midline shift."
        },
        {
            "input": "Please note that contrast was not administered due to inability to obtain\npatient IV access.  The patient is status post left suboccipital craniotomy\nand resection of a left cerebellar hemispheric metastatic lesion with interval\ndecrease in the size of the resection cavity, measuring 1.4 (AP) x 1.4 (TV) x\n1.2 (SI) cm, previously measuring 2.2 (AP) x 1.5 (TV) x 2.2 (SI) cm.  The\namount of pneumocephalus in the resection cavity has decreased.  The\npostoperative fluid collection overlying the craniotomy site is unchanged in\nsize, measuring 2.2 (AP) x 4.1 (TV) x 3.4 (SI) cm.\n\nThe faint T1 hyperintense signal within the resection cavity and peripheral\nrim of slow diffusion surrounding the resection cavity, representing blood\nproducts related to the recent surgery, have decreased in comparison to the\nprior examination.\n\nWithin limits of this noncontrast examination, no definite additional\nintracranial masses are identified.\n\nA new hyperintense focus on the diffusion weighted sequence in the left\noccipital lobe on 302:14 is isointense on the corresponding ADC map on 300:18.\nThe chronic lacunar infarctions in the bilateral corona radiata are unchanged.\nThere is no midline shift.  The patient is status post bilateral cataract\nsurgery.",
            "output": "1. Limited examination in the absence of intravenous contrast.  Please note\nthat contrast was not administered due to inability to obtain IV access.\n2. Status post left suboccipital craniotomy and resection of a left cerebellar\nhemispheric metastatic lesion with interval decrease in the size of the\nresection cavity and amount of hemorrhage within the postoperative bed.\n3. New left occipital probable punctate subacute infarct, with additional mass\nnot excluded on the basis of this examination.  Recommend attention on\nfollowup imaging and correlation with neurologic exam.\n4. Stable postoperative fluid collection overlying left suboccipital\ncraniotomy site.\n\nRECOMMENDATION(S):  New left occipital probable punctate subacute infarct,\nwith additional mass not excluded on the basis of this examination.  Recommend\nattention on followup imaging and correlation with neurologic exam."
        },
        {
            "input": "The patient is status post left subtotal occipital craniotomy and\ncranioplasty.  The resection cavity measures 17 bilateral mm, stable in size\nsince the prior study (series 19, image 50).  There is linear enhancement\nalong the cavity margins as well as a focus of slightly more nodular\nenhancement along the lateral aspect of the cavity measuring 5 x 3 mm, without\nsurrounding edema (series 19, image 52, series 18, image 109).  This most\nlikely represent post treatment changes.\n\nThere are no new enhancing lesions.\n\nThere is no evidence of new blood products or edema.  Scattered foci of\nperiventricular and and subcortical white matter T2 hyperintensities are\nnonspecific but likely sequela of chronic small vessel ischemic disease in\nthis age group.\n\nThe previously noted punctate focus of hyperintensity on the\ndiffusion-weighted images in the left occipital lobe is no longer visualized,\nand there is no corresponding T2/ FLAIR signal abnormality to suggest\nevolution of a prior infarct.  There is no evidence of acute infarct.  A new\npunctate focus of hyperintensity on the diffusion-weighted images projects\nover the left inferior frontal lobe cortex, without a correlate on the ADC\nmap, FLAIR, or post-contrast images, most likely artifactual (series 7, image\n15).   The ventricles and sulci are normal in size.  Major arterial flow voids\nare grossly preserved.  The dural venous sinuses are patent after contrast\nadministration.\n\nA postoperative fluid collection extending from the cranioplasty into the left\nsuboccipital soft tissues is larger compared to ___, with maximum\n___ of 4.4 x 2.8 cm, previously 4.1 x 1.9 cm.\n\nThere is mild mucosal thickening in bilateral anterior ethmoid air cells. \nThere is near complete opacification of the left mastoid air cells and mild\npartial opacification of right mastoid air cells.",
            "output": "1. Minimal nodularity of enhancement along the lateral margin of the left\ncerebellar resection cavity, without surrounding edema, most likely reflects\npost treatment change.  Recommend attention on follow-up studies.\n2. No evidence of new metastatic lesion.\n3. Fluid collection extending from the left cranioplasty site into the left\nsuboccipital soft tissues has increased in size compared to the ___, raising the question of a dural tear with a pseudomeningocele.\n4. Punctate signal abnormality on diffusion tracer images over the left\ninferior frontal cortex, without a correlate on other sequences, is most\nlikely artifactual rather than related to a punctate infarct.  This could be\nreassessed on follow-up imaging.  Previously noted punctate focus of\nhyperintensity on diffusion-weighted images in the left occipital lobe is no\nlonger visualized, and there is no evidence of evolution to a chronic infarct\non T2 weighted/FLAIR images."
        },
        {
            "input": "The patient is status post left occipital craniotomy and cranioplasty, in\ncomparison with the most recent study the previously seen suboccipital fluid\ncollection has resolved, again the surgical bed in the left cerebellar\nhemisphere is unchanged with minimal dural enhancement at the surgical site,\nwith no evidence of abnormal enhancement to indicate recurrent lesion or\nresidual mass, the surgical cavity measures approximately 11 x 18 mm, which is\nsimilar appearance to the prior exam.  On FLAIR sequence, again few scattered\nfoci of high signal intensity identified in the supratentorial region, which\nare nonspecific and may reflect changes due to small vessel disease.  The\nmajor vascular flow voids are patent and demonstrate normal distribution.  The\norbits are unremarkable, the paranasal sinuses are clear, again there is\nopacification of the left mastoid air cells.",
            "output": "1.  Postsurgical changes consistent with left occipital craniotomy and\ncranioplasty, there is interval resolution of the previously seen suboccipital\nfluid collection on the left.  The surgical cavity in the left cerebellar\nhemisphere appears unremarkable with no evidence of abnormal enhancement to\nindicate recurrence or residual mass lesion.\n\n2.  Supratentorially scattered foci of high signal intensity are re-\ndemonstrated in the subcortical and periventricular white matter, which are\nnonspecific and may reflect changes due to small vessel disease.\n\n3.  Unchanged opacities in the left mastoid air cells."
        },
        {
            "input": "There are stable postsurgical changes from left suboccipital craniectomy and\nleft cerebellar hemisphere mass resection.  There is no abnormal enhancement\nwithin the resection bed.  Tiny chronic right cerebellar infarct is new\ncompared the prior examination (14:6).\n\nAgain demonstrated is a prominent, tortuous V4 segment of the left vertebral\nartery which produces unchanged mass effect upon the medulla.  There is no\nevidence of hemorrhage, edema, masses, mass effect, midline shift or\ninfarction.  There is mild prominence of the ventricles and sulci suggestive\ninvolutional changes.  Areas of scattered periventricular, subcortical and\ndeep white matter T2/FLAIR hyperintensity are in a configuration most\nsuggestive of chronic microangiopathy.  .  There is no abnormal enhancement\nafter contrast administration.  The dural venous sinuses are patent on the MP\nrage images.\n\nThere is mild mucosal wall thickening in the inferior aspects of the maxillary\nsinuses as well as the bilateral ethmoid air cells.  The remainder the\nvisualized paranasal sinuses are grossly clear.  There is unchanged fluid\nopacification of the left mastoid air cells.  The orbits are grossly\nunremarkable.",
            "output": "1. Stable postsurgical changes from left suboccipital craniectomy and left\ncerebellar mass resection without abnormal enhancement to suggest recurrence.\n2. No new enhancing mass.\n3. Small, chronic appearing right cerebellar infarct, new compared the prior\nexamination.\n4. Otherwise no acute intracranial abnormality including hemorrhage, acute\ninfarct, or enhancing mass.\n5. Mild global atrophy and white matter signal abnormality suggestive of\nchronic microangiopathy.\n6. Paranasal sinus disease, as described.\n7. Unchanged fluid opacification of the left-sided mastoid air cells."
        },
        {
            "input": "Stable surgical changes status post left suboccipital cranioplasty for a left\ncerebellar mass resection.  There is no abnormal enhancement within the\nresection cavity.  A tiny T2 hyperintense focus in the right cerebellum is\nunchanged from prior exam and likely represents old infarct (6:6; 502:6). \nAgain demonstrated, is a prominent torturous V4 segment of the left vertebral\nartery with unchanged mass effect upon the medulla (10:4).\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor acute infarction.  There is prominence of the ventricles and sulci\nsuggestive of age-related cerebral atrophy.  There are scattered\nperiventricular and subcortical white matter T2/FLAIR hyperintensities which\nare nonspecific, however likely represent sequelae of chronic microangiopathic\nchanges.  The major intracranial flow voids are preserved.  The dural venous\nsinuses are patent on postcontrast MP-RAGE. The orbits are grossly\nunremarkable.  There is no abnormal enhancement after contrast administration.\n\nThere is unchanged mild mucosal thickening of the bilateral maxillary sinuses,\nethmoid air cells and left frontal sinus.  The remainder the paranasal sinuses\nare grossly clear.  Interval decrease in mild fluid within the left mastoid\nair cells, the right mastoid air cells are clear.",
            "output": "1.  Stable postsurgical changes from left suboccipital cranioplasty for left\ncerebellar mass resection without abnormal enhancement to suggest recurrence.\n2. No new enhancing lesions.\n3. No acute intracranial abnormality including hemorrhage, acute infarct, or\nenhancing mass.\n4. Mild global atrophy and probable white matter chronic small vessel ischemic\nchanges."
        },
        {
            "input": "Extensive postsurgical changes are again seen following left suboccipital\ncranioplasty for a left cerebellar mass resection with minimal linear\nenhancement and FLAIR signal changes seen in the resection bed.  There may be\nmildly crease FLAIR hyperintense signal along the anterior aspect of the\nresection margin however this is likely artifactual.  No interval change in\nminimal linear enhancement.  There is no evidence of increasing or nodular\nenhancement concerning for recurrence.  A small T2 hyperintense focus in the\nright cerebellum is stable compared to the prior exam, likely representing old\ninfarct.\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor acute infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  Scattered T2/FLAIR hyperintensities are seen in the\nsubcortical and periventricular white matter, which are nonspecific but likely\ndue to chronic sequela of small-vessel ischemic disease.  The major\nintracranial flow voids are preserved.  There is again prominent and tortuous\nappearance of the V4 segment of the left vertebral artery with mass effect\nupon the medulla.  The dural venous sinuses are patent.\n\nMild mucosal thickening is noted in the ethmoid air cells.  Otherwise, the\nremaining visualized paranasal sinuses, mastoid air cells, and middle ear\ncavities appear clear.  Patient is status post bilateral lens resections.  The\nsoft tissues are grossly unremarkable.",
            "output": "1. Essentially unchanged postoperative appearance following left suboccipital\ncranioplasty without evidence of abnormal enhancement concerning for\nrecurrence.  There is equivocal increased FLAIR hyperintense signal along the\nanterior aspect of the resection margin which is felt to be likely artifactual\nin nature.  However close attention on followup is recommended.\n2. A small chronic infarct in the right cerebellum is unchanged.\n3. Chronic microangiopathy."
        },
        {
            "input": "There is no acute infarction, edema, mass effect, evidence for blood products,\nor other signal abnormalities in the brain parenchyma.  Ventricles, sulci, and\nbasal cisterns are normal in size.  Cerebellar tonsils are normally\npositioned.  Major intravascular flow voids appear grossly preserved, but the\nintracranial vasculature is better assessed on the preceding CTA.  There is\nmild mucosal thickening in several right anterior ethmoid air cells.",
            "output": "No acute infarction and no evidence for other acute intracranial\nabnormalities."
        },
        {
            "input": "MRI BRAIN:\n\nThere is signal abnormality on FLAIR, diffusion weighted, and gradient echo\nimages in the left parietal sulcus, where subarachnoid hemorrhage was\ndemonstrated on the preceding noncontrast head CT.  There is no corresponding\nsignal abnormality on T1 weighted images.\n\nGradient echo images demonstrate no clear evidence for a cavernous\nmalformation or amyloid angiopathy.  No other sites of prior hemorrhage are\nidentified.\n\nThere is no acute infarction.  FLAIR images demonstrate scattered small T2\nhyperintense foci and confluent areas of T2 hyperintensity in the subcortical,\ndeep, and periventricular white matter of the cerebral hemispheres,\nnonspecific but likely sequela of mild to moderate chronic small vessel\nischemic disease in this age group.\n\nVentricles and sulci are age appropriate in size.\n\nThere is evidence of bilateral cataract surgeries.  There is fluid and mucosal\nthickening in bilateral maxillary sinuses, and small mucous retention cysts in\nthe right maxillary sinus.  There is mucosal thickening and dependent\nsecretions in left greater than right frontal sinuses extending into the\nfrontoethmoidal recesses.  There is moderate to severe bilateral anterior\nethmoid air cell opacification.  There is mild mucosal thickening in the\nbilateral posterior ethmoid air cells and left sphenoid sinus, as well as\ntrace aerosolized secretions in bilateral sphenoid sinuses.\n\nMRA NECK:\n\nFat-suppressed axial T1 weighted images of the neck are somewhat limited by\nmotion artifact.  They demonstrate markedly high signal in the distal cervical\nleft internal carotid artery at the skullbase and in the horizontal portion of\nthe petrous segment, as well as a punctate focus of high signal in the\ncavernous segment.  This is consistent with thrombus related to acute to\nsubacute dissection.\n\nGadolinium enhanced neck MRA is limited by suboptimal timing of the scan\nrelative to the contrast bolus as well as by motion artifact.  The left\ninternal carotid artery is small in caliber just distal to its origin to the\nskullbase, with severe narrowing at the skullbase and in the horizontal\nportion of the petrous segment.  The caliber of the left internal carotid\nartery increases in the remainder of the petrous segment, and in the cavernous\nand supraclinoid portions, but it remains smaller than the right.\n\nThere is no evidence of left internal carotid artery stenosis by NASCET\ncriteria on limited evaluation.  Vertebral arteries appear patent without\nflow-limiting stenosis on limited evaluation.\n\nMRA BRAIN:\n\nThe study is limited by motion artifact.  The left internal carotid artery is\nbetter assessed on the gadolinium enhanced neck MRA and axial T1 weighted\nfat-suppressed images.  No evidence for flow-limiting stenosis is seen in the\nright internal carotid artery or other major intracranial arteries.  No\naneurysm larger than 3 mm is detected.  Left ___ complex is again noted,\na normal variant.\n\nMRV HEAD:\n\nThe superior sagittal sinus, the vein of ___, the straight sinus, bilateral\ntransverse sinuses, bilateral sigmoid sinuses and bilateral internal jugular\nveins are patent, as seen on the preceding CTA.  Left transverse and sigmoid\nsinuses are smaller than the right, consistent with normal anatomic variation.",
            "output": "1. Small focus of left parietal subarachnoid hemorrhage is again demonstrated.\nNo evidence for amyloid angiopathy is seen.  No clear evidence for a cavernous\nmalformation is demonstrated.  Please refer to the preceding head CTA report\nfor further observation and recommendations.\n2. Dissection of the distal cervical left internal carotid artery at the\nskullbase and of the horizontal portion of the petrous segment with acute to\nsubacute thrombus.  Other portions of the left internal carotid artery are\nsmall in caliber compared to the right, which may reflect diminished flow\nsecondary to the dissection, but chronic dissection of the more proximal\ncervical internal carotid artery cannot be excluded.\n3. Otherwise, neck MRA is technically limited due to poor timing and motion\nartifact.\n4. The motion limited MRA of the brain demonstrates no evidence for an\naneurysm larger than 3 mm, concordant with the preceding head CTA.\n5. No evidence of major dural venous sinus thrombosis.\n6. Fluid and secretions in the paranasal sinuses may be secondary to prolonged\nsupine positioning in the inpatient setting versus active sinusitis.  Please\ncorrelate with symptoms.\n\nRECOMMENDATION(S):  Please refer to the preceding head CTA report."
        },
        {
            "input": "Diffuse slow diffusion is seen throughout the bilateral basal ganglia, caudate\nnuclei, thalami, hippocampi by and cortex, consistent with anoxic brain\ninjury, associated with diffuse bilateral T2/FLAIR hyperintensity.  Punctate\nfoci of slow diffusion are seen within the left frontoparietal lobes, which\nmay be secondary to a superimposed embolic component.  There is no evidence of\nacute intracranial hemorrhage.  There is mild 5-mm descent of the cerebellar\ntonsils.\n\nSevere mucosal sinus thickening is seen involving the left maxillary sinus and\nmoderate mucositis thickening within the right maxillary sinus.  Moderate\nmucosal sinus thickening is seen involving the ethmoid air cells.  Moderate to\nsevere sinus disease is seen involving the sphenoid sinuses.  The principal\nvascular flow voids are well preserved.",
            "output": "1. Findings consistent with severe diffuse bilateral anoxic brain injury.\n2. Punctate foci of slow diffusion within the left frontoparietal lobes\nsuggests a superimposed embolic foci of infarction.\n3. Note is made of mild 5-mm descent of the cerebellar tonsils. Close clinical\nmonitoring is recommended given possible risk of tonsillar herniation from\ncerebral edema.\n4. No acute intracranial hemorrhage.\n\nNOTIFICATION:  The findings were discussed with Dr. ___. by ___\n___, M.D. on the telephone on ___ at 10:10 am, 5 minutes after\ndiscovery of the findings."
        },
        {
            "input": "Again the suprasellar partially cystic and solid mass identified compressing\nthe floor of the third ventricle. The sella appears normal in size. There is\nno intramuscular extension of the mass seen. The findings are most likely\nsecondary to a craniopharyngioma. Overall, there has been no significant\ninterval change since the previous MRI.",
            "output": "Partially cystic and solid suprasellar mass most likely secondary to\ncraniopharyngioma is again identified and unchanged from the outside MRI\nstudy. Examination is performed for surgical planning."
        },
        {
            "input": "This is a limited examination due to patient motion, only sagittal T1 and\ndiffusion-weighted images were obtained. The patient is status post right\nfrontotemporal craniotomy, small residual pneumocephalus is seen and expected\nafter the surgical procedure, areas of slow diffusion are demonstrated in the\nventral aspect of the right caudate nucleus as well as in the bilateral brain\nconvexities, suggesting acute/ subacute ischemic changes (for example image\n17, series 402 and image 27, series 402). The sagittal T1 weighted sequence is\nlimited due to patient motion, the size and shape of the previously noted\nsuprasellar mass lesion has decreased in size, correlation with axial T1 and\nT2 weighted images is recommended to further characterization.",
            "output": "1. The patient is status post suprasellar mass resection, postsurgical changes\nare visualized consistent with right frontotemporal craniotomy and residual\npneumocephalus as described above.\n\n2. Areas of slow diffusion are visualized in the ventral aspect of the right\nbasal ganglia involving the right caudate nucleus, and likely consistent with\nacute/subacute ischemic changes.\n\n3. The examination is partially limited due to patient motion, only sagittal\nT1 and diffusion weighted images were obtained, please consider repeat this\nstudy an obtained axial and T2 propeller sequences for further\ncharacterization.\n\nNOTIFICATION:  These findings were discovered and communicated in person with\nDr. ___ by Dr. ___ at 15:40 on ___."
        },
        {
            "input": "Patient is status post resection of a craniopharyngioma. Postsurgical changes\nwithin the suprasellar region are noted with blood products adjacent to the\nsurgical resection cavity within the right frontal periventricular white\nmatter. Residual enhancement is noted within the surgical bed. Patient is\nstatus post right frontal craniotomy. Extra-axial fluid collection is present\nmeasuring approximately 8.5 x 1.6 cm. There is associated dural thickening\nwithin this region, postoperative in nature.\n\nThere is no acute infarction or mass effect. The ventricles and sulci are\nnormal in size and configuration. The intracranial vessels are preserved. The\nglobes are intact. The cisterns are patent. There is no diffusion abnormality.",
            "output": "1. Status post resection of a suprasellar craniopharyngioma with expected\npostoperative changes including an extra-axial fluid collection at the right\nfrontal craniotomy site with dural thickening.\n2. Residual enhancement present within the surgical bed. Recommend attention\non followup."
        },
        {
            "input": "Exam is mildly limited by motion artifact.\n\nPostsurgical changes are noted from prior right frontal craniotomy and\ncraniopharyngioma resection. Trace blood products at the prior craniotomy site\nare unchanged. Previously seen right frontal extra-axial fluid collection has\nresolved. There is persistent to minimal dural thickening at the prior site of\ncraniotomy. There is mild residual gadolinium enhancement in the\ncraniopharyngioma resection bed, appearing similar to the prior examination.\n\nThere is no mass effect, or midline shift. Ventricles and sulci are\nage-appropriate.  Nonspecific periventricular white matter FLAIR\nhyperintensities are unchanged. The basal cisterns are patent. There is no\nfocus of slowed diffusion to suggest infarct. The brainstem, posterior fossa\nand cervicomedullary junction are preserved.  There is no new focus of\nintracranial enhancement. Intracranial flow voids are maintained.  Mucous\nretention cysts are noted in bilateral maxillary sinuses. Visualized paranasal\nsinuses are otherwise clear.  Small amount of fluid in the left mastoid air\ncells.",
            "output": "1. Interval resolution of a right frontal extra-axial fluid collection with\notherwise stable postoperative changes from craniopharyngioma resection.\n2. Stable residual enhancement within the resection bed."
        },
        {
            "input": "There has been a right frontotemporal craniotomy.  Enhancement within the\nsuprasellar operative bed is unchanged from MRIs on ___ and ___. There is no hydrocephalus. Ventricles, sulci, and cisterns are\nage-appropriate. Right frontotemporal and right frontal parasagittal\nextra-axial complex fluid/dural thickening is unchanged from MRI on ___. Fluid and dural enhancement are decreased in the right frontal region\ncompared to CT from ___, consistent with resolving postoperative\nchange.  A few foci of gradient susceptibility consistent with chronic\npostsurgical blood products are unchanged from prior MRI.  There is T2/FLAIR\nsignal within the right frontal lobe and right anterior temporal lobe\nsubjacent to the craniotomy, unchanged from prior MRI on ___ and\nconsistent with sequelae of prior surgery.\n\nMajor intravascular flow voids are preserved. There is normal enhancement of\nthe major intracranial arteries and dural venous sinuses following contrast\nadministration.\n\nThere is mucosal thickening of the ethmoid and maxillary sinuses, unchanged.\nThe paranasal sinuses otherwise appear clear. The mastoid air cells appear\nclear. The orbits are normal.",
            "output": "1. Stable residual mass within the suprasellar operative bed, unchanged from\nprior MRIs dating back to the first postoperative MRI with intravenous\ncontrast on ___.\n2.  Postsurgical changes of prior right frontotemporal craniotomy.  Right\nfrontotemporal lobe FLAIR signal is unchanged from prior MRI and consistent\nwith encephalomalacia.  Right frontal extra-axial fluid continues to decrease\nfrom prior MRIs."
        },
        {
            "input": "Please note the study is mildly degraded by motion. Patient is status post\nright frontotemporal craniotomy and resection of a craniopharyngioma. There is\npersistent enhancement within the suprasellar operative bed, not significantly\nchanged in appearance since prior study from ___. Scattered area of\nsusceptibility on gradient echo sequence within the suprasellar space is\nlikely from calcifications and chronic postsurgical blood products.\n\nThere is re-demonstration of a post-surgical right frontal extra-axial fluid\ncollection as well as dural thickening, not significantly changed in size\nsince prior study.\n\nThere is persistent T2/FLAIR hyperintensity within the right frontal lobe and\nright anterior temporal lobe. These are unchanged and consistent with sequelae\nof prior surgery. There are also areas of high signal within the right basal\nganglia, internal and external capsule which are likely areas of gliosis from\nprior infarcts.\n\nThere is no acute infarct, hemorrhage, or mass affect. The ventricles are\nunchanged in size and configuration. Major intracranial vascular flow voids\nare preserved. The dural venous sinuses are patent. There are mucous retention\ncysts within the bilateral maxillary sinuses as well as mucosal thickening in\nthe ethmoid air cells. The globes are unremarkable.",
            "output": "1.  No significant interval change to the residual enhancing mass within the\nsuprasellar operative bed.\n\n2.  Stable postsurgical changes from prior right frontotemporal craniotomy\nwith areas of high T2/FLAIR signal in the right temporal and frontal lobes. No\nsignificant change to the right frontal extra-axial fluid collection and dural\nthickening."
        },
        {
            "input": "Study is moderately degraded by motion.  There is residual cystic and solid\nenhancement centered at the infundibulum measuring 1.1 (AP) x 1.4 (TV) x 1.7\n(SI) cm  (see1300:62, 13:120), which is relatively unchanged.  There foci of\nsusceptibility within the suprasellar space consistent with chronic blood\nproducts and/or calcification.  There is right pterional craniotomy anatomy\nwith subjacent dural enhancement and foci of convexity chronic blood products.\nThere is overlying surgical scar.  There is stable right frontal\nencephalomalacia consistent with postsurgical changes.  There are no new or\nenlarging sites of enhancing disease.  The ventricles and extra-axial spaces\nare unremarkable.  There is no acute infarct, hemorrhage, or mass effect.  The\nvasculature is patent.  There is stable nonspecific dural enhancement on\npostcontrast imaging, which may be postoperative in nature.\n\nThe orbits are unremarkable.  There are bilateral maxillary mucous retention\ncysts versus polyps.  There is a trace left mastoid air cell effusion.",
            "output": "1.  Study is moderately degraded by motion.\n2. Grossly stable residual cystic and solid enhancing disease within the\nsuprasellar operative bed.\n3. Within limits of study, no new or enlarging sites of enhancing disease.\n4. Stable postsurgical changes from right pterional craniotomy.\n5. Paranasal sinus disease as described.\n\nRECOMMENDATION(S):  Recommend clinical correlation and followup imaging."
        },
        {
            "input": "Exam is motion degraded, particularly on the postcontrast sequences.\n\nPostoperative changes are again seen with right pterional craniotomy with\nencephalomalacia in the underlying right frontal lobe, presumably post\ntreatment related.  Thickening of of the pachymeninges underlining the\ncraniotomy is not unexpected.\n\nWithin limitation of motion, there has been no significant interval change. \nPersistent cystic lesion in the region of the infundibulum with areas of\nsurrounding enhancement is grossly unchanged in size and configuration, noting\nthat subtle interval change would be missed.\n\nThere is no acute infarct or visualized new mass.  There is no significant\nmass effect.  There is no new parenchymal signal abnormality.  Major\nintravascular flow voids are preserved.",
            "output": "Motion degraded exam.\nPersistent cystic lesion with regions of enhancement in the suprasellar region\nis grossly unchanged since ___."
        },
        {
            "input": "The patient is status post prior right frontal craniotomy with unchanged right\nfrontal and anterior temporal encephalomalacia and right greater than left\npostsurgical bifrontal dural thickening and enhancement.  Unchanged gradient\necho susceptibility in the suprasellar cistern is compatible with chronic\nhemorrhage product.  Residual heterogeneously enhancing mass with small cystic\ncomponents centered in the suprasellar cistern appears slightly increased in\nsize when compared to examination of ___ measuring approximately\n1.8 x 1.2 x 1.3 cm (TRV, AP, SI).  In particular, nodular component along the\nposterior aspect of the lesion has increased since ___.  Comparison\nto most immediate prior examination of ___ is suboptimal secondary\nto the degree of motion artifact on the prior study.  No new lesions are\nidentified.  There is no acute intracranial hemorrhage or infarct.\n\nThe major cranial flow voids are preserved.  The dural venous sinuses are\npatent.  A small mucous retention cyst in the left maxillary sinus and a\nmoderate mucous retention cyst in the right maxillary sinus is noted.  The\norbits are unremarkable.  The mastoid air cells are clear.",
            "output": "1. Persistent partially cystic enhancing suprasellar lesion measuring\napproximately 1.8 cm appears to demonstrate subtle increased size since\nexamination of ___.  In particular, nodular component along the\nposterior margin appears slightly more prominent.  Close attention on followup\nis recommended.\n2. No new lesions."
        },
        {
            "input": "Study is moderately degraded by motion.  Within these confines:\n\nStable changes status post right frontal craniotomy with associated right\nfrontal and anterior temporal volume loss and bifrontal dural thickening and\nenhancement.  No significant change in the residual heterogeneously enhancing\nmass centered within the suprasellar cistern, measuring 1.3  cm AP x 1.3 cm TV\nx 1.4 cm SI.  Redemonstrated is a small cystic component within the mass.  No\nnew lesions are identified.\n\nMild subcortical and periventricular FLAIR white matter hyperintensity likely\nrepresents a combination of post treatment change and chronic small vessel\nischemic disease given the patient's age.\n\nThere is no evidence of intracranial hemorrhage, midline shift or infarction.\n\nThe major intracranial vascular flow voids are maintained.  The ventricles and\nsulci are normal in caliber and configuration.  There is moderate mucosal\nthickening of the right maxillary sinus with superimposed aerosolized mucosal\nsecretions that can be seen in the setting of acute on chronic sinusitis. \nMinimal nonspecific left mastoid fluid is noted.",
            "output": "1.  Study is moderately degraded by motion.\n2. Grossly stable changes status post right frontal craniotomy for\ncraniopharyngioma resection with unchanged residual heterogeneous mass\ncentered within the suprasellar cistern.  On follow-up imaging, consider\ndedicated sella MRI imaging for further evaluation.\n3.  Paranasal sinus disease suggestive of acute and chronic sinusitis, as\ndescribed.\n4. Nonspecific small left mastoid fluid.\n5. Mild subcortical and periventricular FLAIR white matter hyperintensity\nlikely represents a combination of post treatment change and chronic small\nvessel ischemic disease given the patient's age."
        },
        {
            "input": "MR BRAIN:\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.\n\nThere are T2/FLAIR hyperintensities in the periventricular, subcortical and\ndeep white matter and in the pons, nonspecific, likely secondary to small\nvessel ischemic changes.\n\nNonspecific fluid opacification of bilateral mastoid air cells.  The\nvisualized paranasal sinuses are clear.  The orbits are unremarkable noting\nbilateral prior cataract surgeries.\n\nMRA brain:  There is evidence of vascular flow in both internal carotid\narteries as well as the vertebrobasilar system.  , there is mild irregular\ncontour of the right middle cerebral artery (image 10, series 100), suggestive\nof arthrosclerotic disease similar however less conspicuous findings are\nidentified on the left middle cerebral artery.",
            "output": "1. Findings of small vessel ischemic changes.  Otherwise, unremarkable MRI of\nthe brain.\n2. Arteriosclerotic disease demonstrated by MRA of the head, more significant\nin the middle cerebral arteries as described above, with no aneurysm greater\nthan 4 mm.\n3. Nonspecific bilateral mastoid fluid opacification."
        },
        {
            "input": "There is no abnormal signal on diffusion-weighted imaging to suggest acute\ninfarction. Intracranial flow voids are preserved. Mild periventricular white\nmatter hyperintensities are nonspecific, but could be due to minimal early\nchanges of small vessel ischemic disease. The ventricles and sulci are normal\nin size and configuration. There is no extra-axial fluid collection. Paranasal\nsinuses, mastoid air cells, middle ear cavities are clear.",
            "output": "No evidence of acute infarction."
        },
        {
            "input": "Images of the pituitary appear normal. The pituitary signal intensity appears\nnormal before and after contrast administration. No masses are identified. The\nsuprasellar cistern and cavernous sinuses appear normal. The limited portion\nof the brain included on this study appears normal.\n\nThere is a large retention cyst in the right maxillary sinus and mild mucosal\nthickening in the left maxillary sinus.  There is a small retention cyst and\ntrace mucosal thickening in the left sphenoid sinus.",
            "output": "1. No evidence of a pituitary lesion.\n2. Retention cysts and mucosal thickening in the paranasal sinuses, as\ndetailed above."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.  Retention cyst right maxillary sinus, trace mucosal\nthickening left maxillary sinus.  Clear mastoids.  Preserved vascular flow\nvoids.  Patent dural venous sinuses.",
            "output": "1. Normal intracranial contents.\n2. Paranasal sinus disease."
        },
        {
            "input": "There is no acute infarction, intracranial hemorrhage, extracerebral fluid\ncollection, midline shift or mass effect.  Ventricles and extra-axial spaces\nare normal in size.  Flow voids are maintained. Suprasellar and craniocervical\nregions are unremarkable.\nVisualized paranasal sinuses are clear.",
            "output": "No significant abnormalities are seen on MRI of the brain without gadolinium."
        },
        {
            "input": "There is no evidence of intracranial hemorrhage, edema, masses, mass effect,\nmidline shift or infarction. The pituitary stalk is thickened and measures up\nto 6 mm (900:82), while this finding is nonspecific but may be medication\nrelated, the possibility of hypophysitis is a consideration in the appropriate\nclinical setting, otherwise, there is no evidence of confluent diffusion\nrestriction or increased T2/FLAIR signal within the periventricular or deep\nwhite matter to suggest toxic leukoencephalopathy.  There are few scattered\nbilateral punctate foci of periventricular and subcortical white matter FLAIR\nhyperintensities, most consistent with sequelae of chronic small vessel\nischemic disease.  The ventricles and sulci are prominent, compatible with\nage-related involutional changes.\n\nThere are no osseous lesions.  The orbits are unremarkable.  There is\nincreased T2 signal within the left posterior ethmoid air cell, consistent\nwith mild sinus disease.  Otherwise, the visualized paranasal sinuses are\nunremarkable.  The mastoid air cells and middle ear cavities are clear.",
            "output": "1. Thickening of the pituitary stalk is nonspecific, but may be medication\nrelated, in the appropriate clinical setting hypophysitis is a consideration,\nplease correlate.  No additional findings to suggest toxic\nleukoencephalopathy. If available, comparison with prior MRI imaging can be\nperformed.\n2. No evidence of acute territorial infarction, intracranial hemorrhage, or\nmass identified.\n3. Chronic microangiopathic and involutional changes."
        },
        {
            "input": "There is persistent thickening of the pituitary stalk measuring up to\napproximately 6 mm.  This is similar to the previous examinations.  Elsewhere,\nthere is no abnormal enhancement after contrast administration.\n\nThere is no evidence of hemorrhage, edema, mass effect, midline shift or\ninfarction.   The ventricles and sulci are prominent reflecting volume loss. \nThere are scattered areas of nonspecific T2/FLAIR hyperintensity in the\nsubcortical and periventricular white matter which are nonspecific but\nprobably reflect chronic small vessel disease in this age group.\n\nNo focal osseous lesions are demonstrated.  The major intracranial vascular\nflow voids are preserved.  Orbits are unremarkable.  There is mucosal\nthickening throughout the imaged paranasal sinuses, and fluid in the bilateral\nmaxillary sinuses..",
            "output": "1. Persistent thickening of the pituitary infundibulum.  Differential\nconsiderations are unchanged, again including lymphoma, lymphocytic\nhypophysitis, neurosarcoidosis, metastatic lesions, or medication effects.\n2. No new abnormality or acute intracranial findings.\n3. Paranasal sinus disease with increased mucosal thickening and fluid in the\nmaxillary sinuses."
        },
        {
            "input": "There is a small focus of for slow diffusion in the right occipital lobe best\nvisualized on series 10, image 15 indicative of an acute infarct in the\ndistribution of right posterior cerebral artery.  There are no blood products\nidentified on susceptibility images.  There is no mass effect midline shift or\nhydrocephalus.  Suprasellar and craniocervical regions are unremarkable.\n\nMRA of the head shows normal signal in the arteries of the anterior and\nposterior circulation. No evidence of vascular occlusion stenosis or an\naneurysm greater than 3 mm in size seen.\n\nMRA of the neck shows normal flow in the carotid and vertebral arteries. No\nevidence of stenosis or occlusion or dissection seen.  Fat-suppressed axial\nimages demonstrate no evidence of blood products adjacent to the vertebral\nflow voids to indicate dissection.",
            "output": "Small area of acute infarct in the right posterior cerebral artery\ndistribution in the right occipital lobe.  No significant abnormalities are\nseen on MRA of the head and neck."
        },
        {
            "input": "There is no evidence of acute intracranial hemorrhage or infarction.  There is\nno evidence of midline shift.  Ventricles and sulci are age appropriate. \nPeriventricular deep subcortical FLAIR white matter hyperintensities are\nlikely sequelae of chronic microangiopathy.\n\nA punctate 2 mm enhancing lesion is seen within the right occipital lobe,\nseries 900, image 81 and series 9, image 150, with subtle associated FLAIR\nsignal abnormality.\n\nThe principal dural venous sinuses are patent.\n\nMild mucosal sinus thickening is seen involving the ethmoid air cells. \nRemainder of the visualized paranasal sinuses, mastoid air cells, and middle\near cavities are clear.  The globes are unremarkable.  The principal vascular\nflow voids appear to be well preserved.",
            "output": "1. Focal 2 mm enhancing lesion is seen within the right occipital lobe\n(900;81) and (9;148), with subtle associated increased FLAIR signal\nabnormality.\n2. No acute intracranial abnormalities identified.  Mild chronic\nmicroangiopathy.\n3. Mild paranasal sinus disease.\n\nRECOMMENDATION(S):  A 3-month follow up with brain MRI is recommended for\nfurther evaluation.\n\nNOTIFICATION:  The impression and recommendation above was entered by Dr.\n___ on ___ at 13:38 into the Department of Radiology critical\ncommunications system for direct communication to the referring provider."
        },
        {
            "input": "Images are mildly limited by motion artifact.\n\nIn the right superior cerebellar vermis, there is a 7 mm round lesion with\ncentral fluid signal intensity and eccentric rim enhancement which is most\nthick medially, images 901:89 900:40, 10:8, 7:8, 8:8.  Please note that the\nmeasurement of 7 mm is obtained on the coronal MP RAGE image 901:89.  There is\nno surrounding edema.  No other enhancing lesions are seen.\n\nThere is no pathologic leptomeningeal or pachymeningeal contrast enhancement.\n\nThere is a  developmental venous anomaly in the right cerebellar hemisphere. \nA small focus of susceptibility artifact in the right cerebellar hemisphere\nmedial to the developmental venous anomaly, image 6:6, is suggestive of a\ncavernous angioma given the proximity to the developmental venous anomaly.\n\nNo susceptibility artifact is seen elsewhere in the brain parenchyma.  There\nis no edema or acute diffusion abnormality.\n\nVentricles, sulci, and basal cisterns are age appropriate.\n\nMajor arterial flow voids appear grossly preserved.  Major dural venous\nsinuses appear patent on postcontrast MP RAGE images.\n\nThere is mild mucosal thickening in the ethmoid air cells.  There is moderate\nright and near complete left mastoid air cell opacification.",
            "output": "1. 7 mm round rim enhancing lesion in the right superior cerebellar vermis,\nconcerning for a metastasis, which may be leptomeningeal given the absence of\nsurrounding edema.  No other enhancing lesions and no pathologic\nleptomeningeal contrast enhancement seen.\n2. Developmental venous anomaly in the right cerebellar hemisphere.  Small\nfocus of susceptibility artifact in the right cerebellar hemisphere medial to\nthe developmental venous anomaly is suggestive of a cavernous angioma, given\nthe proximity to the developmental venous anomaly.  A chronic microhemorrhage\nis less likely.\n\nNOTIFICATION:  The impression above was entered by Dr. ___ on\n___ at approximately 09:30 into the Department of Radiology critical\ncommunications system for direct communication to the referring provider."
        },
        {
            "input": "There is a focus of contrast enhancement in the left cerebellar hemisphere,\nseen best on series 900b, image 32, which is not re- demonstrated on the spin\necho postcontrast sequences.  Stable minimal nodular enhancement is noted\nalong the right cerebellar folia, best seen on series 9, image 94 and series\n900b, image 41.  There is a new 0.6 cm x 0.6 cm peripherally contrast\nenhancing mass with minimal surrounding FLAIR hyperintense signal in the right\nsuperior frontal gyrus, seen best on series 900b, image 85, with low signal on\ngradient echo imaging.\n\nThere is no evidence of mass effect, midline shift or infarction.   The\nventricles and sulci are normal in caliber and configuration.  The major\nvascular flow voids are preserved.  A right cerebellar developmental venous\nanomaly is seen.  A focus of low signal is noted in the right cerebellar\nhemisphere, adjacent to the developmental venous anomaly.\n\nThere is heterogeneous signal throughout the calvarium and partially\nvisualized in the upper cervical spine.\n\nThere is partial opacification of the mastoid air cells.  The orbits are\nnormal.  Mild mucosal thickening is seen in the ethmoid sinus.  Degenerative\nchanges with subchondral cysts are noted in the left temporomandibular joint.",
            "output": "1. New 0.6 cm right superior frontal gyral lesion with internal chronic blood\nproducts and minimal surrounding edema, consistent with new metastatic lesion.\nNo new metastatic lesions identified.\n2. Stable leptomeningeal enhancement along the right cerebellar folia,\nconsistent with stable metastatic disease.\n3. Probable right cerebellar cavernoma and adjacent developmental venous\nanomaly.\n4. Abnormal bone marrow signal throughout the calvarium and partially within\nthe visualized upper cervical spine, which may represent infiltrative bony\nmetastatic disease.\n5. Soft tissue enhancement surrounding the spinous process of C2 vertebra as\ndemonstrated on the previous CT of ___.\n\nNOTIFICATION:  The findings were discussed with ___, M.D. by ___\n___, M.D. on the telephone on ___ at 3:57 ___, 5 minutes after\ndiscovery of the findings."
        },
        {
            "input": "In the area of previously demonstrated hyperdensity along the undersurface of\nthe left tentorium, there is an extra-axial soft tissue nodule measuring 8 x 4\nmm (03:18 on sagittal ___, which demonstrates homogeneous enhancement\n(9:65, 901:130).  This soft tissue mass is likely dural-based, adjacent to the\nleft transverse sinus, and not within the sinus.  The dural venous sinuses\ndemonstrate normal enhancement, including the left transverse sinus.  This\nsoft tissue nodule appears stable since ___.\n\nThere is stable minimal enhancement along the right cerebellar folia with a\nprominent vein, likely a DVA (9:83). There is stable focus of susceptibility\nartifact adjacent to the vein (6:8).  The right superior frontal gyrus lesion\nwith nodular enhancement, and demonstrating susceptibility artifact is stable\nand measures up to 6 mm. A focus of contrast enhancement in the left\ncerebellar hemisphere is not demonstrated on today's exam.    The ventricles\nand sulci are normal in caliber and configuration.\n\nHeterogeneous bone marrow signal of the calvarium and included views of the\ncervical spine is likely due to metastatic osseous disease.  T1 hyperintense\nbone marrow signal within the clivus, C1, C2 and part of C3 is likely due to\nprior radiation therapy.  Left mastoid air cell opacification is likely also\nsequela of prior radiation therapy.  The orbits are normal.  Degenerative\nchanges of the left temporomandibular joint is stable.",
            "output": "1. Extra -axial enhancing soft tissue nodule along the left tentorium,\nadjacent to the left transverse sinus, measuring up to 8 mm, presumably\nmetastatic disease from melanoma given the extent of disease elsewhere. \nHowever, the differential includes meningioma.  Stable since ___.\n2. Patent dural venous sinuses.\n3. Stable right superior frontal gyrus lesion.\n4. Stable osseous metastatic disease.\n5. No evidence of infarction."
        },
        {
            "input": "Previously noted enhancement associated with a 6 mm hemorrhagic lesion in the\nright paramedian frontal lobe has decreased (108:115).  A hemorrhagic focus in\nthe right cerebellar hemisphere has slightly increased in size compared to\nprior examination and shows slightly more prominent enhancement, measuring 3\nmm (100a: 66).  At least one additional punctate hemorrhagic focus in the left\ncerebellar hemisphere with equivocal enhancement was not appreciated on the\nprior study (100a:59).\n\nThere is no evidence of acute infarction.  There is no mass effect or shift of\nnormally midline structures.  The ventricles are age-appropriate.  Principal\nintracranial vascular flow voids are preserved.  Dural venous sinuses enhance\nappropriately on postcontrast MP RAGE sequences.  A presumed developmental\nvenous anomaly is again noted in the right cerebellum.\n\nPartially empty sella is unchanged.  Fluid opacification of the left mastoid\nair cells has improved compared to the prior examination.  Opacification of\nthe right mastoids is grossly unchanged.  Orbits are unremarkable.\n\nPartially imaged upper cervical spine demonstrating hypointense signal on T1\nweighted images with heterogeneous enhancement is consistent with known\nmetastatic disease, as seen on recent dedicated cervical spine MRI of ___.",
            "output": "1. No new enhancing lesions are seen.\n2. Slightly decreased enhancement associated with 6 mm hemorrhagic right\nparamedian frontal lesion.\n3. Right cerebellar blood products an associated developmental venous anomaly\nare unchanged although the products are better visualized on the current study\nlikely due to differences in technique\n4. New apparent punctate microhemorrhage in the left cerebellar hemisphere\ncould be at the site of previously treated metastatic disease.\n5. Metastatic disease in partially imaged upper cervical spine.\n6. No evidence of traumatic injury."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.\nThere is no abnormal enhancement after contrast administration.\n\nThe ventricles and sulci are normal in caliber and configuration.\nMajor vascular flow voids are preserved.  Major dural venous sinuses are\npatent.\n\nThere is mild mucosal thickening along the ethmoid air cells and left\nmaxillary sinus.  The mastoid air cells appear centrally clear.  The orbits\nappear grossly unremarkable.",
            "output": "1. No evidence of acute infarction, intracranial hemorrhage or mass.\n2. Patent dural venous sinuses."
        },
        {
            "input": "Please note the study is mildly degraded by motion.\n\nThere is an ill-defined region of FLAIR signal hyperintensity in the right\nperiventricular white matter and corona radiata measuring approximately 2.6\n(AP) x 2.0 (TV) x 1.6 (SI) cm (300:112, 3:112 ).  On the sagittal postcontrast\nimages, the region of FLAIR hyperintensity has an orientation that is\nrelatively perpendicular to the right lateral ventricle.\n\nA smaller region of FLAIR hyperintensity is also present in the superior left\nfrontal subcortical white matter (300:131).  There is no slow diffusion or\ndefinite enhancement in these areas.\n\nThere is no evidence of hemorrhage,  mass, mass effect, midline shift or\ninfarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  Principal intracranial vascular flow voids are preserved and\narteries of the circle of ___ and dural venous sinuses enhance\nappropriately after contrast administration.  There is no abnormal\nenhancement.",
            "output": "1.  Study is mildly degraded by motion.\n2. Please note that no prior imaging was submitted for direct comparison.\n3. Nonspecific nonenhancing white matter lesions as described, compatible with\nreported history of multiple sclerosis.  Differential considerations include\nsequela of prior trauma or infection, history of migraine headaches,\ninflammatory process, and microangiopathic changes."
        },
        {
            "input": "Postcontrast MP RAGE images are limited by motion artifact.\n\nPunctate T2 hyperintense focus in the left parietal deep white matter on\nimages 4:46 and 400:74 is likely unchanged allowing for pulsation artifact in\nthis area on the prior 3D FLAIR images.  Additional foci of high T2 signal in\nthe left posterior frontal subcortical white matter on images 4:58-59 and\n400:85, in the corpus callosum, and right pericallosal white matter (4:98,\n400:77) are also unchanged.  There is no associated contrast enhancement or\nslow diffusion.\n\nSmall T2 hyperintense focus in the right pons on images 4:88, 8:19, was not\ndefinitively seen previously; there is no associated contrast enhancement or\nslow diffusion.\n\nMild thinning of the corpus callosum is nonspecific and may be age-related,\nthough it could be related to demyelinating disease.  Remaining parenchymal\nvolume is normal for age with normal size of the ventricles, sulci, and basal\ncisterns.\n\nThere is no evidence for an intracranial mass, acute infarction, parenchymal\nedema, or blood products.  Major vascular flow voids are grossly preserved. \nDural venous sinuses appear patent on postcontrast MP RAGE images.\n\nMild mucosal thickening in the ethmoid air cells.",
            "output": "1. Stable T2 hyperintense foci in the supratentorial white matter, with\ndistribution compatible with multiple sclerosis, though sequela of chronic\nsmall vessel ischemic disease are also statistically likely in this age group.\n2. New, non-acute, nonenhancing small T2 hyperintense focus in the right pons,\nwhich may represent a new demyelinating lesion versus a new chronic small\nvessel infarct given the patient's age."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  There is prominence of the ventricles and sulci suggestive\ninvolutional changes.  There is a single focus of FLAIR hyperintense signal in\nthe posterior right frontal gyrus rectus (image 14, series 7) which is\nnonspecific and may reflect gliotic change.  There is no abnormal enhancement\nafter contrast administration.  The major vascular flow voids are preserved.\n\nThe orbits, paranasal sinuses and mastoids are normal.  The visualized soft\ntissues are normal.",
            "output": "1. Senescent volume loss with no evidence for an intracranial mass, hemorrhage\nor acute infarct."
        },
        {
            "input": "Study is mildly degraded by motion.\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  The ventricles and sulci are prominent, with the degree of\nprominence of the lateral and third ventricle somewhat disproportionate with\nrespect to the degree of sulcal prominence in the degree of prominence of the\nfourth ventricle although no obstructing lesion is seen at the cerebral\naqueduct.  No increased flow void is seen at the cerebral aqueduct.\n\nThere are patchy T2/FLAIR hyperintensities throughout the subcortical and\nperiventricular white matter and in the pons which are nonspecific but most\nlikely reflect chronic microangiopathy in this age group.  There is a focus of\nsusceptibility in the left frontal operculum on image 12 of series 6. \nAdditional susceptibility in the medial superior left parietal lobe on image\n18 of series 6.  There is no abnormal enhancement after contrast\nadministration.\n\nThe major intracranial vascular flow voids are preserved.  Orbits are\nunremarkable.  There is scattered mucosal thickening throughout the ethmoid\nair cells.  The visualized extracranial soft tissues are unremarkable.",
            "output": "1. Prominence of the ventricles appears somewhat disproportionate with respect\nto the degree of sulcal prominence, which could reflect central atrophy. \nNormal pressure hydrocephalus is also a consideration in the appropriate\nclinical setting.\n2.   Mild to moderate nonspecific white matter signal changes which most\nlikely reflect chronic microangiopathy in this age group.\n3. Punctate areas of susceptibility may reflect chronic microhemorrhage.\n4. No enhancing lesions."
        },
        {
            "input": "The study is limited by motion artifact.  There is no evidence of acute\nhemorrhage, edema, masses, mass effect, midline shift or infarction.  There\nare punctate focus of susceptibility in the left frontal operculum and medial\nsuperior left parietal lobe, unchanged from prior study (11:11, 11:6), there\nare bilateral periventricular and subcortical T2/FLAIR white matter\nhyperintensities, nonspecific but compatible with sequelae of chronic small\nvessel ischemic disease.  The ventricles again demonstrate prominence out of\nproportion to the sulci, without evidence of obstruction and not substantially\nchanged from prior study.  There is no abnormal enhancement after contrast\nadministration.\n\nThe major intracranial flow voids are preserved.  The orbits are unremarkable.\nThe visualized paranasal sinuses, mastoid air cells and middle ear cavities\nare clear.  Mild degenerative changes are visualized at C2-C3 level consistent\nwith posterior disc bulging, partially evaluated this exam.",
            "output": "1. No evidence of acute infarction, intracranial mass, or abnormal\nenhancement.\n2. Redemonstration prominence of the ventricles out of proportion to the sulci\nwithout evidence of obstruction, not substantially changed from prior study\nand suggestive of central atrophy.  Alternatively, findings may represent\nnormal pressure hydrocephalus in the appropriate clinical setting.\n3. Punctate foci of susceptibility in the left frontal and left parietal lobes\nare unchanged, compatible with chronic microhemorrhage.\n4. Stable chronic microangiopathic changes."
        },
        {
            "input": "Multiple periventricular and subcortical white matter foci of T2/FLAIR signal\nhyperintensity, nonspecific and likely sequelae of chronic ischemic\nmicrovascular disease.  There is no evidence of acute intracranial hemorrhage,\nedema, masses, mass effect, midline shift or infarction.  Sulci are slightly\nprominent suggesting mild cortical volume loss, likely involutional nature, no\ndiffusion abnormalities are detected.  There is no abnormal enhancement after\ncontrast administration, specifically there is no evidence of leptomeningeal\nor pachymeningeal enhancement.\n\nThe major vascular flow voids are present and demonstrate normal distribution.\nThe orbits appear normal.  Mild mucosal thickening within the frontal sinus\nand multiple ethmoid air cells is noted.",
            "output": "1. There is no evidence of acute intracranial process or hemorrhage, there is\nno evidence of abnormal enhancement after contrast administration.\n2. Moderate periventricular and subcortical white matter T2/FLAIR signal\nchanges, nonspecific and likely sequelae of chronic microvascular disease in\npatients of this age group.\n3. Paranasal sinus disease as above."
        },
        {
            "input": "Images through the internal auditory canal demonstrates symmetric appearance\nof the seventh eighth nerve complexes.  There is no evidence of abnormal\nenhancement or mass lesion within the internal auditory canals,\ncerebellopontine angles or membranous labyrinth.  The trigeminal nerves are\nnormal in caliber and do not show abnormal enhancement.  There is no evidence\nof vascular compression at the root entry zones of the trigeminal nerves.  No\nother mass lesions are seen within the posterior fossa.\n\nLimited included imaging of the remainder of the brain demonstrates no\nevidence of hemorrhage, edema, masses, mass effect, midline shift or\ninfarction. The ventricles and sulci are normal in caliber and configuration.\nThere is no abnormal enhancement after contrast administration.\n\nNo osseous abnormalities are seen.  There is near-complete opacification of\nthe left maxillary sinus secondary to mucosal thickening.  The orbits are\nunremarkable. The visualized portion of the principle vascular flow voids are\npreserved.\n\nBrain MRA:  There is no evidence of occlusion, flow-limiting stenosis, or\naneurysm involving the circle of ___ and its major tributaries.",
            "output": "1.  No evidence of a cerebellopontine angle mass.  The cisternal portion of\nthe trigeminal nerve and cranial nerve seventh and eighth complexes appear\nnormal.  There is no abnormal enhancement.\n\n2.  There is no evidence of neurovascular compression of the trigeminal\nnerves.\n\n3.  There is near complete opacification of the left maxillary sinus. \nClinical correlation with patient's symptoms is recommended.\n\n4.  Unremarkable brain MRA."
        },
        {
            "input": "There is no acute infarction, intracranial hemorrhage, extracerebral fluid\ncollection, midline shift or mass effect.  The cerebral volume is appropriate\nfor the patient's stated age.  No diffusion abnormalities are detected. Flow\nvoids are maintained.",
            "output": "Unremarkable unenhanced MRI of the brain."
        },
        {
            "input": "There is no evidence of acute intracranial hemorrhage or mass effect. The\nventricles and basal cisterns appear normal.\n\nThere is no evidence of acute ischemia based on diffusion-weighted imaging.\nThere are normal vascular flow voids.  There is subcortical T2/FLAIR white\nmatter hyperintensity which is nonspecific although is presumably sequelae of\nchronic small vessel ischemic disease.\n\nThere is no abnormal brain parenchymal or leptomeningeal enhancement.\n\nThe orbits, skull base, and paranasal sinuses appear unremarkable Ke Ke.",
            "output": "1. No evidence of acute intracranial hemorrhage, mass effect, or acute\nischemia.\n2. Presumed sequelae of chronic small vessel ischemic disease."
        },
        {
            "input": "Motion artifact significantly degrades the diagnostic quality of the imaging.\n\nPRE AND POSTCONTRAST T1 BRAIN IMAGING:\nLeft occipitotemporal intraparenchymal hemorrhage measuring 53 (AP) by 29 (TV)\nby 28 mm (cc) is T2 hypointense, T1 Iso to hyperintense with blooming on the\ngradient echo sequence.  Mass effect with effacement of the inferior aspect of\nthe occipital horn of the left lateral ventricle and displacement of the\nposterior aspect of the falx to the right by 6 mm.  There is intraventricular\nextension of the hemorrhage into the occipital horn of the left lateral\nventricle.  Associated subarachnoid component as evidenced by hyperintense\nsignal intensity in the occipital and temporal sulci bilateral.  Minimal\nsurrounding vasogenic edema.\nPeriventricular and deep white matter hyperintense changes are most likely\nsecondary to microangiopathy.\nNo slow diffusion.  No abnormal enhancing masses in relation to the\nhemorrhage. There is an area of poor opacification of the left transverse\nsinus which is difficult to evaluate due to the significant motion artifact,\nand may represent thrombosis or poor opacification due to mass effect from the\nlocal hemorrhage aggravated by motion artifact.\nThe orbits appear normal.  Mild mucosal thickening involving the ethmoid air\ncells.  The visualized intracranial arteries demonstrate normal T2 flow voids.\n\n\nMRA BRAIN:\nWithin the limitations of the study the intracranial vertebral and internal\ncarotid arteries and their major branchesappear patentwithout evidence\nofsignificant stenosis,occlusion,oraneurysm formation.  No vascular\nmalformation visualized in the area of the left occipitotemporal hemorrhage. \nHypoplastic left A1 segment with an azygos ACA which bifurcates in its A2\nsegment.",
            "output": "1. Left occipitotemporal intraparenchymal hemorrhage measuring 53 x 29 x 28 mm\nwith associated intraventricular extension and subarachnoid component as\ndescribed above.\n2. Please take note of significant image degradation by motion artifact,\nwithin the limitations of the study there is no obvious mass or underlying\nvascular malformation visualized in the area of the hemorrhage.\n3. There is poor opacification of the left transverse sinus which is\nequivocal.  This may be secondary to thrombosis or due to mass effect of the\nhemorrhage on the sinus aggravated by motion artifact.  No obvious features of\ndural sinus thrombosis prior CT done ___"
        },
        {
            "input": "Note is made of cerebellar tonsillar ectopia with the cerebellar tonsils\nextending approximately 3-4 mm below the level of the foramen magnum which\nresult in mild crowding.\n\nThere are innumerable enhancing lesions throughout the cerebellum, within the\nleft aspect of the pons as well as several punctate foci of enhancement\nthroughout the cerebellar hemispheres bilaterally, consistent with metastatic\nlesions.\nSome of these metastatic lesions demonstrate surrounding edema which in\naddition to the crowding at the foramina magnum exhibits some mass effect that\nresults in narrowing of the fourth ventricle.\n\nThe supratentorial ventricular system appears prominent with the third\nventricle measuring up to 10 mm in maximum transverse dimension.  The degree\nof hydrocephalus is unchanged compared to the prior exam.\n\nSingle punctate focus of DWI hyperintensity in the right frontal lobe (series\n4, image 24) without ADC correlate is consistent with a metastatic lesion.\n\nThere are several enhancing scalp lesions with central necrotic component with\nthe largest, partially exophytic lesion arising superiorly to the right ear\nand measuring 2.4 x 2.1 x 2.2 cm (AP X TR X SI) additional lesions are seen in\nthe right frontotemporal region (series 12, image 13) as well as adjacent to\nthe left orbit (series 12, image 11).\n\nThere is a mucous retention cyst along the floor of the right maxillary sinus.\nThere is partial opacification of the bilateral mastoid air cells, left\ngreater than right.  The orbits appear unremarkable.",
            "output": "1. Innumerable infra-and supratentorial metastatic lesions.\n2. Several metastatic scalp lesions identified, with the largest, partially\nexophytic lesion superiorly to the right ear.\n3. Cerebellar tonsillar ectopia with mild crowding at the level of the foramen\nmagnum.\n4. Small fourth ventricle, likely due to a combination of the previously\nmentioned cerebellar tonsillar ectopia and mass effect from the several\ncerebellar metastatic lesions.  Continued close clinical surveillance is\nrecommended given high concern for potential tonsillar herniation.\n5. Prominence of the supratentorial ventricular system suggests obstructive\nhydrocephalus, overall similar in appearance compared to the prior exam.\n\nRECOMMENDATION(S):  Continued close clinical surveillance is recommended given\nhigh concern for potential tonsillar herniation."
        },
        {
            "input": "In comparison with the most recent MRI examination, there is a new focus of\nslow diffusion in the left centrum semiovale, extending inferiorly towards the\ncingulate gyrus suggestive of subacute ischemic changes which is also visible\non T2 and FLAIR images, there is a slightly smaller focus of slow diffusion in\nthe left side of pons (series 502, image 9).  There is interval improvement in\nthe numerous (more than 10 lesions), posterior fossa nodular enhancing\nlesions, with decreased pattern of edema and tonsillar ectopia,\nsupratentorially the previously noted nodular enhancing lesions are less\nconspicuous and difficult to assess, for example the subependymal lesion\nidentified on the lateral aspect of the right lateral ventricle is not longer\nseen 12 focal punctate enhancing lesion in the left parietal convexity appears\nsmaller (series 8, image 135), and measures approximately 2 x 2 mm in\ntransverse dimension.  The ventricles and sulci are slightly prominent\nsuggesting mild cortical volume loss, probably related with posttreatment\nchanges.  The major vascular flow voids are present and demonstrate normal\ndistribution.  There is persistent opacification of the left mastoid air\ncells, the eye globes appear intact, the paranasal sinuses are clear.  Nodular\nscalp and 2 x 2 cm soft tissue lesions identified in the right temporal\nregion,  adjacent to the left orbit (series 10, image 8), anterior to the left\nmasticator space (series 10, image 6), and left inferior sphenoidal wing\n(remain grossly unchanged (series 10, image 12).",
            "output": "1.  Interval decrease in size and edema pattern in the numerous infra and\nsupratentorial metastatic lesions as described detail above.  Grossly no new\nlesions or new areas with abnormal enhancement are seen.\n\n2.  New focus of slow diffusion is identified in the left centrum semiovale\nextending towards the left cingulate gyrus suggestive of subacute ischemic\nchanges, visible on T2 and FLAIR images.\n\n3.  Slightly smaller right pontine focus of slow diffusion.\n\n4.  Soft tissue/scalp and bony lesions in the right temporal region, and\nadjacent to the left orbit/left sphenoid wing remain grossly unchanged."
        },
        {
            "input": "There is a 3 cm lesion with peripheral and internal enhancement within the\nright superior.  The lesion and associated vasogenic edema result in local\nmass effect with leftward displacement of the falx, inferior displacement of\nthe body of the corpus callosum, and narrowing of the right lateral ventricle.\nThe basilar cisterns are patent.\n\nThere is a 3 mm inferiorly directed aneurysm from the supraclinoid segment of\nthe left ICA, likely a superior hypophyseal artery aneurysm (image 3, series\n16).\n\nNo other enhancing lesions are identified.\n\nNo acute infarction is identified.\n\nThe orbits are unremarkable.",
            "output": "1. 3 cm enhancing lesion within the right superior frontal gyrus with marked\nvasogenic edema and trace blood products.  Mass effect with leftward\ndisplacement of the falx, inferior displacement of the body of the corpus\ncallosum, and narrowing of the right lateral ventricle.  The basilar cisterns\nare patent.  Given the clinical history, this lesion is highly suspicious for\nmetastatic disease.\n2. No other enhancing lesions are identified.\n3. 3 mm left superior hypophyseal artery aneurysm."
        },
        {
            "input": "MRI Brain:\nThere is chronic encephalomalacia in the left frontal lobe including the\ninsular cortex with resultant ex vacuo dilatation of the left lateral\nventricle and sylvian fissure.  Asymmetric decrease in size of the left\nmidbrain is seen.  Periventricular and subcortical T2 and FLAIR\nhyperintensities are noted. There is no evidence of hemorrhage, edema, masses,\nmass effect, midline shift or infarction.   The ventricles and sulci are\nprominent.  Minimal fluid is seen in the left mastoid air cells.  Minimal\nmucosal thickening of the ethmoid sinuses is seen.  Bilateral cataract\nextractions are noted.\n\nMRA brain:  There is stable decreased flow related enhancement in the left\npetrous and cavernous internal carotid arteries, as seen on the prior CTA. \nThere is also decreased paucity of flow related signal to the left frontal\nlobe secondary to encephalomalacia.  There is artifactual appearance of a\nsmall outpouching at the left posterior communicating and cerebral artery\njunction secondary to motion artifact.  This was not seen on CTA performed in\n___.  Otherwise, the intracranial vertebral and internal carotid arteries and\ntheir major branches appear normal without evidence of stenosis, occlusion, or\naneurysm formation.\n\nMRA neck:  There is stable complete occlusion of the left common carotid\nartery which reconstitutes at the level of the carotid bulb with diminutive\nappearance of the left internal carotid artery.  The right common, internal\nand external carotid arteries appear normal.  There is no evidence of internal\ncarotid artery stenosis by NASCET criteria.  The origins of the great vessels,\nsubclavian and vertebral arteries appear normal bilaterally.",
            "output": "1. Chronic encephalomalacia in the left frontal lobe with associated wallerian\ndegeneration of the left midbrain.  White matter signal abnormalities most\nconsistent with chronic microvascular ischemic changes.  No acute infarct,\nmass or hemorrhage.\n\n2. Stable complete occlusion of the left common carotid artery reconstituting\nat the level of the carotid bulb with asymmetric decrease in size of the left\ninternal carotid artery which remains patent.  Otherwise, no acute abnormality\non the MRA of the neck and brain."
        },
        {
            "input": "There are scattered bilateral periventricular and subcortical white matter\nhyperintense foci which are nonspecific but likely reflect sequela of chronic\nmicroangiopathy.  Otherwise the parenchymal signal is unremarkable without\nevidence of infarct, hemorrhage, mass, or mass effect.  The ventricles and\ncortical sulci are normal in caliber and configuration.  The extra-axial\nspaces are unremarkable.  The vascular flow voids are preserved.\n\nThe orbits, calvarium, and soft tissues are unremarkable.  There is mild\nmucosal thickening of the frontal and ethmoid sinuses.  There is a small\namount of fluid signal within the left mastoid air cells.  The middle ears are\nclear.",
            "output": "Unremarkable head MRI without infarct, hemorrhage, mass, or mass effect."
        },
        {
            "input": "Axial high-resolution T2 weighted images through the internal auditory canals\ndemonstrate unremarkable seventh and eighth cranial nerve complexes\nbilaterally without evidence of mass or mass effect within the IAC or\ncerebellopontine angle.  The inner ear structures demonstrate normal,\npreserved T2 hyperintense signal and normal morphology bilaterally including\nthe cochlea and semicircular canals.\n\nThere is diffuse enhancement along the course of the left facial nerve\ninvolving the left IAC fundus, as well as all segments of the imaged\ninfratemporal left facial nerve, compatible with stated history of Bell's\npalsy.  There is no evidence of mass along the course the left facial nerve. \nThe left mastoid is unremarkable.  No left parotid gland abnormality\nidentified.  The right facial nerve is unremarkable.  No other abnormal\nenhancement of any additional imaged proximal cranial nerve roots.  No\nabnormal right IAC enhancement.  Meckel's cave is normal bilaterally.\n\nIntracranially, there is no evidence of acute infarction, extra-axial\ncollection, mass effect, or abnormal enhancement.  The ventricles and sulci\nare normal in caliber and configuration.  Major dural venous sinuses are\npatent.  Major intracranial vascular flow voids are preserved.\n\nMucosal thickening and fluid nearly entirely fills the left maxillary sinus. \nThere is mild to moderate ethmoid air cell and mild right maxillary sinus\nmucosal thickening, with a small right maxillary sinus mucous retention cyst. \nFrontal sinus, sphenoid sinus appear clear.  Mastoids appear clear.\n\nApparent FLAIR hyperintensity in the left globe likely represents artifact, as\nno signal abnormality seen on other sequences.  Otherwise, the globes and\norbits appear unremarkable.",
            "output": "1. Diffuse enhancement along the course of the left facial nerve involving the\nleft IAC fundus, as well as all segments of the intratemporal left facial\nnerve, compatible with stated history of Bell's palsy.  Differential includes\n___ Hunt syndrome; correlate clinically with any vesicular rash involving\nthe EAC.\n2. No evidence of perineural tumor spread (although note that the parotid is\nonly partially visualized).  Correlate clinically with any palpable parotid\nabnormality.\n3. Remaining imaged cranial nerve roots are unremarkable.\n4. Paranasal sinus sinus disease as described above."
        },
        {
            "input": "There is a 6 x 3 mm (AP, TRV) CSF intensity focus posterior and inferior to\nthe left internal auditory canal, corresponding to a lucent lesion seen on\nprior CT examination of ___, most compatible with a arachnoid\ngranulation on noncontrast enhanced examination.  There is no evidence of\nassociated diffusion-weighted hyperintense signal.\n\nImages through the internal auditory canal demonstrates symmetric appearance\nof the seventh eighth nerve complexes.  There is no evidence of abnormal mass\nlesion within the internal auditory canals, cerebellopontine angles or\nmembranous labyrinth.\n\nKnown probable dehiscence of the bilateral superior semicircular canals an\napparent atresia of the right oval window with mild pot stapes is much better\nevaluated on CT temporal bone examination of ___.\n\nLimited included imaging of the remainder of the brain demonstrates no\nevidence of hemorrhage, edema, masses, mass effect, midline shift or\ninfarction.  There are a few scattered periventricular and subcortical FLAIR\nwhite matter hyperintensities, which are nonspecific, but commonly seen in\nsetting chronic microangiopathy in a patient of this age.  The ventricles and\nsulci are normal in caliber and configuration. Incidental note is made of a\npartial empty sella.\n\nThe paranasal sinuses, mastoid air cells, and middle ear cavitiesare clear.\nThe orbits are unremarkable. The visualized portion of the principle vascular\nflow voids are preserved.",
            "output": "1. There is a 6 x 3 mm CSF intensity focus corresponding to a recent lesion\nposterior and inferior to the left internal auditory canal seen on prior CT\nexamination.  The findings would suggest arachnoid granulation, although\nsensitivity for small nodular components is limited without contrast."
        },
        {
            "input": "MRI BRAIN:\n\nWithin the right inferior parietal lobe, faintly increased signal is seen on\nthe diffusion tracer images and on the ADC map, as well as on FLAIR images,\nsuggesting T2 shine through.  The high signal on FLAIR images is nonspecific\nbut likely represents sequela of chronic small vessel ischemia, given the\npatient's age.\n\nThe preceding CT raised the question of an acute infarction in the right\npostcentral gyrus and right frontal operculum/ anterior insula, but no\ncorresponding acute infarction is seen.  No evidence for an acute infarction\nis seen elsewhere in the brain parenchyma.\n\nAdditional small foci of high T2 signal in the periventricular and deep white\nmatter of the cerebral hemispheres are nonspecific but likely sequela of\nchronic small vessel ischemic disease in this age group.  There is a prominent\nperivascular space in the left anterior insular subcortical white matter.\n\nThere is global parenchymal volume loss with disproportionate involvement of\nthe superior parietal lobes along the postcentral sulci.\n\nGradient echo images demonstrate linear low signal along the lateral margins\nof the lentiform nuclei, likely secondary to mineralization rather than prior\nhemorrhage, as there is no associated volume loss on other sequences or prior\nCT.  There is no evidence for blood products elsewhere in the brain\nparenchyma.\n\nPrincipal vascular flow voids appear grossly preserved.\n\nThere is mild mucosal thickening in the ethmoid air cells and maxillary\nsinuses, partial right mastoid air cell opacification, mild mucosal thickening\nin the left mastoid air cells, and fluid within the nasopharynx, likely\nsequelae of endotracheal intubation .\n\nMRA NECK:\n\nThe study is technically limited.  There is a 3 vessel aortic arch.  Bilateral\ncarotid bulbs appear irregular, likely due to atherosclerosis.  There may be\nmild, less than 40% right proximal internal carotid stenosis by NASCET\ncriteria.  There is no evidence for left carotid stenosis by NASCET criteria. \nRight vertebral artery origin is suboptimally visualized, and mild stenosis\ncannot be excluded.  Left vertebral artery origin is not included on the\nimages.  Cervical courses of bilateral vertebral arteries are otherwise\npatent.\n\nMRA BRAIN:\n\nImages are limited by motion artifact.  Bilateral carotid siphons appear\nirregular, presumably due to atherosclerosis, without evidence for\nflow-limiting stenosis.  Mild irregularity of the intracranial dominant right\nvertebral artery, without flow-limiting stenosis, may be related to\natherosclerosis or artifact.  There is no evidence for flow-limiting stenosis\nor large aneurysm elsewhere in the intracranial circulation.  Evaluation for\nsmall aneurysms is technically limited .",
            "output": "1. No evidence for acute infarction in the right postcentral gyrus, right\nfrontal operculum, or right anterior insula, where edema was suspected on the\npreceding noncontrast head CT.\n2. Signal abnormality on diffusion tracer sequence and ADC map in the right\ninferior parietal lobe, where there is extensive high T2/FLAIR signal, is most\nconsistent with T2 shine through related to chronic small vessel ischemic\ndisease.  Subacute infarction older than 10 days is less likely, given the\npatient's presentation.  However, comparison with prior studies would be\nhelpful in this regard.\n3. Global parenchymal volume loss with disproportionate involvement of the\nsuperior parietal lobes along the postcentral sulci.\n4. Technically limited neck MRA demonstrates bilateral carotid bulb\nirregularity, presumably atherosclerotic, with mild, less than 40% stenosis by\nNASCET criteria on the right, and no evidence for stenosis by NASCET criteria\non the left.\n5. Right vertebral artery origin is suboptimally visualized, and mild stenosis\ncannot be excluded.  Left vertebral artery origin is not included on the\nimages.\n6. Motion limited brain MRA demonstrates no evidence for flow-limiting\nstenosis or large aneurysm in the major intracranial arteries."
        },
        {
            "input": "Images through the internal auditory canal demonstrates symmetric appearance\nof the seventh eighth nerve complexes.  There is no evidence of abnormal\nenhancement or mass lesion within the internal auditory canals,\ncerebellopontine angles or membranous labyrinth. No other mass lesions are\nseen within the posterior fossa.\n\nLimited evaluation of the brain demonstrates no abnormal enhancement or mass\nlesion.  Very few periventricular and subcortical T2/FLAIR white matter\nhyperintensities are nonspecific, but compatible with chronic microangiopathy\nin a patient of this age.  The sulci, ventricles and cisterns are within\nexpected limits for the patient's mild senescent related global cerebral\nvolume loss.\n\nMild mucosal thickening of the paranasal sinuses.  The orbits are\nunremarkable.  No significant fluid signal is seen in the mastoid air cells.",
            "output": "1. No evidence of IAC or cerebellopontine angle mass.\n2. Very few periventricular and subcortical T2/FLAIR white matter\nhyperintensities are nonspecific, but compatible with chronic microangiopathy\nin a patient this age.  No acute infarct or abnormal enhancement.\n3. Additional findings described above."
        },
        {
            "input": "The examination is minimally motion degraded.  Within these confines:\n\nThere is no intra or extra-axial mass, acute hemorrhage or acute infarct.  The\nsulci, ventricles and cisterns are within expected limits for the patient's\nage.  The major intracranial flow voids are preserved.  The dural venous\nsinuses are patent.  There is no abnormal enhancement.\n\nThe contents of the cerebellopontine angles and internal auditory canals are\nunremarkable.  A branch of the right superior cerebellar artery does cross\nsuperiorly to the root entry zone of the right trigeminal nerve without\nevidence of impingement.\n\nThe paranasal sinuses are clear.  The orbits are unremarkable.  The mastoid\nair cells are clear.",
            "output": "Unremarkable MRA of the head.  No acute infarct or abnormal enhancement."
        },
        {
            "input": "Study is mildly degraded by motion.\n\nMRV BRAIN:\nNormal flow signal is demonstrated within the superior sagittal sinus,\nstraight sinus, transverse sinuses, and sigmoid sinuses. The jugular bulbs and\nproximal jugular veins are patent. Evaluation of the deep venous systems\nreveals normal flow signal in the internal cerebral veins. The vein ___\nis also unremarkable.",
            "output": "1.  Study is mildly degraded by motion.\n2. No evidence for sinus venous thrombosis."
        },
        {
            "input": "The common, internal and external carotid arteries are patent without stenosis\nor occlusion.  There is no evidence of stenosis by NASCET criteria or\ndissection. The origins of the great vessels, subclavian, and vertebral\narteries are not included in the field of view.  The visualized vertebral\narteries are patent throughout their course.\n\nA 2.4 x 3.8 x 3.3 cm round, well-circumscribed anterior mediastinal mass,\ncorresponding to the mass seen on CT, is predominantly T2 hyperintense with a\nnodular T2 iso to hypointense component posteriorly.",
            "output": "1. No evidence of vascular injury.\n2. Partial visualization and characterization of an anterior mediastinal mass.\nCorrelation with prior examinations would be helpful in further evaluation and\nif not available, contrast-enhanced CT of the chest is recommended.\n\nRECOMMENDATION(S):  Partial visualization characterization of an anterior\nmediastinal mass. Correlation with prior examinations would be helpful in\nfurther evaluation and if not available, contrast-enhanced CT of the chest is\nrecommended."
        },
        {
            "input": "There are innumerable foci of parenchymal supratentorial, infratentorial\nmetastases.  Mild associated edema surrounding lesions.  Largest\nsupratentorial metastasis measures 7 mm.  Largest brainstem metastasis\nmeasures 5 mm.  Largest cerebellar metastasis measures 6.5 mm.  No\nhydrocephalus.  No midline shift, no midline shift. Subtle abnormal\nleptomeningeal enhancement along the surface of the cerebellum, bilateral\ninternal auditory canals, along the anterior left temporal lobe best seen on\nFLAIR post gadolinium images, may represent leptomeningeal component of\nmetastatic disease.  Few small enhancing scalp lesions, indeterminate, likely\nmetastases.\n\nSome of the posterior fossa, brainstem metastases were seen on cervical spine\nMRI ___.  Findings are new since ___.  Areas of\ndecreased marrow signal, most prominent in the upper cervical spine,\nconsistent with bone metastases.\n\nMany lesions have mildly increased T1 signal on pre gadolinium images, can be\nseen with subacute blood products, melanin if there is history of melanoma, no\nabnormalities on gradient images.\n\nVascular flow voids are preserved.  Minimal mucosal thickening paranasal\nsinuses.  Clear mastoids.",
            "output": "1. Innumerable supratentorial, infratentorial brain metastases, bone\nmetastases, scalp metastases. Findings consistent with leptomeningeal\nmetastases; infectious, inflammatory processes could have similar appearance.\n2. Findings consistent with small areas of subacute microhemorrhage within few\nparenchymal metastases.  Melanoma could have similar appearance.\n\nNOTIFICATION:  The impression and recommendation above was entered by Dr.\n___ on ___ at 08:44 into the Department of Radiology\ncritical communications system for direct communication to the referring\nprovider."
        },
        {
            "input": "In comparison with the most recent MRI examination, there are numerous infra\nand supratentorial nodular enhancing lesions, some of them with mild vasogenic\nedema which are relatively stable in configuration with no significant mass\neffect or shifting of the adjacent structures, the largest supratentorial\nmetastatic lesion is again seen in the left occipital lobe measures\napproximately 7 mm in transverse dimension (image 89, series 17).  The largest\nnodular enhancing lesion in the posterior fossa is seen in the right\ncerebellar tonsil and measures approximately 7 by 6.5 mm in transverse\ndimension.  No new lesions or new areas with abnormal enhancement are seen. \nNo diffusion abnormalities are detected to indicate acute or subacute ischemic\nchanges.  Please note that some of these lesions demonstrate increased T1 high\nsignal intensity on the pre gadolinium images suggesting underlying blood\nproducts or melanin, no signal abnormality is seen on the gradient echo\nsequences.  There is persistent pattern of enhancement along the internal\nauditory canals suggestive of leptomeningeal metastatic disease (images 44,\nseries 17 and image 92, series 1701), numerous calvarial lesions remain\nunchanged and also are consistent with bone metastatic disease.  The major\nvascular flow voids are present and demonstrate normal distribution.  The\norbits are unremarkable, the paranasal sinuses again demonstrates mild mucosal\nthickening in the floor of the left maxillary sinus, no air-fluid levels are\nseen, the middle ear cavities and mastoid air cells are clear.",
            "output": "1.  Relatively stable numerous infra and supratentorial brain metastatic\nlesions, as well as calvarial metastatic disease.\n\n2.  The appearance and distribution of the nodular enhancing lesions remains\ngrossly unchanged, some lesions demonstrates mild vasogenic edema and\nintrinsic T1 high-signal intensity suggesting hemorrhagic changes or melanin\ndeposit, with no evidence of susceptibility changes.\n\n3.  Similar pattern of enhancement is noted along the internal auditory\ncanals, although this finding is not and specific suggest the possibility of\nleptomeningeal metastatic disease."
        },
        {
            "input": "Right trans frontal ventriculostomy catheter with tip terminating at the\nforamina ___ is unchanged from prior CT examination.\n\nNumerous supra and infratentorial lesions, many of which demonstrating\nintrinsic T1 hyperintense signal are similar to slightly decreased in size\nwhen compared to examination of ___.  No definitive new lesions are\nidentified.  Associated FLAIR signal abnormality has decreased.  There remains\nmild postcontrast enhancement within the internal auditory canals, raising\nconcern for third meningeal involvement, improved from prior exam.\n\nNo acute infarct or intracranial hemorrhage.  The sulci, ventricles cisterns\nare within expected limits for the degree of mild to moderate senescent\nrelated global cerebral volume loss.  The major intracranial flow voids are\npreserved.  The dural venous sinuses are patent.  Bilateral staphyloma and\nlens replacements.  Otherwise the orbits are unremarkable.  No significant\nfluid signal is seen the mastoid air cells.  Metastatic disease of the\nvisualized upper cervical spine is unchanged from prior examination.",
            "output": "1. Numerous supra and infratentorial lesions are slightly smaller to similar\nin size when compared to examination ___.  No new lesions are\nidentified.\n2. No acute infarct or intracranial hemorrhage.\n3. Additional findings as described above."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, or infarction.\nThe ventricles and sulci are normal in caliber and configuration.  The optic\nnerves and optic chiasm are normal in caliber and signal intensity. There is\nno abnormal enhancement. The globes are unremarkable.",
            "output": "Normal MRI of the brain and orbits."
        },
        {
            "input": "There is no infarct, hemorrhage, or mass effect. The ventricles, sulci and\ncisterns are prominent indicative of age related atrophy. There are\nnonspecific periventricular and subcortical white matter\nFLAIR-hyperintensities, likely sequelae of chronic small vessel ischemic\ndisease.  There is an \"empty\" sella turcica, a common variant.  The principal\nintracranial vascular flow voids are present. There are bilateral lens\nimplants. There is mild ethmoid and bilateral maxillary sinus mucosal\nthickening and a small right maxillary sinus mucus-retention cyst. The mastoid\nair cells and visualized soft tissues are unremarkable.",
            "output": "No acute infarct, hemorrhage or mass.\n\nNon-specific white matter abnormalities, likely sequelae of chronic small\nvessel ischemic disease."
        },
        {
            "input": "There is no evidence intracranial hemorrhage, mass, mass effect or shifting of\nthe normally midline structures.  The ventricles and sulci appear slightly\nprominent, likely age related and involutional in nature.  No diffusion\nabnormalities are detected to indicate acute or subacute ischemic changes. \nThe major vascular flow voids are present and demonstrate normal distribution.\nOn the FLAIR sequence, scattered foci and confluent areas of high signal\nintensity are again seen in the subcortical and periventricular white matter,\nwhich are nonspecific and may reflect changes due to small vessel disease. \nThe orbits are unremarkable, the paranasal sinuses are notable for small and\nunchanged mucus retention cyst on the right maxillary sinus, no air-fluid\nlevels are identified.  .  The mastoid air cells are clear.",
            "output": "1.  There is no evidence of acute intracranial process.  No significant\nchanges are demonstrated since the prior MRI examination in ___.\n\n2.  Scattered foci of high signal intensity detected on FLAIR sequence,\ndistributed in the subcortical and periventricular white matter, which are\nnonspecific and may reflect changes due to small vessel disease."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are prominent, likely reflecting\nage-related involutional changes.  There are unchanged T2/FLAIR hyperintensity\nin the periventricular subcortical white matter compatible with chronic\nmicroangiopathy.  The visualized vascular flow voids are grossly preserved. \nThere is mild mucosal thickening of the ethmoid air cells and bilateral\nmaxillary sinuses.  Otherwise the paranasal sinuses and mastoid air cells are\nclear.  Status post bilateral lens replacement.  No abnormal marrow signal is\nidentified.",
            "output": "1. No acute intracranial abnormality.  No evidence of an acute infarct,\nintracranial mass, or hemorrhage\n2. White matter changes of chronic microangiopathy with age-related\ninvolutional changes.  The white matter changes have progressed since ___."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  There is mild periventricular T2/FLAIR hyperintensity,\nnonspecific but likely represents chronic microvascular ischemic disease in\nthis age group.  Again seen is mild prominence of the ventricles and sulci\nconsistent with mild involutional changes.  Otherwise, the ventricles and\nsulci are normal in caliber and configuration.  There is no abnormal\nenhancement after contrast administration.  Hypoenhancing pituitary lesion is\nseen measuring up to 6 mm, incompletely characterized on current exam.",
            "output": "1. No acute intracranial abnormalities identified.  No evidence intracranial\nenhancement.\n2. Hypoenhancing pituitary lesion, incompletely characterized on this exam\nhowever may be secondary to a microadenoma versus pituitary cyst.  Dedicated\npituitary MRI may be helpful for further characterization.\n\nRECOMMENDATION(S):  Dedicated pituitary MRI may be helpful for further\ncharacterization of the pituitary lesion."
        },
        {
            "input": "The patient is status post a suboccipital craniectomy with extensive\npostoperative changes, a pseudomeningocele, a large defect in the right\ncerebellar hemisphere, apparent resection of the right tonsil,  scarring\ninvolving the vermis, and a ventricular catheter entering the right frontal\nhorn.\n\nThere is extensive enhancing material along the posterior margin of the\nresection site underlying the residual occipital bone and bulging into the\npostoperative pseudomeningocele. This material demonstrates the peripheral\nenhancement with a central nonenhancing core. This appears to represent\ndramatic increase in the thickness of enhancing material since the study of ___. The nature of this is uncertain. This would represent\nexuberant postoperative dural reaction, but given the history of cotton balls\nused to control bleeding at the time of surgery, this appears to be the most\nlikely explanation. The material is clearly extra-axial and likely epidural.\nThus, it would be an unusual manifestation of recurrence of this tumor. There\nare no indications to suggest infection.\n\nThe aqueduct appears widely patent. However, the fourth ventricle remains\ndilated and there is a suggestion of possible scarring causing for ventricular\nobstruction. Extensive tissue loss and mild enhancement in the right\ncerebellar hemisphere appear most likely to be postoperative with no evidence\nof residual or recurrent intraparenchymal tumor.",
            "output": "No evidence of intraparenchymal tumor recurrence.\n\nExtensive the dural enhancement surrounding a central nonenhancing core. As\ndiscussed above, this appears most likely to represent exuberant scar\nformation.  This would be an exceedingly unusual manifestation of recurrent\nastrocytoma.\n\nThese findings were discussed with Dr. ___ at 3 pm on ___."
        },
        {
            "input": "Patient is again noted to be status post suboccipital craniectomy. A\nventricular catheter is again noted entering the right frontal horn. There is\na small amount of increased T2/FLAIR signal adjacent to the right ventricular\ncatheter unchanged. Extensive postoperative changes including a\npseudomeningocele, a large defect in the right cerebellar hemisphere, and\napparent resection of the right cerebellar tonsil are again noted.  There is\nstable encephalomalacia changes in the right cerebellum which are unchanged. .\nDilatation of the fourth ventricle is also noted and unchanged.  On\npostcontrast images there is slight enhancement in the operative bed which is\nalso unchanged. There is extensive peripherally enhancing extra-axial epidural\nmaterial seen along the posterior margin of the resection site underlying the\nresidual of occipital bone. This finding appears similar to most recent prior\nstudy.\n\nThere is no acute infarction, intracranial hemorrhage, extracerebral fluid\ncollection, midline shift or mass effect.  No diffusion abnormalities are\ndetected. The cerebral volume is appropriate for the patient's stated age. \nThere are a few scattered foci of T2/FLAIR signal hyperintensity in the\nperiventricular white matter which are nonspecific. These have not\nsignificantly changed compared to prior study. The major vascular flow voids\nare maintained.  The orbits are unremarkable.  There is a mild amount mucosal\nthickening within the ethmoid sinuses. There is a small amount of fluid in the\nright mastoid air cells.",
            "output": "Extensive post surgical changes as detailed above including extensive dural\nenhancement likely representing exuberant fibrous scar tissue. Postsurgical\nchanges have not significantly changed compared to prior study. No evidence of\ntumor recurrence."
        },
        {
            "input": "Patient is again noted to be status post suboccipital craniectomy and left\nparietal craniotomy. There are extensive postoperative changes again noted in\nthe posterior fossa including a pseudomeningocele, unchanged in size and\nconfiguration, and a defect with resection in the right cerebellar hemisphere.\nExtensive enhancing epidural material in the region of the resection\nappearance unchanged and is again felt most likely to represent granulation\ntissue. Ex vacuo dilatation of the fourth ventricle is also stable.\n\nA ventricular catheter is again noted with tip in the frontal horn of the\nright lateral ventricle.\n\nThere is no evidence of acute hemorrhage, edema, masses, shift of midline, or\nacute infarction. The ventricles and sulci are stable in caliber and\nconfiguration.  Vascular flow voids are preserved. There is minimal mucosal\nthickening within the ethmoid air cells. There is trace fluid in the right\nmastoid air cells unchanged. The orbits are unremarkable",
            "output": "1. Patient is status post suboccipital craniectomy with stable postsurgical\nchanges including extensive likely dural scar tissue/postsurgical changes of a\ncontinued followup will be necessary.  No definite evidence of tumor\nrecurrence.\n\n2.  No evidence of acute infarction or acute hemorrhage."
        },
        {
            "input": "There is a right frontal ventriculostomy catheter which terminates in the\nright frontal horn.  The ventricles are stable in size and morphology.  There\nis partially limited evaluation on the lateral right frontoparietal lobes\nsecondary to artifact from the ventriculostomy catheter and reservoir.\n\nOccipital craniotomy changes are seen with extensive postsurgical changes in\nthe posterior fossa.  There is ex vacuo dilatation of the fourth ventricle. \nThere is stable mass like enhancement in the extra-axial spaces of the\nposterior fossa with associated dural enhancement.  No new regions of contrast\nenhancement or intra-axial contrast enhancement are identified.  There is\nunchanged appearance of the pseudomeningocele in the posterior fossa at the\nresection cavity.\n\nAllowing for susceptibility artifact from shunt reservoir, there is no acute\ninfarct or intracranial hemorrhage.  The dural venous sinuses are patent.  The\nmajor intracranial flow voids are preserved.  The paranasal sinuses are clear.\nThe orbits are unremarkable.  Trace fluid signal in the right mastoid tip is\nidentified.",
            "output": "1. Stable postsurgical changes in the posterior fossa.\n2. Stable extra-axial mass like enhancement in the posterior fossa, at the\nresection site, likely representing postoperative granulation tissue.  No new\nsites of contrast enhancement or intra-axial contrast enhancement to suggest\ndisease recurrence or progression."
        },
        {
            "input": "The patient is status post suboccipital craniectomy and resection of a\nposterior fossa mass with unchanged encephalomalacia of the cerebellar\nhemispheres, right greater than left.  The T2/FLAIR hyperintense signal\nsurrounding the resection bed is unchanged.  There is no new or nodular\nenhancement within or surrounding the resection cavity to suggest recurrence. \nThe lobulated, T1 hypointense, enhancing, tubular, extra-axial soft tissue\nposterior and inferior to the resection cavity is unchanged and likely\nrepresents granulation tissue.  The associated ex vacuo dilatation of the\nfourth ventricle is unchanged.  The pseudomeningocele, posterior to the\nresection cavity, is unchanged.\n\nA frontal approach ventriculostomy catheter is unchanged in position,\nterminating within the frontal horn of the right lateral ventricle.  Artifact\nrelated to the shunt reservoir limits evaluation of the right frontal,\nparietal, and temporal lobes.  There is no evidence of acute hemorrhage,\nedema, masses, mass effect, midline shift or infarction.\n\nThe paranasal sinuses are clear.  The orbits are unremarkable.\n\nThe right mastoid air cells are minimally opacified.\n\nThe major intracranial flow voids are preserved.",
            "output": "Stable postsurgical changes with no evidence of residual or recurrent disease.\nThe enhancing material at the surgical site remains most likely scar tissue. \nIt has not progressed since ___."
        },
        {
            "input": "Patient is status post suboccipital craniectomy.  Postsurgical changes in the\nposterior fossa are stable compared to ___, including\nencephalomalacia of the bilateral cerebellar hemispheres, right greater than\nleft.  T2/FLAIR hyperintensity surrounding the resection bed is stable.  There\nis no new masslike enhancement.  Lobulated extra-axial T1 hyperintense, T2\nheterogenous, contrast-enhancing soft tissue, along the craniectomy site is\nunchanged since ___, most consistent with postsurgical granulation/scar\ntissue.  Ex vacuo dilatation of the fourth ventricle is stable. \nModerate-sized pseudomeningocele posterior to the resection cavity is\nunchanged.\n\nA right frontal approach ventriculostomy catheter terminates in the frontal\nhorn of the right lateral ventricle, in unchanged position.  The lateral and\nthird ventricles are stable in size without hydrocephalus.  Susceptibility\nartifact associated with the shunt reserve limits evaluation of the right\nfrontal, parietal and temporal lobes, as before.  Within this limitation,\nthere is no evidence of acute infarct, edema, new blood products, or\nsupratentorial mass.\n\nMajor arterial flow voids are grossly preserved.  The right sigmoid sinus is\nnot well seen on the present or prior postcontrast MP RAGE images.  Right\njugular bulb appears patent.  Other major dural venous sinuses appear patent.\n\nLeft parietal craniectomy changes are again seen.\n\nPartial opacification of the right mastoid air cells is unchanged.  There is\nmild mucosal thickening in the ethmoid air cells.",
            "output": "1. Stable post treatment changes in the posterior fossa.  No evidence for a\nnew mass.\n2. Stable position of right frontal approach ventriculostomy catheter.  Stable\nsize of the lateral and third ventricles without hydrocephalus.  Stable ex\nvacuo enlargement of the fourth ventricle."
        },
        {
            "input": "In the left cerebellar hemisphere, there is a tiny non-enhancing focus which\ndemonstrates low signal on T1 and T2-weighted images, and homogenous negative\nsusceptibility artifact.  These findings, combined with the mildly hyperdense\nappearance on CT indicate that this is likely a small cavernoma or focus of\nchronic microhemorrhage.\n\nNonspecific, non-enhancing FLAIR abnormality is seen in the upper pons.\nNonspecific periventricular and subcortical white matter FLAIR\nhyperintensities are likely a sequela of chronic small vessel ischemic\ndisease.\nPrincipal intracranial flow voids are preserved and dural venous sinuses\nenhance normally without filling defects.\nNo pathologic leptomeningeal or pachymeningeal enhancement.\nThe bone marrow signal is normal.\nNo pathologic upper cervical lymph nodes are appreciated.\nSmall mucous retention cyst is seen in the base of left maxillary sinus,\notherwise the paranasal sinuses are clear.",
            "output": "1. Given the  appearance on CT, along with the signal intensity\ncharacteristics on MRI, the left cerebellar lesion represents chronic blood\nproducts; a small cavernoma or remote focus of microhemorrhage.  Attention on\nfollow up.\n\n2.  Non-specific, non-enhancing FLAIR signal abnormality in the pons may be\ndue to metabolic or electrolyte abnormalities, a demyelinating/inflammatory\nprocess, or a low grade glioma.  Correlation with clinical details is\nrecommended and close followup to assess for interval change as no priors.  If\nworkup for a low grade glioma is desired, the area would be amenable to MR\nspectroscopy for better assessment.\n\nNOTIFICATION:  Findings discussed with Dr. ___ by Dr. ___ telephone\nat ___ ___ on ___."
        },
        {
            "input": "Lateral left frontal cortex, left pre and postcentral gyrus, and left centrum\nsemi ovale restricted diffusion.  There is correlate FLAIR signal\nhyperintensity and no evidence of a hemorrhage.\n\nThere is a focus of FLAIR signal hyperintensity with central CSF signal, at\nthe subcortical white matter of the right frontal cortex consistent with\nremote infectious inflammatory or ischemic process.  The ventricles and\nextra-axial spaces are normal.  The vascular flow voids are preserved.  The\norbits, calvarium, and soft tissues are unremarkable.  There is mild right\nethmoid sinus mucosal thickening.  The mastoid air cells are clear.",
            "output": "1. Acute infarction centered within the left frontal cortex, extending to the\npre and postcentral gyrus and the centrum semiovale corresponding to the MCA\nterritory.  No evidence of hemorrhagic conversion.\n2.  Paranasal sinus disease as described."
        },
        {
            "input": "There is no evidence of edema, masses, mass effect, midline shift or\ninfarction.  The ventricles and sulci are prominent, consistent with global\ncerebral volume loss.  Patchy periventricular T2 hyperintensities are most\nconsistent with chronic microvascular angiopathy.  Foci of microhemorrhages\nare seen in the right frontal and right occipital lobes, likely sequela of\nmicrovascular angiopathy. There is no abnormal enhancement after contrast\nadministration.  There is a small focus of hyperintensity in the right frontal\nsubcortical region near convexity on diffusion images without distinct\nhypointensity on the ADC map (___) likely a subacute infarct.\n\n The paranasal sinuses, mastoid air cells and middle ear cavities are clear. \nThe patient is status post bilateral cataract surgery.",
            "output": "1. Likely a punctate subacute infarct in the right posterior frontal convexity\nregion.  Otherwise, no other acute abnormalities.\n2. Moderate to severe changes secondary to chronic microvascular angiopathy.\n3. Brain and medial temporal atrophy.\n4. No enhancing brain lesions."
        },
        {
            "input": "There is no evidence of hemorrhage, infarction, edema, mass or mass effect. \nPrincipal intracranial vascular flow voids are preserved. No extra-axial blood\nor fluid collection is present. The ventricles and sulci are age appropriate. \nScattered periventricular and subcortical white matter changes are\nnon-specific but could represent small vessel disease.\n\nThere is no pathologic parenchymal, leptomeningeal, or dural focus of\nenhancement after contrast administration. The brainstem, posterior fossa and\ncervico-medullary junction are normal.  The orbits are within normal limits. \nThe paranasal sinuses are clear.  No abnormality of the skull base or calvaria\nis identified.",
            "output": "No evidence of intracranial metastasis."
        },
        {
            "input": "There is scattered bilateral periventricular and subcortical white matter\nFLAIR hyperintense foci, predominantly within the frontal lobes, which are\nrelatively unchanged comparison to are ___.  There is intrinsic T1\nhyperintensity within the bilateral basal ganglia.  There is no acute\nhemorrhage, infarct, mass, or mass effect.  The ventricles and cortical sulci\nare normal in caliber and configuration.  The extra-axial spaces are\nunremarkable.  The vasculature is patent.\n\nThe left lens is absent.  The paranasal sinuses are clear.  There are trace\neffusions within the bilateral mastoid air cells.  The middle ears are clear. \nThe inner ear is unremarkable.  The calvarium is thickened demonstrating low\nT1 marrow signal and heterogeneous postcontrast enhancement.  And there is\nheterogeneous enhancement within the skull base, mandible, and visualized\ncervical spine.",
            "output": "1. No acute intracranial abnormality for intracranial metastatic disease.\n2. Thickened and heterogenous enhancing calvarium addition to heterogeneous\nenhancement within the skullbase, cervical spine, and mandible, suggestive of\ndiffuse osseous metastatic disease.\n3. No evidence of enhancing brain lesions.\n4. Subcortical white matter FLAIR hyperintense foci, likely representing\nsequela of chronic small vessel disease."
        },
        {
            "input": "There is evidence of mild encephalomalacia of the lateral aspect of the right\ncerebellar hemisphere in the AICA territory, likely consistent with sequela of\nan old ischemic insult.  Mild subcortical and deep white matter T2/FLAIR\nhyperintensities are nonspecific but can be seen in the setting chronic small\nvessel disease.  There is a small old left basal ganglia lacunar infarct. \nThere is no evidence of acute intracranial hemorrhage, edema, masses, mass\neffect, midline shift or acute infarction.\n\nThe major intracranial vascular flow voids are maintained.  Note is made of a\nfew bilateral transverse sinus arachnoid granulations.  The ventricles and\nsulci are normal in caliber and configuration for age.  There is no abnormal\nenhancement after contrast administration.",
            "output": "1. No acute intracranial abnormality.\n2. Evidence of a small old right cerebellar infarct in the AICA territory.\n3. Mild white matter chronic microangiopathic changes."
        },
        {
            "input": "Again seen is the posteromedially projecting left paraophthalmic intracranial\nICA saccular aneurysm measuring approximately 4 mm apex to base, 4-5 mm at the\nneck, and 5 mm in maximum diameter (02:53), not appreciably changed in size\nwhen measured in a similar fashion compared with the study of ___.\n\nOtherwise, the remaining components of the intracranial vertebral and internal\ncarotid arteries and their major branches appear normal without evidence of\nstenosis,occlusion,oradditional/new aneurysm formation.",
            "output": "1. 5 mm posteromedially projecting left paraophthalmic intracranial ICA\naneurysm, not appreciably changed compared with ___ when measured in\na similar fashion on that study.\n2. Otherwise, unremarkable circle of ___.  No other aneurysm.  No stenosis\nor occlusion."
        },
        {
            "input": "There is a focus of hyperintense DWI signal abnormality with corresponding\nhyperintense T2/FLAIR and ADC signal within the left aspect of the pons\nimmediately adjacent to the facial colliculus.  There is no associated reduced\nsignal on GRE or enhancement.\n\nThere are a few scattered hyperintense T2/FLAIR signal changes within the\nsubcortical white matter (22:14, 13), without distant periventricular white\nmatter lesion.  There is no abnormal enhancement after contrast\nadministration.  There is no mass effect or midline shift.  The ventricles are\nnormal in size.\n\nThe major intracranial flow voids are preserved.  There is mild partial\nopacification of bilateral maxillary sinuses.  The remaining paranasal sinuses\nand bilateral mastoid air cells appear clear.",
            "output": "1. Focus of diffusion abnormality within the left aspect of the pons with\nhyperintense DWI and ADC signal with corresponding hyperintensity on T2/FLAIR\nsequence, suggestive of subacute infarction.  This is felt atypical for a\ndemyelinating process.\n2. Few scattered hyperintense T2/FLAIR signal changes.  Finding is nonspecific\nand may be a sequela of small vessel microangiopathy.\n\nNOTIFICATION:  The findings were discussed with ___, M.D. by\n___, M.D. on the telephone on ___ at 9:45 AM, 3\nminutes after discovery of the findings."
        },
        {
            "input": "MRA HEAD:\n\nMRA of the circle of ___ was normal flow signal in the arteries of the\nanterior and posterior circulation. There is no evidence of vascular\nocclusion, stenosis or an aneurysm greater than 3 mm in size. No evidence of\nabnormal vascular structures seen.\n\nMRA NECK:\n\nMRA of the neck with contrast demonstrates a normal appearance of the carotid\nand vertebral arteries without stenosis or occlusion dissection.  Narrowing of\nthe left vertebral artery in its horizontal portion at the junction of V3 and\nV4 segment (108 03:17) is artifactual due to incomplete the inclusion of the\nartery.  This area is normal on the source images (8 01:25).",
            "output": "No significant abnormalities are seen on MRA of the head and neck."
        },
        {
            "input": "Previously seen lesion in the left aspect of the pons has decreased,\ndemonstrates mild residual FLAIR hyperintense signal with resolution of\ndiffusion weighted signal abnormality.  There are multiple FLAIR hyperintense\nsubcortical/juxtacortical, deep white matter hyperintensities, with a few new\nlesions identified when compared to ___.  Examples of new\nhyperintensities include foci in the right cerebellum (series 4, image 12), in\nright splenium of the corpus callosum (Series 4, image 21), and a cluster of\nlesions in the left juxtacortical parietal lobe (Series 4, image 26).  There\nis questionable increased signal on diffusion-weighted imaging in the lesion\ninvolving splenium.\n\nAdditionally, there are three small foci of enhancement in the white matter of\nthe left frontal, left parietal lobes, and adjacent to the left insular cortex\n(series 10, image 27, 28, 24), new since prior.\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  The major intracranial flow voids are preserved.  There is no\nabnormal enhancement after contrast administration.  There is mild mucosal\nthickening in the left maxillary sinus, and small submucosal retention cyst\nright maxillary sinus.  Dural venous sinuses are patent.  Mastoid air cells\nare patent.",
            "output": "1. Multiple juxta cortical, deep white matter, infratentorial lesions,\nconsistent with chronic demyelination in the appropriate clinical setting. \nPontine lesion has decreased.  There are multiple small new lesions since\nprior, including 3 enhancing lesions, consistent with active demyelination.\n\nRECOMMENDATION(S):  The findings were discussed with ___, M.D. by J.\n, M.D. on the telephone on ___ at 3:17 ___, 15 minutes after discovery of\nthe findings."
        },
        {
            "input": "There is restricted diffusion in the left MCA territory in the left frontal\nlobe and extending into the head of the caudate.  There are some areas of\nFLAIR hyperintensity in this area consistent with a mixed of acute and\nsubacute infarct.  Flair hyperintensity in the left temporal lobe does not\nhave associated diffusion restriction compatible with chronic infarct.  There\nis no evidence of hemorrhagic conversion.  There is no evidence of hemorrhage,\nedema, masses, mass effect, midline shift or infarction.  There is prominence\nof the ventricles and sulci suggestive involutional changes.  Periventricular\nand subcortical white matter FLAIR hyperintensities are nonspecific but likely\nreflect sequela of chronic small vessel ischemic disease.  The major\nintracranial flow voids appear patent.  The calcified thrombi in distal\narteries were better assessed on the CTA.  The paranasal sinuses and mastoid\nair cells are clear.  The orbits are unremarkable.",
            "output": "1. Acute and subacute infarcts in the left MCA territory in the left frontal\nlobe and left caudate head.\n2. Chronic infarct in the left temporal lobe."
        },
        {
            "input": "There is no evidence of acute hemorrhage. No region of restricted diffusion to\nsuggest ischemia or acute infarction is present.  Ventricles and sulci are age\nappropriate in size and configuration.  There is no shift of normally midline\nstructures. There is no effacement of basal cisterns.  There is no enhancing\nlesion identified.  There is no evidence of pachymeningeal or leptomeningeal\nenhancement.  T2 and FLAIR subcortical white matter hypodensities are\nnonspecific, do not enhance, and do not demonstrate restricted diffusion. \nThere is no extra-axial fluid collection.  Intracranial flow voids are\npreserved.  The dural sinuses are patent.\n\nThe orbits are unremarkable.  Paranasal sinuses demonstrate mild mucosal\nthickening within the right posterior ethmoidal air cells.  Bilateral mastoid\nair cells are clear.",
            "output": "1. There is no evidence of acute intracranial abnormality.\n\n2. A few scattered T2/FLAIR subcortical white matter hyperdensities are\nnonspecific, and while they have been reported in patients with sarcoidosis,\nfindings in a patient of this age likely reflect sequelae of microvascular\ndisease. Findings have additionally been associated with chronic headaches,\nprior trauma related, or secondary to prior infectious or inflammatory\netiologies."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, or acute infarction.  Mild\nprominence of the ventricles and sulci is suggestive of involutional changes.\nThere is no mass effect or midline shift.\n\n Multiple scattered T2 and FLAIR hyperintense foci in the periventricular and\nsubcortical white matter are nonspecific, but likely reflect chronic small\nvessel ischemic changes.\n\nMild mucosal thickening of the left maxillary sinus within septated\nsecretions.  There is trace fluid signal in the bilateral mastoid air cells. \nPostsurgical changes of bilateral lens replacement.\n\nPartially visualized degenerative changes of the upper cervical spine with\ndisc osteophyte complexes indenting the ventral thecal sac at C3-C4 and C4-C5.",
            "output": "1. No evidence of acute infarction or intracranial hemorrhage.\n2. Mild parenchymal volume loss.\n3. Findings of chronic small vessel ischemic disease.\n4. Left maxillary sinus disease."
        },
        {
            "input": "Multiple (approximately 7) bilateral punctate supra and infratentorial acute\ninfarcts.  No hemorrhagic transformation.  Generalized cerebral atrophy with\nex vacuo dilatation of the ventricular system.  Moderate periventricular deep\nwhite matter T2 and FLAIR hyperintense changes are most likely sequela of\nmicroangiopathy.  There is no abnormal enhancement after contrast\nadministration.  The orbits appear normal.  Mild mucosal thickening involving\nthe paranasal sinuses.  The intracranial arteries demonstrate normal T2 flow\nvoids.  The pituitary appears normal.  The craniocervical junction appears\nnormal.",
            "output": "Multiple (approximately 7) bilateral punctate supra and infra tentorial acute\ninfarct.  These are most likely embolic in nature.  No hemorrhagic\ntransformation.\n\nNo intracranial hemorrhage or mass.\n\nGeneralized cerebral atrophy with white matter microangiopathic changes.\n\nNOTIFICATION:  The findings were discussed with ___, M.D. by ___\n___, M.D. on the telephone on ___ at 12:25 pm, 5 minutes after\ndiscovery of the findings."
        },
        {
            "input": "There is no intra or extra-axial mass, acute hemorrhage or acute infarct. \nFLAIR hyperintense signal with associated CSF intensity foci in the right\nbasal ganglia to the centrum semiovale likely represent sequela of prior\nlacunar infarcts and perivascular spaces.  Cortical FLAIR hyperintense signal\nof the right postcentral gyrus (series 10, image 19) likely represents sequela\nprior infarct.   Decreased flow related signal of the left internal carotid\nartery and left MCA is identified, corresponding to findings on MRA brain from\noutside hospital ___.  The orbits are unremarkable.  There is mild\nmucosal thickening of the bilateral maxillary sinuses with dependent fluid in\nthe left maxillary sinus.  The mastoid air cells are essentially clear.",
            "output": "1. No acute infarct or intracranial hemorrhage.\n2. FLAIR hyperintense white matter signal with associated CSF intensity foci\nin the right basal ganglia to centrum semiovale likely represents a\ncombination of prior lacunar infarcts and prominent perivascular spaces. \nCortical FLAIR hyperintense signal the right postcentral gyrus is also\ncompatible with sequela prior infarct.\n3. Decreased flow related signal of the visualize left internal carotid artery\nand left MCA segments are noted, corresponding to MR ___ findings from outside\nhospital ___.\n4. Dependent fluid in the left maxillary sinus may represent acute\ninflammatory process.  Clinical correlation is recommended."
        },
        {
            "input": "There are few non contiguous foci of mildly increased signal on diffusion\nweighted images involving the left periatrial white matter, extending into the\ndeep white matter of the lateral left temporal lobe, with mildly decreased or\nnormalized ADC values, favoring subacute infarcts.  There are no right-sided\nacute or subacute infarcts.  There is no evidence of hemorrhage, edema,\nmasses, mass effect, midline shift.\nThere Is generalized parenchymal atrophy.  There is no hydrocephalus. \nPartially empty sella is again seen.  There are stable chronic infarcts\ninvolving bilateral caudate nuclei, right putamen.  There is chronic cortical\ninfarct involving right middle frontal gyrus, stable.  Probable tiny chronic\ncortical infarct involving medial right postcentral gyrus.  Significantly\ndiminished flow void in the high left cervical ICA, extending to the ICA\nterminus, similar.  Diminutive caliber left MCA branches, similar.  There is\npreserved right ICA, vertebrobasilar and dural venous sinus flow voids.  There\nis mild mucosal thickening of the paranasal sinuses, similar.  Mastoid air\ncells and middle ear cavities are patent.",
            "output": "1. There are few left periatrial and temporal lobe deep white matter subacute\ninfarcts.\n2. There are stable chronic infarcts, and stable significantly diminished left\nICA, MCA flow voids, better evaluated on CTA head and neck ___.  ."
        },
        {
            "input": "There is a large area of slow diffusion in the left MCA territory involving\nthe frontal lobe, parietal lobe, insula, basal ganglia, and a small portion of\nthe temporal lobe.  There is gyriform hemorrhage in the infarcted cortex as\nwell as focal hemorrhage in the left putamen, as seen on the earlier CT done\napproximately 2 hours earlier on ___, not significantly changed\nallowing for differences in modalities.  There is no change in mass effect,\nwith stable minimal rightward shift of the septum pellucidum and third\nventricle, and stable minimal effacement of the left lateral ventricle\ncompared to ___.\n\nThere is loss of the normal flow void in the left internal carotid artery\nincluding the distal cervical, petrous, cavernous, and supraclinoid portions,\nconcerning for recurrent occlusion.  Evaluation of the flow voids of the M1\nsegments of both middle cerebral arteries is limited due to slice selection.\n\nThere is extensive T2 hyperintensity within bilateral pons without acute\ndiffusion abnormality, likely secondary to chronic small vessel changes.\n\nThere is a small disc protrusion at C2-C3 mildly indenting the thecal sac,\nincompletely evaluated.",
            "output": "1. Loss of the normal flow void in the visualized left internal carotid artery\nfrom the distal cervical through the supraclinoid portions, concerning for\nrecurrent occlusion.\n2. Evolving large early subacute infarct in the left MCA territory. \nAssociated minimal mass effect, as well as associated cortical and left\nputaminal hemorrhage, are unchanged compared to the CT from approximately 2\nhours earlier.\n\nNOTIFICATION:  The findings were discussed with ___, M.D. by ___\n___, M.D. on the telephone on ___ at 4:53 pm, 5 minutes after\ndiscovery of the findings."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is a single punctate focus of left frontal corona\nradiata T2/FLAIR hyperintensity, entirely nonspecific and likely of no\nclinical significance.  There is no abnormal enhancement after contrast\nadministration.  There is no abnormal focus of slowed diffusion.  The\nprincipal intracranial vascular flow voids are preserved.\n\nThe paranasal sinuses are grossly clear.  The orbits are grossly unremarkable.",
            "output": "1. No evidence of intracranial metastatic disease.\n2. No acute intracranial abnormality including hemorrhage, infarct, or\nenhancing lesion."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.  There are mild chronic small vessel ischemic changes.  There\nis focus of linear calcification in the inferolateral left cerebellum, stable\nsince prior, no adjacent flow voids, no definite enhancement, may be sequela\nof chronic infarct.  Adjacent dural venous sinuses are patent.  Preserved\nintracranial vascular flow voids.  Clear paranasal sinuses, mastoid air cells,\nmiddle ear cavities.",
            "output": "1. No metastases"
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  There is prominence of the ventricles and sulci suggestive\ninvolutional changes.  Periventricular and subcortical T2 and FLAIR\nhyperintensities are noted. There is no abnormal enhancement after contrast\nadministration.  The major vascular flow voids are preserved.\n\nThe orbits, mastoid air cells and visualized soft tissues are normal.  There\nis mucosal thickening of the right maxillary and ethmoid sinus.",
            "output": "1. No evidence for intracranial metastatic disease.\n2. Nonspecific white matter signal abnormality, likely secondary to chronic\nmicrovascular ischemic changes."
        },
        {
            "input": "Taking into account difference in technique, there is no interval increase in\nsize and number of the several FLAIR hyperintense foci along the callososeptal\ninterface, in the periventricular white matter, compatible with multiple\nsclerosis.  Similarly, there is unchanged linear FLAIR hyperintensity in the\nright middle cerebellar peduncle (100:48).  Some of these lesions demonstrate\nhypointensity on T1 weighted image \"black holes.\"   Although some of these\nlesions demonstrate hyperintensity on diffusion sequences, decreased compared\nto prior MRI, there are no associated hypointensity on ADC map to suggest\ndiffusion restriction.  None of these lesions demonstrate enhancement, and the\npreviously noted linear enhancement along the right middle cerebral peduncle\nhas resolved.\n\nNo new lesions are identified.\n\nThere is no evidence of hemorrhage, mass effect,midline shift or infarction.  \nThe ventricles and sulci are normal in caliber and configuration.\n\nThere is mild mucosal thickening of the ethmoid air cells, otherwise the\nparanasal sinuses and mastoid air cells are clear.  There is no abnormal\nmarrow signal.",
            "output": "1. Stable size and number of the previously noted several FLAIR hyperintense\nfoci in the periventricular and deep white matter, without evidence of\nenhancement to suggest active plaque.\n2. No new lesions are identified."
        },
        {
            "input": "Again seen is an enhancing mass along the inferior left tentorium measuring 14\nx 18 x 17 mm.  The appearance is identical to the study of ___ and\nremains most consistent with a meningioma.  No other masses are detected.\n\nThere is no evidence of hemorrhage, edema, masses, midline shift or\ninfarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  Again seen are white matter hyperintensities on FLAIR of no\ndefinite clinical significance.  They are often attributed to chronic small\nvessel ischemia.",
            "output": "1. No change since ___.  Unchanged left posterior fossa mass, likely a\nmeningioma."
        },
        {
            "input": "MR Head:  Limited examination due to metal artifact from dental hardware. \nSlow diffusion is identified in the vascular territory of the left middle\ncerebral artery, involving the left frontal, temporal and parietal lobes as\nwell as the left frontal parasagittal region, no frank evidence of hemorrhagic\ntransformation is identified or significant mass effect.  On FLAIR and T2\nweighted images the areas of ischemia demonstrates a mild edema and\nhigh-signal intensity.  There is occlusion of the left infra clinoid internal\ncarotid artery.  The orbits are unremarkable, the paranasal sinuses are\nincompletely evaluated due to dental hardware artifact, bilateral opacities\nare seen in the mastoid air cells.\n\nMRA of the head:  There is occlusion of the left internal carotid artery below\nthe clinoid segment, apparently there is collateral vascular flow through the\ncircle ___ via the left posterior communicator artery, however there is no\nsignificant or robust collateral flow throughout the A1 segment, there is also\npoor vascular signal in the distal branches of the left middle cerebral\nartery, suggesting decreased vascular flow.  The posterior circulation appears\npatent with moderate narrowing and the P1 segment on the right, partially\nevaluated in this examination\n\nMRA of the neck: The supra are aortic branches are patent with 3 branching\npattern, there is occlusion of the left internal carotid artery, approximately\nat 15 mm from the bifurcation, the possibility of dissection is a\nconsideration, however, no significant areas of high-signal intensity are\ndemonstrated on the fat suppression sequences at the level of the left\ninternal carotid occlusion.  The right cervical carotid bifurcation appears\nnormal with no evidence of flow stenotic lesions.  Both vertebral arteries are\npatent and codominant.",
            "output": "1.  Acute/subacute ischemic changes identified in the left cerebral\nhemisphere, vascular territory of the left middle cerebral artery as described\nin detail above, with no evidence of hemorrhagic transformation or significant\nmass effect.\n\n2.  Decreased vascularity in the left middle cerebral artery with poor\ncollateral flow via the posterior communicator artery.\n\n3.  Occlusion of the left internal carotid artery above the cervical\nbifurcation, the possibility of dissection is a consideration.  The vascular\nocclusion is extending below the supra clinoid segment.\n\nThe primary team was aware of the ischemic changes since the prior head CT on\n___."
        },
        {
            "input": "Study is moderately degraded by motion.  Within these confines:\n\nThere is chronic encephalomalacia and gliosis in the left frontal and parietal\nlobes related to evolution of left middle cerebral artery territory infarcts\nthat where acute/subacute at the time of ___ MRI.  The smaller\nsize of the left cerebral peduncle and hyperintense FLAIR signal in this\nregion extending superiorly through the posterior limb of the left internal\ncapsule and corona radiata towards the area of infarction is consistent with\nwallerian degeneration (series 11, images 11- 16).  There is no abnormality on\ndiffusion-weighted images to suggest acute infarction.  Curvilinear\nhypointense structures along the periphery of the fluid-filled cavity left\nbehind by the infarcts likely represent prominent vessels or less likely small\namount of hemosiderin deposition (series 9, image ___ and image 16). \nOtherwise, there is no evidence of intracranial hemorrhage.  There is no mass\nor mass effect.  The ventricles and sulci are stable.  Principal intracranial\nvascular flow voids are preserved.  There is paucity of vessels in the region\nof infarction as expected.  The dural venous sinuses enhance appropriately on\npostcontrast MPRAGE sequences. There is no abnormal enhancement.\n\nThere is mild mucosal thickening of the maxillary and ethmoid sinuses.  Fluid\nsignal partially opacifies the right mastoid air cells, unchanged.  There is\nalso fluid signal in a few left mastoid air cells.\n\nThe cerebellar tonsils are noted to be pointed and extend approximately 9 mm\ninferior to the foramen magnum, with questioned elongation of the fourth\nventricle.  Allowing for difference technique, findings are grossly unchanged\ncompared to ___ prior brain MRI.",
            "output": "1.  Study is moderately degraded by motion.\n2. Evolution of chronic left middle cerebral artery territory infarcts as\ndescribed above and associated wallerian degeneration.\n3. No evidence of acute infarction, intracranial hemorrhage, mass or mass\neffect.\n4. Redemonstration of findings suggestive of Chiari 1 malformation.\n5.  Paranasal sinus disease and nonspecific mastoid fluid, as described."
        },
        {
            "input": "There is no evidence of acute territorial infarction.  No intracranial\nhemorrhage.  No mass, mass effect, edema or midline shift.\n\nThe ventricles and sulci are normal, without evidence of hydrocephalus. The\nbasal cisterns are patent.  There is no evidence of impending, downward\nherniation.  There is gross preservation of the principal intracranial\nvascular flow voids.\n\nMucous retention cysts are noted in the left maxillary sinus.  There is\npartial opacification of scattered bilateral ethmoid air cells.  The remainder\nof the visualized paranasal sinuses, middle ear cavities, and mastoid air\ncells are well aerated and clear.  The orbits are within normal limits\nbilaterally.",
            "output": "1. No evidence for acute intracranial infarction or hemorrhage.\n2. Multifocal sinus disease, as detailed above."
        },
        {
            "input": "The study is somewhat limited by patient motion artifact.\n\nThe ventricles and extra-axial CSF spaces are normal in size.  There is no\nhemorrhage, edema, mass or mass effect. There is no acute infarct.  The\ntemporal lobes and hippocampal formations are symmetric and normal in\nmorphology and internal architecture.  There is no evidence of cortical\nheterotopia or other migrational anomaly. The principal intracranial vascular\nflow voids are maintained. Following gadolinium administration there is no\nevidence of abnormal parenchymal, vascular and meningeal enhancement seen. The\nvisualized paranasal sinuses are clear.",
            "output": "1. No acute intracranial abnormality.\n2. No mass or pathologic enhancement.\n3. No anatomic substrate for seizure identified.\n COMMENT:  This study was not performed on a 3T instrument, and is further\nlimited by lack of some of the dedicated seizure imaging sequences (e.g. \ncoronal fSTIR), as well as patient motion artifact. Continued concern for an\nunderlying anatomic cause for seizure, such as focal cortical dysplasia, may\nwarrant consideration of high-resolution imaging at the ___\nBiomedical Imaging (___)."
        },
        {
            "input": "There are a few tiny T2/FLAIR hyperintense foci in the subcortical and\nperiventricular white matter, a nonspecific finding but likely related to\nsmall vessel ischemic disease.  No diffusion abnormalities are detected to\nsuggest acute or subacute infarction.  No encephalomalacic changes.  There is\nno evidence of intracranial hemorrhage, edema, masses, mass effect, or midline\nshift.  The ventricles and sulci are slightly prominent suggesting mild\ncortical volume loss, likely age related and involutional in nature.\n\nThe principal flow voids are preserved.  The visualized paranasal sinuses are\nclear.  The orbits are unremarkable.",
            "output": "1. Mild generalized atrophy.\n2. Small subcortical and periventricular T2/FLAIR hyperintense foci are\nnonspecific, likely related to chronic small vessel ischemic disease.\n3. No evidence of acute territorial infarction or intracranial hemorrhage."
        },
        {
            "input": "There are patchy areas of restricted diffusion throughout the posterior\ninferior right cerebellar hemisphere with corresponding areas of T2 and FLAIR\nhyperintense signal abnormality compatible with early subacute infarction. \nThere is no evidence of hemorrhagic transformation of contrast enhancement. \nNo effacement of the fourth ventricle.  Third and lateral ventricles are\nnormal in size.  There is mild right cerebellomedullary cistern effacement. \nThe cerebellar tonsils are normally positioned.\n\nSmall foci of high signal on T2 weighted and FLAIR images in the predominantly\nsubcortical white matter of the bilateral cerebral hemispheres demonstrate no\ndiffusion abnormality or contrast enhancement.  No evidence for an enhancing\nmass.\n\nThe major intracranial arterial flow voids are preserved.  Flow is seen in the\nright ___ postcontrast MP RAGE images.  The dural venous sinuses are patent\non postcontrast MP RAGE images.\n\nThere are mucous retention cysts and mild mucosal thickening in the maxillary\nsinuses, as well as mild mucosal thickening in the ethmoid air cells.",
            "output": "1. Patchy evolving early subacute infarctions in the posterior inferior\ncerebellar hemisphere, with overall moderate volume.  While no contrast\nenhancement is seen on this exam, late contrast enhancement is seen on neck\nMRA performed 4 hours later on the same day.\n2. No evidence of hemorrhagic transformation.\n3. Mild right cerebellomedullary cistern effacement.  No effacement of the\nfourth ventricle.\n\nRECOMMENDATION(S):  Follow-up brain MRI with and without contrast in\napproximately 6 weeks to ascertain resolution of contrast enhancement."
        },
        {
            "input": "There is conventional 3 vessel branching of the aortic arch.  Common carotid,\ncervical internal carotid, and vertebral arteries appear widely patent without\nevidence for flow-limiting stenosis.  Specifically, no evidence for carotid\nstenosis by NASCET criteria.  Fat-suppressed axial T1 weighted images\ndemonstrate no evidence for intramural hematoma/dissection.\n\nPatchy hyperintensity in the right posterior inferior cerebellar hemisphere on\nthe fat-suppressed axial T1 weighted images corresponds to late contrast\nenhancement of the subacute infarcts detected on the brain MRI with/without\ngadolinium performed approximately 4 hours earlier (without contrast\nenhancement on the initial MRI).  Mild effacement of the right cerebellar\nmedullary cistern is again visualized.\n\nMucous retention cysts and mild mucosal thickening are again noted in the\nincluded portions of the maxillary sinuses.",
            "output": "1. Normal noncontrast neck MRA.  No evidence for vertebral artery intramural\nhematoma/dissection.\n2. Late contrast enhancement of the subacute infarcts detected on the brain\nMRI with/without gadolinium performed approximately 4 hours earlier (without\ncontrast enhancement on the initial MRI).\n\nRECOMMENDATION(S):  Follow-up brain MRI with and without contrast in\napproximately 6 weeks to ascertain resolution of contrast enhancement."
        },
        {
            "input": "There is a moderately enhancing infiltrative mass with internal septations\ncentered in the right ethmoid air cells. The right ethmoid air cells are\ncompletely opacified by this mass. There are areas of cystic changes within\nthis lesion, which also demonstrates restricted diffusion. This lesion is\ncausing erosion  through the right lamina papyracea into the right orbit\nproducing mass effect and displacement of the medial rectus muscle as well as\nthe optic nerve. There is intracranial extension of this mass with invasion\nthrough the cribriform plate in the ethmoid bone into the olfactory groove as\nwell as the straight gyrus in the right frontal lobe. There is associated\nsmall amount of vasogenic edema in the subcortical white matters of the right\nfrontal lobe. This mass also invades through the nasal septum with involvement\nof the left posterior ethmoid air cells. The right superior and middle\nturbinates are also likely involved.  There is also bony erosion of the\nposterior wall of the right sphenoid sinus with tumor involvement.\nThe bilateral sphenoid sinuses are enlarged. There is super-pneumatization of\nthe left sphenoid sinus. The right sphenoid sinus is completely opacified by\nT1 hyperintense material, which likely represents proteinaceous fluid or\ninspissated secretions. The right frontal sinus is also completely opacified\nwith mucosal thickening and enhancement. Enhancement pattern within the right\nfrontal sinus is different from that of the dominant mass, and it is unclear\nwhether this is due to tumor invasion versus incomplete drainage of\nsecretions.\nThere is no evidence of intracranial hemorrhage. The ventricles and sulci are\nnormal in caliber and configuration. The dural venous sinuses are patent.\nMajor intracranial vascular flow voids are preserved. There is no involvement\nof the cavernous sinus by the tumor. The mastoid air cells are normal.",
            "output": "1. Moderately enhancing infiltrative mass centered in the right ethmoid air\ncells with invasion into the right orbit causing mass effect on the medial\nrectus muscle as well as the optic nerve. There is also intracranial extension\nwith erosion of the cribriform plates and involvement of the olfactory groove\nand straight gyrus in the right frontal lobe. This lesion also invades into\nthe nasal septum, left posterior ethmoid air cells, right superior and middle\nturbinates, as well as the posterior wall of the right sphenoid sinus.\nDifferential for this lesion is broad, esthesioneuroblastoma is a\nconsideration given olfactory groove involvement, as well as squamous cell\ncarcinoma. Other neoplasms including metastatic disease or lymphoma. Chronic\ninfectious process is also possible, but less likely.\n2. Proteinaceous or inspissated secretions within the expanded right sphenoid\nsinus likely due to obstruction from the mass. Similarly, the right frontal\nsinus is opacified with mucosal thickening. Enhancement pattern within the\nright frontal sinus is different from that of the dominant mass, and it is\nunclear whether this is due to tumor invasion versus incomplete drainage of\nsecretions."
        },
        {
            "input": "There are areas of restricted diffusion in the bilateral cerebellar\nhemispheres, left greater than right, compatible with acute infarct (4:9,6;\n3:9,6). There are no other concerning areas of restricted diffusion. There is\nno edema or mass identified. A few areas of periventricular and deep white\nmatter hypodensities are nonspecific and may be due to chronic small vessel\nischemic disease. There are no areas of hemorrhage. The paranasal sinuses and\nmastoid air cells are clear.",
            "output": "Areas of restricted diffusion in the bilateral cerebral hemispheres, left\ngreater than right, compatible acute infarcts."
        },
        {
            "input": "There is no acute infarction.  There is no edema, mass effect, or evidence for\nblood products.  No signal abnormalities are seen in the brainstem or\ncerebellum.  There are foci of high T2 signal in the subcortical white matter\nof the cerebral hemispheres, with minimal high T2 signal along the lateral\nventricles, which are nonspecific but likely sequela of chronic small vessel\nischemic disease given the patient's age and cardiovascular risk factors. \nVentricles and sulci are age-appropriate.  Basal cisterns are normal in size.\n\nThere is evidence of bilateral cataract surgery.  There is mild mucosal\nthickening in the ethmoid, maxillary, and sphenoid sinuses, with a small\nmucous retention cyst in the right maxillary sinus and a moderate mucous\nretention cyst in the left maxillary sinus.  There is a tiny focus of air cell\nopacification in the right mastoid tip.",
            "output": "1. No acute infarction.\n2. Scattered signal abnormalities in the subcortical white matter of the\ncerebral hemispheres are nonspecific but likely sequela of chronic small\nvessel ischemic disease, given the patient's age and cardiovascular risk\nfactors."
        },
        {
            "input": "Re-identified is a highly irregular, heterogeneously rim enhancing left\nfrontotemporoparietal mass measuring up to 73 x 48 x 60 mm in maximal\n___.  This mass demonstrates scattered areas of slowed diffusion along\nwith areas of scattered susceptibility artifact suggesting hemorrhage.  There\nis additionally extensive surrounding T2/FLAIR hyperintensity, involving the\nentirety of the frontal lobe, extending superiorly to the left frontal centrum\nsemiovale, also with involvement of the left parietal and occipital lobes,\nindicative of vasogenic edema/infiltration.  There is prominent associated\nmass effect with effacement of the involved sulci, effacement of the left\nlateral ventricle, and up to 4 mm of rightward midline shift.  There is mass\neffect upon the left thalamus and midbrain with effacement of the left\nperimesencephalic cistern, though without frank uncal herniation.\n\nThere is no evidence of infarction.  There is moderate prominence of the\nbackground ventricles and sulci suggestive of age-related involutional change.\nTrace areas of background periventricular and subcortical white matter\nT2/FLAIR hyperintensities most likely reflect the sequela of chronic small\nvessel ischemic disease.  No other enhancing lesions identified.  The\nprincipal intracranial vascular flow voids are preserved.\n\nThere is mild mucosal wall thickening of the left sphenoid sinus, floors of\nthe bilateral maxillary sinuses as well as of the bilateral ethmoid air cells.\nThe frontal sinuses are clear.  The mastoid air cells are clear. There are\nchanges from bilateral lens replacement surgery.  The orbits are otherwise\ngrossly unremarkable.",
            "output": "Irregular, heterogeneously enhancing 73 x 48 x 60 mm left\nfrontotemporoparietal mass with scattered areas of slowed diffusion and\nhemorrhage most likely representing high-grade glioma.  There is extensive\nsurrounding FLAIR signal abnormality throughout the left hemisphere denoting\nvasogenic edema/infiltrative disease, with prominent associated mass effect\nwith up to 4 mm of midline shift."
        },
        {
            "input": "A small area of slow diffusion with associated abnormal T2/FLAIR signal\ninvolves the right parietal cortex ___, 22) compatible with a late acute\nto early subacute infarct.  There is no evidence of hemorrhage, masses, mass\neffect or midline shift.  There are moderate subcortical, deep and\nperiventricular T2/FLAIR white matter hyperintensities compatible with chronic\nsmall vessel ischemic disease given the patient's age.  There is T1/T2\nhyperintensity at the left petrous apex with question of a punctate area of\nassociated diffusion abnormality favored to represent a cholesterol granuloma.\n\nThe major intracranial vascular flow voids are maintained.  There is relative\nprominence of the ventricles relative to the cerebral sulci.  There is\nevidence of a large retrocerebellar arachnoid cyst resulting in mass effect\nand significant atrophy of the cerebellar vermis and to a lesser extent the\nleft and right cerebellar hemispheres..  The paranasal sinuses and mastoid air\ncells are normal.  Status post right lens replacement.",
            "output": "1. Small late acute to early subacute infarct of the right parietal cortex.\n2. Moderate white matter chronic small vessel ischemic disease.\n3. Relative prominence of the ventricles compared to the cerebral sulci can be\nseen in the setting of a communicating type hydrocephalus.\n4. Evidence of a large retrocerebellar arachnoid cyst resulting in mass effect\nand significant atrophy of the cerebellar vermis and to a lesser extent the\nleft and right cerebellar hemispheres.\n5. T1/T2 hyperintensity at the left petrous apex with question of a punctate\narea of associated diffusion abnormality favored to represent a cholesterol\ngranuloma.  Additional differential considerations include petrous apicitis. \nFindings are less likely to be secondary to an underlying mass lesion given\nthe intact peripheral bony cortex.\n\nNOTIFICATION:\nThe acute findings were discussed with Dr. ___, by ___, M.D. on\nthe telephone on ___ at 9:48 pm, 3 minutes after discovery of the\nfindings."
        },
        {
            "input": "Study is mildly degraded by motion, especially on postcontrast imaging. \nWithin these confines:\n\nImages through the internal auditory canal demonstrates symmetric appearance\nof the seventh eighth nerve complexes.  There is no evidence of abnormal\nenhancement or mass lesion within the internal auditory canals,\ncerebellopontine angles or membranous labyrinth. No other mass lesions are\nseen within the posterior fossa.\n\nLimited included imaging of the remainder of the brain demonstrates no\nevidence of hemorrhage, edema, masses, mass effect, midline shift or\ninfarction.  There is no abnormal enhancement after contrast administration.\n\nIncidentally seen is expanded empty sella, grossly unchanged compared to ___ prior exam.\n\nSmall left frontal curvilinear enhancement is noted (see 8:51, 800:52,\n801:24).  Allowing for difference technique, finding may have been present on\n___ prior exam (see 11:10).\n\nAlso seen is minimal T2/FLAIR hyperintensity in the periventricular white\nmatter, nonspecific, likely secondary to small vessel ischemic disease.\n\nNo osseous abnormalities are seen.  Mild mucosal thickening in bilateral\nethmoid air cells.  The remaining visualized paranasal sinuses, mastoid air\ncells, and middle ear cavitiesare clear. The orbits are unremarkable. The\nvisualized portion of the principle vascular flow voids are preserved.",
            "output": "1. Study is mildly degraded by motion.\n2. No evidence of IAC or cerebellopontine angle mass.\n3. Paranasal sinus disease as described.\n4. Limited visualization of nonspecific left frontal curvilinear enhancement\nsecondary to motion degradation.  While finding may represent a developmental\nvenous anomaly, other etiologies, including intracranial metastatic disease,\nis not excluded on the basis examination.  Recommend correlation with\nneurological exam and correlation with oncology history.  If clinically\nindicated, consider repeat exam when patient can tolerate examination.\n\nRECOMMENDATION(S):  Limited visualization of nonspecific left frontal\ncurvilinear enhancement secondary to motion degradation. While finding may\nrepresent a developmental venous anomaly, other etiologies, including\nintracranial metastatic disease, is not excluded on the basis examination.\nRecommend correlation with neurological exam and correlation with oncology\nhistory.  If clinically indicated, consider repeat exam when patient can\ntolerate examination."
        },
        {
            "input": "The intracranial vertebral and internal carotid arteries and their major\nbranches appear normal without evidence of stenosis, occlusion, or aneurysm\nformation.",
            "output": "1. No evidence of aneurysm or AVM.\n2. Patent circle of ___."
        },
        {
            "input": "MRI Brain: There is no evidence of hemorrhage, edema, masses or infarction.\nThere is generalized parenchymal volume loss. There is T2/FLAIR signal\nhyperintensity in the periventricular and subcortical white matter as well as\nwithin the central pons. This is nonspecific but in a patient of this age most\nlikely secondary to chronic small vessel ischemic disease. There is a single\npunctate focus of susceptibility in the right frontal lobe which may represent\nchronic micro hemorrhage or hemosiderin staining from prior trauma.  There is\nno abnormal enhancement on post-contrast images.\n\nMRA brain: The intracranial vertebral and internal carotid arteries and their\nmajor branches appear normal without evidence of stenosis, occlusion, or\naneurysm formation. The right vertebral artery is dominant.\n\nMRA neck: There is irregular plaque at the origin of the right internal\ncarotid artery resulting in approximately 40% stenosis with a possible\nulceration. There is stenosis of the proximal left subclavian artery with\natheromatous plaque seen more distally. Portions of the right brachiocephalic\nartery and vertebral arteries appear unremarkable.\n\nMild grade 1 anterolisthesis of C2 on C3 and pannus surrounding the odontoid\nare noted.",
            "output": "1. Generalized cerebral atrophy. T2/FLAIR signal hyperintensity in the\nperiventricular subcortical white matter as well as the central pons most\nlikely secondary to chronic small vessel ischemic change.\n2. Unremarkable MRA of the brain.\n3. 40% stenosis of the right internal carotid artery at its origin with a\npossible ulceration.\n4. Arthrosclerotic plaque in the left subclavian artery with a proximal\nstenosis"
        },
        {
            "input": "Again seen are chronic infarcts of the left frontal lobe, extending into the\nleft internal capsule, right internal capsule/corona radiata/caudate head,\nright occipital lobe, and right cerebellum and cerebellar peduncle.  There is\nno evidence of acute hemorrhage, edema, masses, mass effect, or midline shift.\n\nThere is mild diffuse increased signal of the cortical sulci diffusion and\nFLAIR images predominantly on the right side but some patchy areas also\nvisualized on the left.  No definite decreased signal identified on ADC map\nfor isointense signal is seen also there is mild diffuse increased signal on\nFLAIR and diffusion images without corresponding low signal on ADC in the left\ncerebral hemisphere.\n\nPartial opacification of the bilateral mastoid air cells.  Mild, left greater\nthan right, mucosal thickening of the bilateral maxillary sinuses, with an\nair-fluid level and aerosolized secretions within the left maxillary sinus. \nAir-fluid levels within the bilateral sphenoid sinuses, against a background\nof mild mucosal thickening.  Partial opacification of the ethmoid air cells. \nSecretions within the nasal cavity.  An ET tube is partially imaged.  The\nbilateral orbits appear unremarkable.  The major intracranial vascular flow\nvoids are preserved.",
            "output": "1. Subtle signal abnormalities on diffusion and FLAIR images predominantly in\nthe right cerebral hemisphere but patchy areas are visualized on the left side\nwith involvement of the left cerebellar hemisphere arch suggestive of subacute\nhypoxic ischemic injury.\n2. Redemonstrated chronic infarcts of the left frontal lobe, right basal\nganglia and deep white matter, right occipital lobe, and right cerebellum.  No\nevidence of new infarct.\n3. Partial opacification of the paranasal sinuses and mastoid air cells,\nlikely sequela of intubation and prolonged supine positioning."
        },
        {
            "input": "There diffusion abnormalities indicative of acute infarct in the right\nposterior inferior cerebellar artery territory left occipital lobe and along\nthese cortical region of the left frontal and parietal lobes. The left and\nright frontal and parietal lobe infarcts are small to characterize but not\nvisualized in the FLAIR indicating acute nature. There is no evidence of blood\nproducts seen. There is no midline shift or hydrocephalus. Mild brain atrophy\nis visualized. The flow void of the right vertebral artery and the left\ninternal carotid artery are not well seen.\n\nMRA of the neck demonstrates nonvisualization of the right vertebral artery\nthroughout the cervical and intracranial region. The left carotid is not\nvisualized distal to the bifurcation. Evaluation of the source images\ndemonstrate no evidence of blood products along the vertebral artery and in\npresence of the occlusion of the left internal carotid from bifurcation, both\nocclusions  appear to be less likely due to dissection and more to\natherosclerotic disease.\n\nMRA of the head demonstrates nonvisualization of the intracranial left\ninternal carotid artery. Diminished flow signal is identified in the left\nmiddle cerebral artery compared to the right side. There is also\nnonvisualization of the right vertebral artery until the vertebrobasilar\njunction. The remaining arteries are patent without evidence of stenosis.",
            "output": "1. Brain MRI shows acute right posterior inferior cerebellar artery infarct\nand small infarcts left frontal and parietal cortical regions and left\noccipital lobe.  No hemorrhage or mass effect.\n2. MRA of the neck and head demonstrate nonvisualization of the right\nvertebral and left internal carotid arteries throughout the cervical and\nintracranial course indicating over occlusion most likely atherosclerotic."
        },
        {
            "input": "MRI BRAIN:\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  Predominantly posterior dural enhancement and dural FLAIR\nhyperintensity is identified.\nScattered and confluent small FLAIR hyperintense foci in periventricular and\ndeep cerebral white matter are nonspecific and may reflect chronic\nmicroangiopathy.  Small focus of blooming artifact on gradient echo sequence\nin the right frontal lobe likely reflects microhemorrhage, possibly in setting\nof hypertension.  Prominent perivascular spaces are noted in bilateral basal\nganglia.  The ventricles and sulci are normal in caliber and configuration.\n\nMRA BRAIN:\nThe intracranial vertebral and internal carotid arteries and their major\nbranches appear normal without evidence of stenosis, occlusion, or aneurysm\nformation.\n\nMRA NECK:\nThe common, internal and external carotid arteries appear normal.  There is no\nevidence of internal carotid artery stenosis by NASCET criteria.  The origins\nof the great vessels, subclavian and vertebral arteries appear normal\nbilaterally.",
            "output": "1. Predominantly posterior intracranial dural enhancement is nonspecific and\nmay be artifactual, although it can reflect inflammatory process.\n2. Major intracranial and cervical arteries are patent without stenosis."
        },
        {
            "input": "The thin line of apparent dural thickening and enhancement seen posteriorly on\nthe prior study is again identified on the conventional T1 weighted images. \nHowever, this disappears on the fat saturated images and is located along the\nright side of the brain on the right to left frequency encoding images.  These\nfindings confirm that this is a chemical shift artifact.",
            "output": "1. The area of possible dural thickening and enhancement noted on the prior\nbrain MR study is confirmed to be chemical shift artifact.."
        },
        {
            "input": "There is unchanged crowding at the level of the foramen magnum with 11 mm\ninferior extension of the cerebellar tonsils, consistent with ___\nmalformation.\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.\n\nThe ventricles and sulci are normal in caliber and configuration.\nThe major vascular flow voids are preserved.\n\nThe paranasal sinuses and mastoid air cells are clear.  The orbits appear\nunremarkable.",
            "output": "1. Unchanged crowding at the level of the foramen magnum with 11 mm inferior\nextension of the cerebellar tonsils, consistent with ___\nmalformation.\n2. Otherwise normal MRI of the head.  No evidence of acute infarction,\nhemorrhage or intracranial mass."
        },
        {
            "input": "Artifact from the patient's ventricular peritoneal shunt partially obscures\nthe right cerebral convexity.  The tip of the shunt catheter is in stable\nposition at the level of the third ventricle.\nPost interventional changes after coil embolization of a fusiform left V4\nsegment aneurysm are again noted.\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor acute infarction.  No diffusion abnormalities are detected.  Unchanged old\nleft chronic cerebellar infarct (series 5, and series 6, image 5).\n\nAllowing for differences in technique, there is no significant change in size\nof the ventricular system.  No midline shift.\n\nUnchanged mucous retention cyst in the left maxillary sinus.  There is mild\nmucosal thickening in the bilateral maxillary sinuses.  The mastoid air cells\nappear clear.  The orbits appear unremarkable.",
            "output": "1. Stable post interventional changes after coil embolization of a fusiform\nleft V4 segment aneurysm.\n2. Stable position of the right frontal approach ventriculoperitoneal shunt\ncatheter with no significant change in size of the ventricular system.\n3. No evidence of acute infarction, hemorrhage or intracranial mass.  The\nbrainstem appears unremarkable without signal abnormality.\n4. Unchanged old left cerebellar  infarct."
        },
        {
            "input": "MRI BRAIN:\nPostsurgical changes after left frontal approach ventriculostomy shunt\ncatheter placement with the tip of the shunt catheter at the level of the\nforamen ___ are again noted.\n\nThere are patchy and punctate areas of DWI hyperintensity in the left\ncerebellar hemisphere, in the medial left occipital lobe as well as in the\nright occipital lobe which for the most part demonstrate ADC and FLAIR\ncorrelates, consistent with recent infarcts.  There is no evidence of\nhemorrhagic transformation.\n\nResidual subarachnoid hemorrhage in the suprasellar cisterns with extension\ninto the basal cisterns is again noted.  There is unchanged intraventricular\nextension with small amount of blood layering in the occipital horns of the\nbilateral lateral ventricles, extending into the fourth ventricle.\nAllowing for differences in technique, there has been decrease in size of the\nventricular system when compared to the most recent CTA with the third\nventricle diameter measuring up to 9 mm from previously 12 mm.\n\nCombination of high-signal intensity in the distal V2 segment (series 22,\nimage 10) as well as in the V4 segment (series 14, image 1 and 2) with a\ndecreased flow in the left vertebral artery is consistent with the previously\nidentified distal left vertebral artery occlusion.\n\nThe remainder of the major vascular flow voids appear preserved.\nThere is mucosal thickening throughout the paranasal sinuses with a 1.7 cm\nmucosal retention cyst in the left maxillary sinus.  There is partial\nopacification of the bilateral mastoid air cells.  The orbits appear grossly\nunremarkable.\n\n\nMRA BRAIN:\nThere is new complete occlusion of the left V4 segment.  Faint partial\nopacification of the distal left V4 segment is likely from retrograde\nperfusion.  The left ___ is not visualized.\nThe intracranial right vertebral and internal carotid arteries and their major\nbranches appear unremarkable without evidence of stenosis,occlusion,or\naneurysm formation.\n\nMRA NECK:\nThere is a decreased contrast opacification of the left vertebral artery with\nnon opacification from the distal V2 segment, consistent with distal left\nvertebral artery occlusion, previously identified on the most recent CTA in\nthe setting of a dissecting left V4 segment aneurysm.\n\nLimited evaluation of the origin of the great vessels due to motion artifact. \nNo definitive high-grade stenosis is identified.  The right vertebral, common,\ninternal and external carotid arteries appear unremarkable.  There is no\nevidence of internal carotid artery stenosis by NASCET criteria.",
            "output": "1. Recent infarctions in the left cerebellum and bilateral occipital lobes.\n2. Occlusion of the left vertebral artery from its distal V2 through V4\nsegment with partial reconstitution of flow in the distal V4 segment from\nretrograde perfusion, similar to prior.  No visualization of the left ___.\n3. Stable postsurgical changes after left frontal approach ventriculostomy\nshunt catheter placement.\n4. Residual subarachnoid hemorrhage, similar to the most recent prior CT, with\noverall improved size of the ventricular system."
        },
        {
            "input": "There is no evidence for intra-axial or extra-axial mass, abnormal\npachymeningeal or leptomeningeal contrast enhancement, edema, abnormal\ndiffusion, or evidence of blood products in the brain parenchyma.  The\nventricles, cerebral sulci, and basal cisterns are normal in size for age.\n\nThere are small foci of high T2/FLAIR signal in the subcortical, deep, and\nperiventricular white matter of the cerebral hemispheres, which are\nnonspecific but may be related to sequela of chronic small vessel ischemic\ndisease in a patient of this age.  Major arterial flow voids are grossly\npreserved.",
            "output": "1. No acute intracranial abnormality identified.\n2. Findings suggestive of chronic small vessel ischemic disease sequelae.\n3. Ventricles and cerebral sulci normal in size for patient's age."
        },
        {
            "input": "Previously identified lesion centered in right temporal/petrous bone at the\nlevel of the jugular foramen is better identified on the CT.  There appears to\nbe a soft tissue component extending further inferiorly and anteriorly which\nis partially visualized and likely demonstrates an area of restricted\ndiffusion (series 502, image 1).  The soft tissue component measures\napproximately 2.3 x 1.8 x 2.9 cm (AP X TR X SI) (series 6, image 2 and series\n4, image 16).  The mass is mostly isointense to muscle on the T1 sequence and\ndemonstrates a slightly heterogeneous signal intensity on the T2 sequence.\nThe mass extends to the right cervical carotid artery with what appears to be\ncomplete encasement of the vessel (series 6, image 51) but preserved right ICA\nflow void.  There is also mild anterior displacement of the cervical right ICA\n(series 4, image 16).\n\nIntracranially, there is no evidence of acute hemorrhage, infarction or\nmidline shift.\n There are scattered T2/FLAIR hyperintensities in the cerebral hemispheres\nbilaterally, a nonspecific finding and likely related to chronic small vessel\nischemic changes.\n\nThe ventricles and extra-axial CSF spaces are age-appropriate.\nNote is made of T1 and T2 hyperintense signal intensity at the level of the\ndistal right transverse sinus and sigmoid sinus which may represent flow\nrelated artifact.  However, are given the absence of IV contrast, no\ndefinitive evaluation of dural venous sinus patency is possible.\nMajor vascular flow voids appear otherwise preserved.\n\nThere is mild mucosal thickening along the ethmoid air cells and in the\nbilateral maxillary sinuses.  There is minimal opacification of the inferior\nbilateral mastoid air cells.  The orbits appear unremarkable.",
            "output": "1. Previously identified lesion centered in the right temporal/petrous bone at\nthe level of the jugular foramen demonstrates a soft tissue component\nextending further inferiorly and anteriorly with encasement and mass effect on\nthe right cervical ICA but with preserved vascular flow void.  Differential\nconsiderations for this lesion include jugular foramen meningioma,\nchondrosarcoma, fibro-osseous lesion,  or metastatic lesion.  Further\nevaluation of this lesion with contrast-enhanced sequences is recommended.  A\nCT of the temporal bone can also be considered for better delineation of the\nosseous involvement.\n2. Hyperintense signal intensity in the distal transverse sinus and sigmoid\nsinus may represent flow related artifact.  However, patency of the dural\nvenous sinuses will need to be evaluated on the postcontrast sequences.\n3. No evidence of acute infarction or hemorrhage.\n4. Nonspecific scattered white matter lesions in the cerebral hemispheres\nbilaterally, likely sequela of chronic small vessel ischemic changes.\n\nRECOMMENDATION(S):  Contrast enhanced MRI sequences are recommended (MRI of\nthe neck with and without contrast) for further evaluation of the skullbase\nlesion.\n\nA CT of the temporal bones can also be considered for better delineation of\nthe osseous involvement."
        },
        {
            "input": "Again identified is the lesions centered in the right temporal/petrous bone at\nthe level of the jugular foramina.  The previously identified soft tissue\ncomponent is again seen which extends inferiorly almost to the level of the\nright carotid bifurcation. The mass measures approximately 2.4 x 1.9 x 4.0 cm\n(AP X TR X SI).  The mass is mostly isointense to muscle on the T1 and T2\nsequences. There is mild enhancement of the lesion after contrast\nadministration.\n\nThere is encasement of the right distal cervical ICA and mild anterior\ndisplacement of the vessel but with preserved flow void, unchanged.\n\nThe mass abuts the right pharyngeal recess with preserved fat planes and no\nevidence of invasion.\nThe salivary glands appear unremarkable.  The parotid glands are normal.\n\nThe right pterygoid muscles appear unremarkable.  There is no cervical\nlymphadenopathy.\n\nAgain noted is mild mucosal thickening in the bilateral maxillary sinuses. \nThere is partial opacification of the bilateral inferior mastoid air cells,\nunchanged.",
            "output": "1. Stable appearance of the right skull base lesion centered in the right\ntemporal/petrous bone.  Extension of the soft tissue component is seen almost\nto the level of the right carotid bifurcation but without adjacent soft tissue\ninvasion.  The mass remains mostly isointense to muscle on the T1 and T2\nsequences and demonstrates mild enhancement after contrast administration. \nDifferential considerations continue to include skull base sarcoma, right\njugular foramina meningioma or possibly a venolymphatic lesion given the\npresence of calcifications on the prior CT.\n2. Stable anterior displacement and encasement of the right internal carotid\nartery with preserved flow void.\n3. No lymphadenopathy."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.\n There are scattered T2/FLAIR hyperintensities in the cerebral hemispheres\nbilaterally, a nonspecific finding but unchanged and likely related to chronic\nsmall vessel ischemic changes.\nIntracranially, there is no abnormal enhancement.\n\nThe ventricles and sulci are age appropriate.\nMajor vascular flow voids are preserved.  There is a filling defect at the\njunction of the right sigmoid sinus into the right jugular vein, consistent\nwith thrombosis (series 9, image 37).  The remainder of the major dural venous\nsinuses is patent.\n\nThere is mild mucosal thickening along the ethmoid air cells and bilateral\nmaxillary sinuses.  There is also partial opacification of the bilateral\ninferior mastoid air cells.\n\nAgain identified is the mildly enhancing right skullbase mass at the right\ntemporal/petrous bone, centered at the level of the jugular foramen. Stable\nsoft tissue component with encasement of the right cervical carotid artery but\npreserved flow void.",
            "output": "1. Sinus venous thrombosis at the junction of the right sigmoid sinus and\njugular vein, likely related to the skullbase mass.\n2. No evidence of intracranial lesions, acute infarction or hemorrhage.\n3. Stable right skullbase mass centered at the right jugular foramen with\ninferiorly and anteriorly extending soft tissue component encasing the right\ninternal carotid artery but with preserved flow void."
        },
        {
            "input": "MR BRAIN:\nThere has been interval increase in size of the medial right temporal lobe\nperipherally enhancing lesion, measuring 1.9 cm x 1.0 cm x 1.8 cm today,\ncompared with 1.4 cm x 0.8 cm x 1.3 cm on ___.  There is thick rim of\nperipheral enhancement, internal microhemorrhage or mineralization.  No\nintrinsic T1 hyperintensity.  There is moderate surrounding FLAIR signal\nabnormality, worsened since prior, extending into the deep white matter of\ntemporal lobe, posterior, inferior sub insula, posterior limb right internal\ncapsule, along the anterior margin of the right periatrial white matter.\n\nThere is no new enhancing focus.\n\nThere is no evidence of recent hemorrhage,mass effect, midline shiftor acute\ninfarction.  The major intracranial vascular flow voids are maintained.\n\nThe paranasal sinuses, mastoid air cells and orbits are normal.\n\nRedemonstrated is a C3 vertebral body metastatic lesion.  Small area of\nsclerosis right calvarial vertex, likely metastasis.\n\nMR ___: No evidence of abnormal perfusion on dynamic perfusion\nimages.\n\nASL Perfusion: No evidence of abnormal perfusion on arterial spin labeled\nimages..\n\nMR Spectroscopy: There is evidence of increased choline with slightly higher\npeak compared with NAA within and surrounding the region of the enhancing\nlesion.  Prominent lipid lactate peak is also seen..",
            "output": "1. Interval increased size of right temporal lobe lesion, mildly worsened\nsurrounding edema.  No abnormality on ASL or DSC, which may favor\npostradiation change.  MR spectroscopy is not typical of radiation necrosis. \nGiven continued increase in size of a lesion over few scans, follow-up MRI in\n___ weeks recommended to exclude tumor.\n2. No new brain lesions.\n3. C3 metastasis, similar.\n\nRECOMMENDATION(S):   Follow-up MRI in ___ weeks"
        },
        {
            "input": "Again identified is an unchanged 7 x 7 mm enhancing nodule in the right medial\ntemporal lobe, which appears to involve the ependymal margin of the lateral\nventricle, appearing inseparable from the choroid plexus.  Surrounding mild\nvasogenic edema appears mildly increased compared to the prior examination.\n\nNonenhancing 12 x 10 mm pineal cyst is unchanged.\n\nThere is no evidence of hemorrhage, new masses, mass effect, midline shift or\ninfarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no new abnormal enhancement after contrast\nadministration.  There is no abnormal focus of slowed diffusion.  The\nprincipal intracranial vascular flow voids are preserved.\n\nThere is minimal mucosal thickening the bilateral maxillary sinuses and\nethmoid air cells.  The sphenoid sinuses are clear.  The orbits are grossly\nunremarkable.  The mastoid air cells are clear.  The known C3 lesion is not\nimaged on the current examination.",
            "output": "1. 7 x 7 mm enhancing nodule in the right medial temporal lobe with minimal\ninvolvement is unchanged in size, though with minimally increased surrounding\nvasogenic edema.\n2. No new enhancing lesion.\n3. The known C3 vertebral body lesion is not imaged on the current study.\n4. Unchanged nonenhancing 12 x 10 mm pineal cyst."
        },
        {
            "input": "There is a left pterional craniotomy with thin subjacent dural enhancement and\na small left frontal subdural fluid collection which measures 2 mm in depth. \nThere is a small focal nodularity of the dural enhancement at the lateral\naspect of the left middle cranial fossa measuring 3 mm (101b:43).  There is no\ncorresponding abnormality at the site on prior CTA.  There is no associated\nslow diffusion or gradient echo blooming.  There is fluid collection\nsuperficial to the craniotomy site measuring up to 3 mm in depth with\nassociated peripheral enhancement enhancement within the overlying scalp soft\ntissues (12:12; 100b:50).\n\nThere is a vascular clip at the anterior communicating artery corresponding to\nsite of treated anterior communicating artery aneurysm.  There is associated\nsusceptibility artifact which mildly obscures adjacent structures.  The\nadjacent vascular flow voids are preserved.\n\nThe parenchymal signal is unremarkable without infarct, hemorrhage, mass, or\nmass effect.  The ventricles and cortical sulci are normal in caliber\nconfiguration.\n\nThe orbits are unremarkable.  There is no abnormal fluid signal within the\nparanasal sinuses, mastoid air cells, or middle ears.",
            "output": "1. Left pterional craniotomy with thin subjacent dural enhancement small left\nfrontal subdural fluid collection, likely arising postsurgical changes\nalthough early infectious process cannot be excluded.  Recommend clinical\ncorrelation.\n2. Small focal nodularity of the dura at the lateral aspect of the left middle\ncranial fossa measuring 3 mm, which may represent postsurgical changes (such\nas a small focus of subacute infarct).  Additional considerations include\ninfectious process, or small dural-based lesion such as a meningioma.  There\nis no corresponding abnormality on prior head CTA.  Recommend follow-up MRI to\ndocument the stability or resolution of this finding.\n3. Trace fluid collection superficial to the left pterional craniotomy with\nmild edema and enhancement within the overlying soft tissues.  Finding may\nrepresent postsurgical changes although infectious process is not excluded. \nRecommend clinical correlation.\n4. Vascular clip at the anterior communicating artery corresponding to site of\ntreated aneurysm causing susceptibility artifact which mildly obscures\nadjacent structures.\n5. No evidence of infarct or hemorrhage.\n\nRECOMMENDATION(S):\n1. Recommend clinical correlation for signs and symptoms of infection given\nthe nonspecific findings of dural enhancement, small subdural fluid\ncollection, small scalp fluid collection, and scalp soft tissue enhancement.\n2. Recommend follow-up head MRI to assess stability or resolution of nodular\ndural enhancement at the left middle cranial fossa.\n\nNOTIFICATION:  The findings were discussed with ___, M.D. by ___\n___, M.D. on the telephone on ___ at 9:34 AM, 10 minutes after\ndiscovery of the findings."
        },
        {
            "input": "There is encephalomalacia and chronic blood products at the right thalamus,\nconsistent with prior hemorrhage.  There is confluent subcortical,\nperiventricular, and deep white matter FLAIR hyperintensity, right greater\nleft, in addition to central and dorsal pontine FLAIR hyperintensity,\ncompatible with sequela of chronic advanced microangiopathy on the left and in\ncombination with prior hemorrhage on the right.  There is a ventricular\ncatheter tract at the right frontal cortex.  There punctate foci of chronic\nblood products within the lateral ventricles.  There is no acute infarct,\nhemorrhage, or mass effect.  There is prominence of the ventricles and\ncortical sulci consistent with volume loss.  The vascular flow voids are\npreserved.  The extra-axial spaces are unremarkable.\n\nThe orbits, soft tissues, and calvarium are unremarkable.  There is a moderate\nmucous retention cyst within the right maxillary sinus.",
            "output": "1. Encephalomalacia and chronic blood products at the right thalamus\nconsistent with sequela of remote hemorrhage.\n2. Extensive confluent periventricular, subcortical, and deep white matter\nFLAIR hyperintensity in addition to central and dorsal pontine FLAIR\nhyperintensity, likely representing sequela of chronic advanced\nmicroangiopathy on the left and in combination with remote hemorrhage on the\nright.\n3. No acute intracranial abnormality without acute infarct, hemorrhage, mass,\nor mass effect."
        },
        {
            "input": "There is a new gradient echo susceptibility artifact overlying the right\nfrontal vertex (series 9, image 19) not seen on prior examination.  Discussion\nwith clinical staff reveals no interval coiling or intervention.\n\nRight frontal lobe encephalomalacia compatible with interval chronic infarct. \nThere are superimposed punctate periventricular and subcortical T2/FLAIR\nnonspecific white matter hyperintensities compatible with chronic\nmicroangiopathy in a patient of this age.  Otherwise, sulci, ventricles\ncisterns are within expected limits for the patient's age.  A gradient echo\nsusceptibility in the left cavernous ICA is compatible with known flow\ndiverting stent placement.  Otherwise, the remainder of the intracranial flow\nvoids are preserved.  The paranasal sinuses are essentially clear.  The orbits\nare unremarkable.  The mastoid air cells demonstrate fluid signal at the tips.\n\nPlease note, evaluation of the intracranial circulation should be performed\nwith MRA and the patient will be called back at no cost.",
            "output": "1. New gradient echo susceptibility focus in the peripheral left frontal lobe.\nThe degree of blooming artifact is concerning for metallic body.  CT is\nrecommended for further evaluation.\n2. Interval chronic right frontal lobe infarct from examination of ___.\n3. The patient will be abrupt back for repeat MRA head with without contrast\nat no cost to the patient.  This has been entered into the radiology callback\nlist.\n\nRECOMMENDATION(S):  CT head without contrast is recommended for further\nevaluation of new gradient echo susceptibility artifact in the left frontal\nlobe.\n\nNOTIFICATION:  The findings were discussed by Dr. ___ with ___\n___ the telephone on ___ at 3:51 ___,  at the time of discovery of\nthe findings.  Results also discussed with Dr. ___ at 16:00"
        },
        {
            "input": "The patient is status post right frontoparietal craniotomy and evacuation of\nhematoma.  Intrinsic T1 hyperintensity within the right frontoparietal lobe,\nis consistent with patient's residual hemorrhage as seen on the prior CT from\n___.  Extensive surrounding vasogenic edema is seen on the FLAIR and\nT2 weighted images, extending inferiorly to the level of the posterior horn of\nthe right lateral ventricle and anteriorly to the level of the right insular\ncortex.  Associated restricted diffusion surrounding the evacuated right\nfrontoparietal cavity, is likely postsurgical in etiology.\n\nPunctate foci of restricted diffusion is seen within the right occipital lobe,\nseries 6, image 12 right frontal lobe, series 6, image 26, left frontal lobe,\nseries 6, image 23 and left precentral gyrus, series 6, image 24.  Given the\nassociated FLAIR changes, this is likely subacute in etiology and sequelae of\npatient's prior angiography.\n\nExtensive susceptibility artifact on the GRE weighted sequences in the right\nfrontoparietal lobe and left frontal lobe is a combination of patient's\nresidual hemorrhage and pneumocephalus is seen on the prior CT.  The\nintravascular flow voids appear to be overall preserved.  No marrow signal\nabnormalities are identified.  The globes are unremarkable.  The visualized\nparanasal sinuses, mastoid air cells, and middle ear cavities are clear. \nAppropriate postsurgical changes are seen status post right sided craniotomy. \nNo definite concerning enhancing lesions are identified, however please note\nthat evaluation is limited for concerning lesions in the acute postoperative\nperiod.  Appropriate postsurgical enhancement is seen within the resection\ncavity.",
            "output": "1. Status post right frontoparietal craniotomy and evacuation of hematoma with\na small amount of residual hematoma and extensive surrounding vasogenic edema.\n2. Appropriate post surgical enhancement is seen within the resection cavity. \nEvaluation for underlying enhancing lesions is difficult given the extensive\nhematoma in the operative bed.  A follow-up MRI after resolution of patient's\nunderlying hematoma is recommended to exclude underlying enhancing lesions.\n3. Subacute foci of infarction within the bilateral frontal lobes and right\noccipital lobe.  No evidence of a large territorial infarction.\n4. Appropriate postoperative pneumocephalus."
        },
        {
            "input": "Redemonstrated are postsurgical changes of right frontoparietal craniotomy and\ncranioplasty for evacuation of a large parenchymal hematoma in this region. \nIn comparison to the prior MR examination of ___, while previously\nnoted immediate postsurgical changes such as scalp swelling and small right\nsubdural fluid collection have results, there has been interval development of\nvolume loss in the region of the hemorrhage with ex vacuo dilatation of the\nright lateral ventricle.  Vasogenic edema has decreased and midline shift has\nresolved.  Residual areas of white matter FLAIR hyperintense signal in the\nsubcortical white matter may represent a combination of gliosis and edema.  A\n13 x 34 mm irregular focus of enhancement in this region abutting the right\nlateral ventricle is probably related to compromise of the blood-brain barrier\ncaused by the extensive hemorrhage and subsequent surgery (13:16).  A rounded\nfocus of low signal on T2 weighted imaging with blooming on the gradient echo\nimages in the left frontal lobe is unchanged the may represent hemosiderin\ndeposition from a chronic hemorrhage.\n\nThere is no evidence of new hemorrhage or acute infarction.  Scattered\npunctate periventricular, subcortical, and deep white matter T2/FLAIR\nhyperintense foci are nonspecific but likely sequelae of chronic\nmicroangiopathy.  Principal intracranial vascular flow voids are preserved and\nthe dural venous sinuses enhance appropriately on postcontrast MP rage\nsequences.  Mild dural thickening and enhancement along the craniotomy margin\nwould be expected.",
            "output": "1. Interval resolution of previously noted immediate postoperative changes in\nthe right frontoparietal region for evacuation of a large intraparenchymal\nhemorrhage in this region as described above.\n2. Expected evolution of hemorrhage and postsurgical changes including volume\nloss, slightly dilatation of the right lateral ventricle, subcortical white\nmatter FLAIR hyperintense signal, and hemosiderin deposition.\n3. An irregular focus of parenchymal enhancement in the region without mass\neffect would be unusual for neoplastic lesion.  However, persistent\nenhancement would require follow-up until resolution to exclude an underlying\nabnormality.  .  There is no additional evidence to suggest an underlying mass\nor vascular malformation and given the presence of chronic blood products in\nthe left frontal region the underlying etiology may be amyloid angiopathy.\n4. No evidence of new hemorrhage or acute infarction.\n\nRECOMMENDATION(S):  Close follow-up to monitor the enhancement in the right\nparietal periatrial region with loss of volume in the region."
        },
        {
            "input": "Study is mildly degraded by motion.\n\nBifrontal nonenhancing white matter lesions are noted (see 4:63, 109; 400:413,\n420).  No lesions demonstrate associated restricted diffusion or increase\nsusceptibility.\n\nThere is no evidence of hemorrhage, masses,mass effect,midline shift or\ninfarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.  Minimal right ethmoid air cell mucosal thickening is present.\nPreviously noted dural calcification overlying right parietal lobe is again\nnoted (see 06:18 on current study and 03:48 on prior exam).  Scattered\nsubcentimeter nonspecific lymph nodes are noted throughout the visualized\nportion of the neck bilaterally, without definite enlargement by CT size\ncriteria.\n\nApproximately 3 mm left choroid fissure cyst is noted (see 07:40 ___ 7\n301:261; 300:260).  Bilateral hippocampal formations and mammillary bodies are\ngrossly preserved in signal and configuration. There is no definite\ndisproportionate medial temporal atrophy. There is no definite focal lobar\nencephalomalacia. There are no focal cortical dysplasias or gray matter\nheterotopia noted.",
            "output": "1.  Study is mildly degraded by motion.\n2. Few nonspecific bifrontal nonenhancing white matter lesions as described. \nDifferential considerations include sequela of prior trauma or infection,\nhistory of migraine headaches, inflammatory or demyelinating process, and\nmicroangiopathic changes.\n3. No definite evidence of intracranial mass or acute infarct.\n4.  Within limits of study, no definite evidence of focal or global\nencephalomalacia.\n\nNOTIFICATION:  The impression and recommendation above was entered by Dr.\n___ on ___ at 10:08 into the Department of Radiology critical\ncommunications system for direct communication to the referring provider."
        },
        {
            "input": "Again seen is left greater than right T2 hyperintensity in the cerebellum and\ndorsal pons along the fourth ventricle, not significantly changed on the left\nbut progressed on the right.  Contrast enhancement is decreased on the left\nbut slightly increased on the right (images 10:9, 900:76).  There are new\nsmall foci of slow diffusion along the posterior margins of bilateral\ncerebellar lesions, images 402:9, 402:8, 400:8, which are more intense than\nthe previously demonstrated slow diffusion in the left cerebellar lesion. \nSmall focus of intrinsic T1 hyperintensity in the left cerebellar lesion,\nwhich may indicate blood products or mineralization, image 5:10, has not\nchanged significantly.\n\nT2 hyperintensity in the left midbrain has decreased, images 8:11 and 06:11,\nwithout associated contrast enhancement.\n\nThere are areas of T2 hyperintensity along the body of the left lateral\nventricle and the left caudate, with decreased caudate hyperintensity compared\nto the prior exam.  There is new T1 hyperintensity on precontrast T1 weighted\nimages (___) and increased contrast enhancement on postcontrast T1\nweighted images (10:15, 10:17), likely due to interim biopsy, as a biopsy\ntrack is seen in the left frontal lobe extending to this lesion.  There is\nalso new low signal on gradient echo images within this lesion, consistent\nwith chronic blood products.  There is persistent abnormal diffusion within\nthis lesion.\n\nThere is high T2 signal in the periventricular white matter along the frontal\nhorn of the right lateral ventricle, extending into the genu of the corpus\ncallosum and into the right caudate, increased in extent compared to the prior\nstudy, but with slightly decreased contrast enhancement.  There is persistent\nabnormal diffusion within this lesion.\n\nThere is new T2 hyperintensity without contrast enhanced in the left lateral\noccipital lobe, involving the subcortical white matter, image 8:14. There is a\nsmall focus of abnormal diffusion in this lesion, image 402:17.\n\nThere is a new T2 hyperintense focus in the left frontal deep white matter on\nimage 8:17, without contrast enhancement.  There is a small focus of abnormal\ndiffusion within this lesion, image 402:19.\n\nThe ventricles are stable in size and age-appropriate.  Major vascular flow\nvoids are preserved.\n\nThere is mucosal thickening in left greater than right ethmoid air cells, as\nwell as mild mucosal thickening in the maxillary sinuses.  There is a small\namount of fluid in the right mastoid.",
            "output": "1. Left greater than right cerebellar and dorsal pons lesion is stable on the\nleft but increased on the right.  New small foci of slow diffusion along the\nposterior margin of bilateral cerebellar lesions may represent active lymphoma\nor small acute infarcts.\n2. New T2 hyperintense, nonenhancing lesions with slow diffusion in the left\nfrontal deep white matter and left occipital subcortical white matter, most\nlikely lymphoma progression rather than acute infarcts.\n3. Post biopsy changes in the lesion along the body of the left lateral\nventricle and left caudate, with new blood products and slightly increased\nenhancement.  Slightly decreased T2 hyperintensity in the left caudate.\n4. Increased extent of T2 hyperintense lesion along the frontal horn of the\nright lateral ventricle and right caudate, with new extension into the genu of\nthe corpus callosum, but with decreased enhancement.\n5. Decreased T2 hyperintensity in the left midbrain without contrast\nenhancement."
        },
        {
            "input": "Wild previously seen multifocal supra and infratentorial FLAIR hyperintense\nfoci involving bilateral caudate nuclei and bilateral cerebellar hemispheres\nas well as the left temporo-occipital subcortical white matter and left\ncentrum semiovale have improved, additional foci of abnormal signal have\ndeveloped.  These new foci include a large portion of the right lentiform\nnucleus, left posteromedial thalamus and a smaller focus in the subcortical\nwhite matter in the posterior left temporal lobe adjacent to the atrium of the\nleft lateral ventricle (series 8, images 12, 13).  These new areas do not show\nslow diffusion.  Mildly prominent vessels in the region of the right lentiform\nnucleus are unchanged compared to the prior study.  There is no definite\nenhancement associated with these new lesions.  There is patchy enhancement\nassociated with residual cerebellar lesions.\n\nSusceptibility artifact in the region of the left caudate nucleus has\ndecreased compared to the prior study and likely represents evolution of\nhemorrhagic products from prior biopsy in this region.  A left frontal burr\nhole and biopsy tract are again noted.  There is no evidence of recent\nhemorrhage or acute infarction.  Ventricles and sulci are stable.  Principal\nintracranial vascular flow voids, including those of the dural venous sinuses\nare preserved.\n\nMultiple lymphoepithelial cysts are again noted in bilateral parotid glands,\nlikely related to the patient's HIV diagnosis (image 102, series 1001).  There\nis no abnormal enhancement along the visualized cranial nerves although the\nsixth cranial nerves are small and not well visualized.",
            "output": "1.  Previously noted multifocal supra and infratentorial lesions as described\nabove have improved, however new ill-defined areas of FLAIR hyperintense\nsignal without definite slow diffusion or enhancement have developed in the\nright lentiform nucleus, left posteromedial thalamus, and left posterior\ntemporal subcortical white matter.  In a patient with HIV, these changes could\nrepresent progression of lymphoma specially since, some of the presumed\nlymphoma lesions previously did not enhance.  Other differential\nconsiderations include infection, inflammation, or drug reaction.\n\n2.  Persistent patchy enhancement in the residual areas of abnormal signal in\nbilateral cerebral hemispheres.\n\n3.  No recent hemorrhage or acute infarction.\n\n4.  Unchanged bilateral parotid lymph or petechial cysts, likely related to\nHIV."
        },
        {
            "input": "The patient is status post left frontal burr hole, previously identified areas\nof left-greater-than-right periventricular white matter FLAIR hyperintensities\nalong with subtle enhancement involving the left frontal corona radiata and\nbody of the right caudate have resolved, with small areas of residual\nencephalomalacia in the areas of prior disease.  Previous identified FLAIR\nhyperintensities within the right basal ganglia and left thalamus have\nsignificantly improved, with punctate focus remaining in the right putamen and\nsubtle, ill-defined FLAIR hyperintensity in the left caudate in area of prior\ndisease involvement.  On additional focus of left occipital subcortical FLAIR\nhyperintensity has also resolved.  FLAIR hyperintensities in the bilateral\ncerebellar hemispheres have also significantly improved, with interval\nresolution of associated subtle enhancement.  No new FLAIR hyperintense\nlesions or abnormal enhancement is seen.\n\nThere is no evidence of hemorrhage, increasing edema, new masses, mass effect,\nmidline shift or infarction.   The ventricles and sulci are normal in caliber\nand configuration.  A tract is seen from prior left frontal ventriculostomy\ncatheter.  There is no abnormal enhancement after contrast administration. \nThe principal intracranial vascular flow voids are preserved.\n\nThere is a small mucous retention cyst in the floor of the left maxillary\nsinus along with trace bilateral ethmoid air cell mucosal wall thickening. \nThe remainder of the visualized paranasal sinuses are otherwise clear.  The\norbits are grossly unremarkable.  The mastoid air cells are clear.",
            "output": "1. Interval resolution of multifocal areas of enhancement with near resolution\nof previously noted FLAIR signal abnormality with minimal residual areas of\nFLAIR hyperintensity in the right putamen, left thalamus and bilateral\ncerebellar hemispheres likely reflecting posttreatment changes.\n2. Otherwise no acute infarct, hemorrhage, or new enhancing lesion."
        },
        {
            "input": "As compared to the prior examination, there has been no significant interval\nchange.  Redemonstrated is minimal residual T2/FLAIR hyperintensities within\nthe right putamen, left thalamus, and bilateral cerebral hemispheres.\n\nThe patient is again status post left frontal burr hole with a pro tract\nidentified extending towards the prior site of left frontal ventriculostomy\ncatheter. There is no evidence of acute infarction.  No acute intracranial\nhemorrhage.  Several small foci low signal on GRE sequences along the left\nperiventricular white matter (06:15) correlates to prior sites of treated CNS\nlymphoma.  No mass, mass effect, edema or midline shift.\n\nThe ventricles and sulci are normal, without evidence of hydrocephalus. The\nbasal cisterns are patent.  There is no evidence of impending, downward\nherniation.  There is gross preservation of the principal intracranial\nvascular flow voids.\n\nFollowing the administration of intravenous contrast material, there is no\nabnormal enhancement.  The dural venous sinuses appear patent on MP-RAGE\nimagine sequences.\n\nThe visualized paranasal sinuses, middle ear cavities, and mastoid air cells\nare well aerated and clear.  The orbits are within normal limits bilaterally.",
            "output": "1. No evidence for acute intracranial process.\n2. Unchanged appearance of T2/FLAIR hyperintensities within the right putamen,\nleft thalamus, and bilateral cerebral hemispheres.  No associated slow\ndiffusion or contrast enhancement.  These findings likely represent stable\npost treatment change.\n3. Small focal areas of low signal on GRE sequences along the left\nperiventricular white matter likely correlate with sites of prior treated CNS\nlymphoma."
        },
        {
            "input": "Status post left frontal burr hole extending toward its prior site of left\nfrontal ventriculostomy catheter.\n\nRedemonstrated is mild FLAIR hyperintensity at the site of the patient's\ntreated left cerebellar hemisphere lesion (8:7).  There is no evidence of\nassociated abnormal enhancement.  No significant change in very subtle FLAIR\nhyperintensity within the left greater than right thalami.  Mild asymmetric\nsize of the left cerebral peduncle likely wallerian degeneration.\n\nPreviously seen FLAIR hyperintensities in the right putamen and right\ncerebellar hemisphere are no longer appreciated.  Redemonstrated are a few\nscattered white matter hyperintensities that are nonspecific and possibly\nrelate to sequela of chronic migraine headaches, old trauma or\ninfection/inflammation.\n\nThere is bilateral increased T2/FLAIR hyperintense signal enlargement of the\ninferior alveolar early nuclei (series 9, image 5; series 8, image 5), similar\nin appearance since examination of ___ compatible with hypertrophic\nolivary degeneration.\n\nNo change in several small foci of low signal on gradient echo images in the\nleft periventricular white matter likely correlating to prior sites of treated\nCNS lymphoma.\n\nThere is no evidence of intracranial hemorrhage or infarction.  The ventricles\nand sulci are normal in caliber and configuration.  There is no abnormal\nenhancement after contrast administration.\n\n The major intracranial vascular flow voids are maintained.  The dural venous\nsinuses are patent.  There is mild mucosal thickening of the visualized\nparanasal sinuses.  The orbits are unremarkable.  Trace fluid signal is seen\nin the right mastoid tip.  Seen on MP-RAGE sequence is a prominent 5 mm right\nparotid cyst, overall similar to prior CTA of ___.",
            "output": "1. Unchanged nonenhancing FLAIR hyperintensities involving the left cerebellum\nand left greater than right thalami.\n2. No longer identified FLAIR hyperintensity within the right putamen and\nright cerebellar hemisphere.\n3. No new enhancing lesions are identified.\n4. Unchanged appearance of bilateral mild enlargement and T2/FLAIR\nhyperintense signal of the inferior olivary nuclei, compatible with\nhypertrophic olivary degeneration.\n5. Additional findings described above."
        },
        {
            "input": "There is an approximately 20 x 24 mm region of ring-like T2/FLAIR hyperintense\nsignal in the left cerebellar white matter abutting the fourth ventricle,\nexerting mild mass effect on the fourth ventricle (108:51).  There is\nassociated peripheral contrast enhancement, which is thinner than the\nring-like T2 hyperintensity, image 102:38.  There also foci of slow diffusion\nwithin the T2/FLAIR hyperintense portion.  Elevated T2/FLAIR signal without\ncontrast enhancement or definite slow diffusion extends into the contralateral\nright cerebellar periventricular white matter, ipsilateral left cerebellar\npeduncle, and left greater than right periventricular dorsal pons, and left\nmidbrain.\n\nThere are additional areas of T2/FLAIR hyperintense signal along the body of\nthe left lateral ventricle, involving the body of the left caudate, and along\nthe frontal horn of the right lateral ventricle.  There is associated contrast\nenhancement, images 102:75, 102:64.  There is a small focus of slow diffusion\nalong the frontal horn of the right lateral ventricle, image 7:19, but\ndiffusion along the body of the left lateral ventricle and body of the left\ncaudate appears fast.\n\nThere is high signal on T2/FLAIR images in the posteromedial left greater than\nright temporal lobes, with cortical involvement.  There is no evidence for\nassociated contrast enhancement or slow diffusion.\n\nThere are small foci high T2 signal in the body and genu of the corpus\ncallosum.  There is a punctate focus of FLAIR hyperintense signal in the right\nfrontal deep white matter (image 5:15).\n\nThere is no evidence of intracranial blood products.  There is no\nhydrocephalus.  Cerebellar tonsils are normally positioned principal\nintracranial vascular flow voids are preserved.  The dural venous sinuses\nenhance appropriately on postcontrast MP rage sequences.\n\nThere is a mucous retention cyst and mild mucosal thickening in the left\nmaxillary sinus.  Multiple bilateral anterior ethmoid air cells are opacified,\nwith mucosal thickening extending into the frontoethmoidal recesses, and other\nbilateral ethmoid air cells demonstrate mild mucosal thickening.  There is\nalso mild mucosal thickening in the right sphenoid and right maxillary\nsinuses.",
            "output": "1. Multiple T2/FLAIR hyperintense lesions involving the left greater than\nright cerebellum along the fourth ventricle, left cerebellar peduncle, left\ngreater than right periventricular dorsal pons, left midbrain, left greater\nthan right posteromedial temporal cortex, periventricular white matter along\nthe body of the left lateral ventricle and in the body of the left caudate,\nperiventricular white matter along the frontal horn of the right lateral\nventricle, and in the corpus callosum.  Left cerebellar periventricular\nlesion, the lesion involving the left periventricular white matter and body of\nthe caudate, in the lesion along the frontal horn of the right lateral\nventricle demonstrate contrast enhancement.  The left cerebellar\nperiventricular lesion and the right frontal periventricular lesion\ndemonstrate contrast enhancement.  Diagnostic considerations include Listeria,\nviral, or mycobacterial infection, Behcet disease, atypical demyelination, or\na paraneoplastic syndrome.\n2. Mild effacement of the left aspect of the fourth ventricle.  No shift of\nmidline structures.  No hydrocephalus.\n\nNOTIFICATION:  The findings were discussed with ___, M.D. by ___\n___, M.D. on the telephone on ___ at 1:08 pm."
        },
        {
            "input": "Please note the study is mildly degraded by motion.\n\nPostoperative changes are noted from left temporal craniectomy and trans\nlabyrinthine approach for resection of vestibular schwannoma with\nmastoidectomy changes and T1 hyperintense fat packing in the mastoid air\ncells.  Thin pachymeningeal enhancement is noted along the left temporal\nconvexity, likely postsurgical in etiology.  There is an extra-axial fluid\ncollection in the soft tissues underlying the surgical site.  There is minimal\nFLAIR hyperintense signal in the lateral left temporal lobe.  There is been\nresection of the enhancing mass in the left internal auditory canal with no\nresidual enhancement identified.  Extensive postoperative changes are noted to\nthe internal auditory canal.  The left seventh and eighth cranial nerves are\nnot well visualized.  The cochlea is seen.  The vestibule and semicircular\ncanals are not seen.\n\n Periventricular and subcortical T2 and FLAIR hyperintensities are noted.  An\nempty sella is seen.  There is a filling defect in the distal left jugular\nvein and transverse sinus with relatively normal opacification of the sigmoid\nsinus.  No acute infarct is seen.\n\nImages through the right internal auditory canal demonstrates normal\nappearance of the seventh and eighth nerve complexes.\n\nThe orbits are unremarkable.  Retention cyst is seen in the right ethmoid\nsinus.",
            "output": "1. Postoperative changes from trans labyrinthine approach resection of left\nvestibular schwannoma with no residual enhancement seen in the region of the\ninternal auditory canal to suggest residual tumor.  Extensive postoperative\nchanges in the inner ear cavity, as described above.\n2. Tandem sinus venous thrombosis in the distal left jugular vein and\ntransverse sinus.\n3. Minimal abnormal high signal in the lateral left temporal lobe, likely\npostsurgical in etiology.\n\nNOTIFICATION:  The results of this study were discussed by Dr. ___ with\nDr. ___ at 8:06 am by phone."
        },
        {
            "input": "There are multiple foci of slow diffusion in the bilateral cerebellar\nhemispheres including the vermis, left greater than right.  A larger area of\nlow diffusion is noted in the right caudate.  There are multiple additional\npunctate foci of slow diffusion in the left frontal, parietal, temporal and\noccipital lobes, including both the gray and white matter, and to a lesser\nextent in the right frontal lobe.  There are multiple punctate foci of\nhemorrhage at the areas of slow diffusion, however the majority of the areas\nof slow diffusion do not demonstrate hemorrhage.  Additional hazy hemorrhage\nis noted along the left parietal lobe.  Multiple additional areas of T1\nhyperintense signal are noted within the gray matter, predominantly of the\nleft parietal, occipital and temporal gray matter, also suggesting hemorrhage.\n\nLeptomeningeal FLAIR hyperintense signal and contrast enhancement is noted\ndiffusely along the convexities, left greater than right.  There is FLAIR\nhyperintense signal with associated sulcal effacement in the a left parietal,\noccipital and posterior temporal lobes and to a lesser extent in the left\nfrontal lobe.  Abnormal FLAIR signal extends into both the gray and white\nmatter.  Additional areas of FLAIR hyperintense signal are noted in the\nperiventricular white matter on the right.  There is mild effacement of the\nleft lateral ventricle.\n\nThe major vascular flow voids are preserved.  The orbits, paranasal sinuses\nand mastoids are normal.  The visualized soft tissues are normal.  Minimal\nlayering fluid is noted in the nasopharynx.",
            "output": "1. Multiple supra and infratentorial subacute infarctions, with associated\npetechial hemorrhage, left greater than right, involving both the gray and\nwhite matter, which may be secondary to an embolic etiology from a cardiac\nsource.  Recommend correlation with echocardiogram.   Associated edema\nresulting in sulcal effacement, predominantly along the left parietal,\noccipital and temporal lobes which may be a sequelae of the evolving infarcts.\nAlternatively, this could represent amyloid associated angiography with\nsuperimposed infarctions.\n2. Multi focal abnormal leptomeningeal signal with associated contrast\nenhancement, which may represent subarachnoid hemorrhage from the infarctions,\nor infection, although infection is less likely given patient's clinical\ncondition.  Leptomeningeal carcinomatosis were inflammation are also less\nlikely given negative results of prior CSF sample from the lumbar puncture. \nInfection could give rise to infarction and hemorrhage.  Carcinomatosis or\ninflammation would be difficult to at reconciled with the evidence of\ninfarction and hemorrhage."
        },
        {
            "input": "As seen on prior head MRI, there are extensive areas of leptomeningeal\nthickening and enhancement, left greater than right.  There is associated mass\neffect with mild effacement of the left lateral ventricle.  These findings\nhave significantly progressed compared to the prior MRI from ___.\nGiven the rapid interval progression, this is favored to be infectious or\ninflammatory in etiology.  The rapid progression and evidence of infarction\nand hemorrhage argue against leptomeningeal carcinomatosis.  Sarcoidosis is\nalso less likely given the absence of any supporting findings on other\nimaging, the cortical infarction and hemorrhage and the rapid interval\nprogression.\n\nThe evaluation of previously seen areas of slow diffusion and extensive areas\nof FLAIR hyperintensity cannot be performed on today's study given the Wand\nprotocol.\n\nThe orbits appear unremarkable.  The visualized paranasal sinuses and mastoid\nair cells are clear.  The dural venous sinuses are patent",
            "output": "1. Marked interval progression of extensive leptomeningeal enhancement with\nareas of nodular thickening and enhancement, left greater than right with some\nmass effect and effacement of left lateral ventricle compared to the prior MRI\nfrom ___.  Given the rapid interval progression, infectious or\ninflammatory etiologies, especially fungal are favored to be most likely.  The\nother possible etiology is leptomeningeal carcinomatosis though favored to be\nless likely given the absence of any primary malignancy identified so far. \nSarcoidosis is unlikely given the rapid progression."
        },
        {
            "input": "Compared to the prior MRI from ___, there has been interval left\nparietal bowel hole for histological sampling.\n\nThere is interval decrease in the amount of leptomeningeal thickening and\nenhancement compared to the prior MRI with persistent left cerebral\nenhancement greater than the right.  There is interval decrease in the amount\nof mass effect on the left lateral ventricle.\n\nThere is associated extensive FLAIR signal abnormality, especially in the left\nparietal temporal lobes, relatively unchanged compared to the prior MRI from ___.  There are some new areas of susceptibility in the left\nparietal lobe near the biopsy tract, likely secondary to post biopsy\nhemorrhage.\n\nThere is interval evolution of the previously seen multiple infarcts in\nbilateral cerebral hemispheres, left greater than right, especially in the\nleft parietal and temporal lobes.  There are few scattered foci of new\ninfarcts in the right frontal centrum semiovale as seen on image 5 02:21 in\nthe right insular cortex on image 502:19.  There are few other new foci of\npunctate infarcts in bilateral cerebellar hemispheres.\n\nThere is interval increase in the areas of T1 intrinsic hyperintensity in the\nleft parietal, temporal add occipital cortex, likely a combination of\nhemorrhage and some areas of the laminar necrosis given the acute infarcts.\n\nThe orbits are unremarkable.  There is mild mucosal thickening in bilateral\nethmoid air cells.  The remaining visualized paranasal sinuses and mastoid air\ncells are clear.  Intracranial flow voids are maintained.",
            "output": "1. Interval decrease in the amount of leptomeningeal thickening and\nenhancement, especially along the left parietal, temporal and occipital lobes.\nRelatively stable surrounding FLAIR signal abnormality and mass effect.\n2. Interval evolution of previously seen multiple foci of infarcts in\nbilateral cerebral and cerebellar hemispheres with few due punctate foci of\ninfarcts.\n3. Interval increase in the about of intrinsic T1 hyperintensity in the left\nparietal, occipital and temporal lobes, likely a combination of laminar\nnecrosis and hemorrhage.\n4. The constellation of findings suggest the possibility of cerebral amyloid\nangiopathy related inflammation."
        },
        {
            "input": "There is motion artifact on the post-contrast MPRAGE sequence which degrades\nspatial resolution.\n\nThere are scattered foci of slow diffusion bilaterally within the cerebellar\nhemispheres, subcortical white matter, and cortices which have overall\nimproved in comparison to prior study.  This slow diffusion is most prominent\nand confluent at the left inferior parietal lobule.  There are new punctate\nfoci of slow diffusion at the anterior right temporal lobe (5 02:11), right\nlateral cerebellar hemisphere (502:8), and at the left anterior centrum\nsemiovale (502:22).  There is unchanged linear gradient echo hypointensity at\nthe left parietal cortex.  There is a punctate focus of gradient echo\nhypointensity at the right parietal cortex (___).  There is cortical\nintrinsic T1 hyperintensity throughout the left parietal cortex, which is\nrelatively unchanged.  There is patchy low a linear cortical enhancement\ninvolving the left parietal cortex.  There is sulcal FLAIR hyperintensity and\nleptomeningeal enhancement throughout the bilateral cerebral convexities, left\ngreater than right, and within the cerebellar folia, which has mildly\nincreased in comparison to prior study.  There is parenchymal enhancement at\nthe anterior right caudate nucleus consistent with subacute infarct.\n\nThere is extensive confluent FLAIR hyperintensity involving the left parietal\nand temporal cortex, without significant mass effect.  There is unchanged\nprominence of the ventricles in comparison ___.  There is\nperiventricular subcortical white matter FLAIR hyperintensity consistent with\nsequela of chronic microangiopathy.  The vascular flow voids are preserved. \nThe dural venous sinuses and cortical veins enhance normally.\n\nThe orbits are unremarkable.  There is a left parietal craniotomy.  There is\nno fluid signal from the paranasal sinuses are mastoid air cells.  The soft\ntissues are unremarkable.",
            "output": "1. Scattered foci of slow diffusion probably involving the left parietal\ncortex with associated linear gradient echo hypointensity and T1\nhyperintensity consistent with petechial hemorrhage and/or laminar necrosis. \nAdditional foci of slow diffusion involving the bilateral cerebellar\nhemispheres and cerebrum.  Overall the extent of slow diffusion as a decreased\nin comparison to prior study consistent with evolving ischemic change, however\nthere several new foci of slow diffusion involving the right cerebellar\nhemisphere, anterior right temporal cortex, and left anterior centrum semi\novale.\n\n2. Leptomeningeal enhancement involving the bilateral cerebral hemispheres and\ncerebellar folia which have mildly increased in comparison to prior study. \nOverall, findings are suspicious for inflammatory cerebral amyloid angiopathy\nwith differential including embolic infarcts, vasculitis, or\nmeningoencephalitis."
        },
        {
            "input": "The examination is moderately motion degraded.  Within these confines:\n\nLeft parietal craniotomy is identified.\n\nSince the prior exam of ___, is interval development of a new 6 mm\nright temporal lobe acute infarct (series 6, image 11).  Additional punctate\nnew foci of slow diffusion of the left frontal lobe (series 6, image 23), left\nanterior temporal lobe (series 6, image 14) and left cerebellar hemisphere\n(series 6, image 6) are identified.  There is now new enhancement of a right\nanterior temporal lobe infarct seen on prior exam (series 13, image 9).\n\nSuperimposed diffusely scattered foci of slow diffusion of the bilateral\ncerebral and cerebellar hemispheres are re-identified, many of which\ndemonstrate postcontrast enhancement.  Unchanged linear gradient echo\nhypointensity of the left parietal cortex with associated patchy cortical\nenhancement.  Additional, punctate peripheral foci of gradient echo\nsusceptibility artifact are also unchanged.  Diffuse enhancing FLAIR\nhyperintense sulcal and leptomeningeal signal is also similar in appearance to\nprior examination.\n\nConfluent FLAIR hyperintense signal of the left parietal and temporal lobes is\nre-identified, with slightly increased involvement of the inferior left\ntemporal lobe, corresponding to regions of new infarct.  Periventricular and\nsubcortical T2/FLAIR white matter hyperintensities are re-identified, which\nare nonspecific but may be seen in the setting of chronic microangiopathy in a\npatient of this age.  The major intracranial flow voids are preserved.  The\ndural venous sinuses are patent.  The paranasal sinuses are essentially clear.\nThe orbits are unremarkable.  The mastoid air cells are clear.",
            "output": "1. Interval development of new infarcts of the right and left temporal lobe,\nleft frontal lobe and left cerebellar hemisphere from examination of ___.  The dominant lesion is in the right temporal lobe measuring\napproximately 6 mm.\n2. Confluent FLAIR hyperintense signal of the left parietal and temporal lobes\nare re-identified, increased in extent along the anterior inferior left\ntemporal lobe, corresponding to regions of new infarct.\n3. Additional regions of previously described infarcts and left parietal\ncortical laminar necrosis and/or petechial hemorrhage are re-identified. \nExpected evolution of prior infarcts, including new enhancement of a right\nanterior temporal lobe infarct is identified.\n4. Leptomeningeal enhancement and FLAIR hyperintense signal of the bilateral\ncerebral and cerebellar hemispheres is similar appearance to prior\nexamination.\n5. The constellation of findings are suspicious for cerebral amyloid angitis\nwith differential considerations including vasculitis, embolic infarcts and\nmeningoencephalitis."
        },
        {
            "input": "The patient had difficulty holding still due to claustrophobia.  Sagittal T1\nweighted and gradient echo images are mildly limited by motion artifact, but\nFLAIR and T2 weighted images were obtained with the available motion reducing\ntechniques.\n\nThere is subarachnoid hemorrhage in the right central sulcus, frontal and\nparietal sulci.  The extent of hemorrhage is better appreciated on MRI than\nCT, as both acute and subacute hemorrhage is seen on MRI.\n\nThere is no evidence for blood products in the brain parenchyma.  There is no\nparenchymal edema or mass effect.  There is no acute infarction.  A small\nchronic right cerebellar hemisphere infarct is noted.  Confluent areas and\ndiscrete foci of high T2 signal in the periventricular, deep, and subcortical\nwhite matter of the cerebral hemispheres are nonspecific but likely sequelae\nof chronic small vessel ischemic disease in this age group.  Prominence of the\nventricles and sulci is unchanged and consistent with age related involutional\nchanges.  There is mild mucosal thickening in the ethmoid sinuses, and small\nmucous retention cysts in the maxillary sinuses.\n\nPrincipal intracranial vascular flow voids are preserved.  Intracranial\nvasculature is better assessed on the concurrent CTA of the head and neck.",
            "output": "1. Right frontal and parietal subarachnoid hemorrhage is again demonstrated. \nThe extent of hemorrhage is better appreciated on MRI than on the preceding\nCT, as both acute and subacute subarachnoid hemorrhage is visible on MRI.\n2. No evidence for parenchymal blood products to clearly indicate amyloid\nangiopathy."
        },
        {
            "input": "There are numerous foci of susceptibility on gradient echo imaging,\npredominantly in the supratentorium with few scattered in the right basal\nganglia.  There are multiple regions of confluent FLAIR hyperintense signal in\nthe subcortical white matter, involving the bilateral frontal lobes, parietal\nlobes, occipital lobes and left temporal lobe, with localized mass effect and\nno midline shift.  Multiple additional areas of subcortical and\nperiventricular T2/FLAIR hyperintensities are seen.  There is no abnormal\nenhancement after contrast administration in the regions of abnormal signal.\n\nThere is no evidence of acute infarction.  There is prominence of the\nventricles and sulci suggestive involutional changes.\n\nThe orbits, paranasal sinuses and mastoid air cells are normal.  The major\nvascular flow voids are preserved.  External stereotactic markers are noted.",
            "output": "1. Numerous supratentorial micro hemorrhages with multi focal subcortical\nedema and no associated contrast enhancement, suggestive of cerebral amyloid\nangiopathy related inflammation.  Neurology consultation is recommended.  No\nevidence for an intracranial mass.\n\nRECOMMENDATION(S):  Neurology consultation recommended."
        },
        {
            "input": "There is no evidence of infarction or hemorrhage.  No mass, mass effect or\nmidline shift is present. The ventricles, cerebral sulci and cisterns are\nprominent, reflecting a mild degree of cerebral atrophy. There are patchy\nareas of T2 and FLAIR hyperintensity within the periventricular, subcortical\nand deep white matter as well as within the pons which likely represent the\nsequela of chronic small vessel ischemic disease, slightly progressed in the\n___ year interim. The cerebellar tonsils protrude approximately 8 mm below the\nlevel of the foramen magnum.\n\nThe visualized orbits and soft tissues are unremarkable.",
            "output": "1. No acute infarct, intracranial hemorrhage or space-occupying lesion.\n2. White matter signal abnormalities are most likely the sequela of chronic\nsmall vessel ischemic disease. Mild cerebral atrophy.\n3. Low-lying cerebellar tonsils."
        },
        {
            "input": "Two foci of T2 and FLAIR high signal intensity are identified in the\nsubcortical white matter, measuring approximately 2 x 3 mm in size (images 14,\n15, series 7 an 8), which are nonspecific and may reflect gliosis. There is no\nacute infarction, intracranial hemorrhage, extracerebral fluid collection,\nmidline shift or mass effect.  No diffusion abnormalities are detected. The\ncerebral volume is appropriate for the patient's stated age.  The major\nvascular flow voids are maintained, there is no evidence of abnormal\nenhancement.\n\nThe orbits are unremarkable, the paranasal sinuses are notable for a mucous\nretention cyst on the right maxillary sinus, mild mucosal thickening on the\nright frontoethmoidal recess, and mucosal thickening in the lateral recess of\nthe sphenoid sinus on the right. The mastoid air cells are clear.",
            "output": "1. Two  small foci of high signal intensity identified on FLAIR and T2\nweighted images in the subcortical white matter on the left, which are\nnonspecific and may reflect gliosis, this finding is not specific, however has\nbeen described in patients with chronic migraines, hypertension, post viral\ninfections and demyelination.\n\n2. Mild mucosal thickening identified in the paranasal sinuses as described\nabove, and right maxillary mucous retention cyst"
        },
        {
            "input": "There are multiple small foci of increased signal on diffusion-weighted\nimaging and low signal on the ADC map images, consistent with acute infarcts\nthe largest is located in the left anterior putamen and measures 1.5 cm\n(04:15).  Others are seen within the right putamen, caudate head, and anterior\nlimb of the internal capsule left caudate, left greater than right frontal\ncortex, right frontal centrum semiovale (04:23), and left postcentral cortex\n(___).  There is no associated mass effect and no evidence for associated\nblood products.\n\nThere are scattered additional faint foci of high signal on the diffusion\ntracer sequence with normal to high signal on the ADC map in the bilateral\ncorona radiata and centrum semiovale, demonstrating a combination of\nencephalomalacia and gliosis on FLAIR images, consistent with chronic infarcts\nwith T2 shine through.  The associated volume loss has progressed compared to\nthe FLAIR images from the ___ MRI.\n\nMild age-related prominence of the ventricles is again seen.  The sulci appear\nage-appropriate.\n\nFlow void of the intracranial left internal carotid artery is narrowed\nincluding the petrous, cavernous, and supraclinoid segments.  Left MCA flow\nvoid is also narrowed.  These findings are better assessed on the CTA from ___.  Intracranial right vertebral artery is small in caliber, as\nseen previously.\n\nSagittal images demonstrate apparent hypointensity in the central spinal cord\nextending inferiorly from C2-C3 level and beyond the inferior margin of the\nimages.  However, there is motion artifact through this area, and these images\nare not optimized for evaluation of the cervical spine.  No abnormality in\nthis area was seen on the sagittal images of the ___ head MRI.\n\nThere is mild mucosal thickening in the ethmoid air cells and sphenoid\nsinuses, as well as trace fluid in the left sphenoid sinus.",
            "output": "1. Multiple small bilateral acute infarcts involving the basal ganglia, left\ngreater than right frontal cortex, as well as a focus in the right frontal\ncentrum semiovale and a focus in the left postcentral cortex.  No associated\nmass effect or evidence for blood products.\n2. Multiple small chronic infarcts in the bilateral corona radiata and centrum\nsemiovale with progression of volume loss compared to ___.\n3. Narrowing of the intracranial left internal carotid artery and left middle\ncerebral artery, better assessed on the preceding CTA from ___.\n4. Apparent hypointensity in the central spinal cord extending inferiorly from\nC2-C3 level and beyond the inferior margin of the images, unclear whether an\nartifact, versus edema or syrinx.\n\nRECOMMENDATION(S):  Cervical spine MRI for further evaluation.\n\nNOTIFICATION:  The findings and recommendations were discussed with ___\n___, N.P. by ___, M.D. on the telephone on ___ at 3:37 pm,\n10 minutes after discovery of the findings."
        },
        {
            "input": "Please note that study is limited given the extensive streak artifact from the\npatient's dental hardware.  Specifically, the diffusion weighted images are\nextremely limited.  In the context of these limitations, the visualized\naspects of the brain demonstrate no evidence of acute intracranial infarction\nor hemorrhage.  The posterior fossa is incompletely evaluated on the FLAIR\nimages given the extensive artifact however no definite FLAIR signal\nabnormalities are identified.  Ventricles and sulci are age appropriate.\n\nMild mucosal sinus thickening seen involving the ethmoid air cells. \nVisualized paranasal sinuses, mastoid air cells, and middle ear cavities are\nclear.  No concerning enhancing lesions are identified.",
            "output": "1. Extremely limited study given the artifact from patient's dental hardware,\nhowever in the context of these limitations, no acute intracranial\nabnormalities identified.  No concerning focal lesions identified."
        },
        {
            "input": "Images through the internal auditory canal demonstrates symmetric appearance\nof the seventh eighth nerve complexes.  There is no evidence of abnormal\nenhancement or mass lesion within the internal auditory canals,\ncerebellopontine angles or membranous labyrinth. No other mass lesions are\nseen within the posterior fossa.\n\nIn the remaining intracranial compartment, there is no evidence for an\nenhancing mass, acute infarction, or edema.  There are scattered small FLAIR\nhyperintense foci in the periventricular, deep, and subcortical white matter\nof the frontal lobes, nonspecific in this age group.  Ventricles, sulci, and\nbasal cisterns are normal in size.  Major vascular flow voids are preserved. \nDural venous sinuses are patent on postcontrast MP RAGE images.\n\nThere is minimal mucosal thickening in the ethmoid air cells.",
            "output": "1. No evidence of IAC or cerebellopontine angle mass.\n2. Scattered small FLAIR hyperintense foci in the bifrontal white matter,\nnonspecific in this age group.  Diagnostic considerations include migraine\nrelated lesions, sequela of prior demyelination or inflammation, or sequela of\nchronic small vessel ischemic disease of the patient has longstanding\ncardiovascular risk factors.  Sequela of vasculitis may also be considered in\nan appropriate clinical setting."
        },
        {
            "input": "Moderate bilateral maxillary, trace sphenoid, trace inferior frontal, moderate\nbilateral ethmoid sinus mucosal thickening is not significantly changed\ncompared to CT sinus from ___, within the limits of comparing\ndifferent modalities.\nFocal area of bone loss in left lateral maxillary sinus wall seen on prior CT\nfrom ___, new since ___, is not well demonstrated on\nthis exam.\n\nNo intracranial abscess or encephalitis is identified.  There is no evidence\nof hemorrhage, edema, masses, mass effect, midline shift or infarction.  Mild\nprominence of ventricles and sulci likely reflect involutional changes.  Mild\nperiventricular scatter small subcortical foci of white matter FLAIR\nhyperintensities are consistent with chronic small vessel disease.  Small\nlacunar infarct is noted at right lentiform nucleus.",
            "output": "1. No intracranial infection is identified.\n2. Paranasal mucosal thickening consistent with sinusitis is not significantly\nchanged compared to ___.\n3. Previously seen focal area of bone loss in left lateral maxillary sinus\nwall on prior CT is not well demonstrated on this exam."
        },
        {
            "input": "No gross abnormalities on the severely motion degraded sagittal T1 imaging. \nRepeat imaging advised.",
            "output": "Repeat imaging advised"
        },
        {
            "input": "There is no intra or extra-axial mass, acute hemorrhage or infarct. The sulci,\nventricles and cisterns are within expected limits for the patient's age.\n\nThere is a single nonspecific 1-2 mm FLAIR hyperintense signal of the right\nposterior centrum semiovale (series 7, image 15).\n\nThe major intracranial flow voids are preserved.  There is mild mucosal\nthickening of the ethmoid air cells.  The orbits are unremarkable.  No fluid\nsignal is seen in the mastoid air cells.",
            "output": "1. No acute intracranial abnormality on noncontrast MRI head.  Specifically no\nintracranial mass, acute hemorrhage or infarct.\n2. A nonspecific 1-2 mm FLAIR hyperintense focus of the right posterior\ncentrum semiovale.  In a patient of this age, the differential consideration\nis broad and may represent sequela of chronic headache such as migraine, prior\ntrauma, infectious/inflammatory etiology.  This is not in a distribution\ntypical for demyelinating disease."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  Periventricular and subcortical T2 and FLAIR hyperintensities\nare noted.  There is minimal focal encephalomalacia in the posterior left\ncerebellar hemisphere, likely from prior infarct.  There is a partially empty\nsella.  There is no abnormal enhancement after contrast administration.  The\nmajor vascular flow voids are preserved.\n\nThe orbits and mastoid air cells are normal.  Minimal mucosal thickening of\nthe ethmoid sinuses seen.  There is a stable 0.7 cm enhancing lesion in the\nskin overlying the right lateral face, at the level of the mandible.\n\nPartially visualized degenerative changes are noted in the upper cervical\nspine.",
            "output": "1. No evidence for intracranial metastatic disease.\n2. Nonspecific white matter signal abnormalities, likely secondary to chronic\nmicrovascular ischemic changes.\n3. A 0.7 cm enhancing skin lesion overlying the right lateral face, at the\nlevel of the mandible.  Recommend correlation with physical exam."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  There is prominence of the ventricles and sulci suggestive\ninvolutional changes.  Periventricular and deep subcortical FLAIR white matter\nhyperintensities are likely sequelae of chronic small vessel ischemic disease.\nThere is no abnormal enhancement after contrast administration.\n\nMild mucosal sinus thickening is seen involving the ethmoid air cells.  The\nmastoid air cells, and middle ear cavities are clear.  The vascular flow voids\nare well preserved.",
            "output": "1. No concerning enhancing lesions identified.  No acute intracranial\nabnormalities identified.\n2. Chronic microangiopathy."
        },
        {
            "input": "Motion artifact degrades the diagnostic quality of the images and renders the\npostcontrast imaging uninterpretable.\n\nWithin this limitation: There is no evidence of hemorrhage, edema, masses,\nmass effect, midline shift or infarction.  There is been interval increase in\nthe periventricular T2 and FLAIR hyperintense changes which are nonspecific. \nNo definite abnormal postcontrast enhancement.  Moderate generalized cerebral\natrophy with ex vacuo dilatation of the ventricular system appears similar\ncompared to prior.  The orbits appear normal.  There is mild mucosal\nthickening of the ethmoid air cells, otherwise, paranasal sinuses are\nessentially clear.  The intracranial arteries demonstrate normal T2 flow\nvoids.  The CP angles are clear.  Partially empty sella.  The craniocervical\njunction appears normal",
            "output": "1. This study is markedly degraded by motion artifact, particularly the\npostcontrast imaging, which is severely degraded.\n2. Within the limitations of the study there is no acute intracranial infarct,\nmass or hemorrhage.  No gross enhancing lesion (this cannot be stated with\ncertainty).\n3. There is interval increase in periventricular T2 and FLAIR hyperintense\nchanges compared to prior imaging which is nonspecific.  These changes do not\nhave the typical distribution of demyelinating disease.\n4. If clinically indicated repeat imaging may be performed."
        },
        {
            "input": "There is no evidence of infarction, hemorrhage, edema, mass, or mass effect. \nNo abnormal enhancement.\n\nThe ventricles and sulci are prominent, compatible with global parenchymal\nvolume loss.\n\nBilateral periventricular and confluent deep white matter foci of T2/FLAIR\nsignal hyperintensity are nonspecific but compatible with moderate to severe\nchanges of chronic white matter microangiopathy.\n\nTrace left mastoid fluid.  Otherwise, the visualized paranasal sinuses and\nright mastoid appear clear.\n\nAside from bilateral lens extraction, the globes and orbits are within normal\nlimits.\n\n Major intracranial vascular flow voids are preserved.\n\n Major dural venous sinuses are patent.",
            "output": "1. No acute intracranial abnormality.  No evidence of intracranial metastases.\n2. Moderate to severe changes of chronic white matter microangiopathy."
        },
        {
            "input": "Evaluation is suboptimal due to motion artifact.  Within this confine:\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  The ventricles and sulci are prominent, consistent with global\ncerebral volume loss.  Patchy periventricular T2 hyperintensities are most\nconsistent with chronic microvascular angiopathy.  There is no abnormal\nenhancement after contrast administration.\n\n The paranasal sinuses, mastoid air cells and middle ear cavities are clear. \nThe patient is status post bilateral cataract surgery.",
            "output": "1. No evidence of metastatic disease.\n2. No acute infarct or intracranial hemorrhage.\n3. Chronic microvascular angiopathy changes."
        },
        {
            "input": "The exam is limited due to motion artifact and was terminated after only a few\nsequences as the patient was unable to cooperate.  Diffusion weighted imaging\ndemonstrates no acute infarct.  There is no obvious mass effect.  Given the\nsevere limitations of study, metastatic disease and hemorrhage cannot be\nexcluded.  However, no definite hemorrhage was identified on same day head CT.",
            "output": "Severely limited study due to motion artifact and patient's inability to\ncooperate for the remainder of the exam.  Within these limitations, there is\nno evidence of acute infarct or mass effect."
        },
        {
            "input": "Multiple new small enhancing lesions are identified measuring 5 mm or smaller\nin size.  The following lesions are apparent:\n\n-Left cerebellum (19:6)\n-Right superior cerebellum (19:8)\n-Left medial temporal lobe (19:10)\n-Left medial thalamus (19:12)\n-Right medial frontal lobe (19:13)\n-Right parietal lobe (19:14)\n-Right side of the splenium (19:14)\n-Left frontal lobe (19:15)\n-Left frontal lobe (7:21 and 15:17) which does not demonstrate definite\nenhancement\nSeveral other punctate foci are visualized on MP rage images which are not\nconfirmed on the T1 spin echo or FLAIR images and could be artifacts or\nvascular structures.\n\nThere is diffuse hyperintense signal in the periventricular white matter which\ncould be due to combination of small vessel disease and prior therapy.  No\nacute infarcts or mass effect is seen.  There is no midline shift.",
            "output": "Multiple small enhancing lesions are new since the previous MRI of ___ indicating metastatic disease.\n\nNOTIFICATION:  The impression and recommendation above was entered by Dr.\n___ on ___ at 16:01 into the Department of Radiology\ncritical communications system for direct communication to the referring\nprovider."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There are nonspecific bilateral frontal lobe small\nhyperintensities on T2W imaging, which likely represent chronic small vessel\ndisease.  There is no abnormal enhancement after contrast administration.",
            "output": "1. No acute intracranial abnormality or abnormal enhancement on\ncontrast-enhanced imaging.\n\n2. Nonspecific bilateral frontal lobe hyperintensities, suggestive of chronic\nsmall vessel disease."
        },
        {
            "input": "The parenchymal signal is unremarkable without acute infarct, hemorrhage,\nmass, or mass effect.  There are no definite FLAIR hyperintense white matter\nlesions or abnormal postcontrast enhancement.  On the 3D FLAIR acquisition, a\nsingle white matter lesion is suggested in the right external capsule with\nadjacent artifact (see 100:95), with no corresponding finding on axial FLAIR\nimaging (see 04:14), suggesting this finding is artifactual.  The ventricles\nand cortical sulci are normal in caliber and configuration.  The extra-axial\nspaces are unremarkable.\n\nThere are short segment FLAIR hyperintense lesions within the cervical cord at\nthe C2 and C3 levels (2: 69, 73), without associated postcontrast enhancement.\nThese are better characterized on prior dedicated cervical spine MRI.\n\nThe right lens is absent and there is a scleral buckle in place, otherwise the\norbits are unremarkable.  The calvarium and soft tissues are unremarkable. \nThe paranasal sinuses mastoid air cells are clear.",
            "output": "1. No acute intracranial abnormality.\n2. No definite evidence of intracranial demyelinating lesions or abnormal\npostcontrast enhancement.\n3. Redemonstration of short segment nonenhancing FLAIR hyperintense cervical\ncord lesions, which are better characterized on prior dedicated cervical spine\nMRI."
        },
        {
            "input": "Study is mildly degraded by motion.  There is no evidence of hemorrhage,\nedema, masses, mass effect, midline shift or infarction.  Periventricular and\nsubcortical T2 and FLAIR hyperintensities are nonspecific but likely represent\nsequelae of chronic small vessel ischemic disease.  There is stable prominence\nof the ventricles and sulci suggestive involutional changes.  There is no\nabnormal enhancement after contrast administration.\n\nThe mastoid air cells and middle ear cavities appear clear.  Patient is likely\nstatus post oral lens replacement surgery.  Right maxillary sinus mucous\nretention cyst versus polyp is noted.",
            "output": "1.  Study is mildly degraded by motion.\n2. No evidence of mass, edema or infarction.\n3. Grossly severe atrophy and probable small vessel ischemic changes.\n4.  Paranasal sinus disease as described."
        },
        {
            "input": "There is no acute infarction, intracranial hemorrhage, extracerebral fluid\ncollection, midline shift or mass effect.  There is mild prominence of\ntemporal horns indicating early changes of medial temporal atrophy.  Flow\nvoids are maintained.  There is thickening of the ligaments at the\ncraniocervical junction resulting in mild-to-moderate narrowing of the spinal\ncanal at foramen magnum and C1 level.  The CSF space surrounding the spinal\ncord is effaced but there is is no compression of the spinal cord seen on the\nsagittal T1 weighted images.  .",
            "output": "No evidence of acute infarct mass effect or hydrocephalus.  Mild medial\ntemporal atrophy.  Extensive degenerative changes the craniocervical junction\nwith narrowing of the spinal canal without  spinal cord compression."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  Prominence of ventricles and sulci are suggestive of\ninvolutional changes.  The temporal horns of lateral ventricles bilaterally\nare focally enlarged, likely reflecting mild medial temporal atrophy.  A\nsingle punctate diffusion-weighted hyperintense focus of the right postcentral\ngyrus is nonspecific, but compatible with chronic microangiopathy in a patient\nof this age.  The major intracranial flow voids are preserved.  Thickening of\ncraniocervical junction ligaments cause moderate narrowing of the spinal canal\nat foramina magnum and C1 level, better evaluated on concurrent MR ___.\nMucosal thickening is mild in bilateral frontal, ethmoid, sphenoid, and\nmaxillary sinuses.  The orbits are unremarkable.",
            "output": "1. No acute infarct is identified.  Additional findings described above.\n2. Bilateral medial temporal atrophy is similar to ___.\n3. Please refer to concurrent MRI cervical spine for additional details."
        },
        {
            "input": "Study is moderately degraded by motion.  Within these confines:\n\nMultiple supratentorial nonenhancing T2 and FLAIR white matter lesions with no\ndefinite associated restricted diffusion or increase susceptibility are noted.\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are preserved in caliber and\nconfiguration.\n\n Within limits of study, there is no definite evidence of mass, or mass effect\nin the medial temporal lobes including the region of the hippocampal heads. \nThere is no definite abnormal enhancement after contrast administration.\n\nThere is extensive mucosal thickening/submucosal edema and fluid opacifying\nthe left maxillary sinus, involving the left more than right ethmoid air\ncells, with more mild sphenoid sinus mucosal thickening.  The frontal sinus is\nclear.  There is mild right maxillary sinus mucosal thickening.  Major\nintracranial vascular flow voids are grossly preserved.  Major dural venous\nsinuses are grossly patent.",
            "output": "1.  Study is moderately degraded by motion.\n2.  No acute intracranial abnormality.\n3. Nonenhancing supratentorial white matter lesions as described. \nDifferential considerations include sequela of prior trauma or infection,\nhistory of migraine headaches, inflammatory or demyelinating process, and\nmicroangiopathic changes.\n4.  Within limits of study, no definite evidence of enhancing intracranial\nmass.\n5. Extensive paranasal sinus disease, as described.\n\nNOTIFICATION:  The impression and recommendation above was entered by Dr.\n___ on ___ at 11:57 into the Department of Radiology critical\ncommunications system for direct communication to the referring provider."
        },
        {
            "input": "Examination is moderately degraded by motion.  Within these confines:\n\nThere is no evidence of restricted diffusion to suggest acute infarction.  No\nevidence of acute intracranial hemorrhage.  Mild prominence of the ventricles\nand sulci is suggestive of involutional changes. There is no mass effect or\nmidline shift.\n\n Periventricular and subcortical T2 and FLAIR hyperintensities are noted which\nmay represent small vessel ischemic and/or treatment related changes.\n\nThere is no abnormal enhancement after contrast administration.\n\nBilateral maxillary sinus and ethmoid air cell mucosal thickening is noted. \nBilateral maxillary sinus probable mucous retention cysts are seen.  The major\nintracranial arterial and venous flow voids are preserved.",
            "output": "1. Examination is moderately degraded by motion.\n2.  No acute intracranial abnormality.\n3.  Within limits of study, no definite evidence of enhancing intracranial\nmass.\n4.  Paranasal sinus disease , as described."
        },
        {
            "input": "Study is moderately degraded by motion, especially on MR angiography.  Within\nthese confines:\n\nMRI BRAIN:\nThere is no evidence of acute intracranial hemorrhage, or infarction.  Mild\nprominence of ventricles and sulci is likely related to age related\ninvolutional changes.  Periventricular and deep subcortical FLAIR white matter\nhyperintensities are likely sequelae of chronic microangiopathy.\n\nMild mucosal sinus thickening is seen involving the ethmoid air cells.  The\nremainder the visualized paranasal sinuses, mastoid air cells, and middle ear\ncavities are clear.  The globes are unremarkable.  The principal vascular flow\nvoids are well preserved.  No concerning enhancing lesions are identified. \nIncidental note is made of a right frontal DVA, series 111 a image 65.\n\nMRA BRAIN:\nA 3 mm outpouching is seen directed medially arising from the supraclinoid\nleft internal carotid artery, series 8, image 114.  Aside from atherosclerotic\nirregularity of the cavernous segment of the left internal carotid artery, the\nleft internal carotid artery is patent.  The left middle cerebral artery is\npatent.  The left anterior cerebral artery is dominant, otherwise the anterior\ncerebral arteries are unremarkable.  The right internal carotid artery is\nnormal.  The vertebral and basilar arteries are grossly patent.  Note is made\nof a fetal type configuration of the left posterior cerebral artery.  The\nright PCA is unremarkable.\n\nMRA NECK:\nMild-to-moderate stenosis is seen along the bilateral vertebral artery\norigins, likely exaggerated secondary to motion artifact.  The vertebral\narteries are otherwise unremarkable, demonstrating appropriate flow.  The\ncommon, internal and external carotid arteries appear normal.  There is no\nevidence of internal carotid artery stenosis by NASCET criteria.  The origins\nof the great vessels, and subclavian arteries are limited in evaluation,\nsecondary to motion artifact.",
            "output": "1. Study is moderately degraded by motion artifact.\n2. No acute intracranial abnormality, with no evidence of acute infarct.\n3. 3 mm outpouching medially directed from the supraclinoid left internal\ncarotid artery, may be secondary to a small aneurysm versus vascular\ninfundibulum.\n4. Intracranial probable atherosclerotic disease as described.\n5. No evidence of internal carotid artery stenosis by NASCET criteria.\n6. Evaluation of the origins of the great vessels limited secondary to motion\nartifact.\n7. Within limits of study, at least moderate stenosis of the origins of the\nvertebral arteries.\n8. Within limits of study, no definite evidence of carotid or vertebral artery\ndissection."
        },
        {
            "input": "There are 5 foci of FLAIR signal abnormality in the left cerebral hemisphere\nwith associated enhancement on postcontrast images.  These lesions include:\n- a lesion in the left parietal lobe on image 1300b:100 measuring 4 mm.\n- a lesion in the left caudate head on image 1300b:92 measuring 5 mm.\n- a lesion in the left frontal cortex on image 1300b:92 measuring 6 mm.\n- a lesion in the left caudate head on image 1300b:90 measuring 4 mm.\n- a lesion in the left parietal lobe on image 1300b:91 measuring 3 mm.\n-a lesion in the left parieto-occipital lobe on image 1300b:87 measuring 3 mm.\n\nAll the lesions other than the basal ganglia are based in the\ncortical/subcortical location. None of these lesions demonstrate slow\ndiffusion or evidence of hemorrhage on gradient echo imaging.  The lesions are\nintrinsically T1 isointense.\n\nIn addition, there are several areas of cortical FLAIR signal abnormality\ninvolving the left frontoparietal lobe.  As seen on image 8:  ___.  Some of\nthese areas correspond to the previously seen hyperdensity on the CT.\n\nA combination of cortical FLAIR signal abnormality with foci of enhancement on\npostcontrast images in the presence of previously seen stenosis of M1 segment\nof the left MCA, these could be subacute infarcts.  However, if these are\nareas of infarction than that the hyperdensity on CT should reflect hemorrhage\nand at the gradient echo images demonstrate no evidence of hemorrhage within\nthese lesions.  The left middle cerebral artery stenosis also raises the\npossibility of herpes zoster ophthalmic thus with intracranial vasculitis and\nresulting infarction.  The normal caliber of the supra clinoid left ICA argues\nagainst this diagnosis.  1 could also consider the possibility of an embolus\nlodged in the M1 segment with small distal emboli accounting for the cortical\ninfarctions.  Possible other differential diagnosis includes intracranial\nmetastasis.  However, this would not explain the middle cerebral artery\nstenosis or in the collection level although lesions in the MCA distribution. \nThe evolution of the lesions on follow-up imaging should distinguished between\ninfarction and tumor.\n\nThe ventricles, cisterns and sulci are patent and symmetric.\n\nThe orbits are unremarkable.  Intracranial flow voids are maintained.  The\nvisualized paranasal sinuses and mastoid air cells are clear.",
            "output": "1. Cortical FLAIR signal abnormality in the left frontoparietal lobe with\nassociated foci of cortically based enhancement on the postcontrast images as\ndescribed above.  These findings in the setting of previously-seen tight\nstenosis of left M1 segment of the MCA are favored to be secondary to subacute\ninfarcts.  Possible other differential diagnosis includes intracranial\nmetastasis.  Clinical correlation, correlation with lumbar puncture and\ncytology and short interval follow up can be performed.\n\nRECOMMENDATION(S):  Clinical correlation, correlation with lumbar puncture and\ncytology and short interval follow up can be performed."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, parenchyma masses, mass effect,\nmidline shift or infarction.   The ventricles and sulci are normal in caliber\nand configuration.  There is no abnormal enhancement after contrast\nadministration.  Mild mucosal thickening maxillary sinus, without fluid. \nOtherwise, paranasal sinuses, mastoids are clear.  Intracranial vascular flow\nvoids are preserved.  Dural venous sinuses are patent.  There is 2 mm\nhypoenhancing nodule in the posterior left paramedian pituitary gland, it may\nrepresent microadenoma or Rathke's cleft cyst, clinically correlate.",
            "output": "1. Normal intracranial contents.\n2. Mild mucosal thickening paranasal sinuses, without fluid.\n3. 2 mm pituitary gland nodule, may represent microadenoma or Rathke's cleft\ncyst, clinically correlate.  If clinically indicated, consider pituitary gland\nMRI."
        },
        {
            "input": "MRI BRAIN:\nAgain demonstrated is a roughly 23 x 7 mm, irregular focus of T2 and T1\nintermediate enhancement, expanding the left cavernous sinus (___),\ntracking along the medial aspect of the left middle cranial fossa, extending\nthrough foramen ovale along V3 at the skullbase, appearing grossly unchanged\ncompared to the prior examination.  No abnormal signal in association with the\nmuscles of mastication on the left which are symmetric when compared to those\nof the right.\n\nPre clival dural thickening and enhancement with enhancement extending into\nright Dorello's canal appears overall unchanged (2002b:40).\n\nThe previously noted punctate foci of enhancement in the orbital apex\nbilaterally are not clearly seen on the current examination.  The orbital fat\nis preserved.  The optic nerves are preserved in caliber and signal without\nabnormal enhancement.  The lacrimal glands are unremarkable.  The extra conal\nmusculature appears symmetric in caliber, without abnormal signal or\nenhancement.  The globes are unremarkable.\n\nThere is no evidence of hemorrhage, edema, significant mass effect, midline\nshift or infarction.  There is mild prominence of the ventricles and sulci,\nsuggestive of involutional change.  Few, punctate scattered areas of\nperiventricular and subcortical white matter T2/FLAIR hyperintensities are in\na configuration most suggestive of chronic small vessel ischemic disease,\nunchanged.  The dural venous sinuses are patent on MP-rage images.  Arachnoid\ngranulations are noted in the bilateral distal transverse venous sinuses.\n\nThere is mild mucosal wall thickening in the posterior aspects of the\nbilateral sphenoid sinuses, a tiny mucous retention cyst in the right\nmaxillary sinus and trace mucosal wall thickening in the ethmoid air cells. \nThe remainder the visualized paranasal sinuses are grossly clear.\n\nT1 and T2 hypointense marrow signal throughout the marrow of the skullbase and\nportions of the upper cervical spine are compatible with known metastases.  Of\nnote dense sclerosis seen on CT also noted to involve the skullbase including\nthe pterygoid process on the left.\n\nMRA BRAIN:\nThe intracranial vertebral and internal carotid arteries and their major\nbranches appear patent without evidence of stenosis, occlusion, or aneurysm\nformation.\n\nMRV BRAIN:\nSlight attenuation of flow related signal within the distal transverse venous\nsinuses correspond to arachnoid granulations on MP RAGE images.  Otherwise\nnormal flow signal is demonstrated within the superior sagittal sinus,\nstraight sinus, transverse sinuses, and sigmoid sinuses. The jugular bulbs and\nproximal jugular veins are patent. Evaluation of the deep venous systems\nreveals normal flow signal in the internal cerebral veins. The vein ___\nis also unremarkable.\n\nMRA NECK:\nThere is a 3 vessel aortic arch.  Apparent focal narrowing of the distal\ncervical segment of the right internal carotid artery on rotation images lack\na correlate on the coronal source images, and is likely artifactual.  The\ncommon, internal and external carotid arteries otherwise appear patent.  There\nis no evidence of internal carotid artery stenosis by NASCET criteria.  The\norigins of the great vessels, subclavian and vertebral arteries appear patent\nbilaterally.",
            "output": "1. Unchanged enhancing lesion measuring 23 x 7 mm in the left cavernous sinus\ntracking along the left middle cranial fossa through foramen ovale, suggesting\na process involving V3 branch of the trigeminal nerve.  Differential\nconsiderations include sarcoid, meningioma, or lymphoma. Given extensive\nsclerosis of the adjacent skull base and interval change between ___ and\n___, metastatic disease would also be possible.\n2. Unchanged pre clival dural thickening and enhancement with extension into\nright Dorello's canal (CN 6) may be related to the process involving the left\ncavernous sinus.  Recommend correlation with CSF studies, if not already\nperformed.\n3. Previously noted punctate foci of enhancement at the level of the orbital\napices are not visualized on the current examination.\n4. No parenchymal enhancing mass.\n5. Patent intracranial arterial vasculature without significant stenosis,\nocclusion, or aneurysm.\n6. No evidence of cerebral venous thrombosis.\n7. Patent cervical arterial vasculature without significant stenosis or\nocclusion."
        },
        {
            "input": "Re-identified is diffusely T1 and T2 hypointense marrow signal throughout the\nskull base and visualized portions of the upper cervical spine compatible with\nknown metastatic disease.  Re-identified is roughly 23 x 7 mm enhancing lesion\nexpanding the left cavernous sinus (10:8), tracking along the medial aspect of\nthe left middle cranial fossa, appearing to extend through the left foramen\novale along the V3 cranial nerve, overall appearing similar to the prior\nstudy.  Minimal pre clival extra-axial dural thickening and enhancement with\nenhancement extending into right Dorello's canal also appears grossly\nunchanged (900:77).  No definite new enhancing lesion is identified.\n\nThere is no evidence of hemorrhage, edema, new masses, mass effect, midline\nshift or infarction.  Mild prominence of the ventricles and sulci suggestive\nof involutional change.  Few punctate scattered areas of white matter T2/FLAIR\nsignal abnormality most likely reflect chronic small vessel ischemic disease. \nThe principal intracranial vascular flow voids are preserved.\n\nThere is a tiny mucous retention cyst in the right maxillary sinus.  There is\ntrace mucosal wall thickening in the floors of the maxillary sinuses,\nbilateral sphenoid and ethmoid air cells.  The frontal sinuses are clear.  The\norbits are unremarkable.  The mastoid air cells are clear.",
            "output": "1. Unchanged enhancing lesion measuring approximately 23 x 7 mm centered in\nthe left cavernous sinus, extending along the left middle cranial fossa, with\nenhancing nodular component exiting through the left foramina ovale suggesting\ninvolvement of the V3 branch of the trigeminal nerve.  Given extensive\nsclerotic bony metastasis throughout the skullbase, metastatic disease is\nlikely.\n2. Unchanged pre clival dural thickening and enhancement with extension into\nright Dorello's canal, likely also reflecting metastatic disease.\n3. Unchanged diffuse sclerotic metastatic involvement of the skullbase, as\npreviously seen.\n4. No new enhancing mass."
        },
        {
            "input": "There are extensive sclerotic osseous calvarial and skullbase metastases,\nincluding involvement of the clivus, sphenoid bone, partially visualized upper\ncervical spine, left mandibular condylar head, lateral wall left orbit,\nsimilar to prior.  There is approximately 2.3 cm x 0.9 cm x 1.6 cm enhancement\nalong the left inferior cavernous sinus, anterior to the Meckel's cave,\nextending into the foramen ovale,, anteromedial floor of the middle cranial\nfossa, compared with 2.3 cm x 1.0 cm by 1.7 cm on ___.  Tumor\nextension into the left pterygopalatine fossa, similar to prior.  There is no\nevidence of intraorbital, or orbital fissure extension. There is no evidence\nof more distal left V3 nerve abnormality to suggest perineural tumor spread. \nDural thickening and enhancement overlying posterior margin of the clivus, and\nextension into the right Durello's canal is similar..  Enhancement of foramen\nrotundum bilaterally, and left vidian canal, consistent with tumor spread.\nFindings likely represent metastatic tumor extension given adjacent osseous\nmetastases.  Other considerations including lymphoma, sarcoid, inflammatory\npseudotumor, meningioma, or possibly subacute to chronic infection is\nunlikely.\n\nThere are mild chronic small vessel ischemic changes.  There is mild\ngeneralized brain parenchymal atrophy.  There is mild paranasal sinus disease,\nwith mucosal thickening, small volume fluid in the sphenoid sinus, which is\nsimilar to prior.\n\nThere is no evidence of hemorrhage, edema, brain masses, mass effect, midline\nshift or infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There are no intracranial metastases.  Visualized upper\nnasopharynx is normal, without mass.",
            "output": "Extensive sclerotic osseous metastases are stable since prior.\nEnhancing tumor along the left cavernous sinus, extending into the multiple\nskullbase foramina, left pterygopalatine fossa is stable since prior, most\nlikely represents metastatic tumor extension.\nThere are no brain parenchymal metastases."
        },
        {
            "input": "Re-identified is diffuse osseous metastatic disease of the skullbase involving\nthe clivus, sphenoid, left mandibular condyle, lateral wall of the left orbit\nis overall similar to prior examination overall similar to prior examination. \nScattered sclerotic lesions of the right mandibular condyle is also similar. \nPartially visualized metastatic disease to the upper cervical spine is also\nre-identified.  Abnormal enhancing soft tissue measuring approximately 1.3 by\n0.4 cm (AP, TRV) of the left cavernous sinus (series 9, image 36), extending\nto the anterior aspect of the Meckel's cave is overall similar to prior\nexamination.  The abnormal enhancement extends into the left foramina ovale,\neffacing the trigeminal fat (series 10, image 36).  There is linear dural\nenhancement along the floor of the left middle cranial fossa, slightly less\nconspicuous compared to prior examination.  Dural thickening and enhancement\nalong the posterior edge of the clivus, with involvement of the right\nDurello's canal (series 9, image 32) is also similar to prior exam.  Abnormal\nenhancement and thickening within the left pterygopalatine fossa and foramen\nrotundum, compatible with tumoral spread, is unchanged.  No definite abnormal\nenhancement of the right foramen rotundum is identified.  There may be mildly\nasymmetric enhancement of the left Vidian canal.\n\nThere is no evidence of intracranial metastatic disease or acute infarct.  The\norbits, orbital apex and supraorbital fissure appear grossly unremarkable. \nThe distal aspects of the left trigeminal nerve appears preserved and\nunchanged.  The internal auditory canals demonstrate no abnormal enhancement\nor mass lesion.  There is no abnormal enhancing lesion within the brain\nparenchyma.  No acute infarct is identified.  Very few scattered punctate\nperiventricular and subcortical T2/FLAIR nonenhancing white matter\nhyperintensities are nonspecific, but compatible with chronic microangiopathy\nin a patient this age.  The visualized intracranial flow voids are preserved. \nThere is mild mucosal thickening of the paranasal sinuses with a small right\nmaxillary sinus mucous retention cyst.",
            "output": "1. Extensive osseous metastatic disease involving the skullbase and visualized\nupper cervical spine is essentially unchanged from prior examination.\n2. Enhancing lesion along the left cavernous sinus with extension into the\nleft pterygopalatine fossa, foramina ovale (with effacement of the left\ntrigeminal fat pad) is overall unchanged from prior examination.  Dural\nthickening along the floor of the left anterior middle cranial fossa, abnormal\nenhancement within the left foramina ovale and vidian canal is re-identified.\n3. The left cavernous sinus lesion also results in dural thickening along the\nposterior edge of the clivus with involvement of the right Durello's canal.\n4. No intra-axial metastatic disease is identified.\n5. Additional findings as described above."
        },
        {
            "input": "There are extensive skull base metastasis, without definite interval change\nfrom the ___ skullbase protocol MRI.  The right hypoglossal canal\nappears similar to the ___ MRI, without high-grade narrowing. There\nis asymmetric enlargement of the intrinsic muscles of the right tongue with\nassociated narrowing of the right glossal tonsillar sulcus.  There may be\nmildly increased signal on fluid sensitive sequences and slightly asymmetric\nenhancement (series 6, image 29; series 10, image 29).   The right posterior\npost styloid parapharyngeal space appears normal.  The right tonsillar pillar,\nlingual tonsil, left tongue, and floor mouth appear normal.\n\nThe orbits and paranasal sinuses are grossly unremarkable.  There is mild\nparanasal sinus mucosal thickening.\n\nThere is residual asymmetric thickening of dura of the left cavernous sinus\nwithin the coronal plane of the foramina ovale, similar to the prior study. \nThere is no abnormal meningeal or parenchymal enhancement.  There is no\nevidence of infarction, hemorrhage, or mass effect.  The major vascular flow\nvoids are preserved.",
            "output": "Interval asymmetric enlargement of the right tongue.  The right tonsillar\npillar, lingual tonsils, and left tongue appear normal.  No fluid collection\nis identified within the floor of mouth.  There are extensive skull base\nmetastasis, without definite interval change and without high-grade narrowing\nof the right hypoglossal canal.  No mass is identified within the right post\nstyloid parapharyngeal space or posterior to the base of tongue along the\nexpected course of the right hypoglossal nerve.  These imaging findings can be\nseen with acute denervation atrophy.  ENT consultation is suggested as\nclinically warranted."
        },
        {
            "input": "Study is moderately degraded by motion, especially the postcontrast skullbase\nimages.\n\nMRI head (accession ___:\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  Prominence of the ventricles and sulci is suggestive of\ninvolutional changes.  The orbits are unremarkable.  Minimal chronic small\nvessel ischemic changes, similar to prior.  There is a small mucous retention\ncyst in the right maxillary sinus.  There is mild mucosal thickening in the\nethmoid air cells and the sphenoid sinuses. There is scattered fluid in the\nmastoid air cells bilaterally.  The appearance of the frontal sinuses is not\nsignificantly changed since ___.  Major arterial vascular flow\nvoids are preserved.\nCentral linear filling defect in the junction of the right transverse and\nsigmoid sinuses is suggestive of nonocclusive thrombus, possibly present on\nprior.\n\nMRI skullbase (accession ___:\nDiffuse bone metastases in the skull base, including the clivus, sphenoid, and\nleft mandibular condyle is again seen.  Metastasis involving left sphenoid\ntemporal buttress has small soft tissue component involving into the supra\nzygomatic temporalis fossa and extraconal space of the left orbit, similar to\nprior.  Extraconal intraorbital soft tissue component measures 1.3 cm x 0.5\ncm, compared with 1.0 cm by 0.5 cm on prior.\n\nMetastases in the cervical spine are partially imaged.  There is no\nsignificant interval change in the appearance of the hypoglossal canals since\n___, with extensive osseous sclerosis on either side of it. \nAtrophy of the right tongue, which shift of the lingual septum to the right,\nand subtle fatty infiltration on axial T1 weighted images, consistent with\ndenervation injury.  No mass between the skullbase and right tongue along the\nexpected course of the hypoglossal nerve.  No brainstem mass or infarct.\n\nAbnormal enhancing soft tissue of the left cavernous sinus measuring\napproximately 0.5 x 2.1 cm measured approximately 0.4 x 1.6 cm on ___ when measured similarly.  Extension into the left foramen ovale (18:33)\nis similar to ___.",
            "output": "1. Findings most consistent with small nonocclusive right transverse, sigmoid\nsinus thrombosis.\n2. Right tongue atrophy, consistent with denervation injury.  This is likely\nfrom tumor involvement at the right hypoglossal canal secondary to adjacent\nosseous metastases.\n3. Extensive osseous metastases, similar.\n4. Osseous metastasis is again seen at left sphenoid temporal buttress with\nmildly increased extraconal orbital soft tissue component.  Left\nparacavernous, foramina ovale involvement is stable.\n\nNOTIFICATION:  Critical results were discussed with ___, M.D. by\n___, M.D. on the telephone on ___ at 10:31 am, 35 minutes after\ndiscovery of the findings."
        },
        {
            "input": "Redemonstrated is diffuse osseous metastatic disease of the skullbase\nincluding the clivus, sphenoid and bilateral mandibular condyles (left greater\nthan right).  No significant change in extensive osseous sclerosis surrounding\nthe hypoglossal canals.\n\nRedemonstrated mild atrophy of the right tongue with shift of the lingual\nseptum to the right and suggestion of fatty infiltration is compatible with\ndenervation injury.  There is no evidence of a brainstem mass or infarct.\n\nNo significant change in abnormal enhancing soft tissue bordering the left\ncavernous sinus measuring approximately 2.1 cm AP x 0.5 cm TV.  There is a\nsimilar degree of extension into the left foramen ovale (11:25).\n\nMinimal enhancement of the left extraconal orbit along the lateral wall\n(series 10, image 44) unchanged from prior exam.\n\nRedemonstrated are scattered osseous metastatic disease involving the\nvisualized portion of cervical spine.\n\nOn limited evaluation of the brain, unchanged trace subcortical and\nperiventricular T2/FLAIR white matter hyperintensities, nonspecific, but\ncompatible with chronic microangiopathy in a patient of this age.  There is no\nevidence for acute infarct or new abnormal enhancement.\n\nThe visualized intracranial flow voids are preserved.  There is mild mucosal\nthickening of the ethmoid air cells.  Small right maxillary sinus mucous\nretention cyst.  There is fluid signal in the bilateral mastoid tips. \nEvaluation for previously described left sigmoid sinus thrombosis cannot be\nmade based on present technique.  The visualized orbits are otherwise\nunremarkable.",
            "output": "1. Stable diffuse osseous metastatic disease of the skullbase involving the\nclivus, sphenoid and bilateral mandibular condyles.\n2. Unchanged abnormal enhancing soft tissue bordering in the left cavernous\nsinus and extending into the foramen ovale.\n3. Redemonstrated scattered osseous metastatic disease involving the cervical\nspine.\n4. Additional findings described above."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   There is mild prominence of the ventricles and sulci\nsuggestive of involutional change.  Very few scattered areas of\nperiventricular and subcortical white matter T2/FLAIR hyperintensity are seen.\nThese appear unchanged compared to the prior exam.  Roughly 20 x 5 mm area of\nextra-axial enhancing soft tissue bordering the left cavernous sinus extending\ninto the left foramen ovale (___) was far better characterized on the\nrecent prior skullbase MR with fat saturation.  Associated enhancement of the\nleft extraconal orbit was also better seen on the prior exam.  There is no\nother abnormal intracranial enhancement after contrast administration.  There\nis an unchanged central linear nonocclusive filling defect at the junction of\nthe right transverse and sigmoid venous sinus.  There is no abnormal focus of\nslowed diffusion.  The principal intracranial vascular flow voids appear\ngrossly preserved.  Prominent right frontal perivascular space is noted.\n\nThere is a small mucous retention cyst in the right maxillary sinus along with\ntrace mucosal wall thickening in the floor of the right maxillary sinus,\nposterior aspect of the bilateral sphenoid sinuses as well as the bilateral\nethmoid air cells.  The frontal sinuses appear clear.  Re-identified is\ndiffuse osseous metastatic disease of the skullbase including the the clivus,\nsphenoid, and bilateral mandibular condyles along with focal areas in the\nvisualized upper cervical spine with low T1 signal indicating sclerosis, also\nbetter characterized on the recent prior skullbase MR. ___ osseous\nsclerosis bordering the hypoglossal canals is again seen.  Atrophy of the\nright tongue is unchanged.",
            "output": "1. Diffuse osseous metastatic disease of the skullbase and upper cervical\nspine is re-identified, better characterized on the recent prior skullbase MR.\n2. Unchanged abnormal enhancing soft tissue bordering the left cavernous sinus\nwith extension into the foramen ovale along with minimal enhancement of the\nleft extraconal orbital fat was also better seen on the recent prior skullbase\nMR.\n3. Unchanged linear central nonocclusive filling defect at the junction of the\nright transverse and sigmoid venous sinus, possibly representing chronic\nnonocclusive thrombus.\n4. Otherwise no hemorrhage, acute infarct, or new intracranial metastatic\nfocus."
        },
        {
            "input": "Again seen is infiltrative T1 hypointense, enhancing soft tissue thickening of\nthe left lateral aspect of the cavernous sinus with extension anteriorly along\nthe medial aspect of the anterior middle cranial fossa dural surface,\ndifficult to measure but spanning up to a 2.8 x 0.7 cm area (11:35 and 09:37).\nCompared with prior exams, this appears larger, with more outwardly convex\nborders and a larger transverse dimension (for example see series 12, image\n31).\n\nThere is extension of this enhancing soft tissue through the left foramen\novale along the course of the left V3 branch, as seen previously, not\nappreciably changed (also 12:31).\n\nThere is extension along the left superolateral orbital roof superolateral to\nthe superolateral recti and abutting and inseparable from the superolateral\nbony orbit (see series 12, image 20 and 11:41), unchanged in appearance.  The\nlateral and superior bony orbit overlying the lesion demonstrates sclerotic\nchange consistent with bony metastatic involvement, as previously. \nInvolvement of the left temporalis muscle (series 11, image 43) seems slightly\nprogressed from prior exam.\n\nAdditionally, there is enhancing T1 hypointense dural thickening along the\nposterior clivus which is more focally nodular in morphology on the right,\njust medial to the porous acousticus; this more nodular area of soft tissue\ndural thickening measures up to 8 x 5 mm, previously 6 x 3 mm when measured in\na similar fashion on the study of ___ (series 8, image 35 on that\nstudy).  This does not extend into the right internal auditory canal. \nRe-identified is abnormal enhancements along the right hypoglossal canal.\n\nThere is unchanged diffuse low signal on all sequences consistent with\nsclerotic metastatic involvement of the ___ including involving this\nclivus and sphenoid.  There are multifocal sclerotic osseous foci within the\nmandible, for example anteriorly (9:6), as well as near the TMJ (09:29). \nThere is patchy multifocal sclerotic metastatic disease involving the\nvisualized upper cervical spine, unchanged.\n\nAgain noted is asymmetric bulk of the tongue, compatible with right fatty\nreplacement and atrophy of hemi-tongue.  Aside from bilateral lens extraction,\nthe globes are intact and unremarkable.  The right orbit is within normal\nlimits.  The cavernous sinus, aside from left-sided soft tissue involvement,\nenhances normally.  The cavernous internal carotid arteries demonstrate\nnormal, preserved flow voids.  The visualized portions of the brain parenchyma\nare within normal limits.  The visualized salivary glands are within normal\nlimits.  Visible upper cervical spinal cord is unremarkable.  There is a small\nmucous retention cyst in the right maxillary sinus laterally; there is trace\nfluid layering in the dependent sphenoid sinuses; otherwise, the visualized\nparanasal sinuses and mastoid air cells appear clear.",
            "output": "1. Mild interval increase in bulk since ___ of the enhancing dural soft\ntissue thickening along the left cavernous sinus and medial left temporal\nfossa, as well as of a more focally nodular area of dural thickening along the\nright posterior clivus just medial to the right porous acousticus.  Possible\nincreased left temporalis muscle involvement adjacent to the left seen a wing\nlesion.\n2. Unchanged extension of disease through the left foramina ovale and along\nthe left superolateral orbit.\n3. Unchanged diffuse sclerosis of the ___ including the clivus and\nsphenoid, with multifocal sclerotic osseous lesions involving the left orbit,\nmandible, and upper cervical spine, compatible with known osseous metastatic\ndisease.\n4. Additional findings described above."
        },
        {
            "input": "Left parietal intraparenchymal subacute hematoma is identified measuring\napproximately 4 x 2.5 cm in size.  There is a area of flow signal adjacent to\nthe hematoma indicative of recent embolization.  Developmental venous anomaly\nis visualized within the basal ganglia as seen previously.  Other small\ndevelopmental venous anomalies are also seen.  There is no mass effect midline\nshift or hydrocephalus.",
            "output": "Examination performed for surgical planning demonstrates left parietal\nintraparenchymal hematoma with associated changes of embolization of\narteriovenous malformation."
        },
        {
            "input": "2.0 cm x 1.6 cm x 1.6 cm peripherally enhancing round mass is identified in\nthe left very posterior temporal lobe.  Inhomogeneous T2 signal is seen\ncentrally, with few thin enhancing septations.  Thin rim of enhancement along\nthe periphery of the lesion, with small areas of associated nodularity, and\nlinear subtle mildly restricted diffusion of the enhancing component. \nAppearance is not consistent with abscess, or late cerebritis, diffusion\nweighted images, T2 weighted images and extent of surrounding edema with\ndifferent appearance.\nMild surrounding nonenhancing T2 signal abnormality.  No internal blood\nproducts.  0.5 cm satellite enhancing nodule along the superolateral margin of\nthe lesion.  Findings likely represent primary glioma, less likely metastasis.\nGiven complete ring of enhancement and some thickened nodular enhancement\nalong the periphery, local mild mass-effect, findings not typical for\ntumefactive demyelination.\n\nMild local mass effect. There is no midline shift or mass effect on the\nventricles.  3 mm focus of hypoenhancement right inferior pituitary gland,\nsuggestive of microadenoma, clinically correlate coronal image 74.  There is\nno evidence of hemorrhage or infarction.  Mild paranasal sinus disease.",
            "output": "1. 2.0 cm posterior left temporal gyrus mass, worrisome for primary high-grade\nglioma, less likely metastasis.  Appearance not consistent with abscess."
        },
        {
            "input": "The 2 cm peripherally enhancing irregular lesion within the posterior left\nsuperior temporal gyrus and the 3 x 6 mm enhancing subcortical satellite\nlesion (series 8, image 68) appear similar to the recent MR from ___.  No new enhancing lesions are identified.\n\nThe ventricles, sulci, and cisterns appear stable.  There is no midline shift.\n\nThe 3 mm focus with lower intensity on postcontrast T1 weighted images within\nthe adenohypophysis to the right of midline may reflect a pituitary\nmicroadenoma, similar to the prior study.\n\nThere are a few paranasal sinus mucosal retention cysts.",
            "output": "2 cm peripheral enhancing irregular lesion within the posterior left superior\ntemporal gyrus and small enhancing satellite nodule appear similar to the MR\nfrom ___.  These findings are most suspicious for a high-grade\nglioma, with metastasis a much less likely consideration."
        },
        {
            "input": "The patient is status post left temporal lobe mass resection, expected\npostsurgical changes are seen consistent with frontal pneumocephalus, residual\nblood products are seen at the surgical site in the temporal region with\nhigh-signal intensity on T1 weighted images without contrast, after the\nadministration of gadolinium no significant change is noted in the surgical\nbed, the previously seen satellite lesion is not clearly seen in the current\nexam, please compare the image number 69, series 8 from ___ with the\ncurrent exam image 97 through 99, series 14.  There is no evidence of\nsignificant mass effect or shifting of the normally midline structures. \nSusceptibility changes are visualized at the surgical cavity consistent with a\ncombination of residual air and blood products (image 12, series 10),\nperipheral slow diffusion is noted towards the left inferior longitudinal\nfascicle and and left periventricular atrium (image 15, series 4), however\nthere is no evidence of territorial infarction.  No new areas of abnormal\nenhancement are seen.  The major vascular are vascular flow voids are present\nand demonstrate normal distribution.  The orbits are unremarkable, the\nparanasal sinuses again demonstrate an unchanged mucous retention cyst on the\nright maxillary sinus.",
            "output": "1.  Postsurgical changes identified in the left temporal lobe, the patient is\nstatus post left temporal lobe mass resection, expected postsurgical changes\nare seen consistent with frontal pneumocephalus and residual blood products at\nthe surgical site, after the administration of gadolinium contrast, there is\nno evidence of significant enhancement at the surgical bed, however close\nfollow-up is recommended until complete resolution of the postsurgical blood\nproducts.\n\n2.  Mild slow diffusion is noted surrounding the surgical bed with no evidence\nof territorial infarction.\n\nNOTIFICATION:  The findings were discussed with ___, M.D. by\n___, M.D. In person on ___ at 08:40 hours.\n\nRECOMMENDATION(S):  Postsurgical changes are visualized in the left temporal\nlobe.  Close follow-up with MRI of the head with and without contrast is\nrecommended to demonstrate evolution of the surgical blood products in the\nleft temporal surgical cavity."
        },
        {
            "input": "The patient is status post left parietal craniotomy for resection of a left\nparietal lobe mass.  Resection cavity is smaller and demonstrates less\nperipheral linear enhancement.   There is slight improvement in the degree of\nsurrounding FLAIR hyperintensity. Superior to the resection cavity is a 1.3 cm\nx 0.8 cm x 0.9 cm homogeneously enhancing nodular component, which is enlarged\ncompared with ___, when it measured 0.9 cm x 0.7 cm x 0.7 cm. \nFindings may represent posttreatment change, focal tumor progression, or\ncombination.  Follow-up ASL, DSC perfusion would be helpful if indicated. \nMildly worsened nonenhancing T2 signal abnormality along the superior margin\nof the treatment bed.  Surrounding T2 signal abnormality at the mid and lower\ntreatment bed is mildly improved.\n\n  The ventricles and sulci are normal in caliber and configuration.  The\nparanasal sinuses, mastoid air cells and middle ear cavities are clear.  The\nintraorbital contents are normal.  Suggestion of 2 mm right paramedian\npituitary macroadenoma, similar.",
            "output": "1. Posttreatment changes.\n2. Increased 1.3 cm solid nodular enhancement at the surgical margin, may\nrepresent posttreatment change, residual tumor, or combination.  Mildly\nworsened surrounding T2 signal abnormality.  ASL, DSC perfusion would be\nhelpful if indicated..\n3. Other posttreatment changes have improved improved.\n\nNOTIFICATION:  The impression and recommendation above was entered by Dr.\n___ on ___ at 13:20 into the Department of Radiology\ncritical communications system for direct communication to the referring\nprovider."
        },
        {
            "input": "Again postsurgical changes are re-demonstrated, the patient is status post\nleft parietal craniotomy and resection of a left parietal lobe mass lesion. \nIn comparison with the most recent examination, the pattern of nodular\nenhancement surrounding the surgical cavity has decreased, however, the\nvasogenic edema FLAIR hyperintensity signal appears slightly more prominent\nwith mild asymmetry of the left ventricular atrium (image 12, series 7),\nsuggestive of posttreatment changes.  New areas of subtle enhancement are seen\nabove the surgical cavity towards the left parietal lobe (image 16, series 6),\nclose attention in follow-up exams is advised.  No diffusion abnormalities are\ndetected.  The major vascular flow voids are present and demonstrate normal\ndistribution.",
            "output": "1.  Postsurgical changes consistent with left parietal craniotomy, the patient\nis status post resection of left parietal mass lesion.\n\n2.  The pattern of nodular enhancement surrounding the surgical cavity has\ndecreased, however the vasogenic edema surrounding the surgical cavity appears\nslightly more prominent with mild asymmetry of the left ventricular atrium as\ndescribed above.\n\n3.  New areas of subtle enhancement in the left parietal region suggest\ntumoral progression (image 16, series 6), close attention in this area is\nadvised.\n\nNOTIFICATION:  The findings were discussed with ___, M.D. by ___\n___, M.D. on the telephone on ___ at 9:17 am, 5 minutes after\ndiscovery of the findings."
        },
        {
            "input": "MR BRAIN: The patient is status post left parietal craniotomy and underlying\nresection of a temporoparietal mass.  Curvilinear enhancement along the\nposterior margins of the resection cavity and surrounding FLAIR edema signal\nis overall similar to prior examination.  However, a new focus of subcortical\nenhancement along the superior margins of the resection cavity (series 12,\nimage 146) is more prominent when compared to prior examination as is\nassociated FLAIR edema pattern.\n\nNo additional regions of abnormal enhancement.  The sulci, ventricles and\ncisterns are within expected limits for the patient's age allowing for\npostsurgical changes.  No new parenchymal FLAIR signal abnormality.  No acute\ninfarct or intracranial hemorrhage.  Major intracranial flow voids are\npreserved.  The dural venous sinuses are patent.  There is mild mucosal\nthickening of the ethmoid air cells.  A mucous retention cyst is noted in the\nright maxillary sinus.  The orbits are unremarkable.  No significant fluid\nsignal is seen in the mastoid air cells.  No suspicious marrow signal.\n\nMR ___: Decreased perfusion in the resection cavity.  No\ndefinite evidence of increased perfusion in the regions of abnormal\nenhancement.\n\nASL Perfusion: No definite increased perfusion in the region of increasing\nabnormal enhancement along the superior margins of the left resection cavity. \nDecreased perfusion along the resection cavity and without definitive\nincreased perfusion along the posterior enhancing margins.\n\nMR Spectroscopy: Single and multi voxel spectroscopy centered along the\nposterior edge of the left temporoparietal resection cavity demonstrates\noverall paucity of metabolites compatible with posttreatment change.  There is\nmildly increased choline to NAA ratio on single voxel spectroscopy potentially\nrepresenting residual tumor.  Multi voxel spectroscopy is technically limited\ndue to artifact.",
            "output": "1. Increasing enhancement and FLAIR signal abnormality in the subcortical\nwhite matter along the superior margins of a left temporoparietal resection\ncavity.  However, no definite increased perfusion on ASL or dynamic\nsusceptibility contrast.  No associated diffusion-weighted signal abnormality.\nAlthough lack of increased perfusion is reassuring and this may represent\nposttreatment change, recommend continued close interval follow-up to exclude\ntumor progression.\n2. Unchanged appearance of curvilinear enhancement along the posterior margins\nof the resection cavity.  No evidence of increased perfusion.  Single voxel\nspectroscopy centered on this region demonstrates overall paucity of\nmetabolites compatible with posttreatment sequela with mildly increased\ncholine to NAA which may represent residual lesion.\n3. No new regions of abnormal enhancement or FLAIR signal abnormality.  No\nacute infarct.\n4. Additional findings described above."
        },
        {
            "input": "Examination is mildly degraded by motion.\n\nPostsurgical changes of left parietal craniotomy and temporoparietal mass\nresection grossly unchanged.  Curvilinear and irregular areas of enhancement\nalong the subcortical/superior aspect of the surgical cavity (image 99 of\nseries 9, image 51 of series 900 on current study and 12:145 on ___ prior exam).  There are subtle associated punctate foci of slow diffusion\nnot definitely seen on most recent prior brain MRI.\n\nOtherwise, there are grossly stable curvilinear enhancement along the\nposterior margin of the resection cavity.\n\nSurrounding FLAIR hyperintense signal abnormalities appear slightly increased\nalong the superior aspect of the resection cavity (images ___ of series 7).\n\nThere is no evidence of restricted diffusion to suggest acute infarction.  No\nevidence of acute intracranial hemorrhage.  The ventricles and sulci are\nstable in size and configuration without midline shift.  The major\nintracranial arterial flow voids are preserved.  The dural venous sinuses are\npatent.\n\nMild mucosal thickening of the ethmoid sinuses.  Small mucous retention cyst\nin the left maxillary sinus inferiorly and tiny mucous retention cyst in the\nright maxillary sinus anteriorly.  Clear mastoid air cells.  Preserved\nintraorbital contents.",
            "output": "1. Examination is mildly degraded by motion.\n2. Increasing degree and extent of enhancement along the superior margins of\nthe left temporoparietal resection cavity with punctate foci of restricted\ndiffusion.  Mildly increased FLAIR hyperintense signal abnormalities along the\nsuperior aspect of the resection cavity as well.  The findings may relate to\npost treatment changes with differential consideration of tumor progression. \nContinued follow-up is suggested.\n3. No evidence of acute infarction or intracranial hemorrhage.\n4. Paranasal sinus disease , as described.\n\nRECOMMENDATION(S):  Increasing degree and extent of enhancement along the\nsuperior margins of the left temporoparietal resection cavity with punctate\nfoci of restricted diffusion. Mildly increased FLAIR hyperintense signal\nabnormalities along the superior aspect of the resection cavity as well. The\nfindings may relate to post treatment changes with differential consideration\nof tumor progression. Continued follow-up is suggested."
        },
        {
            "input": "The left posterior temporal region of residual enhancement underlying the\nsurgical site appears unchanged.  However, the focus of left parietal\nenhancement just cranial to this it has clearly progressed since ___ and\nslightly progressed since ___.  This area was not detected on the brain MR\nof ___.  There has been a progressive increase in FLAIR abnormality\nassociated with the left parietal enhancing mass.  Overall, these Findings\nsuggest tumor progression.\nImages of the remainder of the brain demonstrate no other lesions.  There is\nno evidence of hemorrhage, other masses or infarction.",
            "output": "1. Progressive enhancement and FLAIR abnormality in the left posterior\nparietal region, presumably reflecting tumor progression."
        },
        {
            "input": "MRV: Normal flow signal is demonstrated within the superior sagittal sinus,\nstraight sinus, transverse sinuses, and sigmoid sinuses. The jugular bulbs and\nproximal jugular veins are patent. Evaluation of the deep venous systems\nreveals normal flow signal in the internal cerebral veins. The vein ___\nis also unremarkable.\n\nPRE AND POSTCONTRAST T1 BRAIN IMAGING: There is no abnormal enhancement on\npostcontrast imaging. There is no midline shift, abnormal extra-axial fluid\ncollection, or mass. The ventricles and sulci are normal in caliber and\nconfiguration.",
            "output": "Normal brain MRV."
        },
        {
            "input": "There is no significant change in approximately 1.5 x 2.5 cm hematoma in the\nright caudate head containing acute and early subacute blood with surrounding\nedema.  There is stable effacement of the frontal horn of the right lateral\nventricle.  There is no significant midline shift.  No underlying lesion is\ndiscernible and there is no abnormal vascularity in this region.  There is\nsubtle marginal enhancement around the hematoma likely secondary to\ncompression of surrounding brain parenchyma.  There is no other areas of\nabnormal enhancement after contrast administration.  Several foci of\nperiventricular and subcortical FLAIR hyperintensities are likely the\nsecondary to a chronic small vessel ischemic disease.  There is mild mucosal\nthickening of the anterior ethmoidal air cells.",
            "output": "Stable right basal ganglia intraparenchymal hemorrhage.  No discernible\nunderlying lesion.  If there is persistent concern for underlying lesion,\nconsider repeat imaging after resolution of hemorrhage."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, midline shift or infarction.\n\nThe ventricles and sulci are normal in caliber and configuration.  Flow voids\nare visualized in the major intracranial vessels.\n\nThe patient demonstrates enhancing FLAIR hyperintense pachymeningeal\nthickening involving the bilateral cerebral hemispheres and the posterior\nfossa.  There is also a nonenhancing leptomeningeal FLAIR hyperintense signal\nwithin the bilateral cerebral hemispheric sulci and most prominent at the\nvertex.  These are non-specific findings but possible etiologies include a\nrecent episode of meningitis, chronic meningitis, intracranial hypotension, or\nrecent lumbar puncture.\n\nThere are no diffusion defects.  There is no acute infarct.  The intracranial\nflow voids are preserved.  The dural venous sinuses are patent.  The paranasal\nsinuses and bilateral mastoid air cells appear clear.  Patient has had prior\nbilateral lens replacements.\n\nThere is a left cerebellar developmental venous anomaly (series 10, image 9).",
            "output": "1. There is enhancing FLAIR hyperintense pachymeningeal thickening as well as\nnonenhancing possible leptomeningeal FLAIR hyperintense signal involving the\nbilateral cerebral hemisphere and posterior fossa are non-specific findings\nbut possible etiologies include recent episode of meningitis or chronic\nmeningitis.  Intracranial hypotension may also appear in this manner however\nthere are no secondary signs such as downward displacement of the cerebellar\ntonsils worsening the brainstem.  Inflammatory/infectious etiologies such as\nsarcoid is considered less likely.  There is no nodularity to suggest\nmetastatic disease, and is also considered unlikely but not excluded.\n\n2. A developmental venous anomaly is demonstrated in the left cerebellum.\n\nNOTIFICATION:   The findings were discussed by Dr. ___ with Dr. ___\n___ on the telephone on ___ at 3:41 ___."
        },
        {
            "input": "In comparison to MR from ___, there has been interval resolution of\nthe enhancing FLAIR hyperintense pachymeningeal enhancement, as well as the\napparent nonenhancing leptomeningeal enhancement seen near the vertex.  There\nis no evidence of pachymeningeal or leptomeningeal enhancement or thickening\non the current exam.  Again noted is a decreased medullary-pontine distance\n(series 11, image 13), which may be a residual sign intracranial hypotension.\n\nThere is no evidence of hemorrhage, infarction, edema, mass, or mass effect. \nVentricles and sulci are normal in caliber and configuration.  There are no\nabnormal foci of restricted diffusion.  The major intracranial vascular flow\nvoids are preserved.  The major dural venous sinuses are patent.  Again seen\nis the left cerebellar hemisphere developmental venous anomaly, unchanged in\nappearance since prior study (series 19, image 40).  The frontal sinuses are\nunderpneumatized; otherwise, the imaged paranasal sinuses and mastoid air\ncells are clear.  The globes are intact.",
            "output": "1. Interval resolution of pachymeningeal leptomeningeal thickening and\nenhancement, with persistent decreased medullary-pontine distance, possibly a\nresidual secondary sign of intracranial hypotension.\n2. Unchanged appearance of left cerebellar hemisphere developmental venous\nanomaly."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.  There is stable decreased medullary pontine distance\nmeasuring 5.6 mm.  The major vascular flow voids are preserved.  A\ndevelopmental venous anomaly is again noted in the left cerebellum and appears\nunchanged.\n\nThe orbits and paranasal sinuses are normal.  Partial opacification of the\nright mastoid air cells is seen.  The visualized soft tissues are normal.",
            "output": "1. No new leptomeningeal abnormal signal or contrast enhancement.\n2. Stable decreased medullary pontine distance, which may represent a\nsecondary sign of intracranial hypertension."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is benign developmental venous anomaly in the left\ncerebellum, stable since prior.  Minimal opacification of inferior right\nmastoid air cells.  Intracranial vascular flow voids are preserved.  Clear\nparanasal sinuses.  Patent dural venous sinuses.  Intracranial vascular flow\nvoids are preserved.\n\nPosition of the midbrain, mammillary bodies, cerebellar tonsils are mildly\nimproved since ___, and significantly improved since ___.  Position of the mamillary body and optic chiasm is slightly below\nexpected, stable since prior.  Ponto mammillary distance is 0.70 cm, which is\nnormal, compared with 0.55 cm on ___, and 0.41 cm on ___.  Pontomesencephalic angle is narrowed, similar to most recent\ncomparison, improved since ___.  Optic chiasm is abutting dorsum sella,\nsimilar to most recent comparison.  Minimal flattening of the pons ventrally,\nsimilar to most recent comparison, improved since ___.  There are no\nextra-axial fluid collections today.  There is no tonsillar herniation.  No\nabnormal leptomeningeal or pachymeningeal enhancement.",
            "output": "1. Mildly narrowed pontomesencephalic angle, with normal Ponto mammillary\ndistance.  No abnormal dural enhancement today.  Findings may be residua of\npreviously treated intracranial hypotension, subtle recurrence cannot be\nexcluded in the appropriate clinical setting."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, or infarction.\nThe ventricles and sulci are normal in caliber and configuration.  There are\nno acute infarcts seen. Suprasellar and craniocervical regions are\nunremarkable. Visualized paranasal sinuses are clear. Following gadolinium\nadministration, there is no evidence of abnormal parenchymal, vascular or\nmeningeal enhancement seen.  Elemental venous anomaly in the right cerebellar\nregion is unchanged.\n\nMRA of the head shows normal signal in the arteries of the anterior and\nposterior circulation. No evidence of vascular occlusion stenosis or an\naneurysm greater than 3 mm in size seen.\n\nMRA of the neck shows normal flow in the carotid and vertebral arteries. No\nevidence of stenosis or occlusion or dissection seen.",
            "output": "1. No abnormal enhancement is seen.  Specifically no leptomeningeal\nenhancement is identified.  No acute infarcts mass effect or hydrocephalus.\n2. No significant abnormalities on MRA of the head neck."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.\n\nA developmental venous anomaly is seen in the left cerebellar hemisphere.\n\nThe paranasal sinuses, mastoid air cells and middle ear cavities are clear. \nThe intraorbital contents are normal.",
            "output": "1. No acute intracranial abnormality or evidence of intracranial hypotension."
        },
        {
            "input": "There is no evidence of acute intracranial hemorrhage, mass, mass effect or\nlarge territorial infarction.  There is no evidence of abnormal enhancement\nalong the origin of the trigeminal nerve traversing to the cavernous sinus. \nSubtle T2/FLAIR hyperintensities is likely secondary to chronic small vessel\nischemic disease.\n\nA left maxillary sinus mucous retention cyst is seen measuring 1.2 cm x 1.2\ncm.  No marrow signal abnormalities are identified.",
            "output": "1. No acute intracranial abnormalities identified.\n2. No abnormal signal or enhancement along the trigeminal nerves bilaterally.\n3. Mild sinus disease."
        },
        {
            "input": "Postcontrast MP RAGE images are somewhat limited by motion artifacts, but\npostcontrast axial T1 weighted spin echo images provide adequate diagnostic\nquality.\n\nDiffusion-weighted images demonstrate no acute infarction.  There is no\nevidence for blood products, edema, mass, or other pathologic contrast\nenhancement.  There is mild periventricular white matter T2 hyperintensity\nalong the lateral ventricles, as well as mild right greater than left\noccipital subcortical T2 hyperintensity (corresponding to the hypodensity on\nthe CT from 1 day earlier),  similar to ___, nonspecific but likely\nsequela of chronic small vessel ischemic disease in this age group. \nVentricles and sulci are age-appropriate.  Major intravascular flow voids are\ngrossly preserved.  Major dural venous sinuses are patent on postcontrast MP\nRAGE images.\n\nThere is moderate mucosal thickening in the anterior ethmoid air cells,\nextending into the left frontoethmoidal recess, with mild mucosal thickening\nin the inferior portions of left greater than right frontal sinuses.  There is\nalso minimal mucosal thickening in the maxillary sinuses and along the\nanterior wall of the left sphenoid sinus.\n\nThe patient's gaze appears dysconjugate, similar to prior studies dating back\nto ___.",
            "output": "1. No acute infarction.\n2. Mild supratentorial white matter signal abnormalities, including in the\nright greater than left occipital subcortical white matter, are similar to ___ MRI, nonspecific but likely sequela of chronic small vessel\nischemic disease in this age group.\n3. Chronic dysconjugate gaze dating back to at least ___.\n4. Paranasal sinus disease, as detailed above."
        },
        {
            "input": "There is a 6 mm focus of slowed diffusion with corresponding FLAIR signal\nabnormality in the left temporal lobe along the sylvian fissure, consistent\nwith an acute infarct (series 402, image 20 and series 300b, image 47).  No\nadditional acute infarcts are identified.  There are numerous chronic infarcts\nof the coronal radiata, bilateral basal ganglia, and bilateral thalami.  There\nare numerous patchy and confluent foci of FLAIR hyperintensity in the\nsubcortical, deep, and periventricular white matter, consistent with severe\nchronic microangiopathy.  There may be hemosiderin associated with some of\nthese old infarcts.  There is focal ex vacuo dilatation of the left lateral\nventricle adjacent to old infarcts.  There is moderate generalized chronic\nvolume loss with commensurate prominence of the ventricles, sulci, and\ncisterns.  There is a cavum septum pellucidum et vergae, a developmental\nvariant.\n\nThe V4 segment of the right vertebral artery is occluded, as seen CTA from ___.  The major intracranial vessels otherwise demonstrate normal\npatency.\n\nCoronal high-resolution images asymmetric enlargement of the right temporal\nhorn relative to the left, although the hippocampi by appear normal in\nmorphology and signal.  There is no evidence of migration abnormality\nidentified.",
            "output": "1. Small 6 mm acute to subacute infarct of the left temporal lobe.  No\nassociated mass effect.\n2. Numerous chronic infarcts of the cerebral white matter, bilateral basal\nganglia, and thalami.  Severe chronic microangiopathy.\n3. Moderate generalized parenchymal volume loss.\n4. Asymmetric enlargement of the right temporal horn, although this appears to\nbe due to adjacent temporal lobe volume loss rather than specifically volume\nloss of the right hippocampus.\n5. Occlusion of the V4 segment of the right vertebral artery, unchanged from\nCTA on ___."
        },
        {
            "input": "Compared to ___, again seen are numerous, confluent T2/FLAIR\nhyperintense lesions probably located within the periventricular, pericallosal\nand subcortical white matter.  Several lesions demonstrate associated T1\nhypointensity.  There are 3 new foci, which demonstrate enhancement: a left\nposterior periventricular lesion measures 0.4 cm (___), a 0.5 cm enhancing\nright posterior periventricular lesion (___) and a curvilinear subtly\nenhancing lesion along the anterior margin of a T1 dark spot (series 10, image\n238).  The 2 periventricular lesions demonstrates associated rounded new FLAIR\nhyperintense signal.  There is no evidence of acute large territorial\ninfarction, hemorrhage,or midline shift.\n\nThe ventricles and sulci are slightly prominent for the patient's given age. \nThe basal cisterns are patent.  No evidence of impending, downward herniation.\nThere is apparent preservation of the major intracranial vascular flow voids. \nThe dural venous sinuses appear patent and MPRAGE sequences..  There is mild\nmucosal thickening of the bilateral maxillary sinuses, right frontal sinus and\nethmoidal air cells.  The bilateral orbits are within normal limits.",
            "output": "1. 2 new enhancing periventricular lesions in the right and left parietal\nlobes with associated FLAIR hyperintense signal as well as an additional new\ncurvilinear enhancing lesion along the anterior margins of an existing left\nfrontal T1 hypointense lesion.\n2. Numerous nonenhancing pericallosal, periventricular and subcortical white\nmatter T2/FLAIR hyperintensities, compatible with demyelinating plaques given\nthe history of multiple sclerosis.\n3. Mild prominence of the ventricular system and cerebral sulci, again\nsuggestive of minimal age advanced cerebral atrophic changes.\n4. Additional findings described above."
        },
        {
            "input": "In comparison with the most recent examination dated ___, the 3\npreviously noted foci of enhancement are not longer seen, there are numerous\nrelatively stable  periventricular, juxta cortical, deep, and pericallosal\nT2/FLAIR hyperintense nonenhancing lesions as compared to the prior\nexamination.  No definite new lesion or associated enhancement is identified. \nFew of these lesions demonstrate T1 hypointensity and facilitated diffusion.\n\nThere is no evidence of intracranial hemorrhage,edema,masses,mass effect,\nmidline shift orinfarction.  The ventricles and sulci again appear slightly\nprominent for patient's age suggesting mild cortical volume loss.The principal\nintracranial vascular flow voids are preserved and demonstrate normal\ndistribution, the major dural venous sinuses are patent on the postcontrast\nMPRAGE images.\n\nThe orbits are unremarkable.  Unchanged mucosal thickening is identified in\nthe left maxillary sinus and ethmoidal air cells, no air-fluid levels are\nseen, the mastoid air cells and middle ear cavities are clear.",
            "output": "1. In comparison with the most recent examination dated ___, the 3\npreviously noted foci of enhancement are not longer seen.\n2. Stable demyelinating lesions, as described.  No new lesion or associated\nenhancement.\n3. No hemorrhage, infarct, or enhancing mass.\n\nNOTIFICATION:  These findings were communicated discussed with Dr. ___\n___, by Dr. ___ on ___ at 09:20 hours."
        },
        {
            "input": "Again seen are innumerable white matter hyperintensities on T2 and FLAIR\nimaging compatible with the history of multiple sclerosis there are several T1\nblack holes.  No new lesions are identified.  There is no abnormal enhancement\nafter contrast administration.  The ventricles are mildly enlarged for age,\nunchanged.\nImaging of the brain otherwise appears normal.  There is no evidence of\nmasses, hemorrhage or infarction.",
            "output": "1. Unchanged appearance of numerous white matter lesions compatible with the\nhistory of demyelinating disease.\n2. No evidence of abnormal enhancement or of new lesions."
        },
        {
            "input": "MR BRAIN:\nThere are scattered areas of left pontine, left middle and inferior cerebellar\npeduncle as well as scattered punctate and more confluent areas of left\nposterosuperior cerebellar lobe slowed diffusion, with subtle areas of FLAIR\nhyperintensity compatible with acute to subacute infarct.  Scattered punctate\nareas of encephalomalacia are also noted in the left posterior superior\ncerebellar lobe compatible with chronic infarct.\n\nThere is no evidence of hemorrhage, edema, masses, mass effect,or midline\nshift.  There is prominence of the ventricles and sulci suggestive\ninvolutional changes.   Periventricular and subcortical T2 and FLAIR\nhyperintensities are noted, which may represent small vessel ischemic changes.\n\nThere is mild mucosal wall thickening in the bilateral maxillary sinuses and\nbilateral ethmoid air cells.  The orbits are grossly unremarkable.\n\nMRA brain:  There is a left dominant vertebrobasilar system with hypoplastic\nV4 segment of the right vertebral artery.  Nonocclusive minimal irregularity\nof basilar artery (see 304:14). There is variant fetal type origin of the\nbilateral posterior cerebral arteries.  Bilateral 1 mm lateral outpouchings of\nthe ophthalmic segments of the bilateral internal carotid arteries likely\nrepresent infundibula.  The intracranial vertebral and internal carotid\narteries and their major branches  otherwise appear patentwithout evidence of \nsignificant stenosis, occlusion, or aneurysm formation.  Irregularity of flow\nrelated signal within the right vertebral artery and basilar artery as seen on\nthe prior outside hospital examination is no longer seen.  The visualized\nportion of the bilateral AICAs appear patent.  The PICAs are not clearly\nidentified.",
            "output": "1. Acute to subacute left pontine, left middle and inferior cerebellar\npeduncle and left posterosuperior cerebellar lobe on the background of\npunctate chronic left posterior superior cerebellar lobe infarcts.  Given\nappearance and history, these likely represent foci of embolic infarct in the\nleft ___ territory.  Bilateral AICAs appear patent though the bilateral\n___ are not clearly defined.\n2. No evidence of intracranial hemorrhage.\n3. Previously noted irregular flow related signal in the right vertebral and\nbasilar arteries has resolved.\n4. Nonocclusive minimal irregularity of basilar artery.\n5. Otherwise, circle of ___ grossly patent without definite stenosis,\nocclusion or aneurysm.\n6.  Paranasal sinus disease as described.\n\nNOTIFICATION:  The findings were discussed with ___, M.D. by\n___, M.D. on the telephone on ___ at 9:09 AM, 5 minutes after\ndiscovery of the findings.\n\nFindings were also communicated to and acknowledged by Dr. ___ by ___.\n___, MD 5 minutes after discovery of the findings at 21:15 ___."
        },
        {
            "input": "There is mild motion artifact requiring use of BLADE acquisition technique.\n\nOn the axial T2 and axial FLAIR sequences, there is questionable diffuse mild\nthickening of the cortical gray matter with a mildly indistinct interface with\nthe underlying subcortical white matter.  On corresponding axial T1 and\nsagittal T1 sequences, the gray matter demonstrates normal thickness within\nnormal interface within the subcortical white matter.\n\nOtherwise the parenchymal signal is unremarkable without infarct, hemorrhage,\nmass, or mass effect.  The ventricles and cortical sulci are normal in caliber\nconfiguration.  The extra-axial spaces are unremarkable.  There is normal\ndural venous sinus enhancement.  The vascular flow voids are preserved.\n\nThe orbits, calvarium, and soft tissues are unremarkable.  There is no\nabnormal fluid signal within paranasal sinuses, mastoid air cells, or middle\nears.",
            "output": "1. Mild motion artifact requiring use of BLADE acquisition technique.\n2. Questionable diffuse mild thickening of the cortical gray matter and\nindistinct gray-white interface seen only on the T2 and FLAIR sequences and\nappearing normal on the correlate T1 sequences, therefore likely due to motion\nand BLADE acquisition technique.  Given the clinical setting, however an early\nencephalitis is not entirely excluded.  Consider follow-up imaging if\nclinically warranted.\n3. No acute infarct, hemorrhage, or mass.\n\nRECOMMENDATION(S):  Close follow-up with MRI of the brain with and without\ncontrast as clinically warranted is advised.\n\nNOTIFICATION:  The findings were discussed with ___, M.D. by ___,\nM.D. on the telephone on ___ at 10:02 AM, 10 minutes after discovery of\nthe findings."
        },
        {
            "input": "The parenchymal signal is unremarkable without evidence of acute infarct,\nhemorrhage, mass, or mass effect.  The ventricles and cortical sulci\ndemonstrate normal caliber and configuration.  There is no abnormal\npostcontrast enhancement.  The vasculature is patent.\n\nThe orbits are unremarkable.  There is mild mucosal thickening within the\nbilateral ethmoid air cells.  The mastoid air cells are clear.\n\nThere is an expansile enhancing mass centered at the C1 left lateral mass\nextending anteriorly to the mid anterior arch and posteriorly to the left\nposterior lateral lamina which measures 4.4 AP oblique by 2.3 TV by 2.6 SI cm\n(1001:39; 1000:81).  This involves the left transverse foramen with loss of\nthe normal T2 flow voids within the V2 segment vertebral artery.  The more\ncephalad V4 segment left vertebral artery is diminutive but demonstrates flow\nvoid and postcontrast enhancement.",
            "output": "1. Expansile enhancing mass centered at the left C1 lateral mass suspicious\nfor osseous metastatic disease given patient's history of hepatic cellular\ncarcinoma.  This involves the left transverse foramen and there is\nnonvisualization of the expected T2 flow void which may represent occlusion\nversus slow flow within the traversing left vertebral artery.  The more\ncephalad V4 segment vertebral artery is diminutive, but appears patent. \nConsider CT/CTA for further characterization.\n2. No acute intracranial abnormality.\n\nRECOMMENDATION(S):  Consider CT/ CTA for further characterization of the C1\nbony lesion and the traversing left vertebral artery.\n\nNOTIFICATION:   The impression and recommendation above was entered by Dr.\n___ on ___ at 16:10 into the Department of Radiology critical\ncommunications system for direct communication to the referring provider.\n\nThe findings were discussed by Dr. ___ with Dr. ___ on the telephone on\n___ at 4:15 ___, after discovery of the findings."
        },
        {
            "input": "MRI Brain:  There is no evidence of acute hemorrhage, edema, mass effect  or\nacute infarction.  Ventricles and sulci are normal in caliber and\nconfiguration.\nThere are prior infarctions noted in the left thalamus and in the right\ncoronal radiata. There are scattered foci of T2/FLAIR signal hyperintensity in\nthe periventricular, subcortical, and deep white matter.  There are tiny foci\nof susceptibility artifact in the left temporal lobe and right caudate which\nmay represent tiny regions of chronic micro hemorrhage versus foci of\nmineralization.\nVascular flow voids are preserved.\nThe orbits are unremarkable. There is mucosal thickening within the ethmoid\nair cells and bilateral maxillary sinuses.\nThere is a small amount of fluid again noted in the left mastoid air cells.\n\nMRA brain: The intracranial vertebral and internal carotid arteries and their\nmajor branches appear normal without evidence of focal flow-limiting stenosis,\nocclusion.\nA tiny outpouching is noted at the left middle cerebral artery division,\nmeasuring approximately 2-3 mm, series 13, image 86 ; series 1301, image 10\nwhich can represent a small saccular aneurysm or related to the branching\npoint.\n.\nNo prior studies are available to assess for interval change.\n\nMRA neck:  The common, internal and external carotid arteries and vertebral\narteries appear patent.\nThere is no evidence of focal flow-limiting stenosis.  The origins of the\ngreat vessels, subclavian arteries included appear patent bilaterally.\nCervical spine inadequately assessed as not targeted.",
            "output": "1.  No evidence of new acute infarction. Prior infarctions in the left\nthalamus and right coronal radiata.\n\n2.  T2/FLAIR signal hyperintensity in the periventricular, subcortical, and\ndeep white matter which is nonspecific but may be seen in the setting of\nchronic small vessel ischemic disease.\n\n3.  Patent major intra and extracranial arteries, without focal flow-limiting\nstenosis or occlusion.\n4. A small 2-3 mm saccular outpouching at the left middle cerebral artery\ndivision\n(Se 1301, im 8), can represent a tiny aneurysm or related to the branching\npoint.\nNo prior studies available.\nCorrelation with CT angiogram of the head can be considered for better\nassessment and interventional neuroradiology consult after CTA to decide on\nmanagement"
        },
        {
            "input": "There is no acute infarction, intracranial hemorrhage, extracerebral fluid\ncollection, midline shift or mass effect.  Ventricles and extra-axial spaces\nare normal in size.  A few scattered foci T2 hyperintensity are seen\npredominantly in the subcortical and deep white matter of both cerebral\nhemispheres which are nonspecific and not in the distribution of demyelinating\ndisease.  Findings likely indicate mild changes of small vessel disease.  Flow\nvoids are maintained. Suprasellar and craniocervical regions are unremarkable.",
            "output": "Mild changes of small vessel disease, otherwise, no significant abnormalities\nare seen on MRI of the brain without gadolinium."
        },
        {
            "input": "In comparison with the prior exams, the ventricles and sulci remain prominent,\nout of proportion to sulci rising the possibility of normal pressure\nhydrocephalus in the appropriate clinical setting, however cortical volume\nloss due to involutional changes is also a consideration, the temporal\nventricular horns are not significantly enlarged, please note that the corpus\ncallosum is thin in the sagittal view (image 12, series 3), although this\nfinding is not specific can be seen in patients with ataxia.  Pontine and\nsubcortical periventricular T2/FLAIR hyperintensities are nonspecific and may\nreflect changes due to small vessel disease.  There is no evidence of acute\nintracranial hemorrhage, mass, mass effect or shifting of the normally midline\nstructures.  No diffusion abnormalities are detected, there is no evidence of\nabnormal enhancement after contrast administration.  The major vascular flow\nvoids are present and demonstrate normal distribution, the orbits are normal,\nthe paranasal sinuses and the mastoid air cells are clear.  I",
            "output": "1.  Persistent and grossly unchanged enlarged ventricles, out of proportion to\nsulci rising the possibility of normal pressure hydrocephalus in the\nappropriate clinical setting, however cortical volume loss due to involutional\nchanges is also consideration.\n\n2.  Extensive T2/FLAIR hyperintensities demonstrated in the subcortical and\nperiventricular white matter as well as in the pons, which are nonspecific and\nmay reflect changes due to small vessel disease.\n\n3.  There is no evidence of acute intracranial hemorrhage.  There is no\nevidence of abnormal enhancement after contrast administration."
        },
        {
            "input": "Right frontal approach ventriculostomy is re-demonstrated, causing a\nsignificant amount of artifact in this region.  Within this limitation, no\nlarge territorial infarct, hemorrhage, edema or masses.  Visualized portions\nof the paranasal sinuses are clear.  The ventricles and sulci are normal in\ncaliber and configuration.  Periventricular and subcortical white matter\nT2/FLAIR hyperintensities are nonspecific but likely sequelae of chronic small\nvessel ischemic disease.  Bilateral subdural fluid collections are likely\nhygromas.",
            "output": "Large susceptibility artifact from right sided ventriculostomy limits\nanatomical detail.  Within this limitation, no evidence of infarction."
        },
        {
            "input": "There is a mass enlarging the sella turcica and extending superiorly into the\nsuprasellar cistern.  This measures approximately 15 mm in greatest cranial\ncaudal dimension.  The lesion enhances in homogeneously after contrast\nadministration.  The suprasellar component of the mass elevates and deforms\nthe optic chiasm and the optic nerves.  The hypothalamic stalk is displaced to\nthe right.\nThe most likely diagnosis is a pituitary macro adenoma.  However, the rare\npossibility of a metastasis to the pituitary gland could not be excluded.\nThe emerging of the remainder of the brain otherwise appear normal.  There is\nno evidence of hemorrhage, edema, other masses, mass effect, midline shift or\ninfarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no other abnormal enhancement after contrast\nadministration.",
            "output": "1. 15 mm pituitary lesion that is most likely a macro adenoma.  However, the\npossibility of a metastasis to the pituitary gland could not be excluded.\n2. Otherwise normal study."
        },
        {
            "input": "MRI BRAIN:\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  Moderate periventricular and deep white matter T2 and FLAIR\nhyperintense changes are nonspecific, most likely sequela of microangiopathy. \nIdiopathic basal ganglia calcifications.  Partially empty sella.  The\ncraniocervical junction appears normal.  Heterogeneous and expanded calvarium\nin keeping with history of patient's Paget's disease.  The orbits appear\nnormal.\n\nMRA BRAIN:\nThe intracranial vertebral and internal carotid arteries and their major\nbranches are patent without marked stenosis, occlusion, or aneurysm formation.\nFetal origin of the left PCA.  The right AICA passes into the proximal right\nIAC, but this is seen in a large percentage of asymptomatic patients.\n\nMRA NECK:\nThe common, internal and external carotid arteries are patent.  There is no\nevidence of internal carotid artery stenosis by NASCET criteria.  The origins\nof the great vessels, subclavian and vertebral arteries are patent\nbilaterally.",
            "output": "1. There is no evidence of acute intracranial process or hemorrhage.\n2. Moderate white matter microangiopathic changes.\n3. No intracranial arterial occlusion or aneurysm.  No vascular malformation.\n4. The carotid arteries are patent bilateral.  No proximal ICA stenosis by\nNASCET criteria.\n5. The vertebral arteries are patent bilaterally.\n6. Expanded and heterogeneous calvarium in keeping with history of patient's\nPaget's disease."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.   A couple of punctate periventricular and deep white matter T2\nand FLAIR hyperintensities most likely represent sequela microangiopathy. The\nintracranial arteries demonstrate normal T2 flow voids.  There is a bulbous\noutpouching at the bifurcation of the M1 segment of the left MCA which is\nconcerning for an aneurysm measuring 4 mm in diameter (series 10, image 11). \nAir-fluid level with associated aerated secretions in the left maxillary\nsinus.  Small mucous retention cyst in the right maxillary sinus.  Mild\nmucosal thickening involving the ethmoid and sphenoid sinuses as well as the\nmastoid air cells.  The orbits appear normal.",
            "output": "No acute intracranial infarct.\n\nNo mass or hemorrhage.\n\n4 mm bulbous outpouching at the bifurcation of the M1 segment of the left MCA\nconcerning for an aneurysm measuring 4 mm diameter.\n\nA couple of punctate periventricular and deep white matter T2 and FLAIR\nhyperintensities are nonspecific, but most likely represent sequela of\nmicroangiopathy.\n\nParanasal sinus opacification as described above.\n\nRECOMMENDATION(S):  Neuro interventional consult +/- MRA recommended for\nbetter characterization of the left MCA aneurysm"
        },
        {
            "input": "The web-like filling defect in the right carotid bulb is again noted. There is\nno evidence of stenosis by NASCET criteria. The origins of the great vessels,\nsubclavian, and vertebral arteries appear normal bilaterally.\n\nPlease note that the area of concern was not included in the scan volume of\nthe T1 fat-sat axial imaging.\n\nIncidental finding of a 4 mm bulbous aneurysm arising from the bifurcation of\nthe M1 segment of the left MCA.",
            "output": "1. The web-like filling defect in the right carotid bulb is again noted. \nPlease note that this area of concern was not included in the scan volume of\nthe T1 fat-sat axial imaging.  This finding most likely suggests a web rather\nthan dissection given the location and appearance.\n2. Incidental finding of a 4 mm bulbous aneurysm arising from the bifurcation\nof the M1 segment of the left MCA.\n\nRECOMMENDATION(S):  Neuro interventional consult and MRA to better\ncharacterize the left MCA aneurysm.  At the time of the MRA a repeat T1\nfat-sat should be performed through the right carotid bulb.\n\nNOTIFICATION:  The findings were discussed with ___, M.D. by ___\n___, M.D. on the telephone on ___ at 10:22 am, 10 minutes\nafter discovery of the findings."
        },
        {
            "input": "There is an approximately 5.5 mm left middle cerebral artery bifurcation\naneurysm.\n\nNo other intracranial aneurysm, occlusion or significant stenosis.\n\nThe T1 fat-sat axial imaging done through the right carotid bulb did not\ndemonstrate any hyperintensity to suggest intramural hematoma.  The appearance\nof the right common carotid artery bifurcation on the CTA likely represents a\nweb or ulcerated plaque.",
            "output": "5.5 mm aneurysm at the bifurcation of the left MCA is again noted\n\nThe T1 fat-sat axial imaging done through the right carotid bulb did not\ndemonstrate any hyperintensity to suggest intramural hematoma.\n\nRECOMMENDATION(S):  Neuro interventional consult advised."
        },
        {
            "input": "There is early subacute infarct at the left basal ganglia, involving caudate\nbody, corona radiata, putamen, more apparent compared with ___\nhead CT, not definitely seen on ___ head CT, new since MRI ___.  No hemorrhage.  Postoperative changes, pneumocephalus, left MCA\naneurysm clipping.  Postoperative changes in the scalp, craniotomy.  Small\nfluid collection overlies supra zygomatic temporalis fossa.\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift.\nThe ventricles and sulci are normal in caliber and configuration.  Submucosal\nretention cyst right maxillary sinus.  Essentially clear mastoids. \nIntracranial vascular flow voids are preserved.",
            "output": "1. Early subacute infarct centered on left basal ganglia.  No hemorrhage. \nPostoperative changes intracranially.\n\nNOTIFICATION:  The findings were discussed with ___ NP, by\n___, M.D. on the telephone on ___ at 11:03 pm, 2 minutes\nafter discovery of the findings."
        },
        {
            "input": "MRV:  There is a focal filling defect at the distal right internal jugular\nvein, at the junction with the right sigmoid sinus (series 4, image 55 through\n59; series 11, image 163).  The remaining portions of the right sigmoid sinus\nhowever appear patent.  Normal flow signal is demonstrated within the superior\nsagittal sinus, straight sinus, transverse sinuses, and left sigmoid sinuses. \nThe left jugular bulb and proximal left jugular vein are patent. Evaluation of\nthe deep venous systems reveals normal flow signal in the internal cerebral\nveins. The vein ___ and the straight sinus are also unremarkable.\n\nBrain MRI:  There is no evidence of acute ischemia, hemorrhage, midline shift\nor extra-axial fluid collection.  Confluent T2/FLAIR hyperintensities\ninvolving the subcortical, periventricular and deep white matter are non\nspecific, but likely the sequela of chronic small vessel ischemic disease. \nProminence of ventricles and sulci is consistent with age related involutional\nchanges.  There is focal encephalomalacia involving the right parietooccipital\nlobe with secondary ex vacuo dilation of the right occipital horn.  Changes\nrelated to prior chronic infarction are also present in the left occipital\nlobe.  There is no abnormal enhancement on postcontrast imaging.\n\nThere is complete opacification of the right mastoid air cells, better\nassessed on prior dedicated temporal bone CT.  The left mastoid air cells and\nvisualized paranasal sinuses are clear.  The orbits are grossly unremarkable.",
            "output": "1. Focal filling defect of the distal right internal jugular vein, at the\njunction with the right sigmoid sinus, is highly suspicious for partial\nthrombosis and slow flow.  The possibility of a flow related artifact such as\nturbulence, however remains a consideration, although felt less likely given\nthe corresponding findings seen on the most recent contrast-enhanced temporal\nbone CT.\n2. No evidence for epidural collection, abnormal enhancing lesion or abscess\nformation.\n3. Complete opacification of the right mastoid air cells is better assessed on\nprior dedicated temporal bone CT.\n4. Chronic infarctions involving the right parieto-occipital lobe and left\noccipital lobe.\n\nNOTIFICATION:  The findings were discussed with Dr. ___. by ___\n___, M.D. on the telephone on ___ at 1:08 ___, 15 minutes after\ndiscovery of the findings."
        },
        {
            "input": "MRI brain:  There is chronic encephalomalacia within the bilateral frontal,\nparietal, occipital, and right temporal cortices consistent with remote\ninfarct.  There is no acute infarct, hemorrhage, mass, or mass effect.  There\nis prominence of the ventricles secondary to ex vacuo dilatation.  The\nextra-axial spaces are unremarkable.  The arterial flow voids are preserved.\n\nThe bilateral native lenses are absent.  The soft tissues are unremarkable. \nThere is an endotracheal and oral enteric catheter is in place with fluid\nlayering within the pharynx.  There is mild mucosal thickening within\nbilateral maxillary sinuses.  There is a trace left and mild right mastoid air\ncell effusion without overlying soft tissue fluid collection or abscess. \nApparently there is  improvement in the pattern of pneumatization on the right\nmastoid air cells.\n\nMRV:  There is absence of the right transverse sigmoid, and internal jugular\nvein flow void on the spin echo sequences.  There is corresponding absence of\nflow signal within the left sigmoid and jugular vein with minimal linear flow\nsignal hyperintensity within the right transverse sinus.  On postcontrast\nimaging, there is normal enhancement of the right transverse and sigmoid\nsinus, and internal jugular vein, with a central focal filling defect at the\nright jugular bulb measuring 5 mm (101b:22; 102b:87), which is relatively\nunchanged comparison to prior study.\n\nThe remainder of the major superficial and deep cortical veins, superior\nsagittal sinus, left transverse and sigmoid sinus and internal jugular veins,\ndemonstrate normal enhancement and flow signal hyperintensity.",
            "output": "1. Unchanged small central filling defect of the right jugular bulb, likely\nrepresenting nonocclusive thrombus with associated proximal slow flow within\nthe right transverse and sigmoid sinus and right internal jugular vein.\n2. Trace left and small right mastoid air cell effusions without associated\nepidural or soft tissue abscess.  The degree of right mastoid air cell\nopacification has significantly improved in comparison to ___.\n3. No acute infarct or hemorrhage.\n4. Chronic infarcts, as described."
        },
        {
            "input": "There is a large left MCA territory acute to early subacute infarction much of\nthe left parietal lobe, superior left temporal lobe, insula, and inferior/post\nleft frontal lobe.\n\nThere are small foci of acute to early subacute infarcts with identical signal\ncharacteristics in the anterior right cingulate gyrus (right ACA territory),\nright superior frontal gyrus on images ___ (MCA territory) and in the\nright centrum semiovale white matter (4:26, 24, 23, 22).\n\nNo evidence of blood products.  No significant mass effect.  Specifically, no\ncompression of the ventricles or basal cisterns, and no shift of midline\nstructures.\n\nLoss of the bilateral internal carotid of flow voids with distal supraclinoid\nreconstitution corresponds to non opacification seen on the prior CTA head.\n\nThere is mild-to-moderate mucosal thickening and mucous retention cysts in the\nright maxillary sinus.  There is mild mucosal thickening in the left\nmaxillary, left frontal, and sphenoid sinuses.  There is moderate bilateral\nanterior ethmoid and mild bilateral posterior ethmoid air cell opacification. \nThere is mild partial opacification of the right mastoid air cells.",
            "output": "1. Multifocal acute to early subacute infarctions, moderately large in the\nleft MCA territory, small in the anterior right cingulate gyrus in the right\nACA territory, punctate in the right superior frontal gyrus in the MCA\nterritory, and multiple punctate small acute to early subacute infarcts in the\nright centrum semiovale.\n2. No evidence for blood products.  No significant mass effect.\n3. Occlusion of bilateral internal carotid arteries is again seen with distal\nsupraclinoid reconstitution, better assessed on the ___ CTA."
        },
        {
            "input": "MRI Brain:\nThere are multiple foci of cortical slow diffusion in the posterior left\nfrontal lobe and left parietal lobe with corresponding FLAIR signal\nhyperintensity compatible with subacute infarcts.  There are superimposed\nperiventricular and subcortical foci of T2/FLAIR signal hyperintensity,\nnonspecific and likely sequelae of chronic ischemic microvascular disease. \nThere is no evidence of hemorrhage, edema, masses, mass effect or midline\nshift.  Prominence of the cerebral sulci and ventricles suggestive of\nage-related involutional changes.  A partially empty sella is identified.\n\nMild mucosal thickening within the ethmoid air cells and a left maxillary\nmucous retention cyst is noted.  There are postsurgical changes related to\nlens replacement.\n\nMRA brain: There is irregular narrowing of the left MCA bifurcation and\ninferior division of the left MCA with distal paucity of flow related\nenhancement.  There is irregular narrowing at the right MCA bifurcation wi\nwhich is otherwise patent.  Mild irregularity of the bilateral internal\ncarotid artery siphons is noted, likely related to arthrosclerotic plaque. \nOtherwise, the intracranial vertebral and internal carotid arteries and their\nmajor branches appear normal without evidence of stenosis, occlusion, or\naneurysm formation.\n\nMRA neck: There is mild segmental narrowing of the bilateral vertebral\narteries, likely related to atherosclerotic plaque.  Mild probable\natherosclerotic stenosis of the origins of the external carotid arteries is\nnoted.  Otherwise the common, internal and external carotid arteries appear\nnormal.  There is no evidence of internal carotid artery stenosis by NASCET\ncriteria.  The origins of the great vessels, subclavian and vertebral arteries\nare not well visualized..",
            "output": "1. Subacute infarct involving the posterior left frontal and parietal lobes. \nNo significant regional edema, mass effect or midline shift.\n2. Irregular narrowing of the left MCA bifurcation and inferior division of\nthe left MCA with nonvisualization of distal flow concerning for high-grade\nstenosis or occlusion at the M2 segment.\n3. Otherwise patent intracranial vertebral and internal carotid arteries and\ntheir major branches without evidence of stenosis, occlusion or aneurysm.\n4. Patent common carotid, internal and external carotid arteries without\nevidence of internal carotid artery stenosis by NASCET criteria.\n5. Mild segmental probable atherosclerotic narrowing of the bilateral cervical\nvertebral arteries which are otherwise patent.\n\nNOTIFICATION:   The findings were discussed with Dr.  ___. by ___\n___, M.D. on the telephone on ___ at 12:15 pm, 5 minutes after\ndiscovery of the findings."
        },
        {
            "input": "Study is mildly degraded by motion.\n\nMultiple punctate areas of diffusion restriction in the bilateral cerebellar\nhemispheres, left occipital lobe, bilateral frontal lobes, right parietal\nlobe, and right caudate body are seen.  Some of these lesions demonstrate\nassociated T2 and FLAIR hyperintensity.  There is no definite associated\nincrease susceptibility.  P\n\nPeriventricular and subcortical T2 and FLAIR hyperintensities are noted which\nmay represent small vessel ischemic changes.  There is prominence of the\nventricles and sulci suggestive of involutional changes.  There is no definite\nevidence of intracranial hemorrhage, midline shift, or mass.  Mucous retention\ncyst and mucosal thickening is noted in the in the right maxillary sinus. \nDemonstrate bilateral lens replacement postoperative changes are noted.",
            "output": "1.  Study is mildly degraded by motion.\n2. Bilateral cerebellar hemisphere, left occipital lobe, and right caudate\nbody, punctate acute to subacute infarcts without definite evidence of\nhemorrhagic transformation, concerning for central embolic source.\n3. Global volume loss and probable microangiopathic changes as described.\n4. Paranasal sinus disease, as described."
        },
        {
            "input": "Study is mildly degraded by motion.\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are preserved in caliber and\nconfiguration.\n\nSingle 2mm left frontal superior gyrus enhancing lesion with associated T2 and\nFLAIR hyperintensity is noted (see 12, 13, 15, 16:19; 11:10; 17:138).\n\nFew periventricular and subcortical T2 and FLAIR hyperintensities are noted\nwhich may represent small vessel ischemic changes.  Punctate right parietal\ncalvarium intrinsically T1 hyperintense lesion is noted (see 12:20; 11:15),\nsuggestive of hemangioma.\n\nScattered subcentimeter nonspecific lymph nodes are noted throughout the\nvisualized portion of the neck bilaterally.",
            "output": "1. Study is mildly degraded by motion.\n2. 2 mm left frontal superior gyrus enhancing lesion concerning for metastatic\ndisease.\n3. Limited imaging of the cervical and suboccipital soft tissues suggest\nsubcentimeter nonspecific lymph nodes. If clinically indicated, consider FDG\nPET-CT for further evaluation.\n\nNOTIFICATION:  The impression and recommendation above was entered by Dr.\n___ on ___ at 13:10 into the Department of Radiology critical\ncommunications system for direct communication to the referring provider."
        },
        {
            "input": "There is 0.6 cm left superior frontal gyrus enhancing lesion, most consistent\nwith metastasis, with mild-to-moderate surrounding edema..  It measured 0.2 cm\n___.  There is subtle 1 mm susceptibility within the enhancing\nfocus likely representing blood products (06:20), likely treatment related. \nThere is no new focus of enhancement.\nTiny probable developmental venous anomaly posterior right parietal operculum,\nstable since prior.\nThere is no infarct..  There are minimal scattered subcortical and\nperiventricular white matter FLAIR hyperintensities.  The ventricles and sulci\nare normal in caliber and configuration.\n\nThe major intracranial vascular flow voids are maintained.  The paranasal\nsinuses, mastoid air cells and orbits are normal.",
            "output": "1. 6 mm metastasis left superior frontal gyrus, increased since prior.  Mild\nto moderate surrounding edema.  Punctate focus of microhemorrhage within\nmetastasis, likely treatment related."
        },
        {
            "input": "A 1.7 x 1.8 cm (previously 0.6 cm) left superior frontal gyrus enhancing\nlesion is moderately increased in size.  Surrounding vasogenic edema is\nmoderate and unchanged.  There is no significant mass effect.\n\nAn enhancing focus in the right parietal operculum (series 10, image 91)\nlikely represents a small developmental venous anomaly, unchanged.\n\nNo new intracranial hemorrhage, edema, mass effect or infarction.\n\nAdditional subcortical and periventricular white matter FLAIR hyperintensities\nare nonspecific but likely represent sequela of chronic small vessel ischemic\ndisease.\n\nThe ventricles and sulci are within normal limits.  The major intracranial\nflow voids are preserved.  Dural venous sinuses are patent.  The paranasal\nsinuses and mastoid air cells are clear.  The orbits are unremarkable.\n\nAn intrinsically T1 and T2 hyperintense in the left occipital condyle (series\n5, image 3, series 6, image 3) likely represents a hemangioma and appears\nunchanged from ___.  Similarly, a T1 and T2 hyperintense\nenhancing lesion in the left temporal calvarium (series 10, image 138) is\nunchanged from ___ and is compatible with a hemangioma.",
            "output": "1. Interval increase in a left frontal metastatic lesion, which now measures\nup to 1.8 cm (previously 0.6 cm).  No worsening mass effect or midline shift\nor worsening edema.  Given radiation treatment on ___, this could\npotentially represent sequela of radiation necrosis, however further\nevaluation with MRI spectroscopy and perfusion is recommended.  No new lesions\nidentified.\n2. Unchanged, right parietal operculum enhancing focus felt to be most\ncompatible with a developmental venous anomaly."
        },
        {
            "input": "MR BRAIN:\nThere is 1.6 cm x 1.4 cm x 1.8 cm enhancing d mass left superior frontal\ngyrus, compared with 1.4 cm x 1.2 cm x 1.7 cm on ___.  Mild\nsurrounding edema, minimally worsened.  Enhancing lesion is mildly restricted\ndiffusion with decreased ADC values.\nNo new lesions.\nThere is no evidence of hemorrhage,midline shift or infarction.   The\nventricles and sulci are normal in caliber and configuration.  Vascular flow\nvoids are preserved.  Dural venous sinuses are patent.\n.\nMR ___: Inhomogeneous appearance, with areas of increased\ncerebral blood volume predominantly within periphery of enhancing lesion. \nSome of these findings may represent posttreatment change.\n\nASL Perfusion: 8 mm x 7 mm focus of increased perfusion on ASL along the\nmedial margin of the enhancing abnormality in the left frontal lobe suggestive\nof residual tumor.  Remainder of the abnormality does not show increased\nperfusion, suggesting posttreatment change.\n\nMR Spectroscopy: Elevated choline relative to NAA within enhancing lesion. \nThere is small lactate peak.",
            "output": "1. 1.8 cm enhancing left frontal lobe mass which has increased ASL perfusion\nalong its medial margin, which is suggestive of residual tumor."
        },
        {
            "input": "The left frontal lobe lesion previously seen measures approximately 14 mm\nminimally changed from the previous study.  There is no new area of abnormal\nenhancement identified.  There is no midline shift or hydrocephalus.  No acute\ninfarcts are seen.",
            "output": "Minimally changed left frontal lobe enhancing lesion at the gray-white matter\njunction compared to the previous MRI study.  The examination is performed for\nsurgical planning."
        },
        {
            "input": "The patient is status post recent left frontal craniotomy and resection of\nleft frontal lobe mass.  Intrinsically T1 hyperintense material in the left\nfrontal resection bed (08:11) which demonstrates susceptibility artifact on\ngradient recalled echo images (10:20) is consistent with trace blood products\nfrom resection.  Trace blood products are also seen layering along the\nsuperior falx (10:22), within expected range.  Foci susceptibility along the\nleft frontal convexity may relate to trace residual pneumocephalus, better\nseen on recent CT of the head from ___ (10:16).  T2/FLAIR signal\nhyperintensity in the region of the resection bed and surrounding white matter\nin the left frontal lobe (11:20) is likely related to edema, within expected\nrange.  Similarly, slight left frontal FLAIR hyperintense dural thickening and\nenhancement overlying the resection site is likely reactive to recent surgery.\n\nElsewhere, there is no new superimposed acute intracranial abnormality\nincluding evidence of acute infarction, separate focus of hemorrhage,\nadditional mass, significant mass effect, or additional focus of edema.  The\nbasal cisterns are patent, and there is no shift of the normally midline\nstructures.  The ventricles and sulci are normal in caliber and configuration.\nThe major intracranial vascular flow voids are preserved.  The major dural\nvenous sinuses are patent.",
            "output": "Expected postsurgical findings status post recent left frontal craniotomy and\nresection of left frontal lobe mass, including edema, small volume blood\nproducts, and probable pneumocephalus.  No new superimposed acute intracranial\nabnormality identified."
        },
        {
            "input": "The patient is status post recent left frontal parietal craniotomy and\nresection of a left frontal lobe vertex lesion.  A 1.8 x 1.6 cm (TRV, AP) rim\nenhancing operative bed is identified, slightly more pronounced when compared\nto immediate postoperative examination of ___.  No evidence of nodular\nenhancement.  No new enhancing lesions.\n\nNo acute infarct.  The sulci, ventricles and cisterns are within expected\nlimits for the patient's age.  The dural venous sinuses are patent.",
            "output": "1. 1.8 x 1.6 cm rim enhancing operative bed of the left superior frontal gyrus\nis identified without evidence of nodular component and likely central fluid. \nNo evidence of new enhancing lesion.\n2. Left frontal parietal craniotomy is identified.\n3. Additional findings as described above."
        },
        {
            "input": "Study is mildly degraded by motion.\n\nPituitary is top-normal in size, stable.\n\nPost treatment changes, left frontal lobe, stable.  FLAIR signal abnormality\nsurrounding the resection cavity is stable.  Thin, faint enhancement\nsurrounding the resection site and subjacent to the craniotomy is unchanged. \nNo new enhancement.  No evidence of new enhancing intracranial mass.\n\nThere is no evidence of infarction, hemorrhage, or mass effect.\n\nThe ventricles sulci are grossly stable in caliber and configuration.\n\nThe visualized paranasal sinuses and mastoids appear clear.  The globes and\norbits are preserved.  Major intracranial vascular flow voids are preserved.\nMajor dural venous sinuses are patent.",
            "output": "1. Study is mildly degraded by motion.\n2. Stable postsurgical changes, left frontal lobe, including unchanged extent\nof surrounding parenchymal signal abnormality.\n3. Grossly stable nonspecific minimal enhancement around the resection cavity\nunchanged compared to ___ prior exam.  While findings likely\npostoperative, recurrent or residual tumor is not excluded on the basis of\nthis examination.\n4. Within limits of study, no definite evidence of new intracranial enhancing\nlesion."
        },
        {
            "input": "Postsurgical changes are seen secondary to a left frontal craniotomy for\nresection of a left frontal lobe mass, including focal dural thickening, blood\nproducts and resection cavity.  There is minimal enhancement at the surgical\ncavity (series 10, image 21), likely postsurgical in nature, with adjacent\nareas of FLAIR high-signal intensity, attention in this region in follow-up\nexams is advised.  No diffusion abnormalities are detected or new areas with\nabnormal enhancement.  The ventricles and sulci appear unchanged and are\nnormal in size and configuration.  The orbits are normal, the major vascular\nflow voids are present and demonstrate normal distribution, minimal mucosal\nthickening is noted in the ethmoidal air cells, no air-fluid levels are seen,\nthe middle ear cavities and mastoid air cells are clear.",
            "output": "1. Postsurgical changes identified in the left frontal convexity.\n2. Minimal enhancement is noted in the left frontal surgical cavity, with no\nfrank evidence of residual mass or recurrence, attention in this area is\nrecommended.\n3. Similar pattern of T2 FLAIR high-signal intensity surrounding the surgical\ncavity likely consistent with posttreatment changes.\n4. No acute intracranial abnormality."
        },
        {
            "input": "There are stable postoperative changes from prior left frontal craniotomy and\nresection.  Minimal linear enhancement at the margins of the resection with\nadjacent white matter FLAIR hyperintensity are all unchanged.  No evidence of\nlocal tumor recurrence.\n\nThere are multiple new bilateral lesions centered at the gray-white matter\njunction.  Specifically:\n\n-2 mm, right superior frontal gyrus (17:130), similar compared with ___, not seen on ___\n-5 mm, left middle frontal gyrus (17: 126), it measured 1 mm ___,\nnot seen on ___\n-5 mm, left parietal lobe along the anterior aspect of the postcentral gyrus\n(17:127), it measured 1 mm ___, new since ___\n-2 mm, left temporal lobe (17:69), new since ___\n-2.5 mm metastasis anterolateral left temporal lobe series 17, image 55, new\nsince ___\nThese lesions demonstrate faint, equivocal/barely perceptible FLAIR\nhyperintense signal.\n\nAdditionally there is also a linear, equivocal focus of subtle enhancement\nalong the cortex or cortical gray-white matter junction, anterior margin of\nthe right postcentral gyrus measuring up to 4 mm (17:134),, larger compared to\n___, new since ___, likely metastatic lesion.\n\nPosttreatment change left vertex, stable surrounding linear enhancement, mild\nedema, no new nodularity.\n\nOther:\nElsewhere, there is no evidence of acute infarct, extra-axial collection, or\nmass effect.\n\nThe ventricles and sulci are normal in caliber and configuration.\n\n The visualized paranasal sinuses and mastoids appear clear.  The globes and\norbits are unremarkable.  Major intracranial vascular flow voids are\npreserved.  Major dural venous sinuses are patent.",
            "output": "1. Tumor progression, with worsening small brain metastases since ___.\n2. Stable high left frontal post treatment changes.."
        },
        {
            "input": "Again seen are previously describe small brain parenchymal metastases, similar\nin size.  Tiny cortical lesions at the right vertex series 4, image 313, in\nthe anterior left basal frontal lobe series 4, image 28 are new or better\nseen.  Other lesions are stable as previously described.  Probable small\nhemangioma right parietal bone, similar.  Posttreatment change left vertex,\nstable mild peripheral enhancement.",
            "output": "1. Small brain parenchymal metastases.  2 tiny metastases are new or better\nseen since prior."
        },
        {
            "input": "Again seen are postsurgical changes in the high left frontal lobe with faint\nlinear peripheral enhancement of the surgical cavity without nodularity and\nmild surrounding edema, not significantly changed.\n\nNumerous 1-3 mm previously described enhancing parenchymal foci are again\nnoted, compatible with metastatic disease, not significantly changed in size\nor appearance in comparison to prior study.  Several other punctate\nsubcortical white matter hyperintensities without enhancement are less\nspecific and may reflect chronic microvascular ischemic change.\n\nThere is no evidence of hemorrhage, extra-axial collection, mass effect,\nmidline shift or infarction.   The ventricles and sulci are normal in caliber\nand configuration.\n\nProbable small hemangioma right parietal calvarium appears unchanged.  Trace\nethmoid sinus mucosal thickening.  Otherwise, the paranasal sinuses, orbits\nand globes and mastoid air cells appear clear.",
            "output": "1. Stable postsurgical changes in the high left frontal lobe with faint linear\nperipheral enhancement without nodularity and mild surrounding edema.\n2. Numerous 1-3 mm previously described enhancing parenchymal foci are again\nnoted, compatible with metastatic disease, not significantly changed in size\nor appearance.\n3. No new suspicious lesions identified.\n4. No evidence of hemorrhage, mass effect or infarction."
        },
        {
            "input": "There are again postsurgical changes from high left superior frontal\ncraniotomy.  Resection cavity in the high superior left frontal lobe is again\nseen with faint linear peripheral enhancement but no nodularity or additional\n1-3 mm enhancing parenchymal fossae are again seen, but these appear decreased\ncompared to the previous examination, with some appearing centrally resolved\ncompared to the previous examination, most notably lesions which were\npreviously demonstrated in the superior left frontal lobe and anterior\nparietal lobe on images 116 and 117 of series 9.  These are no longer\nconvincingly demonstrated.  A punctate lesion in the left temporal lobe is\nbarely visible on image 60 of series 16, decreased, and a lesion in the\nsuperior right frontal lobe is barely visible on image 142 of series 16, also\ndecreased.  There are no definite new lesions.\n\nThere are a few scattered punctate foci of nonspecific T2/FLAIR hyperintensity\nin the white matter which may reflect chronic microangiopathy in this age\ngroup.  There is no evidence of acute or subacute infarction.  There are\nchronic blood products at the left frontal surgical site, but no evidence of\nnew or recent hemorrhage.\n\nThe major intracranial vascular flow voids are preserved.  Orbits and\nvisualized extracranial soft tissues are unremarkable.  There are no new\nsuspicious calvarial lesions.  A probable small hemangioma in the right\nparietal lobe is noted",
            "output": "1. Stable postsurgical changes in the superior left frontal lobe with faint\nperipheral enhancement.\n2. The previously described scattered 1-3 mm enhancing parenchymal metastatic\nlesions have decreased in size and number.\n3. There are no new suspicious lesions."
        },
        {
            "input": "Left vertex craniotomy is again seen.  Stable thin marginal enhancement along\nthe left superior frontal surgical cavity without evidence for recurrent\nmasslike enhancement.  Stable mild T2/FLAIR hyperintensity along the left\nsuperior frontal surgical cavity margins.\n\n1.5 mm round enhancing lesion in the left middle frontal gyrus on image\n10:239, with punctate associated FLAIR hyperintensity on image 7:19, is\nslightly more conspicuous compared to ___, but smaller than on\n___ when it measured 4 x 1.5 mm.\n\nThere is a focus of contrast enhancement in the medial right temporal lobe,\nmeasuring 7 x 4 mm in the axial plane on image 10:129, and linear in\nconfiguration on sagittal image 1001:92 and coronal image 1000:77, unchanged\ncompared to ___ but new compared to ___.  This may be\nleptomeningeal rather than parenchymal.  There is no directly corresponding\nFLAIR hyperintensity.  However, there is new FLAIR hyperintensity more\nposteriorly in the medial right temporal lobe, image 7:10, new compared to ___, with faint peripheral contrast enhancement on image 10:125. \nNo associated diffusion signal abnormality.\n\nPreviously seen residual punctate foci of enhancement at the sites of treated\nlesions in the right superior frontal lobe and left temporal lobe are no\nlonger visualized.\n\nNo evidence for an acute infarction or new blood products.  Ventricles and\nsulci are stable in size.  Major vascular flow voids are grossly preserved. \nDural venous sinuses appear patent on postcontrast MP RAGE images.\n\nThere is mild mucosal thickening in the ethmoid air cells.",
            "output": "1. New FLAIR hyperintensity in the right medial temporal lobe, mostly\nposteriorly, with faint peripheral contrast enhancement.  Diagnostic\nconsiderations include new metastatic lesion versus paraneoplastic or\ninfectious encephalitis.  According to Dr. ___ patient does not have\nsymptoms of encephalitis.\n2. Linear enhancement more anteriorly in the right medial temporal lobe is\nstable compared to ___ but new compared to ___,\npossibly leptomeningeal rather than parenchymal.\n3. 1.5 mm round enhancing lesion in the left middle frontal gyrus is slightly\nmore conspicuous than on ___ but smaller than on ___.\n4. Stable post treatment changes at the left frontal vertex without evidence\nfor local recurrence.\n5. Other previously seen small enhancing lesions are no longer visualized.\n\nNOTIFICATION:  The findings in impression item 1 were discussed with ___\n___, M.D. by ___, M.D. on the telephone on ___ at 2:27 pm,\n15 minutes after discovery of the findings."
        },
        {
            "input": "Postsurgical changes are again demonstrated from left vertex craniotomy. \nThere is enhancement subjacent to the craniotomy site and extending into left\nsuperior frontal lobe surgical cavity which appears similar to previous\nexamination, probably postsurgical in nature FLAIR hyperintensity surrounding\nthe surgical site is again demonstrated.\n\nA previous punctate enhancing lesion in the left middle frontal gyrus is no\nlonger visible.\n\nEnhancement overlying the medial right temporal lobe has decreased from the\nprevious examination, now best seen on the axial T1 images, image 9 series 19,\nmeasuring approximately 5 by 3 mm, decreased.  FLAIR hyperintensity in the\nmedial right temporal lobe has also decreased.\n\nElsewhere, there are a few scattered nonspecific T2/FLAIR hyperintensities in\nthe subcortical and periventricular white matter which most likely reflect\nchronic small vessel disease in this age group.  Chronic blood products are\nnoted at the left frontal lobe surgical site.  No evidence of acute or\nsubacute infarction.\n\nThe major intracranial vascular flow voids are preserved.  Orbits and\nvisualized extracranial soft tissues are unremarkable.  There is minimal\nmucosal thickening in the ethmoid air cells.",
            "output": "1. Decreased enhancement overlying the medial right temporal lobe, and\ninterval decrease in the extent of FLAIR hyperintensity involving the medial\nright temporal lobe compared to the previous exam.\n2. Punctate enhancing lesion previously seen in the left middle frontal gyrus\nis no longer apparent.\n3. Stable postsurgical and post treatment changes in the left superior frontal\nlobe at the vertex."
        },
        {
            "input": "Patient is post left frontal craniotomy for left frontal lobe mass resection. \nPeripheral enhancement of the surgical cavity in the left superior frontal\ngyrus with locally increased signal intensity on FLAIR in the surrounding\nparenchyma is unchanged and likely reflects posttreatment change.\n\nThere is a new 1.0 cm area of patchy enhancement and T2/FLAIR signal\nabnormality in the right parietal lobe (10:168).\n\nA 2 mm enhancing focus that is hyperintense on FLAIR in the left middle\nfrontal gyrus (10:231), which was not seen on the ___ study, is\nagain visible and appears similar to the ___ study.\n\nThere are ill-defined areas of enhancement on MPRAGE in the bilateral anterior\ntemporal lobes there are not confirmed on postcontrast T1 spin echo or FLAIR\nsequences and felt to be almost certainly artifactual secondary to pulsation\n(series 10, image 109).\n\nThere is no evidence of recent hemorrhage or infarction.   The ventricles and\nsulci are within expected limits for age.  A few scattered nonspecific\nT2/FLAIR hyperintensities are again seen in the bilateral supratentorial white\nmatter.\n\nThe major intracranial flow voids are preserved.  The dural venous sinuses\nappear patent.\n\nThere is mild mucosal thickening in the ethmoid air cells.  The imaged orbits\nare unremarkable.  No suspicious marrow signal.",
            "output": "1. 1 cm focus of patchy ill-defined enhancement in the right parietal lobe\n(series 10, image 168) with associated subtle FLAIR hyperintense signal.  This\nis not associated with diffusion-weighted hyperintense signal to suggest\ninfarct.  Given the patient's clinical history, a new metastatic lesion is not\nexcluded and close follow-up is recommended.\n2. Ill-defined regions of enhancement in the bilateral anterior temporal lobes\nseen on MPRAGE is not confirmed on postcontrast T1 spin echo or FLAIR\nsequences and is felt to be most certainly artifactual.\n3. Stable post treatment changes at the left frontal lobe resection site.\n4. No acute infarct or new intracranial hemorrhage.\n5. Additional findings as described above."
        },
        {
            "input": "Study is degraded by motion.  Within these confines:\n\nTreatment related changes related to patient's known left frontal metastatic\nlesion are again noted.  Grossly stable T2 and FLAIR hyperintensity\nsurrounding surgical bed and minimal peripheral enhancement is again noted.\n\nRight inferior frontal gyrus T2 and FLAIR hyperintensity with faint\nserpiginous enhancement, and without definite restricted diffusion is again\nnoted (see 12, 13, 15, 16: 14; 17:90; 18:45 on current study and 10:168 on ___ prior exam).  Findings suggestive present on ___\nprior exam (see 17: 95-100 on ___ prior exam).  T2 and FLAIR\nhyperintensity seen on current exam not definitely seen on ___\nprior exam.  (See 15:14 on current study and 15:13 on ___ prior\nexam).\n\nPreviously noted probable artifactual bilateral temporal lobe hyperdensity on\nMPRAGE imaging is not definitely visualized on current exam.\n\nThere is no evidence of mass effect, midline shift or infarction.   The\nventricles and sulci are grossly stable in caliber and configuration. \nPeriventricular and subcortical T2 and FLAIR hyperintensities are noted which\nmay represent small vessel ischemic changes.\n\nGrossly stable left cavernous sinus lateral margin approximately mm enhancing\npunctate asymmetry is again seen, grossly unchanged compared to ___ prior exam (see 19:22 on current study and 19:43 on ___\nprior exam).",
            "output": "1. Study is degraded by motion.\n2. Grossly stable treatment related changes related to patient's known left\nfrontal metastatic lesion.\n3. Grossly stable nonspecific enhancement along surgical bed.  While finding\nmay represent treatment related changes, recurrent residual tumor is not\nexcluded on the basis examination.  Recommend attention on follow-up imaging.\n4. Grossly stable faintly enhancing right inferior frontal gyrus enhancing\nlesion with associated T2 and FLAIR hyperintensity compared to ___ prior exam, suggested to be at least partially present on ___ prior exam, as described.  Differential considerations include capillary\ntelangiectasia and volume averaging of vessels, with metastatic lesion less\nlikely.  Recommend attention on follow-up imaging.\n5. Within limits of study, no definite evidence of new enhancing intracranial\nmass.\n6. Grossly stable left cavernous sinus lateral margin approximately mm\nenhancing punctate asymmetry compared to ___ prior exam.  If not\nvolume-averaging artifact, finding may represent small meningioma.\n\nRECOMMENDATION(S):\n1. Grossly stable nonspecific enhancement along surgical bed. While finding\nmay represent treatment related changes, recurrent residual tumor is not\nexcluded on the basis examination. Recommend attention on follow-up imaging.\n\n\n2. Grossly stable faintly enhancing right inferior frontal gyrus enhancing\nlesion with associated T2 and FLAIR hyperintensity compared to ___ prior exam, suggested to be at least partially present on ___ prior exam, as described.  Differential considerations include capillary\ntelangiectasia and volume averaging of vessels, with metastatic lesion less\nlikely. Recommend attention on follow-up imaging."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.\n\nBilateral hippocampal formations and mammillary bodies are preserved in signal\nand configuration. There is no disproportionate medial temporal atrophy. There\nis no focal lobar encephalomalacia. There are no focal cortical dysplasias or\ngray matter heterotopia noted.\n\nThere is mild mucosal thickening of the maxillary sinuses.",
            "output": "1. Normal brain MRI."
        },
        {
            "input": "MR BRAIN:\nThere is no acute infarct, hemorrhage, mass, or mass effect.  There are\nnonspecific scattered bilateral periventricular white matter FLAIR\nhyperintense foci.  In the ventricles and cortical sulci are normal in size\nand configuration.  The vasculature is patent.\n\nThe bilateral lenses are absent.  There is bilateral maxillary sinus mucosal\nthickening.  There are trace bilateral mastoid air cell effusions.  The\ncalvarium and soft tissues are unremarkable.\n\nOn the post-contrast and delayed sequence, there is peripheral enhancement\nsurrounding the coil pack which is has not changed since the prior study from\n___ and does not represent a patent lumen.\n\nMRA brain:\nThere is low signal within the left anterior cavernous to communicating\nsegment internal carotid artery consistent with susceptibility artifact from\nintravascular stent which limits the evaluation of in-stent stenosis.  There\nis a 1.2 AP by 1.2 TV cm low signal coil pack anterior to the left clinoid\nsegment internal carotid artery consistent with treated aneurysm.  There is a\nsmall focus of intermediate signal within the central aspect of the coil pack\non the noncontrast time-of-flight image which is not visualized on the\npostcontrast time-of-flight sequence, likely representing artifact.  There is\nminimal peripheral high signal on the postcontrast time-of-flight imaging,\nwhich likely represents adjacent soft tissue rather than from lumen\nrecannulization, as described above.\n\nThere is a 3 mm medially projecting aneurysm from the left cavernous segment\ninternal carotid artery (11:86), which is unchanged comparison ___.\n\nThe remainder of the intracranial vasculature is patent without evidence of\nocclusion, dissection, stenosis, or new aneurysm.  .",
            "output": "1. Stent coiled left ophthalmic segment internal carotid artery aneurysm\nwithout evidence of recannulization.\n2. Patent intracranial vasculature without evidence of new aneurysm.\n3. 3 mm medially projecting left cavernous segment internal carotid artery\naneurysm which is unchanged, given differences in technique in comparison to\ncerebral angiogram from ___."
        },
        {
            "input": "MRA brain:\nThere has been interval placement of a right ICA pipeline device.  No residual\nfilling of the known right para ophthalmic artery aneurysm.  The pipeline\ndevice results in decreased flow related enhancement of the right carotid\nsiphon which makes in stent occlusion or stenosis difficult to exclude, but\nthere is normal distal runoff.\n\nCoil pack in situ in the previously stent coiled and re-coiled left\nsupraclinoid ICA aneurysm.  There is mild flow related enhancement seen in the\nproximal aspect of the aneurysm (series 2, image 78 and series 4, image 77)\nwhich is discontinuous with the left ICA, but appears slightly more\nconspicuous compared to prior imaging.\n\nStable 3 mm left cavernous medially projecting left ICA aneurysm.\n\nSuspected 2 mm infundibulum just distal to the right ICA pipeline device\nappear similar compared to prior imaging.\n\nDominant left vertebral artery.  Fetal type origin of the left PCA.\n\nNear complete opacification of the left maxillary sinus.",
            "output": "1. Interval placement of a right ICA pipeline device.  No residual filling of\nthe known right para ophthalmic artery aneurysm.\n2. There is mild flow related enhancement seen in the proximal aspect of the\nstent coiled and recoiled left supraclinoid ICA aneurysm, however this is\ndiscontinuous with the underlying left ICA but appears slightly more\nconspicuous compared to prior imaging, potentially due to difference in\ntechnique.  Attention could be paid to this on follow-up imaging to exclude\nrecanalization.\n3. Stable 3 mm left medially projecting cavernous ICA aneurysm.\n4. Suspected 2 mm infundibulum just distal to the right ICA pipeline device\nappear similar compared to prior imaging.\n5. Additional findings as described above."
        },
        {
            "input": "MR HEAD:  Limited examination due to patient motion. Unchanged right thalamic\nhemorrhage, measuring approximately 19 x 12 mm in transverse dimension with\nassociated vasogenic edema extending into the right posterior limb of internal\ncapsule, right cerebral peduncle, and medial aspect of the right temporal\nlobe. No new areas of hemorrhage are identified. Unchanged lacunar ischemic\nevent is noted in the left pons. There is an unchanged area of ischemia in the\nright central sulcus, with associated vasogenic edema and T2 shine through\neffect on the DWI and ADC maps. Scattered foci of high signal intensity are\nseen in the subcortical white matter and left thalamus, which are nonspecific\nand may reflect changes due to small vessel disease. The orbits are\nunremarkable, the paranasal sinuses and mastoid air cells are clear\n\nMRA OF THE HEAD:  Examination is limited due to patient motion and the distal\nvascular branches are not clearly identified, there is evidence of vascular\nflow in both internal carotid arteries as well as the vertebrobasilar system,\nthere is hypoplasia of the A1 segment on the right, grossly no aneurysms are\nidentified, the anterior, middle and posterior cerebral arteries are not\nclearly seen due to motion.\n\n\nMRA OF THE NECK:  Limited examination of the neck due to patient motion, there\nis patency of the common carotid arteries and vertebral arteries with no frank\nevidence of flow stenotic lesions, however, the left cervical carotid\nbifurcation is partially evaluated due to motion artifacts.",
            "output": "1. Unchanged right thalamic hemorrhage with associated vasogenic edema\nextending into the right cerebral peduncle and medial aspect of the right\ntemporal lobe as described above. No new areas of hemorrhage are identified.\n\n2. Unchanged subacute infarct in the region of the right central sulcus,\nvascular territory of the left mesentery artery.\n\n3. The MRA of the head and neck are limited demonstrating decreased signal in\nthe distal branches of the Circle of ___ due to patient motion."
        },
        {
            "input": "There is high signal on FLAIR images in right greater than left cerebral\nsulci, and in the right aspect of the suprasellar cistern, corresponding to\nthe previously demonstrated subarachnoid hemorrhage.  There is stable blood in\nthe atria and occipital horns of the lateral ventricles.  There is no\nhydrocephalus.\n\nThere are extensive areas of slow diffusion, consistent with acute infarction,\nin the right middle cerebral artery territory involving the right posterior\nfrontal lobe, frontal operculum, insula, portion of the inferior parietal\nlobe, and most of the temporal lobe.  There is another large acute infarct in\nthe left occipital lobe in the left posterior cerebral artery territory. \nThere is a small acute infarct in the body of the left caudate and adjacent\nwhite matter.  Evaluation for additional small cortical infarcts is limited by\nsignal abnormality from subarachnoid hemorrhage in the sulci.\n\nNo evidence of blood products is seen in the left occipital or left caudate\ninfarcts.  Evaluation for hemorrhagic conversion within the right parietal\nportion of the right middle cerebral artery territory infarct is limited by\nadjacent subarachnoid hemorrhage.\n\nThere is no significant mass effect at this time.  There is no ventricular\neffacement or shift of midline structures.\n\nRight middle cerebral artery flow void appears at least partially present.\n\nThere has been prior right cataract surgery.  Endotracheal and enteric tubes\nare partially visualized in the oral cavity.  There is associated fluid in the\nnasopharynx and trace fluid in the left mastoid air cells.  Right mastoid is\nunderpneumatized.\n\nIntracranial flow voids are maintained.",
            "output": "1. Large acute infarcts in the right MCA and left PCA territories, and a small\ninfarcts in the body of the left caudate nucleus and adjacent white matter. \nNo significant mass effect at this time.\n2. Right greater than left convexity subarachnoid hemorrhage is again\ndemonstrated, limiting evaluation for hemorrhagic conversion within the\nparietal portion of the right MCA infarct.  No hemorrhagic conversion is seen\nin the left-sided infarcts.\n3. Stable intraventricular hemorrhage.  No hydrocephalus."
        },
        {
            "input": "Within the right frontal region there is a 0.8 x 1.9 cm extra-axial T2\nhyperintense lesion with slow diffusion and homogeneous enhancement. Findings\nlikely represent a meningioma. There is no abnormal signal within the adjacent\nbrain. There are nonspecific periventricular and subcortical white matter\nT2/FLAIR hyperintensities, likely reflecting sequela of chronic small vessel\nischemic disease. There is no infarct, hemorrhage or mass effect. The\nventricles, and sulci a are prominent indicative of mild parenchymal volume\nloss.\n\nThe principal intracranial flow voids are present. There is mild ethmoid and\nbilateral maxillary sinus mucosal thickening. There is a small amount of fluid\nwithin the right mastoid air cells.",
            "output": "There is 0.8 x 1.9 cm enhancing right frontal extra-axial mass most likely\nrepresenting a meningioma.\n\nNonspecific white matter abnormalities, likely sequela of chronic small vessel\nischemic disease."
        },
        {
            "input": "Study is moderately degraded by motion, especially on noncontrast neck MRA. \nWithin these confines:\n\nMRI BRAIN:\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.\n\nThe focal probable diffusion hyperintensity seen in the right temporal lobe\ncortex is favored to be artifactual near the skullbase rather than true slow\ndiffusion (see 5,6:12), as there is no corresponding ADC abnormality, or\nabnormal signal on corresponding T2/ FLAIR/GRE sequences.\n\nThere is mild mucosal thickening in bilateral maxillary sinuses.  The\nremaining visualized paranasal sinuses are clear.  Minimal mucosal thickening\nin bilateral mastoid air cells.  The orbits are unremarkable.  Intracranial\nflow voids are maintained.  Grossly stable bilateral pneumatized petrous apex\nfluid is again noted.  (See 20:6 on current study, 5:224 on prior CTA, and\n06:12 on ___ prior noncontrast head CT.\n\nMRA BRAIN:\nThe intracranial vertebral and internal carotid arteries and their major\nbranches appear normal without evidence of stenosis, occlusion, or aneurysm\nformation.  Incidentally seen is fetal origin of bilateral posterior cerebral\narteries.\n\nMRA NECK:\nEvaluation of neck vessels is substantially limited due to pulsation and\nmotion artifacts, especially near the origin of the vessels from the aortic\narch.  The common, internal and external carotid arteries appear grossly\npatent.\n\nPartially visualized is the patient's known C4 through C6 anterior spinal\nfusion.",
            "output": "1.  Study is mildly degraded by motion, especially on noncontrast neck MRA.\n2. No acute intracranial abnormality, with no evidence of acute infarct.\n3. Within limits of study, no definite evidence ofaneurysm greater than 3 mm, \ndissection   or significant luminal narrowing.\n4.  Paranasal sinus disease as described.\n\nNOTIFICATION:  The findings were discussed by Dr. ___ with Dr.\n___ on the telephoneon ___ at 6:58 AM, 10 minutes after\ndiscovery of the findings."
        },
        {
            "input": "MRI BRAIN:\nThere is a small chronic lacunar infarct in the left putamen.  Scattered\nperiventricular subcortical white matter foci of FLAIR hyperintense signal\nwithout associated slow diffusion are nonspecific but likely sequelae of\nchronic small vessel ischemic disease in this age group.  Prominence of the\nventricles and sulci is consistent with global atrophy.  There is no abnormal\nfocus of slow diffusion to suggest acute infarction.  There is no hemorrhage. \nThere is no mass or mass effect.  Principal intracranial vascular flow voids\nincluding those of the dural venous sinuses are preserved.  There is a small\nmucous retention cyst in the right maxillary sinus.  There is fluid signal in\na few air cells at the mastoid tips.  Aside from bilateral cataract\nextractions, the orbits are grossly unremarkable.\n\n\nMRA BRAIN:\nThe intracranial vertebral and internal carotid arteries and their major\nbranches appear normal without evidence of stenosis, occlusion, or aneurysm\nformation.\n\nMRA NECK:\nThe common, internal and external carotid arteries appear normal.  There is no\nevidence of internal carotid artery stenosis by NASCET criteria.  The origins\nof the great vessels, subclavian and vertebral arteries appear normal\nbilaterally.",
            "output": "1. No evidence of hemorrhage or acute infarction.\n2. Small chronic lacunar infarct in the left putamen and scattered white\nmatter signal abnormalities, suggestive of chronic small vessel ischemic\ndisease.  Moderate age related involutional changes.\n3. Unremarkable head and neck MRA."
        },
        {
            "input": "Study is degraded by motion.  Within these confines:\n\nMR BRAIN:\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  The ventricles and sulci are prominent, consistent with global\ncerebral volume loss.  Probable chronic infarct is seen in the left precentral\ngyrus (07:20).  Periventricular and subcortical T2 and FLAIR hyperintensities\nare noted which may represent small vessel ischemic changes.\n\nA retention cyst in the right sphenoid sinus appears larger compared to prior\nexam.  There is near complete opacification of the right sphenoid sinus. \nThere is mild mucosal thickening of the maxillary sinuses.  The mastoid air\ncells are clear.  The intraorbital contents are normal.\n\nMRA BRAIN:\nIrregularity of the left greater than right internal carotid artery cavernous\nsegments is noted.  Probable artifacts versus focal occlusion of left mid\ninternal carotid artery cavernous segment versus artifact (see 3: 56, 60). \nThere is also focal narrowing and asymmetric attenuation of signal of the mid\nright M1 segment (303:10) with distal flow.  These findings may be\nartifactual. Additionally, question nonocclusive irregularity of bilateral P1\nP2 segments versus artifact.\n\nThe right A1 segment is dominant, a congenital variant.\n\nOtherwise, the intracranial vertebral and internal carotid arteries and their\nmajor branchesappear preservedwithout definite evidence of stenosis,\nocclusion, or aneurysm formation greater than 3 mm.",
            "output": "1.  Study is degraded by motion.\n2.  No acute intracranial abnormality, with no definite evidence of acute\ninfarct.\n3. Interval progression of right sphenoid sinus disease with a larger\nretention cyst compared to ___ prior exam.\n4. Probable artifacts of bilateral internal carotid artery cavernous segments\nversus focal occlusion with both proximal and distal flow grossly preserved. \nIf clinically indicated, consider CTA head for further evaluation.\n5. Irregularity of bilateral cavernous internal carotid arteries and bilateral\nposterior cerebral arteries, and asymmetric narrow caliber of right M1 segment\nrelative to the left, as described.  While findings may represent artifacts,\nif not artifactual, findings may be related to atherosclerotic changes.  If\nclinically indicated, consider CTA head for further evaluation.\n6. Otherwise, grossly patent circle of ___ as described.\n\nNOTIFICATION:  The impression and recommendation above was entered by Dr.\n___ on ___ at 16:18 into the Department of Radiology critical\ncommunications system for direct communication to the referring provider."
        },
        {
            "input": "The study is limited to T2 and DWI technique. Massive, diffuse bilateral\ncortical high signal on DWI, representing restricted diffusion, and low signal\non ADC suggests hypoxic edema. There is no evidence of masses, mass effect, or\ninfarction. The ventricles and sulci are normal in caliber and configuration.\nFluid is seen in the maxillary sinuses and the left mastoid air cells. Fluid\nlevels are seen in the occipital horns of the lateral ventricles.",
            "output": "Massive, diffuse bilateral cortical edema without hydrocephalus, likely due to\nhypoxia.\n\nNOTIFICATION:  The findings were discussed with ___ on the telephone\non ___ at 4:22 ___."
        },
        {
            "input": "Corresponding to the previously noted dense areas in the cerebral parenchyma,\nthere are foci of negative susceptibility with T1 precontrast hyperintense\nsignal, representing areas of contusion.  No abnormal enhancement is noted\nallowing for the T1 precontrast a appearance to suggest obvious mass lesions.\nModerate surrounding edema noted in the left frontal lobe, with mild rightward\nshift of midline structures, mass effect on the left frontal horn, similar to\nthe recent CT study.\nAssessment on diffusion sequences limited due to presence of blood products.\n\nMildly prominent extra-axial fluid containing spaces, along the right cerebral\nconvexity overlying the frontal and the parietal lobes and minimal on the\nleft, better seen than the prior CT study.\nA few small scattered nonspecific FLAIR hyperintense foci in the cerebral\nwhite matter.\nSella, pineal and the craniocervical junction regions are unremarkable.\nThe venous sinuses appeared unremarkable on the FLAIR sequence.\nThe major intracranial arterial flow voids are noted.\n\nSmall to moderate amount of fluid in the left mastoid air cells.\nMild ethmoidal mucosal thickening.",
            "output": "Multiple foci of altered signal intensity in the brain parenchyma as described\nabove, can relate to areas of contusion/hemorrhage; no significant abnormal\nenhancement.\nModerate edema in the left frontal lobe, with mass effect on the frontal horn\nof the left lateral ventricle and mild rightward shift of midline structures.\nCorrelate clinically for etiology and consider followup evaluation to assess\nfor interval change as needed.\nOther details as above."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, or infarction.\nThe ventricles and sulci are normal in caliber and configuration.  FLAIR\nimages demonstrate no focal abnormalities within the supra or infratentorial\nbrain. Foci of low signal intensities are visualized on the susceptibility\nimages in the left periventricular and right medial parietal lobes best\nvisualized on series 5, image 16. There is mild patchy enhancement seen in\nthis region. An associated developmental venous anomalies are identified.\nThese findings are suggestive of capillary telangiectasia. Relationship of\nthese findings with the patient's seizures is unclear. Correlation with EEG\nfindings is recommended. Coronal other areas of abnormal parenchymal vascular\nor meningeal enhancement seen.\n\nCoronal high-resolution images demonstrate normal appearance of the medial\ntemporal lobe structures. There is no evidence of atrophy or increased signal\nwithin the hippocampal regions.  There is no evidence of migration abnormality\nidentified.",
            "output": "Susceptibility abnormalities and enhancement in the left periventricular\nregion and right medial parietal lobes suggesting a of capillary\ntelangiectasia cf with associated developmental venous anomalies. Relationship\nof these findings with patient's seizures is unclear but clinical correlation\nwith EEG findings is recommended. No other abnormalities are seen."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.\nThere is a heterogenous T1 and T2 hyperintense ovoid lesion in the\ninferoposterior aspect of the sphenoid sinus measuring 20 x 24 x 17 mm (TV by\nAP by CC) which does not show restricted diffusion.  There is mild enhancement\nof the anterior wall of this lesion measuring less than 2 mm in diameter as\nwell as possibly mild linear enhancement in the mid to posterior aspect of the\nlesion.  There is no evidence of bone destruction.  These findings are typical\nof a mucous retention cyst containing inspissated secretions.\nThe pituitary gland is normal.  The adjacent internal carotid arteries are\npatent.\nPneumatized left pterygoid bone.\nThere is no evidence of cerebral hemorrhage, edema, midline shift or\ninfarction.   The ventricles and sulci are normal in caliber and\nconfiguration.",
            "output": "1. Sphenoid sinus mucous retention cyst.\n2. The study is otherwise normal.\n\nRECOMMENDATION(S):  Correlation with CT paranasal sinuses/base of skull for\nbetter evaluation of the sphenoid sinus and clivus (exclude bony destruction)"
        },
        {
            "input": "Postoperative changes paranasal sinuses.  Osseous thickening, likely\nrepresents reactive change chronic periostitis along the posterior, central\nmargin of the sphenoid sinuses similar compared with ___, is new\nsince ___.  Partial opacification, with associated enhancement along\nthe posterior, medial margin of the left sphenoid sinus, similar compared with\n___, likely inflammatory.  Few central foci of decreased signal on\ngradient images, decreased signal on T2 weighted images, few punctate\nassociated calcifications are recent CT scan, can be seen with inspissated\nsecretions, fungal colonization or infection.  Patent cavernous sinus.\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  Benign developmental venous anomaly posterior right temporal\nlobe..  Small benign capillary telangiectasia in the pons.",
            "output": "1. Postoperative changes paranasal sinuses.  Chronic periostitis posterior\nsphenoid sinus.  Adjacent partial sphenoid sinus opacification, enhancement,\nmost likely inflammatory, with appearance of central contents suggestive of\ninspissated secretions, fungal colonization or infection.\n2. No cavernous or parasellar mass."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  Trace mucosal thickening paranasal sinuses.  Clear mastoids. \nPreserved vascular flow voids.",
            "output": "1. Normal intracranial findings."
        },
        {
            "input": "MRA BRAIN:\nA 1 mm superiorly oriented outpouching left P1 segment (series 3, image 73),\nlikely represents an infundibulum, with small aneurysm not entirely excluded. \nThere is also a inferiorly oriented 1 mm outpouching of the right ICA genu\n(series 3, image 51), also felt to be most likely infundibulum.  Otherwise,\nthere is normal flow signal in the intracranial internal carotid arteries.\nThere is normal flow signal in the anterior and middle cerebral arteries\nwithout evidence of focal stenosis or occlusion.  There is persistent fetal\norigin of the right posterior cerebral artery.  The remainder of the posterior\ncirculation is unremarkable.\n\nMRA NECK:\nMRA of the neck is limited due to 2D time-of-flight imaging and motion\nartifact.\nAside from in-plane phase flow/saturation artifact, the common, internal and\nexternal carotid arteries demonstrate flow signal.  No evidence of internal\ncarotid artery stenosis by NASCET criteria.  The origins of the great vessels,\nsubclavian and vertebral arteries are not well evaluated due to motion\nartifact.\nSlight reversal of the normal cervical lordosis.",
            "output": "1. 1 mm superiorly noted outpouching of the left P1 segment, which may be an\ninfundibulum versus small aneurysm.\n2. A 1 mm inferiorly oriented outpouching of the right ICA genu, felt to be\nmost likely an infundibulum, with small aneurysm not entirely excluded.\n3. Allowing for motion degraded noncontrast 2D time-of-flight MRA technique,\ngrossly unremarkable MRA of the neck.  No evidence for dissection."
        },
        {
            "input": "Study is moderately degraded by motion.  Within these confines:\n\nStatus post left frontotemporal craniotomy for mass resection.  A small amount\nof intrinsic T1 hyperintense signal within the resection cavity is compatible\nblood products.  Along the posteromedial resection cavity minimal linear\nenhancement is suggested (see 4, 11:14; 900:100).  Thin peripheral diffusion\nabnormality surrounding the resection cavity is also noted.\n\nNo change to slight decrease in FLAIR signal abnormality surrounding the\nresection cavity with a similar degree of mass effect on the left lateral\nventricle.  The ventricles are grossly stable in size and configuration.\n\n The major intracranial vascular flow voids are maintained.  The mastoid air\ncells and orbits are grossly preserved.  Minimal bilateral ethmoid air cell\nmaxillary sinus mucosal thickening is present.",
            "output": "1.  Study is moderately degraded by motion.\n2. Status post left frontotemporal craniotomy for mass resection with\nassociated probable postsurgical changes as described.\n3. Minimal linear nonspecific enhancement along post room medial surgical\ncavity border.  While finding may be postoperative in nature, residual tumor\nis not excluded on the basis examination.  Recommend attention on follow-up\nimaging.\n4. Prominent slow diffusion medial to the resection cavity which may represent\ntreatment related effects, with differential consideration of infarction.\n5. Grossly stable parenchymal signal abnormality surrounding resection cavity\nwith mass effect on the left lateral ventricle.\n\nNOTIFICATION:  The findings were discussed with ___, N.P. by\n___, M.D. on the telephone on ___ at 9:56 am, 30 minutes\nafter discovery of the findings.\n\n The impression and recommendation above was entered by Dr. ___ on\n___ at 11:54 into the Department of Radiology critical communications\nsystem for direct communication to the referring provider."
        },
        {
            "input": "The patient is status post left frontotemporal craniotomy for mass resection,\nagain residual blood products are visualized in the surgical bed.  After\ncontrast administration, there is abnormal enhancement in the left sylvian\nregion with extension into the brain parenchyma towards the lateral aspect of\nthe caudate nucleus on the left suggestive of residual mass lesion (image 196,\nseries 11, and image 70, series 1100).  Extensive areas of FLAIR high-signal\nintensity are seen in the left centrum semiovale, left sub insular region and\nsurrounding the lateral ventricles likely consistent with post treatment\nchanges with areas of high-signal intensity along the cortical spinal tract in\nthe left cerebral peduncle and pons.  The lateral ventricles are slightly\nprominent, there is no evidence of hydrocephalus.  The ventricles are\nprominent towards the convexity.  Focal areas of high-signal are detected on\nthe DWI maps towards the centrum semiovale (images 23, 26, series 550) which\nare nonspecific, however the possibility of underlying subacute ischemic\nchanges is a consideration.  Small similar area is also identified in the\nright occipital lobe (image 19, series 550) there is no evidence of mass\neffect or hemorrhagic transformation in this areas.  The major vascular flow\nvoids are present and demonstrate normal distribution.  The orbits are\nunremarkable, the paranasal sinuses and the mastoid air cells are clear.",
            "output": "1.  Postsurgical changes are again seen, the patient is status post left\nfrontotemporal craniotomy for mass resection.\n\n2.  Heterogeneous enhancement is identified surrounding the sylvian fissure\nand the subcortical areas towards the body of the caudate nucleus on the left\nsuggesting residual mass lesion.\n\n3.  Extensive areas of FLAIR high-signal intensity are demonstrated in the\ncentrum semiovale, periventricular regions and pons, likely consistent with\nposttreatment changes.\n\n4.  Small foci of slow diffusion identified in the centrum semiovale and right\noccipital lobe as described above suggesting subacute ischemic changes."
        },
        {
            "input": "There is a 2.5 cm irregular peripherally enhancing lesion within the left\noperculum and subinsular region.  The mass and moderate associated vasogenic\nedema result in mild narrowing of the left lateral ventricle, however no\nmidline shift.  There are a few foci of low signal intensity on GRE (series\n10, image 13) that may reflect a small amount of associated hemorrhage.  No\nother enhancing lesions are identified.\n\nThe ventricles, sulci, and cisterns otherwise appear normal.  There is no\nacute infarct.  A few tiny foci of hyperintense signal on T2/FLAIR within the\nsubcortical and periventricular white matter are nonspecific.  The major\nvascular flow voids are preserved.  Dural venous sinuses are patent.  There is\nmild mucosal thickening of the ethmoid air cells.  The orbits are\nunremarkable.",
            "output": "1. 2.5 cm irregular peripheral enhancing mass with moderate associated\nvasogenic edema within the left operculum and subinsular region, most likely a\nmetastatic lesion or glioblastoma.  No other enhancing lesions are identified.\n2. Additional findings as described above.\n\nNOTIFICATION:  The findings above were discussed with Dr. ___ by\nDr. ___ on ___ in person in the neuroradiology reading\nroom."
        },
        {
            "input": "There is encephalomalacia in the left temporal region with postoperative\nchange.  There is no significant interval change.  There is no new area of\nenhancement seen.  Moderate to severe changes of small vessel disease and mild\nbrain atrophy seen.  There is no hydrocephalus or midline shift.",
            "output": "No significant interval change since the previous MRI examinations of  ___ and ___."
        },
        {
            "input": "There is no significant interval change.  Postoperative changes again\nidentified with left anterior temporal encephalomalacia.  Extensive FLAIR and\nT2 hyperintensities in the white matter.  Are unchanged.  There are no acute\ninfarcts or enhancing lesions identified.  No mass effect or hydrocephalus.",
            "output": "Stable appearance compared with ___ in left anterior temporal\nencephalomalacia, postoperative changes and white matter hyperintensities."
        },
        {
            "input": "There has been no significant interval change. Postoperative changes are seen\nin the left temporal region with encephalomalacia. Diffuse hyperintensities in\nthe white matter are also seen.  No abnormal parenchymal vascular or meningeal\nenhancement seen. There is no midline shift, mass effect or hydrocephalus. No\nacute infarcts are seen.",
            "output": "Stable appearance of the brain compared with the previous MRI examination. No\nenhancing lesions are seen. No new abnormalities are identified."
        },
        {
            "input": "Areas of acute hemorrhage in the right frontal lobe and left cerebellar\nhemisphere.  With mild surrounding rim enhancement on post gadolinium images. \nThe right frontal lobe lesion measures approximately 4.5 x 4 cm in the left\ncerebellar lesion measures 4 x 3 cm.  Additional 1 cm or smaller lesions are\nseen in the inferior right cerebellar hemisphere (14:4), inferior left\ncerebellar hemisphere (14:5), inferior left occipital lobe (14:8) and\nconvexity left frontal lobe (14:18) and lateral left frontal lobe (101:73). \nThere is no evidence of restricted diffusion seen within these lesions.  The\nfindings are consistent with metastatic disease.  No abnormalities are seen\nwithin the bony structures.  There is no midline shift or hydrocephalus. \nThere is mass effect on the fourth ventricle by the left cerebellar lesion.",
            "output": "1. Multiple metastatic lesions with largest lesions showing hemorrhage in the\nright frontal lobe and left cerebellar hemisphere.  Mass effect is seen on the\nfourth ventricle by the cerebellar lesion without hydrocephalus.  There is no\nmidline shift.\n2. Postcontrast MPRAGE  images are somewhat limited by motion."
        },
        {
            "input": "Patient is status post left suboccipital craniotomy with mass resection, with\npostoperative dural thickening and enhancement deep to the craniotomy site, as\nwell as small amount of extra-axial fluid and hemorrhage due to the\ncraniotomy.  T1 hyperintensity within the resection bed likely represents\nblood products, and evaluation for residual enhancing tumor is limited in the\nabsence of precontrast images.  1.4 x 1.2 cm residual enhancing tissue along\nthe posterior/superior margin of the resection cavity on image images 4:40,\n400:92 cannot be excluded.  Mass effect on the fourth ventricle has decreased\nbut not resolved.  There is persistent rightward shift of the falx cerebelli\nand partial effacement of the left quadrigeminal plate cistern. There is no\nsupratentorial hydrocephalus.\n\nMultiple additional enhancing lesions are again noted, with the largest right\nfrontal lobe lesion measuring 4.9 x 4 cm.  This lesion has a large area of\ncontact with the dura.  There is associated right frontal sulcal effacement\nand mild mass effect on the frontal horn of the right lateral ventricle.\n\nThe smaller lesions are as follows:\n0.8 x 0.7 cm superficial left frontal lesion, possibly extra-axial, image 4:77\n;\n1.0 x 0.9 cm left posterior temporal lesion along the tentorium, probably\nextra-axial, image 4:46 ;\n1.1 x 0.7 cm right cerebellar hemisphere, image 4:35 ;\n0.9 x 0.8 cm left cerebellar hemisphere, image 04:38.",
            "output": "1. Status post left cerebellar mass resection.  Evaluation for residual tumor\nis limited by T1 hyperintense blood products the surgical bed.  1.4 x 1.2 cm\nresidual enhancing tissue along the posterior/superior margin of the surgical\ncavity cannot be excluded.\n2. Mass effect on the fourth ventricle and left quadrigeminal plate cistern\nhas decreased but not resolved.  No supratentorial hydrocephalus .\n3. Stable size of additional intracranial lesions, many of which may be\nextra-axial.  The largest 4.9 cm right frontal lesion demonstrates unchanged\nmass effect."
        },
        {
            "input": "The patient is status post a left suboccipital craniotomy for resection of\ncerebellar metastatic mass lesion with no significant change since the prior\nexam, residual blood products are again seen in the surgical cavity as well as\nmild vasogenic edema causing mild effacement of the sulci, unchanged enhancing\nmetastatic lesions are again seen cerebellum bilaterally.  Supratentorially\nthe patient is status post right frontal craniotomy and resection of a right\nfrontal mass lesion, expected surgical changes are demonstrated with residual\nblood products in the surgical bed and effacement of the sulci with mild\nvasogenic edema, small subdural blood is noted throughout the right frontal\nregion, better depicted in the axial FLAIR sequence.  There is minimal\nshifting of the normally midline structures towards the left with\napproximately 1.5 mm of deviation (image 14, series 12). Persistent small\nring-enhancing lesions in the left frontal and left temporal lobe appear\nslightly more conspicuous in comparison with the prior exam, for sample left\nfrontal ring-enhancing lesion measuring approximately 6.5 x 6.3 mm in\ntransverse dimension is better depicted in the current exam (image 16, series\n15), no significant vasogenic edema is noted in this region are.  Grossly no\nnew lesions are identified, there is no evidence of diffusion abnormalities to\nindicate acute or subacute ischemic changes.  The major vascular flow voids\nare present and demonstrate normal distribution.  The orbits are unremarkable,\nthe paranasal sinuses and mastoid air cells are clear.",
            "output": "1.  The patient is status post left suboccipital craniotomy for resection of\ncerebellar metastatic mass with no significant change since the prior exam.\n\n2.  Right frontal craniotomy and resection of a right frontal mass lesion with\nexpected postsurgical changes consistent with residual blood products and\nsmall amount of subdural blood along the frontal region, with minimal mass\neffect estimated approximately 1.5 mm of deviation towards the left.\n\n3.  Numerous infra and supratentorial enhancing lesions consistent with\nmetastatic disease involving the cerebellar hemispheres, left frontal and left\ntemporal lobes as described above appear slightly more conspicuous since the\nprior exam, however, no new areas with abnormal enhancement or new lesions are\nseen."
        },
        {
            "input": "Images through the brain demonstrate normal ventricles and extra-axial spaces\nwithout mass effect midline shift or hydrocephalus.  There are no focal  areas\nof chronic or acute blood products seen.  Postcontrast images demonstrate an\nincidental developmental venous anomaly in the right cerebellum.  No areas of\nabnormal enhancement are seen.  The visualized paranasal sinuses are clear.\n\nCoronal images through the temporal lobes and brain with high-resolution\ndemonstrate normal appearance of the medial temporal lobe structures.  There\nis no evidence of mesial temporal sclerosis.  There is no evidence of\nmigration abnormalities.\n\nMRA of the head demonstrates normal flow signal in the arteries of anterior\nand posterior circulation without stenosis or occlusion or an aneurysm greater\nthan 3 mm in size.\n\nMRA of the head demonstrates normal flow signal in the carotid and vertebral\narteries without stenosis or occlusion.  No evidence of dissection.",
            "output": "1. No significant abnormalities on MRI of the brain using seizure protocol.\n2. Normal MRA of the head.\n3. Normal MRA of the neck.\n."
        },
        {
            "input": "The confluent periventricular FLAIR hyperintensities are less obvious than on\nthe previous examination.  Again seen is a focal area of FLAIR hyperintensity\ninvolving the cortex and extending into the deep white matter within the right\nfrontal lobe. There appears to be slightly less cortical swelling when\ncompared with the previous examination. There are slight technical differences\nbetween the way the FLAIR scans were acquired (though the examinations were\nperformed on the same machine) which may have, but are unlikely to have,\ncaused the differences in the contrast on the FLAIR images. The differences\nmay be due to changes in oxygen tension, as the patient is no longer\nintubated. However, the apparent change in the cortical swelling of the right\nfrontal lobe lesion may be real.\n\nThere is no abnormal enhancement.",
            "output": "1. Differences in FLAIR contrast may be due to changes in the oxygen tension\nrather than technical differences. On the current FLAIR images, the white\nmatter signal is not strikingly abnormal and now is now in keeping with what\ncan normally be seen in a ___ patient with small vessel ischemic\ndisease.\n2. The etiology of the right frontal lobe lesion remains unclear though there\nmay be slightly less cortical swelling associated with the lesion, and this\nmay be due to seizure swelling with an area of underlying tissue loss in the\ndeep white matter secondary to previous injury.  There is no abnormal\nenhancement. Followup is recommended."
        },
        {
            "input": "MRI HEAD:  There is no evidence of acute infarction.  The previously seen\nT2/FLAIR abnormality in the medial right temporal lobe, right basal ganglia,\nand right cerebral peduncle has resolved. No new T2/FLAIR abnormality is seen.\nSmall susceptibility in the distribution of the prior enhancement (___)\nwith tiny focal intrinsic T1 hyperintensity (3:11) but no enhancement in the\nright basal ganglia may be a combination of mineralization or prior\nmicrohemorrhage.\n\n\nThere is no mass effect, edema, or hydrocephalus. Ventricles and sulci are\nnormal in size and configuration. Principal vascular flow voids are preserved.\nThere is no abnormal parenchymal, vascular or meningeal enhancement after the\nadministration of gadolinium. Globes and soft tissues are unremarkable.  A\nmucous retention cyst in the right sphenoid sinus is unchanged.",
            "output": "1.  Interval resolution of T2/FLAIR abnormality with no new area of T2/FLAIR\nabnormality.\n\n2.  Mineralization and/or microhemorrhage in the distribution of prior\nenhancement."
        },
        {
            "input": "Patient status post left frontal lobe of biopsy with associated blood products\nin the left frontal lobe. There is a small left subdural hematoma. The\npachymeningeal enhancement has essentially resolved. Also the enhancement in\nthe internal auditory canals is no longer present. There is improved mass\neffect on the left lateral ventricle, and the midbrain. There is persistent\nbut improved bilateral uncal herniation with a better visualization of the\nambient cistern\n\nThere is no infarct.  The principal intracranial flow voids are present. There\nis mild ethmoid mucosal thickening. There is fluid in bilateral mastoid air\ncells.\n\nMulti voxel MR spectroscopy centered at the level of the midbrain and\nbilateral hippocampal- the is unremarkable. There is no elevated choline to\nNAA ratio to suggest a neoplasm.",
            "output": "The pachymeningeal enhancement has essentially resolved. There is improved\nmass effect on the left lateral ventricle, and the midbrain.  There is\npersistent but improved bilateral uncal herniation with a better visualization\nof the ambient cistern.\n\nPosst-operative changes are seen.\n\nMR spectroscopy is unremarkable without evidence of elevated choline to NAA\nratio to suggest a neoplasm."
        },
        {
            "input": "Changes related to a left frontal biopsy are again noted, with small regions\nof gliosis and chronic blood products at the biopsy site.  Given differences\nin technique, diffuse pachymeningeal thickening and enhancement is unchanged. \nAs before, there is partial effacement of the suprasellar cistern with\nbilateral uncal herniation unchanged from the most recent prior examination,\nbut improved compared to more remote exams.\n\nThere is no acute infarct or intracranial hemorrhage. No new regions of\nabnormal signal intensity are present within the brain parenchyma. The\nventricles and cerebral cisterns are age appropriate. The cerebellar tonsils\nare normal in position. The pituitary gland remains prominent for the\npatient's age.\n\nThe visualized orbits and soft tissues are unremarkable.",
            "output": "1. Unchanged pachymeningeal thickening and enhancement.\n2. Bilateral uncal herniation persists, unchanged from the ___\nexamination but improved compared to ___."
        },
        {
            "input": "Again seen are changes related to the left frontal lobe biopsy with regions of\ngliosis and chronic blood products at the biopsy site. This appears unchanged\nwhen compared to most recent study dated ___. Allowing for\ndifferences in technique, diffuse pachymeningeal thickening persists,\nunchanged. Basilar cisterns are patent with partial effacement of the\nsuprasellar cistern compatible with bilateral uncal herniation, stable since\nprior examination.\n\nThere is no acute infarction or intracranial hemorrhage.  No diffusion\nabnormality is identified.  There is no pathologic intracranial enhancement.\nIntracranial flow voids are maintained. Visualized paranasal sinuses and\nmastoid air cells are clear.  The visualized orbits and soft tissues are\nunremarkable.",
            "output": "Unchanged pachymeningeal thickening and bilateral uncal herniation. No new\nacute intracranial abnormality. Re- demonstration of post biopsy changes\nwithin the left frontal lobe, unchanged."
        },
        {
            "input": "Patient is status post left frontal lobe biopsy. Gliosis and and chronic blood\nproducts in this region are unchanged.\n\nThere has been interval worsening of diffuse pachymeningeal thickening and\nenhancement when compared to prior studies, particularly in the posterior\nfossa. There is also increased deformity of the midbrain noted with worsening\nbilateral uncal herniation and recurrent effacement of the basal cisterns.\nHowever, there is no sign of associated parenchymal edema. There is no\nabnormal parenchymal enhancement seen on post contrast images.\n\nSlight asymmetry of the ventricles and a megacisterna magna are again noted. \nThere is no acute infarction, intracranial hemorrhage, or extracerebral fluid\ncollection.  No diffusion abnormalities are detected. The major vascular flow\nvoids are maintained. The orbits are unremarkable, the paranasal sinuses and\nmastoid air cells are clear",
            "output": "Interval worsening of diffuse pachymeningeal thickening and enhancement, and\nbilateral uncal herniation with associated deformity of the midbrain.  Again,\nthese findings may reflect intracranial hypotension, related to occult \"CSF\nleak.\"\n\nNOTIFICATION:  These findings were reviewed in detail with Dr. ___\n___ service) in-person by Dr. ___ at 10:46 am on ___.  Dr.\n___ is considering empiric epidural \"blood patch."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, or infarction.\nThere is asymmetry of the brain with the left lateral ventricle considerably\nsmaller than the right. There appears to be mild left to right midline shift.\nThe medial temporal lobes are displaced medially into the ambient cistern\nbilaterally and slightly inferiorly into the posterior fossa.\n\nPost-contrast images demonstrate diffuse enhancement and thickening of the\npachyeninges.  There is no evidence of intraparenchymal signal intensity\nabnormalities or abnormal enhancement. The medial temporal lobes are displaced\ninto the ambient cistern and below the free edge of the tentorium bilaterally.\nThus, there appears to be a tight supratentorial cavity. However, the degree\nof dural thickening appears insufficient to cause this apparent mass effect.\n\nThe dural thickening is particularly prominent along the tentorium, but is\npresent over the convexities bilaterally and in the posterior fossa. Abnormal\nenhancement extends into the internal auditory canals bilaterally.\n\nThe pattern of diffuse pachymeningeal enhancement has a long differential\ndiagnosis that includes sarcoidosis, lymphoma, other lymphoproliferative\ndisorders, tuberculosis technique meningitis, and syphilis.\n\nThese findings were noticed at 20:40 on ___ and discussed at ___\nwith Dr. ___. The ventricles and sulci are normal in caliber and\nconfiguration. There is no abnormal enhancement after contrast administration.",
            "output": "Tight supra tentorial cavity with extensive pachymeningeal thickening and\nenhancement.\n\nBilateral uncal herniation."
        },
        {
            "input": "MPRAGE sequences are slightly limited by motion artifact. The patient is\nstatus post left frontal craniotomy with biopsy of the left frontal dura.\nThere is a single focus of left frontal diffusion-weighted signal abnormality,\nunchanged from prior exam, consistent with post surgical sequela. No evidence\nfor acute hemorrhage or infarct. Previously noted diffuse pachymeningeal\nenhancement and thickening is essentially resolved current exam, with residual\nmild enhancement in the left IAC (series 15, image 8). Again noted is\nbilateral uncal herniation, unchanged from prior exam.  The major intracranial\nflow voids preserved. Incidental note is made of hyperostosis interna\nfrontalis. Mild mucosal thickening of the paranasal sinuses is noted. The\norbits are unremarkable. There is opacification of right greater than left of\nthe mastoid air cells.",
            "output": "1. Near-complete interval resolution of previously noted diffuse\npachymeningeal thickening and enhancement, with mild residual enhancement\nwithin the left IAC. Unchanged appearance of bilateral uncal herniation.\n2. There is no abnormal signal within the nasal cavity to suggest CSF leak\nhowever, Nuclear Medicine CSF leak study may yield additional information."
        },
        {
            "input": "Redemonstrated is mild pachymeningeal enhancement in the supra and\ninfratentorial region.  This is not significantly changed compared to the MRI\nexamination of ___ and ___.  Although there was reported\ndecrease in enhancement on ___ which was likely secondary to\ntechnical differences.  Again medial displacement of bilateral uncus is seen\nas before.  Deformity of the brainstem is also unchanged.  There is no\nhydrocephalus.  There are no acute infarcts.  A left frontal small bony defect\npresumably secondary to have a biopsy is again visualized.  The visualized\nparanasal sinuses are clear.  Hyperostosis interna predominantly in the\nfrontal region is again noted as an incidental finding.",
            "output": "Essentially unchanged appearance compared to the previous MRI examination is\nof pachymeningeal enhancement both in the supra and infratentorial region with\nmore pronounced changes in the infratentorial region.  Position of the\ntemporal regions bilaterally is also unchanged.  No significant new findings\nare identified."
        },
        {
            "input": "There is redemonstration of intraparenchymal hemorrhage centered in the right\noccipitotemporal region, which demonstrate predominantly hypointensity on T2\nweighted image and heterogeneous hyperintensity on T1 weighted image.  There\nis a mild surrounding vasogenic edema resulting in mild mass effect on the\nadjacent parenchyma.  No evidence of midline shift.  Given the presence of\nintrinsic T1 hyperintensity of the hemorrhage, it is difficult to evaluate the\nextent of enhancement.  The hemorrhage is grossly unchanged in size compared\nto prior CT, and measures 3.0 x 2.3 cm.\nNo additional area of hemorrhage is identified.\n\nThere is no evidence of infarction.  The ventricles and sulci are normal in\ncaliber and configuration.  The visualized major vascular flow voids are\ngrossly preserved.  The paranasal sinuses are clear.  There is mild effusion\nin the left mastoid air cells.  The globes and orbits are unremarkable.  No\nabnormal marrow signal is identified.",
            "output": "1. No significant change in size of the acute intraparenchymal hemorrhage\ncentered in the rightoccipitotemporal region. Given the presence of intrinsic\nT1 hyperintensity of the hemorrhage, it is difficult to evaluate the extent of\nthe enhancement.  Please consider follow-up MRI with contrast after the\nresolution of the hemorrhage to exclude any underlying enhancing lesion.\n2. No evidence of an acute infarct."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  There is no MRI correlate for the high density overlying the\nbilateral cerebellum identified on the recent CT head performed the same day. \nThe ventricles and sulci are normal in caliber and configuration.  There is no\nabnormal enhancement after contrast administration.\n\nThe major intracranial vascular flow voids are maintained.  The paranasal\nsinuses, mastoid air cells and orbits are normal.  Unchanged skin laceration\ndefect overlying the left frontal region.",
            "output": "No acute intracranial abnormality.  Specifically, no MRI correlate for the\nhigh density overlying the cerebellum bilaterally."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.  The major intracranial arteries appear patent without\nsignificant flow limiting stenosis.  The dural sinuses are patent without\nvenous sinus thrombosis.",
            "output": "Dural sinuses are patent without venous sinus thrombosis."
        },
        {
            "input": "A 1.8 x 1.2 cm lesion in the left frontal lobe is heterogeneous in signal with\nareas of T2/T1 hypointensity and hyperintensity.  This lesion has a T2\nhypointense rim.  There is a small amount of adjacent subarachnoid hemorrhage\nin the left frontal sulci.  No new hemorrhages are identified.  There is no\nnodular enhancement within this lesion.  There is minimal, thin peripheral\nenhancement along the inferior aspect of this lesion.\n\nThere is no evidence of edema, masses, mass effect, midline shift or\ninfarction.   The ventricles and sulci are normal in caliber and\nconfiguration.\n\nThe paranasal sinuses and mastoid air cells are clear.  The orbits are\nunremarkable.",
            "output": "Left frontal lobe intraparenchymal hematoma with a small amount of adjacent\nsubarachnoid hemorrhage, containing acute and subacute blood products, which\nmay be due to an underlying occult vascular malformation.  However, the\npossibility of a neoplasm should also be considered.  No nodular enhancement. \nSerial follow-up contrast-enhanced MRI is recommended.\n\nRECOMMENDATION(S):  Serial follow-up contrast-enhanced MRI is recommended."
        },
        {
            "input": "MRI BRAIN:\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are mildly enlarged in an atrophic\npattern.  There is no abnormal enhancement after contrast administration. \nThere is scattered white matter hyperintensity on the FLAIR images of doubtful\nclinical significance.  This is often attributed to mild chronic small vessel\nischemia.\n\nMRA BRAIN:\nThe intracranial vertebral and internal carotid arteries and their major\nbranches appear normal without evidence of stenosis, occlusion, or aneurysm\nformation.\n\nMRA NECK:\nThere is mild atherosclerotic dilatation at the origin of the right internal\ncarotid artery.  Otherwise, the common, internal and external carotid arteries\nappear normal.  There is no evidence of internal carotid artery stenosis by\nNASCET criteria.  The origins of the great vessels, subclavian and vertebral\narteries appear normal bilaterally.",
            "output": "1. Mild atrophy and white matter hyperintensity on FLAIR.  Otherwise normal\nstudy.\n2. No evidence of hemorrhage or infarction.\n3. No evidence of vascular occlusion or stenosis.\n4. Mild dilatation of the proximal right internal carotid artery, likely due\nto atheromatous disease."
        },
        {
            "input": "Please note, only 3D FLAIR and T1 pre and postcontrast sequences were\nobtained.\n\nRe-identified are subcortical and periventricular FLAIR white matter\nhyperintensities, unchanged from examination of ___, and progressed\nfrom examination of ___.  The ventricles sulci and cisterns are within\nexpected limits for the patient's mild senescent related global cerebral\nvolume loss.  No abnormal postcontrast enhancement is identified.  The dural\nvenous sinuses are patent on postcontrast MP rage.  Mild mucosal thickening of\nthe ethmoid air cells and inferior frontal sinuses is noted.",
            "output": "1. No evidence of abnormal enhancement to suggest active process.\n2. Please refer to MRI head without contrast of ___ for additional\ndetails."
        },
        {
            "input": "Within the right centrum semiovale there is FLAIR and faint diffusion\nhyperintensity with foci of low signal on T1 images indicating of a chronic\nsubcortical infarct. There is no acute infarct, hemorrhage, mass effect or\nabnormal enhancement. The principal intracranial flow voids are present.\n\nThe orbits, paranasal sinuses and mastoid air cells are unremarkable.",
            "output": "Late subacute to chronic appearing n infarct in the right cerebral hemisphere\nin the subcortical region. No acute infarcts seen. No enhancing brain lesions\nare identified. No mass effect or hydrocephalus."
        },
        {
            "input": "Multiple punctate areas of acute/subacute infarct identified in the deep\nwatershed distribution of right cerebral hemisphere extending to the\nsuperficial watershed distribution in the right frontal and parietal lobes. \nPunctate focus of acute/subacute infarct is also seen in the left centrum\nsemiovale as well as punctate infarcts are seen in the right periatrial\nregion..  Mild-to-moderate changes of small vessel disease in chronic white\nmatter infarcts are identified.  Increased signal is seen within the right\npetrous carotid region suggestive of occlusion seen on the CT angiography of\nthe neck.\n\n\nThere is mild to moderate brain atrophy.  There is no midline shift or\nhydrocephalus.  No evidence of acute or chronic blood products.  Visualized\nparanasal sinuses are clear.",
            "output": "1. Multiple small acute/subacute infarcts in the deep and superficial\nwatershed distribution of right cerebral hemisphere.\n2. Small punctate infarcts in the left centrum semiovale and right periatrial\nregion.\n3. Absent flow void in the right petrous and cervical internal carotid due to\nocclusion seen on the previous CT angiography."
        },
        {
            "input": "There is region of T2 FLAIR hyperintensity in the left occipital lobe not\npreviously noted on MR from ___ that is concerning for ischemic stroke.\n\nRedemonstration of right mastoidectomy and resection of the right internal\nauditory canal.  Fat packing material within the right mastoid bone, with some\nresorption since ___.  The patient is status post resection of cranial nerves\n7 and 8 on the right side.  There is no residual or recurrent tumor.\n\nRedemonstration of FLAIR hyperintensities in the subcortical and deep white\nmatter that are nonspecific but suggestive of chronic small vessel ischemic\ndisease.  These are unchanged since ___.  There is normal enhancement of the\nmajor intracranial arteries and dural venous sinuses following contrast\nadministration.  The visualized paranasal sinuses do not demonstrate abnormal\nenhancement.",
            "output": "1. Restricted diffusion with FLAIR abnormality in the left occipital lobe\nsuggestive of acute left PCA infarct.\n2. Postsurgical changes secondary to right cerebellopontine angle mass\nresection.  No residual or recurrent mass.\n3. Unchanged FLAIR hyperintensities in the subcortical and deep white matter\nthat are suggestive of early changes of chronic small vessel ischemic disease."
        },
        {
            "input": "There is subtle symmetric elevated FLAIR hyperintense signal involving\nbilateral insula, hippocampi and parahippocampal gyri.  Subtle FLAIR\nhyperintense signal may also be present in the inferior frontal lobes and the\nmammillary bodies.  There is no associated signal abnormality on the remainder\nof the sequences including diffusion.  There is no evidence of mass effect or\nvolume loss in these regions.  There is no hemorrhage.\n\nThere is a small white matter lacunar infarct adjacent to the atrium of the\nleft lateral ventricle (series 4, image 12).  Focal T2 hyperintense signal in\nthe left pons with subtle surrounding FLAIR hyperintense signal also probably\nrepresents a chronic lacunar infarct (series 5, image 8).  There is no\nevidence of acute infarction.  The ventricles and sulci are age-appropriate. \nThere is no disproportionate lobar or mesial temporal volume loss. \nPeriventricular and punctate scattered subcortical white matter foci of FLAIR\nhyperintense signal and those within the pons are nonspecific, but probably\nsequelae of small vessel ischemic disease.  There is no mass, mass effect or\nshift of normally midline structures.  Principal intracranial vascular voids\nare preserved.",
            "output": "1. Subtle symmetric FLAIR hyperintense signal involving bilateral insula,\nhippocampi, and mesial temporal lobes and possibly the inferior frontal lobes\nand mammillary bodies as described above is nonspecific, potentially\nartifactual.  Differential considerations include viral infection,\nparaneoplastic syndrome, or a neurovegetative process.  Symmetric appearance\nand lack of mass effect makes tumor less likely.\n2. No acute infarct or intracranial hemorrhage.\n\nRECOMMENDATION(S):  Short-term follow-up with contrast enhanced MRI is\nrecommended for further evaluation.\n\nNOTIFICATION:  The findings were discussed with ___ as requested\nby ___, M.D. on the telephone on ___ at 1:00 pm, 5 minutes\nafter discovery of the findings."
        },
        {
            "input": "Within the inferior aspect of the left parotid gland, an enhancing, T2\nhyperintense, large left parotid lesion is seen measuring approximately 3.8 cm\nTRV by 3.4 cm AP by 3.8 cm CC, involving both the superficial and deep lobes\nof the parotid gland.  No significant adjacent lymphadenopathy is seen.  The\nlesion appears to abut the angle of the left mandible however there does not\nappear to be frank invasion into the mandible.  There is no evidence of\nperineural spread of enhancement.\n\nThe right parotid gland is unremarkable.  The bilateral submandibular glands\nare unremarkable.  The visualized vascular flow voids appear to be well\npreserved.  No oropharyngeal mucosal mass is identified.",
            "output": "1. 3.8 cm enhancing, large T2 hyperintense lesion within the left parotid\ngland.  Differential considerations include neoplastic etiologies such as\nparotid lymphoma or mucoepidermoid carcinoma.  Other considerations include\npossible pleomorphic adenoma.  Sampling of the left parotid lesion is\nrecommended for further evaluation.\n\nRECOMMENDATION(S):  Sampling of the left parotid lesion is recommended for\nfurther evaluation.\n\nNOTIFICATION:  The impression and recommendation above was entered by Dr.\n___ on ___ at 11:55 into the Department of Radiology critical\ncommunications system for direct communication to the referring provider."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  There are confluent deep and periventricular white matter T2\nsignal abnormalities, most consistent with severe chronic small vessel\nischemic changes, worsened since ___.  Component of chronic demyelination\ncannot be excluded; sequela of distant metabolic or inflammatory process is\nstatistically unlikely.  Brain parenchymal atrophy.  Vascular flow voids are\npreserved.  Minimal paranasal sinus disease.  Minimal opacification right\nmastoids.  Clear left mastoids",
            "output": "1. No acute infarct.\n2. Findings most consistent with severe chronic small vessel ischemic changes.\n3. Brain parenchymal atrophy."
        },
        {
            "input": "There is no evidence of acute infarct on diffusion images.  Moderate brain\natrophy and moderate to severe changes of small vessel disease are seen\nunchanged from the prior study.  Vascular flow voids are maintained. \nSuprasellar and craniocervical regions are unremarkable.  The visualized\nparanasal sinuses are clear.",
            "output": "No acute abnormalities or significant change since the previous MRI of ___."
        },
        {
            "input": "Acute gyriform infarct of the right frontal operculum is identified without\nevidence of hemorrhagic transformation.  No intra or extra-axial mass. The\nsulci, ventricles and cisterns are within expected limits for the degree of\nmild to moderate senescent related global cerebral volume loss.  Right\ntemporoparietal encephalomalacia (series 10, image 11) is noted.  Likely right\nfrontal encephalomalacia (series 10, image 16) is also identified. \nPeriventricular and subcortical moderate T2/FLAIR white matter\nhyperintensities are identified, nonspecific, but compatible with chronic\nmicroangiopathy in a patient of this age.\n\nThe major intracranial flow voids are preserved.  Mild mucosal thickening of\nthe paranasal sinuses with a small partially visualized right maxillary sinus\nmucous retention cyst.  The orbits are unremarkable, noting bilateral lens\nreplacements.  No significant fluid signal is seen in the mastoid air cells. \nNo suspicious marrow signal.",
            "output": "1. Gyriform acute infarct of the right frontal operculum without evidence of\nhemorrhagic transformation.\n2. Right temporoparietal encephalomalacia, likely right frontal\nencephalomalacia.\n3. Periventricular and subcortical moderate T2/FLAIR white matter\nhyperintensities, nonspecific, but compatible with chronic microangiopathy in\na patient of this age.\n4. Additional findings described above."
        },
        {
            "input": "There is no evidence of acute intracranial hemorrhage. The ventricles and\nbasilar cisterns appear normal.\n\nThere is a briskly enhancing, ovoid and smoothly marginated left\ncerebellopontine angle mass which measures 2.6 cm x 1.8 cm and causes mild\nadjacent mass effect on the left cerebellum and brainstem though without\nevidence of ventricular dilatation. There is no apparent extension into the\ninternal auditory canal.  There is mild centrally increased diffusion weighted\nsignal. Overall appearance and location are most suggestive of meningioma.\nWhen compared to prior examination, there is no significant change in size. No\nother lesions are other areas of abnormal enhancement are seen.\n\nThere is no evidence of acute ischemia based on diffusion-weighted imaging.\nThere are normal vascular flow voids. The brain parenchymal volume appears\nwithin normal limits.\n\nThe orbits, skull base, and paranasal sinuses appear unremarkable.",
            "output": "1. Well-marginated, ovoid left cerebellopontine angle mass without apparent\nextension into the internal auditory canal, the appearance of which is most\nsuggestive of meningioma."
        },
        {
            "input": "Again homogeneously enhancing left posterior fossa mass consistent with a\nsmall identified measuring 2.5 cm consistent with a meningioma. Mass effect on\nthe adjacent cerebellar hemisphere is seen.  There is no hydrocephalus.",
            "output": "Left posterior fossa meningioma is again identified for surgical planning."
        },
        {
            "input": "The patient is status post left suboccipital craniectomy for meningioma\nresection. There are expected postoperative changes open including scalp\nswelling and a small amount of air and hemorrhage at the surgical site. Mass\neffect on the left cerebellar hemisphere and cerebellar peduncle has been\nrelieved. There is diffuse posterior fossa dural enhancement, likely\nconsequence of the surgery.  The transverse and sigmoid sinuses appear normal.",
            "output": "Status post left suboccipital craniectomy for meningioma resection with\nexpected postoperative changes."
        },
        {
            "input": "The patient is status post a suboccipital craniectomy for a meningioma\nresection. Since the prior exam, the amount of hypointensities on the gradient\necho sequence in the resection bed have decreased, which is most consistent\nwith a decrease in the amount of surrounding blood products and\npneumocephalus. There are expected postsurgical changes along the resection\ncavity, including mild diffuse posterior dural enhancement. The amount of\nenhancement has decreased since the prior exam. There is no nodular\nenhancement to suggest tumor recurrence. There is no mass effect or abnormal\nsignal in the adjacent cerebellum.\n\nThe remainder of the brain is normal. There is no evidence of an infarct,\nhemorrhage, or other mass lesion. The ventricles and sulci are normal in size\nand configuration. The basal cisterns are patent.\n\nThe paranasal sinuses are clear. There is a small amount of fluid in the left\nmastoid air cells. The right mastoid air cells are clear. The soft tissues are\nunremarkable.",
            "output": "Expected postoperative changes after a left suboccipital craniectomy for a\nmeningioma resection. No evidence of residual or recurrent tumor."
        },
        {
            "input": "The patient is status post left suboccipital craniectomy, cranioplasty, and\nresection of a meningioma with interval decrease in the minimal, smooth dural\nthickening and enhancement underlying the craniectomy site.  There are a small\namount of chronic blood products in the postoperative bed.  There is no\nenhancement in the resection cavity.  No enhancing lesions are identified.\n\nThere is no evidence of edema, masses, mass effect, midline shift or\ninfarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  Scattered T2/FLAIR hyperintensities in the subcortical and\nperiventricular white matter are unchanged and nonspecific, but may represent\nthe sequela of chronic small vessel ischemic disease.\n\nThe left mastoid air cells are partially opacified, improved from the prior\nexamination.  The paranasal sinuses are clear.  The orbits are unremarkable. \nThe major intracranial flow voids are preserved.",
            "output": "1. Postsurgical changes with no evidence of residual or recurrent neoplasm."
        },
        {
            "input": "The left-sided posterior fossa craniotomy is identified.  No evidence of\nrecurrent enhancement is seen.  Postsurgical changes are noted.  The\nventricles and extra-axial spaces are normal in size without midline shift\nmass effect or hydrocephalus.  Subtle area of enhancement in the right frontal\nlobe (16:16) likely representing a developmental venous anomaly is unchanged\ncompared to the prior study.",
            "output": "No signs of tumor recurrence.  Stable appearance of the brain."
        },
        {
            "input": "Study is mildly degraded by motion.  There is no evidence of hemorrhage,\nedema, masses, mass effect, midline shift or infarction.   The ventricles and\nsulci are normal in caliber and configuration.  There is no abnormal\nenhancement after contrast administration.\n\nThe orbits are unremarkable.  Mild mucosal thickening in bilateral ethmoid air\ncells and bilateral maxillary sinuses, unchanged since the prior study from\n___.  The remaining visualized paranasal sinuses and mastoid air cells are\nclear.  Intracranial flow voids are maintained.",
            "output": "1.  Study is mildly degraded by motion.\n2. No evidence of intracranial masses.\n3. Stable paranasal sinus disease as described above.\n4.  No acute intracranial abnormality."
        },
        {
            "input": "There is no evidence of intracranial hemorrhage, edema, masses, mass effect,\nmidline shift or infarction.   The ventricles are normal in size and\nconfiguration, however, a the sulci are slightly prominent for the patient's\nage slightly more significant towards the convexity, although this finding is\nnonspecific suggest mild cortical volume loss, please correlate..  There is no\nabnormal enhancement after contrast administration.\n\nParanasal sinuses and mastoid air cells are unremarkable.  Both globes and\norbits are unremarkable.",
            "output": "1. There is no evidence of acute intracranial process or hemorrhage.\n2. Slightly prominent sulci towards the convexity, this finding is\nnonspecific, however suggest mild cortical volume loss, please correlate.\n3. No diffusion abnormalities or abnormal enhancement after contrast\nadministration.\n\nNOTIFICATION:  The findings were discussed with ___ , M.D. by ___\n___, M.D. on the telephone on ___ at 3:32 pm, 5 minutes after\ndiscovery of the findings."
        },
        {
            "input": "The examination is mildly limited secondary to patient motion.\n\nThere is no evidence of acute infarction.  No intracranial hemorrhage.  No\nmass, mass effect, edema or midline shift.\n\nThe ventricles and sulci are prominent compatible with global cerebral\natrophy.  Scattered periventricular and deep white matter T2/FLAIR\nhyperintensities are nonspecific but likely the sequelae of moderate chronic\nsmall vessel ischemic disease.  The basal cisterns are patent.  There is gross\npreservation of the principal intracranial vascular flow voids.  There is\nsmall chronic infarct in the upper left cerebellum.\n\nThe remainder of the visualized paranasal sinuses, middle ear cavities, and\nmastoid air cells are well aerated and clear.  The orbits are within normal\nlimits bilaterally.  There is benign 3.0 cm x 1.6 cm lipoma at the posterior\nright neck base, just underneath the skin.",
            "output": "1. No evidence for acute intracranial process.\n2. Small chronic left cerebellar infarct.\n3. Mild-to-moderate global cerebral atrophic changes and findings of moderate\nchronic microangiopathy.\n4. Posterior neck benign lipoma."
        },
        {
            "input": "There is a lobulated, 2.8 x 2.1 x 2.3 cm (SI by AP by TV) (6:8 and 5:12)\nsellar mass with suprasellar extension, which demonstrates T2 hyperintensity,\nT1 hypointensity, and heterogeneous enhancement following administration of\ncontrast.  The mass appears to be centered on and arise from the anterior\npituitary, as the normal, intrinsically T1 hyperintense posterior pituitary is\nseen displaced superiorly and posteriorly and laterally to the left, seen\nalong the left superior-posterior margin of the mass, along with leftward\ninfundibular deviation (series 3 and 5, images 14 and 15).\n\nThere is upward mass effect on the optic chiasm, which is contacted and\ndeformed, superiorly displaced, by the mass.  The suprasellar cistern is\nlargely filled by the superior extent of the mass.  The cavernous intracranial\ncarotid flow voids are normal.  Heterogeneous enhancement along the right\ncavernous sinus may reflect some degree of right cavernous sinus involvement\nby the mass (05:12).  The left cavernous sinus appears to enhance normally.\n\nAside from global parenchymal volume loss, the visualized portions of the\nbrain parenchyma appear unremarkable.",
            "output": "1. 2.8 cm lobulated, enhancing sellar mass with suprasellar extension, most\nsuggestive of a pituitary macroadenoma.\n2. Findings suggestive of right cavernous sinus tumor extension.\n3. Mass-effect includes contact and upward displacement and deformation of the\noptic chiasm and effacement of most of the suprasellar cistern.\n4. Posterior pituitary is displaced to the left, at the superior-posterior\nmargin of the mass.\n5. Marked leftward infundibular deviation.\n6. Left cavernous sinus appears normal."
        },
        {
            "input": "The patient's previously noted lobulated sellar mass measures 2.8 x 2.1 x 2.2\ncm with unchanged suprasellar extension is again seen.  There is no midline\nshift and grossly stable upward mass effect on the optic chiasm which is\nsuperiorly displaced by the mass.",
            "output": "Grossly stable 2.8 x 2.1 x 2.2 cm lobular sellar mass with suprasellar\nextension and stable mass effect on the optic chiasm."
        },
        {
            "input": "Small, somewhat wedge-shaped acute infarction in the left find, does not\nextend to the right side.  Addition punctate focus of acute/early subacute\nsmall infarcts in the left sub insula temporal lobe, and left internal\ncapsule.\n\nChronic infarcts have evolved in the right pons and medulla, left thalamus,\nleft internal capsule, and left basal ganglia compared to ___. \nWallerian degeneration left midbrain.\n\nFindings of moderate chronic small vessel ischemic disease.  With areas of\nconfluence in the deep white matter, likely microvascular chronic small vessel\nischemic changes, occasionally similar changes can be seen with metabolic or\ninflammatory etiologies.  Mild-to-moderate involutional changes.  No\nhydrocephalus.  Preserved vascular flow voids, preserved basilar artery flow\nvoid.\n\nMild mucosal thickening of the paranasal sinuses.  Clear mastoid air cells. \nUnremarkable intraorbital contents.",
            "output": "1. Moderate size acute infarct left pons.  Punctate acute/early subacute\ninfarcts left temporal lobe, left internal capsule.\n2. Chronic infarcts left thalamus, internal capsule, globus pallidus, and\nright pons.\n3. No hemorrhage.\n4. Remainder as above.\n\nNOTIFICATION:   The findings were discussed with ___, M.D. by\n___, M.D. on the telephone on ___ at 2:03 pm, 5\nminutes after discovery of the findings."
        },
        {
            "input": "Exam is motion-limited. Restricted diffusion in the left basal ganglia and\nleft hypothalamus is consistent with acute infarct (se 4, im 15, 18). \nBackground bilateral T2/FLAIR prolongation without other correlate are\nnonspecific but may reflect sequelae of chronic small vessel ischemic disease.\nNo gradient echo sequence is available to adequately assess for presence of\nhemorrhage.There is no evidence of masses or midline shift.   The ventricles\nand sulci are normal in caliber and configuration.  The visualized orbits are\nunremarkable.  The visualized portions of the paranasal sinuses are centrally\nclear.  Major intracranial vascular flow voids are preserved.",
            "output": "Acute left basal ganglia and hypothalamic infarct.\n\nNo new GRE sequence was performed to assess for hemorrhage due to patient\ninability to tolerate the entire exam.\n\nNOTIFICATION:   The findings were discussed with ___, M.D. by\n___, M.D. on the telephone on ___ at 2:13 ___, 1 minutes after\ndiscovery of the findings."
        },
        {
            "input": "In comparison with the prior head CT dated ___, and prior\nmaxillofacial CT dated ___, the previously noted right frontal\nsubdural hematoma is thinner measuring approximately 2.5 mm in thickening,\nwith no evidence of mass effect in the adjacent structures (image 16, series\n6).  Postsurgical changes are again seen consistent with right frontotemporal\ncraniotomy for subdural evacuation are again seen. There is marked global\natrophic changes resulting in prominent ventricles and sulci, which appears\nsimilar to the prior exam, there is an unchanged arachnoid cyst in the left\nmiddle cranial fossa.  There is no evidence of acute intracranial hemorrhage\nmass, mass effect or shifting of the normally midline structures.  No\ndiffusion abnormalities are detected to indicate acute or subacute ischemic\nchanges.  The major vascular flow voids are present with significant\ntortuosity of the basilar artery with calcification and no significant changes\nsince the prior exams.  The orbits are grossly unremarkable, with no evidence\nof proptosis as previously seen on the CT dated ___.  The\nparanasal sinuses, middle ear cavities and the mastoid air cells are clear.",
            "output": "1.  There is no evidence of acute intracranial process or hemorrhage.\n\n2.  Slightly thinner right frontal chronic subdural hematoma, measuring\napproximately 2.5 mm in thickening, with no evidence of mass effect.\n\n3..  Chronic changes related to small vessel ischemic disease, global atrophy\nand prior right temporal frontal craniotomy.\n\n4.  Unchanged arachnoid cyst in the left middle cranial fossa."
        },
        {
            "input": "Again noted are postsurgical changes in the right frontotemporal region\ncompatible with craniotomy for subdural evacuation.  There is marked global\natrophy resulting prominent ventricles and sulci, similar in appearance to the\nprior study.  There are patchy and confluent T2/STIRhyperintense areas in\nsubcortical and periventricular white matter, a nonspecific finding. \nAdditionally, there is a 0.4 cm T2 hyperintense focus in the right corona\nradiata that is FLAIR hypointense adjacent the right lateral ventricle likely\nrepresenting a chronic lacunar infarct, unchanged.  When compared to the prior\nstudy, there is no significant change in the right chronic frontal subdural\nhematoma measuring approximately 3 mm in thickness (05:16).  No evidence of\nmass effect on the adjacent structures.  Unchanged arachnoid cyst in the left\nmiddle cranial fossa.  The major vascular flow voids are present with\nsignificant tortuosity of the basilar artery, not significantly changed from\nthe prior study.  There is no abnormal enhancement after contrast\nadministration.\n\nImages through the brainstem demonstrate no focal abnormalities.  Bilateral\nseventh and 8 nerve complexes are well maintained and there is no abnormal\nenhancement or mass lesion.  The tortuous left vertebral artery contacts the\nleft seventh and eighth nerve complex without deformity.  Tortuous right\nvertebral artery slightly indents the right side of the medulla which could be\na variation.  Bilateral cavernous sinuses and orbital abscesses are symmetric\nand there is no mass lesion identified.\n\nThe visualized paranasal sinuses are clear.  The orbits are unremarkable.",
            "output": "1. No mass or abnormal enhancement in the posterior fossa.  Particularly with\nreference to the lower cranial nerves and cerebellopontine angles.\n2. Chronic right frontal subdural hematoma or meningeal thickening is\nunchanged from the prior study.\n3. Chronic changes related to small vessel ischemic disease.\n4. Global atrophy and prior right frontotemporal craniotomy.\n5. Unchanged arachnoid cyst in the left middle cranial fossa."
        },
        {
            "input": "Postsurgical changes related to prior right frontotemporal craniotomy for\nsubdural evacuation are again noted.  There is marked global atrophic change,\nresulting an prominent sulci and ventricles, stable in appearance. \nSignificant periventricular and subcortical white matter T2/FLAIR signal\nhyperintensities reflect the sequelae of chronic small vessel ischemic\ndisease.  Diffuse T2 hyperintense signal throughout the bilateral basal\nganglia, red nuclei, and substantia nigra, possibly from increased iron\ndeposition.  There is no evidence of acute intracranial hemorrhage, edema,\nmasses, mass effect, or infarction.  Susceptibility artifact is noted in the\nregion of the left vertebral artery, compatible with known dense\natherosclerotic calcification (6:8).  A left middle cranial fossa arachnoid\ncyst is unchanged, with adjacent volume averaging from the sphenoid bone.",
            "output": "1.  Chronic changes related to small vessel ischemic disease, global atrophy,\nand prior right frontotemporal craniotomy.\n2.  No acute infarction or hemorrhage.\n3. Diffuse basal ganglia and midbrain T2 hypointensity, suggestive of\nincreased iron depostion, but nonspecific.\n4. Arachnoid cyst in the left middle cranial fossa, unchanged."
        },
        {
            "input": "Previously noted focus of enhancement in the left globus pallidus is less well\nseen. There is patchy signal abnormality and enhancement in the left\ntemporoparietal region with associated FLAIR signal abnormality which is\nrelatively stable.  MR spectroscopy reveals increased choline in this region\nand decreased NAA compatible with neoplasm.  In the globus pallidus, no\nsignificant abnormalities seen on the MR spectroscopy.  MR perfusion is\ntechnically limited\n\nVentricles and sulci are age-appropriate.  Intracranial flow voids are\nmaintained. Visualized paranasal sinuses and mastoid air cells are clear.  No\nevidence for acute ischemia or hydrocephalus",
            "output": "Stable patchy enhancement and FLAIR signal abnormality in the left\ntemporoparietal region. Previously noted enhancement in the globus pallidus\nhas decreased in conspicuity"
        },
        {
            "input": "In the region of the previously seen the enhancing left temporoparietal mass\nis well-circumscribed avidly enhancing lesion which measures 2.5 x 1.7 cm\ncompared to 1.7 x 0.9 cm previously (12a:62) with increased peripheral\nenhancement. Increased FLAIR signal surrounding this mass has significantly\nincreased in comparison to prior study. There is no diffusion abnormality.  No\nother enhancing lesions are identified.\n\nThere is no intracranial hemorrhage. The ventricles and sulci are normal in\nsize and configuration. Prior cerebellar infarcts are again noted. Scattered\nT2/FLAIR hyperintensities in the periventricular and subcortical white matter\nare again noted and suggestive of small vessel ischemic changes. The major\nvascular flow voids are preserved. Orbital soft tissues are unremarkable. The\nvisualized paranasal sinuses and mastoid air cells are clear.",
            "output": "Interval increase in contrast enhancement and peripheral increased FLAIR\nsignal in the region of treated left parieto-temporal astrocytoma which is\nworrisome for tumor progression."
        },
        {
            "input": "Again seen in the left temporoparietal region, there is a 1.9 x 2.6 cm\nwell-circumscribed avidly enhancing lesion, previously 1.9 x 2.4 cm as\nmeasured at approximately the same level allowing for differences in slice\nacquisition. Internal magnetic susceptibility foci are work conspicuous on\ntoday's examination and may reflect foci of calcification. Surrounding\nvasogenic edema (8:19) appears more extensive when compared to prior\nexamination. New since prior examination are punctate foci of restricted\ndiffusion (502:18). No additional enhancing lesion is seen.\n\nPrior cerebellar infarcts are again noted within the left cerebellum and\nsmaller focus within the right cerebellum. Scattered T2/FLAIR hyperintensities\nwithin the periventricular and subcortical white matter are suggestive of\nsmall vessel ischemic changes. There is no significant mass effect or shift of\nmidline structures. Ventricles and sulci are age appropriate in size and\nconfiguration. Intracranial flow voids are maintained. Visualized paranasal\nsinuses and mastoid air cells are clear.",
            "output": "Re- demonstration of left parietal temporal astrocytoma with increased\nsurrounding FLAIR signal, similar degree of enhancement, and new punctate foci\nof restricted diffusion. Tumoral activity cannot be excluded and short term\nfollow up MRI examination is recommended.\n\nNOTIFICATION:  These findings and recommendations were communicated to Dr.\n___ by Dr. ___ telephone at 16:40 on ___ at the time the\nstudy was reviewed."
        },
        {
            "input": "There is re- demonstration of a large left temporal parietal ring-enhancing\nmass with extensive surrounding edema, central necrosis, internal foci of thus\nloaded diffusion with few internal foci of susceptibility artifact. This\nlesion has overall mildly increased in size, today measuring 48 x 46 x 49 mm,\npreviously measuring 42 x 42 x 40 mm. Surrounding edema is more prominent,\ninvolving more of the left frontal and left temporal lobes. There is increased\nassociated mass effect now with 8 mm of rightward shift. There is no downward\nherniation. Despite the increased mass effect, overall configuration and size\nof the ventricles is unchanged with the exception of mildly increased\neffacement of the left lateral ventricle. The basal cisterns remain patent. No\nnew enhancing lesion is identified. There is a stable focus of susceptibility\nartifact in the right occipital lobe. Nonspecific areas of right hemispheric\nperiventricular white matter T2/FLAIR hyperintensity are unchanged. The major\nintracranial vascular flow voids are preserved. The paranasal sinuses and\nmastoid air cells are clear. There is re- demonstration of several foci of\nencephalomalacia in the cerebellum from prior infarcts.",
            "output": "1. Mild interval increase in a size of centrally necrotic, rim enhancing left\ntemporoparietal lesion to 48 x 46 x 49 mm.  There has been interval increase\nin surrounding edema with associated increased mass effect now with 8 mm of\nrightward midline shift.  Basal cisterns remain patent and there is no\ndownward herniation.\n2. No new enhancing lesions.\n3. Chronic bihemispheric cerebellar infarcts."
        },
        {
            "input": "Again seen is a rim enhancing mass within the left parietal region adjacent to\nthe left lateral ventricle which overall demonstrates decreased peripheral\nenhancement and has decreased in size measuring 3.7 x 3.9 cm previously 4.6 x\n4.8 cm. Compared to the prior exam there has also decreased mass effect only 2\nmm of rightward shift of the normally midline structures. The degree of edema\nhas also decreased although some edema does persist within the left\nfrontoparietal region. The mass demonstrates peripheral restricted diffusion\nsimilar to the previous exam which in the absence of antiangiogenic therapy\ncan be an ominous sign.\n\nNonspecific FLAIR and T2 hyperintensity in the periventricular and deep white\nmatter is nonspecific. Areas of encephalomalacia are unchanged likely sequela\nof prior infarcts. The intracranial flow voids are preserved. There is mild\nmucosal thickening in the ethmoid air cells. The remainder of the paranasal\nsinuses are clear. Bone marrow signal within is within normal limits. The\norbits are unremarkable.",
            "output": "1. Decreased in size and peripheral enhancement of the left parietal mass.\nDecreased mass effect and edema since the prior exam. These findings may be\ndue to Avastin therapy or actual tumor response.\n2. No new enhancing lesions."
        },
        {
            "input": "There is a left parietal peripherally T1 hyperintense lesion adjacent to the\nleft lateral ventricle that measures 3.1 x 3.9 cm, slightly decreased in size\nfrom ___ (10:15).  There is likely some degree of peripheral\nenhancement at the anterior margin of the lesion, though assessment is\ndifficult to assess due to intrinsic T1 hyperintense signal (10:14).  There is\nslight interval decrease in the surrounding FLAIR hyperintensity. There are\nalso periventricular and deep white matter FLAIR/ T2 hyperintensities, which\nare nonspecific but may be due to chronic small vessel ischemic disease or\npost-treatment changes. Bilateral cerebellar infarcts are again noted, and a\nstable right occipital area of susceptibility artifact is again seen (6:11).\n\nThere is no new enhancing lesion or mass, hemorrhage or infarct. The principal\nvascular flow voids are patent. The paranasal sinuses and mastoid air cells\nare clear. The globes are intact.",
            "output": "1.  Slight interval decrease in size and surrounding FLAIR hyperintensity of\nthe left parietal lesion.  Otherwise, no significant change.\n2.  No new enhancing lesions.\n3.  Chronic bilateral cerebellar infarcts."
        },
        {
            "input": "An area of diffusion abnormality is again seen in the left parietal region\nwith and surrounding T1 pre gadolinium hyper intensity.  Mild surrounding\nFLAIR hyperintensities are identified.  Overall the configuration and size of\nthe diffusion and FLAIR abnormalities as well as T1 abnormalities have\nremained unchanged compared to the previous MRI of ___.  No new areas\nlamina enhancement or signal abnormalities are seen.  There FLAIR\nhyperintensities extending to the left cerebral peduncle likely representing\nWallerian degeneration.",
            "output": "Stable left parietal changes compared to the previous MRI examination.  No new\nareas of signal abnormalities or enhancement seen."
        },
        {
            "input": "3.2 x 3.1 x 3.3 cm (AP, TRV, SI) left parietal periventricular white matter\nfocus of diffusion-weighted hyperintensity demonstrating peripheral nodular\nenhancement and gradient echo susceptibility is essentially unchanged in size\nand configuration from exam dating back to ___.  Enhancing component\nof the lesion along its inferior aspects at the level of the superior temporal\nlobe, appear slightly more prominent on MPRAGE postcontrast sequences on\ntoday's exam (series 19, image 46) but is unchanged on T1 postcontrast turbo\nspin echo sequences.  It is felt that the MPRAGE findings are likely secondary\nto differences in technique and timing.  The degree of surrounding FLAIR\nhyperintense white matter signal is also unchanged.  Again identified is FLAIR\nhyperintensity extending along the left cerebral peduncle into the pons\ncompatible with wallerian degeneration.\n\nNo new abnormal diffusion-weighted hyperintense signal, enhancing lesions for\nFLAIR abnormality identified.  Gradient echo susceptibility of the right\noccipital lobe (series 14, image 13) is unchanged from prior exam compatible\nwith micro hemorrhage.  Prior cerebellar infarcts are unchanged from prior\nexam.  Superimposed periventricular and subcortical T2/FLAIR white matter\nhyperintensities are identified, which may represent any combination of\nposttreatment changes and small vessel ischemic disease.  No acute\nintracranial hemorrhage or acute infarct.  The major intracranial flow voids\nare preserved.  The dural venous sinuses are patent.  The paranasal sinuses\nare essentially clear.  The orbits are unremarkable.  The mastoid air cells\nare clear.  Left posterior parietal burr hole is identified, sequela of prior\nbiopsy.",
            "output": "1. Essentially stable size of left parietal posttreatment changes when\ncompared to MRI examination dating back to ___, as described above. \nOnly on MPRAGE postcontrast sequences, there is suggestion of subtly increased\nprominence of punctate nodular enhancement along the inferior periphery of the\nlesion at the level of the temporal lobe when compared to the prior exams,\nwhich is felt most likely to represent differences in technique.  However,\nclose attention on followup examination is recommended to document stability\nand exclude disease progression.\n2. No new enhancement or areas of signal abnormality.  Additional chronic\nfindings as described above."
        },
        {
            "input": "3.6x3.8x4.3 cm TRV x AP x CC lesion in the left temporal/parietal lobe in the\nperiatrial area of the left ventricle (04:13) is unchanged in size allowing\nfor differences in slice selection and technique.  As before there is central\nrestricted diffusion and a peripheral rim of intrinsic T1 hyperintensity which\nlikely corresponds to mineralization/calcificaiton seen on recent CT of the\nhead. As before there is equivocal nodular enhancement at the inferior aspect.\n\nSurrounding white matter FLAIR hyperintensities appear unchanged. There is a\nbackground of diffuse periventricular white matter FLAIR hyperintensities\nbilaterally (06:15).\n\nThere is apparent new 12 x 9 mm area with peripheral enhancement in the region\nof the splenium of the corpus callosum (10:14) with minimal associated\ndiffusion restriction extending to the interventricular septum.\n\nThere is an unchanged small focus of susceptibility in the right occipital\nlobe, possibly microhemorrhage.  Areas of encephalomalacia from prior\ncerebellar infarcts re- demonstrated.  Persistent FLAIR hyperintensity\nextending along the left cerebral peduncle into the pons is compatible with\nWallerian degeneration.\n\nThere is no evidence of acute intracranial hemorrhage or infarct.  The basal\ncisterns are clear.  The major intracranial vessel flow voids are preserved.\nThe dural venous sinuses appear patent.  The partially imaged paranasal\nsinuses are grossly clear.",
            "output": "1. Unchanged appearance of left periatrial mass/post treatment changes with\nequivocal nodular enhancement at the inferior border of the lesion. \nPersistent restricted diffusion in the ___ the lesion, in the setting of\nAvastin, is suspicious for pseudo-response.\n2. Apparent new 12 x 9 mm area of peripheral enhancement and faint diffusion\nrestriction in the splenium of the corpus callosum is worrisome for a possible\nnew focus of malignancy.  Close attention on followup is recommended.\n\nNOTIFICATION:  The impression and recommendation above was entered by Dr. ___\n___ on ___ at 14:50 into the Department of Radiology critical\ncommunications system for direct communication to the referring provider."
        },
        {
            "input": "There is stable confluent T2/FLAIR hyperintense signal in the left frontal\nparietal lobe extending into the left occipital and temporal lobe.  Extension\nis also noted in to the posterior left thalamus and cerebral peduncle.  In\naddition, scattered T2/FLAIR hyperintense signal abnormality is noted in the\ncontralateral cerebral hemisphere.  There is intrinsic T1 hyperintense signal\nalong the periphery of the 2.8 cm TR x 3.6 cm SI left ___ atrial lesion with\nquestionable mild contrast enhancement along the anterior inferior margin. \nThis region demonstrates stable restricted diffusion.  In addition, there is\nincreased prominence of the faint intrinsic T1 hyperintense signal and\nprobable peripheral contrast enhancement in the splenium of the corpus\ncallosum with increased size of associated restricted diffusion.\n\nThere is no evidence of hemorrhage, mass effect, midline shift or infarction. \nThere is prominence of the ventricles and sulci suggestive involutional\nchanges.  There is focal encephalomalacia in the left cerebellar hemisphere\nfrom prior infarctions.  There is a stable focus of susceptibility in the\nright occipital lobe.\n\nThe orbits, mastoid air cells the visualized soft tissues are normal.  Mild\nmucosal thickening along the medial left maxillary sinus is partially\nvisualized.\n\nDegenerative changes are noted in the upper cervical spine.",
            "output": "1. Stable appearance of the left periatrial lesion with questionable faint\nperipheral enhancement along the anterior/inferior margin with internal\nrestricted diffusion which may represent post treatment changes versus\nresidual disease.\n2. Increased prominence of the lesion in the splenium of the corpus collosum\nwith internal restricted diffusion and questionable faint peripheral contrast\nenhancement raising concern for progressive disease.\n3. Stable abnormal high signal surrounding the lesion extending into the\nposterior thalamus into the cerebral peduncle, likely representing\nposttreatment changes/Wallerian degeneration."
        },
        {
            "input": "There is motion artifact which significantly degrades spatial resolution.\n\nThere is a peripherally T1 hyperintense lesion within the periatrial white\nmatter extending to the left posterior superior temporal gyrus and the supra\nmarginal gyrus measuring 3.9 cm AP x 4.6 cm SI x 3.2 cm AP (3:6; 04:16).  This\nis relatively unchanged comparison to the prior study.  The remainder of the\nparenchymal T1 signal is unremarkable and demonstrate grossly normal\nmorphology.  There is a small wedge-shaped defect within the left cerebellar\nhemisphere, consistent with an unchanged remote infarction.  There is mild ex\nvacuo dilatation of the left lateral ventricle.  The marrow signal is\nunremarkable.  The soft tissues are unremarkable.",
            "output": "1. Limited study due to patient agitation with only sagittal T1 and axial T1\nweighted sequences acquired.  Significant motion artifact significantly\ndegrades spatial resolution.\n2. Within these limitations, the left periatrial lesion is relatively\nunchanged comparison to prior study by its T1 characteristics.  Recommend\ncompletion MR of the brain when patient can tolerate imaging.\n\nRECOMMENDATION(S):  Recommend completion of brain MRI when patient can\ntolerate imaging."
        },
        {
            "input": "Examination is limited by motion artifact.  Redemonstrated is post treatment\nchange in the left parietal lobe with associated rim enhancement, high FLAIR\nsignal, and hemosiderin deposition.  A punctate focus of enhancement in this\nregion (1000:84) is stable.   Slightly more superiorly along the posterior\ninsular cortex, a 4 mm enhancing focus is more prominent compared to the prior\nexamination (1000:89).  This may be artifactual given the that the images are\nmoderately degraded by motion artifact, but recurrence cannot be excluded. \nThe distribution of FLAIR signal abnormality is unchanged.  Additional\nscattered periventricular, subcortical, and deep white matter foci of\nincreased FLAIR signal without enhancement are grossly unchanged, likely\nsequelae of chronic microangiopathy.  The ventricles are stable.  Major\nintracranial vascular flow voids are preserved.  Intracranial arteries and\ndural venous sinuses enhance normally on postcontrast MPRAGE sequences.",
            "output": "The study is moderately degraded by motion artifact.  Posttreatment changes in\nthe left parietal lobe are grossly similar compared to prior examination,\nhowever a nodular focus of enhancement along the left posterior insula is\nslightly more prominent as compared to the prior examination.  This could be\ndue to motion artifact however close follow-up and attention to this area on\nsubsequent imaging is recommended."
        },
        {
            "input": "The limited obtain sequences are severely limited by motion.  Again identified\nis a left temporoparietal region with a rim of intrinsic T1 hyperintensity,\nwhich grossly appears similar to the precontrast sequence from ___. \nAccurate size measurements are difficult to ascertain given motion\nlimitations.  This region again demonstrates associated slowed diffusion. \nThere is suggestion of slowed diffusion leading to the splenium of the corpus\ncallosum, which is somewhat more apparent than compared to the prior exam. \nThe ventricles and sulci appear prominent, unchanged compared to the prior\nexamination.",
            "output": "1. Please note this is an incomplete examination with only partial acquisition\nof a few of the pre contrast sequences which are severely motion degraded.\n2. Left temporoparietal lesion appears grossly similar to the ___\nexamination, however, confident assessment for stability and/or interval\nchange cannot be performed due to severe motion artifact and lack of post\ngadolinium images.\n\nRECOMMENDATION(S):  Recommend repeating the examination when patient is better\nable to tolerate."
        },
        {
            "input": "Correlating with lesion seen on noncontrast head CT is a dural-based avidly\nenhancing extra-axial mass involving the anterior aspect of the falx in the\ninterhemispheric fissure on the right. It measures 1.5 cm AP x 1.2 cm TRV x\n2.2 cm cc. This is most compatible with a meningioma.  Given differences in\ntechnique, there has been no significant interval change. There is no\nadditional lesion identified.\n\nThere are scattered periventricular, subcortical white matter and pontine\nFLAIR/ T2 hyperintensities which are likely sequela of chronic small vessel\ndisease. There is no acute infarct or mass. There is no hemorrhage. Prominence\nof the ventricles and sulci is compatible global volume loss. Major\nintravascular flow voids including within the major dural venous sinuses are\npreserved.\n\nPost contrast images demonstrate no other abnormal parenchymal or meningeal\nenhancement.\n\nFluid seen within the mastoids bilaterally. Postoperative changes of\nendoscopic sinus surgery are noted.",
            "output": "1.  Unchanged enhancing extra-axial dural-based mass most compatible with\nmeningioma.\n2. Changes suggesting chronic small vessel disease. Otherwise unremarkable MRI\nof the brain."
        },
        {
            "input": "In comparison with the most recent MRI examination, again there is a right\nfrontal avidly enhancingextra-axial dural-based mass, likely consistent with\nmeningioma, attached to the anterior aspect of the falx, measuring\napproximately 13 x 21 mm in sagittal projection and 9 x 14 mm in transverse\ndimension, with no evidence of edema or significant mass effect.  Again\nscattered foci of high signal intensity are re- demonstrated in the pons,\nsubcortical and periventricular white matter, which are nonspecific and may\nreflect changes due to small vessel disease.  The ventricles and sulci appear\nunchanged and are slightly prominent, suggesting by cortical volume loss,\nlikely age related and involutional in nature.  No diffusion abnormalities are\ndetected.  The major vascular flow voids are present and demonstrate normal\ndistribution.  Again mild mucosal thickening is identified in mastoid air\ncells bilaterally, there is mild mucosal thickening in the sphenoid sinus on\nthe right, apparently new since the prior study.",
            "output": "1.  Unchanged avidly enhancing dural-based mass lesion,  attached to the dura\nalong the right median frontal region, likely consistent with meningioma,\nthere is no evidence of significant mass effect or edema surrounding this\nmass.\n\n2.  Unchanged foci of high signal intensity in the subcortical and\nperiventricular white matter, detected on FLAIR and T2 weighted images, which\nare nonspecific and may reflect changes due to small vessel disease."
        },
        {
            "input": "There is punctate slow diffusion in the right hippocampus, image 12 of series\n5 and 6, which can be seen with transient global amnesia.  Focus of\nenhancement along the right frontal calvarium with slow diffusion is noted,\nadjacent thinning and possible enhancement of the adjacent soft tissues. \nOtherwise, no diffusion abnormality is demonstrated.  There is no significant\nmedial temporal lobe atrophy or hippocampal volume loss.  There is no evidence\nof hemorrhage, edema, masses, mass effect, midline shift or infarction.   The\nventricles and sulci are normal in caliber and configuration.  There is\nmucosal thickening within the ethmoid air cells.",
            "output": "1. Slow diffusion in the right hippocampus can be seen with transient global\namnesia.\n2. Nonspecific enhancement in the right frontal calvarium possibly associated\nwith thinning of the adjacent soft tissues.  Please correlate with direct\ninspection."
        },
        {
            "input": "Postcontrast MP RAGE images are limited by motion artifact. Postcontrast axial\nT1 weighted spin echo images provide good diagnostic quality.\n\nThere is no evidence for intra-axial or extra-axial enhancing lesions, and no\nabnormal pachymeningeal or leptomeningeal contrast enhancement, to suggest\nintracranial metastatic disease. There is no evidence for edema, mass effect,\nblood products, or abnormal diffusion in the brain parenchyma. Numerous small\nfoci of high T2 signal are again seen in the subcortical, deep, and\nperiventricular white matter of the cerebral hemispheres, nonspecific but\nlikely sequela of chronic small vessel ischemic disease in a patient of this\nage. A small chronic infarct is again seen in the left putamen on image 9:15.\nProminent perivascular spaces are also again seen in the basal ganglia. Major\nvascular flow voids are grossly preserved. Ventricles, sulci, and basal\ncisterns are normal in size for age.\n\nRight mastoid tip air cells are partially opacified.",
            "output": "No evidence for intracranial metastatic disease."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  There is mild prominence of the ventricles and sulci\nconsistent with age-appropriate involutional changes.  There is no abnormal\nenhancement after contrast administration.  Nonspecific periventricular T2\nwhite matter hyperintensities likely reflect sequela of chronic small vessel\nischemic disease.",
            "output": "1. No evidence of metastatic disease."
        },
        {
            "input": "Study is mildly degraded by motion.  Evaluation for intracranial metastatic\ndisease is limited due to lack of intravenous contrast administration.\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.\n\nThere is bilateral lateral ventricle and cerebral sulci enlargement consistent\nwith age related global involutional changes, similar from prior head CTs. \nPeriventricular and deep white matter T2/FLAIR hyperintensities are\nnonspecific, but most likely reflect chronic small vessel ischemic changes.\n\nFlow voids of the major intracranial vasculature are preserved.  Incidental\nnoting of a right dominant vertebrobasilar system.\n\nThere is mild mucosal thickening of the anterior ethmoid sinuses.  Trace\nnonspecific left mastoid fluid is seen.  Patient is status post bilateral lens\nreplacement.",
            "output": "1.  Study is mildly degraded by motion and limited for evaluation of\nintracranial metastatic disease due to the lack of administration of\nintravenous contrast.  Please note that contrast was not administered due to\npatient refusal of intravenous contrast.\n2. No acute intracranial abnormality, with no definite evidence of acute or\nsubacute infarct.\n3. Within limits of this motion degraded noncontrast brain MRI, no definite\nevidence of intracranial mass.\n4.  Atrophyand probable small vessel ischemic changes as described.\n5.  Paranasal sinus disease and trace nonspecific left mastoid fluid, as\ndescribed."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  Periventricular and subcortical white matter and pontine\nT2/FLAIR hyperintensities are nonspecific but likely sequelae of chronic small\nvessel ischemic disease.  The ventricles and sulci are prominent, indicative\nof involutional change. The major intracranial flow voids are preserved.",
            "output": "1. No evidence of mass, hemorrhage or invarction.\n2. No evidence of metastasis.\n3. Atrophy and probable small vessel ischemic changes are stable."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, or infarction.\nThe ventricles and sulci are dilated in an atrophic pattern. There is\nextensive periventricular white matter hyperintensities on the FLAIR images\nsuggesting chronic small vessel ischemia. Again noted is a cavum septum\npellucidum and vergae",
            "output": "Atrophy and periventricular white matter hyperintensities on FLAIR as\ndescribed above. No evidence of hemorrhage or infarction."
        },
        {
            "input": "Areas slow diffusion are seen involving the left frontal lobe and left\noccipital lobe, with correlating FLAIR hyperintense signal suggesting late\nacute versus early subacute infarcts.\n\nThere is no evidence of hemorrhage, mass, mass effect, edema or midline shift.\nThe ventricles and sulci are mildly prominent.  There is gross preservation of\nthe principal intracranial vascular flow voids.\n\nTrace mucosal thickening is seen within scattered ethmoid air cells.  The\nremainder of the visualized paranasal sinuses, middle ear cavities, and\nmastoid air cells are well aerated and clear.  The orbits are within normal\nlimits bilaterally.",
            "output": "1. Late acute versus early subacute infarcts involving the left frontal and\nleft occipital lobes.\n2. No evidence of hemorrhage.\n3. Mild global parenchymal volume loss."
        },
        {
            "input": "MRI BRAIN:\nThere is slow diffusion surrounding the left paracentral gyrus with associated\nFLAIR hyperintensity.  There is no evidence of intracranial hemorrhage.  There\nis mild diffuse parenchymal volume loss.  There is moderate nonspecific\nperiventricular subcortical FLAIR hyperintensities, likely a sequela of\nchronic small vessel ischemic disease.  There is a focus of chronic infarction\nin the left midbrain (8:8).  The ventricles are normal in size without mass\neffect or midline shift.  The major visualized arterial vascular flow voids\nare preserved.  There is mild mucosal thickening of the bilateral ethmoid air\ncells.  There is a 1.3 x 1.2 cm cystic lesion within the left nasal cavity\nanteriorly demonstrating intrinsic T1 and T2 hyperintensity with layering\nhemorrhagic content, likely representing a nasolabial cyst with proteinaceous\ncontent.\n\nMRA BRAIN:\nThe bilateral intracranial internal carotid arteries and vertebral arteries in\nthe principal intracranial branches appear patent without stenosis, occlusion,\nor aneurysm.\n\nMRA NECK:\nThe bilateral common carotid arteries and internal carotid arteries appear\npatent without internal carotid artery stenosis by NASCET criteria.  The\nbilateral vertebral arteries appear patent.  The bilateral visualized\nsubclavian arteries and origins of great vessels appear patent.",
            "output": "1. Acute to early subacute infarction in the left paracentral gyrus.\n2. No evidence of intracranial hemorrhage.\n3. Diffuse parenchymal volume loss with moderate chronic small vessel ischemic\ndisease.\n4. Focus of chronic infarction in the left midbrain.\n5. 1.3 cm left nasal labial proteinaceous cyst with hemorrhagic content.\n6. MRA brain demonstrates no stenosis, occlusion, or aneurysm of the major\nintracranial branches.\n7. MRA neck demonstrates patency of the bilateral common and internal carotid\narteries and the vertebral arteries.\n\nNOTIFICATION:  The findings were discussed with ___, M.D. by\n___, M.D. on the telephone on ___ at 9:11 am, 2\nminutes after discovery of the findings."
        },
        {
            "input": "MRI HEAD:\nThere is no hemorrhage, infarction, mass effect, masses, midline shift, edema,\nor extra-axial fluid collection.  The ventricles and sulci are normal in size\nand configuration.  The bifrontal volume loss is unchanged.  There is no\nabnormal enhancement.\n\nThe paranasal sinuses and mastoid air cells are clear.  The orbits are\nunremarkable.\n\nThe major intracranial flow voids are preserved.\n\nMRV: Normal flow signal is demonstrated within the superior sagittal sinus,\nstraight sinus, transverse sinuses, and sigmoid sinuses. The jugular bulbs and\nproximal jugular veins are patent. Evaluation of the deep venous systems\nreveals normal flow signal in the internal cerebral veins.",
            "output": "1. No dural venous sinus thrombosis.\n2. No acute intracranial abnormality."
        },
        {
            "input": "MRI BRAIN:\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  There is no abnormal enhancement after contrast\nadministration.  No significant change in mild bifrontal volume loss. The\nventricles and sulci are normal in caliber and configuration. The major\nintracranial vascular flow voids are maintained.  There is mild mucosal\nthickening of the ethmoid air cells. The mastoid air cells and orbits are\nnormal.\n\nMRA brain: The intracranial vertebral and internal carotid arteries and their\nmajor branches appear normal without evidence of stenosis, occlusion, or\naneurysm formation.\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline\nshiftorinfarction.",
            "output": "1. No acute intracranial abnormality.  Specifically, no evidence for dural\nvenous thrombosis.\n2. Patent Circle of ___ without evidence of significant stenosis.\n3. Mild inflammatory changes of the ethmoid air cells.\n4. Unchanged mild bifrontal volume loss."
        },
        {
            "input": "MR BRAIN: There is a posterior paramedian left frontoparietal mixed cystic and\nsolid mass, containing an enhancing nodularity measuring 1.1 cm TV x 1.2 cm AP\nx 1.1 cm SI (___).  There is slight susceptibility artifact\nposterior to this lesion concerning for by blood fluid level (see 18:17).  The\nenhancing nodular component is suggested to demonstrate minimal slow diffusion\n(see 1000, 1002: 33).\n\nA right frontal developmental venous anomaly (17:144).  Otherwise, there is no\nadditional enhancing mass or abnormal enhancement.  There is no evidence of\ninfarction, or other areas of hemorrhage.  The ventricles are normal in size. \nThe major visualized arterial vascular flow voids are preserved.\n\nThere is mild mucosal thickening of bilateral ethmoid air cells.  The\nbilateral mastoid air cells appear clear.\n\nMR CONTRAST PERFUSION: There is enhancing nodularity within the medial aspect\nof the lesion measuring 1.1 cm TV x 1.2 cm AP x 1.1 cm SI (___),\ndemonstrating relative cerebral blood volume similar to white matter (see\n1500:14).\n\nASL PERFUSION: There is decreased cerebral blood flow associated with the left\nfrontoparietal lesion (see 1200:21).\n\nMR SPECTROSCOPY: In the region of the lesion, multi voxel MR spectroscopy is\nnondiagnostic.  Single voxel spectroscopy suggests minimal inversion of\ncholine to creatinine ratio, with preserved NAD creatinine ratio (see 998:45;\n99b:46).",
            "output": "1. Grossly stable left frontoparietal cystic mass with enhancing nodular\ncomponent and associated blood products, without definite increased perfusion\nand nondiagnostic spectroscopy findings.  Differential considerations include\nneoplastic, infectious, and inflammatory etiologies.\n2. No additional enhancing mass or abnormal enhancement."
        },
        {
            "input": "Patient is status post interval parietal craniotomy and resection of a left\nparamedian frontoparietal mass with postoperative changes including scattered\nextra-axial pneumocephalus and trace extra-axial fluid collection.  There are\nblood products within the resection cavity, without definite abnormal\nenhancement to suggest residual tumor.  There is dural thickening and\nenhancement deep to the craniotomy site, likely postoperative.  There is no\nadditional enhancing mass or abnormal enhancement.\n\nThere is no evidence of infarction.  The ventricles are normal in size without\nmidline shift.  The major visualized arterial vascular flow voids are\npreserved.  There is mild mucosal thickening of ethmoid air cells and partial\nfluid opacification of bilateral mastoid air cells, likely reactive.",
            "output": "1. Status post interval resection of a left paramedian frontoparietal mass\nwith blood products in the resection cavity.  No evidence of residual \nenhancement ."
        },
        {
            "input": "There is further interval decrease in the degree of enhancement and\nhyperintense signal on T2/FLAIR within the left posterior cingulate gyrus\nsurgical resection bed.  The left parietal craniotomy is noted.\n\nThe ventricles, sulci, and cisterns appear normal.  There is benign\ndevelopmental venous anomaly in the right frontal lobe, stable since prior. \nPunctate focus of enhancement versus is artifact at the right precentral gyrus\naxial MP rage image 113, attention on follow-up exam is recommended, no\nassociated T2 signal abnormality; not definitely seen on priors.  There is no\nother parenchymal signal abnormality or abnormal enhancement.  There is no\nacute infarct, intracranial hemorrhage, or mass effect.  The major vascular\nflow voids are preserved.\n\nThe orbits unremarkable.\n\nThere is a mucous retention cyst within the left maxillary sinus.",
            "output": "Improved enhancement and T2/FLAIR signal abnormality at the surgical bed.\n\nPunctate focus of enhancement versus artifact right precentral gyrus,\nattention on follow-up exam is recommended.\n\nRECOMMENDATION(S):  Continued follow-up per oncologic protocol."
        },
        {
            "input": "The residual postsurgical FLAIR hyperintense changes in the area of the left\nsub parietal sulcus/posterior left cingulate gyrus demonstrates continued\ninterval improvement compared to prior.  There is no residual enhancement on\nthe T1 MP rage imaging.  Postsurgical changes in relation to the posterior\naspect of the left parietal skull vault and underlying dura is unchanged.  The\nadjacent dural venous sinuses patent.\n\nPreviously noted punctate foci of enhancement present in the right precentral\ngyrus (series 1000, image 129) is less conspicuous compared to prior imaging. \nThere is benign developmental is venous anomaly in the right frontal lobe,\nstable.\n\nThe craniocervical junction is normal.  Partially empty sella.  Small\narachnoid cyst in relation to the anterior aspect of the left middle cranial\nfossa appear similar compared to prior.\n\nThe rest of the findings are unchanged.",
            "output": "Interval improvement at surgical bed, no new enhancement."
        },
        {
            "input": "MRI BRAIN:\n\nThere is a acute infarction in the right middle cerebral artery territory,\nincluding the lentiform nucleus, the body of the caudate, the insular cortex,\nthe frontal lobe, in the anterior parietal lobe including the postcentral\ngyrus.  There also small foci of acute infarction in the left frontal white\nmatter (images 4:22, 4:19), and in the left anterior insular cortex (image\n4:17).  There is no evidence of hemorrhagic conversion.  The body of the right\nlateral ventricle is mildly effaced.  There is no shift of midline structures\nand no mass effect on the basal cisterns.\n\nElsewhere in the brain parenchyma, foci of high T2 signal in the subcortical,\ndeep, and periventricular white matter are nonspecific but likely sequela of\nchronic small vessel ischemic disease in this age group.  Prominent ventricles\nand sulci are consistent with mild age-related involutional changes.\n\nNo osseous abnormality identified. The imaged paranasal sinuses, mastoid air\ncells and middle ear cavities are clear. Visualized portions of the orbits are\nunremarkable.\n\nMRA NECK:\n\nImages at the level of the aortic arch, proximal common carotid arteries, and\nV1 segments of the vertebral arteries are substantially degraded by artifacts.\nV2 and V3 segment of the vertebral arteries demonstrate no evidence for\nflow-limiting stenosis.  There is no evidence for carotid stenosis by NASCET\ncriteria.\n\nMRA BRAIN:\n\nImages are limited by motion artifact.\n\nThere is abrupt cutoff of flow within the right internal carotid artery\nterminus.  No flow is seen in the right middle cerebral artery, and there is\nno evidence for distal reconstitution.  There is also no flow in the proximal\nA1 segment of the right anterior cerebral artery.  Flow in the mid/distal A1\nsegment and A2 segment of the right anterior cerebral artery is less robust\nthan on the left.  The anterior communicating artery is likely patent, though\ndoes not well seen due to motion artifact.  No flow-limiting stenosis is seen\nin the left internal carotid or middle cerebral arteries allowing for motion\nartifact.\n\nNo flow-limiting stenosis is seen in the vertebral and basilar arteries. \nThere is fetal configuration of the right posterior cerebral artery.  Flow in\nproximal P2 segments of bilateral posterior cerebral arteries appears\ndiminished, which may be due to atherosclerosis or motion artifact.  Left ___\na and right AICA are visualized.  Bilateral superior cerebellar arteries are\nonly faintly seen proximally.\n\n3D time-of-flight images demonstrate less flow in the distal cervical and\npetrous right internal carotid artery compared to the left, but this is\nrelated to motion artifact and tilt of the patient's head, as the distal\ncervical and petrous right internal carotid artery demonstrates no\nflow-limiting stenosis on the concurrent gadolinium enhanced neck MRA.\n\nEvaluation for an aneurysm is limited due to extensive motion artifact. \nDistal left anterior cerebral artery appears bulbous on images 9:150 and\n9:153.",
            "output": "1. Acute large right MCA territory infarct.  No evidence of hemorrhagic\nconversion.  Mild effacement of the body of the right lateral ventricle.  No\nshift of midline structures or cisternal compression.\n2. Small acute infarcts in the left frontal white matter and left anterior\ninsular cortex.\n3. Motion limited brain MRA demonstrates occlusion of the right internal\ncarotid artery terminus, occlusion of the right middle cerebral artery without\nevidence for distal reconstitution, and occlusion of the proximal A1 segment\nof the right anterior cerebral artery with diminished flow in the remaining\nright A1 segment and in the right A2 segment compared to the left.\n4. Diminished flow in proximal P2 segments of bilateral posterior cerebral\narteries may be due to atherosclerosis or motion artifact.\n5. Bulbous appearance of distal left anterior cerebral artery may be secondary\nto motion artifact, but evaluation for an aneurysm is limited.\n6. The aortic arch, proximal common carotid arteries, and V1 segments of the\nvertebral arteries are not adequately assessed on the neck MRA.  No evidence\nfor internal carotid stenosis by NASCET criteria.\n\nRECOMMENDATION(S):  CTA head should be considered to exclude distal left\nanterior cerebral artery aneurysm.\n\nNOTIFICATION:  The findings in impression items 1 and preliminary report of\nright MCA occlusion were discussed with ___, M.D. by ___\n___, M.D. on the telephone on ___ at approximately 12:30, 5 minutes\nafter discovery of the findings.\n\n The impression items 3 and 5, and the recommendation above, were discussed\nwith Dr.  ___ by Dr. ___ on the telephone on ___ at 2:16 pm, 10\nminutes after discovery of the findings."
        },
        {
            "input": "There are postoperative changes in the left frontal lobe after tumor\nresection. There is high signal intensity on the FLAIR images surrounding the\nsurgical site, unchanged since the ___ study.  A small amount of fluid in\nthe surgical cavity has decreased in volume since the previous study.  There\nis a minimal amount of enhancement along the posterior medial aspect of the\nsurgical cavity combine likely due to a postoperative enhancement.  There is\nno evidence of tumor progression.  No new lesions are detected.  No other\nareas of abnormal enhancement are noted. There is no evidence of infarction.",
            "output": "Slight decrease in the volume of fluid at the surgical site since the study of\n___. There are been no other significant changes status post\nresection of a left frontal neoplasm.  No evidence of tumor progression."
        },
        {
            "input": "Again seen are postsurgical changes after resection of a left frontal\nneoplasm.  There are no findings to suggest tumor recurrence. There is minimal\npostoperative enhancement at the surgical site.  There is FLAIR hyperintensity\nat the surgical site, unchanged since ___.  There is a small amount of\nhemorrhage at the surgical site, unchanged. The remainder of the brain appears\nnormal with no other findings to suggest tumor. There is no evidence of\ninfarction or hemorrhage.",
            "output": "Status post resection of left frontal lobe tumor, unchanged since ___.  No evidence of tumor progression."
        },
        {
            "input": "The patient is status post left frontal craniotomy resection of a left frontal\nlobe mass. There is unchanged appearance of encephalomalacia and gliosis of\nthe left frontal lobe with mild associated ex vacuo dilatation of the anterior\nhorn of the left lateral ventricle. There remains some mild dural thickening\nalong the resection site, without evidence of abnormal nodular enhancement or\nresidual enhancing mass lesion. The there is a single nonspecific T2/FLAIR\nwhite matter hyperintensity of the right posterior temporal lobe (series 8,\nimage 11) which is unchanged dating back to exam of ___. Allowing\nfor postsurgical changes, sulci, ventricles and cisterns are within expected\nlimits. The major intracranial flow voids are preserved. No evidence of acute\nhemorrhage or infarct. Mucous retention cysts in the left maxillary sinus is\nnoted. Otherwise remainder of the paranasal sinuses are essentially clear. The\norbits are unremarkable. The mastoid air cells are clear.",
            "output": "Unchanged appearance of left frontal craniotomy and resection bed without\nevidence of residual or recurrent tumor."
        },
        {
            "input": "There has been no significant interval change. There frontal postoperative\nchanges are identified. T2 hyperintensities.  Mild dural enhancement is\nidentified in this region with a small focus of enhancement adjacent to the\nleft side of the falx. This finding is essentially unchanged. There is no new\narea of enhancement or signal abnormality. No evidence of acute or chronic\nhemorrhage are identified. There is no midline shift mass effect or\nhydrocephalus. No acute infarcts are seen. Previously noted parotid gland\nlesion is less apparent on the current study.",
            "output": "No significant interval change since the previous MRI examinations.  No\nsignificant new abnormalities are seen."
        },
        {
            "input": "Patient is status post left frontal craniotomy with expected stable\npostsurgical changes including stable susceptibility artifact from hemosiderin\ndeposition and stable T2/FLAIR signal in the left frontal lobe. There is\nunchanged dural enhancement and an unchanged small focus of enhancement\nadjacent to the left side of the falx (series 17, image 19).  There is no new\nenhancement to suggest residual or recurrent tumor.\n\nThere has been a slight interval decrease in size and previously noted\nenhancing lesion in left parotid gland which measured 11 mm AP x 11 mm SI x 9\nmm TV and today measures 9 mm AP x 8 mm SI x 4 mm TV.  The morphology of this\nlesion has also changed now appearing more reniform rather than rounded as on\nprior studies suggesting that this finding represents an intra parotid lymph\nnode.\n\nThere is no evidence of acute infarction, midline shift, or mass effect. The\nventricles and sulci are stable in caliber and configuration. Major vascular\nflow voids are preserved. The orbits are unremarkable. The paranasal sinuses\nand mastoid air cells are clear.",
            "output": "Patient is status post left frontal craniotomy for prior astrocytoma resection\nwith stable post operative changes.  No new enhancement is identified."
        },
        {
            "input": "Left frontal craniotomy is identified. There hyperintensities and meningeal\nenhancement in the region again identified. There is no evidence of new signal\nabnormality or abnormal enhancement identified.  There is no mass effect,\nmidline shift or hydrocephalus.  The right posterior frontal developmental\nvenous anomaly is incidentally seen.",
            "output": "Stable appearance of postoperative changes in left frontal lobe.  No\nsignificant new abnormalities."
        },
        {
            "input": "The patient is status post left frontal craniotomy and resection of a left\nfrontal lobe mass.  Left frontal FLAIR hyperintense signal in the surgical\nsite well as mild overlying dural thickening and enhancement is unchanged from\nprior exams.  There is no evidence of residual nodular enhancement within the\nresection cavity.\n\nThere is no acute intracranial hemorrhage or infarct.  Allowing for\npostsurgical changes, sulci, ventricles cisterns are within expected limits. \nNo new lesions are identified.  Incidental note is made of stable right\nposterior frontal and right cerebellar developmental venous anomalies and a\nsmall pineal cyst.  The major intracranial flow voids are preserved.  The\ndural venous sinuses are patent.  The paranasal sinuses are clear. The orbits\nare unremarkable.  The mastoid air cells are clear.",
            "output": "Stable postoperative findings of the left frontal lobe without evidence of\ndisease progression."
        },
        {
            "input": "There have been no significant changes since the prior studies.  Again seen\nare postoperative changes after a left frontal craniotomy.  There is\nhyperintensity in the left frontal white matter on the FLAIR images at the\nsurgical site.  Considering the diagnosis, this likely represents a\ncombination of treatment effect and residual tumor.  There is no evidence of\ntumor progression.  There is no abnormal parenchymal enhancement after\ncontrast administration.  There is a focal area of unchanged dural thickening\nand enhancement underlying the surgical site.  There is no evidence of\nabnormal slow diffusion at the tumor bed.\nImages of the remainder of the brain appear normal with no other areas of mass\nor abnormal enhancement.",
            "output": "Stable appearance of left frontal postoperative change and presumed residual\ntumor.  No evidence of tumor progression."
        },
        {
            "input": "Postoperative changes are identified on the left frontal region.  FLAIR\nhyperintensities are seen.  No abnormal enhancement are identified.  There is\nno significant change.  There are no other focal abnormalities, acute infarcts\nmass effect hydrocephalus or abnormal enhancement.",
            "output": "Stable appearance of left frontal postoperative changes and FLAIR\nhyperintensities without enhancement compared with previous MRI examination. \nNo definite new abnormalities are seen."
        },
        {
            "input": "Postsurgical changes involve a left frontal craniotomy and resection of left\nfrontal mass.  Comparison is made to most recent examination dated ___.  Pachymeningeal thickening and enhancement subjacent to the\ncraniotomy site is stable.  There is no abnormal enhancement identified at the\nresection site.  T2 and FLAIR hyperintensities within the left frontal lobe\nare unchanged.  There is no abnormal diffusion or evidence of hemorrhage.\nHigh-signal within the bilateral parotid glands on the diffusion sequences are\nmost consistent with intra parotid lymph nodes.\n\nVentricles are stable in size and configuration. There is no shift of normally\nmidline structures. There is no effacement of basal cisterns.  There is no\nextra-axial fluid collection.\n\nMajor intracranial flow voids are preserved.  Dural sinuses are grossly patent\non the postcontrast MP rage sequence.",
            "output": "Stable appearance of left frontal postoperative changes and FLAIR\nhyperintensities. No new enhancement relative to most recent MR examination\ndated ___.  No acute abnormality."
        },
        {
            "input": "The piece patient is status post left frontal craniotomy for resection of left\nfrontal lobe mass.  Stable postoperative changes include FLAIR/T2 signal\nabnormality in the left frontal lobe with ex vacuo dilatation of the frontal\nhorn of left lateral ventricle.  Adjacent pachymeningeal thickening and\nenhancement is also stable.  There is no new or nodular enhancement concerning\nfor recurrence.\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are stable in caliber and\nconfiguration.  Multiple small oval foci of restricted diffusion the parotid\nglands bilaterally likely represent intraparotid lymph nodes.  There is no\nabnormal enhancement after contrast administration.  A very small right\nparietal developmental venous anomaly, a normal variant, is noted (series\n100b, image 123).  Mucosal thickening is noted on the right mastoid air cells,\napparently new since the prior exam.",
            "output": "1. Stable appearance of left frontal postoperative changes new or without\nconcerning enhancement.\n2. No acute intracranial abnormality.\n3. Mucosal thickening is noted in the right mastoid air cells, new since the\nprior exam."
        },
        {
            "input": "Left frontal postoperative changes and mild extra-axial meningeal enhancement\nare again identified.  FLAIR hyperintensities are seen in the left frontal\nlobe.  New since the prior study is rim enhancement along the anterior left\nlateral ventricle (10:15).  Given the duration of stability on prior scans,\nthis appears to suggest tumor recurrence.  There is no acute infarct mass\neffect or hydrocephalus seen.",
            "output": "1. New enhancement along the anterior horn of the lateral ventricles\nsuspicious for tumor progression.\n2. At that time of interpretation of this finding, a neuro oncology clinical\nnote suggests that the clinical team is aware of this finding."
        },
        {
            "input": "Postoperative changes in the left frontal region again identified.  FLAIR\nhyperintensities are seen in the left frontal region.  Subtle linear\nenhancement in the subependymal region of the anterior horn of the left\nlateral ventricle is again seen.  There is no significant interval change.  No\nacute infarcts are seen",
            "output": "Stable appearance compared to the prior study.  No new findings are\nidentified."
        },
        {
            "input": "Again postsurgical changes consistent with left frontal craniotomy are seen,\nin comparison with the most recent exam, there are stable postsurgical changes\nin the left frontal region including T2/FLAIR high-signal intensity and mild\nex vacuo dilatation of the left frontal ventricular horn.  There is an\nunchanged subtle linear of enhancement in the subependymal region of the left\nfrontal ventricular horn (image 17, series 6).  No diffusion abnormalities are\ndetected.  There is no evidence of intracranial hemorrhage.  The major\nvascular flow voids are present and demonstrate normal distribution. The\norbits are unremarkable, the paranasal sinuses and mastoid air cells are\nclear.  Unchanged foci of slow diffusion in both parotid glands, stable since\n___, suggestive of slightly prominent intraparotid lymph nodes.",
            "output": "1.  Stable appearance of the left frontal surgical cavity, and similar areas\nof encephalomalacia in the left frontal lobe consistent with posttreatment\nchanges.  There is no evidence of new lesions or new areas with abnormal\nenhancement.\n\n2.  Unchanged subtle linear enhancement adjacent to the left frontal\nsubependymal region."
        },
        {
            "input": "There are postoperative changes in the anteromedial left frontal lobe, with\nleft frontal craniotomy.  New enhancing 4.0 cm x 3.6 cm x 3.4 cm mass has\ndeveloped in the left frontal lobe white matter abutting left frontal horn,\nwith areas of intrinsic T1 signal shortening, consistent with blood products. \nThere is irregular, thick peripheral enhancement, with lack of central\nenhancement.  Extensive nonenhancing FLAIR hyperintensity has developed in the\nleft frontal lobe extending to the left precentral gyrus posteriorly, in the\ncentrum semiovale, corona radiata, external capsule, sub insula, upper basal\nganglia, anterior limb left internal capsule.  T2 signal partially extends\ninto the left corpus callosum, without extension across midline.  Left frontal\nhorn is nearly obliterated.  There is 0.5 cm left-to-right midline shift, new\nsince prior suprasellar cistern is partially effaced.  There is no uncal\nherniation.  On preoperative exam from ___, primary brain tumor\nshows no enhancement.  There is mild dural enhancement overlying surgical\ncavity.  There are no other areas of abnormal enhancement.\nThere is no evidence of infarction.  There is no hydrocephalus.  Few small\nenhancing nodules are seen in the bilateral parotid glands, likely represent\nlymph nodes.  Intracranial vascular flow voids are preserved.  Dural venous\nsinuses are patent.",
            "output": "1. New 4 cm mass has developed in the left frontal lobe with thick peripheral\nenhancement and extensive surrounding nonenhancing FLAIR hyperintensity, and\nnew 0.5 cm left to right midline shift.  Differential considerations include\nradiation necrosis versus tumor progression.  MR spectroscopy, perfusion\nrecommended in further evaluation.\n\nRECOMMENDATION(S):  MR spectroscopy, MR perfusion including ASL and DSC\nperfusion.\n\nNOTIFICATION:  The impression and recommendation above was entered by Dr.\n___ on ___ at 16:43 into the Department of Radiology\ncritical communications system for direct communication to the referring\nprovider.\nAccording to clinical notes, clinical service is aware of the imaging findings\nat the time of interpretation."
        },
        {
            "input": "MR BRAIN: Right frontal craniotomy is re-identified with 3.7 x 3.2 (AP, TRV)\nperipherally enhancing lesion adjacent to the frontal horn of the left lateral\nventricle extending to the subependymal surface, and prominent surrounding\nfrontal edema pattern is overall similar to most recent prior examinations,\nwith minimal effacement of the frontal horn of the left lateral ventricle. \nAssociated peripheral rim of gradient echo susceptibility artifact compatible\nwith micro hemorrhages is similar from prior exam allowing for technical\ndifferences.  Diffusion-weighted hyperintense signal along the central aspect\nof the lesion is also unchanged.  Minimal 2 mm rightward midline shift is also\nessentially unchanged.  Mild dural thickening and enhancement with cystic\nencephalomalacic changes of the left anterior frontal lobe is also unchanged.\n\nThere is no acute infarct or intracranial hemorrhage.  Incidental note is made\nof a right precentral gyrus developmental venous anomaly (series 1200b, image\n112).  No new enhancing lesions are identified.  The major intracranial flow\nvoids are preserved.  The dural venous sinuses are patent on postcontrast\nMP-RAGE.  The orbits are unremarkable.  There is mild mucosal thickening of\nthe ethmoid air cells and maxillary sinuses.  No significant fluid signal is\nnoted in the mastoid tips.\n\nMR ___: No definite increased perfusion on dynamic contrasted\nsusceptibility.\n\nASL Perfusion: No definite increased perfusion on ASL.\n\nMR Spectroscopy: On single voxel spectroscopy, there is no elevated choline to\nNAA centered over the central portion of the peripherally enhancing lesion. \nOn multi voxel spectroscopy, there is overall paucity of metabolites with\nincreased lactate, compatible with posttreatment changes..",
            "output": "1. Re-identified is a 3.7 cm peripherally enhancing lesion adjacent to the\nfrontal horn of the left lateral ventricle, unchanged from prior examination\nof ___.  Surrounding FLAIR white matter edema pattern is also\nsimilar.\n2. There is no increased perfusion on the noncontrast susceptibility or ASL. \nMulti voxel spectroscopy demonstrates overall paucity of metabolites with\nminimally increased lactate.\n3. The overall findings are suggestive of radiation necrosis.\n4. Additional findings as described above.\n5. Continued follow-up is recommended."
        },
        {
            "input": "There is no acute infarction, edema, mass effect, evidence for blood products,\nor other signal abnormalities in the brain parenchyma.  The ventricles are\nnormal in size for age.  Extra-axial spaces in the supratentorial and\ninfratentorial compartments are prominent, suggesting parenchymal involutional\nchange.  The corpus callosum is mildly thin.  The cerebellar tonsils are\nnormally positioned.  Major intracranial vascular flow voids are grossly\npreserved.",
            "output": "1. No evidence for signal abnormalities in the brain parenchyma on noncontrast\nMRI.\n2. Mild global parenchymal involutional change."
        },
        {
            "input": "There is no evidence of acute infarction.  No intracranial hemorrhage. No\nmass, mass effect, edema or midline shift.\n\nThe ventricles and sulci are mildly prominent.  There is a right-sided\ndominant vertebral basilar system, with a diminutive left V4 segment, which is\nunchanged from ___.  Otherwise, the remainder of the principal intracranial\nvascular flow voids appear preserved.\n\nTrace mastoid fluid is seen bilaterally.  The remainder of the visualized\nparanasal sinuses and middle ear cavities are grossly clear.  The patient is\nstatus post bilateral lens replacement.",
            "output": "1. No evidence for acute intracranial hemorrhage or infarction.\n2. Age advanced, mild-to-moderate global parenchymal volume loss.\n3. Trace bilateral mastoid fluid.\n4. Additional findings, as above."
        },
        {
            "input": "There is chronic infarct in the right posterior cerebral artery distribution\ninvolving the occipital, parietal, and temporal lobes.  No acute infarct is\nseen.  Low GRE signal throughout this area is consistent with blood products,\nprobably chronic hemorrhage.  There is extensive tissue loss in this area. \nSmall chronic infarct in the left frontal lobe is also demonstrated.\n\nMild prominence of the ventricles and sulci suggestive of age-related volume\nloss.  Periventricular and subcortical T2 and flair hyperintensities are\nnonspecific but likely represent small vessel ischemic disease.\n\nThere is mild mucosal thickening of the ethmoidal air cells.  The maxillary\nsinuses and mastoid air cells are clear.  The orbits are unremarkable.",
            "output": "1. No acute infarct.\n2. Chronic infarct in the right posterior cerebral artery distribution\ncontaining blood products, likely chronic hemorrhage.  No mass effect or\nmidline shift."
        },
        {
            "input": "The ventricles and sulci are enlarged likely reflective of age related\nparenchymal volume loss. There is no evidence of hemorrhage, edema, masses,\nmass effect, or acute infarction. There is confluent T2/FLAIR signal\nhyperintensity in the periventricular, subcortical, and deep white matter\nwhich is nonspecific but likely on the basis of chronic small vessel ischemic\ndisease. There is also mild T2/FLAIR signal hyperintensity in the central pons\nwhich also is likely secondary to chronic small vessel ischemic disease. There\nis a more focal region of T2 hyperintensity in the pons (series 9, image 11)\ndisease which may reflect a prior region of infarction.  There are a few\nscattered foci of susceptibility artifact in the right insula, medial left\ntemporal lobe, palms, and right cerebellar hemisphere. There is a prominent\nCSF space intensity noted in the right aspect of the sella which may represent\na partially empty sella versus a sellar arachnoid cyst. Vascular flow voids\nare preserved. Patient is status post right lens replacement. There is mucosal\nthickening within the ethmoid air cells. The remaining paranasal sinuses are\nclear. There is a small amount of fluid in the right mastoid air cells.",
            "output": "1.  No evidence of acute infarction or acute hemorrhage.\n\n2.  Generalized parenchymal volume loss.\n\n3.  Confluent T2/FLAIR signal hyperintensity in the white matter of the\nbilateral cerebral hemispheres which is nonspecific but likely on the basis of\nchronic small vessel ischemic disease.\n\n4.  Multiple small foci of susceptibility artifact in the bilateral cerebral\nhemispheres and pons as detailed above. Findings may represent chronic\nmicrohemorrhage or amyloid angiography.\n\n5.  Slightly prominent empty sella versus arachnoid cyst. If clinical concern\nover this finding warrants, a dedicated MR of the pituitary gland could be\nobtained for further evaluation."
        },
        {
            "input": "There is a 3 mm T1 hyperintense structure in subarachnoid space of the right\nparietal lobe (10:20) with associated susceptibility artifact and FLAIR\nhyperintensity.\n\nSingle subcortical T2/FLAIR hyperintensity in the left frontal lobe without\nenhancement (07:26) is entirely nonspecific, potentially due to small vessel\ndisease.  Otherwise there is no focal parenchymal signal abnormality.  No\nabnormal enhancement.  There is no infarct, mass effect or midline shift. \nVentricles and sulci are age appropriate.  Major intravascular flow voids\nincluding within the major dural venous sinuses are preserved.\n\nNo abnormal signal in the paranasal sinuses or mastoids.",
            "output": "A focus of T1 and FLAIR hyperintensity with associated susceptibility on\ngradient echo sequences in the subarachnoid space of the right parietal lobe. \nExact etiology is uncertain, potentially calcification and unlikely to\nrepresent metastatic disease.  Consider unenhanced head CT for further\ncharacterization.  Otherwise unremarkable MRI of the brain."
        },
        {
            "input": "Previously noted focus of susceptibility artifact along the right parietal\ndura corresponds to a 5 mm dural calcification on recent CT examination\n(6:16), without evidence of contrast enhancement on MP RAGE images (10:139). \nThere is no evidence for an enhancing mass or abnormal meningeal contrast\nenhancement.  There is no evidence for edema, acute infarction, or new blood\nproducts.  Ventricles and sulci are normal in size.  A single punctate focus\nof left frontal subcortical white matter FLAIR hyperintensity is unchanged,\nnonspecific, though may reflect changes from chronic small vessel ischemic\ndisease (7:20).\n\nThe principal intracranial vascular flow voids are preserved.  Dural venous\nsinuses appear patent on postcontrast MP RAGE images.\n\nThis routine brain MRI is not optimized for detailed evaluation of the\ncavernous sinuses.  The cavernous sinuses appear normal in size without\nevidence for a large mass.",
            "output": "No evidence for intracranial metastatic disease.  5 mm right parietal dural\ncalcification versus completely calcified meningioma is stable.\n\nRECOMMENDATION(S):  If clinically warranted, a dedicated cavernous sinus\nprotocol MRI with fat-suppressed postcontrast images could better assess the\ncavernous sinuses."
        },
        {
            "input": "Numerous supratentorial periventricular enhancing lesions with low T2 signal\nand mildly slow diffusion are new compared to the prior examination. Signal\ncharacteristics and periventricular distribution are characteristic of\nlymphoma.  A lesion centered in the mid fornix measures approximately 15 x 10\nmm (___).  Other smaller enhancing lesions are noted within the\nfornix including a 4 x 3 mm lesion anteriorly (10:97) and a 5 x 2 mm lesion\nposteriorly (10:100).  A lesion in the left caudate body measures 10 x 7 mm\n(1000:101).  Another lesion abutting the left splenium of the corpus callosum\nmeasures 12 x 6 mm (1000:102).  There are left periatrial enhancing lesion\nwith the dominant lesion measuring 23 x 13 mm (1000:96); surrounding vasogenic\nedema causes effacement of the occipital horn of the left lateral ventricle. \nOther satellite enhancing lesions in the left periatrial region measures 6 mm\n(1000:99) 3 mm (1000:102) 5 mm (1000:101 and 2 mm (1000:94).  There also new\nareas of nodular periventricular/appended mole enhancement along the lateral\nventricles bilaterally, most prominent the frontal horns (09:13). 7 x 5 mm\nenhancing lesion is noted in the pineal gland (10:114).\n\nPunctate area of susceptibility artifact along the right parietal dura\ncorresponds to a 5 mm dural calcification on prior CT examination, and no\ndefinite correlate is seen on the postcontrast images.\n\nPunctate focus of high signal on diffusion in the right medial parietal cortex\n(___), lacks correlate on ADC map or FLAIR images.  It may represent a\npunctate subacute infarct or artifact.\n\nThere is no evidence of new blood products.  The background ventricles and\nsulci are normal in size for age.  The principal intracranial vascular flow\nvoids are preserved.",
            "output": "1. Numerous new supratentorial periventricular enhancing lesions, with\ndistribution and signal characteristics which are characteristic of lymphoma. \nThe dominant lesion in the left periatrial white matter is associated with\nedema, causing effacement of the occipital horn of left lateral ventricle.  No\nshift of midline structures.\n2. Punctate focus of high signal on diffusion tracer sequence in the right\nmedial parietal cortex without correlate on other sequences may represent a\npunctate subacute infarct or artifact.  If there is continued concern,\nshort-term follow up MRI may be helpful for differentiation.\n3. Unchanged 5 mm right parietal dural calcification versus calcified\nmeningioma."
        },
        {
            "input": "Study is moderately degraded by motion.  Within these confines:\n\nThere are multiple enhancing lesions demonstrating hypointense T2 signal with\nsurrounding FLAIR hyperintensity and mildly slow diffusion, as follow:\n-increase; 1.5 cm TV x 1.4 cm AP x 1.2 cm SI mid fornix (900:99), previously\n1.2 cm TV x 1.3 cm AP x 1.1 cm SI.\n-decrease; 0.5 cm TV x 0.7 cm AP x 0.4 cm SI adjacent to the tectum (900:89),\npreviously 0.7 cm TV x 0.8 cm AP x  0.6 cm SI.\n-decrease; 0.6 cm TV x 0.7 cm AP x 0.6 cm SI left caudate body (900:99),\npreviously 0.7 cm TV x 1.0 cm AP by 0.7 cm SI.\n-decrease; 0.9 cm TV x 0.6 cm AP x 0.7 cm SI adjacent to the splenium\n(900:100), previously 1.2 cm TV by 0.6 cm AP x 1.0 cm SI.\n-increase; 0.8 cm TV x 0.7 cm AP x 0.8 cm SI left periatrial lateral ventricle\n(900:95), previously 0.7 cm TV x  0.6 cm AP x 0.7 cm SI.  Additional left\nperiatrial enhancing nodule is not well visualized on this study.\n-decrease; 1.4 cm TV x 2.0 cm AP x 2.0 cm SI left occipital horn of the\nlateral ventricle (900:91), previously 1.4 cm TV x 2.4 cm AP x 2.3 cm SI.\n\nAgain seen is FLAIR hyperintensity surrounding the atrium and occipital horn\nof the left lateral ventricle with slight increase in FLAIR hyperintensity in\nthe splenium.  The left caudate body FLAIR hyperintensity has slightly\ndecreased.  Otherwise, there is no significant interval change.\n\nThe ventricles are normal in size without mass effect or midline shift. \nAdditional scattered foci of FLAIR hyperintensity within the periventricular\nsubcortical white matter is not significantly changed.\n\nThere is no evidence of infarction.  There is an unchanged right occipital GRE\nhypointense focus similar to the prior study, likely dural calcification\nversus calcified meningioma.  The paranasal sinuses and bilateral mastoid air\ncells appear clear.",
            "output": "1.  Study is moderately degraded by motion.\n2. Multiple enhancing intraparenchymal lesions likely related to known\nlymphoma, with mixed interval change in size and white matter changes, as\ndescribed above."
        },
        {
            "input": "Compared to prior MRI from ___, there is been significantly\ndecreased enhancement and size of the majority of the enhancing\nperiventricular enhancing lesions compatible with CNS lymphoma. \nRepresentative lesions are described below:\n\n-previously seen 1.5 x 1.4 x 1.2 cm mid fornix lesion has nearly resolved,\ndemonstrating trace associated subtle postcontrast enhancement (series 1000,\nimage 107).\n-0.5 x 0.5 x 0.3 cm lesion adjacent to the tectum (1000:94, 10:93) measured\n0.5 x 0.7 x 0.4 cm.\n-previously seen 0.6 x 0.7 x 0.6 cm left caudate body lesion has resolved.\n-0.5 x 0.7 x 0.7 cm lesion adjacent to the splenium (1000:106, 10:101)\npreviously measured 0.9 x 0.6 x 0.7 cm.  Moderate associated FLAIR\nhyperintensity associated with this lesion has slightly increased since prior\nexam (7:14).\n-previously seen distinct left periatrial and occipital horn lesions appear\nmore confluent, with the left periatrial component now measuring approximately\n1.2 x 1.0 x 1.6 cm, previously 0.8 x 0.7 x 0.8 cm (1000:99, 10:126) and the\nleft occipital horn lesion now measuring 1.0 x 0.5 x 1.0 cm (1000:100, 10:26),\nwith patchy enhancement along the ependymal surface.  The degree of FLAIR\nhyperintensity surrounding these two lesions has significantly improved since\nprior MRI from ___, now mild-to-moderate overall (___).\n\nNo new enhancing intraparenchymal lesions identified.\n\nThe ventricles are normal in size and configuration.  There is no mass effect\nor midline shift.  Basal cisterns remain non-compressed.\n\nScattered periventricular and subcortical white matter FLAIR hyperintensities\nare unchanged and likely reflect a chronic combination of posttreatment change\nand small vessel microangiopathy.\n\nThere is no evidence of infarction or hemorrhage.  Right occipital hypointense\nGRE focus, likely reflecting dural calcification versus calcified meningioma,\nunchanged over multiple prior exams.  The major intracranial flow voids are\npreserved.  The dural venous sinuses are patent on postcontrast MP-RAGE.\n\nNo osseous abnormality identified.  Extracranial soft tissues are grossly\nunremarkable.  There is mild mucosal thickening of the ethmoid air cells. \nOtherwise, the remainder the paranasal sinuses, mastoid air cells and middle\near cavities are clear.  The orbits are unremarkable.",
            "output": "1. Compared to prior MRI from ___, significant improvement in size\nor near-complete resolution of multiple enhancing periventricular lesions,\ncompatible with known lymphoma, with significantly decreased associated FLAIR\nedema pattern.\n2. Left periatrial and occipital horn lesions however are more confluent in\nnature, with the periatrial component larger in size when compared to prior\nexamination with patchy enhancement along the ependymal surface.  The degree\nof surrounding white matter FLAIR hyperintensity is significantly improved. \nThis may represent posttreatment change, however attention on followup is\nrecommended to exclude progression.\n3. No new enhancing lesions identified.\n\nNOTIFICATION:  The findings were discussed with ___, N.P. by\n___, M.D. on the telephone on ___ at 10:37 am, 3 minutes after\ndiscovery of findings, per request for wet read."
        },
        {
            "input": "Compared to most recent prior MRI there has been slightly increased\nenhancement of several periventricular lesions.  In particular:\n-lesion adjacent to the left occipital horn and left periventricular atrium,\nappears much more prominent and confluent with increased enhancement and\nmeasures 1.4 x 2.9 cm, previously up to 2.3 cm.  There is increased FLAIR\nsignal surrounding this lesion compared to the prior exam.\n-a lesion adjacent to the splenium measures 1.0 x 1.4 cm, previously up to 0.7\ncm.\n-lesion in the mid fornix shows increased enhancement and measures\napproximately 0.6 x 1.3 cm, previously only faintly visible on most recent\nprior.\n-lesion adjacent the tectum measures up to 0.5 cm, not significantly changed\nfrom prior\n-lesion anterior to the frontal horn of the left lateral ventricle is more\nprominent compared to prior and measures up to 0.7 cm\n\nThese lesions are not associated with significant mass effect. The ventricles\nand sulci are normal in size and configuration.\n\nRight occipital hypointense GRE focus is stable from prior exams.\n\nThere is no evidence of infarction.  The major intracranial flow voids are\npreserved.  The dural venous sinuses are patent on postcontrast images.   The\nbasal cisterns are patent.  The paranasal sinuses and bilateral mastoid air\ncells appear clear.",
            "output": "1. Interval increase in size and enhancement of several periventricular\nlymphoma lesions, compared to most recent prior exam.\n2. Increase in associated edema around the largest lesion near the left\noccipital horn and left periventricular atrium."
        },
        {
            "input": "Compared to the most recent prior exam from ___, there appears to be a\nchange in morphology and interval progression of the multiple intracranial\nlesions, with increased signal on the diffusion-weighted images.\n\n-along the body of the corpus callosum, a heterogeneously enhancing, FLAIR\nhyperintense mass has increased in size, as well as demonstrates increased\nFLAIR signal abnormality compared to the prior exam, now measuring 2.7 cm TRV\nby 2.4 cm AP by 1.3 cm cc, previously measuring up to 2 cm.  Increased signal\non the diffusion weighted images appears slightly progressed compared to the\nprior exam.\n\n-heterogeneously enhancing lesion along the periatrial region of the left\noccipital horn of the lateral ventricle, now appears less confluent and more\nheterogeneous with grossly stable surrounding FLAIR signal abnormality, with\nthe nodular enhancing components in aggregate measuring up to 4.2 cm TRV by\n2.7 cm AP by 3.5 cm cc, compared to the prior exam at which time this measured\nup to 2.1 cm in the craniocaudal dimension, series 800, image 90.\n\n-increased FLAIR signal abnormality and worsening heterogeneous, nodular\nenhancement is seen within the splenium of the corpus callosum, with increased\nsignal on the diffusion weighted images.\n\n-an enhancing lesion within the left genu of the corpus callosum measures 0.8\ncm, slightly increased in size compared to the prior exam from ___ now\nmeasuring up to 0.6 cm, with interval increase in surrounding FLAIR signal\nabnormality.\n\n-a focal area of nodular enhancement is seen within the left internal auditory\ncanal, series 800, image 61, is more conspicuous when compared to prior exam\nbut felt likely to represent venous structure.\n\n-an enhancing lesion adjacent to the tectum measures 0.4 cm, series 8 image\n111, unchanged compared to the prior exam.\n\n-ependymal enhancement along the occipital horn of the left lateral ventricle\nappears grossly similar compared to the prior exam, however demonstrates\nslight interval increase in the extent of slow diffusion.\n\nThere is unchanged nonenhancing 2 mm focus centered between the anterior and\nposterior pituitary, likely representing a Rathke's cleft cyst.\n\nThere is no evidence of acute intracranial infarction.  Ventricles and sulci\nare age appropriate.  Additional periventricular and deep subcortical FLAIR\nwhite matter hyperintensities are likely secondary to chronic microangiopathy.\nA right occipital hypointense focus likely reflects dural calcification versus\ncalcified meningioma.  The dural venous sinuses are patent postcontrast MPRAGE\nimages.  Mild mucosal sinus thickening is seen involving the ethmoid air\ncells.  The remainder of the visualized paranasal sinuses, mastoid air cells,\nand middle ear cavities are clear.  The globes are unremarkable.  The\nprincipal vascular flow voids appear to be well preserved.",
            "output": "1. Overall, compared to the most recent prior exam from ___, there\nappears to be slight interval progression of the heterogeneous multiple\nenhancing periventricular lesions, with interval increase in heterogeneity and\nsurrounding FLAIR signal abnormality.  Although this could be secondary to\nsequelae of post treatment changes, given the interval increased signal on the\ndiffusion weighted images of many of these lesions, progression of disease\nremains of concern.\n2. Focal area of nodular enhancement within the left internal auditory canal,\nappears new compared to the prior exam, may represent a venous structure. \nClose attention on followup is recommended.\n3. Stable 0.4 cm enhancing lesion adjacent to the tectum.\n4. Additional findings as described above."
        },
        {
            "input": "Compared to ___, there has been interval decrease in the multiple\nintracranial lesions that demonstrate enhancement and slow diffusion. For\nexample, the splenium of the corpus callosum demonstrated punctate foci of\nenhancement, previously showed 8 mm enhancing nodule on the right (900:91). \nSmall foci of enhancement in the periatrial region of the left occipital horn\nof the lateral ventricle measures up to 9 x 8 mm, previously 19 x 17 mm with\nnodular border, extending to the left splenium (900:84).  Small foci of\nenhancement in the body of the corpus callosum now measures up to 9 mm,\npreviously more confluent and nodular, measuring up to 17 mm (900:102).  Focus\nof enhancement in the genu of the corpus callosum has decreased, now\ndemonstrating more hypointensity (900:86).\n\nWhile T2/FLAIR hyperintensity surrounding the above-described lesions has,\nmild T2/FLAIR hyperintensity has increased in the midline and right genu of\nthe corpus callosum is new, image 7:15.\n\nEpendymal enhancement along the occipital horn of the left lateral ventricle\nhas decreased.\n\nPeripheral enhancement in the pineal region on image 9:128 is unchanged.\n\nThe left internal auditory canal linear enhancement is overall similar\n(900:57), thought to represent venous structure.\n\nNonenhancing millimetric focus between in the pituitary is thought to\nrepresent a Rathke's cleft cyst, unchanged (9:130).\n\nThere is no acute infarction.  Mild global parenchymal volume loss with\nprominent ventricles and sulci are again seen.  The major intracranial flow\nvoids are maintained.  The dural venous sinuses enhance normally on\npostcontrast MP RAGE images.\n\nThere is mild mucosal thickening of the ethmoid air cells.\n\nOvoid 13 mm enhancing nodule within the left parotid tail is unchanged,\ncompatible with an enlarged lymph node (900:19).",
            "output": "1. Multiple bilateral periventricular enhancing lesions corresponding to the\nknown lymphoma have decreased in size with decreased adjacent T2/FLAIR\nhyperintensity.\n2. While no new enhancing lesion is seen, there is mild new T2/FLAIR\nhyperintensity in the midline and right genu of the corpus callosum, of\nuncertain significance.\n3. Stable nonspecific peripheral enhancement in the pineal region.\n4. Stable nonenhancing focus in the central pituitary, compatible with a\nRathke's cleft cyst.\n5. Stable 13 mm enhancing left parotid tail nodule, compatible with an\nenlarged lymph node."
        },
        {
            "input": "Re-identified is masslike FLAIR hyperintensity involving the periventricular\nwhite matter of the occipital horn of the left lateral ventricle, crossing\nmidline at the splenium of the corpus callosum appears similar to the prior\nexamination demonstrating slowed diffusion.  Additional involvement of the\nbody of the corpus callosum and pericallosal white matter appearing slightly\ndecreased as compared to the prior examination, demonstrating associated\nslowed diffusion.  Additional involvement is seen in the periventricular white\nmatter of the frontal horn of the left lateral ventricle, extending to the\ngenu of the corpus callosum, which appears somewhat decreased as compared the\nprior examination.  Several nodular enhancing lesions in the left occipital\nperiventricular region have decreased in size, for example the largest\nenhancing lesion in this area measuring 8 x 5 mm previously measured 9 x 8 mm\n(900:94).  Additional punctate enhancing lesions adjacent to the frontal horn\nof the left lateral ventricle have also decreased in conspicuity as compared\nthe prior examination.  Additional enhancing lesions seen in the pericallosal\nwhite matter adjacent to the body have also decreased in conspicuity, for\nexample on the left a 7 x 2 mm enhancing component previously measured 10 x 5\nmm (900:109).\n\nThere is no evidence of hemorrhage, significant mass effect, midline shift or\ninfarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no new enhancing lesion.  The principal intracranial\nvascular flow voids are preserved.\n\n The visualized paranasal sinuses are grossly clear.  The orbits are grossly\nunremarkable.  There is nonspecific fluid opacification of a few right-sided\nmastoid air cells.  The left mastoid air cells are clear.",
            "output": "1. Masslike left posterior temporal and occipital periventricular white matter\nFLAIR signal abnormality with slowed diffusion crossing midline at the\nsplenium of the corpus callosum appears similar to the prior examination,\nthough with decrease of enhancing nodular components, in keeping with given\nhistory of CNS lymphoma.\n2. Additional involvement of the body of the corpus callosum and pericallosal\nwhite matter appears slightly decreased, with decrease of enhancing component.\n3. Additional involvement of the left frontal periventricular white matter\nwith extension to the genu of the corpus callosum has also decreased, with\ndecrease of enhancing component.\n4. Otherwise no infarct, hemorrhage, or new enhancing lesion."
        },
        {
            "input": "Multiple enhancing supratentorial cerebral parenchymal nodules are increased\nin number and size compared to prior with associated surrounding edema.  Many\nof these have a perivascular growth pattern that would be typical of lymphoma.\nFor example:\nLeft optic radiation enhancing lesion adjacent to the left occipital horn\ncurrently measures 9 x 9 mm previously measuring 8 x 5 mm.\nEnhancing nodule in the right splenium of the corpus callosum measures 6 mm in\ndiameter (previously ___ m).\nMarked T2 and FLAIR edema persists surrounding the left occipital horn as well\nas in the splenium of the corpus callosum with associated slow diffusion as\ndescribed below.\nIncreased ependymal enhancement in the posterior aspect of the left occipital\nhorn suggesting involvement of the ventricle.\nMultiple new enhancing nodules in the left frontal lobe adjacent to the left\nfrontal horn are increased in size and number.\nThe enhancing nodule in the body of the left corpus callosum is slightly\nincreased in size currently measuring 5 mm diameter.\nAreas of slow diffusion present in the splenium of the corpus callosum, in the\nleft ___ horn area as well as in the body of the left corpus\ncallosum.\nSlow diffusion in the left frotal lobe (___) as well as in the\nbody of the right corpus callosum appears improved compared to prior.\n\nThe paranasal sinuses are clear.  No orbital abnormalities.  No posterior\nfossa lesions.  No cerebellopontine angle masses.  No findings to suggest\nhydrocephalus.",
            "output": "1. Interval progression of multiple supratentorial enhancing lesions\ncompatible with the history of lymphoma.\n2. Areas of slow diffusion are again noted in the splenium of the corpus\ncallosum, body of left corpus callosum and left perirectal area, also typical\nof lymphoma."
        },
        {
            "input": "There is persistent sulcal enhancement within the left frontal and left\ncerebral hemispheres, not significantly changed when compared to prior exam. \nAdditionally, there is confluent T2/FLAIR signal hyperintensity/edema centered\npredominantly within the left parietal lobe which is increased when compared\nto prior exam.  There are foci of gradient signal hypointensity throughout the\nbilateral cerebral hemispheres indicating chronic microhemorrhage.  There is\nnew gradient signal hypointensity within the left parietal lobe, indicating\ninterval hemorrhage.  The overall appearance may represent metastatic disease\nversus amyloid angiopathy related inflammation, less likely sarcoid or\nlymphoma.\n\nThere are normal vascular flow voids.  There is no evidence of acute infarct\nbased on diffusion-weighted imaging.  Cerebral form foci of slow diffusion\nwithin the left cerebral hemisphere may be related to subarachnoid blood\nproducts.  There are additional punctate in confluent subcortical and\nperiventricular T2/FLAIR hyperintensities which are nonspecific though may\nrelate to sequelae of chronic small vessel ischemic disease.  There is diffuse\nbrain parenchymal volume loss.\n\nThe orbits, skull base, and paranasal sinuses appear unremarkable.",
            "output": "1. Persistent left cerebral hemisphere sulcal effacement with interval\nincrease and left frontal and left parietal lobe edema, subarachnoid blood\nproducts, and areas of more chronic micro-hemorrhage within the bilateral\ncerebral hemispheres, including a new focus within left parietal lobe.  The\noverall findings may represent metastatic disease versus amyloid angiopathy\nrelated inflammation, less likely sarcoid or lymphoma."
        },
        {
            "input": "There is a new area of slow diffusion seen within the medial right occipital\nlobe (4:9) in the PCA territory.  Several additional punctate areas of slow\ndiffusion within the posterior parietal lobe, right occipital lobe, and\nbilateral cerebellar hemispheres also appear new from the prior examination.\n\nThere is no large intracranial hemorrhage.  Several micro hemorrhages are seen\nwithin the cerebellar vermis (10:8), posterior left parietal lobe (10:12),\nright frontal operculum (10:15), and within the left middle cerebellar\npeduncle (10:6).  These appear relatively unchanged from the prior\nexamination.\n\nPatchy areas of T2/FLAIR hyperintensity within the bilateral periventricular\nwhite matter appears similar.  FLAIR hyperintensity is also seen within the\nright anterior paramedian frontal lobe, similar to the prior examination.\n\nThere is extensive leptomeningeal enhancement with associated FLAIR signal\nabnormality again seen coating the bilateral cerebellar hemispheres, overall\nsimilar to the previous examination.  Pachymeningeal enhancement is most\nprominent overlying the left frontoparietal convexity, and appears more\nconspicuous as compared to the previous examination.\n\nThe ventricles and sulci are prominent the basal cisterns are patent.  There\nis gross preservation of the principal intracranial vascular flow voids. The\ndural venous sinuses appear patent on MP-RAGE imagine sequences.\n\nMild mucosal thickening is seen within the right maxillary sinus and scattered\nethmoid air cells.  Fluid signal is seen within the bilateral mastoid air\ncells.  The remainder of the visualized paranasal sinuses, middle ear\ncavities, and mastoid air cells are well aerated and clear.  The patient is\nstatus post bilateral lens resections.",
            "output": "1. New, focus of slow diffusion within the right medial occipital lobe, with\nnumerous additional punctate areas of slow diffusion within the posterior\nright parietal lobe, right occipital lobe, and bilateral cerebellar\nhemispheres.  Findings are concerning for interval infarction, likely\nsecondary to vascular involvement of the patient's known meningitis.\n2. Multiple micro hemorrhages are stable from the prior examination.\n3. Increasingly prominent pachymeningeal enhancement, with a relatively stable\ndegree of leptomeningeal enhancement.  Findings are compatible with known\nunderlying meningitis, likely with the superimposed effect of multiple\ninterval lumbar punctures.\n4. Diffuse patchy T2/FLAIR signal abnormalities within the right frontal lobe\nand bilateral periventricular white matter.  These findings are minimally\nprogressed from the prior examination, and of uncertain etiology.  They may\nrepresent areas of active infection, a secondary superinfection, or treatment\nrelated effects.  Additional diagnostic considerations include missed prior\nwhite matter infarctions secondary to vasculitis in the setting of meningitis.\n\nNOTIFICATION:  Updated findings were conveyed by Dr. ___ to Dr. ___\nphone at 10:55 on ___, 2 minutes after discovery."
        },
        {
            "input": "There is an acute to subacute infarct along the right ACA territory. \nOtherwise, no evidence of hemorrhage, edema, masses, mass effect, or midline\nshift. Prominence of the ventricles and sulci are are compatible with age\nrelated involutional changes. Encephalomalacia and T2 signal abnormality is\nnoted in the left MCA territory, compatible with prior infarct. Mild\nperiventricular T2 signal abnormality is compatible with chronic sequela of\nischemic changes.  The visualized paranasal sinuses, mastoid air cells, and\nmiddle ear cavities appear grossly unopacified.  Patient is status post lens\nresections.",
            "output": "1. Acute to subacute infarct is seen in the right ACA territory.  No evidence\nof hemorrhagic conversion.\n2. Encephalomalacia and T2 signal abnormality seen in the left MCA territory\nis compatible with old prior infarct.\n\nNOTIFICATION:  The findings were discussed with ___, M.D. by ___\n___, M.D. on the telephone on ___ at 1:50 pm, 2 minutes after discovery\nof the findings.  Attempted to contact ED Resident, but she was unavailable\ndue to concurrent trauma arrival in ED."
        },
        {
            "input": "MRI BRAIN:\nThere is a T1 hyperintense T2 hypointense enhancing extra-axial collection\nwith restricted diffusion overlying the posterior right occipital convexity. \nThere is associated susceptibility artifact consistent with acute blood\nproducts.\n\nThere is a similar T1 isointense/T2 hypointense extra-axial collection\noverlying the left occipital convexity.  There is susceptibility artifact\nconsistent with blood products.\n\nThere is T2/FLAIR signal hyperintensity in the right medial frontal gyrus\nconsistent with encephalomalacia resulting from a chronic infarct in the right\nACA territory.  There is a similar area of partially cystic encephalomalacia\nwith T2/FLAIR hyperdensity in the left frontal and superior temporal lobes\nconsistent with a chronic infarct in the left MCA territory.  Small focus of\nsusceptibility artifact is in the superior left frontal lobe, likely\nrepresenting a small area of chronic hemorrhage.  There is a chronic infarct\nin the right cerebellar hemisphere.\n\nThere is a punctate area of susceptibility artifact in the superior right\ncerebellar hemisphere and numerous enhancing vessels overlying the folia of\nthe right cerebellar hemisphere, which likely represents a developmental\nvenous anomaly with a small cavernoma (110:68, 111:91).\n\nThere is no evidence of acute infarct, edema, midline shift or mass effect.\nThere are punctate and confluent regions of T2/FLAIR hyperintensity in the\nsubcortical, periventricular and deep white matter, which are nonspecific but\nlikely reflect chronic small vessel ischemic disease in this age group. \nVentricles and sulci are prominent, consistent with age-related global\nparenchymal loss.\n\nMRA BRAIN:\nThe intracranial vertebral and internal carotid arteries and their major\nbranches appear normal without evidence of occlusion.  A 2 mm aneurysm is seen\narising medially from the left ICA (___ 78).  There is mild stenosis of the\nhorizontal segment of the right MCA.  There is attenuation of the distal right\nanterior cerebral artery (101:8).  There is mild stenosis of the left P1\nsegment of the PCA; the distal left posterior cerebral artery is otherwise\npatent.  There is a fetal origin of the right posterior cerebral artery with a\nhypoplastic right P1 segment.\n\nMRA NECK:\nThere is mild-to-moderate stenosis at the origin of the right vertebral\nartery.  The origins of the great vessels, subclavian and left vertebral\narteries otherwise appear normal.  The common, internal and external carotid\narteries appear normal.  There is mild-to-moderate stenosis of the proximal\nleft internal carotid artery.",
            "output": "1. Extra-axial blood products overlying the bilateral occipital convexities,\nright greater than left, likely represent subarachnoid hemorrhage with a small\nsubdural component.  No evidence of aneurysm or vascular anomaly is noted in\nthis location.\n2. 2 mm aneurysm is seen arising from the medial aspect of the left ICA (___\n78).\n3. Chronic infarcts in the right anterior cerebral artery and left middle\ncerebral artery territories.  Small lacunar infarct in the right cerebellar\nhemisphere.\n4. Incidental note is made of a developmental venous anomaly and cavernoma in\nthe right cerebellar hemisphere.\n5. Mild stenosis in the horizontal segment of the right MCA.  There is\nattenuation of the distal right anterior cerebral artery.  No evidence of\naneurysm or occlusion in the ___.\n6. There is stenosis at the origin of the right vertebral artery.  Mild\nstenosis of the proximal left internal carotid artery.\n7. Additional findings as described above."
        },
        {
            "input": "There are multiple cortical foci of increased signal intensity on the\ndiffusion-weighted images in a watershed distribution between the left ACA and\nMCA territories (302:20 - 27). These correlate with small foci of decreased\napparent diffusion coefficient. There is marked T2 and FLAIR signal\nhyperintensity surrounding a region of encephalomalacia in the posterior left\nfrontal lobe (06:20). Periventricular and deep white matter FLAIR signal\nhyperintensities are compatible small-vessel ischemic disease. There is an\nisolated focus of signal loss within a posterior frontal lobe gyrus (07:22),\nbetter seen on the susceptibility weighted gradient echo images compared with\nspin echo images\n\nThere is no intracranial mass, mass effect, or midline shift. Ventricles and\nsulci are mildly enlarged.  Intracranial flow voids are maintained. Visualized\nparanasal sinuses and mastoid air cells are clear. Osseous and soft tissue\nstructures are unremarkable.",
            "output": "1. Multiple foci of ischemia in a left ACA - MCA watershed distribution\n2. Old left frontal infarct\n3. Isolated tiny focus of intraparenchymal hemorrhage in a posterior left\nfrontal gyrus might be related to the new or old ischemia"
        },
        {
            "input": "There is no evidence of hemorrhage, edema, mass, or acute infarction.  The\nventricles and sulci are age-appropriate.  There is no mass effect or midline\nshift.  There is no abnormal parenchymal, leptomeningeal, or pachymeningeal\nenhancement.  There is no partial empty sella.\n\nThe paranasal sinuses, mastoid air cells, and intraorbital contents are\nunremarkable.  No torturous optic nerve sheath complex is identified.  The\nmajor intracranial arterial flow voids are preserved.  The dural venous\nsinuses are patent.  There is mild narrowing of the bilateral transverse and\nsigmoid sinus junction.",
            "output": "1. Unremarkable MRI of the brain with no evidence of acute infarction,\nintracranial hemorrhage, or mass.\n2. There is mild narrowing of the bilateral transverse and sigmoid sinus\njunction, which may be associated with pseudotumor cerebri in the appropriate\nclinical setting.  However, no other secondary signs are identified including\nno partial empty sella and no tortuosity of the optic nerve sheath complexes."
        },
        {
            "input": "Carotid and vertebral arteries demonstrate normal flow signal. There is no\nevidence of vascular, stenosis or dissection. The. The thoracic aorta and its\nmajor branches also demonstrate normal appearances. The vertebral artery\nartery origins are patent.",
            "output": "No significant abnormalities are seen on MRA of the neck."
        },
        {
            "input": "The patient has undergone left frontal craniotomy.Again noted are\npost-treatment changes in the left frontal lobe and basal ganglia. This\nincludes encephalomalacia and ex vacuo dilatation of the left lateral\nventricle.  Susceptibility artifact within this region is from chronic blood\nproducts.  Extensive confluent white matter FLAIR hyperintensities are\nunchanged and consistent with prior radiation therapy and/or chronic small\nvessel ischemic disease.\n\nThere is no hemorrhage, mass effect, or evidence of acute infarction. The\nprincipal intracranial vascular flow voids are maintained. Following\ngadolinium administration, there is no  abnormal parenchymal, vascular, or\nmeningeal enhancement. The visualized paranasal sinuses are clear.",
            "output": "Stable post-treatment changes without evidence of residual or recurrent\ndisease."
        },
        {
            "input": "There has been no significant interval change. Postoperative changes are\nidentified in the left frontal region with an area of encephalomalacia and\ndiffuse hyperintensities. There is ex vacuo dilatation of the anterior horn of\nthe left lateral ventricle. There is moderate ventriculomegaly including\nprominence of temporal horns and sulci indicating brain atrophy. Following\ngadolinium no abnormal enhancement is identified. In particular, no abnormal\nenhancement is seen in the left frontal region. There are subtle foci of T1\nhyperintensity on post gadolinium images in both temporal lobes best\nvisualized on series 14, image 10 which appear to be due to pulsation\nartifacts as they are not visualized on the MPRAGE images.",
            "output": "No significant change from the previous MRI examination. No signs of recurrent\nmass lesion identified. Brain atrophy and small vessel disease.\nEncephalomalacia in the left frontal region."
        },
        {
            "input": "The postsurgical changes in the left frontal calvarium with a left frontal\nburr hole and a linear tract in the left frontal lobe related to prior biopsy\nare unchanged.  The encephalomalacia in the left frontal lobe and left basal\nganglia is unchanged.  There is associated ex vacuo dilatation of the frontal\nhorn and body of the left lateral ventricle, unchanged from prior.\n\nA new, intra-axial, oval T1 hypointense, T2 hypointense, enhancing lesion in\nthe right occipital lobe measures 3.3 x 2.0 by 2.5 cm.  Curvilinear\nenhancement extends from this lesion into the subependymal regions of the\noccipital horn of the right lateral ventricle.  Portions of this lesion\ndemonstrate slow diffusion.  This lesion is associated with extensive\nsurrounding edema and local mass effect with effacement of the sulci.  The\nedema in the right occipital lobe extends into the right parietotemporal lobes\nand effaces the occipital horn of the right lateral ventricle.  No other\nenhancing lesions are identified.\n\nThe confluent T2/FLAIR periventricular hyperintense signal in the left\nfrontoparietal and right frontal lobes are unchanged.\n\nThere is no evidence of hemorrhage, midline shift or infarction.\n\nThe paranasal sinuses and mastoid air cells are clear.  The orbits are\nunremarkable.\n\nThe major intracranial flow voids are preserved.",
            "output": "1. New enhancing right intra-axial lesion in the right occipital lobe with\nadjacent subependymal extension and associated local mass effect and edema,\nconsistent with recurrent lymphoma.\n2. Stable postsurgical changes in the left frontal lobe.\n\nNOTIFICATION:  The findings were discussed by Dr. ___ with ___\n___ RN on the telephoneon ___ at 4:12 ___, 20 minutes after discovery\nof the findings."
        },
        {
            "input": "Again seen are a left frontal burr hole and presumed biopsy site, extensive\nwhite matter hyperintensities on the T2 weighted images and a focus of\nhemorrhage adjacent to the dilated portion of the left lateral ventricle. \nAgain seen is chronic hemorrhage and enhancement along the occipital horn of\nthe right lateral ventricle.  These findings have not changed since the prior\nstudy.  No new lesions are detected.  No masses are detected.",
            "output": "1. Unchanged appearance of severe white matter hyperintensity, likely\ntreatment related, and residual enhancement along the occipital horn of the\nright lateral ventricle.  No evidence of new lesions or disease progression."
        },
        {
            "input": "The previously seen enhancing lesion in the right occipital lobe adjacent to\nthe occipital horn of the right lateral ventricle has decreased in size.  The\nadjacent subependymal enhancement although still present has also decreased. \nThe FLAIR hyperintensities have also decreased.\n\nThere is no change in appearance of encephalomalacia and postoperative changes\nin the left frontal lobe with ex vacuo dilatation.  No enhancing lesion is\nseen in this region.  There are no other areas of abnormal enhancement.  There\nis no midline shift or hydrocephalus.  There are no diffusion abnormalities.",
            "output": "Decrease in size of the enhancing lesion and surrounding edema in the right\noccipital lobe adjacent to the occipital horn with decrease in size of \nadjacent subependymal enhancement.  No new enhancing lesions are seen."
        },
        {
            "input": "Again seen is left frontal tissue loss with dilatation of the frontal horn of\nthe left lateral ventricle.  Again seen is extensive white matter\nhyperintensity on the T2 weighted images, presumably treatment related. Again\nseen is a focus of enhancement adjacent to the occipital horn of the right\nlateral ventricle.  The volume of enhancing material appears slightly greater\nthan on the study of ___.  There have been no other changes since the\nrecent prior studies.  However, the white matter abnormality on FLAIR imaging\nappears somewhat more extensive than in ___, particularly in the right\nhemisphere.\nAre identified.\nGeneralized ventricular prominence and sulcal prominence indicating atrophy\nappear stable across these examinations.  There is a small amount of chronic\nhemorrhage at the left frontal surgical site with no evidence of new\nhemorrhage.  There is no evidence of infarction.",
            "output": "1. Slight increase and enhancing material adjacent to the occipital horn of\nthe right lateral ventricle, presumably lymphoma.\n2. Gradually increase in the prominence of white matter hyperintensity on T2\nweighted images, most notable in the right hemisphere.\n3. No evidence of new lesions."
        },
        {
            "input": "MR BRAIN:  The study is moderately limited by motion.  Again, there are\npostsurgical changes from left frontal craniotomy and mass resection with\nassociated dilatation of the frontal horn of the left lateral ventricle. \nExtensive and diffuse white matter FLAIR hyperintensity is unchanged, likely\ntreatment related.  A 20 x 11 mm focus of enhancement adjacent to the\noccipital horn of the right lateral ventricle is unchanged compared to ___ (1200b:69).  In the region of the left parahippocampal gyrus, there is a\nnew 8 x 6 mm focus of enhancement demonstrating a rim of T2 hyperintensity\nwith suspected diffusion restriction (1200b:61).\n\nThere is no evidence of acute hemorrhage,  mass effect, midline shift or\ninfarction.  Prominence of the ventricles and sulci is unchanged compared to\nthe prior examination, related atrophy.  Paranasal sinuses are grossly clear. \nThe principal intracranial vascular flow voids are preserved.\n\nMR ___: Contrast perfusion images are limited however\ndemonstrate no definite increased blood flow to either of the above described\nenhancing lesions..\n\nASL Perfusion: ASL perfusion images demonstrate no definite increased\nperfusion to either of the above described enhancing lesions..\n\nMR Spectroscopy: Single and multi voxel spectroscopy was obtained for the\nright occipital lesion demonstrating no abnormal metabolite peak.  Note that\nspectroscopy was not performed on the new left parahippocampal gyrus lesion..",
            "output": "1. New 8 mm enhancing lesion in the left parahippocampal gyrus without\nincreased perfusion, concerning for lymphoma recurrence.\n2. Stable 20 mm enhancing lesion adjacent to the occipital bone of the right\nlateral ventricle demonstrating inconclusive metabolites peak on MR\nspectroscopy without increased profusion.  While MR spectroscopy suggests\nagainst malignant etiologies such as high-grade glioma, this lesions still\nlikely represents lymphoma, particularly with interval development of a new\nlesion.\n3. Stable postsurgical changes from left frontal craniotomy and mass\nresection.\n4. Stable diffuse white matter FLAIR hyperintensities, likely representing\nposttreatment change."
        },
        {
            "input": "There are stable postsurgical changes from left frontal craniotomy and mass\nresection with associated ex vacuo dilatation of the frontal horn of the left\nlateral ventricle.  There is no residual or recurrent enhancement in the\nresection bed.\n\n9 x 6 mm homogeneously enhancing lesion in the region of the left\nparahippocampal gyrus is minimally increased in size compared to the prior\nexamination where it measured 7 x 6 mm (1000:94).\n\nHeterogeneously rim enhancing 31 x 21 mm right periatrial lesion has\nintervally increased in size, previously measuring roughly 21 x 11 mm\n(1000:101).  There are scattered areas of slowed diffusion within this mass,\nand there is extension of this mass to the right splenium of the corpus\ncallosum, new compared to the prior examination.  There has been prominent\ninterval increase in surrounding vasogenic edema, with increased localized\nmass effect with effacement of the occipital horn of the right lateral\nventricle.  No new enhancing mass is identified.\n\nThere is no evidence of hemorrhage, midline shift or infarction.  Moderate\nventriculomegaly is unchanged compared to prior examination.  Diffuse areas of\nwhite matter T2/FLAIR hyperintensity are unchanged compared the prior\nexamination, with the exception of increased edema around the right periatrial\nlesion.  The principal intracranial vascular flow voids are preserved.\n\nThe visualized paranasal sinuses are grossly clear.  The orbits are grossly\nunremarkable.",
            "output": "1. Prominent interval increase in size of a 31 x 21 mm heterogeneously\nenhancing right periatrial lesion with extension to the right splenium of the\ncorpus callosum, with areas of internal diffusion restriction and prominent\nincrease in surrounding vasogenic edema and localized mass effect.  Given\nappearance, this may represent either progressive lymphoma, or radiation\nnecrosis.\n2. Minimal interval increase in size of a homogeneously enhancing lesion in\nthe region of the left parahippocampal gyrus.\n3. No new enhancing mass, or infarct.\n4. Diffuse white matter signal abnormality, likely representing posttreatment\nchange."
        },
        {
            "input": "MR BRAIN:  Limited obtained FLAIR sequence again demonstrates postsurgical\nchange from left frontal craniotomy and mass resection.  Prominent ventricles\nand sulci are unchanged in size and configuration from prior examination. \nThere is unchanged ex vacuo dilatation of the frontal horn of the left lateral\nventricle.  Diffuse areas of white matter T2/FLAIR hyperintensity are once\nagain demonstrated.  A heterogeneous area of surrounding the occipital horn of\nthe right lateral ventricle corresponds to area of enhancement on the recent\nprior examination.\n.\nASL Perfusion: Perfusion images are limited by motion, however demonstrate\nquestionable areas of increased perfusion in area of enhancing lesion.\n\nMR Spectroscopy: Single voxel spectroscopy demonstrates mildly increased\ncholine peak in the areas of enhancement in bilateral periatrial white matter.\nMulti voxel spectroscopy in area of right periatrial enhancement demonstrates\nmildly elevated choline peak, decreased NAA peak, and prominently elevated\nlipid peak.",
            "output": "1. Area of right periatrial enhancement as seen on prior examination\ndemonstrates questionable increased perfusion with metabolites profile most\nsuggestive of recurrent/progressive lymphoma.\n2. Area of left periatrial enhancement demonstrates nonspecific metabolites\nprofile, though likely also represents recurrent/progressive lymphoma, given\nfindings elsewhere in the brain."
        },
        {
            "input": "The patient is status post left frontal craniotomy.  Ex vacuo dilatation of\nthe left lateral ventricle with encephalomalacia in the left frontal\nperiventricular white matter and left basal ganglia is stable from prior\nexamination.  Diffuse left greater than right frontal parietal white matter\nedema pattern is similar to prior examination.\n\nThere is a new ring-enhancing 6 mm lesion of the right frontal lobe (series 4,\nimage 70) demonstrating slow diffusion.  Periventricular region of nodular\nenhancement along the right occipital horn measuring approximately 3.2 x 2.1\ncm is similar in size to prior examination, with increased central\nhypoenhancement and decreased peripheral rind of nodular enhancement. \nAssociated diffusion-weighted hyperintense signal is now confluent.  There is\ndecreased size of left ___ enhancement measuring approximately 9 mm,\nalong the posterior insula (series 4, image 54).\n\nIncidental note is made of a partial empty sella.  The dural venous sinuses\nare patent on postcontrast MP-RAGE.",
            "output": "1. There is new ring-enhancing 6 mm lesion of the right frontal lobe (series\n4, image 70) with associated slow diffusion.\n2. Right periventricular lesion is grossly unchanged in size measuring\napproximately 3.2 cm, with decreased peripheral enhancement.  However, there\nis now avid confluent slow diffusion centrally, concerning for progression.\n3. Decreased enhancement and size of left periatrial lesion, now measuring\napproximately 9 mm."
        },
        {
            "input": "MR BRAIN:\nThe patient is status post left frontal craniotomy with a linear track within\nthe left frontal lobe with adjacent encephalomalacia and ex vacuo dilatation\nof the left lateral ventricle.\n\nThere is interval decrease in enhancing left temporal periatrial lesion,\nmeasuring 0.6 x 0.4 cm (1100b:60), previously 0.9 x 0.7 cm.\n\nThere is unchanged right frontal lobe ring-enhancing lesion measuring 0.8 x\n0.6 cm with corresponding slow diffusion and incomplete peripheral rim of\nsusceptibility artifact.\n\nThere is unchanged peripherally enhancing right periventricular\nparietal/occipital lesion measuring 3.2 x 2.6 cm contiguous with the occipital\nhorn of the right lateral ventricle, with unchanged confluent slow diffusion\nand peripheral rim of susceptibility artifact.  Surrounding T2 hyperintensity\nhas decreased compared to ___.\n\nConfluent T2 hyperintensity elsewhere in the cerebral hemispheres is similar\nin extent compared to ___.  There is unchanged diffuse parenchymal\nvolume loss with prominence of the ventricles, sulci, and cisterns.  There is\nno evidence for acute infarction or new blood products.\n\nThe dural venous sinuses appear patent. The principal intracranial vascular\nflow voids are preserved.\n\nThere is mild mucosal thickening in the ethmoid air cells.\n\nMR CONTRAST PERFUSION:\n\nThere is no evidence for increased cerebral blood volume in the region of the\ncerebral lesions.\n\nASL PERFUSION:\n\nThere is no evidence for increased perfusion in the region of the cerebral\nlesions.\n\nMR SPECTROSCOPY:\n\nThe multi voxel spectroscopy in the right periatrial region demonstrates\nmarkedly elevated NAA, without increased choline to NAA ratio (series 1600).\n\nSingle voxel spectroscopy in the right frontal and left temporal lobe\ndemonstrate no elevated choline to NAA peak (series 99).",
            "output": "1. Slight interval decrease in enhancing left temporal periatrial enhancing\nlesion.  No evidence for increased MR perfusion or abnormal single voxel MR\nspectroscopy.\n2. Stable size of rim enhancing right periventricular parietal/occipital\nlesion, with decreased surrounding T2 signal abnormality compared to ___.  No increased MR perfusion.  While slow diffusion in the setting of\nAvastin use could indicate viable tumor, multi voxel MR spectroscopy\ndemonstrates no evidence for tumor.\n3. Stable small rim enhancing right frontal lesion.   No evidence for\nincreased MR perfusion or abnormal single voxel MR spectroscopy.\n4. No evidence of new enhancing lesions."
        },
        {
            "input": "MR BRAIN: The examination is mildly to moderately motion degraded.  Within\nthis confine:\n\nLeft frontal craniotomy and underlying left frontal lobe encephalomalacia with\nex vacuo dilatation of the left lateral ventricle is unchanged from prior\nexamination.  Confluent bihemispheric white matter FLAIR hyperintensity is\noverall similar in appearance to examination ___ allowing for\nmotion degradation, compatible with a combination of posttreatment change and\nchronic small vessel ischemic disease.\n\nSuperimposed FLAIR hyperintense signal of the right periatrial white matter\nappears mildly more confluent, involving more of the lingual gyrus, compared\nto prior examination allowing for differences in patient angulation, measuring\napproximately 2.5 x 2.5 cm (series 10, image 13).  Associated\ndiffusion-weighted hyperintense signal appears slightly more prominent and\nconfluent along the inferior aspects when compared to the prior examination.\n\nDiffusion-weighted hyperintense signal associated with a previously described\nring-enhancing right frontal corona radiata lesion is less conspicuous when\ncompared to prior exam (series 502, image 21).  No new diffusion-weighted\nhyperintense signal.\n\nNo new hemorrhage product is identified.  Hemosiderin within the left basal\nganglia biopsy bed is unchanged.  The major intracranial flow voids are\npreserved.  Mild mucosal thickening of the ethmoid air cells identified.  The\norbits are unremarkable.  Minimal fluid signal is noted in the mastoid tips. \nNo focal suspicious marrow lesion.\n\nMR ___: MRI perfusion study is nondiagnostic secondary to lack\nof IV contrast.\n\nASL Perfusion: Motion degraded examination without definitive evidence of\nincreased perfusion.",
            "output": "1. No postcontrast sequences or spectroscopy performed as the examination was\nterminated early secondary to patient request.\n2. Right periatrial white matter FLAIR hyperintense signal appears slightly\nmore confluent when compared to prior examination of ___, with\noverall minimally increased STIR hyperintense signal along its inferior\naspects.  While this may represent posttreatment effect and differences in\ntechnique, diffusion-weighted hyperintense signal in the setting of Avastin\ncould represent pseudo response and close interval follow-up, with\ncontrast-enhanced study and spectroscopy is recommended.\n3. Overall decreased diffusion-weighted hyperintense signal associated with a\npreviously described right frontal corona radiata ring-enhancing lesion.  No\nnew regions of diffusion-weighted hyperintense signal identified.\n4. No definite increased perfusion on motion degraded ASL.\n5. Additional findings described above.\n\nRECOMMENDATION(S):   Recommend repeat examination with pre and post axial T1,\npostcontrast MP-RAGE, DSC and MRI spectroscopy is recommended for more\ndefinitive comparison to prior examination."
        },
        {
            "input": "There is small focus of mildly increased signal on diffusion weighted images\nin the right Corona radiata, less conspicuous compared with ___,\nwith associated mild enhancement, which has improved since ___. \nThere is 2.9 cm x 2.5 cm right periatrial masslike FLAIR abnormality, with\nintermediate T2 signal, compared with 2.8 cm x 2.5 cm on ___. \nThere is associated zone of periventricular restricted diffusion.  Enhancement\nseen on ___ has significantly improved with minimal residual\ndiscontinuous enhancement on today's exam, with some intrinsic T1\nhyperintensity evident on pre gadolinium images.  Previously seen small focus\nof enhancement posterior to the left insula has nearly resolved, without\nassociated restricted diffusion on today's scan.  There is generalized brain\nparenchymal atrophy.  There are extensive confluent T2 signal abnormalities in\nbilateral cerebral hemispheres, likely posttreatment change.  Postoperative\nchange of prior left frontal drain placement with focus of encephalomalacia\nalong the drain tract.  There is stable chronic infarct in the left basal\nganglia.\nThere is no evidence of new mass or infarct.  No new enhancing abnormalities. \nParanasal sinuses, mastoid air cells are clear.  Preserved intracranial\nvascular flow voids.",
            "output": "1. There has been near resolution of right periatrial enhancement since ___.  Persistent stable periatrial FLAIR masslike hyperintensity and\nassociated restricted diffusion may be treatment related or pseudo response,\nand is unchanged since ___.\n2. Interval decrease of small focus of enhancement in the right Corona\nradiata, and near resolved small focus of enhancement posterior to the left\ninsula.\n3. Extensive confluent parenchymal T2 hyperintensities, likely treatment\nrelated.  Chronic encephalomalacia left frontal lobe, with chronic left basal\nganglia infarct, stable.\n4. No new infarcts."
        },
        {
            "input": "When compared to previous exam, there has been no significant interval change.\nMasslike FLAIR hyperintensity in the periatrial white matter of the right\nlateral ventricle with associated restricted diffusion is unchanged.  There is\nno associated enhancement noting slight associated peripheral T1\nhyperintensity on the precontrast exam.\n\nPreviously seen enhancing focus in the corona radiata on the right is no\nlonger enhancing the faint punctate focus of high signal on diffusion remains.\n\nLeft frontal encephalomalacia and left basal ganglia lacunar infarcts are\nchronic.  Extensive periventricular and subcortical white matter T2/FLAIR\nhyperintensities are again noted.  Enlargement of the ventricles and sulci is\ncompatible global volume loss.\n\nMajor intravascular flow voids are preserved.\n\nVisualized paranasal sinuses and mastoid air cells are clear.",
            "output": "1. No significant interval change since prior.  Right periatrial masslike\nFLAIR hyperintensity with associated restricted diffusion but no enhancement. \nNo progression of disease or new lesion.\n2. Interval resolution of previously seen enhancing focus in the corona\nradiata on the right."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.\nThere is redemonstration of extensive confluent T2/FLAIR hyperintensities in\nthe cerebral hemispheres bilaterally and in the pons, a nonspecific finding\nbut similar in extent to the prior CT and likely related to severe chronic\nsmall vessel ischemic changes.\nThere is no abnormal enhancement after contrast administration.\n\nThere is generalized parenchymal volume loss which is most likely age related.\nProminence of the ventricular system and extra-axial CSF spaces appears\nsimilar to prior and is consistent with the previously mentioned parenchymal\nvolume loss.\nMajor vascular flow voids appear preserved.  Major dural venous sinuses are\npatent.\n\nThere is mild mucosal thickening along the ethmoid air cells and in the right\nmaxillary sinus.  There is trace fluid in the left mastoid air cells.",
            "output": "1. No evidence of infarction, hemorrhage or mass.\n2. Unchanged extensive confluent white matter changes the cerebral hemispheres\nbilaterally and in the pons, nonspecific but most likely related to severe\nchronic microangiopathy."
        },
        {
            "input": "There is geographic slow diffusion involving the right frontal operculum and\nright insular cortices.  There are numerous small punctate foci of slow\ndiffusion within the right temporo-occipital cortex (___).  There small\nfoci of slow diffusion within the posterior right external capsule and\nanterior limb right internal capsule (302:17, 14).  There is correlate FLAIR\nhyperintensity and mild mass effect correspond next to the sites of slow\ndiffusion, without evidence of hemorrhage.\n\nThere are background periventricular and subcortical white matter FLAIR\nhyperintense foci, likely representing sequela of chronic microangiopathy. \nThe ventricles and cortical sulci are normal in caliber and configuration. \nThe extra-axial spaces are unremarkable.  The vascular flow voids are\npreserved.\n\nThe orbits, calvarium, and soft tissues are unremarkable.  There is mild\nmucosal thickening within the paranasal sinuses with a left maxillary mucous\nretention cysts.  The mastoid air cells and middle ears are clear.",
            "output": "1. Territorial acute infarction involving the right frontal operculum and\ninsular cortices corresponding to the middle cerebral artery.\n2. Numerous punctate infarcts involving the right temporo-occipital cortex. \nPunctate infarcts involving the right anterior limb internal capsule and\nposterior external capsule.  No evidence of hemorrhagic conversion.  The\nparietal infarcts may be in watershed distribution.\n3. Background sequela chronic microangiopathy."
        },
        {
            "input": "There is a partially calcified vein running adjacent to the corpus callosum\nand anterior to the vein of ___, which is patent and empties at the junction\nof the vein ___ and ___ sinus.  This represents a developmental\nanomaly and correlates to the curvilinear hyperdensity seen on prior CT head\ndated ___.  The vein ___ and bilateral internal cerebral veins,\nas well as the straight, inferior, and superior sagittal sinuses are patent\nwithout evidence of thrombosis.  There is no evidence of an AVM.  There is no\nevidence of hemorrhage, edema, masses, mass effect, midline shift or\ninfarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.",
            "output": "1. Partially calcified, patent vein anterior to the vein ___ correlates\nto the abnormality seen on head CT dated ___ and likely represents a\ndevelopmental anomaly.\n2. No evidence of thrombus in the major intracranial veins and sinuses.\n3. No evidence of hemorrhage, mass, or infarction."
        },
        {
            "input": "The bilateral common,internal carotid, and external carotid arteries appear\nnormal.  There is no evidence of stenosis of the internal carotid arteries\nbilaterally, by NASCET criteria.\n\nThe origins of the great vessels, subclavian, and vertebral arteries appear\nnormal bilaterally.  The common carotid bifurcations appear normal.",
            "output": "1. No evidence of stenosis of the internal carotid arteries bilaterally.\n2. The vertebral arteries bilaterally are unremarkable."
        },
        {
            "input": "Multiple foci of bilateral, slightly more prominent on the left, hemispheric\nfrontal and parietal cortical, white matter and splenium of the corpus\ncallosum diffusion-weighted hyperintensity with associated ADC hypointensity,\nsome of which demonstrate pseudo normalization compatible with late acute to\nsubacute infarcts of multiple vascular distribution are identified.  Similar\nfindings of the bilateral cerebellar hemispheres are noted.  The largest\ninfarcts are along the bilateral ACA territory and can be seen on prior CT\nexaminations.\n\nFLAIR hyperintensity interdigitating within the bilateral convexities are\ncompatible with residual subarachnoid hemorrhage.  Small subdural hematomas\nare noted and unchanged from prior exam allowing for technical differences. \nGradient echo susceptibility within the occipital horns of the lateral\nventricles corresponds to known interventricular hemorrhage.  A right trans\nfrontal ventriculostomy with tip terminating at the level of the foramen of\n___ is identified which demonstrates hemorrhage product and edema along its\ntract, similar in appearance to CT examination of ___.\n\nGradient echo susceptibility artifact within the expected location of the ACA\naneurysm coil packing limits evaluation of the surrounding parenchyma.  The\nremainder of the intracranial flow voids are preserved.\n\nThe ventricles are unchanged in configuration from the prior exam.  The\npatient is intubated with fluid within the nasopharynx.  Partial opacification\nof the ethmoid air cells and of the sphenoid sinuses as well as mild\nopacification of the frontal sinuses are noted.  The orbits are unremarkable. \nThe mastoid air cells demonstrate fluid signal.",
            "output": "1. Re- demonstrated are large bilateral ACA territory infarcts, seen on prior\nCT examinations.  In addition, there are scattered cortical and subcortical\nwhite matter bihemispheric as well as bilateral cerebellar late acute to\nsubacute infarcts, not readily visualize on prior CT examinations.\n2. Multi compartment hemorrhages as described above similar appearance to CT\nexamination.\n3. Gradient echo susceptibility artifact from ACA aneurysm coil packing is\nidentified."
        },
        {
            "input": "There is no intracranial mass, mass effect, or midline shift. Ventricles and\nsulci are age-mildly prominent.\nThere is mild T2/FLAIR signal hyperintensity in the periventricular,\nsubcortical, and deep white matter which is nonspecific but in a patient of\nthis age likely secondary to chronic small vessel ischemic disease. There is\nno pathologic intracranial enhancement. Intracranial flow voids are\nmaintained.  The orbits are unremarkable. Visualized paranasal sinuses and\nmastoid air cells are clear.\nA small fat deposit/hemangioma in the right posterior parietal parasagittal\nbone, hyperintense on T1 pre and pos-contrast sequences.",
            "output": "No acute infarction or hemorrhage.  No evidence of intracranial mass\n\nMild T2/FLAIR signal hyperintensity in the bilateral cerebral hemisphere white\nmatter which is nonspecific but could be secondary to chronic small vessel\nischemic changes, etc."
        },
        {
            "input": "The study is degraded by motion.\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  Scattered bilateral periventricular and subcortical white\nmatter T2/FLAIR hyperintensities are nonspecific, but may represent a sequela\nof chronic small vessel ischemic changes.  No abnormal FLAIR signal within the\nbasal ganglia or pons to suggest osmotic demyelination syndrome.  The\nventricles and sulci are prominent, somewhat out of proportion for patient's\nage, but is suggestive of atrophy.  There is no abnormal enhancement after\ncontrast administration.\n\nMajor intracranial vascular flow voids are preserved.\n\nVisualized paranasal sinuses, mastoid air cells and middle ear canals are\nclear. The orbits are unremarkable.",
            "output": "1.  No evidence of central osmotic demyelination syndrome.\n2.  No evidence of ischemia or hemorrhage.\n3. Atrophy, slightly out of proportion to patient's age."
        },
        {
            "input": "MRI Brain:\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  There are extensive white matter hyperintensities on FLAIR\nimaging.  Although nonspecific, these are often attributed to chronic small\nvessel ischemia.  The ventricles and sulci are enlarged in an atrophic\npattern.  .  There is no abnormal enhancement after contrast administration.\n\nMRA brain: The intracranial vertebral and internal carotid arteries and their\nmajor branches appear normal without evidence of stenosis, occlusion, or\naneurysm formation.  There are bilateral infundibulum at the origins of the\nposterior communicating arteries from the internal carotid arteries\n\nMRA neck:  The study is limited, being performed only without contrast.  The\nfindings suggest possible atherosclerotic plaque involving the proximal left\ninternal carotid artery without evidence of stenosis by NASCET criteria. \nImages of the right common and internal carotid arteries appear normal within\nthe severe limitations of this technique.  Vertebral artery imaging appears\nnormal.  The common, internal and external carotid arteries appear normal. \nThere is no evidence of internal carotid artery stenosis by NASCET criteria. \nThe origins of the great vessels are not included in this examination.",
            "output": "1. Atrophy and findings suggesting chronic small vessel ischemia.  No evidence\nof hemorrhage or infarction.\n2. Bilateral peak come origin infundibulum.  Otherwise normal intracranial\nMRA.\nLimited noncontrast neck MRA suggests atheromatous plaque at the origin of the\nleft internal carotid artery without stenosis by NASCET criteria."
        },
        {
            "input": "There is a large area of slow diffusion with associated FLAIR signal elevation\ninvolving the  head of the left caudate nucleus, anterior limb of the left\ninternal capsule, and portions of the left putamen.  Additional foci of slow\ndiffusion are present in the left centrum semiovale, left frontal, parietal,\ntemporal and temporo-occipital region, in the left MCA distribution.  A very\nfew scattered punctate periventricular and subcortical superimposed T2/FLAIR\nwhite matter hyperintensities are nonspecific, but likely sequela of chronic\nmicroangiopathy.  There is no hemorrhage.  There is no mass or mass effect. \nThe ventricles and sulci are age-appropriate.  Principal intracranial vascular\nflow voids are preserved.  There is mild mucosal thickening in the ethmoid air\ncells.",
            "output": "Late acute infarcts involving the left basal ganglia and left temporal and\nparietal lobes with a punctate focus also seen in the left frontal lobe are\nconsistent with embolic phenomena in the left MCA distribution.  No\nhemorrhage."
        },
        {
            "input": "MRI BRAIN:\nAn irregular elongated area of restricted diffusion in the right cerebellar\nhemisphere extending into the right middle cerebellar peduncle is compatible\nwith acute infarction, similar to prior CT dated ___.  No additional\nsites of infarction are noted.\n\nThere is no evidence of acute intracranial hemorrhage.  The ventricles and\nsulci are age-appropriate.  No mass effect or midline shift.\n\nThere is a partially empty sella.  Mild mucosal thickening of the ethmoid\nsinuses.  Mucous retention cyst in the inferior right maxillary sinus. \nPostsurgical changes of bilateral lens replacement.\n\nMRA BRAIN:\n Examination is mildly degraded by motion.\n\nThere is luminal irregularity involving the bilateral M1 segments, which may\nbe related to motion artifact versus atherosclerotic disease.  Otherwise,\nthere is normal flow signal in the anterior and middle cerebral arteries. No\nfocal stenosis, occlusion, or aneurysm demonstrated.\n\n There is persistent fetal origin of the right posterior cerebral artery.\n\nThere is a linear hypointense filling defect involving the proximal portion of\nthe basilar artery after the confluence of the vertebral arteries (images\n___ of series 10).  On the postcontrast neck MRA images reconstruction in\naxial plane there is no filling defect identified, however.  This findings\nsuggest that the filling defect is likely due to flow related artifact distal\nto severe stenosis of the basilar artery rather than a chronic thrombosis.\nThere is normal flow signal in both posterior cerebral arteries.\n\nMRA NECK:\nMRA of the neck is limited due to timing of the contrast bolus.  There is\nstandard 3 vessel aortic arch anatomy.  The common carotid arteries and\ninternal carotid arteries demonstrate flow signal.  There is no evidence of\ninternal carotid artery stenosis by NASCET criteria.  The vertebral arteries\ndemonstrate flow signal.  No focal stenosis or occlusion.",
            "output": "1. Acute infarction right cerebellar hemisphere.\n2. High-grade stenosis of the proximal basilar artery with a linear filling\ndefect distally likely secondary to flow related artifact on noncontrast 3D\nMRA of the head which is not confirmed on postcontrast images.  A chronic\ndissection with flow within the false as well as true lumina appears less\nlikely from the appearances on postcontrast images.\n3. Patent anterior, middle, and posterior cerebral circulation.  No \nocclusion.\n4. Patent neck vasculature with no evidence of focal stenosis or occlusion,\nwithin limitations."
        },
        {
            "input": "There is no evidence of acute intracranial hemorrhage, mass, mass effect or\ninfarction.  The ventricles and sulci are normal in size and configuration. \nThe basilar cisterns are patent.  No enhancing lesions are identified.  The\nmajor vascular flow voids are well preserved.\n\nThe visualized paranasal sinuses are clear.",
            "output": "No acute intracranial abnormalities identified.  No enhancing lesions\nidentified."
        },
        {
            "input": "There is a left occipital infarct in the distribution of posterior cerebral\nartery. Multiple small infarcts are identified in the left frontal and\nparietal lobes adjacent to the previously seen chronic infarct. In addition,\nseveral punctate areas of infarction are seen in the right cerebral hemisphere\ninvolving the frontal and occipital lobe. There is a chronic left middle\ncerebral artery anterior division infarct visualized. Mild atrophy and small\nvessel disease seen. No evidence of acute or chronic blood products.",
            "output": "Acute left occipital lobe posterior cerebral artery territory infarct.\nMultiple small infarcts in the left frontal parietal lobes as well as in the\nright cerebral hemisphere. Given bilateral involvement, the infarcts rmay be\nelated to cardioembolic source."
        },
        {
            "input": "The masticator, temporalis, lateral pterygoid and medial pterygoid muscles are\nbilaterally symmetric and normal in bulk. No masses or mass effect are seen\nalong the course of the trigeminal nerves or near either foramen ovale.  There\nis no evidence of hemorrhage, edema, or infarction. The ventricles and sulci\nare normal in caliber and configuration. There is no abnormal enhancement\nafter contrast administration.",
            "output": "Normal contrast-enhanced examination of the head. No enhancing lesion near the\nforamen ovales or along the proximal course of the trigeminal nerves. The\nmuscles of mastication appear normal in bulk and are bilaterally symmetric."
        },
        {
            "input": "MR Head:  Evolving subacute ischemic changes are redemonstrated in the left\nparietal lobe with associated foci of slow diffusion, suggestive of embolic\netiology in the left cerebellar hemisphere, left occipital lobe. There is no\nevidence of hemorrhagic transformation. Multiple foci of high signal are\ndemonstrated on T2 in the subcortical white matter and cerebellum, consistent\nwith chronic lacunar ischemic changes and microvascular ischemic disease. The\nventricles and sulci are slightly prominent, suggesting mild cortical volume\nloss. The orbits are unremarkable, the paranasal sinuses and mastoid air cells\nare clear.\n\nMRA Head:  There is evidence of vascular flow in both internal carotid\narteries as well as the vertebrobasilar system, there is narrowing of the\ndistal branches of the Circle of ___, more significant on the left, with\nsignificant narrowing at the superior division of the left middle cerebral\nartery The basilar artery appears patent, there is dominance of the left\nvertebral artery. The right posterior communicating artery demonstrates fetal\npattern, the distal branches of the posterior cerebral arteries are not\nclearly identified, probably related with arteriosclerotic disease. No\naneurysms are detected.\n\nMRA of the neck: Both common carotid arteries are patent with no evidence of\nstenosis at the carotid cervical bifurcations. The vertebral arteries are\npatent with no evidence of flow stenotic lesions, the left vertebral artery\nappears dominant.",
            "output": "1. 1. Evolving subacute ischemic changes in the left parietal lobe with\nassociated foci of slow diffusion, suggesting embolic etiology as can detail\nabove, involving the left cerebellar hemisphere and left occipital lobe. There\nis no evidence of hemorrhagic transformation or mass effect.\n2. Scattered foci of high signal intensity identified in the subcortical and\nperiventricular white matter as well as in the cerebellum, likely consistent\nwith a combination of small vessel disease and lacunar ischemic changes.\n3. Segmental narrowing in the distal branches of the Circle of ___, more\nsignificant on the left middle cerebral artery and posterior cerebral\narteries, likely consistent with arteriosclerotic disease as described above.\n4. The cervical carotid arteries, and the vertebral arteries are patent with\nno evidence of flow stenotic lesions."
        },
        {
            "input": "New areas of slow diffusion predominantly involving the right posterior\nparietal cortex with additional punctate focus of slow diffusion within the\nleft posterior parietal cortex. Previously described infarct within left\nparietal region again shows increased diffusion signal and is compatible with\nnow subacute to chronic infarct. Given distribution, findings are suggestive\nof a central source.\n\nThere is no evidence of acute intracranial hemorrhage or mass effect. White\nmatter signal abnormality is presumably on the basis of chronic small vessel\nischemic disease, in combination with multiple bilateral lacunar infarcts.\n\nThe orbits and paranasal sinuses are unremarkable.\n\nEvaluation of the intracranial vasculature demonstrates no large vessel\nocclusion, aneurysm, or vascular malformation. The distal intracranial vessels\nare not well-visualized which is potentially on an artifactual basis although\natheromatous narrowing is also possible. Incidental note is made of fetal\norigin of right PCA.\n\nEvaluation of vasculature within the neck on 2D time-of-flight images\ndemonstrates no large vessel occlusion or vascular malformation.",
            "output": "1. New areas of slow diffusion within the bilateral parietal lobes, right\ngreater than left, compatible with acute ischemia. Pattern, in combination\nwith prior findings, is suggestive of central source.\n2. No pathologic large vessel occlusion or vascular malformation within the\nhead or neck.\n3. Distal intracranial vessels are not well visualized which is potentially an\nartifactual basis although atheromatous narrowing is possible."
        },
        {
            "input": "MRI Brain:  There is no evidence of hemorrhage, edema or recent infarction. \nVentricles and sulci are enlarged in an atrophic pattern.  There is\nperiventricular white matter hyperintensity suggesting chronic small vessel\nischemia.  There is a 14 mm enhancing dural-based mass adjacent to the\nsuperior sagittal sinus, apparently arising from the left side of the falx.\nThis presumably represents a meningioma.\n\nMRA brain: The intracranial vertebral and internal carotid arteries and their\nmajor branches appear normal without evidence of stenosis, occlusion, or\naneurysm formation.  There are possible small infundibulum at the origins of\nthe posterior communicating arteries bilaterally.\n\nMRA neck:  Images of the vasculature of the neck are limited by poor timing of\nthe contrast bolus. However, these lower quality images demonstrate apparent\nnormal CT of the major arteries.  There is no evidence of internal carotid\nartery stenosis by NASCET criteria.",
            "output": "No no evidence of hemorrhage or infarction.  14 mm dural based meningioma with\nno evidence of brain compression.\n\nPossible small infundibulum at the origins of the posterior communicating\narteries bilaterally.\n\nNo evidence of arterial stenosis or occlusion."
        },
        {
            "input": "There is an 8mm focus of slow diffusion in the right frontal lobe adjacent to\nthe central sulcus which may represent acute or subacute ischemic changes,\ncorrelate clinically.  No evidence of large vascular territory infarct.\n\nThere are several foci of susceptibility on the gradient echo images (11; 16,\n18) within the right cerebral hemisphere which may represent microhemorrhagic\nchanges or less likely calcifications.  No significant intracranial hemorrhage\nis noted.\n\nThere is no evidence of edema, masses, mass effect, or midline shift.  There\nare scattered FLAIR hyperintensities in the periventricular and subcortical\nwhite matter which are nonspecific but may represent chronic microvascular\nchanges.  The ventricles and sulci are prominent in size and configuration\nconsistent with age-related atrophy and involutional changes.\n\nThere is a rounded 9 mm T2 hyperintense foci in the right nasal turbinate (12;\n5) which may represent proteinaceous material.  There is a mucous retention\ncyst in the right maxillary sinus.",
            "output": "1. Small focus of of slow diffusion in the right frontal lobe adjacent to the\ncentral sulcus, may represent acute or subacute ischemic changes, correlate\nclinically.  No large vascular territory infarct.\n2. Several foci of susceptibility on GRE in the right cerebral hemisphere\nwhich may represent micro hemorrhagic changes or less likely calcifications. \nNo significant intracranial hemorrhage."
        },
        {
            "input": "Slow diffusion is identified on the right frontal lobe with gyriform pattern\nand punctate area of high-signal intensity on the DWI sequence (image 22,\nseries 502), suspicious for subacute ischemic change, previously demonstrated\nby head CT of ___.  There is an unchanged right frontoparietal and\ntemporal subdural hematoma, extending the right parasagittal region, causing\nsimilar mass effect and shifting of the normally midline structures towards\nthe left with approximately 3.3 mm of shifting (image 13, series 4).  No new\nareas of hemorrhage are seen.",
            "output": "1.  Slow diffusion identified in the right frontal lobe with gyriform pattern\nand punctate area of restricted diffusion, likely consistent with subacute\nischemic changes.\n\n2.  Unchanged right frontoparietal and temporal subdural hematoma, with\nsimilar pattern of mass effect shifting of the midline structures towards the\nleft.\n\nNOTIFICATION:  The findings were discussed by Dr. ___ with Dr.\n___ on the telephoneon ___ at 10:20 AM, 5 minutes after\ndiscovery of the findings.\n\nRECOMMENDATION(S):  Limited examination the patient cannot hold still or lay\nflat due to altered mental status change, only axial sagittal T1, axial\ngradient echo and axial diffusion-weighted images were obtained.  Please\nconsider repeat this study under anesthesia if clinically warranted."
        },
        {
            "input": "Please note the study is degraded by motion. There is prominence of the\nventricles and sulci suggestive involutional changes. Periventricular and\nsubcortical T2 and FLAIR hyperintensities are noted, which may represent small\nvessel ischemic changes. There is a punctate focus of hemorrhage within the\nleft frontal lobe (see series 7, image 15), that is new since the ___\nprior brain MRI.\n\nThere is an approximately 1.5 cm left parietal wedge-shaped area of subacute\ninfarct. Additional punctate acute infarcts are noted within the left frontal,\nleft occipital and right parietal lobes.\n\nThere is no evidence of  edema, masses, mass effect.  There is a chronic right\ncerebellar infarct again noted. There is a stable right maxillary sinus mucous\nretention cyst versus polyp. The visualized portion of the orbits are\npreserved. Small nonspecific left mastoid fluid is present.",
            "output": "1. Study is degraded by motion.\n2. Wedge shape subacute left parietal infarct as described.\n3. Punctate left frontal, left occipital, and right parietal acute infarcts. \nIn the setting of atrial fibrillation, findings concerning for embolic\netiology. Recommend clinical correlation.\n4. Atrophy and small vessel ischemic changes as described.\n5. Paranasal sinus disease as described.\n\nNOTIFICATION:   The findings were discussed by Dr. ___ with Dr. ___ on\nthe telephone on ___ at 5:55 ___, immediately after discovery of the\nfindings."
        },
        {
            "input": "MRI Brain:  There is no evidence of hemorrhage, edema, masses or infarction. \nVentricles and sulci are normal in caliber and configuration.  There is no\npathologic enhancement. There are multiple foci of T2/FLAIR hyperintensity in\nthe subcortical, deep, and periventricular white matter. There is no lesion of\nthe brainstem or corpus callosum. Major intravascular flow voids are\npreserved.\n\nThere is minimal mucosal thickening of the ethmoid sinuses the paranasal\nsinuses are otherwise clear. The mastoid air cells are clear. The orbits are\nnormal.\n\nMRA brain: The intracranial internal carotid arteries and their major branches\nappear normal without evidence of stenosis, occlusion, or aneurysm formation. \nThere is a right fetal type PCA, a developmental variant. There is congenital\nhypoplasia of the left vertebral artery, as seen on CTA from ___.\nThe intracranial vertebral arteries are otherwise unremarkable.\n\nMRV head: The dural venous sinuses and major cerebral veins are patent.\n\nMRA neck: The origins of the great vessels, subclavian and vertebral arteries\nappear normal bilaterally.\n\nThe right common, internal and external carotid arteries appear normal.  There\nis no evidence of right internal carotid artery stenosis by NASCET criteria.\n\nThe left common carotid artery is normal. There is mild atherosclerotic\nirregularity of the left proximal internal carotid artery, as seen on CTA from\n___. There is no evidence of left internal carotid artery stenosis\nby NASCET criteria. The left external carotid artery appears normal.\n\nThe left vertebral artery is nondominant, as seen on CTA from ___.\nThe right vertebral artery is dominant.\n\nThe bilateral internal jugular veins, brachiocephalic veins, and visualized\nSVC are normal.",
            "output": "1. No intracranial hemorrhage or acute infarct.\n2.  Multiple scattered T2/FLAIR hyperintensity is in the cerebral white\nmatter. These are nonspecific and are commonly seen due to chronic small\nvessel ischemic disease.\n3.  Normal MRA head with developmental variants detailed above.\n4.  No dural venous sinus or major cortical vein thrombosis.\n5.  Mild atherosclerosis of the left proximal internal carotid artery,\nunchanged from CTA on ___.\n6.  Hypoplastic left vertebral artery, as seen on recent CTA."
        },
        {
            "input": "Limited study as patient was unable to continue the exam.\n\nAllowing for this, there is evidence of slow diffusion correlating to the\npreviously described hypoattenuation involving the left temporal, parietal and\noccipital lobes.  No additional areas slow diffusion are identified.\n\n Prominence of the ventricles and cerebral sulci are compatible with age\nrelated involutional changes.",
            "output": "1. Acute infarct within the left parieto-occipital and temporal lobes.\n2.  Generalized parenchymal volume loss, likely age related."
        },
        {
            "input": "Multiple calvarial metastases, examination limited by the absence of\nintravenous contrast, which was not administered due to the patient reported\nallergy.  The dominant lesion is located in the right temporal region,\nmeasuring approximately 5.4 x 3.2 cm with mass effect on the adjacent right\ntemporal lobe.  The lesion is heterogeneous with internal foci of hemorrhage\ncompatible with reported diagnosis of primary thyroid malignancy.  Despite\nmass effect, there is no significant midline shift and only minimal effacement\nof the right lateral ventricle occipital horn.  Multiple smaller lesions are\nlocated in the left frontoparietal region (series 10, images 15, ___ and\nright occipital region (series 10, image 17).  A particularly prominent second\nlesion measuring 1.3 x 0.4 cm breaches the inner table of the left parietal\nbone with adjacent dural thickening (series 10, image 15).  No intra-axial\nlesions identified within limitations of this noncontrast examination.\n\nNo evidence of intracranial hemorrhage or infarction.  The major intracranial\nflow voids are preserved.  Excepting minimal effacement of the right lateral\nventricle, the ventricles are normal in size and configuration.  The basal\ncisterns are patent.  Mild rightward nasal septum deviation anteriorly.  There\nis an air-fluid level in the right sphenoid sinus.",
            "output": "1. Multiple calvarial metastases measuring up to 5.4 cm with mass effect on\nthe right temporal lobe. The dominant metastasis demonstrates foci of\nhemorrhage consistent with documented  thyroid primary malignancy.  No midline\nshift or herniation.\n2. No intra-axial metastases identified.\n3. No intracranial hemorrhage or infarction."
        },
        {
            "input": "Stable postoperative changes from right frontal craniotomy and resection of a\nmeningioma. The T2/FLAIR hyperintensity in the subjacent brain parenchyma is\nunchanged. There is no abnormal enhancement. There is no infarct, hemorrhage\nor mass effect. The ventricles and sulci are appropriate for age.\n\nThe principal intracranial flow voids are present. Of the orbits are\nunremarkable. There is small amount of fluid in the mastoid air cells\nbilaterally. There is mild ethmoid mucosal thickening.",
            "output": "Stable postoperative changes from right frontal meningioma resection without\nevidence of recurrent or residual mass."
        },
        {
            "input": "The patient is status post right frontal craniotomy and resection of a\nmeningioma, with the expected postoperative changes, similar in appearance\ncompared to ___. Again seen is T2/FLAIR hyperintensity in the subjacent\nbrain parenchyma, unchanged in appearance and distribution. There is no\nenhancing mass in this region to suggest local recurrence. No new focus of\nenhancement is identified.\nThere is no evidence of hemorrhage, edema, or infarction. The ventricles and\nsulci are normal in caliber and configuration. There is no abnormal\nenhancement after contrast administration.  The principal intracranial flow\nvoids are preserved.  There is mild mucosal thickening within the the left\nmaxillary and frontal sinus, as well as scattered anterior and posterior\nethmoid air cells.",
            "output": "Similar appearance of the right frontal craniotomy and resection of\nmeningioma, with the expected postoperative changes.  No evidence of\nrecurrent/residual mass or new mass."
        },
        {
            "input": "Again seen are postsurgical changes related to prior right frontal craniotomy\nand resection of right frontal meningioma.  There are associated postsurgical\nchanges with FLAIR signal abnormality in the superior right frontal lobe,\nunchanged compared to the prior study.  There is no nodular enhancement to\nsuggest recurrent tumor.\n\nThere is no evidence of acute hemorrhage, edema, masses, mass effect, midline\nshift or infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.\n\nThere is mild mucosal thickening in bilateral anterior ethmoid air cells.  The\nremaining visualized paranasal sinuses are clear.  Minimal nonspecific fluid\nopacification of bilateral mastoid air cells.  Intracranial flow voids are\nmaintained.",
            "output": "1. Stable changes related to prior right frontal craniotomy and meningioma\nresection with expected postoperative changes.  No recurrent tumor is seen.\n2. Otherwise, unremarkable MRI of the brain."
        },
        {
            "input": "There is no intra or extra-axial mass, acute hemorrhage or infarct. There are\nscattered periventricular and subcortical T2/FLAIR white matter\nhyperintensities, which are nonspecific, but commonly seen in setting of\nchronic microangiopathy.  The ventricles and sulci are normal in caliber and\nconfiguration.\n\nAgain noted is downward displacement of the cerebellar tonsils pole measuring\napproximately 9 mm with \"kinking\"  of the medulla.  A large syringohydromyelia\nbeginning at the C2 level is partially visualized, similar in appearance to\noutside hospital MRI.\n\nThere is no abnormal enhancement after contrast administration.  Incidental\nnote is made of a 1 cm left occipital subperiosteal lipoma.  Mild mucosal\nthickening of the paranasal sinuses are noted.  The orbits are unremarkable. \nThe mastoid air cells are clear.\n\nAlthough CSF phase contrast images demonstrate bidirectional CSF flow at the\nlevel of the pons, midbrain and anterior cervical medullary junction, there is\nstenosis and slowed flow at the level of the anterior cervical medullary\njunction.  There is also decreased bidirectional CSF flow at the posterior\ncervical medullary junction.  Unremarkable bidirectional flow of the aquaduct\nand fourth ventricle.",
            "output": "1. ___ malformation with 9 would mm downward herniation of the cerebellar\ntonsils and \"kinking\" of the brainstem.\n2. Bidirectional CSF flow anteriorly with slowed flow at the level of anterior\ncervicomedullary junction.  Decrease bidirectional flow at the posterior\ncervicomedullary junction."
        },
        {
            "input": "Secondary to patient allergy to gadolinium containing contrast media, no\nintravenous contrast was administered.\n\nSurgical fiducial markers are present about the calvarium.  Ventricles and\nsulci are normal in size and configuration.  There is no shift of normally\nmidline structures.  Basal cisterns are patent.  There is no extra-axial fluid\ncollection.\n\nAgain identified is downward displacement of the left cerebellar tonsil\napproximately 9 mm below the level of the foramen magnum (___:92).  The\nright cerebellar tonsil is additionally downward displaced approximately 5 mm.\nApparent \"kinking\"  of the mid to lower brainstem is similar to prior\nexamination.  A syringohydromyelia begins at the C2 level, partially imaged,\nsimilar to prior examination.  Again identified is a left occipital\nsubperiosteal lipoma which measures approximately 1.3 cm.\n\nIntracranial flow voids are preserved.  The orbits are unremarkable.  Mastoid\nair cells are clear.  Mucosal thickening involves the anterior ethmoidal air\ncells.",
            "output": "Chiari type 1 malformation with approximate 9 mm downward herniation of the\nleft cerebellar tonsil and kinking of the brainstem, unchanged in appearance\nrelative to prior examination dated ___.  Partially imaged\nsyringohydromyelia begins at the C2 level and is additionally unchanged."
        },
        {
            "input": "Suboccipital craniotomy and C1 laminectomy changes are seen with decreased\ncrowding of the posterior fossa.  Angulation of the cervicomedullary junction\npersists.  Small focus of encephalomalacia in the inferior left cerebellar\nhemisphere is new.  The ventricles are normal in size.  The fourth ventricle\nis minimally larger than prior to surgery, consistent with decompression, and\nthe third and lateral ventricles are stable in size.  There is no acute\ninfarction or parenchymal edema.  All total T2 hyperintense foci again seen in\nthe periventricular, deep, and subcortical white matter of the cerebral\nhemispheres, nonspecific in this age group.  The major vascular flow voids are\npreserved.\n\nThe cervical spinal syrinx is better assessed on the concurrent cervical spine\nMRI.\n\nThere is stable prominence of the adenoids.  The orbits and visualized soft\ntissues are normal.  There is mild mucosal thickening in the bilateral\nmaxillary and right sphenoid sinuses.",
            "output": "1. S/p Chiari 1 decompression with decreased crowding in the posterior fossa.\n2. Cervical spinal syrinx is better assessed on the concurrent cervical spine\nMRI.\n3. New small focus of encephalomalacia in the left inferior cerebellar\nhemisphere.  No acute infarction.\n4. Stable supratentorial white matter signal abnormalities, which are\nnonspecific in this age group.  Diagnostic considerations include chronic\nmicrovascular ischemic changes (unusual for age with possible if the patient\nhas longstanding hypertension or diabetes), sequela of demyelination, sequela\nof inflammation/infection, or sequela of vasculitis."
        },
        {
            "input": "The patient is status post suboccipital craniotomy and resection of the\nposterior C1 arch for Chiari decompression, overall similar in appearance to\nprior examination.  There remains syringohydromyelia measuring up to 3 mm in\nAP diameter of the visualized upper cervical spine, unchanged from prior\nexaminations.  There is no acute infarct or intracranial hemorrhage. \nPeriventricular and subcortical punctate T2/FLAIR white matter\nhyperintensities are nonspecific, but compatible with chronic microangiopathy\nin a patient of this age, unchanged from prior examination.  Left inferior\ncerebellar hemisphere infarct is unchanged from prior examination.  The major\nintracranial flow voids are preserved.  There is mild mucosal thickening of\nthe ethmoid air cells and bilateral maxillary sinuses.  The orbits are\nunremarkable.  No fluid signal is seen in the mastoid air cells.\n\nCSF phase contrast images demonstrate normal CSF flow in the biphasic CSF flow\nof the prepontine cistern, anterior cervicomedullary junction and posterior\ncervicomedullary junction as well as through the fourth ventricle.",
            "output": "1. The patient is status post suboccipital craniotomy and resection of the\nposterior C1 arch for Chiari decompression, overall similar to prior MRI.\n2. There remains syringohydromyelia of measuring up to 3 mm in AP diameter of\nthe visualized upper cervical spine, unchanged from prior examination.\n3. CSF phase contrast flow study demonstrates biphasic CSF flow in the\nprepontine cistern, anterior and posterior cervicomedullary junctions."
        },
        {
            "input": "The patient is status post a Chiari decompression surgery.  CSF spaces seen\ninferior to the cerebellum.  A syrinx is visualized in the upper cervical\nspinal cord extending to C4 level with the upper extent does not appear to be\nsignificantly changed compared to the previous MRI of ___.  There\nis a focus of FLAIR hyperintensity in the right parietal lobe with several\nother foci of FLAIR hyperintensity indicating mild changes of small vessel\ndisease which are unchanged compared to the prior study.  Postcontrast images\ndemonstrate no abnormal enhancement.\n\nPhase contrast images demonstrate normal flow with at the craniocervical\njunction synchronized with the cardiac cycle.  Normal bidirectional flow is\nseen also at the 4 foramina image in the inferior fourth ventricle.  Normal\nflow signal is also identified within the aqueduct and the upper fourth\nventricle as well as in the basal cisterns and upper cervical spine.",
            "output": "1. Status post Chiari decompression with patent CSF pathways at the foramen\nmagnum.  Normal bidirectional CSF flow is seen at the foramen magnum without\nevidence of impairment.\n2. Unchanged upper cervical spine syrinx compared with the cervical spine MRI\nof ___.  The lower extent of the syrinx is not assessed on this\nstudy.\n3. No acute infarcts or enhancing brain lesions.  Changes of small vessel\ndisease as before."
        },
        {
            "input": "There is an area of slow diffusion in the left posterior putamen/external\ncapsule leading to the left posterior frontal corona radiata with additional\npunctate areas in the right splenium of the corpus callosum and numerous\npunctate areas in the right occipital lobe with corresponding T2/FLAIR\nhyperintensity, compatible with late acute to early subacute infarct.\n\nThere is no evidence of hemorrhage, masses, mass effect, or midline shift. \nThere is moderate prominence of the ventricles and sulci suggestive of\ninvolutional change.  Scattered areas of periventricular, subcortical and deep\nwhite matter T2/FLAIR hyperintensities are in a configuration most suggestive\nchronic small vessel ischemic disease.  The principal intracranial vascular\nflow voids are preserved.\n\nThere is a small mucous retention cyst in the right maxillary sinus.  There is\ntrace mucosal wall thickening in the bilateral anterior ethmoid air cells\nalong with a another small mucous retention cyst in the right frontal sinus. \nThere are changes from bilateral lens replacement surgery.  The orbits are\notherwise grossly unremarkable.  The mastoid air cells are clear.",
            "output": "1. Small late acute to early subacute infarcts in the left posterior\nputamen/external capsule leading to the left posterior frontal corona radiata,\nright splenium of the corpus callosum, and right occipital lobe, as described.\nThe distribution is suggestive of an embolic etiology.\n2. No hemorrhage or suggestion of mass.\n\nNOTIFICATION:   The findings were discussed by Dr. ___ with Dr. ___\n___ on the telephone on ___ at 2:01 am, 5 minutes after discovery of\nthe findings."
        },
        {
            "input": "The ventricles and extra-axial spaces are normal in size. There is no evidence\nof midline shift, mass effect or hydrocephalus. There are no acute infarcts. \nA few nonspecific foci of T2 hyperintensity are seen.  There is a 1.5 cm area\nof low signal in the extra-axial space in the left anterior temporal region on\nthe T2 weighted images which demonstrates enhancement of a small incidental\nmeningioma.  No mass effect is seen in the adjacent temporal lobe or brain\nedema identified.  There are no areas of abnormal parenchymal enhancement\nseen.  On the spin echo T1 axial images areas of apparent enhancement in both\ntemporal lobes are secondary to pulsation artifacts which are not visualized\non the MPRAGE images.  The vascular flow voids are maintained. The visualized\nparanasal sinuses are clear. .",
            "output": "1. 1.5 cm left anterior temporal meningioma without significant mass effect on\nthe adjacent brain or brain edema.\n2. No abnormal parenchymal or leptomeningeal enhancement.\n3. No acute infarcts."
        },
        {
            "input": "Limited research examination protocol MRI was performed, and the examination\nis degraded by patient motion.\n\nThe patient remains status post right frontal craniotomy with right frontal\napproach ventriculostomy catheter, unchanged in position.  Susceptibility\nartifact from embolization coils is seen in the anterior suprasellar region.\n\nThere is a background of large subacute right MCA territory infarction. \nMultiple sites of restricted diffusion are seen throughout the left basal\nganglia, external capsule, and centrum semiovale, compatible with late acute\nto early subacute infarcts.\n\nRedemonstrated are areas of subarachnoid hemorrhage seen anteriorly along the\nfalx, around the right ventriculostomy catheter tract, and throughout the\nright sylvian fissure and basal cisterns.  The overall extent of this appears\nsimilar to the recent CT examination.  Dependent bilateral intraventricular\nhemorrhage is also unchanged.\n\nFLAIR hyperintensity extending along the right cerebral peduncle into the\nright midbrain likely reflects wallerian degeneration.  A FLAIR hypointense\nfocus in the right cerebellar hemisphere (4:6) may reflect a small chronic\ninfarct.\n\nThere is ex vacuo dilatation of the right lateral ventricle, chronic in\nappearance.  Areas of chronic encephalomalacia and infarct are also seen\nwithin the right frontal lobe and periventricular white matter.\n\nOtherwise the background ventricles and sulci are mildly prominent diffusely,\nsuggesting global parenchymal volume loss.  Periventricular and subcortical\nwhite matter FLAIR hyperintensities are noted, a nonspecific finding that most\nlikely represents the sequelae of chronic small vessel ischemic disease.\n\nMucosal thickening is seen in the left maxillary sinus.  The remainder of the\nparanasal sinuses and mastoid air cells are grossly clear. Orbits are\nunremarkable bilaterally.",
            "output": "1. Research protocol MRI degraded by patient motion.\n2. Late acute to early subacute scattered infarcts involving the left basal\nganglia, corona radiata, and centrum semiovale.\n3. Diffuse subarachnoid and intraventricular hemorrhage, similar to the recent\nprior examinations.\n4. Subacute to early chronic right MCA territory infarction with ex vacuo\ndilatation of the right lateral ventricle and associated wallerian\ndegeneration.\n5. Small, punctate probable chronic infarct of the right cerebellar\nhemisphere.\n6. Additional findings as above."
        },
        {
            "input": "Limited research examination protocol MRI.\n\nThe patient remains status post right frontal craniotomy with right frontal\napproach ventriculostomy catheter, unchanged in position.\nSusceptibility artifact from embolization coils seen in the anterior\nsuprasellar region.\n\nThere is background of large chronic right MCA territory infarct with\nresultant encephalomalacia.\n\nLeft basal ganglia and left centrum semiovale infarcts are less conspicuous\ncompared to prior.\n\nSubarachnoid hemorrhage in the suprasellar cistern, right sylvian fissure as\nwell as anterior interhemispheric fissure is again noted and improved compared\nto prior.  Hemorrhage in the occipital horns of the lateral ventricles are\nimproved compared to prior.  Small amount of right subdural hemorrhage is\nagain noted.\n\nFLAIR hyperintensity extending along the right corticospinal tracts into the\nright cerebral peduncle likely reflects Wallerian degeneration.\n\nAsymmetrical ventriculomegaly of the right lateral ventricle being increased\ncompared to the left is again noted and appears fairly similar compared to\nprior imaging.\n\nWhite matter microangiopathic changes are stable.\nSmall chronic right cerebellar insult is unchanged.",
            "output": "Research protocol MRI.\n\nNo new intracranial hemorrhage or infarct.\n\nInterval improvement in the subarachnoid hemorrhage.  Vascular coil results in\nsusceptibility artifact in the anterior aspect of the suprasellar cistern.\n\nDecrease in conspicuity of the known left MCA territory infarct.\n\nChronic right MCA territory infarct is unchanged.\nVentriculomegaly with right frontal ventriculostomy catheter is unchanged."
        },
        {
            "input": "Examination is moderately degraded by motion and large area of susceptibility\nartifact from right VP shunt catheter.\n\nMRI BRAIN:\n\nA right frontal approach ventriculoperitoneal shunt catheter terminates near\nthe foramina of ___, similar to prior exam.  Postsurgical changes of prior\nright frontal craniotomy.  There is also a small area of susceptibility\nartifact in the anterior suprasellar region from embolization coils.\n\nThere are new small bilateral subdural fluid collections along the bilateral\ncerebral convexities, measuring up to 6 mm in maximal thickness along the left\nposterior frontal convexity.  Nonspecific diffuse pachymeningeal enhancement\nis noted.\n\nThere is unchanged moderate ventriculomegaly with ex vacuo dilatation of the\nright lateral ventricle.  Question decreased left lateral ventricle size\ncompared to ___ prior exam.  There is encephalomalacia and volume\nloss in the distribution of the right MCA territory.  Patchy to confluent\nareas of T2 and FLAIR hyperintense signal abnormalities in the periventricular\nand subcortical white matter are nonspecific, but likely reflect a combination\nof small vessel ischemic changes and chronic infarct.\n\nChronic right cerebellar blood products versus mineralization is again seen. \nIn the right cerebellar hemisphere. Otherwise no other evidence of acute\nintracranial hemorrhage.  Within the confines of artifact, no evidence of\nrestricted diffusion.\n\nMild mucosal thickening in the left maxillary sinus.  Minimal mucosal\nthickening of the ethmoid sinuses.  The mastoid air cells are grossly clear.\n\nMRA BRAIN:\n\nThere is susceptibility artifact from embolization coils in the region of the\nproximal anterior cerebral arteries.  Postcontrast images demonstrate partial\nfilling of the aneurysm along the proximal A2 segment of the left anterior\ncerebral artery (images 54-58 of series 4).\n\nThe right M1 segment remains smaller than the left M1 segment when compared to\nprior CTA head.  Otherwise, the intracranial vertebral and internal carotid\narteries and their major branches are grossly preserved without definite\nevidence of stenosis, occlusion, or new aneurysm formation.",
            "output": "1. Examination is moderately degraded by motion and susceptibility artifact.\n2. Partial filling of the aneurysm along the proximal A2 segment of the left\nanterior cerebral artery status post vascular coiling.\n3. Otherwise, patent circle of ___ with no evidence of occlusion or new\naneurysm formation.\n4. New small bilateral subdural fluid collections along the cerebral\nconvexities, nonspecific bilateral pachymeningeal enhancement and question\ninterval decrease in size of left lateral ventricle compared to ___\nprior exam.  While findings are nonspecific, they may be seen in the setting\nof overshunting.\n5. Unchanged moderate ventriculomegaly in the setting of a right frontal\napproach VP shunt catheter.\n6. Chronic right MCA territory infarct.\n\nNOTIFICATION:  The impression and recommendation above was entered by Dr.\n___ on ___ at 21:12 into the Department of Radiology critical\ncommunications system for direct communication to the referring provider."
        },
        {
            "input": "There is no evidence of brain edema, masses, mass effect, midline shift or\ninfarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is linear parafalcine T2 on an FLAIR hyperintensity\nmeasuring 0.3 cm in maximum thickness, with mild associated enhancement, may\nrepresent sequela of subacute subdural hemorrhage.  Differential\nconsiderations include infection, neoplasm, and are less likely unless\nstrongly clinically suspected.  .  There was no bright signal on the\ncomparison head CT from ___.  There are no other areas of abnormal\nenhancement or gradient abnormality.  There are no other areas of abnormal\nenhancement.  Paranasal sinuses are clear.  Mastoid with air cells are clear. \nIntracranial vascular flow voids are clear.",
            "output": "1. There is no brain edema.\n2. Linear, enhancing small parafalcine abnormality, likely represents subacute\nsubdural hematoma given clinical history.  Infection, neoplasm are less likely\nunless clinically suspected."
        },
        {
            "input": "There is a focus of slow diffusion in the left parietal white matter that is\nnot accompanied by a evidence of hemorrhage and is faintly visible on the\nFLAIR images.  This finding suggests subacute infarction.  The FLAIR images\ndemonstrate numerous areas of deep and subcortical white matter hyperintensity\nbilaterally.  These findings suggest old infarction.  No masses are\nidentified.  The ventricles and sulci are normal in caliber and configuration.",
            "output": "1. Left parietal white matter lesion likely subacute infarction.\n2. Multiple deep and subcortical lesions most likely representing chronic\ninfarction."
        },
        {
            "input": "The common, internal and external carotid arteries appear normal.  There is no\nevidence of stenosis by NASCET criteria. The origins of the great vessels,\nsubclavian, and vertebral arteries appear normal bilaterally.  Previously\ndescribed left cervical ICA dissection is not appreciated on this exam.  The\ncommon carotid bifurcations appear normal.",
            "output": "Previously described left cervical ICA dissection is not visualized on this\nexam."
        },
        {
            "input": "Images through the internal auditory canal demonstrates symmetric appearance\nof the seventh eighth nerve complexes.  There is no evidence of abnormal\nenhancement or mass lesion within the internal auditory canals,\ncerebellopontine angles or membranous labyrinth. No other mass lesions are\nseen within the posterior fossa.\n\nLimited included imaging of the remainder of the brain demonstrates no\nevidence of hemorrhage, edema, masses, mass effect, midline shift or\ninfarction. There is prominence of the ventricles and sulci suggestive\ninvolutional changes.  Few scattered subcortical and periventricular T2/FLAIR\nhyperintensities are seen, most consistent with chronic microvascular ischemic\nchanges.  There is no abnormal enhancement after contrast administration.\n\nNo osseous abnormalities are seen. The  mastoid air cells, and middle ear\ncavitiesare clear. The orbits are unremarkable. The visualized portion of the\nprinciple vascular flow voids are preserved.  T2 hypo intense, T1 hyperintense\nsignal is noted in the sphenoid sinus.  Degenerative changes are partially\nvisualized in the upper cervical spine.",
            "output": "1. No evidence of IAC or cerebellopontine angle mass.\n2. Senescent volume changes with minimal white matter signal abnormality,\nconsistent chronic microvascular ischemic changes.\n3. Inspissated mucus in the sphenoid sinus."
        },
        {
            "input": "There is a 2.4 x 2.3 x 1.4 cm (transverse x AP x craniocaudal) subcortical\nlikely intra-axial mass in the right frontal lobe.  There is no \"CSF cleft\" or\ndefinite dural tail.  Superiorly it grows up to and thickens the dura, likely\ntransgressing the subarachnoid space. The mass is heterogeneous but\nintrinsically T1 bright on precontrast sequences. Following administration\nthere is definite enhancement. There are rounded central intra- and medial\nparalesional cystic spaces.  There are regions of susceptibility compatible\nwith hemorrhage. There is extensive vasogenic edema about the mass involving\nthe right frontal and parietal lobes (07:25).\n\nThere are other scattered T2/FLAIR subcortical and more confluent\nperiventricular white matter hyperintensities with and a few foci in the\nbrainstem which are nonspecific but likely reflect chronic microvascular\nischemic disease. There is no evidence of acute infarct. The ventricles and\nsulci are prominent suggesting age-related atrophy. The intracranial flow\nvoids are preserved. The paranasal sinuses and mastoid air cells are clear.",
            "output": "1. Intrinsically T1-hyperintense but enhancing intra-axial lesion with cystic\nnecrotic components consistent with a solitary hemorrhagic metastasis, from\nsuspected renal cell carcinoma.\n2. The lesion extends peripherally and causes dural thickening, and may\ntransgressing the subarachnoid space, with direct tumoral involvement."
        },
        {
            "input": "The right frontal lobe enhancing lesion has decreased in size compared to the\nprior exam measuring 17 x 19 mm previously 22 x 23 mm.  The surrounding\nvasogenic edema has also decreased. There are no new enhancing lesions\nidentified. Extensive periventricular white matter FLAIR hyperintensities are\nunchanged and likely due to chronic small vessel ischemic disease.  There is\nno acute infarction or hemorrhage. The ventricles and sulci are prominent\nconsistent atrophy.  The intracranial flow voids are preserved.  Inspissated\nsecretions in the left sphenoid sinus are new since the previous exam.",
            "output": "1. Right frontal lobe enhancing lesion has decreased in size as has\nsurrounding edema. No new enhancing lesions.\n2. New inspissated secretions in the sphenoid sinus. Correlate clinically for\na noninvasive fungal infection."
        },
        {
            "input": "Interval decrease size of a heterogeneously enhancing and hemorrhagic right\nfrontal lesion measuring approximately 1.7 x 1.1 cm which previously measured\napproximately 1.9 x 1.6 cm. In addition, there is decreased surrounding FLAIR\nhyperintense signal.\n\nMedial to the occipital horn of the left lateral ventricle, a is now a\nhemorrhagic lesion demonstrating intrinsic T1 hyperintensity measuring\napproximately 1.6 x 1.4 cm demonstrating mild enhancement (series 10, image\n12) with mild surrounding FLAIR hyperintense edema pattern and not seen on\nprior exam of ___.\n\nThere is a new 3 mm T1 intrinsically hyperintense nodule of the left anterior\nparietal parafalcine vertex, making evaluation for enhancement difficult. \nThis is presumably hemorrhagic given the intrinsic T1 hyperintensity (series\n10, image 21).\n\nSingle punctate focus of gradient echo susceptibility blooming of the left\nfrontal lobe (series 6, image 17) is similar appearance to prior exam. No\nother new enhancing lesions are noted.\n\nNo evidence of acute infarct. Prominent confluent subcortical and\nperiventricular white matter T2/FLAIR hyperintensities are seen unchanged in\ndistribution in configuration from prior exam, likely representing sequela of\nchronic small vessel ischemic disease in a patient of this age.  More focal T2\nhyperintensities in the basal ganglia are noted bilaterally as well as pons,\nlikely representing sequela of prior lacunar infarcts. The major intracranial\nflow voids preserved. A mucous retention cyst is seen in the left maxillary\nsinus. Otherwise the remainder of the paranasal sinuses are essentially clear.\nThe orbits are unremarkable. The mastoid air cells are clear.",
            "output": "1. A new subtly enhancing intrinsically T1 hyperintense lesion medial to the\noccipital horn of the left lateral ventricle measuring approximately 1.6 cm in\ngreatest dimension, compatible with a hemorrhagic metastatic lesion.\n2. A second new 3 mm T1 hyperintense nodule of the left parafalcine parietal\nlobe is noted.\n3. Interval decrease size of a heterogeneously enhancing hemorrhagic right\nfrontal lobe lesion now measuring approximately 1.7 cm in greatest dimension\nwith decreased surrounding FLAIR intense signal."
        },
        {
            "input": "There is a new enhancing lesion seen in the right occipital lobe measuring\napproximately 6 mm ( series 11, image 10). There has been an interval decrease\nin size of an enhancing lesion in the left frontal lobe which today measures 9\nx 8 mm. Enhancing lesions in the right frontal lobe and along the left\nparietal parafalcine vertex are unchanged in size.\n\nThe ventral and sulci are prominent consistent with age-related parenchymal\nvolume loss. There are unchanged confluent subcortical and periventricular\nwhite matter T2/FLAIR signal hyperintense lesions likely secondary to chronic\nsmall vessel ischemic disease. Vascular flow voids are preserved. Orbits are\nunremarkable. There is a small mucous retention cyst in the left maxillary\nsinus. The remaining paranasal sinuses and mastoid air cells are clear.",
            "output": "New enhancing lesion in the right occipital lobe.  Slight interval decrease in\nsize of enhancing lesion in the left occipital lobe. Remaining lesions are\nstable in size."
        },
        {
            "input": "Multiple enhancing supratentorial lesions are again identified. Enhancing\nlesions in the right occipital lobe and left parietal lobe are stable to\nslightly increased in size. Previously seen enhancing lesion in the medial\nleft occipital lobe is not present on today's study. However, there is\nevidence of blood products in this region consistent with prior hemorrhage. \nEnhancing lesions in the right frontal lobe and left parietal parafalcine\nvertex are unchanged in size. No new enhancing lesions are seen.\n\nThe ventricles and sulci are again noted to be prominent consistent with\nage-related parenchymal volume loss. There is periventricular and subcortical\nT1 hypointensity which again is felt to be secondary to chronic small vessel\nischemic disease and unchanged.  There is no evidence of acute infarction. The\norbits are unremarkable. There is new mucosal thickening in the left maxillary\nsinus with an air fluid level. There is additional mucosal thickening noted in\nthe left frontal sinus and ethmoid air cells. The mastoid air cells are clear.",
            "output": "1.  Multiple enhancing supratentorial lesions consistent with history of\nmetastatic disease. Right sagittal and left parietal lobe lesions are stable\nto slightly increased in size. Previously identified medial left occipital\nlobe enhancement has resolved and residual blood products are seen in this\nregion consistent with prior hemorrhage.  Remaining lesions are unchanged. No\nnew enhancing lesions are identified.\n\n2. Stable chronic small vessel ischemic disease.\n\n3. Paranasal sinus disease as detailed above."
        },
        {
            "input": "There is no evidence of acute intracranial hemorrhage. The ventricles and\nbasal cisterns appear stable. There are normal vascular flow voids. There is\nno evidence of acute infarct based on diffusion-weighted imaging.\n\nThere are several supratentorial intrinsically T1 hyperintense lesions which\nappear slightly increased in size when compared to ___ and ___. Right frontal lesion measures 2.2 cm in maximal AP dimension,\npreviously 1.8 cm. Left posterior parietal lesion now measures 0.8 cm,\npreviously 0.5 cm. Left parietal parafalcine lesion measures 0.7 cm,\npreviously 0.6 cm right occipital lesion measures 0.9 cm, previously 0.7 cm no\nnew lesions are seen. There is new gradient signal hypointensity within the\nright occipital lesion which may reflect sequelae of treatment or interval\nhemorrhage. Chronic blood products are again seen within the right frontal,\nleft parietal, and left occipital lesions which may relate to prior treatment.\nThere is no clear enhancement within the left occipital lesion.\n\nThere is diffuse brain parenchymal volume loss. There is extensive subcortical\nand periventricular T2/FLAIR signal hyperintensity which likely reflects a\ncombination of sequelae of chronic small vessel ischemic disease and post\ntreatment related change.\n\nThere is opacification of the left frontal sinus and anterior left ethmoid air\ncells.",
            "output": "1. Multiple supratentorial T1 hyperintense lesions with some enhancement,\nprogressively increasing in size when compared to prior two exams.  The\nincrease in size of lesions can be attributed to interval hemorrhage which\nlimits evaluation for change in enhancement."
        },
        {
            "input": "Please note the study is degraded by motion.\n\nAgain seen is intraparenchymal hemorrhage with an associated hematocrit level\narising from the region of a known left posterior parietal lobe mass lesion,\nmost consistent with interval hemorrhage of a metastatic focus. Overall, this\narea measures 2.9 x 2.7 x 3.5 cm. There is a small amount of surrounding\nedema.\n\nAdditionally, there are several supratentorial intrinsically T1 hyperintense\nlesions which are overall similar in size as compared to ___. The\nright frontal lesion measures 2.5 cm in maximal AP dimension, previously 2.2.\nThe left parietal parafalcine lesion measures up 8 mm, previously 7 mm. The\nright occipital lesion measures 8 mm, previously 9 mm.  No new lesions are\nidentified. Gradient signal hypointensity within these lesions may reflect\nsequela of treatment,  old hemorrhage or mineralization.\n\nAgain seen is diffuse brain parenchymal volume loss. There is extensive\nsubcortical and periventricular T2/FLAIR signal hyperintensity, which may\nreflect combination sequela of chronic small vessel ischemic disease and\nposttreatment related change.\n\nDiffusion weighting imaging does not demonstrate evidence of acute infarct.\nThe major intracranial vessels exhibit the expected signal void related to\nvascular flow.\n\nThe sella turcica, craniocervical junction, and orbits are unremarkable. \nSinus mucosal thickening is seen within the left frontal sinus, left sphenoid\nsinus, and multiple anterior ethmoid air cells.",
            "output": "1. Study is degraded by motion.\n2. Intraparenchymal hemorrhage with associated hematocrit level arising from\nthe region the known left posterior parietal lobe mass lesion concerning for\ninterval hemorrhage of a metastatic focus.\n3. Other previously noted supratentorial T1 hyperintense enhancing metastatic\nlesions are grossly stable in size compared to the prior exam, as described\nabove.\n4. No new lesions identified."
        },
        {
            "input": "Hemorrhagic enhancing lesions are identified in both cerebral hemispheres. The\nlesions seen in the left parietal lobe near the convexity demonstrate\nincreased in size.  There is also increase in blood products.  There is also\nslight increase in size and blood products in the left frontal and right\nposterior temporal  lesions.  The previously seen right frontal lobe lesions\nhave not significantly changed in size.  There is brain atrophy seen. Edema in\nthe left parietal lesions may produce mass effect on the left lateral\nventricle which has slightly increased but there is no midline shift.  No\ndefinite new areas of enhancement seen. Soft tissue changes are seen in the\nleft frontal sinus as before.",
            "output": "Increase in size and blood products within previously identified lesions in\nthe left parietal, frontal and right temporal regions. There is increase in\nedema about the left parietal lesion with mass effect on the left lateral\nventricle but no midline shift.  Examination is limited by motion."
        },
        {
            "input": "MR BRAIN:\n Again seen are areas of late acute to early subacute infarction involving the\nleft occipital lobe.  No evidence for hemorrhagic transformation at this time.\nChronic infarcts are seen in the left cerebellar hemisphere, right medial\ntemporal lobe, and posterior left superior frontal lobule in the precentral\ngyrus.\n\nThere is no evidence for acute intracranial hemorrhage.  However, a punctate\nfocus of susceptibility artifact within the right inferior parietal lobe\n(13:14) may represent a punctate chronic microhemorrhage.  A larger area of\nsusceptibility artifact in the left cerebellar hemisphere is unchanged from\nprevious examination, and may represent an additional area of microhemorrhage\nversus cavernoma.\n\nThe ventricles and sulci are enlarged compatible with global parenchymal\nvolume loss.  Periventricular and subcortical white matter FLAIR\nhyperintensities are noted, a nonspecific finding that most likely represents\nthe sequelae of chronic small vessel ischemic disease.\n\nMild mucosal thickening is seen throughout scattered ethmoid air cells\nbilaterally.  The remainder of the visualized paranasal sinuses, middle ear\ncavities, and mastoid air cells are well aerated and clear.  The orbits are\nwithin normal limits bilaterally.\n\n\nMRA brain:\nThe intracranial portions of the carotid arteries appear grossly patent.  The\nvertebrobasilar system is left-sided dominant with a diminutive right\nvertebral artery.\n\nThe distal left posterior cerebral artery demonstrates focal narrowing\nadjacent the area of infarction, better assessed by CT.  The remainder of the\nintracranial vasculature is otherwise grossly patent without additional sites\nof high-grade stenosis or occlusion.\n\nRedemonstrated is a somewhat ovoid irregular shaped focus of T2 hypointensity\nwith flow related signal seen on the MRA images adjacent the cerebellar vermis\non the left (8:94).  This focal dilation appears to connect to a vascular\nstructure with increased flow related signal that subsequently connects to the\nvein of ___ sinus, suggesting a developmental venous anomaly.",
            "output": "1. Late acute versus early subacute infarctions within the left occipital lobe\nin the distribution of the left posterior cerebral artery.\n2. Focal severe narrowing versus occlusion of the distal left posterior\ncerebral artery, somewhat better seen on CT examination.\n3. Probable left cerebellar cavernous malformation, unchanged since the prior\nexamination.\n4. Flow related signal on MR angiogram images involving and irregular ovoid\nlesion in the left posterior fossa, which connects back to the venous system\nvia the vein of ___ sinus.  This finding is suggestive of a\ndevelopmental venous anomaly, an incidental finding and could be related to\nthe cavernous malformation.\n5. Additional findings, as above."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, or infarction.\nThe ventricles and sulci are normal in caliber and configuration. There is\nscattered foci of FLAIR hyperintensity in the subcortical, deep, and\nperiventricular white matter, most consistent with chronic small vessel\nischemic disease in a patient of this age. Major intravascular flow voids are\npreserved.\n\nThere is mild mucosal thickening of the ethmoid sinuses. The paranasal sinuses\nand mastoid air cells are otherwise clear. The orbits are normal.",
            "output": "1. No evidence of hemorrhage or infarction.\n2. Scattered foci of FLAIR hyperintensity in the cerebral white matter, most\nconsistent with chronic small vessel ischemic disease in a patient of this\nage."
        },
        {
            "input": "Numerable T1 hypointense, enhancing lesions with restricted diffusion are\nseen, with the largest measuring up to 2.5 x 2.8 x 2.5 cm (AP x TV x CC)\n(9:77, 900:72) involving the left occipital lobe and corpus callosum along the\nmedial aspect of the posterior horn of the left lateral ventricle.\n\nAdditional suspicious lesions include:\n5 mm parasagittal left parietal lobe (9:121),\n1.1 cm posterior left parietal lobe (9:111),\n1.1 x 1.5 cm left lateral ventricle (9:102),\n1.8 x 2 cm left tail of the caudate nucleus with mass-effect upon the\nposterior horn of the left lateral ventricle (9:96),\n2 x 2 cm left external capsule (9:89),\nenhancing soft tissue density also occupies the bilateral frontal horns\n(9:88),\n2 x 1.6 cm right temporal lobe (9:61),\n1 x 0.9 cm hypothalamic (9:67).\n\nThere is also enhancement lining the ependymal wall the frontal horns of the\nlateral ventricles.\nThere is enhancement along the bilateral internal auditory canals along the\nseventh and eighth nerve complexes worrisome for tumor.\n\nSusceptibility artifacts within the dominant lesion on the medial aspect of\nthe posterior horn of the left lateral ventricle likely represents internal\nblood products.\n\nCalcified (by prior CT) dural-based lesion overlying the left posterior\nfrontal cortex, stable from ___, likely represents a meningioma\n(9:139).\n\n  No large intracranial hemorrhage or infarction.  No midline shift despite\nthe numerable lesions listed above.  The ventricles and sulci are mildly\nprominent, likely reflective of age related involutional changes.  Moderate\nperiventricular and subcortical T2/FLAIR hyperintensities are nonspecific but\nlikely reflective of chronic microangiopathy.  The major intracranial arterial\nflow voids are preserved.  The dural venous sinuses are patent.\n\nThe calvarium and overlying soft tissues are normal.  Mild mucosal thickening\nof the ethmoid air cells.  The remaining paranasal sinuses and mastoid air\ncells are clear.  Unremarkable orbits and retro-orbital structures.",
            "output": "1. Numerable enhancing and restricting lesions, with the largest measuring up\nto 2.8 cm, highly concerning for malignancy.  Ependymal enhancement lining the\nfrontal horns of the lateral ventricles and enhancement along internal\nauditory canals along the seventh and eighth nerve complexes.  Given history\nof primary malignancy, metastatic disease is possible though lymphoma is also\nin the differential diagnosis given imaging characteristics.  No evidence of\nmidline shift or hydrocephalus.\n2. Stigmata of age-related involutional changes and chronic microangiopathy.\n3. Left parietal extra-axial lesion most likely a meningioma."
        },
        {
            "input": "In the subcutaneous tissues of the left posterior aspect of the neck overlying\nthe paraspinal muscles there is a 2.3 x 1.3 x 1.8 cm lesion (TR, AP, CC\n___, with thin septations (3:22) that demonstrates high T1/T2 signal\nand suppresses on fat saturation sequences. No nodular soft tissue is\nidentified within the lesion and there is no invasion of underlying tissues.\n\nThere is no cervical lymphadenopathy. No abnormal fluid collection is\nidentified. The pharyngeal mucosal space has a normal appearance. Structures\nof the nasopharynx, oropharynx, hypopharynx and larynx are symmetric and\nappear normal. The parotid, submandibular, and sublingual glands and spaces\nhave a normal appearance. The major vessels of the neck appear unremarkable.\nMasticator, parapharyngeal, and retropharyngeal spaces appear normal. The\nparanasal sinuses, mastoid air cells and airways are clear. The visualized\nsegments of the orbits, globes, and intracranial compartment are unremarkable.\nMultiple T2 hyperintense lesions are seen in the thyroid, more prominently in\nthe right thyroid lobe where a 2.5 x 2.1 cm nodule is identified (4:31).\n\nDegenerative changes of the cervical spine are mild and incompletely\ncharacterized with this non-dedicated protocol.  Heterogeneously high T1/T2\nsignal intensity in the vertebral body of T1 is incompletely evaluated",
            "output": "1. Lesion with thin septations in the left posterior aspect of the neck that\ndemonstrates high T1/T2 signal and suppresses on fat saturation sequences is\nmost likely a lipoma. However, a thorough evaluation of a neck mass would\ninclude contrast-enhanced sequences that would provide clues of alternative\ndiagnoses which were not performed in this patient due to patient's\ndiscomfort.\n\n2. Multiple T2 hyperintense thryoid nodules should be further assessed with\nultrasound if not previously performed and if clinically indicated.\n\n3. Inhomogeneous marrow signal in the vertebral body of T1 is incompletely\nevaluated with this exam. Further assessment with a dedicated cervical spine\nprotocol could be performed if clinically indicated."
        },
        {
            "input": "The examination is motion degraded.  Within these confines:\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are patent and prominent in keeping\nwith age-related volume loss. There is no abnormal enhancement after contrast\nadministration.\n\nThere are extensive areas of T2/FLAIR hyperintensity in the periventricular,\nsubcortical and deep white matter, nonspecific, likely secondary to small\nvessel ischemic changes.\n\nThe orbits are unremarkable noting prior bilateral cataract surgeries.  Mucous\nretention cyst in the right maxillary sinus with mucosal thickening.  The\nremaining visualized paranasal sinuses and mastoid air cells are clear. \nIntracranial flow voids are maintained.  The osseous structures are\nunremarkable.  Incidental note is made of a left trapezius intra muscular\nlipoma.",
            "output": "1. Findings of small vessel ischemic changes.\n\n2. No acute intracranial abnormality.  Specifically, no abnormal enhancement\nor leptomeningeal thickening is seen.\n\n3. There is global cerebral volume loss, compatible with age-related\ninvolutional changes, without specific pattern to suggest etiology of\ndementia."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   Prominence of the ventricles and cerebral sulci are\ncompatible with age related involutional changes.   There is no abnormal\nenhancement after contrast administration.\n\nThere are mild-to-moderate subcortical and periventricular white matter FLAIR\nhyperintensities compatible with small vessel disease.\n\nThe major intracranial vascular flow voids are maintained.  There is a\nmoderate and mild amount nonspecific fluid within the left and right mastoid\nair cells, respectively.",
            "output": "1. No acute intracranial abnormality.\n2. Mild white matter small vessel disease.\n3. Generalized parenchymal volume loss, likely age related."
        },
        {
            "input": "There are approximately seven small bifrontal subcortical white matter\nT2/FLAIR hyperintensities.  Without prior exam for direct comparison,\nevaluation for change cannot be performed.  There is no associated restricted\ndiffusion with these lesions nor susceptibility artifact.\n\nThere is no intracranial mass, mass effect, or midline shift. Ventricles and\nsulci are age-appropriate.  There is no restricted diffusion to suggest acute\ninfarct. No abnormal susceptibility artifact identified. Major intravascular\nflow voids are preserved including within the major dural venous sinuses.\n\nMucous retention cyst is noted in the left sphenoid sinus.  Otherwise,\nvisualized paranasal sinuses and mastoid air cells demonstrate no abnormal\nsignal.",
            "output": "Small bifrontal subcortical white matter T2/FLAIR hyperintensities.  By report\nthese were present on prior though without images for direct comparison,\ncannot evaluate for interval change.  Regardless, these are nonspecific and\ndifferential considerations are similar to previously reported.  These are\ncommonly seen in the setting of chronic small vessel disease though without\nappropriate history, additional etiologies such as vasculitis or migraine\nheadaches are possible, among others.  Demyelination is possible though\nappearance and distribution is not typical."
        },
        {
            "input": "There is no evidence of intracranial hemorrhage, edema, masses, mass effect,\nmidline shift or infarction.  The sulci appear slightly prominent, likely age\nrelated and involutional nature, suggesting mild cortical volume loss, there\nis mild asymmetry of the lateral ventricles, probably developmental in nature,\nthere is no evidence of hydrocephalus.  There are mild foci of periventricular\nand subcortical white matter T2/FLAIR signal hyperintensity, nonspecific and\nlikely sequelae of chronic microangiopathy.  There is no abnormal enhancement\nafter contrast administration.  There are postsurgical changes related to\nbilateral lens replacement.",
            "output": "1. No intracranial masses, hemorrhage, infarction or abnormal enhancement.\n2. Mild periventricular and subcortical white matter changes, nonspecific and\nlikely related to chronic microangiopathy."
        },
        {
            "input": "There is unchanged minimal linear enhancement along the posterior planum\nsphenoidale.  There is no evidence for a new intracranial mass. The pituitary\ngland is not evaluated with dedicated high-resolution images, with appears\nunchanged in shape and size compared to ___. There is no evidence for\nedema, mass effect, abnormal diffusion, or blood products in the brain\nparenchyma. There are few scattered punctate foci of high T2 signal in the\nbifrontal subcortical, deep, and periventricular white matter, slightly\nprogressed compared to ___ and ___. Ventricles, sulci, and basal cisterns\nare normal in size. Cerebellar tonsils are normally positioned. Major arterial\nflow voids are grossly preserved. Major dural venous sinuses are patent.",
            "output": "1. Stable postsurgical change along the posterior planus vena dull eighth. No\nevidence for new intracranial mass.\n2. Few scattered punctate foci of high T2 signal in the bifrontal white\nmatter, slightly progressed compared to ___ and ___, compatible with sequela\nof mild chronic small vessel ischemic disease, given the patient's age and\ncardiovascular risk factors, or migraine-related lesions, given the patient's\nreported history of migraines."
        },
        {
            "input": "Study is mildly degraded by motion.\nGrossly stable postoperative changes related to patient's known right frontal\nsuprasellar meningioma resection are again noted.  Grossly stable minimal\nnonspecific linear enhancement along the planum sphenoidale is again seen. \nWithin limits of this nondedicated examination, limited imaging of pituitary\ngland is grossly stable compared to ___ prior exam.\n\nThere is no evidence of hemorrhage, edema, mass effect, midline shift or\ninfarction.   The ventricles and sulci are stable in caliber and\nconfiguration.  Few periventricular and subcortical T2 and FLAIR\nhyperintensities are noted which may represent small vessel ischemic changes.",
            "output": "1. Study is mildly degraded by motion.\n2. Postoperative changes related to patient's known right frontal suprasellar\nmeningioma resection.  Minimal nonspecific enhancement along planum\nsphenoidale, unchanged compared ___ prior exam, which may be postoperative.\n3. Within limits of study, no definite evidence of new enhancing intracranial\nmass.  If continued concern for sella enhancing mass, consider dedicated\ncontrast sella MRI for further evaluation.\n4. Grossly stable minimal probable microangiopathic changes as described."
        },
        {
            "input": "There are multiple small punctate left parietal foci of slow diffusion and\nsome of them show corresponding reduced signal on susceptibility weighted\nimages.  These may be intraparenchymal within the cortex, suggesting multiple\nsmall acute infarction or in the subarachnoid space suggesting foci of\nsubarachnoid hemorrhage.\n\nRedemonstration of left subdural T1 isointense and T2 hyperintense signal\nintensity which is not completely suppressed on FLAIR sequence along left\ncerebral convexity with layering fluid/fluid levels, foci of slow diffusion\nand septations posteriorly; essentially unchanged in size since ___. \nDescribed findings likely related to different ages subdural hematoma.  There\nis underlying exerted mass-effect on the opposing brain parenchyma with no\nmidline shift.\n\nThere is minimal left parietal subarachnoid hemosiderin staining likely\nrelated to remote subarachnoid hemorrhage.\n\nThere is no evidence of edema, masses, mass effect or midline shift.  The\nventricles and sulci are stable in caliber and configuration.\n\nStatus post right lens surgery removal.  Otherwise both orbits and globes are\nnormal.  Mild mucosal thickening involving bilateral mastoid air cells. \nParanasal sinuses are normal.",
            "output": "1. Multiple small foci of slow diffusion in left parietal region, which may\nreflect small cortical infarctions or small amounts of subarachnoid\nhemorrhage..\n2. Redemonstration of left cerebral convexity different ages subdural hematoma\nwith underlying mass effect on opposing brain parenchyma with no midline\nshift.  Unchanged in size since ___."
        },
        {
            "input": "There are innumerable supra and infratentorial rim enhancing metastatic\nlesions with slowed diffusion and surrounding vasogenic edema, with more\npronounced number of lesions within the cerebellum.  Lesions are also seen\nwithin the right midbrain and right pons.  The dominant lesion in the left\ncerebral hemisphere is in the left middle frontal lobe measuring 14 x 12 mm\nwith moderate surrounding vasogenic edema (1200:122).  The dominant lesion in\nthe right cerebral hemisphere is in the right superior frontal lobe measuring\nup to 17 x 13 mm (1200:137) with moderate surrounding vasogenic edema.  The\ndominant cerebellar lesion is located in the midline measuring 16 x 12 mm\n(1200:79).  A single left occipital lesion measuring 13 x 13 mm demonstrates\npunctate area of associated susceptibility artifact (10:8, 7:8), suggestive of\nhemorrhage.  The remainder of the lesions appear nonhemorrhagic.\n\nThere is no evidence of midline shift or acute territorial infarct.  The\nbackground ventricles and sulci are normal in caliber and configuration.  The\ndural venous sinuses appear patent on MP-RAGE images.  The principal\nintracranial vascular flow voids appear preserved.\n\nThere is opacification of posterior right ethmoid air cells and right sphenoid\nsinus.  There is mild mucosal thickening of the right maxillary sinus.  There\nis mild mucosal thickening in the left frontoethmoidal recess.  There are\napparent changes from functional endoscopic sinus surgery.  The orbits are\ngrossly unremarkable.  The mastoid air cells are clear.\n\n11 x 10 mm T1 hypointense lesion abutting the inferior endplate of the C2\nvertebral body, with some enhancement of the inferior aspect on MP-RAGE\nimages, is suspicious for osseous metastasis.",
            "output": "1. Innumerable enhancing supra and infratentorial metastatic lesions, as\ndescribed, additionally with involvement of the midbrain and pons.  Many of\nthese lesions demonstrate vasogenic edema with associated localized mass\neffect.  Of these, a single left occipital lesion appears hemorrhagic.\n2. 11 x 10 mm lesion abutting the inferior endplate of the C2 vertebral body\nis suspicious for osseous metastasis.  This can be further evaluated with\ncontrast-enhanced dedicated cervical spine MR, if indicated.\n3. Paranasal sinus disease, as described, with postsurgical changes from FESS."
        },
        {
            "input": "MR BRAIN:\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.\n\nThe left orbit is proptotic.  Adjacent T2 and FLAIR hyperintense signal in the\npreseptal soft tissues is consistent with edema.  On on axial T1 fat-sat\npostcontrast images, asymmetric post septal enhancement within the retrobulbar\nare fat of the left orbit abuts the optic nerve (19:12).  There is extraconal\ninflammatory stranding/phlegmon of the left medial orbit and roof, exerting\nmass effect on the adjacent extra-ocular eye muscles.  Mild inflammatory\nenhancement of the left superior and medial rectus is noted.  The globe itself\nappears normal.  Asymmetric pachymeningeal and leptomeningeal enhancement\nsuperior to the orbit along the left frontal lobe is present without fluid\ncollection/empyema (19:1, 20:23, 20:15).\n\nThe left V1 nerve division passes through soft tissue edema superior to the\nleft orbit.  There is no asymmetric FLAIR signal or enhancement of the V2\nnerve division on coronal images.  Possible asymmetric enhancement is seen on\naxial images of the left V2 nerve division as it approaches the infraorbital\nforamen although there is no evidence of abnormal enhancement in Meckel's\ncave, the pterygopalatine fossa, foramen rotundum, or the Vidian canal\n(19:16).\n\nThere is extensive sinus disease.  For example, near complete opacification of\nleft ethmoid air cells with mucosal thickening of the right ethmoid, bilateral\nsphenoid, bilateral maxillary, and bilateral frontal sinuses which enhance on\npostcontrast images.\n\nMRV brain:  There is no evidence of cavernous or dural venous sinus\nthrombosis.  The intracranial flow voids are present and normal.",
            "output": "1. Left orbital cellulitis with associated superficial soft tissue\ninflammation and edema of the left face.  There is abnormal enhancement and\ninflammatory stranding of both the intra and extraconal fat.  There is\ninflammatory enhancement of the left superior and medial rectus as well as\nsuperior oblique.\n\n2. Extraconal inflammatory stranding/phlegmon of the orbital roof and medial\norbit exerts mild mass effect on the extraocular eye muscles without rim\nenhancing collection to suggest abscess at this time.\n3. Adjacent left frontal meningitis suggests intracranial extension of\ninfection without evidence of abscess or empyema.\n4. No evidence of cavernous sinus thrombosis.\n5. Extensive sinus disease, as described, a possible infectious source.\n6. Left V1 and V2 nerve divisions pass near these periorbital inflammatory\nchanges, which may correlate to the patient's facial paresthesias.  There is\nquestionable asymmetric enhancement of the left V2 nerve division, not\nconfirmed on coronal sequences.\n\nNOTIFICATION:  The findings were discussed with ___, M.D. by ___\n___, M.D. on the telephone on ___ at 2:50 ___, 2 minutes after\ndiscovery of the findings."
        },
        {
            "input": "There is redemonstration of subarachnoid hemorrhage within the anterior\ninterhemispheric fissure, sylvian fissures, and sulci.  Parenchymal hematoma\nin the anterior corpus callosum is also again seen.  There is stable blood in\nthe occipital horns of the lateral ventricles.  The ventricles are stable in\nsize.  Prominence of the ventricles and cerebral sulci is congruent with mild\nparenchymal volume loss.  There is mild confluent periventricular T2\nhyperintensity, a nonspecific finding.  A track from prior right frontal\napproach ventriculostomy catheter is noted.\n\nPrior CTs suggested a thin subdural hematoma along the posterior falx, but\nthere is no corresponding signal abnormality on FLAIR images.\n\nThere is a punctate focus of high signal on diffusion-weighted images within\nthe left frontal centrum semiovale (302:24), without a clear colored on the\nADC map, with corresponding hyperintensity on T2 weighted and FLAIR images.\n\nThe major vascular vascular flow voids are visualized.  The intracranial\narteries are better assessed on the CTA from 1 day earlier from ___.\n\nThere is mild mucosal thickening of the right maxillary sinus and ethmoid air\ncells and a mucous retention cyst within the right maxillary sinus.  There is\nnear complete opacification of bilateral mastoid air cells.",
            "output": "1. Punctate early subacute infarction in the left frontal centrum semiovale.\n2. Subarachnoid hemorrhage with anterior interhemispheric fissure\npredominance, parenchymal hemorrhage in the anterior corpus callosum, and\nintraventricular hemorrhage are stable.\n3. Stable size of the ventricles."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.\n There are scattered T2/FLAIR hyperintensities in the cerebral hemispheres\nbilaterally, a nonspecific finding and likely related to chronic small vessel\nischemic changes.\n\nThere is mild generalized parenchymal volume loss, most likely age related. \nMild prominence of the ventricular system and extra-axial CSF spaces\nconsistent with the previously mentioned parenchymal volume loss.\nMajor vascular flow voids appear preserved.\n\nThe paranasal sinuses and mastoid air cells appear centrally clear.  The\norbits appear grossly unremarkable.",
            "output": "1. No evidence of acute infarction, hemorrhage or intracranial mass.\n2. Scattered white matter changes in the cerebral hemispheres bilaterally,\nlikely sequela of chronic microangiopathy."
        },
        {
            "input": "There is no intra or extra mass, acute hemorrhage or infarct.  No evidence of\nabnormal enhancement.  No suspicious parenchymal FLAIR signal abnormality. \nThere is mild intrinsic T1 hyperintense signal of the bilateral globus\npallidus, similar to prior examination, compatible with given history\ncirrhosis.  The sulci, ventricles and cisterns are within expected limits for\nthe degree of moderate senescent related global cerebral volume loss,\nunchanged from prior exam.  Minimal periventricular and subcortical T2/FLAIR\nwhite matter hyperintensities are nonspecific, but compatible with chronic\nmicroangiopathy in a patient of this age.  The major intracranial flow voids\nare preserved.  The dural venous sinuses are patent on MP rage.  There is\ndependent aerosolized mucous in the right maxillary sinus and mild mucosal\nthickening of the remainder the visualized paranasal sinuses, progressed from\nprior exam.  The orbits are unremarkable noting right lens replacement.  Trace\nfluid signal is seen the bilateral mastoid air cells.  No suspicious marrow\nsignal.",
            "output": "1. No acute intracranial abnormality on contrast enhanced MRI brain. \nSpecifically, no evidence of abnormal intracranial enhancement or suspicious\nparenchymal FLAIR signal abnormality.\n2. Mild T1 intrinsic hyperintense signal of the globus pallidus, compatible\nwith given history of cirrhosis, unchanged from prior exam.\n3. No evidence of dural venous thrombosis.\n4. Paranasal sinus disease and fluid in the mastoid air cells.  Additional\nfindings described above."
        },
        {
            "input": "Examination is mildly degraded by motion.  There is no evidence of hemorrhage,\nedema, masses, mass effect, midline shift, or infarction..  The ventricles and\nsulci are slightly prominent, likely secondary to involutional change. \nScattered periventricular and subcortical FLAIR signal hyperintensities are\nnonspecific but may reflect the sequelae of chronic microvascular ischemic\ndisease.  The major vascular flow voids appear preserved.\n\nThe visualized paranasal sinuses and mastoid air cells are clear.  The orbits\nare unremarkable.",
            "output": "1. White matter hyperintensities suggesting chronic small vessel ischemia. \nOtherwise normal brain MRI."
        },
        {
            "input": "No evidence of acute territorial infarction, hemorrhage, masses or midline\nshift.  Ventricles and sulci are slightly prominent, likely due to\ninvolutional changes.  Intrinsic T1 hyperintensity within the bilateral basal\nganglia is likely secondary to mineralization.  Periventricular and\nsubcortical white matter T2/FLAIR hyperintensities are nonspecific but likely\nsequelae of chronic small vessel ischemic disease.  The major flow voids are\npreserved.  Mild maxillary sinus disease.",
            "output": "1. No acute infarction or hemorrhage.\n2. Evidence of chronic ischemic vessel disease."
        },
        {
            "input": "There is no diffuse signal abnormality to suggest acute infarction. Multiple\nsmall scattered foci of increased susceptibility artifact on gradient echo\nimages in the cerebrum, cerebellum, right thalamus, and pons are consistent\nwith micro hemorrhages.  Confluent periventricular subcortical white matter\nT2/FLAIR hyperintensities are nonspecific but likely sequelae of chronic\nmicroangiopathy. There is no evidence of acute hemorrhage, edema, masses, or\nmass effect.  There is prominence of the ventricles and sulci suggestive\ninvolutional changes, advanced for age.  The intracranial vascular flow voids\nare preserved.  Mucosal thickening and mucous retention cysts are present in\nthe maxillary sinuses bilaterally.  In the right posterior ethmoid air cells\nare opacified and there is fluid in the nasopharynx.  Distal right vertebral\nartery demonstrates diminished flow void (9:4) which may be due to\natherosclerotic disease.",
            "output": "1.  No evidence of acute hemorrhage or infarction.  No mass or mass effect.\n\n2.  Scattered foci of increased susceptibility artifact on gradient echo\nimages in the cerebrum, cerebellum, right thalamus, and pons are consistent\nwith micro hemorrhages likely from hypertension.\n\n3.  Moderate white matter microvascular ischemic change including scattered\nchronic lacunar infarcts in the basal ganglia and thalami.\n\n4.  Global atrophy is advanced for age."
        },
        {
            "input": "Some of the sequences have been degraded by movement artifact.\n\nThere is a 4 mm focus of enhancement in the left cerebellar hemisphere\nsuperiorly, abutting the left tentorium cerebelli.  There is no surrounding\nedema.  There is no abnormal leptomeningeal enhancement.  There is\nencephalomalacia in the right parietal and superior aspect of the right\noccipital lobe, and also in the splenium of the corpus callosum, in keeping\nwith the previous hemorrhage.  There is surrounding T2/FLAIR hyperintensity,\nwhich likely represents gliosis.  There is hemosiderin staining on gradient\necho sequence at the periphery of the area of encephalomalacia, in keeping\nwith previous hemorrhage.  There are a few foci of blooming in the right\nfrontal lobe, in keeping with previous microhemorrhage.  There is no evidence\nof mass effect, midline shift or infarction.  There is ex vacuo dilatation of\nthe trigone and occipital horn of the right lateral ventricle secondary to the\nadjacent encephalomalacia.",
            "output": "-4 mm focus of enhancement in the left cerebellar hemisphere superiorly\nabutting the left tentorium cerebelli.  Differential considerations include a\nbenign process such as a small meningioma, however a focal solitary metastatic\nlesion cannot definitively be excluded.\n-Encephalomalacia and surrounding gliosis in the right parietal and superior\naspect of the right occipital lobe, in keeping with previous hemorrhage.\n-There are few foci of blooming on gradient echo within the right frontal\nlobe, in keeping with previous microhemorrhage.\nRecommendations:\n\nThree-month follow-up with MRI of the head is recommended to evaluate for\ninterval change."
        },
        {
            "input": "Study is severely degraded by motion, especially on postcontrast images. \nWithin these confines:\n\nRight parieto-occipital remote hemorrhage related encephalomalacia.  Grossly\nstable nonspecific curvilinear enhancement within the area of encephalomalacia\nis again seen (see 100:115 current study and 101:111 on prior exam). \nAdditional punctate right frontal focus of chronic blood products versus\nmineralization is noted (see 10:15).\n\nLeft cerebellar approximately 4 mm focal enhancement is again seen on\npostcontrast imaging (see 13:7; 17:62; series 18 on current study and 14:64;\n15:8 on ___ prior exam).\n\nThere is no evidence of hemorrhage, edema, mass effect, midline shift or\ninfarction.   The ventricles and sulci are stable in caliber and\nconfiguration.",
            "output": "1. Study is severely degraded by motion.\n2. No definite evidence of acute infarct.\n3. Grossly stable approximately 4 mm left cerebellar enhancing mass.  While\nfinding may represent artifact, or dural-based mass such as meningioma,\nmetastatic disease is not excluded on the basis of this examination.  Again,\nrecommend three-month follow-up evaluation for stability or comparison with\noutside contrast brain MRI if available for comparison.\n4. Right parieto-occipital remote hemorrhage related encephalomalacia.\n5. Grossly stable right frontal punctate chronic blood products versus\nmineralization.\n\nRECOMMENDATION(S):  Grossly stable approximately 4 mm left cerebellar\nenhancing mass. While finding may represent artifact, or dural-based mass such\nas meningioma, metastatic disease is not excluded on the basis of this\nexamination. Again, recommend three-month follow-up evaluation for stability\nor comparison with outside contrast brain MRI if available for comparison."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction. The ventricles and sulci are prominent for the patient's age,\nsuggesting cortical volume loss.  No diffusion abnormalities are detected. \nThe major vascular flow voids are present and demonstrate normal distribution.\n\nThe paranasal sinuses and mastoid air cells are clear, the orbits are\nunremarkable.",
            "output": "1. No acute intracranial abnormality."
        },
        {
            "input": "There is normal gray-white matter signal without acute infarct, hemorrhage,\nmass, or mass effect.  The ventricles and extra-axial spaces are unremarkable.\nThe vascular flow voids are preserved.  The orbits, calvarium, and soft\ntissues are unremarkable.  The paranasal sinuses and mastoid air cells are\nclear.",
            "output": "Normal brain MRI.  No evidence of stroke."
        },
        {
            "input": "There is no evidence of intracranial hemorrhage, mass, mass effect or shifting\nof the normally midline structures.  The ventricles and sulci are normal in\nsize and configuration for patient's age.  On the axial FLAIR and T2 weighted\nimages, there is a single focus of high signal intensity identified in the\nsubcortical white matter of the right parietal lobe measuring approximately\n2.8 x 6.5 mm in transverse dimension (image 15, series 15), with no evidence\nof abnormal enhancement after contrast administration, and no diffusion\nabnormalities, likely reflecting sequela of chronic microvascular ischemic\nchange, however this finding is nonspecific.  The major vascular flow voids\nare present and demonstrate normal distribution, the orbits are unremarkable,\nthe paranasal sinuses demonstrate mild mucosal thickening in the ethmoidal air\ncells, no air-fluid levels are seen, the middle ear cavities and mastoid air\ncells are clear.",
            "output": "1.  There is no evidence of intracranial process or hemorrhage.\n\n2.  Single focus of T2/FLAIR high-signal intensity identified in the\nsubcortical white matter of the right parietal lobe as described detail above\n(image 15, series 15, with no evidence of abnormal enhancement after contrast\nadministration, although this finding is nonspecific suggests sequela of\nchronic microvascular ischemic change."
        },
        {
            "input": "Multiple bilateral diffusion abnormalities involving the cerebellum, left\nfrontal cortex and bilateral parietal cortices, none with ADC correlate,\nprobably suggest subacute cardioembolic infarcts.  The infarcts are\nnonenhancing and there is no GRE correlate.  No abscess formation identified. \nNo leptomeningeal enhancement.\n\nModerate periventricular and subcortical white matter T2/FLAIR\nhyperintensities are nonspecific but likely sequelae of chronic small vessel\nischemic disease.  Ventricles and sulci are prominent consistent with\ninvolutional changes.\n\nThere is mucosal thickening and a fluid level seen in the right maxillary\nsinus.  There is extensive unilateral opacification of the right mastoid air\ncells with extension into the middle ear.  No obvious asymmetry of the\nnasopharynx to suggest malignancy.",
            "output": "1. Multiple multifocal nonenhancing subacute infarcts are likely\ncardio-embolic in origin.  No other signs of infectious etiology, including no\nGRE correlate, no abscess formation, and no leptomeningeal enhancement.\n2. Moderate small vessel ischemic disease.\n3. Extensive unilateral opacification of the right mastoid air cells and right\nmaxillary sinus mucosal thickening with an air-fluid level."
        },
        {
            "input": "The common, internal and external carotid arteries appear normal. There is no\nevidence of stenosis by NASCET criteria. The origins of the great vessels,\nsubclavian, and vertebral arteries appear normal bilaterally.  The common\ncarotid bifurcations appear normal.\n\nStatus-post endoscopic sinus surgery, better characterized on prior head and\nneck CTA.  Mild maxillary sinus mucosal thickening, small right maxillary\nsinus mucous retention cyst, and partial ethmoid air cell opacification.",
            "output": "Essentially normal MRA neck."
        },
        {
            "input": "There is no evidence of acute infarction.  There are numerous tiny T2\nhyperintense foci throughout the basal ganglia and thalami which suppress on\nFLAIR and are compatible with prominent perivascular spaces.  Additional FLAIR\nT2 hyperintensities within the bilateral cerebellar hemispheres are compatible\nwith chronic infarcts.  Similarly, additional periventricular and subcortical\nwhite matter T2/FLAIR hyperintensities are likely sequela of chronic small\nvessel disease.  No intracranial hemorrhage. No mass, mass effect, edema or\nmidline shift. There is no abnormal enhancement.  The dural venous sinuses\nappear patent.\n\nThe ventricles and sulci are prominent compatible with global parenchymal\nvolume loss, not out of per patient for patient's age.  There is gross\npreservation of the principal intracranial vascular flow voids.\n\nMild mucosal thickening is noted in scattered ethmoid air cells.  The\nremainder of the visualized paranasal sinuses, middle ear cavities, and\nmastoid air cells are well aerated and clear.  The patient is status post\nbilateral lens resections.",
            "output": "1. No evidence for acute intracranial hemorrhage, infarction, or abnormal\nenhancement.  Specifically, patent basal cisterns without evidence for mass or\nmass effect.\n2. Global parenchymal volume loss and evidence of chronic small vessel\nischemic disease."
        },
        {
            "input": "The study is motion degraded. Within these confines:\n\nThere is no evidence of mass, hemorrhage or infarct. Sulci, ventricles and\ncisterns are within expected limits for the patient's age. There are unchanged\nperiventricular and subcortical T2/FLAIR white matter hyperintensities, which\nare nonspecific.  The major intracranial flow voids are preserved. The dural\nvenous sinuses are patent. There is no abnormal enhancement. Moderate mucosal\nthickening of the left maxillary sinus is new since prior exam. There are\nbilateral lens replacements otherwise orbits are unremarkable. The mastoid air\ncells are clear.",
            "output": "1. Motion degraded study.\n2. Allowing for this, there is no evidence of intracranial metastatic disease.\n3. Nonspecific T2/FLAIR white matter hyperintensities, commonly seen in\nsetting of chronic microangiopathy."
        },
        {
            "input": "Please note, FLAIR images were not acquired during this study.\n\nThe patient is status post interval resection of a left frontal lobe mass with\npostsurgical changes including blood products within the resection cavity,\nbifrontal pneumocephalus with small amount of extra-axial fluid/hemorrhage,\nand linear dural thickening enhancement deep to the craniotomy site, likely\npostoperative.  There is slow diffusion surrounding the resection cavity,\nwhich may represent postoperative ischemia.\n\nThere is a nodular focus of enhancement along the posterior aspect of the\nresection cavity (600:120), measuring 7 mm TV x 1 cm AP x 0.9 cm SI.  There is\ndecrease in mass effect on the adjacent superior sagittal sinus.  Otherwise,\nthere is no evidence of acute infarction, new enhancing mass or additional\nareas of abnormal enhancement.  Again seen is a nodular nonenhancing focus\nwithin the posterosuperior sagittal sinus, likely arachnoid cyst.  There is\nmild mucosal thickening of bilateral ethmoid air cells with a small left\nmaxillary sinus mucosal retention cyst.  There is trace fluid opacification of\nbilateral mastoid air cells.  The orbits appear unremarkable.",
            "output": "1. Postsurgical changes as described above related to interval resection of a\nleft frontal lobe mass, likely a meningioma.  Small nonspecific enhancing\nnodular focus along the posterior aspect of the resection cavity, may\nrepresent tiny residual tumor.  Attention on follow-up is recommended.\n2. No new enhancing mass or additional abnormal enhancement.\n3. Small amount of slow diffusion surrounding the resection cavity may\nrepresent postoperative ischemia."
        },
        {
            "input": "Left frontal craniotomies identified.  Extensive dural enhancement is seen in\nthis region.  Encephalomalacia is identified.  Postcontrast images demonstrate\na in area of nodular enhancement adjacent to the left side of the superior\nsagittal sinus (1001:65) measuring 19 x 15 mm which appears to have slightly\nincreased since the prior study when it measured 13 x 12 mm.  No other areas\nof abnormal enhancement seen.  No acute infarcts are identified.",
            "output": "Slight  interval increase in size of residual nodular enhancing lesion in the\nleft parafalcine region since the MRI of ___.  Close follow-up\nrecommended."
        },
        {
            "input": "The left frontal para falx meningioma measuring 29 x 17 mm in the coronal\nplane appears similar  to the most recent prior imaging ___.  The\nlesion is T2 hypointense and demonstrates loss of signal on the gradient echo\nin keeping with calcification.  It demonstrates homogeneous enhancement\npostcontrast.  The lesion abuts the adjacent superior sagittal sinus and\nappears to have invaded cluded.  Surrounding FLAIR edema appears fairly\nsimilar compared to prior.  Overlying postsurgical changes are stable.\n\nProminent arachnoid granulation in relation to the posterior aspect of the\nsuperior sagittal sinus is again noted and is unchanged.  The rest of the\nbrain is normal in morphology.  No other abnormal enhancing lesions.  The\nventricular profile is appropriate for age.  Partially empty sella.  Bilateral\nchoroid plexus xantho granulomas.  The craniocervical junction appears normal.\nThe intracranial arteries demonstrate normal T2 flow voids.  Orbits appear\nnormal.  Small mucous retention cyst present in the inferior aspect of the\nleft maxillary sinus.  Minimal mucosal thickening involving the ethmoid air\ncells.",
            "output": "The left frontal para falx meningioma appears similar compared to most recent\nprior imaging done ___.  The lesion appears stable to minimally\nincreased in size compared to first postoperative MRI done ___.\nThe lesion appears to invade the superior sagittal sinus"
        },
        {
            "input": "At the left parasagittal vertex, there is a 5.2 x 4.3 x 4.2 cm (AP x TV x SI)\nextra-axial mass, abutting the dura with evidence of mild dural thickening\nwith narrow genius enhancement, most consistent with a meningioma.  Blooming\nartifacts on gradient echo is most consistent with calcifications, as seen on\nprior CT from ___.  There is associated mass effect in the adjacent\nleft frontal lobe and mild vasogenic edema.\n\n\nThere are choroid plexus cysts bilaterally.\n\nMild periventricular white matter T2/FLAIR hyperintensities are nonspecific,\nhowever likely due to small vessel ischemic disease in this age group.\n\nThere is mild bilateral ethmoid air cell and frontal sinus mucosal thickening.\nOtherwise, the paranasal sinuses, mastoids and middle ear cavities are clear.\n\nThe imaged globes are unremarkable.\n\nThe intracranial flow voids are maintained.  There is intrinsically T1 and T2\nhypointense, nonenhancing filling defect in the posterior sagittal dural\nsinus, most likely representing arachnoid granulation (21:101).  Dural venous\nsinuses are patent otherwise.",
            "output": "1. 5.2 x 4.3 x 4.2 cm extra-axial mass left parasagittal, causing mass effect\non the left frontal lobe at the vertex with associated dural tail, most\nconsistent with a meningioma.  There is mild vasogenic edema.\n2. Although the mass is attached to the wall of the sinus, the superior\nsagittal sinus is patent."
        },
        {
            "input": "There is no evidence of hemorrhage or infarction.  The ventricles and sulci\nare mildly prominent in size and configuration with no mass effect or midline\nshift.  Scattered patchy FLAIR hyperintense periventricular and subcortical\nwhite matter foci are nonspecific, but most likely related to chronic small\nvessel ischemic disease.\n\nThe major intracranial arterial flow voids are maintained.  The intraorbital\ncontents are normal.  There is mild mucosal thickening of the ethmoid sinuses.\nThe mastoid air cells are clear.",
            "output": "1. No evidence of hemorrhage or infarction.\n2. Mild cerebral atrophy and chronic small vessel ischemic disease."
        },
        {
            "input": "Study is slightly motion limited.  There is no evidence of hemorrhage, edema,\nmasses, mass effect, midline shift or infarction.  Ventricles, sulci and\ncisterns demonstrate similar mild involutional changes.  Subcortical and\nperiventricular white matter T2/FLAIR hyperintensities are again noted.  There\nis similar signal abnormality within the pons.  No associated enhancement is\nseen.  These likely represent microvascular ischemic change.  There is no\nabnormal enhancement after contrast administration.  Partially empty sella\nturcica is similar.  T2 hyperintensities again noted within the right petrous\napex.  Small retention cyst is present in the right maxillary sinus.\n\nMild ethmoid air cell mucoperiosteal thickening is noted.",
            "output": "1. Mildly motion limited study.\n2. No convincing metastatic involvement of the brain.\n3. Similar appearance of probable microvascular ischemic change.\n4. Similar appearance of T2 hyperintense focus within the right petrous apex\nwhich could be related to effusion."
        },
        {
            "input": "MRI BRAIN:\n\nThere is no slow diffusion to suggest acute infarction.  Multiple focal areas\nof fast diffusion (low signal on DWI, high signal on the ADC map) along the\nperiphery of the cerebellar hemispheres bilaterally are consistent with\nchronic infarcts (___).  Susceptibility artifact in the basal ganglia\nbilaterally, particularly on the right, probably represents mineralization. \nMultifocal punctate and more confluent periventricular and subcortical foci of\nhigh T2/FLAIR signal are nonspecific but likely sequelae of chronic\nmicroangiopathy in a patient of this age.  Prominence of the ventricles and\nsulci is in keeping with global atrophy.  Intracranial vascular flow voids are\npreserved.  The orbits are unremarkable.\n\nMRA BRAIN:\nThe intracranial vertebral and internal carotid arteries and their major\nbranches appear normal without evidence of stenosis, occlusion, or aneurysm\nformation.\n\nMRA NECK:\nThere is a central filling defect in the proximal left internal carotid artery\non the arterial phase postcontrast sequences (22:18).  The right internal\ncarotid artery demonstrates normal caliber and signal intensity distal to this\narea.  A similar finding is noted in the proximal left external carotid artery\non the same sequence.  Both filling defects are no longer visualized on the\nmore delayed coronal sequence and are consistent with flow related artifact. \nThe internal and external carotid arteries otherwise appear normal.  There is\nno evidence of internal carotid artery stenosis by NASCET criteria.  The\norigins of the great vessels, subclavian and vertebral arteries appear normal\nbilaterally.",
            "output": "1. Global atrophy, chronic small vessel ischemic change, and chronic\ncerebellar infarcts.  No acute infarction.\n2. Susceptibility changes in the basal ganglia and may represent changes due\nto mineralization.  No intra or extra-axial hemorrhage otherwise.\n3. Unremarkable brain MRA.\n4. Unremarkable neck MRA."
        },
        {
            "input": "There is no intra or extra-axial mass, acute hemorrhage or infarct. The sulci,\nventricles and cisterns are within expected limits for the patient's mild\nsenescent related global cerebral volume loss.  Mild to moderate\nperiventricular and subcortical T2/FLAIR nonenhancing white matter\nhyperintensities are nonspecific, but compatible with chronic microangiopathy\nin a patient of this age.  The major intracranial flow voids are preserved. \nThe dural venous sinuses are patent.  Incidental note is made of a partial\nempty sella.  The orbits are unremarkable, noting bilateral lens replacements.\nThere is mild mucosal thickening of the ethmoid air cells.  The remainder the\nparanasal sinuses are essentially clear.  No significant fluid signal is seen\nin the mastoid air cells.  No suspicious osseous lesion.  Degenerative changes\nat the craniocervical junction include a prominent pannus posterior to the\ndens, minimally remodeling the cervicomedullary junction as well as a disc\nprotrusion at C3-C4 which appears to result in moderate to severe spinal canal\nnarrowing, remodeling the cord.",
            "output": "1. No evidence intracranial metastatic disease at this time.  No abnormal\npostcontrast enhancement.\n2. No acute infarct or intracranial hemorrhage.  Periventricular and\nsubcortical T2/FLAIR white matter hyperintensities are nonspecific, but\ncompatible with chronic microangiopathy in a patient of this age.\n3. There appears to be at least moderate to severe spinal canal narrowing with\nremodeling of the cord at C3-C4.  If the patient is clinically symptomatic,\nrecommend further evaluation with MRI cervical spine.\n4. Additional findings described above."
        },
        {
            "input": "There is an 8 mm focus of enhancement at the right frontal convexity regions\nseen on series 10, image 22 and additional 5 mm focus of enhancement\nidentified at the right inferior cerebellum best seen on series 10, image 5. A\npunctate area of enhancement is also seen in the right as well as in the left\ntemporal lobe on series 10 image 10. There is no leptomeningeal enhancement\nseen. There is no mass effect, midline cyst or hydrocephalus. Changes of small\nvessel disease are again identified. Soft tissue changes are seen within the\nleft sphenoid sinus with inspissated secretions.",
            "output": "No foci of enhancement as described above since the previous MRI of ___ but the largest focus of enhancement in the right frontal convexity\nmeasuring 8 mm. Findings are consistent with metastatic disease."
        },
        {
            "input": "There infarction involving the majority of the right posterior cerebral artery\nterritory including the medial occipital and temporal lobes, right cerebral\npeduncle and right thalamus.  There is hemorrhage within the right thalamic\ninfarct.\n\n The ventricles and sulci are prominent, consistent with global cerebral\nvolume loss.  Patchy periventricular T2 hyperintensities are most consistent\nwith chronic microvascular angiopathy.\n\nModerate opacification of the left maxillary sinus is seen with internal blood\nproducts, likely due to the patient's known left orbital blowout fracture. \nThere is moderate mucosal thickening of the ethmoid and sphenoid sinuses with\nair-fluid levels within the sphenoid sinuses.\n\nA large scalp hematoma is seen over the left frontal region.  A large\nsubgaleal collection is seen in the left frontoparietal region.\n\nThe mastoid air cells are clear.  The patient is status post right lens\nreplacement.\n\nEndotracheal and oro-enteric tubes are partially visualized.",
            "output": "1. Right PCA territory infarction with hemorrhage in the right thalamic\ninfarct.\n2. Acute left maxillary and bilateral ethmoid and sphenoid sinus disease with\nblood products in the left maxillary sinus, likely related to the patient's\nknown left orbital blowout fracture.\n3. Large left frontal scalp hematoma and large left frontoparietal subgaleal\ncollection, likely posttraumatic."
        },
        {
            "input": "There is no evidence of acute intracranial hemorrhage or mass effect. The\nventricles and basal cisterns appear normal.\n\nThere is nonspecific T2/FLAIR signal hyperintensity within the subcortical and\nperiventricular white matter which is presumably on the basis of chronic small\nvessel ischemic disease. There are normal vascular flow voids. There is no\nevidence of acute ischemia based on diffusion-weighted imaging.\n\nThere is gradient signal hypointensity within the right occipital lobe which\ncould represent a vascular malformation such as a cavernoma or telangiectasia\nversus prior remote hemorrhage. There is no clear abnormality seen in this\nregion on other sequences. Recommend correlation with additional post-contrast\nimaging and SWI technique (please protocol on ___ magnet for this specific\nsequence).\n\nThere is diffuse paranasal sinus mucosal thickening with air-fluid levels\nwithin the bilateral maxillary sinuses and sphenoid sinuses.",
            "output": "1. No evidence of acute intracranial hemorrhage, mass effect, or acute\nischemia.\n2. Gradient signal hypointensity within right occipital lobe could represent a\nvascular malformation such as a cavernoma or telangiectasia versus prior\nremote hemorrhage. Recommend correlation with additional post-contrast imaging\nand SWI technique (see above).\n3. Brain parenchymal volume loss and presumed sequelae of chronic small vessel\nischemic disease.\n\nNOTIFICATION:   The impression above was entered by Dr. ___ on\n___ at 15:55 into the Department of Radiology critical communications\nsystem for direct communication to the referring provider."
        },
        {
            "input": "There is no evidence of acute infarction.  No intracranial hemorrhage.  No\nmass, mass effect, edema or midline shift.\n\nThere is minimal asymmetry of the right temporal ventricular horn extending to\nthe right choroidal fissure (image 11, series 13, and image 60, series 18),\nsuggestive of choroidal fissure cyst, measuring approximately 10 x 6 mm in\ncoronal projection.  The basal cisterns are patent.  There is no evidence of\nimpending, downward herniation.  There is apparent preservation of the\nprincipal intracranial vascular flow voids.  No diffusion abnormalities are\ndetected.\n\nFollowing the administration of intravenous contrast material, there is no\nabnormal enhancement.  The dural venous sinuses appear patent on MP-RAGE\nimagine sequences.\n\nMucosal thickening is seen involving the bilateral ethmoidal with possible\ninspissated secretions in the posterior ethmoidal air cells on the right\n(image 15, series 6), mucosal thickening is also noted in the maxillary\nsinuses and right frontal sinus extending towards the frontal ethmoidal recess\non the right.  A small mucous retention cyst is noted in the left sphenoid\nsinus.  The mastoid air cells are well aerated and clear.  The orbits are\ngrossly unremarkable.",
            "output": "1.  There is minimal asymmetry lateral to the right temporal ventricular horn\nsuggestive of small choroidal fissure cyst with no evidence of mass effect or\nedema.\n\n2.  Paranasal sinus disease, as detailed above.  Otherwise, unremarkable MRI\nexamination of the brain."
        },
        {
            "input": "There is encephalomalacia in the inferomedial left cerebellar hemisphere. \nThere is no evidence of acute intracranial infarction, hemorrhage, edema,\nmass, or mass effect.  The ventricles and sulci are within normal limits with\nrespect to caliber and configuration.\n\nThe visualized paranasal sinuses and mastoid air cells appear clear.  The\nglobes and orbits are unremarkable.  Major intracranial vascular flow voids\nare grossly preserved.",
            "output": "1. No acute intracranial abnormality.\n2. Inferomedial left cerebellar hemisphere encephalomalacia, consistent with\nsequelae of chronic infarct."
        },
        {
            "input": "The subarachnoid hemorrhage in the suprasellar and pre pontine cisterns is\nunchanged. There are also unchanged bilateral small intraventricular\nhemorrhages. There is no new hemorrhage. There is no infarct, or mass effect.\nThe principal intracranial flow voids are present.\n\nThere is complete opacification of the right maxillary sinus with moderate\nmucosal thickening and fluid.  There are findings suggestive of enlargement of\nthe right maxillary sinus accessory ostium and chronic osteitis, but it better\nappreciated on CT dated ___. The orbits, mastoid air cells and\nvisualized soft tissues are unremarkable.",
            "output": "Subarachnoid hemorrhage in the suprasellar and prepontine cisterns, unchanged,\nwith a small amount of intraventricular blood. There is no new hemorrhage, and\nno evidence of acute infarct or abnormal enhancement.\n\nComplete opacification of the right maxillary sinus with moderate mucosal\nthickening and retained fluid.  There are also findings suggestive of\nenlargement of the right maxillary sinus accessory ostium and thickening of\nits walls, suggestive of chronic osteitis, better-appreciated on the CTA."
        },
        {
            "input": "MRA Head: There is mild prominence of the left MCA bifurcation, in correlation\nwith prior CTA findings, although no discrete aneurysm  seen on current study\nor prior cerebral angiogram. There is otherwise no clear evidence of\nintracranial aneurysm, vascular malformation, or pathologic large vessel\nocclusion within the intracranial vasculature. The anterior communicating\nartery and bilateral posterior communicating arteries are seen. The left A1\nsegment is hypoplastic.\n\nThere is a small right maxillary sinus mucosal retention cyst.  The remaining\nimaged portions of the intracranial contents are unremarkable.\n\nMRA neck: The aortic arch demonstrates conventional three-vessel branch\nconfiguration. The vertebral arteries are codominant. There is no evidence of\ndissection, hemodynamically significant stenosis, or pathologic large vessel\nocclusion within the vessels of the neck.",
            "output": "1. No clear evidence of aneurysm, hemodynamically significant stenosis, or\npathologic large vessel occlusion within the vasculature of the head and neck."
        },
        {
            "input": "There are postoperative changes of a prior left frontal craniotomy with\nunderlying encephalomalacia.  The associated there signal abnormality in the\npostoperative site is unchanged when compared to prior exam.  There is no\nevidence of acute intracranial hemorrhage or mass effect. The ventricles and\nbasal cisterns appear stable in size.\n\nThere is no evidence of acute ischemia based on diffusion-weighted imaging.\nThere is extensive subcortical and periventricular T2/FLAIR signal\nhyperintensity which is presumably on the basis of chronic small vessel\nischemic disease.\n\nThere is minimal dural enhancement subjacent to the craniotomy site though\nthere is otherwise no evidence of abnormal brain parenchymal or leptomeningeal\nenhancement to suggest residual or recurrent intracranial disease.\n\nThere is a right maxillary sinus air-fluid level, which could represent a\ncomponent of acute sinusitis. The orbits are unremarkable.",
            "output": "1. Postoperative change of prior left frontal craniotomy with underlying\nencephalomalacia.\n2. No evidence of abnormal brain parenchymal or leptomeningeal enhancement to\nsuggest recurrent intracranial metastatic disease.\n3. Stable extensive presumed sequelae of chronic small vessel ischemic\ndisease.\n4. Right maxillary sinus air-fluid level which could represent a component of\nacute sinusitis."
        },
        {
            "input": "In comparison will multiple prior examination, again postsurgical changes are\nre- demonstrated, consistent with left frontal craniotomy. There are stable\npost radiation induced changes in the subcortical white matter of both\ncerebral hemispheres, more significant on the left. There is not evidence of\nabnormal enhancement to indicate residual mass, recurrence or metastatic\ndisease.  No diffusion abnormalities are detected to indicate acute or\nsubacute ischemic changes.  The ventricles and sulci remain unchanged and\nappear slightly prominent, suggesting cortical volume loss. Additional\nscattered areas of high-signal intensity in the subcortical white matter may\nrepresent changes due to small vessel disease, however, this finding is\nnonspecific. The major vascular flow voids are present and demonstrate normal\ndistribution. The orbits are unremarkable, the paranasal sinuses are notable\nfor mucous retention cyst on the right maxillary sinus, which is unchanged. \nThe mastoid air cells are clear.",
            "output": "1. In comparison with the most recent examination, no significant changes are\nidentified, there are stable postsurgical and post radiation induced changes\nin the left frontal lobe, and associated areas of encephalomalacia in the\nsubcortical white matter bilaterally.\n\n2. There is no evidence of residual mass, recurrence or new metastatic\ndisease.\n\n3.  Scattered foci of high signal intensity in the subcortical white matter\nare unchanged, and are nonspecific, suggestive of chronic microvascular\nischemic disease."
        },
        {
            "input": "Left frontoparietal craniotomy changes are seen with unchanged appearance of\nthe underlying left frontal resection cavity.  Stable FLAIR hyperintense\nsignal surrounds the resection cavity with no new or residual abnormal\ncontrast enhancement.  Confluent stable periventricular and subcortical\nT2/FLAIR hyperintense signal is noted throughout the remainder of supra\ntentorium.  There is a focus of FLAIR hyperintense signal in the medial left\ncerebellar hemisphere with no associated contrast enhancement, series 8, image\n7, stable since ___.\n\nThere is no evidence of hemorrhage, mass effect, midline shift or infarction. \nThere is prominence of the ventricles and sulci suggestive involutional\nchanges.  There is no abnormal enhancement after contrast administration.  The\nmajor vascular flow voids are preserved.\n\nBilateral cataract extraction changes are seen.  An air-fluid level is noted\nin the right maxillary sinus.  Minimal mucosal thickening of the ethmoid\nsinuses seen.  The mastoid air cells are normal.  Fatty replacement of the\nbilateral parotid glands is seen.  The remainder the visualized soft tissues\nare normal.\nIntrinsic T1 hyperintense signal is noted in the visualized upper cervical\nspine and clivus, likely secondary to fatty marrow hyperplasia from prior\nradiation.",
            "output": "1. Stable postsurgical and post radiation changes, as described above with no\nnew contrast enhancing lesion or abnormal high signal identified, to suggest\nrecurrent or residual disease metastatic disease.\n2. Stable paranasal sinus disease."
        },
        {
            "input": "Study is mildly degraded by motion.  Patient is status post left\nfrontoparietal craniotomy with stable postsurgical changes.  There is T2 FLAIR\nhyperintensity within the surgical bed that is unchanged.  There is a\nconfluence of T2 FLAIR hyperintensity of the periventricular and deep\nsubcortical white matter that is left hemisphere dominant, which is stable\ndating back to ___ studies.\n\nThere is no evidence of new masses.  There is no evidence of hemorrhage,\nedema, mass effect, midline shift or infarction.  There is prominence of the\nventricles and sulci suggestive age-related involutional changes.  There is no\nabnormal enhancement after contrast administration.\n\nThere is right maxillary sinus mucous retention cyst.",
            "output": "1.  Study is mildly degraded by motion.\n2. Stable postsurgical and radiation changes, as described.\n3.  Within limits of study, no definite evidence of recurrent or residual\nmetastatic disease.\n4. Stable paranasal sinus disease as described above."
        },
        {
            "input": "Patient is status post left frontoparietal craniotomy with stable postsurgical\nchanges.  Posttreatment changes within the adjacent left frontal lobe surgical\nbed is again demonstrated.  There is no evidence of recurrent tumor.  The\nregions of T2 FLAIR hyperintensity in the periventricular and deep subcortical\nwhite matter, left greater than right, is stable.  Area of subcortical FLAIR\nhyperintensity in the posterior frontal lobe, probably involving lateral\nprecentral gyrus is stable since ___, there is no associated enhancement.\n\nThere are no new masses or mass effect.  There is no evidence of hemorrhage,\nterritory infarction, or midline shift. There is no abnormal enhancement after\ncontrast administration.\n\nThe ventricles and sulci are prominent in caliber and configuration,\nsuggestive of age related atrophy and involutional changes.  The major\nintracranial vascular flow voids are preserved.  The dural venous sinuses\nappear patent.\n\nAgain demonstrated is a right maxillary mucous retention cyst.  There is mild\nanterior nasal septum deviation to the left.  Otherwise, the paranasal\nsinuses, bilateral mastoid air cells and middle ear cavities are clear..",
            "output": "1. There is no evidence of new or recurrent mass.\n2. There are no acute intracranial changes.\n3. Stable posttreatment changes."
        },
        {
            "input": "MRI BRAIN:\nRe-demonstration of left frontoparietal craniotomy changes.  There is no\nevidence of recurrent tumor.  The regions of T2 FLAIR hyperintensity in the\nperiventricular and deep subcortical white matter, left greater than right, is\nstable compared to prior MR exam performed ___.  Area of\nhigh-intensity in the left postcentral gyrus on axial DTI (series 7, image\n26), does not demonstrate enhancement or surrounding edema on postcontrast\nimaging and is obscured by surgical artifact on other sequences.  Since is\ncorrelates with the area of hyperdensity on CT, this likely corresponds to an\narea of subarachnoid hemorrhage.  Otherwise there is no abnormal enhancement\nafter contrast administration.  The ventricle and sulci are prominent in\ncaliber and configuration, suggestive of age related atrophy and involutional\nchanges.  There is no evidence of recurrent tumor.\n\nMRA BRAIN:\nThere is irregularity of the bilateral M2 segments without evidence of\nocclusion.  Otherwise intracranial vertebral and internal carotid arteries and\ntheir major branches appear normal without evidence of stenosis, occlusion, or\naneurysm formation.\n\n\nMRA NECK:\nThere is mild narrowing of the left vertebral and internal carotid arteries at\ntheir origin.  There is signal loss of the left common carotid bifurcation\nextending into the left internal carotid artery on contrast-enhanced MRA, but\n2D time-of-flight MRA and MPrage postcontrast images show the vessel to be\nnormal without evidence of stenosis; it is speculated that the signal loss is\nartificial.  There is no evidence of internal carotid stenosis by NASCET\ncriteria.",
            "output": "1. Area of high intensity in the left postcentral gyrus on axial DTI, does not\ndemonstrate enhancement or surrounding edema on postcontrast imaging and is\nobscured by surgical artifact on other sequences. This likely corresponds to\nan area of subarachnoid hemorrhage as seen on prior CT head performed ___.\n2. Re-demonstration of left frontoparietal craniotomy changes as well as T2\nFLAIR hyperintensity in the periventricular deep subcortical white matter,\nleft greater than right, that is stable compared to prior MR exam on ___.\n3. There is irregularity of the bilateral M2 segments without evidence of\nocclusion.\n4. There is signal loss of the left common carotid bifurcation extending into\nthe left internal carotid artery on contrast-enhanced MRA, but 2D\ntime-of-flight MRA and MPrage postcontrast images show the vessel to be normal\nwithout evidence of occlusion; it is speculated that the signal loss is\nartificial."
        },
        {
            "input": "MRA NECK:\nEvaluation of the aortic arch and great vessel origins is limited by artifact.\nRemaining cervical courses of the common carotid arteries, as well as the\ninternal carotid arteries, appear widely patent without evidence for stenosis\nby NASCET criteria.  Evaluation of vertebral artery origins and V1 segments is\nalso limited by artifacts.  Remaining courses of bilateral vertebral arteries\nappear widely patent.\n\nMRA BRAIN:\nThere is mild motion artifact.  The intracranial vertebral and internal\ncarotid arteries and their major branchesappear widely patent without evidence\nfor flow-limiting stenosis or aneurysm.",
            "output": "1. Technically limited evaluation of the great vessel origins and vertebral\nartery origins.  Otherwise, unremarkable neck MRA.\n2. Unremarkable brain MRA allowing for mild motion artifact."
        },
        {
            "input": "MRI BRAIN:\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.\n There are noted to severe patchy T2/FLAIR hyperintensities in the cerebral\nhemispheres bilaterally, a nonspecific finding and likely related to chronic\nsmall vessel ischemic changes.\n\nThere is no abnormal enhancement after contrast administration.\n\nIncidental note is made of a partially empty sella.\n\nThe ventricles and sulci are age appropriate.  Well preserved brain parenchyma\nfor patient's age.\nMajor vascular flow voids are preserved.  Major dural venous sinuses are\npatent.\n\nThere is mild mucosal thickening along the ethmoid air cells.  There is near\ncomplete opacification of the right maxillary sinus with appearance of sinus\natelectasis.  The mastoid air cells appear clear.  The orbits appear\nunremarkable.\n\nMRA BRAIN:\nThe intracranial vertebral and internal carotid arteries and their major\nbranches appear normal without evidence of stenosis, occlusion, or aneurysm\nformation.\n\nMRA NECK: Dynamic examination is motion degraded.  Within this confine:\nThe common, internal and external carotid arteries appear normal.  There is no\nevidence of internal carotid artery stenosis by NASCET criteria.  The origins\nof the great vessels, subclavian and vertebral arteries appear normal\nbilaterally.",
            "output": "1. No acute intracranial abnormality on contrast enhanced MRI brain.  No\nevidence of acute infarction, hemorrhage or mass.\n2. Moderate to severe nonspecific patchy white matter changes in the cerebral\nhemispheres bilaterally, likely sequela of chronic small vessel ischemic\nchanges.\n3. Patent intracranial and cervical vasculature without evidence of stenosis,\ndissection, occlusion or aneurysm formation.\n4. Near complete opacification of the right maxillary sinus with appearance of\nsinus atelectasis and mild mucosal thickening along the ethmoid air cells.\n5. Additional findings described above."
        },
        {
            "input": "There is a 3.4 x 3.1 x 2.6 cm (AP X TR X SI) predominantly ring enhancing\nlesion in the right frontal lobe, corresponding to the previous abnormality on\nthe CTA which is new when compared to the prior exam from ___.  The\nmass demonstrates predominantly slow diffusion and speckled areas of\nsusceptibility artifact which most likely represent intratumoral hemorrhage.\nThere are some areas of fast diffusion is centrally within the necrotic\nportion of the tumor.  There is faintly high-signal intensity on the\nprecontrast T1 sequence which correspond to the area of high density on the\nprior noncontrast CT.\n\nThe mass demonstrates significant surrounding edema which does not infiltrate\nthe corpus callosum.  There is partial effacement of the right frontal lobe\ngyri and sulci as well as of the right lateral ventricle with associated 4 mm\nleftward midline shift which is, allowing for differences in technique,\nsimilar to the prior CT.  The ventricular system is otherwise stable in size\nand configuration.  The basal cisterns remain patent.\n\nCombination of imaging findings including high density on prior noncontrast\nCT, faintly high signal intensity on precontrast T1, slow diffusion and\nsomewhat low signal intensity on T2 weighted imaging could be seen with\nlymphoma. However, the prominent vascularity surrounding the lesion can be\nseen with metastatic disease.  The extremely rapid progression would be\nunusual for even a grade IV glioma, as would be the lack of infiltration into\nthe corpus callosum.  Thus, although a glioblastoma remains a diagnostic\nconsideration, lymphoma or metastasis appears more likely.\n\nAdditional patchy T2/FLAIR hyperintensities in the cerebral hemispheres\nbilaterally, a nonspecific finding and likely related to chronic small vessel\nischemic changes.\nMajor vascular flow voids appear preserved.  Major dural venous sinuses are\npatent.\n\nThere is mild mucosal thickening along the ethmoid air cells and partial\nopacification of the right maxillary sinus.  The mastoid air cells appear\ncentrally clear.  The orbits appear grossly unremarkable.",
            "output": "1. Predominantly ring-enhancing lesion in the right frontal lobe, new from\n___ and demonstrating slow diffusion and intratumoral hemorrhage as\nwell as significant surrounding edema.  Findings are concerning for a primary\nbrain malignancy such as lymphoma or an intracranial metastatic lesion and\nless likely a high-grade glioma.\n2. Edema surrounding the mass results in partial effacement of the right\nlateral ventricle and associated 4 mm leftward midline shift, allowing for\ndifferences in technique, not significantly changed from the prior CT.  Patent\nbasal cisterns.\n3. Additional nonspecific white matter changes in the cerebral hemispheres\nbilaterally, likely sequela of chronic microangiopathy."
        },
        {
            "input": "Again seen is 3.7 cm x 3.3 cm x 2.7 cm mass right frontal lobe, involving\noperculum, upper sub insula, extending into basal ganglia, local mass-effect..\nFindings stable since ___.  Restricted diffusion of the enhancing\ncomponent.  Inhomogeneous enhancement centrally, consistent with cystic change\nor necrosis.  Stable local mass-effect, stable mild midline shift.  No other\nmasses.\n\nComplete opacification with moderate atelectasis and volume loss of the right\nmaxillary sinus.",
            "output": "1. Large right frontal lobe mass, likely glioma, possibly metastasis."
        },
        {
            "input": "Postsurgical changes after right frontal craniotomy for subtotal resection of\na predominantly peripherally enhancing mass are noted.  There are blood\nproducts and fluid as well as a small amount of air within the resection\ncavity.  A small amount of devitalized tissues noted around the resection\ncavity.\nThere is residual nodular enhancement superiorly, along the medial and\nposterior inferior aspect of the resection cavity (series 15, image 95, 102\nand 107) which corresponds to residual tumor.\nA small extra-axial collection subjacent to craniotomy site with slight\nextension into the right middle cranial fossa is noted measuring up to 4 mm in\nmaximum thickness and likely postsurgical in etiology.\n\nThere is persistent extensive edema surrounding the residual mass and site of\nsurgery, similar to prior and with unchanged associated 4 mm leftward midline\nshift and partial effacement of the right lateral ventricle.  The basal\ncisterns remain patent.  There is no crowding at the level of the foramen\nmagnum.\nThe ventricular system is otherwise stable in size and configuration.\n\nThere are additional patchy T2/FLAIR hyperintensities in the cerebral\nhemispheres bilaterally, a nonspecific finding but unchanged and likely\nrelated to chronic small vessel ischemic changes.\nMajor vascular flow voids appear preserved.  Major dural venous sinuses are\npatent.\n\nThere is unchanged complete opacification of the maxillary sinus.  The\nremainder of the paranasal sinuses and mastoid air cells appear clear.  The\norbits appear grossly unremarkable.",
            "output": "1. Expected postsurgical changes after subtotal resection of a right frontal\nlobe mass.\n2. Residual nodular enhancement superiorly to the resection cavity, along its\nmedial and posterior inferior border are consistent with residual tumor.\n3. Unchanged extensive edema in the right frontal lobe surrounding the\nresection cavity and residual mass with stable 4 mm leftward midline shift and\npartial effacement of the right lateral ventricle.\n4. Unchanged nonspecific additional patchy white matter changes in the\ncerebral hemispheres bilaterally, likely sequela of chronic microangiopathy."
        },
        {
            "input": "Expected evolution of postsurgical changes after right frontal craniotomy for\nsubtotal resection of a predominantly peripherally enhancing mass are noted.\n\nThe resection cavity appears slightly more expanded with fluid contents. \nAreas of residual nodular enhancement superiorly as well as along the medial\nand posterior inferior aspect of the resection cavity are again identified.\n\nOverall, the enhancement surrounding the resection cavity appears more\nwell-defined when compared to the prior examination which could reflect\npostsurgical enhancing.  There is a slightly more nodular area extending\nsuperiorly along the lateral border of the resection cavity (series 900, image\n105 and series 9, image 107) which could reflect a an area of collapsed\nresection cavity.\n\nThere has been slight decrease in the amount of confluent FLAIR\nhyperintensities throughout the right cerebellar hemisphere.  As a result,\nthere is also decreased leftward midline shift now measuring up to 3 mm from\npreviously 4 mm.  There is also slightly improved mass-effect on the right\nlateral ventricle.  The basal cisterns remain patent.  There is no crowding at\nthe Level of the foramina magnum.  The ventricular system is otherwise stable\nin size and configuration.\n\nThere are additional patchy T2/FLAIR hyperintensities in the cerebral\nhemispheres bilaterally, a nonspecific finding but unchanged and likely\nrelated to chronic small vessel ischemic changes.  Major vascular flow voids\nare preserved.  Major dural venous sinuses appear patent.\n\nThere is unchanged complete opacification of the right maxillary sinus.  The\nremainder of the paranasal sinuses and mastoid air cells appear clear.  The\norbits appear grossly unremarkable.  Clear",
            "output": "1. Expected evolution of postsurgical changes after right frontal craniotomy\nfor subtotal resection of a right frontal lobe mass.\n2. More well-defined enhancement surrounding the resection cavity may be\nsurgery related.\n3. An area of increased nodularity extending superiorly along the lateral\nborder of the resection cavity could reflect a collapsed portion of the\nresection cavity.\n4. Additional areas of previously noted nodular enhancement appear similar to\nprior and are consistent with residual tumor.\n5. Overall slight decrease in the amount of confluent FLAIR hyperintensities\nin the right cerebellar hemisphere with decrease in leftward midline shift now\nmeasuring up to 3 mm from previously 4 mm and slight improvement of\nmass-effect on the right lateral ventricle."
        },
        {
            "input": "There is significant interval enlarged in size of previously partially\nresected right frontal mass lesion measuring approximately 54 x 35 mm in\ntransverse dimension.  The mass lesion show more extensive and thick irregular\nmarginal enhancement.  There is interval increased surgical margin irregular\nand nodular diffusion restriction.  There is no significant interval change of\nleftward midline shift by 5 mm AP. There is effacement of the right lateral\nventricle due to mass effect there is no uncal herniation or tonsillar\nherniation. The basal cisterns remain patent.\n\nThere is significant interval increase of perilesional T2 FLAIR hyperintense\nsignal intensity with associated  locoregional mass effect as well as mass\neffect on the right lateral ventricle.\n\nThere are additional patchy T2/FLAIR hyperintensities in the cerebral\nhemispheres bilaterally, a nonspecific finding but unchanged and likely\nrelated to chronic small vessel ischemic changes.\n\nUnchanged osseous postsurgical changes consistent with right craniotomy, major\nvascular flow voids are preserved.  Major dural venous sinuses appear patent.\n\nThere is unchanged complete opacification of the right maxillary sinus.  The\nremainder of the paranasal sinuses and mastoid air cells appear clear.  The\norbits appear grossly unremarkable.",
            "output": "1. Interval increase in size of the previously seen intra-axial enhancingmass\nlesion, with increased perilesional edema, and locoregional mass effect. \nDescribed findings suggests progression.  For follow-up with advanced MR\ntechniques (MR perfusion and spectroscopy) is recommended\n\nRECOMMENDATION(S):  If clinically warranted for follow-up with brain tumor\nperfusion and spectroscopy protocol is recommended."
        },
        {
            "input": "There is no edema, mass effect, abnormal diffusion, evidence for blood\nproducts, or other signal abnormalities in the brain parenchyma. Ventricles,\nbasal cisterns, and cerebral sulci are normal in size for age.  Cerebellar\ntonsils extend by 1 mm into the foramen magnum.  The appear morphologically\nnormal, and there is no kinking of the cervicomedullary junction.",
            "output": "1 mm ectopia of the cerebellar tonsils without stigmata of a Chiari 1\nmalformation. Otherwise, unremarkable noncontrast brain MRI."
        },
        {
            "input": "There is no acute infarction, intracranial hemorrhage, extracerebral fluid\ncollection, midline shift or mass effect.  No diffusion abnormalities are\ndetected. The cerebral volume is appropriate for the patient's stated age. \nComparison with the prior MRI examination dated ___, again there\nare few scattered foci of high signal intensity detected on FLAIR sequence in\nthe right frontal subcortical white matter (image 15, series 9), and above the\nright subinsular region images (15, 16, series 9), apparently slightly more\nnumerous since the prior exam which are nonspecific, however this type of\nfindings can be seen in patients with chronic migraines, there is no evidence\nof abnormal enhancement.  The major vascular flow voids are maintained, and\ndemonstrate normal distribution.  The orbits are unremarkable, the paranasal\nsinuses and mastoid air cells are clear.  Mild degenerative changes are\nvisualized in the upper cervical spine, partially evaluated in this exam,\nhowever previously demonstrated by MRI of the cervical spine in ___.",
            "output": "Few scattered foci of FLAIR high signal intensity  detected in the subcortical\nwhite matter of the right frontal lobe and above the right sub insular region,\napparently are slightly more numerous since the prior exam,  these findings\nare nonspecific and can be seen in patients with chronic migraines.  There is\nno evidence of abnormal enhancement or acute or subacute intracranial process."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  Mild prominence of the ventricles and sulci is consistent with\nage-appropriate involutional changes.  Mild nonspecific periventricular and\nsubcortical FLAIR hyperintensities are suggestive of chronic small vessel\nischemic disease.\n\nThere is a tiny focus of enhancement without correlate on additional sequences\nis noted in the left head of the caudate.  This is new since the study of ___.  In the absence of abnormality in this location on the other\nimages, neoplasm or infection appear quite unlikely.  It is possible this is\nrelated to small vessel ischemia, as suggested by the other scattered white\nmatter hyperintensities.  If the etiology is not apparent, a follow-up\nexamination in 2 months may be helpful.\nOtherwise, there is no abnormal enhancement after contrast administration. \nThere is mild mucosal thickening of the right frontal sinus.  Otherwise\nparanasal sinuses and mastoid air cells are clear.",
            "output": "Tiny area of enhancement in the left caudate head may reflect focal small\nvessel ischemia.  The absence of associated abnormalities on other images\nargues against a more aggressive etiology.  If the nature of this finding is\nunknown, consider a repeat MR in 2 months.\nThere are scattered white matter hyperintensities suggesting chronic small\nvessel ischemia.\nThe study is otherwise normal.\n\nRECOMMENDATION(S):  Consider a repeat MR with contrast in 2 months."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  There is mild prominence of the ventricles and sulci\nsuggestive mild involutional changes..  There is mucosal thickening in the\nleft maxillary and bilateral ethmoid sinuses.",
            "output": "1. No acute intracranial abnormality.\n2. No evidence of acute infarct.\n3.  Paranasal sinus disease as described."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.",
            "output": "1. Normal brain MRI."
        },
        {
            "input": "Central skullbase:\nPosttreatment, post resection changes of central skullbase chordoma, with\nclival involvement.  Areas of marrow replacement, erosion and enhancement at\nthe clivus is stable since ___.  Mild retro clival enhancement, enhancement\nabout basilar artery, ventral pons, stable.  Stable abnormal signal,\nenhancement bilateral cavernous sinus, about both cavernous segment ICA,\nlikely residual tumor.  Moderate brainstem, cerebellar atrophy.\n\nOther pending:\nVP shunt, mild gliosis around shunt tract the frontal lobe white matter.  No\nhydrocephalus.  Mild chronic small vessel ischemic changes.  No acute infarct,\nhemorrhage.  Preserved vascular flow voids.  Moderate opacification paranasal\nsinuses.  Fluid left maxillary sinus, suggestive of acute sinusitis.  Mild\nopacification bilateral mastoids..  Patent dural venous sinuses.",
            "output": "1. Posttreatment changes central skullbase, with probable small areas of\nresidual tumor, stage since ___.\n2. Moderate brainstem, cerebellar atrophy.\n3. Findings consistent with acute paranasal sinusitis."
        },
        {
            "input": "No focus of slow diffusion to suggest acute infarct in the brain parenchyma.\nNo focus of negative susceptibility to suspect intracranial hemorrhage.\n\nThere are extensive T2-FLAIR hyperintense foci noted in the cerebral white\nmatter in the frontal and the parietal lobes on both sides, periventricular\nand subcortical in location as well as in the centrum semiovale and in the\ncorona radiata and a few subtle foci in the occipital lobes on both sides and\nin the pons, nonspecific in appearance and may relate to small vessel ischemic\nchanges.\nThese have progressed compared to the prior study of ___.\nA tiny cyst or chronic lacune in the right cerebellar hemisphere.\nThere is moderate dilation of the lateral and the third ventricles along with\nprominent Sylvian fissures and cerebral sulci, related to diffuse parenchymal\nvolume loss.\nIndentation and thinning of the corpus callosum by the dilated lateral\nventricles.\n\nThe major intracranial arterial flow voids are noted and better assessed on\nthe same day CT angiogram study.  A small tiny outpouching is noted from the\nright middle cerebral artery series 10, image 11.\nModerate left maxillary sinus mucosal  thickening, with likely retention\ncyst/fluid.\nMinimal ethmoidal mucosal thickening on both sides.\nThe mastoid air cells are grossly clear.\nStatus post bilateral lens replacement.  The included orbits are unremarkable.\n\nSlightly hypointense marrow signal.\nMultilevel, multifactorial degenerative changes are noted in the cervical\nspine with disc osteophyte complex causing indentation on the thecal sac\noutline, with moderate canal narrowing, not adequately assessed as not\ntargeted.",
            "output": "1. No acute infarct or mass effect.\n2. Extensive cerebral white matter T2 FLAIR hyperintense foci, likely related\nto small vessel ischemic changes, with some progression compared to the prior\nstudy.       Mild to moderate diffuse parenchymal volume loss without\nsignificant change.\n3. Tiny outpouching from the right middle cerebral artery division;\nintracranial arteries are better assessed on the same day CT angiogram study.\n4. Left maxillary sinus fluid/mucosal thickening/retention cyst.\n\n5. Slightly hypointense marrow signal and  degenerative changes in the\ncervical spine."
        },
        {
            "input": "There is no intra or extra-axial mass effect, acute hemorrhage or infarct. \nThere are a very few nonspecific subcortical and periventricular T2/FLAIR\nwhite matter hyperintensities, which may be seen in the setting of chronic\nmicroangiopathy.  There is ventriculomegaly, unchanged from prior examinations\ndating back to ___.  Allowing for the ventriculomegaly, sulci and cisterns\nare within expected limits for the patient's age.  The major intracranial flow\nvoids are preserved.  The paranasal sinuses are essentially clear.  The orbits\nare unremarkable allowing for bilateral lens replacements.  Fluid signal is\nseen in the right mastoid tip.  Incidental note is made of a metopic suture.",
            "output": "1. There is no acute infarct or intracranial hemorrhage."
        },
        {
            "input": "There is mild-to-moderate generalized cerebral atrophy.  There is moderate\nsymmetric dilatation of the ventricles, unchanged since the CT of the head\nperformed ___.  There is no evidence hemorrhage, edema, masses,\nmass effect, midline shift or infarction.  There is mild residual bilateral\nethmoid sinus mucosal thickening.  There are normal flow voids within the\nintracranial arterial circulation suggestive for patency.  The orbits are\nunremarkable.  The mastoid air cells are clear bilaterally.",
            "output": "1. Generalized cerebral atrophy.\n2. Moderate symmetric dilatation of the ventricles unchanged.  This raises the\npossibility of communicating hydrocephalus.\n3. No evidence of acute intracranial hemorrhage or infarction."
        },
        {
            "input": "Regions of increased T2/FLAIR signal hyperintensity are again noted within the\nbilateral white matter predominantly within the parietal lobes likely\nrepresenting cortical tubers in this patient with reported history of tuberous\nsclerosis. A small 7 mm ring enhancing subependymal mass is again noted\nadjacent to the right lateral ventricular wall. There is also nodularity of\nthe lateral ventricles likely secondary to additional tiny subependymal\nnodules.  There is no enhancing mass obstructing the foramen of ___. There\nis no hydrocephalus. There are no new lesions identified. Susceptibility\nartifact is again noted within the left cerebellum and is also unchanged.\nAccounting for differences in technique, these findings are unchanged.\n\nThere is no acute infarction, intracranial hemorrhage, extracerebral fluid\ncollection, or midline shift. No diffusion abnormalities are detected. The\ncerebral volume is appropriate for the patient's stated age.  The major\nvascular flow voids are maintained, there is no evidence of abnormal\nenhancement. The orbits are unremarkable, the paranasal sinuses and mastoid\nair cells are clear",
            "output": "1. Stable bilateral subcortical T2/FLAIR signal abnormalities consistent with\ncortical tubers/tuberous sclerosis.  No new lesions are identified.\n2.  Stable 7 mm right lateral ventricle ring-enhancing lesion due to\nsubependymal nodule.\n3.  No mass identified near foramen ___."
        },
        {
            "input": "MRA brain:  There is mild irregularity of the distal cervical internal carotid\narteries.  Otherwise, the intracranial vertebral and internal carotid arteries\nand their major branches appear normal without evidence of stenosis,\nocclusion, or aneurysm formation.\n\nMRA neck: The common, internal and external carotid arteries appear normal. \nThere is no evidence of stenosis by NASCET criteria. The origins of the great\nvessels, subclavian, and vertebral arteries appear normal bilaterally.  The\ncommon carotid bifurcations appear normal.",
            "output": "1. Mild irregularity of the distal cervical internal carotid arteries, likely\nsecondary to a combination of atherosclerotic calcification and motion\nartifact.  Otherwise, no acute abnormality on the MRA of the neck and brain. \nNo evidence for dissection."
        },
        {
            "input": "Study somewhat limited due to motion related artifacts on multiple sequences.\n\nLarge heterogeneously enhancing mass, approximately 6.5AP x 4.7CCx4.7TR cm,\nlikely intra-axial, with extensive surrounding vasogenic edema centered in the\nbifrontal region, left more than right and causing effacement and exerting\nlocal mass effect on the bilateral frontal horns of the lateral ventricles and\nbody of left lateral ventricle and rightward shift of midline structures. \nThere is indentation node invasion into the anterior part of the corpus\ncallosum. These also displacement of the A2 segments of the anterior cerebral\narteries towards the right side by the mass. Mild drooping of the optic\nnerve/optic chiasm due to the mass effect. Multiple flow voids seen within\nthis lesion. Areas of negative susceptibility, may represent some hemorrhage\nor mineralization within the lesion. Findings concerning for an aggressive\nmalignancy such as a high-grade glioma.\n\nThe major intracranial arterial flow voids are noted.\nVenous sinuses are unremarkable.\nSella, pineal gland, craniocervical junction regions are unremarkable.\nThe imaged paranasal sinuses and the mastoid air cells are grossly clear.\nThe imaged orbits are unremarkable.\nBone marrow signal is unremarkable.",
            "output": "Large heterogeneously enhancing mass, approximately 6.5AP x 4.7CCx4.7TR cm,\nlikely intra-axial, with extensive surrounding vasogenic edema centered in the\nbifrontal region, left more than right and causing effacement and exerting\nlocal mass effect as described above. Correlation with noncontrast CT can be\nhelpful for hemorrhage versus mineralization.\nDifferential diagnosis includes GBM, lymphoma, metastasis, etc.\nNeurosurgery consult, further workup and followup as needed."
        },
        {
            "input": "Again seen is an irregular, rim enhancing mass involving bilateral medial\nfrontal lobes and the corpus callosum, more extensive on the left than right,\nwith extensive vasogenic edema. The mass effaces the frontal horns and\nanterior bodies of the lateral ventricles and causes left-to-right subfalcine\nherniation with rightward shift of the midline structures as well. There is no\nuncal herniation or compression of the basal cisterns. Otherwise,\ncomprehensive evaluation of the brain parenchyma is not performed with this\nlimited exam which is targeted for surgical planning.",
            "output": "Rim enhancing mass involving bilateral medial frontal lobes on the corpus\ncallosum is again demonstrated for surgical planning. Diagnostic\nconsiderations include glioblastoma, or lymphoma if the patient is\nimmunocompromised. Metastasis less likely."
        },
        {
            "input": "When compared to prior, there has been interval decrease in size of the\nperipherally enhancing mass lesion in the parasagittal frontal lobes, left\ngreater than right.  Overall the peripheral enhancing lesion measures 4.5 cm\nAP x 3.1 cm cc x 2.6 cm TRV, previously 6.2 x 4.8 x 3.3 cm when measured in\nsimilar locations in similar planes.  The degree of surrounding FLAIR\nhyperintensity has also decreased, there is resolution of previously seen\neffacement of the frontal horns of the lateral ventricles.  There is no\nmidline shift.\n\nSingle subcortical white matter FLAIR hyperintensity in the right frontal lobe\nis noted, unchanged.  There is no new parenchymal signal abnormality.  There\nis no acute infarct.  Susceptibility artifact compatible with blood products\nseen within the mass and along the prior left frontal approach biopsy tract.\n\nThere is no new abnormal enhancement.  Major intravascular flow voids are\npreserved.\n\nParanasal sinuses and mastoids are essentially clear.",
            "output": "Interval decrease in size of peripherally enhancing bifrontal mass lesion with\ndecreased mass effect."
        },
        {
            "input": "Left trans frontal biopsy of a 2.5 x 1.6 x 2.7 cm (TRV, AP, SI) left medial\nfrontal lobe peripherally enhancing mass with extension across the midline\nalong the genu of the corpus callosum to the medial right frontal lobe is\nslightly smaller in size when compared to examination of ___.  The\ndegree of surrounding left frontal white matter FLAIR edema pattern is similar\nin configuration and distribution.  Re-identified is peripheral gradient echo\nsusceptibility along the biopsy track and of the lesion, compatible with\nhemorrhage product, similar in extent from the prior exam.\n\nThere no new enhancing lesions or FLAIR signal abnormalities.  Sulci,\nventricles and cisterns are within expected limits for the patient's age\nallowing for the left frontal mass.  The major intracranial flow voids are\npreserved.  The dural venous sinuses are patent.  The paranasal sinuses are\nclear.  The orbits are unremarkable.  The mastoid air cells are clear.",
            "output": "1. Continued decrease in size of a lobulated peripherally enhancing left\nmedial frontal lobe mass with extension across the midline to the right\nfrontal lobe along the genu of the corpus callosum.\n2. No new lesions."
        },
        {
            "input": "Postcontrast MPRAGE sequences are motion degraded.  Within these confines:\n\nPrior left frontal burr hole and biopsy track extending to the frontal horn of\nthe left lateral ventricle are unchanged from prior exam.  Gradient echo\nsusceptibility along the biopsy represents hemorrhage product.  Re-identified\nis a lobulated 2.8 x 2.5 x 2.3 cm (AP, TRV, SI) left medial frontal lesion\nextending across the midline along the genu of the corpus callosum to the\nmedial right frontal lobe is essentially unchanged in size when compared to\nexamination of ___ but smaller when compared to posttreatment\nexamination of ___.  The lesion demonstrates intrinsic peripheral T1\nhyperintense signal and gradient echo susceptibility compatible with\nhemorrhage product with postcontrast regions of nodular enhancement, similar\nin appearance to the prior exam.  The degree of surrounding left frontal white\nmatter FLAIR edema pattern is essentially unchanged in configuration in\ndistribution.\n\nNo new enhancing lesions or FLAIR abnormality.  Allowing for posttreatment\nchanges and left frontal mass, the sulci, ventricles and cisterns are within\nexpected limits for the patient's age.  No acute intracranial hemorrhage or\ninfarct.  The major intracranial flow voids are preserved.  The orbits are\nunremarkable.  The paranasal sinuses are clear.  The mastoid air cells are\nclear.",
            "output": "1. Unchanged size of left frontal mass demonstrating peripheral nodular\nenhancement and hemosiderin rim extending across the midline along the corpus\ncallosum to the right frontal lobe when compared to examination of ___.\n2. No new lesions."
        },
        {
            "input": "Motion artifact slightly limits evaluation.  Stable postsurgical changes\nfollowing right frontal craniotomy for meningioma resection, with minimal\nunderlying dural thickening and enhancement, and susceptibility on the\ngradient echo sequence, in keeping with postoperative blood products.  No new\nenhancing mass or other new abnormal enhancement is identified.\n\nThere is no evidence of infarction.  There is a small chronic infarct in the\nhead of the right caudate nucleus, which was not present on the most recent\nMRI Head dated ___.  There are nonspecific bilateral\nsupratentorial white matter T2/FLAIR hyperintensities, which most likely\nrepresent the sequelae of chronic microangiopathy in this age group. \nParenchymal volume is age-appropriate with stable size of the ventricles and\nsulci.\n\nMajor vascular flow voids are grossly preserved.  Dural venous sinuses appear\npatent on postcontrast MP RAGE images.\n\nStable appearance of the defect in the left lamina papyracea, with medial\nherniation of left orbital fat, without herniation of the left medial rectus\nmuscle.",
            "output": "1. Stable post treatment changes following right frontal craniotomy and\nmeningioma resection.  No evidence of residual or recurrent mass.\n2. Small chronic infarct in the head of the right caudate nucleus, new\ncompared to the last MRI from ___.  No acute infarction.\n\nNOTIFICATION:  The impression above was entered by Dr. ___ on\n___ at 11:37 into the Department of Radiology critical communications\nsystem for direct communication to the referring provider."
        },
        {
            "input": "There are stable postsurgical changes from right frontal craniotomy and\nmeningioma resection with minimal underlying dural thickening and enhancement\nand chronic blood product.  There is no new focus of enhancement to suggest\nrecurrence.\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  Few scattered areas of periventricular and subcortical white\nmatter T2/FLAIR hyperintensity appear slightly more numerous than compared to\nprior examination and likely represent the sequela of chronic small vessel\nischemic disease.  There is no abnormal enhancement after contrast\nadministration.  There is no abnormal focus of slowed diffusion.  The\nprincipal intracranial vascular flow voids are preserved.  The dural venous\nsinuses are patent on postcontrast MP-RAGE.\n\nThe paranasal sinuses are grossly clear.  The orbits are grossly unremarkable.",
            "output": "1. Stable postsurgical changes from right frontal craniotomy and meningioma\nresection without evidence of residual or recurrent disease.\n2. No hemorrhage, infarct, or enhancing mass.\n3. Few scattered areas of white matter signal abnormality, slightly more\nnumerous compared to the prior examination, likely reflective of chronic small\nvessel ischemic disease."
        },
        {
            "input": "Enhancing T2 hyperintense focus is seen in the left adenohypophysis (5:8, 4:8,\n7:8), measuring 2 mm x 4 mm x 1 mm (AP x TV x SI).\n\nOtherwise the pituitary signal intensity appears normal before and after\ncontrast administration.  The pituitary stalk appears midline and enhance\nnormally.  The suprasellar cistern and cavernous sinuses appear normal. The\nlimited portion of the brain included on this study appears normal.",
            "output": "1. 2 mm enhancing T2 hyperintense lesion in the left adenohypophysis,\nsuspicious for microadenoma.  No mass effect."
        },
        {
            "input": "There is no evidence of hemorrhage or mass effect.  The ventricles appear\nnormal.\n\nThere are normal vascular flow voids.  There is no evidence of acute infarct\nbased on diffusion-weighted imaging.  There is diffuse brain parenchymal\nvolume loss.  There is subcortical and periventricular T2/FLAIR signal\nhyperintensity with additional involvement of the brainstem which is\nnonspecific though is most often ascribed to sequelae of chronic small vessel\nischemic disease.\n\nThere is no abnormal brain parenchymal or leptomeningeal enhancement.  There\nis a left parietal developmental venous anomaly.\n\nThe orbits, paranasal sinuses, and mastoid air cells appear unremarkable.",
            "output": "1. No hemorrhage, mass effect, or acute infarct.\n2. No evidence of intracranial metastatic disease.\n3. Left parietal developmental venous anomaly.\n4. Brain parenchymal volume loss and probable sequelae of chronic\nmicroangiopathy."
        },
        {
            "input": "There is no intra or extra-axial mass, acute hemorrhage or infarct. Sulci,\nventricles and cisterns are within expected limits for the patient's age. \nThere are scattered T2/FLAIR subcortical and periventricular white matter\nhyperintensities, which are nonspecific, unchanged from prior exam and\ncommonly seen in setting of chronic microangiopathy.  There is no abnormal\nenhancement.  No T1 intrinsic signal abnormality within the basal ganglia to\nsuggest hepatic encephalopathy on imaging.  The major intracranial flow voids\nare preserved.  The dural venous sinuses are patent.  Allowing for bilateral\nlens replacements, the orbits are unremarkable.  The frontal sinuses are not\npneumatized.  Otherwise, the remainder the paranasal sinuses are clear.  The\nmastoid air cells are clear.",
            "output": "1. There is no intra or extra-axial mass, acute hemorrhage or infarct.  No\nabnormal enhancement.\n2. No T1 intrinsic hyperintense signal within the basal ganglia to suggest\nimaging findings of hepatic encephalopathy.\n3. There are nonspecific T2/FLAIR white matter hyperintensities which are\nnonspecific, but commonly seen with chronic microangiopathy in a patient of\nthis age."
        },
        {
            "input": "Study is moderately degraded by motion.  Within these confines:\n\nThere is an approximately 7 (AP) x 5 (TV) x 5 (SI) mm right parasagittal\npericallosal FLAIR and T2 hyperintense lesion, T1 hypointense with minimal\nadjacent vessels and no definite associated restricted diffusion or increase\nsusceptibility (see 4:112; 3:110; 300:280; 7:71; 550:32; 6,8:17).\n\nMultiple bifrontal probable prominent perivascular spaces are noted.\n\n\nBilateral hippocampal formations and mammillary bodies are preserved in signal\nand configuration. There is no disproportionate medial temporal atrophy. There\nis no focal lobar encephalomalacia. There are no focal cortical dysplasias or\ngray matter heterotopia noted.\n\nThere is no evidence of hemorrhage, mass effect, midline shift or infarction. \nThe ventricles and sulci are normal in caliber and configuration.  Cavum\nseptum pellucidum is noted (see ___.\n\nPatient's previously noted parasagittal suboccipital approximately 1.9 x 0.9\ncm lipoma.  4 mm pineal cyst is noted.  Bilateral maxillary, sphenoid, and\nfrontal sinus mucosal thickening is present.  Right maxillary sinus mucous\nretention cyst is present.",
            "output": "1. Study is moderately degraded by motion.\n2. Right parasagittal pericallosal single 7 mm largely CSF signal structure\nwith increased FLAIR signal which may be related to 3D CUBE FLAIR technique. \nWhile findings are suggestive of prominent perivascular space, differential\nconsiderations include arachnoid cyst, demyelinating lesion, and sequela of\nprior trauma or infection.  Consider correlation with prior brain MRI, if\navailable.  If clinically indicated, consider noncontrast routine brain\nimaging that includes standard axial T2 and axial 2D FLAIR imaging.\n3. Paranasal sinus disease, as described.\n4. 1.9 cm parasagittal suboccipital scalp lipoma.\n5. 4 mm pineal cyst."
        },
        {
            "input": "In comparison with the prior examination, again there is a 7 mm CSF signal\nstructure along the right parasagittal pericallosal region (image 16, series\n5), please note that this cystic appearing structure appears is slightly less\nconspicuous, likely due to different magnetic field strength at 1.5 tesla and\npreviously at 3 tesla.  There is no evidence of mass effect or shifting of the\nnormally midline structures in this region, and probably this cystic\nappearance structure represent small arachnoid, cyst which was also visible on\nthe prior CT of the head dated ___ on the image 47, series 602. \nOtherwise no significant changes are visualized to the entire brain or new\nlesions, no diffusion abnormalities are detected.  Mild mucosal thickening is\nseen in the frontal sinus and frontoethmoidal recesses as well as anterior\nethmoidal air cells, no air-fluid levels are seen, the mastoid air cells are\nclear.",
            "output": "1.  Unchanged cystic appearing structure in the right parasagittal region\nabove the splenium of the corpus callosum, measuring approximately 7 mm in\nanterior-posterior dimension, which appears slightly less conspicuous since\nthe prior study, likely due to the difference in the magnetic field strength,\nand probably consistent with small arachnoid cyst with no evidence of mass\neffect or edema.\n\n2.  Mild paranasal sinus disease involving the frontal sinus, and the\nethmoidal air cells as described above."
        },
        {
            "input": "Study is mildly degraded by motion.  There is no evidence of hemorrhage,\nedema, masses, mass effect, midline shift or infarction.   The ventricles and\nsulci are normal in caliber and configuration.  Right maxillary sinus mucous\nretention cyst versus polyp is noted.  Periventricular and subcortical T2 and\nFLAIR hyperintensities are noted, which may represent small vessel ischemic\nchanges.  A partially empty sella is noted.",
            "output": "1. Study is mildly degraded by motion.\n2. No acute intracranial abnormality, with no evidence of acute infarct.\n3. Paranasal sinus disease as described."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor acute infarction.  Findings consistent with severe chronic small vessel\nischemic changes cerebral hemispheres, brainstem.  Probable chronic lacunar\ninfarct right basal ganglia.  Benign-appearing, 10 x 8 mm nonenhancing left\nsphenoid wing lesion follows CSF on all sequences, compatible with a small\nmeningocele (series 8, image 7).  The ventricles and sulci are normal in\ncaliber and configuration.  Mineralization within the basal ganglia\nbilaterally.  There is no abnormal enhancement after contrast administration. \nPreserved vascular flow voids, dural venous sinuses are patent.\n\nMajor intracranial vessels are patent.  Orbits are unremarkable.  Partial\nopacification right mastoids,, less than 50% volume, of doubtful significance.\nSmall suboccipital lymph nodes are not pathologically enlarged.",
            "output": "1. No metastases.\n2. Probable 10 mm left sphenoid wing meningocele.\n3. Findings consistent with severe chronic small vessel ischemic change.\n4. Chronic lacunar infarct right basal ganglia.\n5."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor acute/subacute infarction.  There is a left sphenoid meningocele which is\nunchanged.  Adjacent encephalomalacia in the anterior inferior temporal lobe. \nOtherwise, the ventricles and sulci are normal in caliber and configuration. \nThere are patchy areas of T2/FLAIR hyperintensity in the subcortical and\nperiventricular white matter as well as in the pons which are nonspecific but\nlikely reflect chronic small vessel disease in this age group.  Chronic\nlacunar infarct in the right basal ganglia.  Basal ganglia mineralization\nagain noted.  There is no abnormal enhancement after contrast administration.\n\nThe major intracranial vascular flow voids are preserved.  Orbits and\nvisualized extracranial soft tissues are unremarkable.  There is a\nquestionable area of T2 hyperintensity in the upper cervical spinal cord at\nthe C1-C2 level, partially imaged.",
            "output": "1. No acute intracranial abnormality.  No intracranial enhancing lesions to\nsuggest metastatic disease.\n2. Nonspecific white matter signal changes most likely reflecting advanced\nsmall vessel disease in this age group.\n3. Chronic lacunar infarct in the right basal ganglia.\n4. Redemonstrated left sphenoid wing meningocele with encephalomalacia in the\nadjacent temporal lobe.\n5. There is a questionable partially imaged T2 hyperintense lesion in the\nupper cervical spinal cord at the C1-C2 level.  Although possibly artifactual,\nand intramedullary spinal cord lesion is not excluded and further assessment\nwith cervical spine MRI is recommended.\n\nNOTIFICATION:  The impression and recommendation above was entered by Dr. ___\n___ on ___ at 12:08 into the Department of Radiology critical\ncommunications system for direct communication to the referring provider."
        },
        {
            "input": "There are numerous small areas of slowed diffusion in the bilateral frontal,\nbilateral parietal, bilateral occipital lobes and bilateral cerebellar\nhemispheres with associated FLAIR hyperintensity, compatible with acute to\nsubacute infarcts, likely of embolic etiology.\n\nThere is no evidence of hemorrhage, masses, mass effect, or midline shift. \nThere is mild prominence of the ventricles and sulci suggestive involutional\nchanges.  The background areas of periventricular and subcortical white matter\nT2/FLAIR hyperintensity, apart from the areas of infarct likely represent the\nsequela of chronic small vessel ischemic disease.  The principal intracranial\nvascular flow voids are preserved.  A punctate focus of susceptibility\nartifact is noted in the left frontal lobe, compatible with chronic\nmicrohemorrhage (07:17).\n\nThere is minimal mucosal thickening in the bilateral maxillary sinuses and\nbilateral ethmoid air cells.  The remainder the visualized paranasal sinuses\nare clear.  There is minimal opacification of the left-sided mastoid air\ncells.  The right-sided mastoid air cells are clear.  There are changes from\nbilateral lens replacement surgery.  The orbits are otherwise unremarkable.  .",
            "output": "Numerous acute to subacute infra- and supratentorial infarcts in all vascular\ndistributions, as described, with configuration suggestive of embolic\netiology.\n\nNOTIFICATION:  The neurology service was aware of these findings at time of\ndictation per OMR progress note."
        },
        {
            "input": "There is no acute infarction, intracranial hemorrhage, extracerebral fluid\ncollection, midline shift or mass effect.  Ventricles and extra-axial spaces\nare normal in size.  Flow voids are maintained. Suprasellar and craniocervical\nregions are unremarkable.",
            "output": "No significant abnormalities are seen on MRI of the brain without gadolinium."
        },
        {
            "input": "MRI Brain:\nThere is no intra or extra-axial mass, acute hemorrhage or infarct.  Sulci,\nventricles and cisterns are within expected limits for the patient's age. \nThere is no abnormal enhancement.  There are a very few periventricular and\nsubcortical T2/FLAIR nonspecific white matter hyperintensities.  The major\nintracranial flow voids are preserved.  The dural venous sinuses are patent. \nThere is moderate mucosal thickening of the left maxillary sinus.  The\nremainder of the paranasal sinuses are clear.  The orbits are unremarkable. \nThe mastoid air cells are clear.\n\nMRA brain:  There is a 1 mm posterior projecting triangular outpouching of the\nleft carotid terminus most likely representing a small infundibulum.  An\nidentical appearing outpouching is noted on the right, however a definitive\nsmall-vessel can be seen arising from it.  Otherwise, the intracranial\nvertebral and internal carotid arteries and their major branches appear normal\nwithout evidence of stenosis, occlusion, or aneurysm formation larger than 3\nmm.\n\nMRA neck:  There is common origin of the right brachiocephalic and left common\ncarotid arteries, a very common anatomic variant.  The common, internal and\nexternal carotid arteries appear normal.  There is no evidence of internal\ncarotid artery stenosis by NASCET criteria.  The origins of the great vessels,\nsubclavian and vertebral arteries appear normal bilaterally.",
            "output": "1. No acute intracranial hemorrhage or infarct.\n2. There are a very few periventricular subcortical T2/FLAIR nonspecific white\nmatter hyperintensities, commonly seen in setting chronic microangiopathy in a\npatient of this age.\n3. Essentially unremarkable MRA of the brain.  There is a 1 mm posterior\nprojecting triangular outpouching of the left carotid terminus, most\ncompatible with a small an infundibulum as an identical appearing focus is\nnoted on the right carotid terminus where a definitive small-vessel can be\nseen arising from it.\n4. Unremarkable MRA of the neck."
        },
        {
            "input": "Smaller subcentimeter focus of diffusion-weighted signal abnormality at the\ngenu of the left internal capsule, compatible with an acute lacunar infarct.\nAdditional chronic lacunes of the bilateral basal ganglia are noted, involving\nthe bilateral putamina and anterior limbs of the internal capsules and right\nglobus pallidus.  There is subtle 1 cm enhancing focus in the right globus\npallidus with associated gradient echo susceptibility artifact, compatible\nwith calcifications noted on prior CTs, essentially unchanged in size allowing\nfor technical differences, which may represent a cavernous malformation or\npotentially sequela of prior trauma. There are scattered punctate foci of\ngradient echo susceptibility artifact, which may represent chronic\nmicrohemorrhages. Calcifications of the pons and bilateral basal ganglia are\nalso seen. Superimposed moderate periventricular and subcortical nonspecific\nT2/FLAIR white matter hyperintensities are also noted, commonly seen in the\nsetting of small vessel ischemic disease.\n\nThere is prominence of the ventricles, greater within expected for the\npatient's age, although this is unchanged since CT exam of ___. Otherwise\nsulci and cisterns are within expected limits. The major flow voids are\npreserved.\n\nThe paranasal sinuses are well-aerated. The orbits are unremarkable. There is\nfluid signal, right greater than the left, within the mastoid air cells.",
            "output": "1.  Acute lacunar infarct of the left basal ganglia, closely apposed to the\ngenu of that internal capsule.\n\n2.  Sequelae of small vessel ischemic disease, as well as multiple chronic\nlacunar infarcts as described above.\n\n3.  1 cm enhancing focus in the right globus pallidus with associated chunky\ncalcification, unchanged in size when compared to prior exam, which may\nrepresent cavernous malformation, sequelae of prior trauma, or relate to #4,\nbelow.\n\n4.  Again noted are widely-distibuted and roughly symmetric bilateral basal\nganglionic as well as pontine and centra semiovale calcifications, suggestive\nof systemic metabolic process such as so-called \"LCC\" (leukoencephalopathy,\ncerebral calcifications, and cysts), though no cysts per se are seen.The\noverall pattern would be unusual for Fahr disease."
        },
        {
            "input": "There are 2 subcentimeter areas of restricted diffusion in the right frontal\nlobe, 1 more rounded appearing in the subcortical ___ matter and 1 linear\narea based in the cortical gray matter (402: 22, 24). Both of these areas\ndemonstrate FLAIR hyperintensity as well as subtle post gadolinium enhancement\nwith appearance most suggestive of subacute infarcts. However, given the\nhistory of new diagnosis lung cancer, metastatic lesions cannot be excluded. \nThere is no mass effect, or midline shift. Ventricles and sulci are\nage-appropriate. There is no pathologic intracranial enhancement. Intracranial\nflow voids are maintained. The brainstem, posterior fossa and cervicomedullary\njunction are preserved. The orbits, periorbital and paracavernous spaces are\npreserved.  Visualized paranasal sinuses and mastoid air cells are clear.",
            "output": "1. Two subcentimeter foci of restricted diffusion based in the cortex and\nsubcortical ___ matter of the right frontal lobe demonstrating restricted\ndiffusion, FLAIR hyperintensity and subtle post gadolinium enhancement in a\nconfiguration most suggestive of subacute infarct. However, metastatic lesions\ncannot be excluded and short-term interval repeat MR with gadolinium in 8\nweeks is recommended to confirm etiology. Infarcts should demonstrate\nevolution in appearance whereas metastatic lesions will show no change or\nprogression.\n\nNOTIFICATION:  The findings were discussed by Dr. ___ with Dr. ___ on the\ntelephone on ___ at 2:03 ___, 30 minutes after discovery of the\nfindings."
        },
        {
            "input": "MRA head: The intradural segments of the vertebral arteries are normal; the\nvertebral arteries are codominant. The basilar artery is normal. The superior\ncerebellar and posterior cerebral arteries are normal.  The right posterior\ncommunicating artery is partially visualized and is normal. The left posterior\ncommunicating artery is not visualized.\n\nThe intracranial internal carotid arteries are tortuous but demonstrate normal\npatency. The middle cerebral arteries are normal and demonstrate symmetric\narborization. The anterior cerebral arteries and anterior communicating artery\nare normal.\n\nNo stenosis, aneurysm greater than 3 mm, or arteriovenous malformation is\nidentified.\n\nMRA neck:  There is bovine aortic arch anatomy, a developmental variant. The\norigins of the major brachiocephalic vessels are normal.\n\nThe visualized left subclavian artery is normal. The left vertebral artery is\nnormal.\n\nThe visualized right subclavian artery is normal. The right vertebral artery\nis normal.\n\nThe left common, internal, and external carotid arteries are normal.\n\nThe right common, internal, and external carotid arteries are normal.\n\nNo stenosis (by NASCET criteria), dissection, or pseudoaneurysm is identified.\n\nThere is a right pleural effusion, as seen on recent CT from ___.",
            "output": "1.  No steno-occlusive disease with of the head and neck carotid and\nvertebrobasilar systems.\n2.  Right pleural effusion."
        },
        {
            "input": "The two lesions mentioned on prior study in the right frontal lobe are again\nseeen.  The cortical lesion continues to show enhancement but is unchanged in\nsize.   The subcortical lesion is less prominent on T2 and diffusion weighted\nimages and no longer demonstrates enhancement.  No surrounding edema.  There\nis a new subependymal enhancing focus posterior to the head of the left\ncaudate nucleus which is bright on FLAIR, measuring 3 x 6 mm, not definitely\nseen on prior study however this may be due to slice selection. There is no\nevidence of hemorrhage, edema, or mass effect. The ventricles and sulci are\nnormal in caliber and configuration.",
            "output": "The previously questioned areas in the right frontal lobe are again seen.  The\nsubcortical lesion is less prominent and most likely represents evolving\ninfarct.  The cortical lesion continues to enhance, and metastasis cannot be\nruled out.  There is also a new subependymal enhancing focus posterior to the\nhead of the left caudate nucleus, concerning for metastastic disease. \nRecommend follow up MR to assess for evolution."
        },
        {
            "input": "2 previously noted linear foci of high T2 signal in the right frontal cortex\nand subcortical white matter, images 7:21 and 7:20, are stable in size on\nFLAIR/ T2 weighted images compared to ___. The no longer\ndemonstrate contrast enhancement or abnormal diffusion, consistent with\nexpected evolution of infarcts, which are now chronic.\n\nPreviously noted small rim enhancing lesion in the body of the left caudate\nnucleus now demonstrates punctate residual enhancement, image 10:18, and\ndecreased extent of high T2 signal, image 7:18, compared to ___.\nIt does not demonstrate abnormal diffusion today, but demonstrated a punctate\nfocus of high signal on the diffusion tracer sequence on ___.\nThis may also represent an evolving infarct or a metastasis responding to\ntherapy.\n\nNo new enhancing lesions are seen. There is no acute infarction, edema, or\nevidence for new blood products in the brain parenchyma. Ventricles and sulci\nare normal in size for age. Major arterial flow voids are grossly preserved.\nMajor dural venous sinuses are patent.\n\nThere are small mucous retention cysts in the maxillary sinuses.",
            "output": "1. The small linear T2 hyperintense lesions in the cortex and subcortical\nwhite matter of the right frontal lobe are stable in size on FLAIR/T2 weighted\nimages, but no longer demonstrate contrast enhancement or abnormal diffusion,\nconsistent with expected evolution of infarcts.\n2. The small enhancing lesion in the body of the left caudate has decreased in\nsize with decreased associated high T2 signal, and at no longer demonstrates\nabnormal diffusion, compatible with an evolving infarct, though a metastasis\nresponding to therapy may have a similar appearance.\n3. No evidence for new enhancing intracranial lesions.\n4. No evidence for an acute infarct or other acute intracranial abnormality."
        },
        {
            "input": "There is no evidence of acute intracranial hemorrhage. The ventricles are\nstable in size.\n\nThere are normal vascular flow voids.  There is no evidence of acute infarct\nbased on diffusion-weighted imaging. There is mild diffuse brain parenchymal\nvolume loss.  There is mild subcortical and periventricular T2/FLAIR signal\nhyperintensity which may reflect sequelae of chronic microangiopathy.  There\nis additional T2/FLAIR signal hyperintensity within the cortex and subcortical\nwhite matter of the right frontal lobe which appears unchanged and may\nrepresent chronic infarcts.  Apparent increase signal in the left cerebellum\non FLAIR images appears to be due to pulsation artifacts.\n\nThere are no new lesions or areas of abnormal brain parenchymal or\nleptomeningeal enhancement.\n\nThere is a left maxillary sinus air-fluid level.  The orbits and mastoid air\ncells are unremarkable.",
            "output": "1. No evidence of acute intracranial hemorrhage, mass effect, or acute\ninfarct.\n2. Signal abnormality within the right frontal lobe is unchanged and may\nreflect sequelae of prior infarct.\n3. No areas of abnormal brain parenchymal or leptomeningeal enhancement.\n4. Brain volume loss and presumed sequelae of chronic microangiopathy.\n5. Paranasal sinus disease.\n6.  Reviewed with Dr. ___."
        },
        {
            "input": "Please note that the inferior cerebellar hemispheres were not included on\ndiffusion weighted, T2 weighted, FLAIR, gradient echo, precontrast and\npostcontrast T1 weighted images, though they are included on the postcontrast\nMP RAGE images.\n\nMotion artifact also limits evaluation on multiple sequences.\n\nThere is a right occipital craniotomy, likely related to recent surgical\nresection of a neoplasm within the right occipital lobe given the clinical\nhistory.  There is encephalomalacia in the posterior right occipital lobe,\nlikely representing the surgical cavity, with surrounding T2 hyperintensity\nextending to the atrium of the right lateral ventricle.\n\nThere is a large late subacute intraparenchymal hemorrhage within the right\noccipital and posterior temporal lobes, with partial effacement of the\noccipital horn of the right lateral ventricle.  Prior CTs demonstrate expected\nevolution of blood products between ___.  No nodular\nenhancement is identified.  No shift of midline structures or compression of\nbasal cisterns.\n\nNo acute infarction is identified in the visualized portion of the brain.\nThere are multiple small foci of hyperintense signal on T2 weighted images\nwithin the bilateral cerebral hemispheres and pons, nonspecific but likely the\nsequela of mild chronic small vessel disease and/or treatment related change.\n\nThe major vascular flow voids are preserved.",
            "output": "1. Large late subacute intraparenchymal hemorrhage within the right occipital\nand posterior temporal lobes, with partial effacement of the occipital horn of\nthe right lateral ventricle, but no shift of midline structures or mass effect\non basal cisterns.\n2. Encephalomalacia in the posterior right occipital lobe likely represents\nthe surgical cavity.  Surrounding T2 hyperintensity extending to the atrium of\nthe right lateral ventricle, without prior MRI for comparison.  No nodular\nenhancement is identified.\n3. Please note that the inferior portions of the cerebellar hemispheres are\nnot adequately imaged.\n\nRECOMMENDATION(S):  Recommend follow up MRI with and without contrast after\nresolution of blood products."
        },
        {
            "input": "Again noted are postsurgical changes related to right parietal craniotomy with\nresection of the previously noted large right temporoparietal mass with stable\nmild ex vacuo dilatation of the right occipital horn. There is minimal dural\nthickening and enhancement subjacent to the craniotomy site as well as thin\nlinear enhancement along the inferolateral margin of the resection cavity\n(10:72), which appears unchanged comparison to the prior study dated ___.  There has been interval decrease in size of a rounded nonenhancing\nfocus within the dependent aspect of the anterior resection cavity, now\nmeasuring 8 x 9 mm, previously measuring 17 x 16 mm on ___.  Findings\nlikely reflect clotted blood products with interval partial resorption.  The\nextent of the right parietal, occipital and temporal lobe FLAIR signal\nabnormality surrounding the resection cavity appears unchanged, as does the\nslight FLAIR hyperintense signal within the splenium of the corpus callosum\nextending along the occipital horn of the left lateral ventricle.\n\nThere is no evidence of acute intracranial hemorrhage, hydrocephalus, midline\nshift or acute territorial infarction.\n\nThe paranasal sinuses, mastoid air cells, orbits and globes appear within\nnormal limits.",
            "output": "1. Redemonstrated postsurgical changes related to resection of previously\nnoted right temporoparietal mass.\n2. Thin linear enhancement along the inferolateral margin of the resection\ncavity appears unchanged.\n3. The extent of FLAIR hyperintense signal surrounding the resection cavity\nand involving the splenium of the corpus callosum and white matter along the\nleft occipital horn appears unchanged.\n4. Interval decrease in size of a rounded nonenhancing focus within the\ndependent resection cavity, mild measuring 9 mm, previously measuring 17 mm on\n___.  Findings likely reflect clotted blood products with interval\npartial resorption.\n5. No new region of FLAIR signal abnormality or enhancement is seen."
        },
        {
            "input": "MRI Brain:\nThere is small focal less than 3 mm of T2 FLAIR hyperintensity with increased\nDWI signal intensity with corresponding faint decreased ADC value (series 4,\nimage 21) at the left posterior frontal lobe, most likely a subacute\ninfarction.  Also there is questionable tiny focal area of slow diffusivity at\nlateral margin of the left hippocampus (series 4, image 12); which could be\nartifactual in origin however may reflect a second focus of infarction.\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor brain herniation.  The ventricles and sulci are age appropriate in caliber\nand configuration.  Are bilateral periventricular and deep white matter\nmultifocal T2 FLAIR hyperintensities; nonspecific in appearance and could be\nrelated to chronic microangiopathy.\n\nStatus post lens removal surgery of both globes.  Otherwise both orbits appear\nnormal.  There is mild mucosal thickening involving ethmoid air cells and\nmaxillary sinuses as well as bilateral mastoid air cells.\n\nMRA brain:\nThe right ophthalmic artery is poorly visualized.  This is at the limit of\nreliable resolution of MRA.  However, the left ophthalmic artery is well seen\nand appears normal.  Thus, this may reflect stenosis or occlusion of the right\nsided artery.\n\nThe intracranial vertebral and internal carotid arteries and their major\nbranches appear patent without evidence of severe stenosis, occlusion, or\naneurysm formation.\n\nMRA neck:\nThere is short segment of severe luminal narrowing of the proximal right\ninternal carotid artery starting from about 1 cm from carotid bifurcation. \nThere is complete signal loss at this level, presenting a measurement.  This\ndramatic finding typically requires at least 70% stenosis.  Otherwise the neck\nvessels appear normal.\n\nThere is no evidence of left internal carotid artery stenosis by NASCET\ncriteria.",
            "output": "1. Small focal left frontal juxtacortical white matter faint slow diffusivity\nsuggestive of subacute infarction.\n2. Questionable punctate focal area of slow diffusivity along the lateral\nmargin of left hippocampus that may reflect another small infarction.\n3. Poor visualization of the right ophthalmic artery raises the possibility of\nstenosis or occlusion.\n4. Short segment of signal loss of the proximal right internal carotid artery\nsuggests at least 70% stenosis.  The vessel is widely patent distal to this."
        },
        {
            "input": "The patient is status post left frontoparietal decompression craniectomy. The\ncutaneous surgical clips overlying the left scalp results in susceptibility\nartifact.  The frontal and parietal lobes is seen herniating through the\ndefect.\nLarge left MCA infarct is again visualized involving the left frontal and\nparietal lobes as well as the left basal ganglia and extending into the\ncorticospinal tracts into the left cerebral peduncle.  There is also slow\ndiffusion involving the splenium of the corpus callosum.  Punctate areas of\nslow diffusion also seen in the left superior frontal gyrus as well as in the\nhigh posterior aspect of the right frontal lobe and left occipital lobe.  Mild\nmass effect with midline shift to the left by 4 mm.\nNo posterior fossa infarcts.\nMultiple punctate areas of susceptibility artifact within the infarct in\nkeeping with hemorrhagic transformation.  Loss of the left M2 vessels flow\nvoid in keeping with occlusion.\n\nSusceptibility artifact in the right basal ganglia most likely represents\nidiopathic mineralization.\n\nMild moderate opacification of the paranasal sinuses.  Retained fluid present\nin the nasopharynx is most likely secondary to nasopharyngeal instrumentation.\nThe orbits appear normal.  The craniocervical junction appears normal.  The\npituitary appears normal.",
            "output": "The patient is status post left frontoparietal decompression craniectomy. \nLarge left MCA infarct as well as scattered infarcts in other vascular\ndistributions.  Punctate areas of hemorrhagic transformation of the left MCA\ninfarct.  Mild mass effect with midline shift to the left by 4 mm."
        },
        {
            "input": "There is a T2 bright, T1 isointense to dark well-circumscribed extra-axial\nmass in the floor of the anterior cranial fossa measuring 3.7x3.3x2.5 cm TRV x\nAP x CC (13:105 and 100b:60).  The mass appears to be arising from the dura\nwith thin enhancing dural tails extending over the bifrontal convexities\n(101b:92).  There is mass effect on the bilateral inferior frontal lobes\nwithout evidence of parenchymal invasion.\n\nThe ventricles and sulci are prominent suggesting age-related involutional\nchanges.  Periventricular and deep white matter FLAIR hyperintensities are\nnonspecific but suggest sequela of chronic microvascular ischemic disease. \nThe basal cisterns are clear.  There is no evidence of central herniation. \nThere is no evidence of intracranial hemorrhage or infarct.\n\nThere are T1 dark to isointense, T2 bright enhancing foci in the calvarium\nmeasuring 10 x 5 mm in the left parietal skull (13:49 and 12:19) and 6 x 4 mm\nfocus in the left frontal skull (13:74 and 101b:76).  These correspond to\ncalvarial lucencies seen on recent CT of the head and are also unchanged since\n___\n\nIn comparison to the adjacent subcutaneous fat a right parietal scalp\nlobulated well-circumscribed lesion is T1 dark and T2 isointense to\nhypointense (03:20) with enhancement following contrast administration.  The\nlesion measures approximately 2.8 x 1.1 x 0.9 cm.  Overall this is unchanged\nsince CT head of ___\n\nThere is significant mucosal thickening of the left maxillary sinus and T2\nsignal filling several left ethmoidal air cells similar to recent CT.  The\nremaining paranasal sinuses are grossly clear.",
            "output": "1. Avidly enhancing extra-axial mass in the floor of the anterior cranial\nfossa most compatible with olfactory groove meningioma without evidence of\nadjacent parenchymal invasion.\n2. Two small indeterminate T2 bright, T1 dark enhancing foci in of the left\nparietal and left frontal skull are unchanged in size since at least ___. \nLong-term stability and well-circumscribed sclerotic margins on CT suggests a\nbenign etiology.  While somewhat atypical in appearance these could reflect\nhemangiomas.\n3. Well-circumscribed lobulated lesion in the right parietal scalp unchanged\nsince ___ likely reflects a benign granuloma."
        },
        {
            "input": "There is a 3.3 x 3.1 cm rim enhancing mass in the left posterior temporal\nregion with surrounding edema and chronic associated blood products.  The mass\ndemonstrates intrinsic low signal intensities on T2 and FLAIR images.\nIncreased signal along the periphery seen on the diffusion images with\ndecreased ADC.  Small focus of hyperintensity on diffusion images in the right\nfrontal lobe (04:17) has corresponding subtle FLAIR abnormality but no\ndefinite enhancement is identified.  Given significant motion on postcontrast\nimages assessment of other subtle areas of enhancement is limited.\n\nThere is no midline shift or hydrocephalus.",
            "output": "Approximately 3.5 cm left temporal rim enhancing lesion with chronic blood\nproducts and surrounding edema suggestive of metastatic disease. E no other\ndefinite lesions are seen but valuation  is limited due to motion on\npostcontrast images."
        },
        {
            "input": "Heterogeneously enhancing 3.5 x 3.0 cm (AP, TRV) left temporal parietal mass,\nwith prominent surrounding edema pattern resulting in effacement of the left\nlateral ventricle trigone is unchanged.  In addition, there is a right frontal\nsubtly enhancing 4 mm lesion (series 3, image 81; series 10, image 17)\ncorresponding to diffusion-weighted hyperintense signal, better seen on the\ncurrent exam compared to the prior.  No additional enhancing lesions are\nidentified.  No evidence of acute infarct.  There is scattered opacification\nof right sided ethmoid air cells.  Mild mucosal thickening of the remainder\nthe paranasal sinuses is noted.  The dural venous sinuses are patent.  No\ndefinite osseous lesions.",
            "output": "1. Unchanged 3.5 cm left temporal parietal mass with associated edema pattern.\n2. Unchanged 4 mm enhancing lesion of the right frontal lobe.\n3. No other definite enhancing lesions are identified.\n4. No interval change from prior examination on pre-surgical planning\nexamination."
        },
        {
            "input": "Patient is status post left parietal craniotomy for resection of left parietal\nlesion with postsurgical changes visualized in the resection cavity including\nblood products with adjacent diffuse parietal lobe edema with an area of focal\nslowed diffusion surrounding the resection cavity.  Expected thin rim of\nperipheral enhancement in the resection cavity, compatible with breakdown of\nblood brain barrier is identified without nodularity or masslike enhancement. \nExpected left hemispheric dural thickening and enhancement.  No midline shift.\nThere is minimally increased effacement of the occipital horn of the left\nlateral ventricle, secondary to postoperative edema.  There is no evidence for\nacute infarct..  The ventricles and sulci are otherwise stable in caliber and\nconfiguration.\n\nUnchanged 4 mm enhancing focus of the right frontal lobe, concerning for an\nadditional lesion.  No other definite abnormal enhancement visualized.\n\nThe major vascular flow voids are preserved.  The dural venous sinuses are\npatent.  There is a small right maxillary mucous retention cyst otherwise the\nimaged paranasal sinuses and mastoid air cells are clear.  The orbits are\nunremarkable",
            "output": "1. Status post left parietal craniotomy for resection of left parietal lesion\nwith postsurgical changes in the resection cavity, as described above, without\nclear evidence of residual lesion within the resection cavity.\n2. Unchanged 4 mm enhancing focus of the right frontal lobe concerning for an\nadditional lesion.\n3. Additional findings described above."
        },
        {
            "input": "Again seen is residual enhancing tumor at the left temporal resection site. \nThe degree of enhancement has increased since that time.  It is difficult to\ndetermine whether this increase in enhancement is due to true tumor\nprogression, or simple evolution of postoperative enhancement.  The thickness\nand nodularity of the greater enhancement suggests that tumor progression is\nmore likely.  Similarly, the volume of slow diffusing material has increased\nsince the prior study.  This is not typical postoperative change.\nThe volume of perifocal edema and the left hemispheric mass effect have\ndecreased since the prior study.  There is no left-to-right midline shift.\nNo new lesions are identified.  There is expected of postoperative dural\nenhancement at the left temporal surgical site.",
            "output": "1. Increased volume of enhancement and slow diffusion of the residual left\ntemporal lobe tumor at the surgical site.  These findings are concerning for\ntumor progression rather than simple expected postoperative change.\n2. Decrease in edema and local mass effect since the study of ___."
        },
        {
            "input": "The patient is status post left parietal craniotomy for resection of left\ntemporoparietal lesion, with postsurgical changes visualized in the resection\ncavity including blood products with an area of restricted diffusion\nsurrounding the resection cavity, both appearing slightly improved compared to\nmost recent MRI done ___. There is persistent fairly diffuse temporal\nand parietal edema with unchanged thick, irregular enhancement about the\nresection cavity.  The enhancement abuts the left temporal lobe.  Small\noverlying extra-axial/subdural collection measuring 3 mm in diameter is also\ndecreased in size compared to prior (previously 5 mm).\n\nPreviously noted ring enhancing lesion in the right frontal lobe is again\nvisualized, and appears slightly larger and more conspicuous, measuring\napproximately 5 mm in transverse dimension (image 17, series 14), previously\n3.5 mm in ___, suspicious for an additional metastatic lesion, no\nmidline shift or significant mass effect is seen adjacent to this lesion.  The\npituitary appears normal.  The craniocervical junction appears normal.  The\norbits appear normal.  The paranasal sinuses are essentially clear.  The\nintracranial arteries demonstrate normal T2 flow voids.",
            "output": "1.  The patient is status post left parietal craniotomy for resection of a\nleft temporoparietal lesion.\n\n2.  Compared to most recent MRI done ___ the postsurgical changes in\nthe form of blood in the resection cavity as well as restricted diffusion\nsurrounding the resection cavity both appear slightly improved.  However there\nis persistent fairly diffuse temporal and parietal edema with unchanged thick\nirregular enhancement about the resection cavity which is concerning for\nresidual disease.\n\n3.  Also compared to MRI done ___ the restricted diffusion and\nenhancement about the resection cavity is increased concerning for residual\ndisease/disease progression.\n\n4.  Overlying extra-axial/subdural collection is slightly decreased in size\ncurrently measuring 3 mm.\n\n5.  Unchanged ring enhancing lesion in the right frontal lobe, which is also\nsuspicious for metastatic disease.  No new lesions are identified."
        },
        {
            "input": "Postoperative changes are again seen in the left temporal region with a rim\nenhancing area at the surgical site.  The previously seen blood products have\nevolved but mild blood products are still visualized at the level. \nSurrounding FLAIR hyperintensities are seen.  Compared to the previous MRI\nstudy the thickness of the rim enhancement as well as the surrounding FLAIR\nhyperintensities have decreased.\n\nThe previously seen rim enhancing right frontal lobe lesion has minimally\nincreased from 5 mm on the previous study 2 7 mm on the current study\npredominantly due to increase in central hypointensity.  No definite new areas\nof abnormal enhancement are seen.  There are no acute infarcts.  Diffusion\nabnormality at the surgical site appears to be related to blood products.",
            "output": "1. At the site of surgical changes enhancement is decreased with evolution of\nblood products and decrease in FLAIR hyperintensities.  Rim enhancement at the\nsurgical margin persists.\n2. Minimally increased size of the right frontal lobe rim enhancing lesion.\n3. No definite new enhancing lesions."
        },
        {
            "input": "Evaluation is suboptimal due to motion artifact.\n\nThe patient is post left parietal craniotomy.  A resection cavity is seen in\nthe temporal lobe.  There is thick peripheral worsening enhancement\nsurrounding surgical cavity, with restricted diffusion, there is moderate,\nworsening edema involving the left temporal and parietal lobes, extending to\ninvolve the anterior left temporal lobe and left posterior corona radiata. \nThere is effacement of the left occipital and temporal horns.  No midline\nshift is seen.  Area of enhancement measures 4.7 cm x 3.4 cm today, compared\nwith 3.4 cm x 2.8 cm on ___, with much more thick enhancement along\nthe periphery today.  Mild edema is suggested in the right lateral cerebellum\nwith 6 mm focus of enhancement, this area is motion degraded.\n\nA new 1.5 x 1.4 cm lesion is seen along the left anteromedial temporal lobe\nseries 13, image 8.\n\nPreviously seen enhancing lesion at the right anterior frontal lobe has\ndecreased, decreased surrounding edema.  The lesion appears extra-axial\nhowever evaluation is difficult given the motion artifact.\n\n The ventricles and sulci are prominent, consistent with global cerebral\nvolume loss.  The paranasal sinuses, mastoid air cells and middle ear cavities\nare clear.  The intraorbital contents are normal.  Preserved vascular flow\nvoids.",
            "output": "1.  Significant worsening of enhancing mass surrounding surgical cavity,\nworsened surrounding edema, likely represents tumor progression.  ASL, DSC\nperfusion would be helpful to exclude radiation necrosis.\n2.  New 1.5 cm left middle cranial fossa mass consistent with metastasis.\n3.  Suggestion of small inferior right cerebellar lesion, area is motion\ndegraded.\n4.  Improved right frontal lesion."
        },
        {
            "input": "Study is mildly degraded by motion.  There is restricted diffusion in the left\npre and postcentral gyrus with associated T2/FLAIR signal abnormality and\nenhancement (06:25).  Increase susceptibility within this central sulcus\ncorresponding to hyperdensity seen on previous outside noncontrast head CT is\nagain seen (see 10:20 on current study and 201:89 on prior outside exam).\n\nThere is a additional small focus of CSF signal intensity adjacent to the\nfrontal horn of the left lateral ventricle with surrounding FLAIR signal\nhyperintensity, without restricted diffusion or enhancement suggestive of\nchronic infarct (11:16).  There is a chronic left inferior frontal cortical\ninfarct overlying this region.\n\nThere is linear FLAIR signal with associated low signal on GRE sequences in a\nright frontal sulcus, likely due to a small thrombosed venous branch verus a\nsmall focus of subarachnoid hemorrhage (11:20, 10:19).  There is no definite\nevidence of ventriculomegaly.\n\nThere is thrombosis of the superior sagittal sinus extending to the torcula,\nleft transverse sinus, left sigmoid sinus and visualized portion of the left\ninternal jugular vein.  Additionally, there is thrombosis of multiple\nbilateral cerebral veins at the vertex bilaterally.  The straight sinus, right\ntransverse sinus, right sigmoid sinus and visualized portion of the right\ninternal jugular vein are patent.  Intracranial flow voids in the circle of\n___ are preserved.\n\nThere is minimal mucosal thickening in the ethmoid air cells and partial\nopacification the left mastoid air cells.  The orbits are grossly preserved.",
            "output": "1.  Study is mildly degraded by motion.\n2. Dural venous sinus thrombosis involving the superior sagittal sinus, left\ntransverse sinus, left sigmoid sinus, proximal left internal jugular vein, and\nmultiple bilateral cerebral veins at the vertex.\n3. Left frontoparietal acute to subacute infarct with adjacent subarachnoid\nhemorrhage as described.\n4. Right frontal thrombosed vessel versus small subarachnoid hemorrhage as\ndescribed.\n5. Additional chronic left frontal infarcts.\n6. Partial opacification of the left mastoid air cells is nonspecific and\nappears increased compared with outside CT head performed earlier on same day,\nsuggesting it is possibly due to patient's left-sided dural venous sinus\nthrombosis, however mastoiditis as a source of the dural sinus venous\nthrombosis cannot be excluded.\n\nNOTIFICATION:  The wet read findings were discussed with ___, M.D.\nby ___, M.D. on the telephone on ___ at 9:21 pm, 5 minutes\nafter discovery of the findings.\n\n The impression and recommendation above was entered by Dr. ___ on\n___ at 09:27 into the Department of Radiology critical communications\nsystem for direct communication to the referring provider."
        },
        {
            "input": "There is no evidence of infarction, hemorrhage, edema, mass, or mass effect.\nThe ventricles and sulci are prominent, compatible with global parenchymal\nvolume loss.\n\nBilateral periventricular and deep white matter foci of T2/FLAIR signal\nhyperintensity are nonspecific but compatible with mild changes of chronic\nwhite matter microangiopathy, similar to prior exam of ___.\n\nThe visualized paranasal sinuses and mastoids appear clear. The globes and\norbits are unremarkable.  Major intracranial vascular flow voids are\npreserved.\n\nHypointense right frontal calvarial 10 mm focus (08:19) is unchanged since\n___, nonspecific, likely benign given stability and lack of enhancement on\nthe prior study, possibly a bone island.",
            "output": "1. No acute intracranial abnormality.\n2. Chronic findings include global parenchymal volume loss and mild changes of\nchronic white matter microangiopathy."
        },
        {
            "input": "There is no evidence of acute infarction, edema, mass effect, or intracranial\nblood products..  Mild periventricular and subcortical white matter T2/FLAIR\nhyperintensities are again seen, nonspecific but likely sequelae of chronic\nsmall vessel ischemic disease.  The ventricles and sulci are mildly prominent,\nindicative of chronic involutional change.\n\nEvaluation of the bilateral supraclinoid internal carotid flow voids, and of\nthe right cavernous carotid and proximal middle cerebral artery flow voids, is\nlimited by volume averaging artifact.  However, the intracranial arteries are\nbetter assessed on the ___ CTA.\n\nThere is a persistent air-fluid level in the nasopharynx, likely secondary to\nthe endotracheal intubation.",
            "output": "No acute infarction or evidence of other acute intracranial abnormalities."
        },
        {
            "input": "No evidence of hemorrhage, edema, masses, or acute infarction.  The ventricles\nand sulci remain prominent consistent with involutional changes.  No mass\neffect or midline shift.  Findings of chronic small vessel ischemic disease.\n\nThere is no abnormal parenchymal enhancement after contrast administration. \nThe major intracranial arterial flow voids are preserved.  The dural venous\nsinuses are patent.\n\nSmall focus of dural thickening and mild enhancement left vertex overlying\nmiddle frontal gyrus, series 7, image 22, series 10, image 143, series 1001,\nimage 67, nonspecific, could be posttraumatic, inflammatory, neoplastic. \nFindings are new since brain MRI without and with gadolinium ___.  Abnormality measures 2-3 mm in thickness, 2 cm length.\n\nMinimal mucosal thickening of the paranasal sinuses.  Clear mastoid air cells.\nUnremarkable intraorbital contents.  Preserved vascular flow voids.  Dural\nvenous sinuses are patent.",
            "output": "Small area of dural thickening, enhancement left vertex, nonspecific,\ndifferential considerations include posttraumatic change, recent lumbar\npuncture, inflammatory, neoplastic etiology.  Follow-up brain MRI without and\nwith gadolinium recommended."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are mildly prominent reflecting\nvolume loss.  There are a few mild scattered areas of nonspecific T2/FLAIR\nhyperintensity in the subcortical and periventricular white matter which\nlikely reflect chronic small vessel disease in this age group..  There is no\nabnormal enhancement after contrast administration.  The previous area of\ndural thickening/enhancement at the left vertex has resolved.\n\nThe major intracranial vascular flow voids are preserved.  Orbits and\nvisualized extracranial soft tissues are unremarkable.",
            "output": "1. No acute intracranial abnormality.\n2. Interval resolution of the previous area of dural thickening/enhancement at\nthe left vertex.\n3. Nonspecific white matter signal changes likely reflecting chronic small\nvessel disease in this age group.\n4."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.  Unchanged appearance of the T1 and T2 hypointense sclerotic\nright frontal calvarial lesion, measuring 1.3 cm.  There is a nonenhancing\nright parietal calvarial focus that is hyperintense on diffusion-weighted\nimaging corresponds to lucency on the CT head dated ___, that is\nunchanged since ___, but appears new since ___.  This may\nrepresent another focus of myeloma.  No additional calvarial lesions are\nidentified.",
            "output": "1. No acute intracranial abnormality or intracranial mass is identified.\n2. Unchanged appearance of the T1 and T2 hypointense sclerotic right frontal\ncalvarial lesion, measuring 1.3 cm.\n3. Nonenhancing right parietal calvarial focus that is hyperintense on\ndiffusion-weighted imaging, corresponding to lucency on the CT head dated ___, that is unchanged since ___, but appears new since\n___. This may represent another focus of myeloma.\n4. No additional calvarial lesions are identified."
        },
        {
            "input": "There is no acute infarction, intracranial hemorrhage, extracerebral fluid\ncollection, midline shift or mass effect.  No diffusion abnormalities are\ndetected. The cerebral volume is appropriate for the patient's stated age. \nThe major vascular flow voids are maintained. There is no evidence of abnormal\nenhancement. The orbits are unremarkable, the paranasal sinuses and mastoid\nair cells are clear",
            "output": "Essentially normal MRI of the brain with and without contrast, there is no\nevidence of acute or subacute intracranial process"
        },
        {
            "input": "The intracranial vertebral and internal carotid arteries and their major\nbranches appear patent without evidence of flow-limiting stenosis or aneurysm\ngreater than 3 mm.  There is fetal type configuration of the left posterior\ncerebral artery with a hypoplastic P1 segment and a large left posterior\ncommunicating artery.  The right posterior communicating artery is not seen,\neither absent or hypoplastic.",
            "output": "No evidence of an intracranial arterial aneurysm greater than 3 mm."
        },
        {
            "input": "In the left frontal lobe near the convexity (11:272 and 1101:68) there is an\napproximately 8 mm enhancing lesion near the surface of the brain. There is no\nadjacent brain edema identified.  No adjacent dural enhancement is noted.  On\nthe axial images the lesion appears somewhat triangular similar to an\nextra-axial mass such as meningioma but on the coronal and sagittal images it\nhas a rounded configuration and appears to be intra-axial.\n\nIn the left frontal lobe more laterally and inferiorly there is faint area of\nsusceptibility (7:15) with the linear enhancement (10:15 and 11:175)\nindicative of a developmental venous anomaly with adjacent capillary\ntelangiectasia.  No other enhancing lesions are identified.\n\nThe ventricles and extra-axial spaces are normal in size without midline shift\nmass effect or hydrocephalus.  Vascular flow voids are maintained.  Visualized\nparanasal sinuses are clear.  No abnormal signal is seen in the visualized\nbony structures.",
            "output": "1. 8 mm cortical enhancing lesion difficult to characterize as intra or\nextra-axial given its small size ( metastasis versus meningioma ) but given\nrounded shape on the sagittal and coronal images favors intra-axial location.\n2. If patient has prior brain MRI studies, comparison would be helpful.  If\nnone are available short-term follow-up in ___ weeks could help for assessment\nof interval change."
        },
        {
            "input": "In the left superior frontal gyrus/superior frontal sulcus, there is a 7 x 6 x\n8 mm (AP by transverse by SI close) enhancing nodule.  Appearance is not\nsignificantly changed from prior examination.\n\nThere is a linear region enhancement in the inferior left frontal lobe, likely\nrepresenting developmental venous anomaly, unchanged.\n\nThere is focal dilation of a venous structure in the right posterior fossa at\nthe level of the foramen magnum, probably an occipital emissary vein (series\n18, image 29).\n\nThere is no evidence of hemorrhage, edema, mass effect, midline shift or\ninfarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no other abnormal enhancement after contrast\nadministration.  The major intracranial vascular flow voids are preserved.",
            "output": "1. 8 mm probable lesion either involving/adjacent to the superior left frontal\ngyrus is unchanged from prior examination, and it remains difficult to\ncharacterize as intra or extra-axial.  Differential diagnosis remains\nmetastasis versus meningioma."
        },
        {
            "input": "There is extensive bilateral background cortical siderosis consistent with\nprior subarachnoid hemorrhages.  There is sulcal FLAIR hyperintensity within\nthe right central sulcus, precentral sulcus, and superior frontal sulcus with\ncorresponding leptomeningeal enhancement.  There is a small focus of\nleptomeningeal enhancement at the posterior left frontal superior gyrus\n(100:94).\n\nThere is extensive bilateral confluent periventricular and subcortical white\nmatter FLAIR hyperintensity consistent with sequela of chronic\nmicroangiopathy.  There is no acute infarct follow mass, or mass effect. \nThere is prominence of the ventricles and cortical sulci consistent with\nvolume loss.  The vasculature is patent.\n\nThe orbits, calvarium, and soft tissues are unremarkable.  There is mild\nmucosal thickening within the frontal and ethmoid sinuses.  The mastoid air\ncells and middle ears are clear.",
            "output": "1. Sulcal FLAIR hyperintensity and leptomeningeal enhancement involving the\nright central, precentral and superior frontal sulci. Additional focus of\nleptomeningeal enhancement at the left frontal superior gyrus. Findings may\nrepresent reactive changes secondary to subarachnoid hemorrhage versus\nleptomeningeal carcinomatosis, given clinical history of lung cancer. \nConsider correlation with CSF cytology and/or follow up imaging to\ncharacterize the evolution of these findings.\n2. Extensive bilateral cortical siderosis consistent with prior subarachnoid\nhemorrhages.\n3. No discrete parenchymal lesion."
        },
        {
            "input": "Images through the internal auditory canal demonstrates symmetric appearance\nof the seventh eighth nerve complexes.  There is no evidence of abnormal\nenhancement or mass lesion within the internal auditory canals,\ncerebellopontine angles or membranous labyrinth. No other mass lesions are\nseen within the posterior fossa.\n\nLimited included imaging of the remainder of the brain demonstrates a focal\narea of encephalomalacia in the right pons, unchanged.  No evidence of\nhemorrhage,edema, or mass.  Mild global parenchymal volume loss is noted. \nThere is no abnormal enhancement after contrast administration.\n\nNo osseous abnormalities are seen.  There is partial opacification of the\nbilateral mastoid air cells.  The paranasal sinuses, andmiddle ear cavitiesare\nclear. The imaged portions of the orbits are unremarkable. The visualized\nportion of the principle vascular flow voids are preserved.",
            "output": "1. No evidence of ___ or cerebellopontine angle mass.\n2. Unchanged focal area of encephalomalacia in the right side of the pons."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, mass, or infarction. The ventricles\nand sulci are age-appropriate.  There is no mass effect or midline shift.\n\nScattered T2 and FLAIR hyperintense foci in the periventricular and\nsubcortical white matter are nonspecific, but likely reflect chronic small\nvessel ischemic changes.\n\nThere is mild mucosal thickening of the paranasal sinuses.  There is mild\nfluid signal in the left mastoid air cells.  The intraorbital contents are\nunremarkable.",
            "output": "1. No evidence of mass, hemorrhage or infarction."
        },
        {
            "input": "There is no intracranial mass, mass effect, or midline shift. Ventricles and\nsulci are age-appropriate.  Incidentally noted is a cavum septum pellucidum et\nvergae.  There is no focal parenchymal signal abnormality. There is no region\nof restricted diffusion or abnormal susceptibility artifact. Major\nintravascular flow voids are preserved.\n\nPost contrast images demonstrate no abnormal parenchymal or meningeal\nenhancement.\n\nVisualized paranasal sinuses and mastoid air cells demonstrate no abnormal\nsignal.",
            "output": "Normal MRI of the brain."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, mass, mass effect, or infarction.\nThe ventricles and sulci are normal in caliber and configuration.  A 1cm cavum\nseptum pellucidum et vergae is incidentally noted indenting the lateral\nventricles.\nThere is no abnormal parenchymal signal or enhancement after contrast\nadministration.  Major vascular flow voids are preserved.\nThe orbits are unremarkable.\nThere is mild mucosal thickening within the frontal sinuses.  There is\nmoderate mucosal thickening within the ethmoid air cells and mucosal\nthickening and fluid signal within the left greater than right maxillary and\nsphenoid sinus.  There is fluid signal and secretions noted in the\nnasopharynx.\nSmall amount of fluid in the mastoid air cells on both sides.\nSlightly hypointense marrow signal.",
            "output": "1.  No evidence of acute infarction, hemorrhage, or enhancing mass lesion.\n1 cm cavum septum pellucidum et vergae\n\n2.  Paranasal sinus disease and small amount of fluid in the mastoid air\ncells, right more than left.\n\n3. Slightly hypointense marrow signal.  This can relate to cellular red marrow\nin a young patient; however, correlate with hematology labs for anemia,\nsystemic disease, marrow disorder, etc.\nOther details as described above."
        },
        {
            "input": "Trigeminal nerves and the cavernous sinuses are symmetric.  There is no\ndeformity or fullness identified.  No abnormal enhancement is seen.  There is\nno evidence of neural vascular deformity of the trigeminal nerves.  No\nevidence of infiltrative process of the skullbase, parapharyngeal regions or\nnasopharynx.  Both orbits are symmetric in appearance.\n\nImages through the brain demonstrate moderate atrophy and small vessel\ndisease.  No abnormal enhancement is seen within the brain",
            "output": "1. No mass lesion or abnormal enhancement seen in relation with the trigeminal\nnerves or cavernous sinuses.\n2. Moderate brain atrophy and small vessel disease.\n3. No enhancing brain lesions."
        },
        {
            "input": "The study was terminated prematurely due to patient's inability to cooperate. \nOnly sagittal and axial T1 precontrast imaging was performed.\n\nMild prominence of the ventricles and sulci likely represents age-related\ninvolutional change.  No obvious mass or large intracranial hemorrhage.\n\nLimited assessment of the orbits is unremarkable.  Paranasal sinuses and\nmastoid air cells are grossly clear.",
            "output": "1. The study was terminated prematurely due to patient's inability to\ncooperate and is moderately limited by motion.  Only sagittal and axial T1\nprecontrast imaging was performed.\n2. Within the above limitations, no definite large hemorrhage or intracranial\nmass identified. Please see the subsequent complete MRI that was obtained on\nthe same date."
        },
        {
            "input": "Study is moderately limited by patient motion, within the limitations of this\nexam:\n\nA punctate area of slow diffusion within the posterior right putamen (series\n502, image 17) without a definite corresponding low signal on the ADC map,\nconcerning for subacute infarct.\n\nFour punctate cortical areas of slow diffusion in the bilateral occipital and\nright frontal lobes (series 502, image 11, 14, 12, 17) without definite\ncorrelates on the ADC map are also concerning for subacute infarcts.\n\nCorresponding to the right parietal sulcal hyperdensity on prior CT, there is\ntrace sulcal, linear susceptibility on the gradient echo imaging, compatible\nwith trace subarachnoid hemorrhage (series 10, image 16).  A right cerebellar\nfocus susceptibility (series 10, image 5), likely represents a chronic\nmicrohemorrhage.  Bilateral basal ganglia lacunar infarcts noted.\n\nPontine, periventricular and deep white matter FLAIR hyperintensities are\nnonspecific, but likely represent sequelae of chronic small vessel ischemic\ndisease.  Prominence of the ventricles and sulci, are compatible with\nage-related involutional change.\n\nThe ocular lenses have been surgically replaced.  The orbits are otherwise\nunremarkable.  There is mild mucosal thickening in the ethmoid air cells.  The\nmastoid air cells are clear.",
            "output": "1. Trace right parietal subarachnoid hemorrhage, corresponding to the\nhyperdensity seen on prior CT.  No new or worsening hemorrhage.\n2. Punctate right putaminal, right frontal and bilateral occipital subacute\ninfarcts.\n3. Pontine, periventricular and deep white matter FLAIR hyperintensities are\nnonspecific but likely represent sequela of chronic microangiopathy.\n\nNOTIFICATION:  The findings were discussed with ___, M.D. by ___,\nM.D. on the telephone on ___ at 10:16 am, 5 minutes after discovery of\nthe findings."
        },
        {
            "input": "Study is mildly degraded by motion.\n\nMRI BRAIN:\nThere are several areas of slow diffusion with associated T2/FLAIR high signal\nall within the left parieto-occipital cortex extending to the deep white\nmatter as well as punctate foci of slow diffusion in the left frontal lobe\n(series 7, images ___.  Susceptibility on gradient echo imaging in the left\nparieto-occipital region is compatible with a small amount of blood products.\n\nThe major intracranial vascular flow voids are maintained.  The ventricles and\nsulci are normal in caliber and configuration.  There is no abnormal\nenhancement after contrast administration.  There is minimal 1-2 mm cerebellar\ntonsillar ectopia.\n\nThere is moderate mucosal thickening of the ethmoid air cells.  There is a\nsmall amount of fluid within the left mastoid air cells.  The orbits are\nnormal.\n\nMRA BRAIN:\nQuestion minimal nonocclusive narrowing at left P1-2 junction versus artifact.\nLeft proximal A1 segment not well visualized, and asymmetric decreased caliber\nof left A1 segment relative to right A1 segment is noted (see 2: 96-99).\n\nThe intracranial vertebral and internal carotid arteries and their major\nbranches appear patent without evidence of stenosis, occlusion, or aneurysm\nformation.  There is a right dominant vertebrobasilar system with the left\nintracranial vertebral artery terminating into the left ___.",
            "output": "1.  Study is mildly degraded by motion.\n2.  Left PCA distribution parieto-occipital with small areas of blood products\nand additional punctate deep white matter ACA and MCA watershed distribution\nleft frontal acute to subacute infarcts, as described.\n3. Question minimal nonocclusive narrowing at left P1-2 junction versus\nartifact.\n4. Limited visualization of proximal left A1 segment, and diminutive left A1\nsegment relative to right A1 segment.  While findings may represent normal\nvariant superimposed with artifact, steno-occlusive disease is not excluded on\nthe basis examination.\n5. Otherwise, grossly patent circle of ___ without definite evidence of\nocclusion or aneurysm.\n6. Paranasal sinus disease, as described.\n\nNOTIFICATION:  The impression and recommendation above was entered by Dr.\n___ on ___ at 12:34 into the Department of Radiology critical\ncommunications system for direct communication to the referring provider."
        },
        {
            "input": "MR BRAIN:\nThere is a subacute infarction within the left parietal occipital lobe\ndemonstrating surrounding vasogenic edema and internal hemorrhagic components.\nThe extent of internal hemorrhage has increased from the prior examination.\n\nAdditional areas of enhancement with FLAIR/T2 hyperintensity and\nhyperintensity and diffusion weighted imaging are seen within the left centrum\nsemiovale extending into the left posterior parietal subcortical and cortical\nfibers, suggestive of additional areas of infarction with several areas of\ninternal hemorrhage that are also slightly more conspicuous as compared to the\nprior examination.  Several additional punctate areas of slow diffusion is\nseen within the left frontal lobe white matter.\n\n There is no evidence for new areas of interval infarction.  No areas of\nadditional parenchymal enhancement or hemorrhage.\n\nThe ventricles and sulci are mildly prominent.  The basal cisterns are patent.\nThere is gross preservation of the principal intracranial vascular flow voids.\nThe dural venous sinuses appear patent on MP-RAGE imagine sequences.\n\nMucosal thickening is seen within scattered ethmoid air cells and sphenoid\nsinuses, with nonspecific fluid signal seen in the left mastoid air cells. \nThe remainder of the visualized paranasal sinuses, middle ear cavities, and\nmastoid air cells are well aerated and clear.  The orbits are within normal\nlimits bilaterally.\n\n\nMR ___: There are several areas of central increased mean\ntransit time within the left posterior parietal and left occipital infarcts. \nAdditionally, there is evidence of decreased cerebral blood volume throughout\nthe majority of the left occipital infarct.\n\n\nASL Perfusion: Several areas of increased perfusion are noted within the left\noccipital and parietal lobes, correlating to the areas of increased FLAIR\nsignal abnormality and enhancement.\n\n\nMR Spectroscopy: Multi voxel MR spectroscopy is limited secondary to\nhemorrhagic products within the site of infarction.  Allowing for this,\ninterrogation of the surrounding areas of FLAIR hyperintensity within the left\nparietal occipital lobe demonstrate several areas of increased creatinine and\ncholine, with CC/Naa ratios of 1 or less.  Many these areas also demonstrate\nincreased MI/Cr ratios of 1 or slightly above 1, in addition to increased\nlipids and lactate.",
            "output": "1. Interval evolution of a dominant left parieto-occipital infarction with\nincreasing internal hemorrhagic products, with surrounding edema and\nenhancement.\n2. Multiple additional areas of known subacute infarction, as above, several\nof which also demonstrate increasing internal hemorrhagic components.\n3. MR contrast perfusion of the dominant infarct demonstrates increased mean\ntransit time and areas of decreased cerebral blood volume, compatible with\ninfarction.\n4. ASL perfusion demonstrates several areas curvilinear and focal increased\nperfusion, generally involving the smaller, more superior areas of infarction\nand correlating with areas of enhancement.  These findings may represent\nreactive changes in the setting of recent ischemia.\n5. MR spectroscopy of the dominant left parieto-occipital infarct is limited\nsecondary to extensive hemorrhagic products within the lesion.  Allowing for\nthis, there are increased choline and creatinine levels, although the\ncholine/NAA ratio remains at 1 or below.  Associated areas of increased\nMI/creatinine ratio are suggestive of a non neoplastic etiology such as\ninfarction, including the possibility of a cortical hemorrhagic venous\ninfarct.  Increased lipids and lactate likely correlate with areas of necrosis\nfollowing infarction.\n6. These findings taken together are suggestive of areas of evolving\nischemia/infarction, some of which contain internal hemorrhagic components, a\nvenous hemorrhagic cortical infarction is a consideration, recommend attention\nat follow-up imaging to further exclude any underlying mass."
        },
        {
            "input": "A tracheostomy is noted. There is a T1 hypointense, T2 hyperintense enhancing\nglottic and subglottic circumferential laryngeal mass asymmetric to the right\nwhich appears similar to size as on prior CTA study. There is signal\nabnormality and enhancement seen within the hyoid bone.  There is a focal loss\nof the prevertebral fat plane at C5-C6 level (Se 8, im 13; Se 9, im 21).\nTherefore, the invasion of this fat plane by neoplasm cannot be completely\nexcluded though this can relate to slice thickness and volume averaging.\nHowever, the ALL appears grossly  intact without obvious disruption and there\nis no abnormal signal within the bones of the cervical spine.\nAssessment of the aerodigestive tract is limited due to intubation.\n\nThere is no pathological adenopathy by imaging criteria.  Neck vessels are\npatent.\nThe salivary glands and unremarkable.",
            "output": "Enhancing laryngeal soft tissue mass consistent with history recurrent tumor.\nThere is a focal loss of prevertebral fat plane at C5-C6 and therefore the\ninvasion of this space by tumor cannot be excluded; however, this can also\nrelate to slice thickness and volume averaging.  However, the ALL appears\ngrossly intact and there is no abnormal signal within the osseous cervical\nspine.\n(It is unclear if loss of clear fat plane by itself should preclude surgery as\nthere is no obvious involvement of the vertebrae at these levels- correlate\nwith surgical consult)"
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  There is prominence of the ventricles and sulci suggestive\ninvolutional changes.\n\nModerate mucosal sinus thickening is seen involving the ethmoid air cells. \nMild sinus disease is seen involving the maxillary sinuses.  Mild sinus\ndisease is seen involving the left frontal sinus.  The sphenoid sinus is\nclear.  The principal vascular flow voids are well preserved.  There is mild\natrophy of the hippocampal formations bilaterally.",
            "output": "1. Mild atrophy of the hippocampal formations bilaterally.\n2. No acute intracranial abnormalities identified."
        },
        {
            "input": "MR BRAIN:\nThere is no evidence of hemorrhage, edema, masses, mass effect, or midline\nshift.  There are a few scattered areas of cortically based diffusion\nabnormality in the bilateral frontal and parietal lobes near the vertex, for\nexample images 20, 26 and 25 of series 4.  However, there are no corresponding\ndefinite T2 signal changes these regions, and there is no did decreased\ndiffusion involving the hippocampal formations or basal ganglia.  There are\nfew scattered minimal nonspecific T2/FLAIR hyperintense foci in the\nsubcortical and periventricular white matter which may reflect chronic small\nvessel disease in this age group. The ventricles and sulci are mildly\nprominent reflecting volume loss.\n\nThe major intracranial vascular flow voids are preserved.  Orbits are\nunremarkable.  There is patchy fluid signal in the bilateral mastoid air\ncells, there is mild scattered mucosal thickening throughout the paranasal\nsinuses.\n\nMRA brain: The intracranial vertebral and internal carotid arteries and their\nmajor branches appear normal without evidence of stenosis, occlusion, or\naneurysm formation.  Slightly dominant left vertebral artery.  There is a\npatent posterior communicating artery on the right and possibly also with\nsmall patent posterior communicating artery on the left.",
            "output": "1. There are questionable areas of cortically based diffusion abnormality in\nthe superior parietal and frontal lobes.  This could be artifactual given the\nlack of associated T2 signal changes, but subtle findings of hypoxic injury\ngiven the history of cardiac arrest are also possible. Consider short-term\nfollow-up exam to assess evolution.\n2. Unremarkable MR angiography of the head."
        },
        {
            "input": "There is motion artifact which degrades image quality particularly on the pre\nand postcontrast axial T1, postcontrast MP rage, and axial T2 sequences.\n\nThere is diffuse leptomeningeal pachymeningeal nodular enhancing disease\nconsistent with lymphoma, as follows:\n\nThere is nodular extra-axial enhancing disease at the anterior left frontal\noperculum (30 01:15), anterior parafalcine left frontal cortex (___),\nsuprasellar cistern, ambient cistern, cerebellopontine angles, fourth\nventricle, and posterior cranial fossa base.  There is diffuse nodular\nenhancement coating the posterior fossa structures including the midbrain,\npons, medulla, and visualized upper cervical spine.  There is enhancing\ndisease involving the expected course of multiple cranial nerve courses,\nforamen of Luschka and Magendie, however the fine detail is obscured by motion\nartifact.  There is enhancing disease within the right internal auditory\ncanal, indicated leptomeningeal disease.  There is mass like enhancing disease\nwithin the spinal canal at the C3 level which extends across the near entirety\nof the spinal canal either infiltrating or compressing the traversing cervical\ncord and producing spinal cord edema.  This measures 1.0 cm x 1.7 by 1.1 cm\n(101:20).\n\nThere is no acute hemorrhage, territorial infarct, or shifting of the normally\nmidline structures.  The ventricles are unremarkable.  The orbits and soft\ntissues are unremarkable.  The paranasal sinuses and mastoid air cells are\nclear.  There is diffuse T1 hypointensity of the calvarial marrow.",
            "output": "1. Study is limited by motion artifact, as described, limiting the spatial\nresolution.\n2. Diffuse nodular enhancing disease involving the leptomeningeal and\npachymeningeal extra-axial spaces, as described, predominantly within the\nbasal cisterns consistent with intracranial lymphoma.\n3. Mass like enhancing disease within the visualized upper cervical canal from\nC1 through C3 levels, which may be compressing or infiltrating the adjacent\ncervical cord.\n4. Low signal within the cranial marrow which is nonspecific and may be seen\nwith hematopoetic marrow or infiltration.\n\nNOTIFICATION:  The findings were discussed by Dr. ___ with Dr. ___ on the\ntelephone on ___ at 9:18 AM, 10 minutes after discovery of the findings."
        },
        {
            "input": "There is markedly improved but persistent leptomeningeal and pachymeningeal\nnodular enhancement in the pre pontine cistern, along the foramen of Luschka,\nsuprasellar cistern, anterior cranial fossa, cerebellar folia and anterior to\nthe temporal lobes.  Minimal partially visualized circumferential enhancement\nin the upper cervical spine is seen, with some areas of more masklike\nnodularity, also improved in comparison to the prior MRI.  The nodular\nenhancement on the right extends into the right internal auditory canal.\n\nThere is no evidence of hemorrhage, edema, mass effect, midline shift or\ninfarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  Periventricular and subcortical T2 and FLAIR hyperintensities\nare noted.  The major vascular flow voids are preserved.\n\nMinimal fluid is seen in the right mastoid air cells.  The orbits are normal. \nThere is minimal mucosal thickening of the ethmoid sinuses.",
            "output": "1. Markedly improved but persistent leptomeningeal and pachymeningeal nodular\nenhancement at the skullbase, visualized upper cervical spine and anterior\ncranial fossa, as described above.\n2. No new sites of abnormal contrast enhancement."
        },
        {
            "input": "There is no intracranial mass, mass effect, or midline shift. Ventricles and\nsulci are age-appropriate. There is no focal parenchymal signal abnormality. \nRight basal ganglia prominent perivascular space is incidentally noted.  There\nis no region of restricted diffusion or abnormal susceptibility artifact.\nMajor intravascular flow voids are preserved.\n\nPost contrast images demonstrate subtle pachymeningeal enhancement along the\nfloor of the anterior cranial fossa (103A: 51).  The amount of thickening and\nenhancement along the anterior margin of the left middle cranial fossa and\nadjacent to the Meckel's cave on the left has decreased (103A: 39 and 37). \nThere is still persistent but also decreased abnormal enhancement along the\nanterior and posterior aspects of the upper cervical cord best seen on the\nsagittal MPRAGE images.\n\nVisualized paranasal sinuses and mastoid air cells are clear.",
            "output": "Interval decrease of previously seen abnormal enhancement along the anterior\nand middle cranial fossae and abutting the upper cervical cord."
        },
        {
            "input": "There is re- demonstration of a 26 x 24 mm acute left cerebellar\nintraparenchymal hematoma with associated T2 prolongation and signal void on\ngradient echo. This hemorrhage is unchanged in size compared with earlier same\nday examination.  Trace peripheral enhancement is likely related to the bleed.\nThere is no definite underlying mass. Associated surrounding mass effect\nappears similar to the prior study with effacement of the fourth ventricle. \nOverall configuration of the ventricles and sulci is unchanged compared to the\nprior examination remaining prominent, likely secondary to age related\ninvolutional change.  There is no hydrocephalus.  There is mild surrounding\nvasogenic edema.  Other scattered punctate foci of subcortical and deep white\nmatter and T2 prolongation are nonspecific.  There is no abnormal focus of\ndiffusion restriction. T2 \"dark through\" effect is seen in the region of\nintraparenchymal hemorrhage on diffusion-weighted images.  There is otherwise\nno definite focus of abnormal post gadolinium enhancement.  There is no\nabnormality of the skull base or calvarium. The orbits, periorbital and\nparacavernous spaces are unremarkable. The major intracranial vascular flow\nvoids are preserved.  Mucosal wall thickening is noted in the bilateral\nfrontal sinuses, bilateral ethmoid air cells, bilateral sphenoid air cells and\nbilateral maxillary sinuses.",
            "output": "1. No significant interval change of a 26 x 24 mm acute left cerebellar\nintraparenchymal hematoma with associated mass effect and effacement of the\nfourth ventricle. No definite underlying mass with trace peripheral post\ngadolinium enhancement likely secondary to bleed."
        },
        {
            "input": "MR BRAIN:\nThere is no evidence of intracranial hemorrhage,edema,masses,mass effect,\nmidline shift or infarction.   The ventricles and sulci are normal in caliber\nand configuration.  No diffusion abnormalities are detected.\n\nBoth orbits and globes are unremarkable.  Paranasal sinuses and mastoid air\ncells are unremarkable.\n\nMRA brain: The intracranial vertebral and internal carotid arteries and their\nmajor branches appear normal without evidence of stenosis, occlusion, or\naneurysm formation.",
            "output": "1. Unremarkable MRI and MRA of the brain.  There is no evidence of acute\nintracranial process or hemorrhage\n2. There is no evidence of abnormal enhancement after contrast administration"
        },
        {
            "input": "There is no intracranial hemorrhage.\n\nDiffusion weighting imaging does not demonstrate evidence of acute infarct.\n\nThe major intracranial vessels exhibit the expected signal void related to\nvascular flow.\n\nGray white matter differentiation is otherwise maintained.\n\nVentricles and extra axial CSF spaces are within normal limits.\n\nThe sella turcica, craniocervical junction, and orbits are unremarkable.\n\nThe paranasal sinuses and mastoid air cells demonstrate normal signal.",
            "output": "Unremarkable, unenhanced MRI examination of the brain."
        },
        {
            "input": "In the left posterior fossa, there is a round 3.2 x 2.9 x 3.0 cm dural-based\nmass inseparable from the left tentorium, abutting the superolateral aspect of\nthe left cerebellar hemisphere, presumably meningioma. It is isointense to\ngray matter on T1 and T2 weighted imaging with homogeneous avid enhancement. \nThere is regional T2 prolongation within the left cerebellar hemisphere\nconsistent with vasogenic edema with and mild effacement of the fourth\nventricle.  No hydrocephalus.  No evidence of hemorrhage or infarction.\n\nThe left transverse sinus is hypoplastic.  The left distal transverse sinus\nand sigmoid sinus do not enhance and may be compressed or occluded by the\npresumed meningioma.  The left internal jugular vein traits postcontrast\nenhancement.  The remainder of the dural venous sinuses are patent.",
            "output": "Dural-based mass in the left posterior fossa, consistent with a meningioma. \nThere is regional vasogenic edema with mild effacement of the fourth ventricle\nbut no obstructing hydrocephalus.  No definite enhancement of the distal left\ntransverse sinus and sigmoid sinus which may be severely compressed with\nocclusion a possibility.  There is reconstitution of contrast enhancement of\nthe left internal jugular vein."
        },
        {
            "input": "Slight increase in size of a 3.6 x 2.9 cm enhancing lesion abutting the\ntentorium causing mass effect on the left cerebellum and effacing the fourth\ncompatible with an atypical meningioma.  Of note, a nonenhancing portion of\nthe mass likely represents necrotic tissue days new since ___. \nThere has been an increase in the extensive associated edema within the left\ncerebellar hemisphere extending to the left pons.  There is increased mass\neffect on the left pons/midbrain.  No evidence of hemorrhage or infarction.\n\nThe mass abuts the left transverse sinus and the process sinuses difficult to\ndistinguish in this region from the mass.  Although the transverse sinuses\nvisual lies distally as well as the sigmoid sinus is seen on MP rage axial\npost gadolinium images, the mass appears to be invading the sinus in the\nlateral portion.  A small defect proximally in left transverse sinus (900:70)\nis of low signal and most likely due to an arachnoid granulation rather than a\nthrombus.\n\nThere is no evidence of hemorrhage or infarction.  There is an empty sella.\n\nThe major intracranial vascular flow voids are maintained.  The ventricles and\nsulci are normal in caliber and configuration.  The paranasal sinuses, mastoid\nair cells and orbits are normal.",
            "output": "1. Slight increase in size of the mass abutting the left tentorium\ndemonstrating interval development of necrotic change and slight worsening of\nsurrounding edema and mass effect on the left cerebellar hemisphere, left\nmidbrain and pons.  There is persistent effacement of the fourth ventricle.\n2. The mass appears to be invading the left transverse sinus but proximal and\ndistal flow remains,\n3. No intracranial hemorrhage or acute infarction."
        },
        {
            "input": "No significant change in the 3.6 x 2.9 cm enhancing lesion abutting the\ntentorium and causing mass effect on the left cerebellum with effacement of\nthe fourth ventricle compatible with an atypical meningioma.  Redemonstrated\nis a nonenhancing portion of the mass likely representing necrotic tissue.  No\nchange in the degree of extensive associated edema within the left cerebellar\nhemisphere and extending into the left pons.  There is no evidence of\nhemorrhage or infarction.  There is no new enhancing focus.\n\nThe mass continues to abut the left transverse sinus and appears to be\ninvading the sinus at the lateral portion (08:31).  As before, adjacent focus\nof hypoattenuation overlying the lateral aspect of the left transverse sinus\nis favored to represent an arachnoid granulation rather than any thrombus.",
            "output": "1. No change in size of the mass abutting the left tentorium with associated\nmass effect on the left cerebellar hemisphere, midbrain and pons, effacement\nof the fourth ventricle and a stable degree of edema within the left\ncerebellar hemisphere.  Findings are compatible with an atypical meningioma.\n2. No evidence of intracranial hemorrhage or acute infarction."
        },
        {
            "input": "Postoperative changes related to a left suboccipital craniectomy for resection\nof a left cerebellar mass.  A thin rim of diffusion abnormality surrounding\nthe resection cavity is compatible with expected postoperative changes. \nIntrinsic T1 signal and susceptibility within the resection cavity is\ncompatible with blood products.  There is a small amount of pneumocephalus in\nthe region of the resection cavity.  Mild peripheral enhancement surrounding\nthe resection cavity is likely postoperative, however, residual disease cannot\nbe entirely excluded.  Mild expected postoperative dural thickening and\nenhancement overlying the left tentorium is noted.\n\nNo significant change in left hemispheric T2/FLAIR abnormal signal.  There has\nbeen interval improvement in mass effect on the left midbrain and pons.  New\nedema/enhancement of the visualized left neck muscles is likely reactive from\nrecent surgery.  Subcutaneous left parietal drainage catheter is re-identified\n\nThe major intracranial vascular flow voids are maintained.  The dural venous\nsinuses remain patent.  The ventricles and sulci are normal in caliber and\nconfiguration.  The paranasal sinuses and orbits are normal.  There is a small\namount of nonspecific fluid within the left mastoid air cells.",
            "output": "1. Postoperative changes related to a left suboccipital craniectomy for\nresection of a left cerebellar mass with mild expected postoperative\nenhancement surrounding the resection cavity although subtle residual disease\ncannot be entirely excluded for which continued follow-up was recommended.\n2. New edema/enhancement of the visualized left neck muscles, presumably\nreactive from recent surgery.\n3. Additional findings described above."
        },
        {
            "input": "Status-post left occipital craniectomy and cranioplasty.  There is very mild\ndural irregularity and enhancement at the surgical site.  There is no evidence\nfor an enhancing mass at the surgical site, nor elsewhere in the intracranial\ncompartment.  Compared to the ___ MRI, T1 hyperintense blood\nproducts in the surgical bed have resolved.  Mild T2/FLAIR hyperintensity in\nthe lateral left cerebellar hemisphere along the surgical bed has decreased in\nextent compared to the prior MRI with resolution of mass effect.  Previously\nseen rightward shift of midline structures in the posterior fossa and\neffacement of the fourth ventricle have resolved.  The ventricles and sulci\nare now normal in size.\n\nThere is non opacification of the left sigmoid sinus and the left transverse\nsinus at the level of the surgical bed, similar to the presurgical MRI exams. \nMedial aspect of the left transverse sinus is small but patent, unchanged. \nVisualized upper portion of the left internal jugular vein appears patent. \nOther dural venous sinuses opacify with contrast on MP RAGE images, as\nexpected.  Major arterial flow voids are preserved.\n\nThere is mild mucosal thickening in the ethmoid air cells.  A cluster of left\ndependent mastoid air cells near the cranioplasty is opacified, similar to the\n___ CT.",
            "output": "1. No evidence for residual or recurrent tumor.\n2. Resolution of mass effect in the posterior fossa.\n3. Non opacification of the left sigmoid sinus and left transverse sinus at\nthe level of the surgical bed, with patency of the medial left transverse\nsinus and the visualized upper internal jugular vein, unchanged compared to\nthe presurgical MRIs prior to mass resection."
        },
        {
            "input": "There are central pontine and periventricular and subcortical white matter\nFLAIR hyperintense foci, which are relatively unchanged comparison to ___.  There are larger FLAIR hyperintense white matter lesions\nperpendicular to the right lateral ventricular body (08:15) and within the\nleft frontal subcortical white matter (08:15).  There is a solitary gradient\necho hypointense focus at the right temporal subependymal parenchyma (7:  8),\nwhich is unchanged.  Otherwise the parenchymal signal is unremarkable without\nacute infarct, hemorrhage, mass, or mass effect.  There is mild prominence of\nthe ventricles and cortical sulci consistent with volume loss, without lobar\npredominance.\n\nThe extra-axial spaces are unremarkable.  The vascular flow voids are\npreserved.  The orbits, calvarium, and soft tissues are unremarkable.  There\nis no fluid signal within the paranasal sinuses, mastoid air cells, or middle\nears.",
            "output": "1. Scattered bilateral periventricular subcortical white matter and central\npontine FLAIR hyperintense foci with larger FLAIR hyperintense lesions in the\nright periatrial white matter and left frontal subcortical white matter, which\nare unchanged comparison ___.  Findings are nonspecific, typically\nseen in the setting of chronic microangiopathy, with differential\nconsiderations including prior trauma, prior infection, history of migraine\nheadaches, or demyelinating process.  Recommend clinical correlation.\n2. Unchanged mild diffuse volume loss, without lobar predominance.\n3. Unchanged solitary punctate chronic microbleed in the right temporal\nperiventricular white matter.\n4. No acute intracranial abnormality without infarct, hemorrhage, or mass\neffect."
        },
        {
            "input": "There is a developmental venous anomaly involving the left gyrus rectus and\nthe more superior aspect of the left medial frontal lobe, with a 3.5 mm venous\naneurysm in the left gyrus rectus on images 19:60 and 18:37.\n\nIn the medial aspect of the left superior cerebellum, there is a punctate\nfocus of susceptibility artifact, image 14:9, with a small blood vessel\ndemonstrated in this air on post-contrast T1 weighted and MP RAGE images\n___, 17:69-70).  There is no associated signal abnormality on T2 weighted\nor FLAIR images, though these images demonstrate pulsation artifact\nimmediately anterior to this area.  It is not clear the susceptibility\nartifact is related to a tiny cavernous malformation or slow venous flow.\n\nPostcontrast MP RAGE images also demonstrate a punctate focus of enhancement\nin the left middle cerebellar peduncle, images 19:42 and 17:72, without a\ncorrelate on any other sequences.  This is most suggestive of a capillary\ntelangiectasia.\n\nThere is no evidence for an intracranial mass.  There is no edema or acute\ndiffusion abnormality in the brain parenchyma.  8 mm fluid signal intensity\nlesion in the left putaminal is compatible with a chronic infarct or a\nprominent perivascular space.  There are multiple small foci of high T2 signal\nin the subcortical, deep, and periventricular white matter of the cerebral\nhemispheres, nonspecific but likely sequela of chronic small vessel ischemic\ndisease in a patient of this age.  Ventricles and sulci are normal in size for\nage.\n\nMajor arterial flow voids are grossly preserved.  Major dural venous sinuses\nappear patent on postcontrast MP RAGE images.\n\nThere is a moderate mucous retention cyst along the floor of the right\nmaxillary sinus and minimal mucosal thickening along the floor of the left\nmaxillary sinus.",
            "output": "1. Developmental venous anomaly in the medial left frontal lobe with a 3.5 mm\nvenous aneurysm in the left gyrus rectus.\n2. Punctate focus of susceptibility artifact in the medial aspect of the left\nsuperior cerebellum, with a small blood vessel seen on postcontrast images. \nIt is not clear whether the susceptibility artifact is related to a tiny\ncavernous malformation or slow venous flow.\n3. Punctate focus of contrast enhancement in the left middle cerebellar\npeduncle, seen on postcontrast MP RAGE images only, is most suggestive of a\ncapillary telangiectasia."
        },
        {
            "input": "MRI BRAIN:\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  No hydrocephalus.  Mild chronic small vessel ischemic changes.\nThere are moderate chronic small vessel ischemic changes.  Chronic lacunar\ninfarct left putamen, anterior limb left internal capsule, similar to prior. \nTiny chronic lacunar infarcts bilateral centrum semiovale, 1 on each side,\nsimilar to prior.  There is large benign developmental venous anomaly in the\nanterior left frontal lobe, extending into the orbital frontal gyri, with\nassociated 0.3 cm venous varix.  There is no evidence of of cavernoma. \nSuggestion tiny developmental venous anomaly in the left cerebellum, stable. \nDural venous sinuses are patent.  Partial opacification right maxillary sinus\nfloor, otherwise patent paranasal sinuses, mastoids.\n\nMRA BRAIN:\nPatient motion mildly compromises exam.  Patent A-comm, left PCOM.  Dominant\nright vertebral artery.  Probable mild atherosclerotic narrowing right P1\nbilateral P2 segments of hypoplastic right A1 segment.  PCA, accentuated by\nimage related artifact.  Probably mild bilateral M 2, M3 segment\natherosclerotic disease, ext did by artifact at this level.  Otherwise, the\nintracranial vertebral and internal carotid arteries and their major branches\nappear normal without evidence of occlusion, or aneurysm formation.\n\nMRA NECK:\nThere is significant motion artifact at the thoracic inlet and aortic arch. \nAt the level of the mid neck and superiorly exam is of diagnostic quality\nwithout much motion.\n\nThere is atherosclerotic narrowing of the proximal right ICA, with\napproximately 25% narrowing by NASCET criteria.\n\nMinimal atherosclerotic irregularity in the proximal left ICA, no evidence of\nstenosis by NASCET criteria.\n\nV1 and proximal V2 segments of vertebral arteries are attenuated, partially\nfrom technique, however, there is probably moderate right and moderate to\nsevere left vertebral artery narrowing.  Remaining portion of V2, V3, V4\nsegments of the dominant right vertebral artery is normal.  Areas of moderate\natherosclerotic narrowing involving left V2, V3 segment.\n\nOtherwise the origins of the great vessels, subclavian, common carotid\narteries appear normal",
            "output": "1. Moderate chronic small vessel ischemic changes, with few small chronic\nlacunar infarcts, stable since prior.\n2. Probable mild intracranial atherosclerotic disease, accentuated by artifact\non the source images.\n3. Significant narrowing of the proximal bilateral vertebral arteries,\nprobably moderate on the right and moderate to severe on the left. \nApproximately 25% narrowing right proximal ICA."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction. The ventricles and sulci are normal in caliber and\nconfiguration. There is periventricular and subcortical white matter\nhyperintensity on the FLAIR images suggesting chronic small vessel ischemia.\n\nNo osseous abnormalities seen. The paranasal sinuses, mastoid air cells, and\nmiddle ear cavities are clear. The visualized portion of the orbits are\nunremarkable. The visualized portion of the vascular flow foids are preserved.",
            "output": "1. Findings suggesting chronic small vessel ischemia.  Otherwise normal study\nwith no evidence of hemorrhage or infarction"
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.   The ventricles and sulci are normal in caliber and\nconfiguration.\n\nThe visualized paranasal sinuses and mastoid air cells are clear.  The orbits\nare grossly unremarkable.  The major intracranial vascular flow voids are\npreserved.",
            "output": "Normal brain MRI."
        },
        {
            "input": "The images are mildly degraded by motion artifact.  There is no diffusion\nabnormality.  No evidence of hemorrhage, edema, mass effect, or acute\ninfarction.  Prominence of the ventricles and sulci is consistent with age\nrelated involutional change.  A few scattered punctate white matter FLAIR\nhyperintensities are nonspecific.  Principal intracranial vascular flow voids\nare preserved.  There is mild mucosal thickening in the left maxillary sinus. \nThe orbits are unremarkable.",
            "output": "No evidence of hemorrhage, edema, mass, mass effect, or acute infarction."
        },
        {
            "input": "Motion artifact moderately limits evaluation.\n\nNo evidence for an acute infarction, intracranial mass, edema, or blood\nproducts.  There is mild T2/FLAIR hyperintensity along the lateral ventricles\nand few scattered small T2/FLAIR hyperintensities in the supratentorial white\nmatter, nonspecific but likely sequela of mild chronic small vessel ischemic\ndisease in this age group.  There is mild-to-moderate global parenchymal\nvolume loss with prominent ventricles and sulci.\n\nMajor arterial flow voids are grossly preserved.  Dural venous sinuses are\npatent on postcontrast MP RAGE images.\n\nThere is partial opacification of bilateral underpneumatized mastoids, which\nmay be secondary to prolonged supine positioning in the inpatient setting. \nThere is also mild-to-moderate mucosal thickening in the left maxillary sinus",
            "output": "Moderately motion limited exam. No evidence for an acute infarction or other\nacute intracranial abnormalities."
        },
        {
            "input": "There are multiple punctate foci of slow diffusion throughout both cerebral\nhemispheres including the right frontal lobe, bilateral parietal lobes,\nbilateral occipital lobes and right temporal lobes as well as in the right\nlentiform nucleus and bilateral cerebellar hemispheres.  The largest focus is\nin the right temporal lobe (4:15).  There are confluent periventricular,\nsubcortical and deep white matter areas of T2/FLAIR hyperintensity, likely\nrelated to severe chronic small vessel ischemia.  There is prominence of the\ncerebral sulci, lateral and third ventricles suggestive of age-related\ninvolutional changes.  There is no evidence of hemorrhage, masses, mass effect\nor midline shift.\n\nThere is mild mucosal thickening in multiple ethmoid air cells.  Trace fluid\nsignal is noted in the right mastoid air cells.  Visualized orbits are\nunremarkable except for bilateral lens replacement.",
            "output": "1. Multiple scattered punctate acute to subacute infarcts throughout the\nbilateral cerebral hemispheres, right lentiform nucleus and bilateral\ncerebellar hemispheres suspicious for a cardioembolic etiology.  No evidence\nof hemorrhagic conversion, mass effect or midline shift.\n2. Global parenchymal volume loss with sequelae of chronic small vessel\nischemia in the supratentorial white matter."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.\n\nThe ventricles and sulci are normal in caliber and configuration.  There is a\n5 mm retention cyst within the right maxillary sinus.  There is a mild amount\nof nonspecific fluid within the mastoid air cells.  There is no abnormal\nenhancement after contrast administration.\n\nFor details of the cervical spine please refer to the concurrently performed\nMRI cervical spine study.",
            "output": "1. No acute intracranial abnormality.\n2. For details of the cervical spine please refer to the concurrently\nperformed MRI cervical spine study."
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor infarction.  Small vague area of enhancement in the left cerebellum (18:6)\nseen on T1 weighted spin echo does not have any correlate on other sequences. \nThe ventricles and sulci are normal in caliber and configuration.  The orbits\nare unremarkable.  Approximately 6 mm retention cyst in the right maxillary\nsinus is again seen.  There is mild fluid in the mastoid air cells.  There is\nno abnormal enhancement after contrast administration.",
            "output": "1. No definite brain lesions.\n2. Small vague area of enhancement in the left cerebellum on a single T1\nweighted spin echo image does not have any correlate on other sequences and is\nlikely artifactual, but attention on follow-up is suggested (18;6)."
        },
        {
            "input": "Linear focus of leptomeningeal enhancement posterior, medial right parietal\nlobe, seen on post gadolinium in FLAIR images, stable since ___.  Stable mild linear pachymeningeal enhancement floor of the\nleft middle cranial fossa compared to prior exams.  No other areas of abnormal\nenhancement intracranially.\n\nThere is no evidence of hemorrhage, edema, parenchyma masses, mass effect,\nmidline shift or infarction.   The ventricles and sulci are normal in caliber\nand configuration.  Intracranial vascular flow voids are preserved.  Trace\nmucosal thickening paranasal sinuses.  Clear mastoids dural venous sinuses are\npatent.\n\nMild cerebellar tonsillar ectopia, similar to prior.  Marrow signal\nabnormality in the visualized upper cervical spine was better seen on recent\nMR cervical spine ___.  Inhomogeneous enhancement of the central\npituitary gland is suggestive of microadenoma, measuring 5 mm, similar to\nprior.",
            "output": "1. 2 small areas of meningeal enhancement, stable since ___. \nDifferential considerations include neoplastic infiltration, inflammatory\nprocess, possibly underlying vessels or reactive change.  Infection is\nunlikely.\n2. Suggestion of pituitary microadenoma."
        }
    ]
}