Text_summarization/task91_mimic_mri_brain_summarization.json

{
    "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 Brain into a concise conclusion."
    ],
    "Reasoning": [],
    "Input_language": [
        "English"
    ],
    "Output_language": [
        "English"
    ],
    "Instruction_language": [
        "English"
    ],
    "Domains": [
        "Medicine",
        "Clinical Reports",
        "MRI",
        "Brain"
    ],
    "Positive Examples": [],
    "Negative Examples": [],
    "Instances": [
        {
            "input": "MRI BRAIN:  Multi-lobulated right posterior cerebral artery aneurysm arising\nfrom the right P1 segment is partially thrombosed, and in comparison to ___, the overall measurements are 26 x 26 mm(111a:41) (previously 28 x 25 mm)\nwith a true lumen measuring 16 x 14 mm (previously 16 x 15 mm), with a roughly\n4 mm narrow neck. Again seen is resultant mass effect on the pons and\nmidbrain.  FLAIR hyperintensity in the mid brain in conjunction with residual\ndiffusion abnormality corresponds to the subacute infarction seen on the prior\nMRI, which is now evolving.  There is mild effacement of the right\npre-pontine, crural, and ambient cisterns as results of the mass-effect from\nthe aneurysm. 3 mm aneurysm at the junction of the right P1 and P2 segments is\nstable in size.\nArea of prior early subacute infarction in the right thalamus demonstrates\nhigh signal on the diffusion-weighted sequence, likely T2-shinethrough effect,\nwith subtle enhancement, indicative of an evolving recent infarct.  Prior\ninfarct in the left parietal lobe continues to evolve, with some residual\nsubtle enhancement seen on the current study.\nLayering fluid is seen in the right maxillary sinus and mild mucosal\nthickening is noted in the left maxillary sinus. Partially lobulated mucosal\nthickening is noted in the sphenoid sinus.  The ventricles and sulci are\nnormal in size and configuration. No mass or diffusion abnormality is\nidentified.\n\nMRA BRAIN:  The bilateral internal carotid and middle cerebral arteries and\ntheir branches are patent. The right A1 segment is poorly visualized as on the\nprior MRA and corresponds to hypoplasia seen on the prior CT. The left A1\nsegment is normal, as is the anterior communicating artery complex. Large\npartially thrombosed aneurysm arising from the right P1 segment is described\nabove. 3 mm aneurysm at the junction of the P1 and P2 segments of the right is\nalso described above. The lack of flow-related enhancement in the right P2\nsegment is likely secondary to slow flow. The posterior circulation is\notherwise normal.",
            "output": "1.  Unchanged size of large right P1 segment aneurysm with stable size of the\ntrue lumen and continued partially thrombosed appearance.\n2.  Stable 3mm right P1-P2 segment aneurysm.\n3.  Evolution of infarcts in the right thalamus, left parietal cortex, and\nmidbrain."
        },
        {
            "input": "The examination is motion degraded.\n\nMRA head:  Re-identified is a right P1/posterior communicating artery 3.1 x\n1.8 x 3.7 cm (TRV, AP, SI) partially thrombosed aneurysm with gradient echo\nsusceptibility from coil embolization of the distal posterior communicating\nartery (i.e. series 5c, image 81). There is postcontrast enhancement at the\naneurysm base (series 6c, image 78 through 83) not seen on pre contrast\nimages, compatible with residual flow. The aneurysm is similar in size when\ncompared to the prior exam.\n\nThe right P1 segment is no longer visualized. Trace postcontrast opacification\nof the right posterior communicating artery is noted (series 6c, image 81),\nnot seen on pre contrast sequences. There is a paucity of flow related signal\nof the distal right P3 through P4 segments, which does demonstrate asymmetric\npostcontrast opacification, compatible with slow flow.\n\nAllowing for motion artifact, the remainder of the intracranial circulation is\nunremarkable without evidence of stenosis, occlusion or other aneurysm.\n\nMRI head: There is no acute intracranial hemorrhage or infarct. Right\ncerebellar hemisphere encephalomalacia is unchanged from prior exam. There is\nT1 hyperintense signal along the superior margin of the encephalomalacia,\nunchanged from prior exam compatible with residual blood\nproduct/demineralization. FLAIR hyperintense signal of the right thalamus\nextending along the cortical spinal tract into the right midbrain, left\nfrontal FLAIR hyperintense signal at the level of the anterior superior\nfrontal gyrus and pontine hyperintense FLAIR signal are slightly less\nconspicuous when compared to the prior exam. Again noted is a right\nP1/posterior communicating artery segment aneurysm as described in the MRA\nsection of the exam. The remainder the intracranial flow voids are preserved.\nRight greater than left mucosal thickening of the maxillary sinuses and\npartial desiccation of ethmoid air cells are unchanged. The orbits are\nunremarkable. The mastoid air cells are clear. The dural venous sinuses are\npatent. There is no abnormal enhancement.",
            "output": "1. Right P1/ posterior communicating artery 3.7 cm partially thrombosed\naneurysm is unchanged in size from most recent prior exam.\n2. The patient is status post coil embolization at the level of the distal\nright posterior communicating artery.\n3. There is residual flow at the base of the aneurysm on postcontrast MRA.\n4. The right P1 segment is no longer visualized, likely thrombosed. There\nremains opacification of the majority of the right posterior communicating\nartery.\n5. No acute intracranial hemorrhage or infarct.\n6. Additional findings as described."
        },
        {
            "input": "MRI BRAIN: 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 in the brain enhancement after\ncontrast administration.\n\nInnumerable round, T1 hypointense, T2 hyperintense, enhancing lesions are\nscattered throughout the calvarium, mandible, left temporomandibular joint,\nand visualized upper cervical spine.  Slightly expansile, T1 hypointense,\nheterogeneously enhancing mass in the clivus, extending into the occipital\ncondyles, abuts the cavernous internal carotid arteries and does not extend\ninto the sphenoid sinuses.  This mass also extends into the right sella and\nslightly displaces the pituitary gland to the left.\n\nThe maxillary sinuses contain mucus retention cyst.  The mastoid air cells are\nclear.  The major intracranial flow voids are preserved.\n\nMRI ORBITS:  A lobulated, T1 hypointense, T2 hyperintense, heterogeneously\nenhancing, left intraconal mass in the left superior orbit measures 2.5 x 1.3\nx 1.4 cm.  This mass is indistinguishable from the superior rectus and\nsuperior oblique muscles and and also abuts the medial rectus muscle and left\noptic nerve.  This mass extends to the orbital apex.  The intra orbital optic\nnerve is displaced inferiorly with effacement its CSF sheath.  The left optic\nnerve is slightly enlarged without T2 hyperintense signal or enhancement\nwithin the nerve itself, however, there is a surrounding rim of enhancement\nalong the sheath of the left intraorbital optic nerve.  The right orbit and\noptic nerve are normal.  There is mild left preseptal soft tissue swelling and\nmild left proptosis.",
            "output": "1. Enhancing left superior orbital, intraconal mass, indistinguishable from\nthe superior rectus and superior oblique muscles, extending to the orbital\napex and displacing the left optic nerve inferiorly, most likely representing\na plasmacytoma given the patient's history of multiple myeloma.\n2. Effacement of the CSF nerve sheath of the left optic nerve with a\nperipheral rim of enhancement along the nerve sheath of the left intraorbital\noptic nerve, which may represent inflammation related to the compression by\nthe mass or direct infiltration.\n3. Slightly expansile, enhancing mass in the clivus, extending into the right\nsella turcica, occipital condyles, and abutting the cavernous internal carotid\narteries, also likely representing a plasmacytoma.\n4. Numerous, round enhancing lesions scattered throughout the calvarium and\nupper cervical spine, consistent with the patient's history of multiple\nmyeloma.\n\nNOTIFICATION:  The findings were discussed with Dr. ___. by ___,\nM.D. on the telephone on ___ at 8:44 AM, 10 minutes after discovery of\nthe findings."
        },
        {
            "input": "Again seen is a left frontal surgical cavity with a tiny enhancing nodule at\nthe deep medial aspect of the cavity. This corresponds to an area of\nhemorrhage seen on the prior examinations. Again seen is extensive white\nmatter hyperintensity on FLAIR imaging in the left frontal lobe surrounding\nthe surgical cavity. Given the diagnosis, this likely represents a combination\nof tumor infiltration and treatment effect. There has been no progression of\nthis abnormality since the prior study. There is no evidence of abnormal blood\nflow or blood volume the associated with this lesion.\n\nMR spectroscopy is limited by and delays, presumably due to blood products.\nThere is mild choline elevation, but not sufficient to suggest malignancy.\n\nAgain seen is far less dramatic white matter abnormality in the right frontal\nlobe. This is presumably related to prior radiation and also appears stable.\n\nThere are no findings to suggest tumor progression. No new lesions are\nidentified. There is no other evidence of abnormal enhancement. There is no\nevidence of infarction. Here have been no significant changes since the prior\nstudy.",
            "output": "Stable appearance of left frontal postoperative changes, surgical cavity,\nFLAIR hyperintensity, and a small peripheral nodule.  No evidence of tumor\nprogression."
        },
        {
            "input": "The left frontal lobe surgical cavity is similar to multiple prior exams. A T2\nhypointense nodule along the posterior medial portion of the cavity continues\nto have mild enhancement. There is a T2 hypointense layering fluid level.\nExtensive adjacent subcortical white matter T2 and FLAIR signal hyperintensity\nis similar.\n\nCompared with the prior exam, there is now new gyriform, nodular, cortical\nenhancement surrounding the surgical resection cavity (11:19 -22). Posterior\nto the resection bed, there is a new cortical region of increased signal\nintensity on the arterial spin labeling perfusion sequence (04:19).\nPost-contrast perfusion data confirm increased blood flow (800: 16) and blood\nvolume (800:37) to this region. There is no abnormal diffusion. Single voxel\nspectroscopy data were acquired posterior to the resection cavity shows\nelevated choline and decreased N-acetylcysteine peaks which is similar to the\nprior exam in ___.\n\nThere is no acute infarct, hemorrhage, intracranial mass, mass effect, or\nshift of the normally midline structures. Ventricles and sulci moderately\nenlarged, compatible with atrophy. Periventricular FLAIR signal hyperintensity\nis compatible with small-vessel ischemic change. There is no abnormal contrast\nenhancement. Principle intracranial flow voids are maintained. Visualized\nparanasal sinuses and mastoid air cells are clear. Osseous and soft tissue\nstructures are unremarkable.",
            "output": "Frontal lobe surgical resection cavity with new surrounding gyriform, nodular\ncortical enhancement, increased perfusion, and abnormal spectroscopy. These\nfindings are concerning for, although not specific for the local tumor\nrecurrence."
        },
        {
            "input": "Brain MRI:\n\nAn area of FLAIR abnormality in the right parietal lobe demonstrates rim\nenhancement within it with restricted diffusion in the area as well as blood\nproducts on susceptibility images.  In the adjacent brain a rim enhancing\ndural-based lesion is identified (602:22 and 12:19) with intrinsic restricted\ndiffusion.  A third area of restricted diffusion with rim enhancement is seen\nin the right occipital lobe (602:12 and 12:11).  An additional punctate area\nof diffusion abnormality is seen in the right periventricular region (602:21).\nThere is no midline shift or hydrocephalus.\n\nMRA head:\n\nMRI is limited by motion.  In the right parietal region in the area of\nhemorrhage (4:116) there is focal vascular ectasia suspicious for a mycotic\naneurysm.  Otherwise the MRA is 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.",
            "output": "1. Extremely limited study due to motion.  Particularly, the postcontrast\nimages and MRA are limited by motion.\n2. Right parietal and occipital abscesses with hemorrhage in the right\nparietal region at the site of suspicious mycotic aneurysm.  Additional\npunctate foci of acute infarcts."
        },
        {
            "input": "There is an unchanged large left temporoparietal arteriovenous malformation,\napparently the majority the drainage is superficial, there is ectasia of the\nleft arterial vessels, and prominent vascular cortical draining veins.  The\narterial spin labeling sequence (ASL), shows increased perfusion in the\nvascular nidus, more significant in the prominent veins. The tractography\nshows mild deviation of the association, commissural and cortical spinal\ntracts adjacent to the vascular nidus, note is made of minimal medial\ndeviation of the superior longitudinal fasciculus.\n\nThe functional MRI demonstrates the expected activation areas during the\nmovement of the hands, feet and tongue. The primary motor cortex activation\nappears anterior to the vascular nidus during the moment of the right hand.\nDuring the movement of the right foot, areas of activation are visualize\nmedial and anterior to the vascular nidus (image 71, series 26).\n\nThe functional paradigm for the language shows the majority of the BOLD\nactivation on the left cerebral hemisphere, likely related with dominance. The\nBroca's area BOLD activation is adequately visualized on the paras opercularis\nand pars triangularis within the inferior frontal gyrus, and corresponds to\nthe Brodmann areas the BA 44 and the BA 45, all of them anterior to the\nvascular nidus. The Wernicke's BOLD activation area is visualized inferior to\nthe vascular nidus on the left.",
            "output": "1. Unchanged large left temporoparietal arteriovenous malformation with\nincreased perfusion in the vascular nidus, as demonstrated on the arterial\nspin labeling sequence.\n\n2. The functional MRI demonstrates the primary motor activation areas anterior\nto the vascular nidus during the moment of the right hand. During the movement\nof the right foot, areas of activation are visualize medial and anterior to\nthe vascular nidus.\n\n3. The Broca's area BOLD activation is adequately visualized on the paras\nopercularis and pars triangularis within the inferior frontal gyrus, and\ncorresponds to the Brodmann areas the BA 44 and the BA 45, all of them\nanterior to the vascular nidus. The Wernicke's BOLD activation area is\nvisualized inferior to the vascular nidus on the left.\n\n4. The tractography shows mild deviation of the association, commissural and\ncortical spinal tracts adjacent to the vascular nidus, there is minimal medial\ndeviation of the superior longitudinal fasciculus."
        },
        {
            "input": "The patient is status post right lens surgery.  Scattered FLAIR/T2 bright foci\nwithin the cerebral white matter are likely incidental regions of mild\nage-related microvascular changes, similar to prior.  The punctate left\nparietal infarct seen on the prior examination is no longer evident.  There is\nno evidence of interval infarct, hemorrhage, or mass.  There is no pathologic\nenhancement.  Major intracranial flow voids are preserved.  Ventricles,\ncisterns, and sulci again show mild symmetric age-related prominence.",
            "output": "1.  No evidence of interval hemorrhage, infarct, or mass.  No evidence of\nmetastasis.\n2.  Expected evolution of the very small left parietal infarct seen on the\n___ examination, which is no longer evident."
        },
        {
            "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.\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\nMRV of the head demonstrates normal flow in the superior sagittal and\ntransverse sinuses as well as in the deep venous system.",
            "output": "No significant abnormalities are seen on MRI of the brain without gadolinium.\nNo significant abnormalities are seen on MRA of the head.  Normal MRV of the\nhead."
        },
        {
            "input": "Multiple bilateral small supra and infratentorial infarcts are again\nidentified on diffusion and FLAIR images.  Overall there are fewer apparent\ninfarcts seen on diffusion images on the current study compared to the prior\nstudy but some of the infarcts in the periventricular region (04:21) appears\nslightly larger which could be secondary to evolution of these infarcts. \nHowever, a left posterior periventricular infarct (04:21) seen on the current\nstudy appears to be not present on the  previous study.  No evidence of blood\nproducts seen on the susceptibility images.  Periventricular hyperintensities\nindicating small vessel disease are unchanged.\n\nFluid is seen in both middle ears as well as mastoid air cells.\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.  Small protuberance of 1 mm at the\nposterior aspect of both supraclinoid internal carotid arteries appear to be\ndue to incidental infundibula.  No abnormal protuberance is are seen along the\nperipheral vascular structures to suggest mycotic aneurysms within the limited\nresolution of MRA.",
            "output": "1. Multiple bilateral supra and infratentorial small infarcts are identified\nsome of which are less apparent due to evolution.\n2. Possible new small infarct in the left posterior periventricular region.\n3. No significant abnormalities on MRA."
        },
        {
            "input": "MRV BRAIN WITHOUT CONTRAST: There is normal flow in the main venous sinuses as\nwell as the internal cerebral veins and vein of ___. No filling defect\nconcerning for thrombosis is identified. There is good visualization of the\ndistal ICA's, vertebral and basilar arteries as well as the vessels of the\ncircle of ___ and there is no gross evidence of flow stenotic lesions or\naneurysms larger than 3 mm in size are seen.\n\nMRI BRAIN WITHOUT CONTRAST: There is no evidence of acute intracranial\nhemorrhage, mass, mass effect or shifting of the normally midline structures.\nThe ventricles and sulci are slightly prominent, likely reflecting cortical\nvolume loss, apparently age related and involutional. Multiple foci of high\nsignal intensity are identified in the subcortical and periventricular white\nmatter on T2 and FLAIR sequences, which are nonspecific and may represent\nchanges due to small vessel disease. 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 orbits are within normal limits.  Mild concentric mucosal thickening is\nseen in all paranasal sinuses and the mastoid air cells. A T1 bright area in\nthe vertebral body of C3 (series 4 image 13), is stable since MR from ___ and\nlikely benign such as fatty marrow.",
            "output": "1. Normal brain MRV.  No evidence of venous sinus thrombosis.\n\n2. No evidence of acute intracranial process. Multiple foci of high signal\nintensity are identified in the subcortical and periventricular white matter\non T2 and FLAIR sequences, which are nonspecific and may represent changes due\nto small vessel disease.\n\n3. Mild concentric mucosal thickening is seen in all paranasal sinuses and the\nmastoid air cells."
        },
        {
            "input": "MRI BRAIN:\n\nThere is symmetric restricted diffusion involving the bilateral caudate heads\nand putamen, sparing the globus pallidus.  Equivocal areas of restricted\ndiffusion within the bilateral hippocampi are also noted.\n\nNo evidence for acute intracranial hemorrhage.  A punctate focus of\nsusceptibility artifact within the right cerebellar hemisphere is noted, with\na smaller 1 seen in the right parietal white matter.  These findings may\nreflect the sequelae of chronic microhemorrhage.  No mass, mass effect, edema\nor 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\nMucosal thickening is seen in the bilateral maxillary sinuses, scattered\nethmoid air cells, and right sphenoid sinus, with an air-fluid level in the\nright sphenoid sinus.  Mastoid fluid is seen bilaterally, presumably secondary\nto recent intubation.  The orbits are grossly unremarkable bilaterally.\n\n\nMRI ORBITS:\nThe bony orbits and preseptal soft tissues are normal. The globes are intact\nand normal in appearance. The optic nerves and complex are normal, without\nabnormal signal/edema.  The extraocular muscles are uniform in size and normal\nin signal. The lacrimal apparatus is normal. Retrobulbar soft tissues are\nnormal.",
            "output": "1. Symmetric restricted diffusion involving the bilateral caudate heads and\nputamen, sparing the globus pallidus, with equivocal involvement of the\nbilateral hippocampi.  These imaging findings taken together with the\npatient's clinical presentation are most compatible with methanol poisoning. \nDifferential considerations also include anoxic brain injury.\n2. No evidence for acute intracranial hemorrhage or vascular territorial\ninfarction.\n3. Paranasal sinus disease and bilateral mastoid fluid, as above.\n4. Essentially unremarkable noncontrast MR examination of the orbits."
        },
        {
            "input": "FLAIR images again demonstrate to of foci of hyperintensity indicative of mild\nchanges of small vessel disease in the white matter.  Mild brain atrophy seen.\nThere is no midline shift mass effect or hydrocephalus.  Following contrast\nadministration a faint area of enhancement in the right posterior temporal\nlobe is again identified consistent with a previously suggested diagnosis of\ncapillary telangiectasia.  Unchanged since the previous MRI of ___.  No other areas of abnormal parenchymal vascular or meningeal\nenhancement seen.\n\nImages through the internal auditory canal demonstrates symmetric appearance\nof the seventh eighth nerve complexes.  No evidence of abnormal enhancement or\nmass lesion seen within the internal auditory canals, cerebellopontine angles\nor membranous labyrinth.  No other mass lesions are seen within the posterior\nfossa.",
            "output": "1. No evidence of abnormal signal or enhancement or mass lesion in relation\nwith the internal auditory canals or membranous labyrinth.\n2. Mild changes of small vessel disease.  Unchanged right temporal capillary\ntelangiectasia.  No other abnormal enhancing brain lesions."
        },
        {
            "input": "Please note the study is mildly degraded by motion.\n\nORBITS:  Please note evaluation of the cavernous sinuses and Meckel's cave on\ncoronal images (series 10) is limited due to artifact.  These areas are imaged\non series 9.  The bony orbits and preseptal soft tissues are normal.  The\nglobes are intact and normal in appearance. The optic nerves and complex are\nnormal, without edema or abnormal enhancement. The extraocular muscles are\nuniform in size and normal in signal. The lacrimal apparatus is normal.\nRetrobulbar soft tissues are normal.\n\nOTHER FINDINGS:\n\n\nRight frontal (see 08:23), left parietal (see 08:21) white matter\nhyperdensities are present on FLAIR imaging.\n\nThe imaged portion of the brain is normal, without focal lesion, abnormal\nenhancement, or edema. The cavernous sinus is unremarkable. The imaged\nparanasal sinuses and mastoid air cells are clear.  A 5 mm mucous retention\ncyst versus polyp is noted at the right fossa of ___ (see 9:2).",
            "output": "1.  Study is mildly degraded by motion.\n2. Normal MRI of the orbits.\n3. Right frontal and left parietal nonspecific white matter hyperdense\nlesions.  While differential considerations include prior trauma, infection,\nhistory of migraine headaches, or microangiopathic changes, demyelinating\nprocess is not excluded on the basis of this examination.  Recommend clinical\ncorrelation.\n\nRECOMMENDATION(S):\n1. Right frontal and left parietal nonspecific white matter hyperdense\nlesions. While differential considerations include prior trauma, infection,\nhistory of migraine headaches, or microangiopathic changes, demyelinating\nprocess is not excluded on the basis of this examination.  Recommend clinical\ncorrelation ."
        },
        {
            "input": "Subacute blood products are seen with surrounding hemosiderin deposition in\nthe left insular region extending to the left frontal parietal region. \nSuperficial siderosis is seen within the left sylvian fissure and along the\nsulci of the left cerebral hemisphere.  Artifacts obscure the details of the\nright frontal lobe and parietal lobe presumably secondary to a shunt catheter.\nThe shunt catheter is seen within the anterior horn of the right lateral\nventricle.  There is ventriculomegaly indicating communicating hydrocephalus\nwith ventricular size appears to have increased from the previous CT.  No\nacute infarcts are seen.  Restricted diffusion in the left insular and frontal\nlobe regions is secondary to blood products.\n\nMRA of the head with and without contrast is limited by motion.  Motion limits\nevaluation for the recanalization.  There is subtle hypointensity in the\nregion of anterior communicating artery no definite coil pack is seen in this\nregion no aneurysm is identified in this region.  There is a coil pack in the\nregion of left middle cerebral artery bifurcation.  On the precontrast images\nthere are no signs of recanalization.  However, the motion limited\npostcontrast studies subtle enhancement following pack (06:52).  It is unclear\nwhether this is secondary to surrounding brain enhancement or due to\nrecanalization.",
            "output": "1. Motion limited MRA study .  On the precontrast MRA no definite signs of\nrecanalization are seen in the left middle cerebral artery coil embolization. \nHowever, on postcontrast MRA subtle signal is seen within superior portion of\ncoil pack which could be secondary to recanalization or enhancement of the\nsurrounding brain.\n2. Ventriculomegaly with slightly increased ventricular size since the\nprevious CT of ___.\n3. Left insular and frontal lobe subacute hematoma and superficial siderosis\nsecondary to prior hemorrhage."
        },
        {
            "input": "MRV: Normal flow signal is demonstrated within the superior sagittal sinus,\nstraight sinus, right transverse sinus, and sigmoid sinuses.  No flow related\nsignal seen in the left transverse sinus which, as described below\ndemonstrates normal enhancement MPRAGE sequences.  Overall, this appears is\nsimilar when compared to prior.  The jugular bulbs and proximal jugular veins\nare patent. Evaluation of the deep venous systems reveals normal flow signal\nin the internal cerebral veins. The vein ___ is also unremarkable.\n\nPRE AND POSTCONTRAST T1 BRAIN IMAGING:  There are persistent blood products\nwith regions of T1 hyperintensity and peripheral enhancement in the right\nfrontal lobe, in regions of prior hemorrhagic infarct.  There is associated ex\nvacuo dilatation of the frontal horn of the right lateral ventricle. \nEncephalomalacia is also noted in the left frontal lobe, unchanged.  Gyriform\nT1 hyperintensity with T2 hypointensity in the left temporal lobe is also\ncompatible with cortical laminar necrosis in the setting of prior infarct,\nunchanged.  There is no evidence of new hemorrhage.\n\nTiny extra-axial fluid collection just deep to the right-sided craniotomy\nalong the right cerebral convexity is significantly smaller now measuring up\nto 8 mm, previous 14 mm.   Patient is status post right craniotomy.\nPostoperative right cerebral dural thickening and enhancement persists.   The\nright temporal lobe appears to herniate at the site of prior craniotomy within\na small gap at the posterior skull flap margin (05:15), unchanged.\n\nThe ventricles and sulci are stable in size and configuration.  The basal\ncisterns are patent.  There is no evidence of new infarct.",
            "output": "1. Evolving blood products in the bilateral frontal lobes and left\ntemporoparietal region.\n2. Minimal residual subdural fluid along the right cerebral convexity.\n3. The dural venous sinuses including the left transverse sinus are patent.\n4. Unchanged small herniation of the temporal lobe within a small gap at the\nposterior skull flap margin."
        },
        {
            "input": "MRI head: Patient is status post left suboccipital craniotomy for resection of\npreviously demonstrated left CP angle mass. There are expected postoperative\nchanges including overlying soft tissue swelling and fluid collection and\npostoperative blood products. There is a small region of slow diffusion in the\nlateral left cerebellar hemisphere adjacent to the region of resection with\ncorresponding subtle T2/FLAIR signal hyperintensity (series 6, images ___. On\npost-contrast images, there is no evidence of a residual tumor.\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 in the left mastoid air cells.\n\nMRA head:  The major intracranial arteries appear normal with no evidence of\nstenosis, occlusion, or aneurysm formation.\n\nRECOMMENDATION(S):",
            "output": "1. Patient is status post left occipital craniotomy for resection of\npreviously demonstrated left CP angle mass with expected postoperative\nchanges.  There is no evidence of residual tumor. There is a region of slow\ndiffusion in the left cerebellar hemisphere adjacent to the resection site\nconsistent with postoperative change.\n\n2.  Unremarkable MRA of the head without evidence of stenosis, occlusion, or\naneurysm formation."
        },
        {
            "input": "MRI BRAIN:\nA 1.4 x 1.3 cm enhancing lesion in the right cerebellar hemisphere (series 10,\nimage 7) is unchanged from ___.  Mildly worsened surrounding FLAIR\nabnormality.\n\nMultiple additional subcentimeter foci of nodular enhancement in the temporal\nlobes, bilaterally (series 10, image 12, 14, 9, series 12 image 11, 12), the\nbilateral insula (series 12, image 16, 17) and the right greater than left\nmedial both anterior and posterior frontal lobes, and medial parietal lobes\n(series 10, image 18, series 11, image 6), similar compared with ___.  Findings may represent Leptomeningeal metastatic disease.  Component of\nenhancing subacute infarcts is possible given apparent cortical enhancement in\nsome areas, including temporal lobes and insula.  Nodular components of\nenhancement involving paramedian frontal and parietal lobes is more suggestive\nof metastatic disease.  Infection or inflammatory process such as sarcoid\ncould have similar appearance.  Clinically correlate.\n\nThere is no midline shift or mass effect associated with these lesions.\nProbable sebaceous cyst left vertex..  Brain parenchymal atrophy. \nPeriventricular and deep white matter FLAIR hyperintensities are nonspecific,\nbut likely represent sequela of moderate to severe chronic small vessel\nischemic disease and appear unchanged from ___.\n\n\nMRI ORBITS:\nA left globe prosthesis is noted.  Atrophic left optic nerve.  Mild prominence\nof the left medial rectus is unchanged and likely secondary to the placement\nof the left globe prosthesis. The extraocular muscles are otherwise uniform in\nsize and normal in signal.  Cavernous sinus is normal.\n\nThe bony orbits and preseptal soft tissues are normal.  The right globe is\nintact and normal in appearance. The optic nerves and complex are normal,\nwithout edema or abnormal enhancement.  The lacrimal apparatus is normal.\nRetrobulbar soft tissues are normal.",
            "output": "1. A right cerebellar mass, similar in size, mildly worsened edema.\n2. Areas of superficial, probably combination leptomeningeal and cortical\nenhancement bilateral cerebral hemispheres.  Some areas are nodular and are\nsuggestive of metastatic disease.  Some are more linear and limited to cortex,\nand component of subacute enhancing infarcts is possible.  Differential\nconsiderations include infection, inflammatory process including sarcoid.  No\nsignificant change since prior.\n3. Unremarkable appearance of the right orbit.\n\nRECOMMENDATION(S):  Follow-up MRI brain without and with contrast in 8 weeks\nif clinically appropriate."
        },
        {
            "input": "The FLAIR hyperintense lesion noted in the right middle cerebellar\npeduncle and extending into the posterior pons and anteromedial cerebellar\nhemisphere is similar to the recent MRI from ___. \nCorrelating with that examination, this lesion shows no restricted diffusion\nand does not enhance.  Other scattered FLAIR hyperintensities within the\ncerebral white matter are likely incidental.  There are no other masses. \nThere is no abnormal intracranial enhancement.  The dural venous sinuses and\nmajor intracranial arteries are patent.",
            "output": "Nonenhanceing FLAIR bright mass centered in the right cerebellar\npeduncle.  The imaging characteristics are most suspicious for a low-grade\nglial tumor.  Lack of enhancement makes a tumefactive demyelinating or\ninflammatory lesion far less likely.  Infratentorial location, lack of\nenhancement and lack of diffusion restriction makes lymphoma highly unlikely."
        },
        {
            "input": "MR BRAIN:\nPatchy areas of slow diffusion is seen in the bilateral pons, right cerebellar\nhemisphere, left cerebellar hemisphere, bilateral medial occipital lobes, and\na punctate focus on the right thalamus anteriorly consistent with late acute\nto subacute infarcts.  This correlates with the suspected basilar artery\nthrombosis seen on the prior CTA.\n\nA punctate focus of GRE susceptibility in the medial right cerebellar\nhemisphere may represent a focus of prior microhemorrhage.\n\nThe ventricles and sulci are prominent, consistent with global cerebral volume\nloss.  Patchy periventricular T2 hyperintensities are most consistent with\nchronic microvascular ischemic disease.  A 1.5 cm T2 hyperintense focus in the\nleft caudate body likely represents a chronic infarct.  Small chronic infarcts\nin the right cerebellar hemisphere are also noted.\n\nThere is mucosal thickening of the maxillary and ethmoid sinuses.  The mastoid\nair cells and middle ear cavities are clear.  The intraorbital contents are\nnormal.\n\n\nMRA BRAIN:\nThere is near complete attenuation of the flow related signal within the\nposterior cerebral arteries, proximal basilar artery and the intracranial\nright vertebral artery.\n\nThere is moderate narrowing of the cavernous segments of the bilateral\ninternal carotid arteries, likely due to atherosclerotic disease.\n\nThere is moderate narrowing of the distal segments of the bilateral middle\ncerebral arteries.  Incidental note is made of a hypoplastic right A1 segment.",
            "output": "1. Late acute to subacute infarcts involving the pons, bilateral cerebellar\nhemispheres and bilateral medial occipital lobes.\n2. Near-complete attenuation of flow related signal within the posterior\ncerebral arteries, proximal basilar artery and intracranial right vertebral\nartery.\n3. Moderate narrowing of the cavernous segments of the bilateral ICAs and\ndistal segments of the bilateral MCAs."
        },
        {
            "input": "There continues to be ill-defined mild enhancement in the left frontal lobe,\nsimilar to prior MR exam.  MR spectroscopy shows elevated choline ratio along\nthe left frontal lobe and corpus callosum in the area of mild enhancement.  No\nelevated blood flow is seen on ASL imaging.",
            "output": "Spectroscopy findings in the left frontal lobe and corpus callosum concerning\nfor malignant process such as lymphoma versus GBM."
        },
        {
            "input": "The patient is status post right frontal craniotomy.  Since the most recent\nMRI examination, there is an unchanged left frontal heterogeneous enhancing\nmass lesion.  The arterial spin labeled sequence is notable for a small focus\nof increased perfusion in left frontal lesion (image 10, series 19).  The\ntractography color maps demonstrate mild deviation towards the midline of the\nmajor corticospinal,  association and commissural tracts.\n\nThe functional MRI demonstrates BOLD activation areas during the movement of\nthe hands, feet and tongue.  No significant areas of activation are adjacent\nto the left frontal  mass lesion during movement of the hands tongue and feet.\n\nThe language paradigm demonstrates the propagation of activation in the\nconvexity with the majority of the BOLD activity on the left cerebral\nhemisphere, likely related with dominance, with scatter areas of activation\nadjacent to the mass lesion as demonstrated on the images ___, series 31.",
            "output": "1. Unchanged right frontal arteriovenous malformation as described in detail\nabove, with increased perfusion in the superior aspect of the vascular nidus. \nThere is mild deviation towards the midline of the major corticospinal,\nassociation and commissural tracts.\n\n2. Decreased BOLD signal in the right cerebral hemisphere, this finding is\nmore obvious during the movement of the left hand, with shifting of the\nprimary motor cortex activation medially and superiorly.\n\n3. The language paradigm demonstrates the propagation of activation in the\nconvexity with the majority of the BOLD activity on the left cerebral\nhemisphere, likely related with dominance, few scattered foci of activation\nare visualized adjacent to the left frontal mass lesion."
        },
        {
            "input": "The patient is status post trans-sphenoidal resection of a large pituitary\nadenoma with a combination of residual enhancing soft tissue and hemorrhage\nproducts measuring a conglomerate 3.2 x 1.2 x 2.4 cm (TRV, AP, CC) within an\nexpanded sella. The enhancing soft tissue abuts the bilateral carotid siphons\nwithout encasement. The degree of hemorrhage products has dramatically\nimproved since prior exam. A ovoid enhancing nodular soft tissue component\nanterior to the infundibulum measuring 1.3 x 1.2 x 0.9 cm (CC, TRV, AP) is \nslightly smaller when compared to prior exam. There is downward traction of\nthe optic chiasm and residual mass, new from prior exam, presumably secondary\nto continue resolution of blood products and postsurgical edema and scarring.\nThere remains expansion of the\n\nThe visualized intracranial flow voids are preserved. The infundibulum is\nroughly midline.\n\nThe visualized paranasal sinuses are unremarkable. The limited portion of the\nbrain included on this study appears normal.",
            "output": "1. Decrease in residual enhancing soft tissue within an expanded sella is\nnoted with interval decrease in extent of soft tissue edema and hemorrhage\nproducts.  There is a superimposed nodular soft tissue component anterior to\nthe infundibulum, essentially unchanged from prior exam.\n2. There is now downward traction of the infundibulum, presumably secondary to\na combination scarring and evolving hemorrhage products and edema."
        },
        {
            "input": "MRA head:  The major intracranial arteries appear normal with no evidence of\nstenosis, occlusion, or aneurysm formation.  A fetal type right PCA is\nincidentally noted.\n\nMR brain:  There is no evidence of hemorrhage, edema, masses, mass effect, or\ninfarction. The ventricles and sulci are stable in caliber and configuration. \nThere is stable T2/FLAIR signal hyperintensity in the periventricular,\nsubcortical, and deep white matter. There is no abnormal enhancement after\ncontrast administration.",
            "output": "1.  No acute infarction or enhancing mass lesion.\n\n2.  Unchanged T2/FLAIR hyperintensity in the periventricular, subcortical, and\ndeep white matter unchanged and likely reflecting chronic small vessel\nischemic disease.\n\n3.  Unremarkable MRA of the head without aneurysm, malformation, or stenosis."
        },
        {
            "input": "Slow diffusion within right parietal and right inferior frontotemporal regions\nwith corresponding marked cortical T2/ FLAIR signal abnormality and new\nhemorrhage compatible with acute/subacute infarction. The ventricles and\nbasilar cisterns are patent.\n\nNo clear evidence of dural sinus thrombosis. Attenuated left transverse sinus\nis presumably on a developmental hypoplastic basis as this does not correspond\nwith contralateral area of ischemia. Given overall FINDINGS, area of infarct\nmay be arterial, likely right MCA territory.\n\nOrbits and paranasal sinuses are unremarkable.",
            "output": "1. Acute/subacute right MCA territory infarct with associated hemorrhage.\n2. No clear evidence of dural venous thrombosis -- attenuated left transverse\nsinus is presumably on a developmental, hypoplastic basis.\n\nNOTIFICATION:  Findings were discussed with the ___, by Dr.\n___ the telephone, at approximately 1234 ___."
        },
        {
            "input": "Again seen is an irregular inhomogenoeously enhancing right temporal lobe mass\nwith surrounding edema.  The volume of enhancing material has increased\nsomewhat since the study of ___ and markedly since ___.  This\nincrease is also associated with a small increase in edema.\n\nThe ASL perfusion demonstrates mild elevation of blood flow, unchanged.\n\nThe Spectroscopy demonstrates choline and ___ elevation in multiple voxels\nacross the enhancing part of the lesion.\n\nDiffusion in the region of the tumor appears normal or fast.",
            "output": "Progressive enlargement of the enhancing right temporal lobe mass with\nincreased edema.  Elevated perfusion appears stable since ___.  Overall,\nthe findings indicate progressive tumor."
        },
        {
            "input": "ORBITS:\nThere is enhancing STIR hyperintense signal of the right intraconal fat as\nwell as enhancement of the right optic nerve sheath complex compatible with\nperineural neuritis.  There is subtle STIR hyperintense signal of the right\nextra-ocular eye muscles, most notable involving the medial, lateral and\ninferior rectus (series 11, image 11; series 13, image 11), although these\ndemonstrate equivocal enhancement.  There is postcontrast enhancement of the\nright orbital apex and supraorbital fissure (series 13, image 11).  There is\nalso enhancement of the right infraorbital fissure and foramen rotundum,\nextending into the right pterygopalatine fossa (series 13, image 15).  The\nright globe is unremarkable.\n\nThe right superior ophthalmic vein remains distended.  On postcontrast\nsequences, there may be a subtle linear nonocclusive filling defect near the\norbital apex (series 14, image 15; series 13, image 8), potentially\nrepresenting thrombus.\n\nThere is very subtle pachymeningeal enhancement along the bilateral posterior\nrectus gyri (series 14, image 19), extending along the right orbital frontal\nlobe, potentially representing pachymeningitis.\n\nThere is mild enhancing STIR hyperintense signal of the right medial and\nlateral pterygoid muscles (series 14, image 16), potentially reactive.\n\nRe-identified is right greater than left mucosal thickening of the maxillary\nsinuses and left-greater-than-right partial opacification of the sphenoid\nsinuses.  Polypoid near complete opacification of the posterior ethmoid air\ncells is identified.  This is overall similar in appearance to prior\nexamination.\n\nThe left orbit is unremarkable.\n\nLimited evaluation of the brain demonstrates punctate diffusion-weighted\nhyperintense signal of the right postcentral gyrus and left aspect of the\npons, compatible with late acute to subacute infarcts, per better described on\nprior MRI.  No evidence of interval acute infarct",
            "output": "1. Enhancing STIR hyperintense signal of the right intraconal fat and right\noptic nerve sheath complex with enhancement of the right supra and infra\norbital fissure is identified.  Mild STIR hyperintense signal and possible\nenlargement of the extra-ocular eye muscles, predominantly involving the\nmedial, lateral and inferior recti muscles are identified.\n2. Given the severe pansinus disease as described above and the patient's\nclinical history of diabetes myelitis, the orbital findings are presumed\ninfectious in nature, potentially fungal.  No evidence of hypoenhancement or\ndevitalized tissue.\n3. Apparent nonocclusive focal filling defect within the right superior\nophthalmic vein, concerning for possible thrombus.\n4. There is mild dural enhancement of the posterior bilateral rectus gyri and\nright orbitofrontal lobe, likely representing pachymeningitis.\n5. There is enhancement along the right foramina rotundum into the\npterygopalatine fossa.  Mild STIR hyperintense enhancement of the right medial\nand lateral pterygoid muscles is identified, potentially reactive.\n\nNOTIFICATION:  The findings were discussed with ___, M.D. by ___\n___, M.D. on the telephone on ___ at 1:16 pm, 10 minutes after\ndiscovery of the findings."
        },
        {
            "input": "MRI: The T2-weighted sequence is degraded by motion and was not repeated.There\nis focal encephalomalacia surrounded by more extensive subcortical gliosis,\nmanifesting as hyperintense signal on FLAIR sequences, in the right frontal\nlobe (___).  This likely corresponds to the parenchy al hemorrhage noted\nin the history. There is additional gliosis involving the bilateral gyri recti\nin the inferior frontal lobe (8:15).  There is Wallerian degeneration of the\nright corticospinal tract, to a much greater extent than expected for the size\nof the right frontal insult, suggesting more extensive cerebral injury, occult\nby imaging.\n\nThere is no acute intracranial hemorrhage or chronic blood products present. \nThere is no edema or mass effect.  There is frontal and parietal atrophy much\nmore than expected for the patient's age.\n\nThere is minimal mucosal thickening in bilateral maxillary sinuses and ethmoid\nair cells. The paranasal sinuses are otherwise clear.\n\nMRA: The circle of ___ and its principal intracranial branches are widely\npatent, without vascular malformation or significant steno-occlusive disease. \nIncidentally noted is an intradural left internal carotid artery 2.5 mm\naneurysm, in the carotid cave (5:67, 505:6).  The dural venous sinuses are\npatent.",
            "output": "1. Focal encephalomalacia with surrounding gliosis in the right frontal lobe\nrelated to the remote parenchymal hemorrhage mentioned in the history.  The\nsurprising extent of Wallerian degeneration in the right corticospinal tract\nsuggests more extensive cerebral underlying injury than is apparent by\nimaging.\n2. Additional foci of gliosis in the inferior frontal gyri recti, bilaterally,\nalso likely related to remote brain trauma.\n3. Frontoparietal cortical atrophy much more than expected for the patient's\nage, likely related to above.\n4. Incidental 2.5 mm aneurysm, intradural, in the left carotid cave."
        },
        {
            "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\nMRV of the head shows normal flow signal in the superior sagittal and\ntransverse sinuses as well as in the deep venous system.",
            "output": "No significant abnormalities are seen on MRI of the brain without gadolinium. \nNormal MRV of the head.  No evidence of venous sinus thrombosis."
        },
        {
            "input": "MR:  Multiple enhancing intraparenchymal lesions are again seen.  A dominant\nlesion in the right parietal lobe (1100b:79) measures 1.6 x 2.6 cm, previously\n3.2 by 2.0 cm.  The degree of surrounding vasogenic edema has not changed.\n\nAdditional lesions are as follows:\nTwo punctate enhancing foci in the high right parietal lobe (1100 B:  103,\n104), unchanged.\nLeft parasagittal left frontal lesion measuring 3 mm (1100b:93), unchanged.\nA peripherally enhancing lesion in the right caudate head (1100b:74) measuring\n9 x 9 mm, previously uniformly enhancing and 11 x 9 mm.  This lesion\ndemonstrates decreased surrounding vasogenic edema.\nAdditional 2 mm focus in the right caudate head (1100d:68), unchanged.\nA left temporoparietal lesion (1100b:72) measuring 10 x 6 mm, not\nsignificantly changed in size though demonstrating decreased surrounding\nvasogenic edema.\nA 8 x 7 mm left frontal lesion, unchanged\nA 3 mm lesion in the right putamin (1100b:62), unchanged\nA left parasagittal left parietal lesion measuring 5 mm (1100b:89), unchanged\nA 4 mm lesion in the superior left cerebellum, unchanged (1100b:52)\nTwo adjacent 7 mm lesions in the right cerebellar hemisphere (1100 P: 32)\nunchanged.\nThere is a punctate focus of enhancement within the genu of the corpus\ncallosum on the left (1100b:69) which was also faintly visualized on prior. \nTwo punctate foci of enhancement in the left caudate head (1100b:64 and 65)\nare also unchanged.\n\nThere is a punctate focus of enhancement within the pons to the right of\nmidline (1100b:45) not definitively identified on prior.\n\nThere is no new parenchymal signal abnormality.  A few scattered\nperiventricular and subcortical white matter T2 FLAIR hyperintensities which\nmay be due to chronic small vessel disease.  There is no acute infarct. \nSusceptibility artifact seen in association with the dominant right parietal\nand right caudate head lesions indicating blood products.\n\nMultiple rounded hypointense lesions within the bony calvarium suspicious for\nmetastases are grossly unchanged.\n\nMRA: Intracranial vascular structures are unremarkable without evidence of\nsignificant stenosis, aneurysm, or occlusion.",
            "output": "1. Supra and infratentorial enhancing metastatic lesions.  Dominant right\nparietal lesion demonstrates interval decrease in size though similar degree\nof surrounding vasogenic edema.\n2. New punctate enhancing lesion within the pons to the right of midline. \nOtherwise no new lesion identified.\n3. There is decreased central enhancement and mild decreased surrounding\nvasogenic edema surrounding right caudate head lesion.  Decreased surrounding\nedema surrounding a left temporal lesion.  Otherwise no change in the numerous\nother lesions.\n4. Bony metastatic disease similar in burden compared to prior.\n5. Normal MRA of the brain."
        },
        {
            "input": "There is no infarct, hemorrhage or mass.  The ventricles, cisterns\nand sulci are age appropriate.  There is no abnormal enhancement.  The seventh\nand eighth cranial nerve are normal in their cisternal and canalicular\nportions.  The inner ear structures have normal MR appearance.",
            "output": "No evidence of metastases, no abnormality of the seventh or\neighth cranial nerve is noted."
        },
        {
            "input": "There is a postoperative cavity in the left parietal lobe. There is increasing\nnodular enhancement along the medial aspect of the postoperative cavity\nmeasuring 11 x 14 mm. Increased FLAIR hyperintensity in the same region.\nIncreased subependymal enhancement along the left occipital horn. Post\ntreatment changes in the white matter are stable.\n\nMR Perfusion:  No significant increase perfusion\n\nMRS:  Limited due to technique\n\nIntracranial flow voids are maintained. Visualized paranasal sinuses and\nmastoid air cells are clear.",
            "output": "Increased nodular enhancement in the left parietal lobe along the medial\naspect of the cavity. Findings are concerning for tumor recurrence."
        },
        {
            "input": "Again demonstrated are post-surgical and -treatment changes in the left\nparieto-occipital region. There are similar sites of nodular enhancement at\nthe margin of the resection and anteriomedially in the subependymal region of\nthe occipital horn of the left lateral ventricle.  This site demonstrates\nassociated abnormal Choline peak on MRS, suspicious for residual tumor.\nCompared to the contralateral side there is increased blood flow in the region\nsurrounding the resection cavity, also suspicious for tumor.\n\nThere is gyriform leptomeningeal enhancement in the left occipital lobe with a\nnodular component (1200b:50 and 12:60) similar to the  most recent study, but\nnew since ___, suspicious for subarachnoid space involvement by\ntumor.  No MRS ___ this site was performed.\n\nThere is a new focus of intrinsic T1-hyperintensity in the lateral aspect of\nthe left putamen, measuring 8 x 7 mm (1200b:60).  There is no associated\nenhancement and no increased perfusion, and no \"blooming\" abnormality on the\nGRE sequence. There are relatively symmetric bihemispheric white matter\nFLAIR-hyperintensities, likely reflecting prior whole brain radiation.\n\nSingle voxel spectroscopy just medial to the resection bed reveals no\nsignificant inversion of the choline and creatinine peak. Multi voxel\nspectroscopy shows inversion of the creatinine peaks in the region of interest\n3, 5, and 10. NAA is a low in region of interest 5 and 10.",
            "output": "1. Allowing for the extensive treatment-related changes, there are persistent\nnodular foci of enhancement, at the margin of the resection and anteromedially\nin the subependymal aspect of the left lateral ventricular occipital horn,\nwith highly abnormal MRS, suspicious for residual tumor.\n\n2. Additional region of leptomeningeal enhancement in the medial left\noccipital, similar to the prior study but new since ___, lobe\nsuspicious for subarachnoid space involvement, as suggested previously.\n\n3. Round intrinsic T1-hyperintense focus in the lateral left putamen is new,\nbut does not show appreciable enhancement or abnormal perfusion.\n\nThis is indeterminate in nature, but may represent hemorrhagic lacune or\nradiation-related vascular abnormality. Close attention to this site on\nfollow-up MRI is recommended."
        },
        {
            "input": "Small acute infarcts are noted in the medial right temporal lobe\n(series 14 and 15 images 11 and 10), with very mild associated\nFLAIR-hyperintensity. There is no evidence of hemorrhage or mass.  Scattered\nFLAIR/T2-bright foci within the cerebral white matter are compatible with\nunderlying chronic microvascular ischemic disease.",
            "output": "Small acute infarcts in the right medial temporal cortex."
        },
        {
            "input": "MR BRAIN:\nEncephalomalacia in the left inferior frontal lobe is likely related to a\nchronic infarction.  Scattered foci of T2/FLAIR hyperintensities in the\nperiventricular, subcortical, and deep white matter are nonspecific.\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline shift\nor  acute infarction.   The ventricles and sulci are prominent, related to\nage-appropriate volume loss.\n\nThe left maxillary sinus contains a moderate mucous retention cyst.  The\nmastoid air cells are clear.  The patient is status post bilateral cataract\nsurgery.\n\nMRA brain:  The left distal M1 segment is severely, focally narrowed.  There\nis mild narrowing of the right mid to distal P1 segment and moderate,\nmultifocal narrowing and irregularity of the left P1 and P2 segments.  The\nintracranial internal carotid, bilateral vertebral, basilar, right middle\ncerebral, and bilateral anterior cerebral arteries are patent and otherwise\nwithout evidence of stenosis or occlusion.  No aneurysms are identified.",
            "output": "1. No acute infarctions.\n2. Chronic infarction in the left inferior frontal lobe.\n3. Probable sequela of mild to moderate chronic small vessel ischemic disease.\n4. Severe, focal stenosis of the left distal M1 segment, mild stenosis of the\nright mid to distal P1 segment, and moderate multifocal narrowing irregularity\nof the left P1 and P2 segments, likely related to atherosclerotic disease."
        },
        {
            "input": "MRI BRAIN: 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 evidence of abnormal atrophy of the brainstem,\ncerebellum or middle cerebellar peduncles.  The posterior pituitary bright\nspot is not visualize, of uncertain clinical significance.  There is no\nabnormal enhancement after contrast administration.  The intracranial arteries\ndemonstrate normal T2 flow voids.  The dural venous sinuses are patent.  The\nparanasal sinuses are essentially clear.  The mastoid air cells are clear.\n\nMRI ORBITS: The bony orbits and preseptal soft tissues are normal. The globes\nare intact and normal in appearance.  There is an 8 mm segment of the right\noptic nerve in the posterior aspect of the orbit just proximal to the apex\nwhich demonstrates increased T2 signal and demonstrates postcontrast\nenhancement.  The nerves appear slightly smaller than would be expected for\nage, but is symmetrical in size.  No evidence of diffusion-weighted\nhyperintense signal.  The extraocular muscles are uniform in size and normal\nin signal. The lacrimal apparatus is normal. Retrobulbar soft tissues are\nnormal.",
            "output": "1. Short-segment of T2 high signal of the right optic nerve in the posterior\naspect of the orbit which demonstrates postcontrast enhancement.  Clinical\ncorrelation for posterior ischemic optic neuropathy is recommended.  The\nnerves are symmetric in size, but slightly smaller than would be expected for\nage, compatible with given history of optic atrophy.\n2. No incidental intracranial findings of note.  The pituitary bright spot is\nnot visualize, of uncertain clinical significance.  Of note, the brainstem,\ncerebellum and middle cerebellar peduncles are unremarkable."
        },
        {
            "input": "MRI brain:\n\nA chronic right basal ganglia infarct is identified extending to the\nperiventricular region.  A chronic right cerebellar infarct is also noted. \nThere is no mass effect midline shift or hydrocephalus.  No acute infarct is\nidentified.  There are no micro hemorrhages.  The ventricles and extra-axial\nspaces are normal in size.  Following gadolinium administration, there is no\nevidence of abnormal parenchymal vascular or meningeal enhancement seen.  Mild\nmucosal thickening is seen in the ethmoid air cells and sphenoid sinuses.\n\nMRI orbit:\n\nImages through the orbits demonstrate symmetric appearance is of the optic\nnerves and extraocular muscles.  No mass lesion or abnormal enhancement is\nseen.  There is no compression of the optic chiasm or intra cranial optic\nnerves.  No abnormal signal within the optic nerves identified.",
            "output": "1. Chronic right basal ganglia and cerebellar infarcts.  No acute infarcts.\n2. No enhancing brain lesions mass effect or hydrocephalus.\n3. No significant abnormalities on MRI of the orbits."
        },
        {
            "input": "MRI BRAIN WITHOUT IV CONTRAST:\nMultiple foci of slow diffusion are noted in the left MCA territory, in the\nleft frontal and the parietal lobes, without significant change compared to\nthe recent study of ___.\nNo significant surrounding edema or mass effect.\nNo focus of negative susceptibility within to suggest hemorrhage. On the FLAIR\nsequence, multiple small scattered FLAIR hyperintense foci are noted in the\nfrontal and the parietal lobes on both sides without signific moderate\nethmoidal and mild-to-moderate sphenoidal mucosal thickening.\nThe mastoid air cells the fluid on both sides.\nSella, pineal gland and the craniocervical junction regions are unremarkable.\nAnt change compared to the recent study.\n\nMR ANGIOGRAM OF THE HEAD WITHOUT IV CONTRAST:\nThere is narrowing of the left middle cerebral artery, M1 and M2 segments,\nwith decreased visualization of the M2 and more distal branches.\nThese are better assessed on the prior CT angiogram study.\nRest of the intracranial arteries appear patent without focal flow-limiting\nstenosis or occlusion or aneurysm more than 3 mm within the resolution.",
            "output": "1.  Multiple infarcts in the left MCA territory without significant change\ncompared to the recent MRI study of ___.\n2. Narrowing of the M1 and M2 segments of the left middle cerebral artery\nalong with decreased visualization of the M 2 segments and more distal\nbranches.  The arteries are better assessed on the source images than the MIP\nreformations.\nPlease see recent CT angiogram study for better assessment of the arteries."
        },
        {
            "input": "MRI brain:\n\nThere is a right parietal intraparenchymal hematoma measuring approximately 25\nmm AP x 27 mm TV x 28 mm SI. There is no significant change in size compared\nto prior study. Signal abnormality is noted on diffusion-weighted images;\nassessment for ischemic changes is confounded by the presence of blood\nproducts. On post-contrast images, there is a thick, slightly irregular rind\nof heterogeneous peripheral enhancement, approx.  1.1cm in thickness.\nThere is surrounding vasogenic edema. There is local mass effect with sulcal\neffacement and narrowing of the atrium and occipital horn of the right lateral\nventricle.\nThere is no shift of midline structures.\nThe sulci and vetricles are normal elsewhere.\nThere is a small right subdural fluid collection or hemorrhage.\nThere are scattered foci of T2/FLAIR signal hyperintensity in the\nperiventricular, deep, and subcortical white matter which is nonspecific but\nlikely secondary to chronic small vessel ischemic disease.\n\nThe major vascular flow voids are maintained.\nThe orbits are unremarkable.\nThere is minimal mucosal thickening within the paranasal sinuses. The mastoid\nair cells are clear.\n\nMRV brain:\nThe superior sagittal sinus, straight sinus, transverse sinuses, sigmoid\nsinuses, and the visualized internal jugular veins are patent without filling\ndefect to suggest thrombosis. The visualized deep cerebral veins are also\npatent. The vein ___ is unremarkable.",
            "output": "1. Right parietal  intraparenchymal hematoma, 2.8x2.5x2.7cm,  unchanged\ncompared to prior CT.  Thick rind of slightly irregular and heterogeneous\nperipheral enhancement seen in/surrounding the hematoma on post-contrast\nimages. This could be a finding seen with a subacute hematoma, however an\nunderlying mass lesion cannot be completely excluded, given the thickness and\nirregularity.  Close Followup is recommended to assess for interval change.\n\n2.  T2/FLAIR signal hyperintense focii in the periventricular, deep, and\nsubcortical white matter which are nonspecific but most likely secondary to\nchronic small vessel ischemic disease.\n\n3.  Patent major dural venous sinuses"
        },
        {
            "input": "There is an unchanged right parietal enhancing lesion with minimal edema\nmeasuring approximately 23 x 25 mm in transverse dimension. No new lesions are\nidentified since the prior examination. On the ASL sequence, there is a\npunctate area of hyperperfusion within the mass lesion (image 27, series 10). \nThe tractography shows minimal deviation of the corticospinal, association an\ncommissural tracts.\nThe expected activation areas during the movement of the hands, feet, tongue\nwere demonstrated. The functional MRI during the movement of the left hand\ndemonstrate BOLD activation at less than 1 cm from the mass, the majority of\nthe activation appears anterior. No other areas of BOLD activation are\nadjacent to the mass lesion.",
            "output": "1. Unchanged right parietal enhancing lesion with punctate area of avid\nenhancement demonstrated on the ASL sequence.\n\n2. The functional MRI during the movement of the left hand demonstrate BOLD\nactivation at less than 1 cm from the mass, the majority of the activation\nappears anterior. No other areas of BOLD activation are adjacent to the mass\nlesion."
        },
        {
            "input": "MRI BRAIN:  There is mild artifact related to dental work.  There is no\nevidence of hemorrhage, edema, masses, mass effect, midline shift or\ninfarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  Minimal scattered punctate FLAIR hyperintensities in the\nperiventricular white matter are nonspecific, are consistent with chronic\nsmall vessel ischemic disease.  There is small focus of decreased signal on\nFLAIR images involving anteromedial right frontal lobe, most consistent with\nencephalomalacia related to prior trauma, or possibly neuroglial cyst in the\nabsence of history of trauma.  No abnormal enhancement, no associated edema. \nThere is tiny benign capillary telangiectasia or developmental venous anomaly\nin the right frontal lobe series 11, image 18.  There is no abnormal\nenhancement after contrast administration.\n\nMRI ORBITS: The bony orbits and preseptal soft tissues are normal. The globes\nare intact and normal in appearance. The optic nerves and complex are normal,\nwithout edema or abnormal enhancement. The extraocular muscles are uniform in\nsize and normal in signal. The lacrimal apparatus is normal. Retrobulbar soft\ntissues are normal.",
            "output": "Normal orbits.\nBenign-appearing small cystic change in the anterior right frontal lobe, most\nconsistent with posttraumatic encephalomalacia."
        },
        {
            "input": "Normal flow signal is noted in the petrous, cavernous, and supraclinoid\nportions of the internal carotid arteries. The anterior and middle cerebral\narteries are normal. The anterior communicating artery region is normal.\n\nAgain identified is inhomogeneous susceptibility in the region of the right\nmid-V4 segment with T1 hyperintensity at the base of the coil pack/ mouth of\nthe aneurysm which appears prominent and enlarged, similar to prior MRA ___ and conventional angiogram ___.  Again noted is the right ___\n___ from the neck of the aneurysm. There is persistent narrowing of\nthe V4 segment distal to this region.\n\nThe posterior communicating arteries are prominent bilaterally with a\ndiminutive left P1 segment. The posterior cerebral arteries and basilar artery\nare otherwise unremarkable. The superior cerebellar arteries are normal. The\nintradural segments to the left vertebral artery is patent.\n\nNo arterial stenosis, other saccular aneurysm, or AVM is identified. Flow is\nsymmetric.",
            "output": "Stable appearance of T1 hyperintensity at the mouth/base of the previously\ncoiled the mid right V4 vertebral artery aneurysm."
        },
        {
            "input": "Study is mildly degraded by motion.\n\nThere is a hypoenhancing solid pituitary mass with a cystic peripherally\nenhancing component which extends superiorly into the pituitary stalk into the\nsuprasellar cistern.  Total SI dimension of this mixed solid and cystic mass\nlikely measures 1.4 cm, with maximal transverse dimension measuring 0.9 cm\n(4:8) and maximal AP dimension measuring 0.8 cm (8:9).  This structure\ndemonstrates FLAIR hyperintensity.  Question minimal associated fine\ncalcifications on prior outside head CT versus artifact (see 203:42; 202:38). \nQuestion enhancing rim of compressed pituitary around nonenhancing cyst (7:8).\n\nA small amount of likely normal pituitary parenchyma is seen predominantly\nalong the along the right lateral aspect of the pituitary mass.\n\nAgain, there is extension into the suprasellar cistern with displacement and\nmild compression of the optic chiasm (7:8).  The cavernous internal carotid\narteries and cavernous sinuses are grossly preserved.  The infundibulum is\ndeviated towards the left.\n\nThe limited portion of the brain, paranasal sinuses, and orbits included on\nthis study appears normal.",
            "output": "1.  Study is mildly degraded by motion.\n2. 1.4 x 0.9 x 0.8 cm hypoenhancing mixed solid and cystic pituitary mass with\nquestioned fine associated calcification versus artifact on prior outside head\nCT as described, concerning for craniopharyngioma, with differential\nconsiderations of Rathke's cleft cyst and cystic macroadenoma.\n3. Extension of mass cystic component into the midline suprasellar cistern\nwith mass effect and mild displacement of the optic chiasm."
        },
        {
            "input": "Compared to ___, there has been slight interval decrease in\nsize of the right frontal mass.  There is a persistent thick rind of enhancing\ntissue that shows restricted diffusion.  Compared to the prior examination,\nthere are now linear regions of susceptibility artifact within the central\naspect of the mass and a central region of T2 hyperintense and T1 moderately\nintense material.  In addition, there is evidence of interval craniotomy\nadjacent to the mass.  Adjacent FLAIR/T2 hyperintensity is unchanged. \nModerate maxillary sinus mucosal thickening is again demonstrated.",
            "output": "Evidence of interval right frontal craniotomy, with slight\ninterval decrease in size of the right frontal mass, with evidence of central\nnecrosis or hemorrhage."
        },
        {
            "input": "In comparison with the most recent head CT examination, there is a grossly\nunchanged 35 x 30 mm right frontal intraparenchymal hematoma, associated with\nan underlying arteriovenous malformation, there is no significant mass effect\nor shifting of the normally midline structures.  The vascular drainage for\nthis vascular malformation apparently is superficial.  No new areas of\nabnormal enhancement are demonstrated in this short interval.\nThe ASL sequence demonstrates a punctate focus of increased perfusion in the\nvascular nidus (series 9, images 25 through 29).\nThe tractography color maps demonstrate mild medial deviation of the right\nsuperior longitudinal fascicle fibers, as well as some fibers of the corpus\ncallosum towards the right.\n\nThe functional MRI demonstrates the expected areas of BOLD activation during\nthe movement of the right hand, feet, and tongue.  Please note that the\npatient was unable to move the left arm or hand, however slightly open and\nclose her fist, limiting the evaluation for the primary motor cortex, which\napparently is projected and migrated towards the left cerebral hemisphere,\nalso please note there is increased BOLD signal within the hematoma and in the\ncentral aspect of the vascular nidus consistent with venous contamination\n(series 5000, images 16 and 17).\nDuring the movement of the tongue, the BOLD activation appears inferior to the\nhematoma, and  is more significant on the right (series 5000, image 21).\n\nThe word generation paradigm demonstrates the majority of the activation in\nthe right cerebral hemisphere, including the Broca's area..\n\nThe activation areas during the movement of the right hand, right toe appear\nin the expected locations, with no evidence of areas of activation adjacent to\nthe vascular nidus and the right frontal hematoma.",
            "output": "1.  Unchanged right frontal intraparenchymal hematoma with associated\narteriovenous malformation as described detail above.\n\n2.  There is a small focus of increased perfusion in the vascular nidus, as\nwell as venous contamination demonstrated on the BOLD images within the\nvascular malformation.\n\n3.  Please note that the patient was unable to move the left arm and left\nhand, however it was capable to open and close her fist, projecting the\nmajority of the bold activation for the movement of the left hand in the left\ncerebral hemisphere.\n\n4.  The language paradigm demonstrates the majority activation in the right\ncerebral hemisphere including the Broca's area.\n\n5.  The tractography demonstrates mild deviation of the superior longitudinal\nfascicle medially, as well as mild medial deviation of some fibers from the\ncorpus callosum medially."
        },
        {
            "input": "Study is mildly degraded by motion.\n\nMRI BRAIN:\nThere are numerous T1 hypointense, T2 hyperintense, enhancing lesions\nthroughout the calvarium consistent with known metastatic osseous disease,\nwithout evidence of extra osseous extension.  The largest on the left is\nwithin the parietal calvarium measuring 2.5 cm (08:21.  The largest on the\nright is at the right parietal calvarium measuring 4.1 cm (08:15).  There is\nan additional enhancing lesion at the dens measuring 1.1 cm (12:104).\n\nNonspecific periventricular and subcortical T2 and FLAIR hyperintensities are\nnoted, which may represent small vessel ischemic changes or treatment related\neffects.   There is no acute infarct, hemorrhage, or mass effect.  The\nventricles and cortical sulci are normal caliber and configuration.  There are\nprominent nonenhancing cysts within the choroid plexus of the lateral\nventricular atria, right greater than left, which are unchanged.  The\nextra-axial spaces are unremarkable.  The vascular flow voids are preserved. \nThere is normal dural venous enhancement.\n\nThe previously noted right middle cranial fossa area of enhancing soft tissue\n(see 400:88, 5:8 on ___ prior exam) is smaller compared to prior\nexaminations, measuring approximately 1.4 (AP) x 11 (TV) x 11 (SI) mm (see\n09:12, 12:148-150 on current study and 16:8 on ___ prior exam, and\n5:8 on ___ prior exam).  The soft tissue density measured\napproximately 4 (AP) x 17 (TV) x 13 (SI) mm on ___ prior exam (see\n17:121, 16:8).\n\nStable approximately 17 (AP) x 19 (TV) x 9 (SI) mm right middle cranial fossa\nprobable arachnoid cyst is again noted (see 8:10, 12:155 ).\n\nBilateral maxillary sinus and ethmoid air cell mucosal thickening is present. \nNonspecific right mastoid fluid is noted.  Partially visualized is an\napproximately 3 x 8 mm  T1, STIR, FLAIR hypointense nonenhancing structure\nlateral to the right maxillary molars and gingiva (see 6, 7, 10:6, 8:1).\n\nA grossly stable approximately 1.5 x 2.0 cm right lateral ventricle probable\nchoroid plexus cyst is again noted (see 08:12, 4 02:16, 1200:87).\n\nMRI ORBITS:\nThe bony orbits and preseptal soft tissues are normal. The globes are intact\nand normal in appearance. The optic nerves and complex are normal, without\nedema or abnormal enhancement. The extraocular muscles are uniform in size and\nnormal in signal. The lacrimal apparatus is normal. Retrobulbar soft tissues\nare normal.",
            "output": "1. Study is mildly degraded by motion.\n2. Numerous lesions throughout the calvarium and within the odontoid process\nconsistent with osseous metastatic disease, which is relatively unchanged\ncomparison to prior study.\n3. Interval decrease sinus of enhancing right middle cranial fossa soft tissue\noverlying right temporal pole as described.\n4. No evidence of intraorbital metastatic disease, with no definite right\nsuperior orbital fissure mass.\n5. No acute intracranial abnormality.\n6.  Paranasal sinus disease as described.\n7. Nonspecific nonenhancing structure lateral to right maxillary molars in\ngingiva.  Question dental hardware.  Recommend correlation with surgical\nhistory and physical exam."
        },
        {
            "input": "Please note the study is mildly degraded by motion. The intracranial vertebral\nand internal carotid arteries and their major branches appear normal without\nevidence of stenosis, occlusion, or aneurysm formation.  Area of previous\nconcern identified adjacent to cavernous segment of left internal carotid\nartery, with no definite flow related intensity (see series 3 image 109).",
            "output": "1. No definite aneurysm identified.\n2. Previously noted 5 mm hypointense structure suggested to be adjacent to\ncavernous segment of left internal carotid artery, with no definite flow\nrelated enhancement. While finding likely represents a pneumatized posterior\nclinoid process, differential considerations include thrombosed aneurysm.\nRecommend clinical correlation. If clinically indicated, consider head CTA for\nfurther evaluation.\n\nRECOMMENDATION(S):  If clinically indicated, CTA can be considered for further\nevaluation."
        },
        {
            "input": "8 mm focus of central and right paramedian pituitary gland T2 signal\nabnormality,.  On post gadolinium images there is 3.5 mm focus of decreased\nenhancement within the abnormality, similar..  Findings most consistent with\npituitary microadenoma, similar.  No contact of the optic chiasm.  Normal\ncavernous sinus.  Normal ICAs, clivus, sphenoid sinus..\n\nVisualized intracranial structures, upper neck soft tissues are normal.",
            "output": "1. Findings consistent with pituitary microadenoma, similar."
        },
        {
            "input": "MRA 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.  No abnormal vascular structures are seen\nwithin the internal auditory canals.  Source images demonstrate fluid within\nthe right mastoid air cells.",
            "output": "No significant abnormalities are seen on MRA of the head.  Fluid within the\nright mastoid air cells."
        },
        {
            "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 T2\nhyperintensity of nonspecific nature are seen.\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.",
            "output": "Most significant abnormalities are seen on MRI of the brain with and without\ngadolinium. No significant abnormalities are seen on MRA of the head."
        },
        {
            "input": "There is no evidence of mass, hemorrhage, or acute infarcts. \nScattered punctate FLAIR hyperintensities within the cerebral white matter are\ncommon and likely incidental finding in a patient of this age.  Major\nintracranial flow voids are preserved.  Partial opacification of the bilateral\nmastoid air cells is incidentally noted.",
            "output": "No suspicious interval change to suggest metastasis."
        },
        {
            "input": "There are 3 unchanged ring enhancing lesions, 2 of them in the right frontal\nand 1 in the right parietal lobe. The ASL sequence shows increased perfusion\nin these lesions (image 24 series 3a).  The tractography demonstrates minimal\ndeviation of the adjacent commissural and association tracts, note is made of\ncorticospinal tracts adjacent to the frontal and parietal mass lesions\nposteriorly.\n\nThe functional MRI shows the expected BOLD activation areas in the primary\nmotor cortex during the movement of the hands, feet and tongue.  During the\nmovement of the left hand and left foot, the BOLD activation is localized\nposterior lateral to the right parietal enhancing lesion at less than 1 cm\n(image 76, series 1205 and image 79, series 1209). The language paradigm shows\nthe majority of the BOLD activity in the left cerebral hemisphere, likely\nrelated with dominance.",
            "output": "1. Unchanged 3 ring-enhancing lesions, 2 of them in the right frontal and 1 in\nthe right parietal lobe as described above with increased perfusion on the ASL\nsequence and minimal deviation of the adjacent tracts.\n\n2. During the movement of the left hand and left foot, the BOLD activation is\nlocalized posterior lateral to the right parietal enhancing lesion at less\nthan 1 cm (image 76, series 1205 and image 79, series 1209)."
        },
        {
            "input": "MRI BRAIN:\nA punctate focus of DWI hyperintensity in the left corona radiata (series 402,\nimage 21) does not demonstrate a definitive ADC correlate and therefore most\nlikely represents T2 shine through.\n\nNote is made of several T2/FLAIR hyperintense periventricular lesions some of\nwhich are perpendicularly oriented and at the callosal septal interface,\nconsistent with demyelinating plaques.  There is no abnormal enhancement after\ncontrast administration.  Some of these lesion demonstrate intrinsic T1\nhypointensity, suggestive of chronicity.\n\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.\nMajor vascular flow voids are preserved.  Major dural venous sinuses are\npatent.\n\nThe paranasal sinuses and mastoid air cells appear clear.\n\nMRI ORBITS:\nNote is made of mild enhancement involving the left optic nerve (series 10,\nimage 12), consistent with optic neuritis.\nThe right optic nerve and complex is normal, without edema or abnormal\nenhancement.\n\nOtherwise, the bony orbits and preseptal soft tissues are normal. The globes\nare intact and normal in appearance.  The extraocular muscles are uniform in\nsize and normal in signal. The lacrimal apparatus is normal. Retrobulbar soft\ntissues are normal.",
            "output": "1. Several nonenhancing, partially perpendicularly oriented periventricular\nlesions, some of which are along the callosal septal interface, are consistent\nwith demyelinating plaques, likely in the setting of multiple sclerosis.\n2. Enhancement of the left optic nerve, consistent with optic neuritis.\n3. No evidence of infarction, hemorrhage or mass."
        },
        {
            "input": "MRI OF THE HEAD WITHOUT AND WITH IV CONTRAST:\n\nA few scattered abnormalities are noted as described below, of uncertain\netiology.\nOn the DWI sequence, there is linear hyperintense signal in the right\ncerebellar hemisphere on series 5, image 7, without significant signal change\non the ADC sequence. There is subtle FLAIR hyperintense signal, series 18,\nimage 7 along with hypointense signal on the MPRAGE sequence series 106, image\n40; series 107, image 100. This can be located in the parenchyma/ adjacent\nfolia or both. The nature of this finding is uncertain, however,\ninflammation/blood products to be considered; no abnormal enhancement, no\nsurrounding edema or mass effect.\nOn the DWI sequence, there is another small round focus noted anterosuperiorly\nseries 5, image 9 without corresponding abnormality on the ADC or the FLAIR\nsequence.\nOn the FLAIR sequence, there is slightly increased signal intensity in the\nright posterior insula series 18, image 16, 17 unclear if this is in the\nparenchyma or related to enhancement of the adjacent vessel.\nSlight increased signal intensity in the interpeduncular fossa, can relate to\nenhancement of the vascular structures.\nSubtle increased signal intensity in the left frontal vertex series 18, image\n21 question related to volume averaging or pulsation artifact from the vessel.\nSlightly increased signal intensity in the falx superiorly on the FLAIR\nsequence- series 18, image 19, 20.\nA slightly prominent venous tributary, in the right posterior parietal lobe,\nlikely variant.\nRest of the brain parenchyma is unremarkable.\nSella, pineal gland and the craniocervical junction regions are unremarkable.\nThe cerebellar tonsils are located at the level of the foramen magnum.\n\nThe ventricles, the extra-axial CSF spaces on the sulci are otherwise\nunremarkable.\nMinimal fluid noted in the mastoid air cells on both sides, left more than\nright.\nModerate ethmoidal and mild to moderate sphenoidal mucosal thickening noted.\nFluid in the nasopharynx and nasal cavity related to intubation. The included\norbits are grossly unremarkable.\n\n3D TOF MR ANGIOGRAM OF THE HEAD WITHOUT IV CONTRAST:\nThe major intracranial arteries of the anterior and the posterior circulation\nare patent, without focal flow-limiting stenosis, occlusion or aneurysm more\nthan 3 mm within the resolution of the study. The left MCA division is\nslightly prominent without obvious outpouching.\nThe posterior inferior cerebellar arteries and the cavernous carotid segments\nare slightly tortuous in course.\nThe left distal cervical internal carotid artery is tortuous in course.\n\nPHASE CONTRAST MR VENOGRAM OF THE HEAD:\nThe major venous sinuses are patent.",
            "output": "1.  A few scattered abnormalities on the diffusion and the FLAIR sequences as\ndescribed above, in the right cerebellar hemisphere and in the right posterior\ninsula- of uncertain etiology, considerations include inflammation, infection\nor blood products or mineralization, toxic, etc.  Correlate clinically and\nwith EEG and consider close followup to assess for interval change and better\ncharacterization.  No abnormal enhancement, no surrounding edema or mass\neffect.\n2. Patent major intracranial arteries as described above.  Tortuous left\ndistal cervical internal carotid artery- correlate clinically for any vascular\ndisorders given the young age of the patient.\n3.  Patent major dural venous sinuses.\nOther details as above\n\nNOTIFICATION:  D/w ___ by Dr. ___ phone on ___ soon after\nreview at approx.  11am."
        },
        {
            "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\nMRA: Intracranial vascular structures are unremarkable without evidence of\nsignificant stenosis, aneurysm, or occlusion.",
            "output": "Normal MRI and MRA of the head."
        },
        {
            "input": "Subtle assymetric increased DWI, decreased ADC and increased FLAIR\nsignal is seen within the left medial temporal lobe (700:13, 702:13), possibly\nartifactual. There is no evidence of blood products or mass effect. \nVentricles, cisterns and sulci show symmetric prominence compatible with\nglobal volume loss, similar to the prior CT.  Intracranial flow voids are\npreserved, though there is some likely atherosclerotic irregularity of the\nintracranial arteries, most prominent in the basilar.",
            "output": "Focus of slow diffusion versus an artifact in the medial left\ntemporal lobe. However, post-ictal changes or a small acute infarct cannot be\nexcluded. If clinically warranted, a short-interval follow-up MRI could be\nobtained for reassessment."
        },
        {
            "input": "There is been no significant interval change. Again approximately 5-6 mm\nanterior communicating artery aneurysm identified which is unchanged in\nappearance and size. No vascular occlusion or stenosis seen.",
            "output": "No significant interval change since the previous MRI examination. 5-6 mm\nanterior communicating artery aneurysm is again seen."
        },
        {
            "input": "MRI BRAIN: Right frontal parietal burr hole.  No significant change in\nminimally enhancing bifrontal lesions with involvement and extension across\nthe genu of the corpus callosum and left cingulate gyrus, and separate lesion\nat the anterior left centrum semiovale, which have areas of intrinsic T1\nhyperintensity.  Again seen small foci of susceptibility abutting the frontal\nhorn of the right lateral ventricle compatible with old blood products.  There\nis a similar degree of bifrontal FLAIR signal abnormality.  Bifrontal atrophy.\nLess conspicuous is a previously identified linear focus of sulcal FLAIR\nhyperintensity in the left precuneus.\n\nThere is no evidence of new hemorrhage or infarction.  The ventricles and\nsulci are normal in caliber and configuration.\n\nThe major intracranial vascular flow voids are maintained.  Patent dural\nvenous sinuses.  No significant change in complete opacification of the left\nfrontal sinus, left ethmoid air cells and left maxillary sinuses, with areas\nof restricted diffusion and peripheral enhancement, worrisome for sinusitis. \nThere is mild mucosal thickening of the right ethmoid air cells and maxillary\nsinus.  There is trace nonspecific fluid within the left mastoid air cells.\n\nMRI ORBITS: There is persistent left orbital preseptal swelling/inflammation\nand enhancement.  Tiny pocket of mildly restricted diffusion in the left\nperiorbital soft tissues, may be involving inferior left eyelid series 502,\nimage 10, may represent small abscess, measuring 0.4 cm series 9, image 10. \nNo definite infiltration of intraorbital fat.  Opacification and enhancement\nof the left frontal, ethmoid, maxillary sinuses, with enhancement of the left\nmedial orbital wall, consistent sinusitis.  Obstruction should be excluded. \nNormal cavernous sinus.  Patent superior ophthalmic vein.\n\nThe globes are intact and normal in appearance. The optic nerves and complex\nare normal, without edema or abnormal enhancement. The extraocular muscles are\nuniform in size and normal in signal. The lacrimal apparatus is normal.\nRetrobulbar soft tissues are normal.",
            "output": "1. Persistent left periorbital preseptal swelling compatible with preseptal\ncellulitis, with suggestion of 0.4 cm microabscess.\n2. Stable extensive left frontal, ethmoid, maxillary sinusitis. Obstruction\nshould be excluded, recommend ENT consult.\n3. Unchanged minimally enhancing bifrontal lesions.  No new enhancement.\n4. Similar degree of bifrontal FLAIR signal abnormality.\n5. Improved previously described abnormality in the left precuneus.\n\nNOTIFICATION:  The findings were discussed with ___, M.D. by\n___, M.D. on the telephone on ___ at 11:45 am, 15 minutes\nafter discovery of the findings."
        },
        {
            "input": "MRI HEAD WITHOUT AND WITH IV CONTRAST\n\nNo focus of slow diffusion in the brain parenchyma to suggest acute infarct.\nNo focus of negative susceptibility to suggest suspicious intracranial\nhemorrhage.\nOn the FLAIR sequence, no obvious focal lesions are noted.\nNo focus of abnormal enhancement is noted in the brain parenchyma or meninges.\nThe ventricles and the cerebral sulci are normal.\nProminent posterior fossa CSF spaces can relate to ___ cisterna magna.\n\nThe major intracranial arterial flow voids are noted. Fetal PCA pattern on\nboth sides.\nMildly prominent pituitary gland can be within normal limits given the\npatient's age.\nPineal gland and the craniocervical junction regions are unremarkable.\n\nSmall to moderate amount of fluid noted in the right mastoid air cells.\nMildly prominent adenoids. Small retention cysts in the maxillary sinuses.\nSphenoid sinus septation inserts on the right carotid groove.\nThe imaged orbits are unremarkable on the routine study.\nLimited assessment of the optic nerves as not targeted.\n\nTOF MRV HEAD WITHOUT CONTRAST\n\nThe major dural venous sinuses are patent.  No obvious filling defect noted.\nSlightly decreased signal intensity in the transverse sinus/ sigmoid sinus\nregion bilaterally and at the torcula can be artifactual related to volume\naveraging or flow related artifacts appear.\nRight transverse and sigmoid sinuses and right internal jugular vein are\ndominant.",
            "output": "1.  No acute infarct or mass effect or enhancing lesions in the brain\nparenchyma.\n2. Patent major dural venous sinuses as described above.\n3. Small to moderate amount of fluid in the right mastoid air cells, mildly\nprominent adenoids\nCorrelate clinically for etiology.\nLimited assessment of the orbits for signs of intracranial hypertension.\nCorrelate clinically."
        },
        {
            "input": "MRI HEAD:\n\nThere is no evidence of edema, mass effect, abnormal diffusion, or blood\nproducts in the brain parenchyma.  There is no pathologic extra-axial\ncollection. The ventricles and basal cisterns appear normal.  There is 3 mm\nectopia of the cerebellar tonsils. However, the cerebellar tonsils appear\nmorphologically normal. The pituitary gland is not evaluated in\nhigh-resolution detail, but its size and contours appear grossly unremarkable\nfor the patient's age and gender.\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 for age.\n\nThe orbits, skull base, and paranasal sinuses appear normal.\n\nMRA HEAD:\n\nThe study is mildly limited by motion artifact. There is no evidence of an\naneurysm or hemodynamically significant stenosis within the intracranial\nvasculature. The anterior communicating artery is unremarkable. The bilateral\nposterior communicating arteries are small.  Right ___ complex is noted,\na normal variant.",
            "output": "1. 3 mm ectopia of the cerebellar tonsils could represent normal anatomic\nvariation. However, in the setting of headaches, intracranial hypotension or\nidiopathic intracranial hypertension may be considered. Contrast enhanced MRI\ncould evaluate for other signs of intracranial hypotension. If the patient has\nsymptoms of intracranial hypertension, then correlation with lumbar puncture\nwould be helpful.\n2. Mildly motion-limited brain MRA without evidence for aneurysm."
        },
        {
            "input": "The intracranial vertebral and internal carotid arteries and their major\nbranches appear normal without evidence of stenosis, occlusion, or aneurysm\nformation.",
            "output": "Normal study"
        },
        {
            "input": "Again seen are masses surrounded by vasogenic edema in the left temporal lobe\nand extending into the left putamen.  There is extensive vasogenic edema. The\nlesions enhance inhomogeneously after contrast administration, but there are\nno definite areas of necrosis. There is no evidence of leptomeningeal seeding\nof tumor.  As previously noted, the diffusion coefficient is relatively slow\nwithin these masses.\n\nMR spectroscopy demonstrates choline and lipid lactate elevation with\ndepression of NAA. These findings are consistent with a malignant neoplasm.\n\nImages of the remainder of the brain demonstrate scattered periventricular and\nsubcortical white matter hyperintensities on FLAIR suggesting chronic small\nvessel ischemia.\n\nAgain seen is a right petroclinoid enhancing mass most likely a meningioma.",
            "output": "The masses previously identified in the left temporal lobe and putamen enhance\nafter contrast administration and demonstrate elevation of the choline and\nlipidand lactate. Diffusion is relatively slow. These findings strongly\nsuggest a malignant neoplasm. The diffusion findings favor lymphoma. The\ncluster of multiple enhancing lesions with extensive surrounding vasogenic\nedema favor malignant glioma. Metastatic disease is the less likely\nalternative.\n\nUnchanged right meningioma."
        },
        {
            "input": "There is normal variant right dominant vertebrobasilar system.  The\nintracranial vertebral and internal carotid arteries and their major branches\nappear normal without evidence of stenosis, occlusion, or aneurysm formation.\n\nSmall mucous retention cysts are noted in the bilateral maxillary sinuses as\nwell as minimal mucosal wall thickening in the right frontal sinus.",
            "output": "Normal brain MRA.  No aneurysm identified."
        },
        {
            "input": "MRI BRAIN:\nThere is no intra or extra-axial mass, acute hemorrhage or infarct.  The\nsulci, ventricles and cisterns are within expected limits for the degree of\nmoderate senescent related global cerebral volume loss.  There are mild\nperiventricular and subcortical T2/FLAIR white matter hyperintensities, which\nare nonspecific, but compatible with chronic microangiopathy in a patient of\nthis age.  No abnormal postcontrast enhancement.  The major intracranial flow\nvoids are preserved.  The dural venous sinuses are patent.  The patient is\nstatus post bilateral antrostomy and ethmoidectomies with apparent resection\nof the left superior and middle turbinates.  There remains moderate mucosal\nthickening of the visualized maxillary sinuses and right residual ethmoid air\ncells.  The orbits are unremarkable noting bilateral lens replacements.  No\nsignificant fluid signal is seen in the mastoid air cells.\n\nMRI ORBITS: The bony orbits and preseptal soft tissues are normal. The globes\nare intact and normal in appearance. The optic nerves and complex are normal,\nwithout edema or abnormal enhancement. The extraocular muscles are uniform in\nsize and normal in signal. The lacrimal apparatus is normal. Retrobulbar soft\ntissues are normal.  The optic chiasm and optic tracts are unremarkable.  The\ncavernous sinuses are unremarkable.",
            "output": "1. No acute intracranial abnormality on contrast enhanced MRI brain. \nSpecifically no abnormal enhancement or mass lesions.\n2. Unremarkable MRI orbits.\n3. Additional findings 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.  There are\nno acute infarcts seen. Suprasellar and craniocervical regions are\nunremarkable. Visualized paranasal sinuses are clear.\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.",
            "output": "No significant abnormalities are seen on MRI of the brain without gadolinium.\nNo significant abnormalities are seen on MRA of the head."
        },
        {
            "input": "MRI Head: There is no evidence of hemorrhage, edema, masses, mass effect, or\ninfarction. The ventricles and sulci are normal in caliber and configuration.\nA cavum septum pellucidum et vergae is incidentally noted. There are a few\nnonspecific scattered foci of T2/FLAIR signal hyperintensity in the\nperiventricular, subcortical, and deep white matter of the bilateral frontal\nlobes. There is no abnormal enhancement after contrast administration. The\norbits are unremarkable. There is mucosal thickening within the ethmoid air\ncells and a mucous retention cyst in the right maxillary sinus. The mastoid\nair cells are clear.\n\nMRA head:  There is a 3 mm outpouching arising from the proximal left\ncavernous internal carotid artery and projecting posteriorly (series 10, image\n65) which may reflect the known aneurysm mentioned in patient history. No\nprior studies available for direct comparison. The remaining major\nintracranial arteries appear normal with no evidence of stenosis, occlusion,\nor new aneurysm formation.",
            "output": "1.  Unremarkable MRI of the head without evidence of acute infarction, acute\nhemorrhage, or mass lesion.\n\n2.  Few scattered nonspecific foci of T2/FLAIR signal hyperintensity in the\nwhite matter of the bilateral frontal lobes ambulatory changes of small vessel\ndisease.\n3.  3 mm outpouching arising from the posterior left cavernous internal\ncarotid artery. This likely represents the aforementioned previously known 3\nmm left ICA aneurysm. No direct studies are available for comparison however.\nNo definite new aneurysms detected."
        },
        {
            "input": "There is left basal ganglia hemorrhage present with minimal surrounding edema.\nThe surrounding diffusion abnormality could be related to blood products or\nassociated ischemia. Mild changes of small vessel disease are seen. There is\nno midline shift or hydrocephalus. No ab no abnormal vascular structures are\nseen.\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.",
            "output": "Small area of acute hemorrhage in the left posterior limb of internal capsule\nwith mild diffusion abnormality likely related to blood products. Minimal\nsurrounding edema. No evidence of other micro hemorrhages. Mild brain atrophy.\nNo significant abnormalities are seen on MRA of the head."
        },
        {
            "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\nIntracranial arterial flow voids are maintained.  The orbits are unremarkable.\nThere is mucosal thickening with partial opacification of right ethmoid air\ncells.  The remaining visualized paranasal sinuses are clear.  The mastoid air\ncells are clear.\n\nMRV brain:  There is minimal flow related signal in the left transverse sinus\nalong its entire course.  No definite blooming identified on gradient echo. \nThere is FLAIR signal hyperintensity localizing to the left transverse sinus\nwhich can indicate slow flow or thrombosis. The left sigmoid sinus and left\ninternal jugular vein however demonstrate expected flow related signal,\npotentially due to prominent vein of ___.  This decreased flow related\nsignal in the left transverse sinus is likely due to its hypoplastic size.\n\nThe remaining dural venous sinuses including the superior sagittal sinus, the\ntransverse sinus, the vein ___ and bilateral sigmoid sinuses are patent\nwith flow related enhancement.",
            "output": "1. Unremarkable MRI of the brain.\n2. Thin, minimal flow related signal in the left transverse sinus.  While this\nis most likely secondary  to markedly hypoplastic left transverse sinus with\nslow flow, underlying transverse sinus thrombosis is not entirely excluded. \nIf desired, CT venogram could be performed to more clearly delineate."
        },
        {
            "input": "There is a small focus of chronic blood products in the right thalamus, which\ncorresponds with the hyperdense focus seen on recent CT.  No other focus of\nhemorrhage is seen.  There is no evidence of mass, mass effect, or infarct.\n\nThe major intracranial arteries appear normal with no evidence of stenosis,\nocclusion, or aneurysm formation.  Prominent ventricles and sulci suggest age\nrelated atrophy.  Periventricular T2 hyperintensity is consistent with small\nvessel ischemic disease.",
            "output": "Stable small focus of hemosiderin indicating chronic blood products in the\nright thalamus corresponding with a hyperdense focus seen on recent CT.  No\nother focus of acute hemorrhage.  Severe changes of small vessel disease and\nbrain atrophy including severe medial temporal atrophy.  No significant\nabnormalities on MRA of the head."
        },
        {
            "input": "MRI HEAD and IAC:  There is no intra or extra-axial mass. Incidental note is\nmade of a partial empty sella. No acute intracranial hemorrhage. No evidence\nof acute infarct.\n\nThere is a 5 mm FLAIR hyperintense and enhancing focus adjacent to the\noccipital horn of the left lateral ventricle (series 22, image 13, series\n1038, image 90, series 6, image 17 and series 5, image 17)) which demonstrates\nassociated diffusion-weighted and ADC map hyperintense signal.  A small focus\nof FLAIR hyperintensity and enhancement is seen adjacent to posterior left\nlateral ventricle (22 and 24:15).\nThere is a punctate focus of very subtle diffusion-weighted hyperintense\nsignal of the left medial frontal lobe and an additional foci posterior to the\noccipital horn of the left lateral ventricle, without corresponding\nhypointense signal on ADC map, compatible with \"T2 shine through\" artifact.\nThere are a few left hemispheric predominant white matter periventricular\nT2/FLAIR punctate hyperintensities. Sulci, ventricles cisterns are within\nexpected limits for the patient's age. The major intracranial flow voids are\npreserved. The dural venous sinuses are patent. There is no evidence for\ncavernous sinus thrombosis.\n\nThere is no abnormal enhancement. The contents of the cerebellopontine angles,\nIAC including the ___ nerve complex, CN 3, 5 and 6 are unremarkable.  The\nvisualized optic nerves and orbital apex are unremarkable. No abnormal\nenhancement along the course of the seventh cranial nerve. The inner ear\nstructures are unremarkable.\n\nSmall mucous retention cyst in the right sphenoid sinus is noted. Mild mucosal\nthickening of the ethmoid air cells is also seen. Otherwise, the paranasal\nsinuses are clear. Under pneumatization of the left frontal sinus is\nincidentally noted. The mastoid air cells are clear. The orbits are\nunremarkable.\n\nMRV: No venous sinus thrombosis.",
            "output": "1. A few punctate foci of  FLAIR hyperintensity are seen predominantly in the\nperiventricular region with two of the foci showing enhancement and restricted\ndiffusion seen in one of the lesions.  The differential diagnosis includes\ndemyelinating disease with subacute infarcts considered less likely.\n2. No signal abnormalities, acute infarcts or enhancement within the brain\nstem\n3. Unremarkable examination of the cerebral pontine angle and IAC.\n4. The optic nerves and orbital apex are unremarkable. The orbits are\nunremarkable.\n5. No sinus venous thrombosis. No evidence of cavernous sinus thrombosis."
        },
        {
            "input": "MRA and MRV BRAIN: There is evidence of vascular flow in both internal carotid\narteries as well as the vertebrobasilar system, no flow stenotic lesions or\naneurysms larger than 3 mm in size are seen. The anterior, middle and\nposterior cerebral arteries are patent with no evidence of narrowing or\nstenosis. The basilar artery appears patent, with no evidence of flow stenotic\nlesions. Absent posterior communicating arteries bilaterally, a normal\nvariant. There is normal flow within the main venous sinuses. There is no\nevidence of venous sinus thrombosis.\nMRI BRAIN WITH CONTRAST: There is no acute infarct or intracerebral\nhemorrhage. 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. No diffusion abnormality is detected. No\nintracranial mass is identified. There is no pathologic parenchymal,\nleptomeningeal, or dural focus of enhancement after contrast administration.\nThe brainstem, posterior fossa and cervical medullary junction are preserved.\nThe orbits are normal. There is mild mucosal thickening in the left frontal\nsinus. The remaining paranasal sinuses are clear. No abnormality of the skull\nbase or calvaria is identified.",
            "output": "1. Normal brain MRA. .\n2. No evidence of cerebrovascular disease, venous sinus thrombosis, or\nposterior reversible encephalopathy syndrome."
        },
        {
            "input": "The left dural arteriovenous fistula is better demonstrated on the\nprior angiograms. This examination demonstrates intense, but decreased\ncompared to ___, cortical enhancement and engorged vessels, probably\nveins, within the left lateral temporal lobe. There is flow related\nenhancement within the engorged left vein of ___, compatible with retrograde\nflow, from the left sigmoid sinus at the site of the AVF. In addition, engored\nveins extend medially with deep drainage via left lateral ventricular\nsubependymal veins eventually into the straight sinus. Coil packs within\nexternal carotid branches are seen as tubular regions of suceptability. the\nremaining intracranial arteries show no evidence of flow limiting stenosis or\naneurysm. Edema within the left temporal lobe persists, but is not well\nevaluated without FLAIR or T2 sequences.",
            "output": "Left temporal dural AV fistula with venous engorgement, edema,\nand enhancement. This was a limited study for surgical planning. Enhancement\nhas decreased slightly compared to ___. Retrograde flow into an engorged\nleft vein ___ is demonstrated."
        },
        {
            "input": "The right parietal resection cavity is similar to prior with nodular, cortical\nenhancement that is unchanged compared to ___, but increased compared to\n___.  The presumed left medial high parietal convexity meningioma\n(rounded 12-mm extra-axial homogeneously enhancing dural-based mass) is\nsimilar to the prior, as is adjacent cortical and subcortical enhancement. \nRight temporal/parietal inner table calvarial enhancement (11:70) is similar\nto prior and remains suspicious.  Focal CSF intensity along the medial left\ntemporal lobe is similar to prior and may represent post-treatment changes or\nan arachnoid cyst.  Right greater than left hemispheric white matter FLAIR/T2\nhyperintensity, likely post-treatment changes, are also similar to prior.\n\nParanasal sinus mucosal reaction, most prominent in the left maxillary sinus,\nhas increased compared to prior.  The patient is status post bilateral lens\nsurgery.",
            "output": "1.  Nodular cortical enhancement in the right parietal operative bed is\nsimilar to the most recent examination of ___, but increased compared to\n___.  Continued followup is suggested.\n2.  Presumed left high parietal convexity meningioma with adjacent cortical\nenhancement, unchanged in appearance.\n3. Persitent inner table right temporal/parietal calvarial enhancement remains\nsuspicious for an agressive process. If warranted, thin slice CT with bone\nalgorhythm would further evaluate.  \n4. Other chronic post-treatment and post-surgical changes, similar to prior."
        },
        {
            "input": "MRI BRAIN WITHOUT AND WITH IV CONTRAST\n\nNo acute infarct, mass effect, shift of normally midline structures.\nOn the FLAIR sequence, a few small focal hyperintense foci are noted in the\nfrontal lobes on both sides, in the centrum semiovale, and in the posterior\nparietal/ occipital lobes series 7, image 13 nonspecific in appearance.\nNo abnormal enhancement is noted in these foci or elsewhere in the brain\nparenchyma or meninges.\n\nThe ventricles, the extra-axial CSF spaces and the sulci are unremarkable.\nThe left hippocampus is smaller compared to the right on some of the coronal\nimages.\nThis may relate to decrease in size or positional.\n\nThe major intracranial arterial flow voids are noted.\nThe venous sinuses are unremarkable.\nThe sella, pineal gland and the craniocervical junction regions are\nunremarkable.\n\nSmall retention cyst in the right maxillary sinus.\nMild ethmoidal mucosal thickening, with a small retention cyst with dense\ncontents on the left side. Mild frontal sinus mucosal thickening.\nThe sphenoid sinus septation inserts on the left carotid groove.\nVery minimal fluid noted in the mastoid air cells.\n\nMR ANGIO BRAIN\n\nThe major intracranial arteries of the anterior and the posterior circulation\nare patent, without focal flow-limiting stenosis, occlusion or aneurysm more\nthan 3 mm within the resolution of the study.\nPosterior communicating arteries are patent,  left prominent compared to the\nright.\nThe anterior inferior cerebellar arteries are not well seen likely diminutive.\nLeft vertebral artery is dominant.",
            "output": "MRI BRAIN:  No acute infarct or mass effect or abnormal enhancement.\n\nMRA BRAIN:  Patent major intracranial arteries, without focal flow-limiting\nstenosis, occlusion or aneurysm more than 3 mm within the resolution of the\nstudy.\n\nOther details as above.\nPL.  See MRA NECK study performed and reported separately."
        },
        {
            "input": "Images through the brain demonstrate  chronic infarcts in a watershed\ndistribution in the right parietal lobe and right frontal lobe which are new\nsince the MRI of ___.  Punctate areas of high signal on\ndiffusion images in the right parietal and frontal cortical region at the site\nof chronic infarct appear to be due to T2 shine through.  The previously seen\nacute infarct in the right frontal lobe has evolved.  There is no midline\nshift or hydrocephalus.  No enhancing brain lesion is identified.\n\nMRA of the head demonstrates stent assisted coiling of the right middle\ncerebral artery aneurysm seen on the previous study.  There is some residual\nfilling of the medial anterior and posterior aspect of the aneurysm (4:67) is\nvisualized.  No vascular occlusion or stenosis is seen.",
            "output": "1. Stent assisted coiling of the right MCA aneurysm with residual filling of\nthe medial aspect.  No vascular occlusion or stenosis.\n2. Right parietal and frontal watershed infarcts although new since the prior\nstudy appear late subacute to chronic."
        },
        {
            "input": "There is asymmetry and enlargement of the left temporal ventricular horn with\napparently a cystic formation within, additionally there is a enhancing nodule\nin the posterior aspect of this lesion of (image number 14, series 15), which\napparently is more conspicuous is the most recent examination and ___, there is no significant mass effect or midline shifting of the normally\nmidline structures. No other lesions or areas with abnormal enhancement are\nidentified. On the ASL sequence, there is no significant hyperperfusion.  .\n\nThe functional MRI of the brain demonstrate the expected activation areas in\nthe primary motor cortex during the movement of the hands, with no significant\nactivation adjacent to the enhancing lesion on the left temporal region.\n\nDuring the movement of the tongue there is activation adjacent to the left\ntemporal ventricular horn as demonstrated on the image 29, series 1606.\n\nThe language paradigms demonstrates the majority of the lesion on the left\nwith no significant activation adjacent to the mass lesion.\n\nThere tractography shows minimal deviation of the left inferior longitudinal\nfascicle.",
            "output": "Enlargement of the left temporal ventricular horn with a cystic lesion\nwithinnodular enhancement as described in detail above. There is no\nsignificant perfusion in this lesion. No diffusion abnormalities are detected.\nThe functional images demonstrate activation adjacent to the mass lesion\nduring the tongue as described above\n\nNOTIFICATION:  These findings were communicated Dr. ___ by Dr. ___ on\n___ at 11:30 hr"
        },
        {
            "input": "MRI head: The patient is status post left pterional craniotomy with resection\nof a predominately cystic temporal lobe mass.  Since the most immediate prior\nexam, there has been significant decrease in degree of left temporal horn\nexpansion, FLAIR hyperintense signal and enhancement within the surgical bed. \nThere is improvement in degree of dural thickening and enhancement overlying\nthe resection site.  However, there is apparent relative increased conspicuity\nof post contrast enhancement of the posterior aspect of the temporal horn\n(series 1200b, image 45), which maybe artifactual secondary to overall\ndecreased size of the temporal horn.  No new enhancing lesions are noted. \nInterval resolution of post operative pneumocephalus.\n\nThere is no acute infarct of new intracranial hemorrhage.  Sulci, ventricles\nand cisterns are with expected limits for the patient's age, allowing for post\nsurgical changes. 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.\n\nMRI perfusion:  There is no increased perfusion on ASL or dynamic\nsusceptibility sequences.\n\nMRI spectroscopy:  Background noise renders single voxel spectroscopy\nnondiagnostic.  On multivoxel spectroscopy there is overall decreased\nmetabolites, with increased choline to NAA on voxels 3, 9, 11, although these\nvoxels are peripheral to the region of increased enhancement and partially\ncentered over the Sylvian fissure and these values are susceptible to volume\naveraging errors.",
            "output": "1. There is near complete resolution of previously described left temporal\nhorn expansion.  There is apparent increased prominence in a region of\nperipheral enhancement of the posterior aspect of the temporal horn, although\nthis is felt to be artifactual from decrease in size of the temporal horn\nrather than recurrent or residual tumor.  Close attention to this region on\nfollowup exams is recommended.\n2. Otherwise, there is significantly decreased FLAIR hyperintense signal and\nenhancement (of the remainder of the resection site) when compared to prior\nexam.\n3. No new enhancing lesions are noted.  No acute hemorrhage or infarct.\n4. No increased perfusion on ASL or DSC.\n5. There is no clear evidence for increased choline to NAA ratio of the loft\ntemporal lobe."
        },
        {
            "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.  Incidental developmental venous anomaly seen in\nthe left parietal region.\n\nMR venogram 3 with gadolinium enhanced impeded images demonstrate no evidence\nof dural venous sinus thrombosis.  Superficial as well as the deep venous\nsystems are patent.",
            "output": "No significant abnormalities are seen on MRI of the brain with and without\ngadolinium.  Normal MRV of the head.  No evidence of dural venous sinus\nthrombosis."
        },
        {
            "input": "MRI head:  There is no evidence of hemorrhage, edema, masses, mass effect, or\ninfarction. The ventricles and sulci are normal in size and configuration.\n\nThere is left frontal sinus mucosal thickening. The orbits and skull base are\nunremarkable.\n\nMRA/MRV head: There is no aneurysm, pathologic large vessel occlusion, or\nvascular malformation within the intracranial arterial vasculature. The dural\nsinuses appear patent without evidence of dural venous sinus thrombosis or\nabnormal expansion.",
            "output": "1. No evidence of hemorrhage, mass effect, or infarction.\n2. No evidence of dural venous sinus thrombosis."
        },
        {
            "input": "MRI head: External electrodes and endotracheal tube are noted.  There is no\nintra or extra-axial mass, mass effect, acute infarct or major hemorrhage.\nThere is leptomeningeal nonenhancing FLAIR hyperintense signal, most prominent\nat the bilateral vertex.  Mild periventricular hyperintense signal is also\nnoted.\nSulci, ventricles and cisterns are within expected limits otherwise.\n\nThe major intracranial flow voids are preserved. The dural venous sinuses are\npatent.\nThe paranasal sinuses are clear. The orbits are unremarkable. Fluid signal in\nthe mastoid air cells is likely secondary to intubation.\n\nMRA head: The major intracranial arteries appear normal with no evidence of\nstenosis, occlusion, or aneurysm formation more than 3mm.  Left posterior\ncommunicating artery is well, seen right is faintly seen.",
            "output": "1. Nonenhancing leptomeningeal FLAIR hyperintense signal in the sulci most\npredominantly at the bilateral vertex, can be artifactual or real; if real,\ncan be  secondary to increased oxygenation from intubation, propofol,\ntoxic-metabolic causes, inflammatory/infectious, causes etc. Clinical\ncorrelation and correlation with laboratory values is recommended and followup\nas needed.\n2. Mild periventricular hyperintense signal; attention on followup as needed.\nRemainder of the MRI head is unremarkable otherwise.\n3. Unremarkable MRA head."
        },
        {
            "input": "There is an unchanged right frontal arteriovenous malformation. Prominent\ndilated veins are seen along the right frontal temporal region, consistent\nwith superficial drainage of the vascular malformation.  The arterial spin\nlabeled sequence is notable for increased perfusion in the most superior\naspect of vascular malformation, extending in the periventricular region\n(image 20, series 10).  The tractography color maps demonstrate mild deviation\ntowards the midline of the major corticospinal,  association and commissural\ntracts.\n\nThe functional MRI demonstrates BOLD activation areas during the movement of\nthe hands, feet and tongue.  Note is made of decreased BOLD signal in the\nright cerebral hemisphere, this finding is more obvious during the movement of\nthe left hand with shifting of the primary motor cortex activation medially\nand superiorly (images 71-81, series 1106).  During the tongue movement the\nmajority of the BOLD activity appears on the left cerebral hemisphere with\nareas of lower signal surrounding the vascular nidus on the right (image 67,\nseries 1109).\n\nThe language paradigm demonstrates the propagation of activation in the\nconvexity with the majority of the BOLD activity on the left cerebral\nhemisphere, likely related with dominance.",
            "output": "1. Unchanged right frontal arteriovenous malformation as described in detail\nabove, with increased perfusion in the superior aspect of the vascular nidus. \nThere is mild deviation towards the midline of the major corticospinal,\nassociation and commissural tracts.\n\n2. Decreased BOLD signal in the right cerebral hemisphere, this finding is\nmore obvious during the movement of the left hand, with shifting of the\nprimary motor cortex activation medially and superiorly.\n\n3. The language paradigm demonstrates the propagation of activation in the\nconvexity with the majority of the BOLD activity on the left cerebral\nhemisphere, likely related with dominance."
        },
        {
            "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\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.  Slight tortuosity of the anterior\ncommunicating artery is incidentally noted.",
            "output": "No significant abnormalities are seen on MRI of the brain with and without\ngadolinium. No significant abnormalities are seen on MRA of the head."
        },
        {
            "input": "Hyperintense, known to be enhancing lesion is again seen within the foramen of\nMagende measuring 9 x 8 x 15 mm which is unchanged when compared to prior when\nmeasured in similar ___.  There is no secondary hydrocephalus.  There\nis no other abnormal enhancement.",
            "output": "Unchanged enhancing lesion in the foramen of Magende as previously seen."
        },
        {
            "input": "MRI HEAD:\n\nImages are limited by motion artifact. There are normal vascular flow voids. \nThere is a punctate focus of possible slow diffusion within the inferior right\nfrontal cortex, versus artifact, (series 902, image 16). There is associated\nhigh signal on FLAIR images (series 11, image 13) which appears new from prior\nexam. This suggests an acute to subacute infarct. There is extensive\nsubcortical, deep and periventricular white matter T2/FLAIR signal\nhyperintensity, similar to prior exam, which is nonspecific though presumably\non the basis of sequelae of chronic small vessel ischemic disease. There is\ndiffuse brain parenchymal volume loss with associated prominence of the\nventricles and sulci.  There is no evidence for intracranial blood products.\n\nMRA HEAD:\n\nMRA images are degraded by motion artifact, limiting detection of small\naneurysm. There is no evidence of large aneurysm. Major intracranial arteries\ndemonstrate no evidence for occlusion. There is moderate narrowing of the mid\nand distal M1 segment of the left middle cerebral artery which appears\nunchanged from ___. There are fetal-type posterior cerebral arteries\nbilaterally.",
            "output": "1. Probable punctate acute or subacute infarct in the cortex of the inferior\nright frontal lobe.\n2. Extensive supratentorial white matter signal abnormalities are nonspecific\nbut likely sequela of chronic small vessel ischemic disease, similar to the ___ MRI.\n3. Unchanged narrowing of the mid/distal M1 segment of the left middle\ncerebral artery, presumably atherosclerotic."
        },
        {
            "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.  No focal parenchymal signal abnormality.  There is no\nmidline shift, abnormal extra-axial fluid collection,infarct, ormass.  The\nventricles and sulci are normal in caliber and configuration.\n\nMucous retention cysts noted in the maxillary sinuses.  Other paranasal\nsinuses and mastoids demonstrate no abnormal signal.",
            "output": "1. Normal MRI of the brain.  No focal parenchymal signal abnormality.\n2. Normal MRV of the brain."
        },
        {
            "input": "The major intracranial arteries appear normal with no evidence of stenosis,\nocclusion, or aneurysm formation. There is no evidence of hemorrhage, edema,\nmasses, mass effect, or infarction. The ventricles and sulci are normal in\ncaliber and configuration. There is no abnormal enhancement after contrast\nadministration.  The orbits are unremarkable. The major vascular flow voids\nare preserved.  There is a small mucous retention cyst in left maxillary\nsinus. The remaining paranasal sinuses and mastoid air cells are clear.",
            "output": "1. No acute infarction, hemorrhage, or enhancing mass lesion.\n\n2.  Unremarkable MRA of the head."
        },
        {
            "input": "Exam is limited secondary to motion. Within this limitation, the following\nobservations are made:  The pituitary gland is unremarkable and enhances\nhomogeneously. The infundibulum is in the midline.  Posterior pituitary T1\nbright spot is normal.\n\n The optic nerves and chiasm appear normal.  The cavernous sinuses are\nunremarkable and the cavernous ICA intravascular flow voids are preserved. \nThere is no parenchymal signal abnormality. There is no restricted diffusion.\n\nPostcontrast exam is extremely limited. No abnormal enhancement is noted.",
            "output": "No evidence of intracranial abnormality or pituitary abnormality within the\nlimitation of a motion degraded exam."
        },
        {
            "input": "ORBITS: There is mildly increased STIR hyperintense signal of the right\nretro-bulbar optic nerve, with associated fatty inflammatory stranding of the\norbital fat (series 13, image 9; series 11, image 9).  Associated enhancement\nof the right optic nerve and nerve sheath complex (series 13, image 8; series\n14, image 11) is noted.  Mild apparent inflammatory stranding of the\nright-sided palpebrae is identified.  Otherwise, the remainder the bony orbits\nand left preseptal soft tissues are unremarkable.  The globes appear intact. \nThe extraocular eye muscles are uniform in size and normal in signal. The\nlacrimal apparatus is unremarkable.  The left orbit is unremarkable.  There is\nno signal abnormality of the left optic nerve, bilateral canalicular,\ncisternal optic nerves or of the optic chiasm or optic tracts.\n\nOTHER FINDINGS: \n\nThere is no evidence of acute infarct or abnormal enhancing mass.   There are\nvery few scattered punctate periventricular and subcortical 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 within expected limits for the patient's age. The visualized intracranial\nflow voids are preserved. There is near complete opacification of the ethmoid\nair cells and of a left frontal sinus. Mild mucosal thickening of the\nmaxillary sinuses is noted.",
            "output": "1. Findings compatible with mild right optic neuritis and ___.  Mild\nright orbital fatty inflammatory stranding is noted.  Overall the findings are\ncompatible with given history of sarcoidosis.  Clinical correlation is\nrecommended.\n2. The left orbit, bilateral cisternal orbital nerves, optic chiasm and optic\ntracts are unremarkable.\n3. There is no evidence of intracranial abnormal enhancement.  No acute\ninfarct.\n4. Minimal periventricular and subcortical T2/FLAIR white matter\nhyperintensities are nonspecific, but compatible with chronic microangiopathy\nin a patient of this age.\n5. Paranasal sinus disease as described above.\n\nNOTIFICATION:  The findings were discussed with Dr. ___. by ___\n___, M.D. on the telephone on ___ at 9:03 am, 20 minutes after\ndiscovery of the findings."
        },
        {
            "input": "MRI BRAIN:\nThere is area of asymmetric enhancement involving right cavernous sinus,\nencircling carotid artery, slightly bowing into the sella, measuring 1 cm x 1\ncm by 0.5 cm.  No definite associated restricted diffusion.  Subtle\nenhancement extends into the very proximal superior orbital fissure. \nDifferential considerations include lymphoma, meningioma, inflammatory process\nincluding sarcoid, inflammatory pseudotumor.  Metastasis is less likely. \nInfection is unlikely.  Underlying clivus is normal, normal adjacent sphenoid\nsinus, without opacification.  No enhancement of the skullbase foramina,\npterygopalatine fossa to suggest perineural tumor.\nNo definite abnormality left cavernous sinus.\n\nThere is no evidence of hemorrhage, edema,parenchymal masses,mass\neffect,midline shift or infarction.   The ventricles and sulci are mildly\nprominent in caliber, likely reflecting involutional changes.  Periventricular\nand subcortical white matter FLAIR hyperintensities are likely due to moderate\nchronic small vessel disease.\nDegenerative changes in the cervical spine with probably moderate central\ncanal narrowing C3-C4 level, suggestion of central disc protrusion.\n\nMRI ORBITS: The bony orbits and preseptal soft tissues are normal. The globes\nare intact and normal in appearance. The optic nerves and complex are normal,\nwithout edema or abnormal enhancement. The extraocular muscles are uniform in\nsize and normal in signal. The lacrimal apparatus is normal. Retrobulbar soft\ntissues are normal.",
            "output": "1. Asymmetric enhancing soft tissue right cavernous sinus, in the region of\nthe expected course of the third cranial nerve, consider lymphoma, meningioma,\ninflammatory process including sarcoid, inflammatory pseudotumor, metastasis.\n2. Moderate chronic small vessel ischemic changes.\n3. Probably moderate central canal narrowing C3-C4 level, suggestion of\ncentral disc protrusion."
        },
        {
            "input": "There are multiple areas of restricted diffusion identified. A large area of\nrestricted diffusion is seen in the right parietal lobe with low ADC\nconsistent with an acute or early subacute infarct. Several other smaller\nareas of restricted diffusion are seen in the left frontal lobe both parietal\nlobes right occipital lobe and left temporal lobe which are too small to\ncharacterize on ADC. There likely represent subacute infarcts.\n\nThere are bilateral subdural collections identified. On the left side\npostoperative changes are seen with a small residual subdural approximately 5\nmm in the left frontal parietal occipital region. There is also a small 5 mm\nchronic subdural in the right frontal region. Subdural also extends to the\nposterior falx and right tentorium.  Accounting for differences in technique\ncompared to the prior CT dated there is no significant change in the size of\nsubdurals.\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.  The distal right vertebral artery is\nnot visualized which could be secondary to congenital variation or occlusion\nin the neck. This can be further evaluation with MRA of the neck if clinically\nindicated.",
            "output": "1. Multiple acute/ subacute infarcts are visualized in both cerebral\nhemispheres with largest lesion in the right parietal lobe.\n2. Bilateral small subacute /chronic subdural hematoma is identified which\nafter accounting for differences compared to prior CT have not changed but can\nbe further followed up with a CT scan if indicated.\n3. The MRA shows no significant abnormalities except for nonvisualization of\nthe right distal vertebral artery which could be a congenital variation but\nfurther evaluation could be obtained with MRI of the neck if clinically\nindicated."
        },
        {
            "input": "There is an unchanged left middle cerebral artery aneurysm, projected in the\nleft temporal region with avid enhancement (image 60, series 11).  The\narterial spin labeled sequence is notable for mild increased perfusion in this\narea (image 12, series 10). The tractography color maps demonstrate no\nsignificant deviation of the major corticospinal,  association and commissural\ntracts, the aneurysm appears inferior to the left inferior longitudinal\nfascicle.\n\nThe functional MRI during the movement of the left hand demonstrates the\nexpected activation area with no significant activity adjacent to the\naneurysm. The functional MRI demonstrates BOLD activation areas during the\nmovement of the hands, feet and tongue.  During the tongue movement the BOLD\nactivity appears in both cerebral hemispheres, with activation areas superior\nto the aneurysm on the left (image 23, series 23).\n\nThe language paradigm demonstrates the propagation of activation in the\nconvexity with the majority of the BOLD activity on the left cerebral\nhemisphere, likely related with dominance, with no significant areas of\nactivation adjacent to the aneurysm.",
            "output": "1. Unchanged left MCA aneurysm, with avid perfusion on ASL and no significant\ndeviation in the tractography maps.\n\n2.  The suspected activation areas of activity are demonstrated by functional\nMRI with BOLD activity superior to the aneurysm during the movement of the\ntongue."
        },
        {
            "input": "MRI HEAD: No evidence of intra or extra-axial mass, acute hemorrhage or\ninfarct. There is global cerebral volume loss. Sulci, ventricles and cisterns\nare prominent, however within expected limits for the degree of volume loss.\nThere is a single punctate gradient echo susceptibility focus of the left\ncoronal radiata (series 13, image 18) which may represent sequela of prior\nmicrohemorrhage. The major intracranial flow voids are preserved. Mild mucosal\nthickening of the paranasal sinuses is noted. Incidental note is made of\nbilateral lens replacements, otherwise orbits are unremarkable. The mastoid\nair cells are clear.\n\nHEAD MRA: The bilateral proximal A2 segments are slightly bulbous in\nappearance. Otherwise, normal flow related enhancement is seen in the\nintracranial internal carotid, middle cerebral and anterior cerebral arteries\nwithout significant mural irregularity or stenosis. There is normal symmetric\narborization of the MCA branches. There is no aneurysm greater than 3 mm. A\npatulous basilar tip is incidentally noted.  Normal flow related signal is\nseen in the right codominant intracranial vertebral arteries, the basilar\nartery, and the bilateral superior cerebellar and posterior cerebral arteries.\n\n.",
            "output": "No evidence of acute infarct.\nEssentially unremarkable MRA of the head."
        },
        {
            "input": "There is an unchanged hemorrhagic lesion centered in the lower aspect of the\nleft temporal lobe with tangle of vessels adjacent to this lesion, consistent\nwith hemorrhagic AVM, previously demonstrated by MRI, MRA and cerebral\nangiogram. On the ASL there is increase perfusion in the left temporal lobe\nAVM and on the left transverse sinus (image 7, series 9.\n\nThe functional MRI demonstrates the expected activation areas during the of\nmovement of the hands in the primary motor cortex, with no significant BOLD\nsignal or activation adjacent to the left temporal lobe AVM.\n\nThe functional MRI paradigm during the movement of the tongue shows areas of\nactivation bilaterally, slightly more significant on the right (image 54,\nseries 27), there is some motor BOLD activation anterior to the left temporal\nhematoma (image 32 conus series 27).\n\nThe language paradigm demonstrates bilateral BOLD activity, however the\nmajority of the activation appears on the left cerebral hemisphere, for\nexample image 55 series 20, with no significant activation adjacent to the\nleft temporal lobe AVM.\n\nThe tractography color maps shows minimal medial displacement of the left\ninferior longitudinal fasciculus.",
            "output": "1. Unchanged hemorrhagic lesion identified in the left temporal lobe,\nconsistent with hemorrhage AVM. There is avid perfusion in the vascular nidus\ndemonstrated by ASL technique.\n\n2. The functional paradigms demonstrates the expected activation areas during\nthe movement of the hands in the primary motor  cortex, with no significant\nareas of active lesion adjacent to the left temporal lobe AVM.\n\n3. The functional MRI paradigm during the movement of the tongue shows areas\nof activation bilaterally, slightly more significant on the right (image 54,\nseries 27), there is some motor BOLD activation anterior to the left temporal\nAVM/hematoma (image 32 conus series 27).\n\n4.  The language paradigm demonstrates bilateral BOLD activity, however the\nmajority of the activation appears on the left cerebral hemisphere, for\nexample image 55 series 20, with no significant activation adjacent to the\nleft temporal lobe AVM."
        },
        {
            "input": "A small amount of filling is seen at the base of the previously coiled basilar\ntip aneurysm, similar to prior imaging from prior angiography. Signal loss\nrelated to a stent is seen in the left posterior communicating artery. \nOtherwise, the major intracranial arteries appear normal with no evidence of\nstenosis, occlusion, or aneurysm formation.\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, or infarction.\nThe ventricles and sulci are mildly prominent, consistent with patient's age. \nSmall FLAIR hyperintensities are noted in the periventricular white matter,\nconsistent with small vessel ischemic disease.",
            "output": "Small amount of filling at the base the previously coiled basilar tip\naneurysm, unchanged from prior angiography images.  Otherwise normal\nvasculature."
        },
        {
            "input": "There is no acute infarct identified on diffusion weighted images.  Mild to\nmoderate brain atrophy and small vessel disease are seen.  There is no midline\nshift or hydrocephalus.  A partially empty sella is visualized.  Visualized\nparanasal sinuses are clear.\n\nMRA is limited by motion.  The distal vertebral arteries are not well\nvisualized but flow is visualized bilaterally.  Otherwise the MRA shows no\nevidence of vascular occlusion or stenosis or an obvious aneurysm within the\nlimitations.",
            "output": "No acute infarcts mass effect or hydrocephalus.  Motion limited shows flow\nwithin the arteries of the anterior and posterior circulation without obvious\nabnormalities with limited evaluation of distal vertebral arteries.  ."
        },
        {
            "input": "There is no evidence of acute hemorrhage or infarction.  The ventricles and\nsulci are prominent, suggestive of involutional change.  Extensive\nperiventricular FLAIR hyperintensities are nonspecific, likely sequela of\nchronic ischemic small vessel disease.  There appears to be mild dural\nthickening, which may represent sequela of prior lumbar puncture.\n\nNonspecific FLAIR hyperintense signal along the bilateral frontal parietal\nsulci (series 11, image 23) is identified without evidence of associated\nenhancement, potentially representing sequela of intubation and propofol.  No\nevidence of acute infarct.  No intracranial hemorrhage.  The sulci, ventricles\nand cisterns are within expected limits for the patient's age.  Confluent\nperiventricular and subcortical mild to moderate T2/FLAIR white matter\nhyperintensities are nonspecific, but commonly seen in setting chronic\nmicroangiopathy in a patient this age.\n\nThere is diffuse mucosal thickening involving the right maxillary sinus and\nethmoid air cells, with nonenhancing slightly central heterogeneous fluid.  No\nevidence of osseous erosion or dehiscence.  No evidence of periosteal abscess\nalong the right orbital wall.\n\nThere is a punctate focus of diffusion-weighted hyperintense signal at the\nroot entry zone of the right nerve (series 602, image 12).  The right\ntrigeminal nerve cisternal segment as well as V3 demonstrates postcontrast\nenhancement on MPRAGE (series 1501, image 79 and series 15, image 51) which\nextends into Meckel's cave.\n\nA T2 hyperintense fluid collection demonstrating peripheral enhancement\nmeasuring approximately 1.6 cm in maximal thickness (11:14) tracks along the\nright lateral calvarium, extending to the lateral right orbit, as seen on the\nprior CT.  There is bilateral preseptal periorbital stranding and edema.\n\nThere is mild enhancement and enlargement of the right superior rectus.  Right\nperineural right is (series 9, image 11) is identified.  The optic nerve\nitself appears spared.  There is subtle retro-bulbar and intraconal\ninflammatory stranding.  The orbital apex on the right appears grossly\npreserved.  There is questionable enlargement of the medial and inferior\nrectus muscle as well as T2 hyperintense signal.\n\nA lipoma overlying the left frontal calvarium is again seen.  The left orbit\nappears unremarkable.  A trace amount of fluid is within the left mastoid air\ncells.  The right mastoid air cells are clear.",
            "output": "1. Findings of right ___ as well as inflammatory stranding of the\nretro bulbar fat.  Thickening and enhancement of the right superior rectus\nmuscle with no involvement of the remainder the right extra-ocular eye\nmuscles.  The right orbital apex appears grossly intact.\n2. Punctate focus of diffusion-weighted hyperintense signal at the root entry\nzone of the right trigeminal nerve as well as abnormal enhancement of the\ncisternal trigeminal nerve and right V3 with extension into the Meckel's cave.\n3. No evidence of acute intracranial hemorrhage or infarct.\n4. Overall the findings may suggest herpes zoster given extensive trigeminal\nnerve involvement.\n5. No evidence of acute infarct or intracranial hemorrhage.  No definite\nabnormal postcontrast enhancement within the brain.\n6. Diffuse mucosal thickening of the right maxillary sinus extending into the\nnasal cavity and right ethmoid air cell without evidence of definitive osseous\ndestruction.  There is central hyperintense fluid, compatible with hemorrhage\nproduct and protein compatible with known history of recent surgery.\n7. Stable, peripherally enhancing fluid collection along the right lateral\ncalvarium.  Prominent bilateral preseptal periorbital edema.\n8. Additional findings as described above."
        },
        {
            "input": "In comparison with the prior MRA and CTA of the head dated ___,\nagain vascular flow voids are re- demonstrated in the left posterior cerebral\nartery and apparently more distal and in the left occipital lobe, with small\ntangle of vessels suggesting an underlying arteriovenous malformation.  The\narterial spin labeled sequence is notable for decreased perfusion in the right\ncerebral hemisphere.  The tractography color maps are grossly unremarkable,\nwith no significant deviation of the of the major corticospinal,  association\nand commissural tracts.\n\nThe functional MRI demonstrates the expected BOLD activation areas during the\nmovement of the hands, feet and tongue, with no significant areas of\nactivation adjacent to the left posterior cerebral artery and left occipital\nlobe.  The visual paradigms shows the expected activation areas in the primary\nvisual cortex with and activation anterior to the left posterior cerebral\nartery aneurysm or vascular dilatation as demonstrated on the image 17, series\n1302.  The distal aspect adjacent to the left transverse sinus and torcula\nappear unremarkable with no significant areas of BOLD activation.\n\nThe language paradigm demonstrates the propagation of activation in the\nconvexity with bilateral areas of activation, with no evidence of dominant\narea.",
            "output": "1.  In comparison with the prior examinations, no significant changes are\nvisualized in the left posterior cerebral artery aneurysm or vascular\ndilatation with increased angle vessels more distally in the left occipital\nlobe, suggestive of small  AVM.\n\n2.  The visual paradigm shows the expected activation areas in the primary\nvisual cortex, with BOLD  activation anterior to the left posterior cerebral\nartery aneurysm or vascular dilatation as demonstrated on the image 17, series\n1302.  The distal aspect adjacent to the left transverse sinus and torcula\nappear unremarkable with no significant areas of BOLD activation.\n\n3. The language paradigm demonstrates the propagation of activation in the\nconvexity with bilateral areas of activation, with no evidence of dominant\narea."
        },
        {
            "input": "The single FLAIR sequence is markedly limited by motion artifact. \nThis reveals prominence of the ventricles, cisterns and sulci for age with no\nevidence of large mass or midline shift.",
            "output": "Incomplete, nondiagnostic MRI of the brain.  The patient could\ntolerate only a single coronal FLAIR sequence which was markedly limited by\nmotion artifact.  Repeat examination with apprpriate sedation is suggested."
        },
        {
            "input": "MRI BRAIN:  When compared to prior examination of ___, prominent\nperiventricular, subcortical and deep white matter T2/FLAIR hyperintensities,\nmany of which correspond to T1 dark holes, is essentially unchanged in\nconfiguration from prior examination, although there appears to be a single\nnew nonenhancing FLAIR hyperintense lesion of the left orbital frontal lobe\n(series 4, image 14).\n\nThere is a 1-2 mm punctate enhancement of the right pre central sulcus (series\n102b, image 94) and supplemental motor area (series 102b, image 103), without\ncorresponding FLAIR abnormality, most compatible with vessel enhancement.\n\nThere is no intra or extra-axial mass, acute hemorrhage or infarct.  Sulci,\nventricles and cisterns are mildly prominent secondary to global cerebral\nvolume loss greater than would be expected for the patient's age, but\nunchanged from prior exam.  The major intracranial flow voids are preserved. \nMild mucosal thickening of the left maxillary sinus is identified.  The\nmastoid air cells are essentially clear.\n\nMRI ORBITS:  Unchanged from most recent CT sinus and head of ___, is a\npredominantly left intraconal T1 isointense to extra-ocular eye muscle, T2\nhyperintense essentially homogeneously enhancing 1.2 x 0.6 x 1.1 cm (AP, TRV,\nSI) mass which may represent a hemangioma, although the homogeneous\nenhancement does raise the possibility of a schwannoma.  The lesion is located\nbetween the medial and inferior rectus muscles, abutting the medial aspect of\nthe left globe without evidence of significant mass effect.\n\nThere is very mild asymmetric an nonenhancing STIR hyperintense signal of the\nleft orbital optic nerve (series 13, image 12).  The bony orbits and preseptal\nsoft tissues are normal. The globes are intact and normal in appearance. The\nright optic nerves and complex are normal, without edema or abnormal\nenhancement. The extraocular muscles are uniform in size and normal in signal.\nThe lacrimal apparatus is normal.",
            "output": "1. There is subtle asymmetric nonenhancing STIR hyperintense signal of the\nleft optic nerve (series 13, image 12).  Clinical correlation is recommended.\n2. Unchanged appearance of a predominantly left intraconal T1 isointense and\nT2 hyperintense homogeneously enhancing 1.2 cm lesion, likely representing a\ncavernous orbital hemangioma.  Differential consideration would include\nschwannoma.\n3. Essentially unchanged configuration and number of nonenhancing\nperiventricular, subcortical and deep white matter T2/FLAIR hyperintensities,\ncompatible with demyelinating plaques given the history of multiple sclerosis.\nThere may be interval development of a nonenhancing single left orbital\nfrontal lesion since examination of ___."
        },
        {
            "input": "MRI BRAIN:\nThere is 1.0 cm x 0.7 cm x 0.6 cm intracranial, extra-axial enhancing mass\nalong the right sphenoid bone, the exerting mild mass effect on the adjacent\nright posterior orbital gyrus and anterior inferior insula, with slight dural\ntail.  Findings most consistent with meningioma.  Tiny benign developmental\nvenous anomaly left vertex.\nThere is no evidence of hemorrhage, edema,scratched midline shift or\ninfarction.   The ventricles and sulci are normal in caliber and\nconfiguration.  There is no abnormal enhancement after contrast\nadministration.  There are severe confluent chronic small vessel ischemic\nchanges mild paranasal sinus mucosal thickening.  Clear mastoids.\n\nMRI ORBITS:\nThe bony orbits and preseptal soft tissues are normal. The globes are intact\nand normal in appearance. The optic nerves and complex are normal, without\nedema or abnormal enhancement. The extraocular muscles are uniform in size and\nnormal in signal. The lacrimal apparatus is normal. Retrobulbar soft tissues\nare normal.",
            "output": "1. Findings consistent with 1 cm right sphenoid wing meningioma.\n2. Severe chronic small vessel ischemic changes.\n3. Mild paranasal sinus disease."
        },
        {
            "input": "Images through the brain demonstrate normal ventricles and extra-axial spaces\nwithout midline shift mass effect hydrocephalus or focal abnormalities. \nPostcontrast images demonstrate no abnormal enhancement.\n\nImages through the internal auditory canals demonstrate an approximately 3 x 5\nmm left vestibular schwannoma within the lateral portion of the internal\nauditory canal which is unchanged compared to the previous MRI examination. \nNo definite enhancement of the cochlea seen.  The signal intensities of\ncochlea and vestibule on high-resolution T 2 images are symmetric and normal\nin appearance.",
            "output": "Unchanged appearance and size of left-sided vestibular schwannoma compared\nwith previous MRI examinations of ___ and ___."
        },
        {
            "input": "This study is limited by motion artifact. The intracranial internal carotid\nand vertebral arteries, and their major branches, are patent without evidence\nfor flow-limiting stenosis. There is a stable 2 mm laterally projecting\noutpouching at the junction of the left posterior cerebral artery with the\nleft posterior communicating artery, images ___ and 100:10. There is no\naneurysm at either the left or right posterior communicating artery origin.\nThe ___ MRA suspected a small aneurysm at the right posterior communicating\nartery origin based on the MIPS, but this is felt to be related to tortuosity\nof the internal carotid artery, as no aneurysm is seen on the source data. No\nnew aneurysm is seen.",
            "output": "Stable 2 mm aneurysm at the junction of the left posterior cerebral artery\nwith the left posterior communicating artery.  No evidence for a new aneurysm\non motion limited evaluation."
        },
        {
            "input": "Postcontrast images are limited by motion artifact.\n\nThere is a ventral epidural rim enhancing fluid collection extending from the\nbase of the dens superiorly along the posterior aspect of the clivus to the\nlevel of the pons, larger on the right than left. Its superior extent was not\nincluded on the ___ cervical spine MRI. Its inferior extent has\ndecreased in size since ___ with resolution of mass effect on the\nmedulla. This fluid collection demonstrates T2 hyperintensity and slow\ndiffusion, consistent with an abscess.\n\nIn addition, there is a 5 x 4 mm focus of enhancement within the right\nanterior cerebellar hemisphere with mild surrounding T2 hyperintensity, but no\ndiffusion abnormality. This may represent a septic embolus, or contrast\nenhancement related to a sterile subacute infarct which no longer demonstrates\nabnormal diffusion. Given the surrounding T2 signal abnormality, a capillary\ntelangiectasia is unlikely.\n\nThere is no evidence for intracranial blood products. Diffusion weighting\nimaging does not demonstrate evidence of acute infarct. There is nonspecific\nbihemispheric periventricular T2/FLAIR hyperintensity which may reflect\nchronic microvascular ischemic changes. Ventricular, cisternal, and sulcal\nprominence indicates parenchymal volume loss. The major intracranial vessels\nexhibit the expected signal void related to vascular flow.\n\nThe paranasal sinuses demonstrate scattered areas of mucosal thickening. There\nis fluid in some mastoid air cells bilaterally.",
            "output": "1. Ventral epidural abscess extending from the base of the dens superiorly\nalong the posterior aspect of the clivus to the level of the pons. Its\nsuperior extent was not imaged on the prior cervical spine MRI from ___. Its inferior extent has decreased with resolution of mass effect upon\nthe medulla. This collection is contiguous with the atlantoaxial joint, as\nseen previously. Please see concurrent cervical spine MRI report for findings\nrelated to the atlantoaxial joint.\n2. Small enhancing focus in the anterior right cerebellar hemisphere with mild\nsurrounding T2 hyperintensity. This may represent a septic embolus, or\ncontrast enhancement related to a sterile subacute infarct which no longer\ndemonstrates abnormal diffusion. Malignancy is not excluded. Given the\nsurrounding T2 signal abnormality, a capillary telangiectasia is unlikely.\nRecommend follow-up MRI in 2 weeks.\nThe findings were discussed by Dr. ___ with Dr. ___ telephone on\n___ at 11:34 AM."
        },
        {
            "input": "Postoperative changes are seen in the left suboccipital region with\nencephalomalacia in the left cerebellar hemisphere.  There is no residual\nparenchymal enhancement identified.  Previously seen subtle enhancement has\ndecreased.  There is FLAIR hyperintensity which is unchanged.  A filling\ndefect within the left sigmoid and distal transverse sinuses is again seen. \nHowever, this filling defect appears to have slightly decreased in size more\nmedially.\n\nSmall area of enhancement within the right internal canal indicative of a\nvestibular schwannoma is unchanged from the prior study.  No other areas of\nabnormal enhancement seen.  There are no acute infarcts identified.\n\nMRV of the head demonstrates normal flow in the superior sagittal sinus and\nright transverse sinus.  There is decreased flow within the left transverse\nsinus secondary to thrombus seen on the MP rage images..",
            "output": "1. Decrease of enhancement in the left cerebellar hemisphere with FLAIR\nhyperintensities in the left cerebellum.  No new areas of enhancement seen.\n2. Filling defect in the left transverse and sigmoid sinuses have slightly\ndecreased in size but there remains a thrombus within this region.\n3. Unchanged right vestibular schwannoma.\n4. No acute infarct or other areas of abnormal enhancement."
        },
        {
            "input": "MRI BRAIN:\n\nThere are multiple T2 hyperintense lesions in the subcortical, deep, and\nperiventricular white matter of the cerebral hemispheres, including callosal\nand pericallosal lesions, consistent with the known multiple sclerosis. \nSeveral lesions are new since ___, for example in the right frontal centrum\nsemiovale (13:18, 12:50), right genu of the corpus callosum (13:17, 12:53),\nleft frontal centrum semiovale (13:9, 12:77), left paracentral corona radiata\n(13:16, 12:81 and 13:17, 12:84).  These do not demonstrate contrast\nenhancement.  The larger of the two new left paracentral corona radiata\nlesions, image 13:16, demonstrates very high signal on the diffusion tracer\nsequence, 5:21, without low signal on the ADC map, which may indicate subacute\netiology.  No infratentorial lesions are seen.\n\nParenchymal volume is age-appropriate.  There is no acute infarction or\nenhancing intracranial mass.\n\nThere is mild mucosal thickening in the ethmoid, frontal, and maxillary\nsinuses.\n\nMRI ORBITS:\n\nThe left optic nerve is slightly larger than the left, best seen on coronal\nSTIR images, with contrast enhancement best seen on coronal postcontrast\nimages, series 15.  This is compatible with optic neuritis.  The right optic\nnerve appears unremarkable.  Extraocular movement muscles and globes are\nunremarkable.  There is no evidence for an intraorbital mass.  Cavernous\nsinuses appear unremarkable.",
            "output": "1. Supratentorial demyelinating disease with several new lesions compared to\n___.  No enhancing lesions. The larger of the two new left\nparacentral corona radiata lesions demonstrates very high signal on the\ndiffusion tracer sequence without low signal on the ADC map, which may\nindicate subacute etiology.\n2. Left optic neuritis."
        },
        {
            "input": "There is no evidence of intracranial hemorrhage, infarct, or mass. \nVentricles, cisterns, and sulci are age appropriate.  There is no abnormal\nintracranial enhancement.  There are fluid-fluid levels in the sphenoidal\nsinuses, opacification of a number of ethmoidal air cells, and of the right\ngreater than left mastoid air cells with T2 bright material.",
            "output": "No acute intracranial abnormality.  Paranasal sinus mucosal\nreaction with fluid-fluid levels in the sphenoidal sinuses and mastoid\nopacification.  This may be secondary to intubation."
        },
        {
            "input": "There isartifact from a pipeline embolization stent extending from the right\nparaclinoid internal carotid artery to the region of the right internal\ncarotid artery terminus. There is no evidence of abnormal flow-related\nenhancement surrounding the region of the stent. There is an aneurysm arising\nfrom the origin of the left ophthalmic artery which projects anteriorly and\nsuperiorly and measures 5 mm in maximal dimension.\n\nNo additional aneurysms are seen. There is no evidence of pathologic large\nvessel occlusion or hemodynamically significant stenosis within the\nintracranial vasculature.",
            "output": "1. Artifact from right internal carotid artery pipe line embolization stent\nwithout evidence of abnormal flow-related enhancement surrounding the stent.\n2. 5 mm aneurysm which projects anteriorly and superiorly arising from the\norigin of the left ophthalmic artery. Comparison with prior studies would be\nuseful in determining stability."
        },
        {
            "input": "MRA 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.",
            "output": "No significant abnormalities are seen on MRA of the head."
        },
        {
            "input": "Study is degraded by motion.\n\n.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 masses,mass effect, midline shift or infarction.  There is\nprominence of the ventricles and sulci suggestive of involutional changes. \nPeriventricular and subcortical T2 and FLAIR hyperintensities are noted which\nmay represent small vessel ischemic changes. There is no abnormal enhancement\nafter contrast administration.\n\n OTHER:\nLimiting the parotid glands demonstrate bilateral subcentimeter nonspecific\nprobable lymph nodes.\n\n Minimal nonspecific right mastoid fluid is seen.",
            "output": "1.  Study is degraded by motion.\n2. No evidence of IAC or cerebellopontine angle mass.\n3. Global volume loss and probable microangiopathic changes as described.\n4. No definite evidence of acute infarct.\n5. Minimal nonspecific right mastoid fluid."
        },
        {
            "input": "MRI BRAIN: There is no hemorrhage, edema, mass, mass effect, or infarct. The\nventricles and sulci are normal in size and configuration. The basal cisterns\nare patent. The paranasal sinuses and mastoid air cells are clear. The orbits\nand soft tissues are unremarkable.\n\nMRV BRAIN: There is normal flow in the main venous sinuses as well as the\ninternal cerebral veins and vein of ___.  No filling defect concerning for\nthrombosis is identified.  There is good visualization of the distal ICA's,\nvertebral and basilar arteries as well as the vessels of the circle of ___,\nand there is no gross evidence of flow stenotic lesions or aneurysms larger\nthan 3 mm in size are seen.",
            "output": "Normal brain MRI and MRV. No evidence of a venous sinus thrombosis."
        },
        {
            "input": "MR BRAIN:\nIncomplete and limited MRI of the brain demonstrates prominence of the\nventricles and sulci suggestive involutional changes.  Small bilateral\ncerebellar hemisphere chronic infarcts are noted.   No midline shift or large\ncompressive mass is identified, although limited examination given incomplete\nstudy.  There is no acute infarct.\n\nMRA brain:  This portion of the exam is limited due to motion however, there\nis stable appearance of the 4 mm anteriorly oriented outpouching off of the\nanterior communicating artery, series 3, image 96, as is seen on the prior\nCTA.  Minimal irregularity of the cavernous internal carotid arteries is seen,\nconsistent with atherosclerotic calcification.  There is markedly diminutive\nin size of the right A1 segment.  There is minimal irregularity in narrowing\nof the left PCA similar to prior CTA.  Otherwise, the intracranial vertebral\nand internal carotid arteries and their major branches appear normal without\nevidence of stenosis, occlusion, or additional aneurysm formation.",
            "output": "1. Limited and incomplete MRI of the brain with no contrast administered\nsecondary to patient claustrophobia.  No acute infarct or large compressive\nmass identified on the limited sequences.  A repeat completion MRI can be\nacquired if clinically indicated.\n2. 4 mm anterior communicating artery aneurysm again seen, better visualized\non the dedicated CTA of the head."
        },
        {
            "input": "Study is degraded by motion.\nMRI head: The study is slightly motion degraded. Within these confines:\n\nThere is no acute infarct, intra or extra-axial mass or hemorrhage. Sulci,\nventricles and cisterns are within expected limits for the patient's age. A\nleft paraclinoid ICA aneurysm, measuring approximately 1.2 x 0.9 cm (AP, TRV)\non axial T2 weighted sequences is enlarged when compared to prior examination\nof ___ even allowing for technical differences. This is better\nevaluated on CTA performed on ___.\n\nThere are mild periventricular and subcortical T2/FLAIR nonspecific white\nmatter hyperintensities, which are nonspecific, but may be seen in the setting\nof chronic microangiopathy.\n\nThere is a 1.5 x 1.0 x 1.5 cm (SI, AP, TRV) left occipital subcutaneous\nnodule, increased in size from prior exam of ___ likely representing a\nsebaceous cyst. Clinical correlation is recommended.\n\nThe paranasal sinuses are clear. The orbits are unremarkable. The mastoid air\ncells are clear.\n\nMRV: There is lack of flow related signal of the left transverse sinus which\nreconstitutes at the level of the sigmoid sinus and internal jugular vein.\nThis is felt to be secondary to slow flow as the left transverse sinus was\nwidely patent on CTA examination of ___ (see series 5 images 210-217\non prior CTA exam). The remainder of the dural venous sinuses are patent.",
            "output": "1. Study is degraded by motion.\n2. No acute infarct or hemorrhage.\n3. Interval enlargement of a left paraclinoid ICA aneurysm from prior exam of\n___. This is better evaluated on CTA performed on ___. \nNeurosurgery consultation recommended.\n4. Limited visualization of left transverse sinus on MRV, with reconstitution\nat sigmoid sinus, likely artifactual, as left transverse sinus is noted to be\nwidely patent on CTA examination from earlier in same day.\n5. Mild interval enlargement of a left occipital subcutaneous nodule\npresumably a sebaceous cyst. Clinical correlation is recommended.\n\nRECOMMENDATION(S):   RE 2:  Neurosurgery consultation recommended..\n RE 4:  Recommend clinical correlation.\n\nNOTIFICATION:   The findings were discussed by Dr. ___ with Dr. ___\n___ on the telephone on ___ at 11:00 AM, at the time of discovery of\nthe findings."
        },
        {
            "input": "ORBITS MRI:  Optic nerves, extraocular movement muscles, and superior\nophthalmic veins appear normal and symmetric.  No mass, inflammatory change,\nor other abnormalities seen within the orbits.  The left cavernous sinus is\nslightly expanded by the recently treated aneurysm of the cavernous left\ninternal carotid artery, as seen on the brain MRI from ___.  No other\nabnormality of the left cavernous sinus is seen.  The aneurysm is difficult to\nmeasure precisely on the images provided, but appears to measure 10 mm\ntransverse by 10 mm AP on the present exam and on the ___ brain MRI,\ncompared to 11 mm on the ___ CTA.\n\nBRAIN MRA:  There is evidence of a pipeline stent in the left cavernous and\nparaclinoid internal carotid artery, with low signal in the walls of the\nstent.  Flow is visualized within the stent.  Within the treated aneurysm of\nthe cavernous left internal carotid artery, there is a 4 x 3 mm focus of flow\nnear the aneurysm neck, image 3:50, with curvilinear extension on image 3:54,\nas well as more peripheral curvilinear focus of flow, image 3:51.\n\nAnterior and middle cerebral arteries appear widely patent.  Right internal\ncarotid artery appears widely patent.\n\nLeft vertebral artery is dominant.  Left V3 segment is again noted to follow\nan aberrant course, exiting the left T1 transverse foramen and coursing under\nthe left posterior arch of C1 prior to entering the dura, better seen on the\n___ CTA.  There is no flow-limiting stenosis in the posterior\ncirculation.\n\nNo new aneurysm is seen.",
            "output": "1. The pipeline stent in the cavernous and paraclinoid left internal carotid\nartery appears patent.\n2. 4 x 3 mm focus of flow in near the neck of the cavernous left internal\ncarotid artery aneurysm with adjacent curvilinear extension, as well as a\nseparate focus of curvilinear flow within the more peripheral portion of the\naneurysm.\n3. The left cavernous sinus remains slightly expanded by the aneurysm.\n4. Aberrant course of the V3 segment of the left vertebral artery is again\nnoted."
        },
        {
            "input": "A chronic infarct of the medial right cerebellar hemisphere is similar to\nprior.  There is no evidence of mass or acute hemorrhage or acute infarct. \nThere is mild hemosiderin adjacent to the encephalomalacia in the right\ncerebellar hemisphere.  Ventricles, cisterns and sulci otherwise show\nsymmetric, age-related prominence.  There are scattered FLAIR/T2\nhyperintensities within the cerebral white matter likely representing\nmicrovascular ischemic changes.",
            "output": "1.  No acute interval change.\n\n2.  Chronic infarct of the medial right cerebellar hemisphere.\n\n3.  Underlying microvascular changes."
        },
        {
            "input": "MRI BRAIN:  There is no hemorrhage, mass or infarct.  The ventricles, cisterns\nand sulci are age appropriate.  Chronic right mastoid effusion and mild\nparanasal sinus mucosal thickening is incidentally noted.  There is\nsusceptibility artifact from the coiling of the right internal carotid artery\nophthalmic segment aneurysm.  There is no abnormal enhancement within the\nbrain.\n\nMRA HEAD:  There is a thin region of linear enhancement within the neck of the\ncoiled right internal carotid artery ophthalmic segment aneurysm.\n\nThe approximately 3-mm aneurysm arising from the ventral paraclinoid portion\nof the left internal carotid artery, projecting inferomedially, is similar to\nthe prior examinations.\n\nThere are no new aneurysms and there is no significant stenosis of the\nintracranial arteries.",
            "output": "1.  Thin, linear filling adjacent to the coiled right internal carotid artery\nophthalmic segment aneurysm. Continued follow up recommended.\n2.  Unchanged appearance of the left paraclinoid internal carotid artery\naneurysm, 3 mm diameter."
        },
        {
            "input": "Large, enhancing extra-axial mass within the left frontal lobe, measures 7.3\ncm in maximal dimension, and is unchanged when compared to prior exam. Mass\nappears to arise from the dura of the greater wing of the sphenoid bone. There\nis unchanged severe mass effect with rightward midline shift and effacement of\nthe left lateral ventricle. The mass demonstrates heterogenous enhancement,\nmore greater inferiorly, where there is also associated increased profusion as\ndepicted on arterial spin labeled imaging.\n\nTractogrpahy demonstrates posterior displacement of the fibers of the cortical\nspinal tract and associated fibers.  The majority of the BOLD activation\nduring assessment of language function is within the left cerebral hemisphere;\nhowever, there is no significant activity identified adjacent to the mass\nlesion. Additionally, during evaluation hand, foot, and tongue activity, there\nis normal BOLD activation in expected locations although without activity\nadjacent to the lesion.",
            "output": "1.  Unchanged large extra-axial mass with heterogenous enhancement, increased\nperfusion, and mass effect within the left frontal lobe including posterior\ndeviation of the fibers of the corticospinal tract.\n2. The majority of BOLD activation during assessment of language function is\nseen within the left cerebral hemisphere; however, there is no significant\nactivity identified adjacent to the mass lesion."
        },
        {
            "input": "Status post coil embolization of ruptured left posterior\ncommunicating artery aneurysm. A 2-mm focus of flow-related enhancement along\nthe posterior medial aspect of the base of the coil pack is suspicious for a\nsmall amount of flow.  No new aneurysms are seen.  Major intracranial vessels\nare otherwise patent.\n\nThe brain is significant for extensive microvascular ischemic changes\nmanifested by T2/FLAIR hyperintensities within the cerebral white matter. \nThere is no evidence of interval hemorrhage or acute infarct or mass.  The\npatient is status post bilateral lens surgery.",
            "output": "1.  Status post coil embolization of ruptured left posterior communicating\nartery aneurysm.  A tiny focus of flow-related enhancement along the medial\naspect of the base of the coil pack is suspicious for a small amount of\nresidual or recanalized flow.\n2.  No evidence of new hemorrhage, acute infarct, or mass."
        },
        {
            "input": "BRAIN MRI:  There is no acute infarction, edema, mass effect, or evidence for\nintracranial blood products. Again seen are extensive 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.  Multiple prominent perivascular spaces are\nalso again seen in bilateral supratentorial white matter.  Moderate global\ncerebral atrophy with associated enlargement of the ventricles and sulci is\nagain noted.\n\nBRAIN MRA:  Flow is visualized within the intracranial internal carotid and\nvertebral arteries, and their major branches, without evidence of\nflow-limiting stenosis.  Amount of flow related enhancement within the\npreviously coiled aneurysm of the communicating segment of the left internal\ncarotid artery has increased on both the precontrast and post-contrast MRAs\ncompared to ___. No new aneurysm is seen.",
            "output": "Increased recanalization of the previously coiled aneurysm of the\ncommunicating segment of the left internal carotid artery.\nStable appearance of the brain.\n\nNOTIFICATION:  The impression above was entered by Dr. ___ on\n___ at 17:27 into the Department of Radiology critical communications\nsystem for direct communication to the referring provider."
        },
        {
            "input": "There is no hemorrhage, mass, or mass effect identified.  No abnormal\nparenchymal enhancement is identified. The ventricles are normal in size and\nshape. There is no shift of normally midline structures. Intracranial flow\nvoids are maintained. No diffusion abnormality is identified. No evidence of\nintra or extracranial fluid collection.\n\nNote is made of fluid within the left mastoid air cells as well as right\nmaxillary sinus with mucosal thickening, present on prior CT dated ___. The orbits are unremarkable.",
            "output": "Unchanged fluid within the left mastoid air cells as well as right maxillary\nsinus with mucosal thickening. No evidence of intra or extracranial\nhemorrhage."
        },
        {
            "input": "Postoperative changes are noted in the sphenoid sinus.  Again seen, is an\nenlarged sella containing an intrinsically T1 hyperintense cystic lesion. \nThere is no associated enhancement.  Overall size has not significantly\nchanged given differences in technique, with the lesion measuring 19 x 19 x 9\nmm (AP x transverse x CC), previously 18 x 18 x 8 mm.  There is some internal\nlow T2 signal intensity, likely internal debris.  There is no invasion of\nadjacent structures.  The pituitary stock is unchanged.  The suprasellar\ncistern and cavernous sinuses appear normal.\n\nLimited portions of the brain demonstrate a nonspecific T2/FLAIR\nhyperintensities in the right frontal lobe (series 6, image 16).  Ventricles\nare normal in size and configuration.  Intracranial flow voids are preserved. \nThere is mild mucosal thickening in the ethmoid air cells.",
            "output": "No significant change to cystic lesion located in an enlarged sella. \nIntrinsic T1 hyperintense signal within the cyst, represents proteinaceous\ndebris versus is blood product, and is also unchanged."
        },
        {
            "input": "MRA 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.",
            "output": "No significant abnormalities are seen on MRA of the head."
        },
        {
            "input": "Time-resolved 2D phase contrast images, including re-phased, phase, and\nmagnitude images were reviewed.  Images demonstrate normal biphasic, pulsatile\nCSF flow within the pre medullary, prepontine cisterns and anterior to the\ncervicomedullary junction and surrounding the upper cervical spinal cord. \nThere is normal biphasic pulsatile CSF flow within the foramina of ___,\nthird ventricle, cerebral aqueduct and fourth ventricle.  However, flow is not\nseen in the inferior fourth ventricle, nor in the retro-cerebellar CSF space\nand posterior to the cervical spinal cord at the level of the foramen magnum,\nlikely related to patient's known Chiari 1 malformation.\n\nThere is protrusion of the cerebellar tonsils through the foramen magnum, up\nto 17 mm on the right and 12 mm on the left with effacement of the CSF space\nsurrounding the cervicomedullary junction, compatible with Chiari 1\nmalformation.\n\nThere is no hydrocephalus.  Aside from effacement of the inferior fourth\nventricle, the ventricles and sulci are normal in caliber and configuration.\n\nThere is no evidence of infarction, hemorrhage, edema, mass, or mass effect.\n\nThere are prominent dilated perivascular spaces in the basal ganglia\nbilaterally.\n\nThere is pansinus mucosal thickening, worst in the maxillary sinuses.  There\nis evidence suggestive of prior endoscopic sinonasal surgery including defects\nin the medial maxillary sinus walls.  No air-fluid levels.  Mastoids appear\nclear.\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. No acute intracranial abnormality.\n2. Chiari 1 malformation.  No hydrocephalus.\n3. Apparent obstruction of CSF flow in the inferior fourth ventricle and the\nretro-cerebellar CSF space, as well as posterior to the spinal cord and\ncerebellar tonsils at the level of the foramen magnum.\n4. Pansinus mucosal thickening.\n5.  Please see separate report for details of findings from same-day MRI\ncervical spine."
        },
        {
            "input": "MRI brain:\n\nNo acute infarcts are seen.  There is no midline shift or hydrocephalus. \nPostsurgical changes are identified in the left temporal region.  Residual rim\nenhancement is identified in this region extending to the internal auditory\ncanal are after resection of the previously seen with vestibular schwannoma.\n\nWithin the left transverse sinus there is a filling defect identified on the\npost gadolinium MP rage images (23: 35-62).  There is also low signal on\nsusceptibility images.  The findings are suggestive of venous sinus\nthrombosis.  The thrombosis extends to thus torcula region.  The superior\nsagittal and right transverse sinuses are patent.\n\nMRV of the head:\n\nThe MRV demonstrates absence of flow signal within the left transverse sinus\nconsistent with thrombosis.\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.",
            "output": "1. Postoperative changes of vestibular schwannoma resection in the left\ntemporal region with the postoperative changes identified with fluid and air\nin the area.\n2. Acute left transverse sinus thrombosis extending to left jugular vein\nproximally within the visualized portions.\n3. No acute infarcts are seen."
        },
        {
            "input": "The images are significantly motion degraded. Increased T2/FLAIR signal and\nold hemorrhage in the left frontal lobe is consistent with an old left frontal\ninfarct, with encephalomalacia and ex vacuo dilation of the frontal horn of\nthe left lateral ventricle and Wallerian degeneration of the left pyramidal\ntract. No acute stroke, new hemorrhage, edema, or mass effect is seen. There\nis no abnormal enhancement after IV contrast administration. Periventricular,\nsubcortical, and deep white matter T2 FLAIR hyperintensities are consistent\nwith chronic small vessel ischemic disease.  The ventricles and sulci are\nprominent, suggestive of age-related involutional change.  Intracranial\nvascular flow voids are preserved.  On time-of-flight images, there is no\nflow-limiting stenosis, occlusion, dissection, or aneurysm greater than 3 mm.\n\nOn 3D reconstructed images, the carotid arteries appear normal.  There is\nmarked irregularity of the intracranial vessels both proximally and distally. \nThis appearance on a good quality MRA would represent severe atheromatous\ndisease. However, this exam is severely degraded by motion artifact, and could\nbe entirely secondary to motion alone.  Attenuation of the superior division\nof the left MCA does appear to be real, and could be a consequence of the\nprior stroke.",
            "output": "1. Exam limited by motion artifact. An old left frontal infarct is unchanged.\nNo pathologic focus of enhancement.\n2. Irregularity of the intracranial vessels, if seen on a good quality MRA,\ncould represent severe atheromatous disease. However, this exam is severely\ndegraded by motion, and thus this appearance could be entirely due to motion\nartifact.\n3. Attenuation of the superior division of the left MCA could be a consequence\nof the prior stroke."
        },
        {
            "input": "Scattered, punctate FLAIR/T2 hyperintensities within the cerebral\nwhite matter, non-enhancing are likely incidental.  There is no evidence of\nmass, hemorrhage or acute infarct.  The ventricles, cisterns and sulci are age\nappropriate.\n\nMRV HEAD:  The dural venous sinuses and major intracranial veins are patent. \nA partially empty sella is incidentally noted.",
            "output": "1.  No intracranial mass, hemorrhage or acute infarct.\n2.  No venous thrombosis."
        },
        {
            "input": "MRI BRAIN: There is no evidence of hemorrhage, edema, masses, mass effect,\nmidline shift orinfarction.  There is prominence of the ventricles and sulci\nsuggestive of age-related involutional changes.  Subcortical and\nperiventricular FLAIR signal hyperintensities are nonspecific, however likely\nrepresent sequela of chronic small vessel ischemic disease.  There is no\nabnormal enhancement after contrast administration.\n\nMRI ORBITS: Patient is status post bilateral lens replacement.  The bony\norbits and preseptal soft tissues are normal. The globes are intact and normal\nin appearance. The optic nerves and complex are normal, without edema or\nabnormal enhancement. The extraocular muscles are uniform in size and normal\nin signal. The lacrimal apparatus is normal. Retrobulbar soft tissues are\nnormal.",
            "output": "1. No findings to explain patient's symptoms.\n2. Atrophy and likely chronic small vessel ischemic disease."
        },
        {
            "input": "BRAIN MRI:  There is no abnormal parenchymal, leptomeningeal, or\npachymeningeal contrast enhancement.  There is no acute infarction, edema,\nmass effect, or evidence for blood products in the brain parenchyma.  There\nare multiple small chronic infarctions in the cerebellar hemispheres, more\nnumerous on the left. There are foci of high T2 signal in the subcortical,\ndeep, and periventricular white matter of the cerebral hemispheres, as well as\nin the pons, likely sequela of chronic small vessel ischemic disease in a\npatient of this age. There is age-related cerebral atrophy with associated\nprominence of the ventricles and sulci. Major arterial flow voids are grossly\npreserved. There is mild mucosal thickening in the ethmoidal air cells.\nEndotracheal and orogastric tubes are noted.\nBRAIN MRV:  Superior sagittal sinus, transverse sinuses, sigmoid sinuses, and\nupper internal jugular veins appear patent without evidence for thrombosis.\nLeft transverse sinus is hypoplastic, as seen on the conventional MR images,\nabnormal ovarian.  Flow in the straight sinus has lower signal intensity than\nflow in the other major dural venous sinuses, which may be related to its\nsmall size, as it appears patent on the postcontrast MP RAGE images.",
            "output": "1. No acute infarction and no evidence for intracranial malignancy.  No other\nseizure source is identified.\n2. Multiple small bilateral cerebellar infarcts. Supratentorial white matter\nsignal abnormalities are likely sequela of chronic small vessel ischemic\ndisease, given the patient's age.\n3. No evidence for major dural venous sinus thrombosis."
        },
        {
            "input": "MRI HEAD:\n\nThere is no evidence of acute infarct based on diffusion-weighted imaging.\nThere is no evidence for intracranial blood products. There are numerous small\nfoci of T2/FLAIR signal hyperintensity throughout the periventricular and\nsubcortical white matter with additional involvement of the central pons,\nwhich are unchanged, nonspecific but most likely sequelae of chronic small\nvessel ischemic disease. There are multiple prominent perivascular spaces\nwithin the basal ganglia.  There is a small chronic right occipital cortical\ninfarct with associated focal volume loss, as seen previously.  There is\nmoderate age-related global parenchymal volume loss.\n\nMRA HEAD:\n\nThere is no evidence of aneurysm flow-limiting stenosis within the\nintracranial vasculature.",
            "output": "1. No evidence of acute infarct or other acute intracranial abnormalities.\n2. Small chronic right occipital infarct is again seen. Supratentorial white\nmatter signal abnormalities, grossly unchanged, nonspecific but likely sequela\nof chronic small vessel ischemic disease.\n3. No evidence of aneurysm or flow-limiting stenosis within the intracranial\nvasculature."
        },
        {
            "input": "Limited examination due to patient motion, within this limitation, there is\nevidence of slow diffusion involving the left occipital lobe, vascular\nterritory of the left posterior cerebral artery, areas of high-signal\nintensity in the left suboccipital lobe are also visible on T2 and FLAIR\nsequences suggesting a subacute ischemic event, after contrast administration,\nthere is gyriform pattern of enhancement in the left occipital lobe (series\n10, images 10 through 15).  No other areas of abnormal enhancement are\nvisualized throughout the brain or orbits.  Within the limits of this exam,\nthere is no evidence of hemorrhagic transformation, subcortical and\nperiventricular areas of high-signal intensity are demonstrated on FLAIR and\nT2 weighted images, which are nonspecific and may reflect changes due to\nchronic small vessel disease, similar findings are also visible in the pons. \nThe ventricles and sulci are prominent suggesting cortical volume loss, except\nfor mild effacement of the sulci in the left occipital lobe related with\nacute/subacute ischemic changes.  The major vascular flow voids are present\nand demonstrate normal distribution.\nThe orbits demonstrate bilateral lens replacement, otherwise are unremarkable.\nWithin the limits of this examination, there is no evidence of orbital\nretrobulbar lesions or evidence of intra or extraconal orbital lesions.  There\nis mild mucosal thickening in the ethmoidal air cells, no air-fluid levels are\nseen, the maxillary sinuses are clear, the middle ear cavities and mastoid air\ncells are normally pneumatized.",
            "output": "1.  Areas of slow diffusion are visualized in the left occipital lobe, which\nare also visible on T2 and FLAIR sequences, consistent with acute/subacute\nischemic changes.\n\n2.  Gyriform pattern of enhancement is identified in the left occipital lobe,\nwithin the limits of this examination, grossly there is no evidence of\nhemorrhagic transformation.\n\n3.  Limited views of the orbits are unremarkable, with no evidence of abnormal\nenhancement throughout the orbits.\n\n4.  T2/FLAIR subcortical and periventricular areas of high-signal intensity \nare nonspecific and may reflect changes due to chronic small vessel disease.\n\nNOTIFICATION:  These findings were communicated via phone call to ___\nMD, by ___ MD, at 16:00 hours on ___, 5 minutes after\ndiscovery of the findings.  Per Dr. ___ patient needs to return to the\nemergency room for further evaluation related with acute/subacute ischemic\nchanges in the left occipital lobe."
        },
        {
            "input": "MRI brain: No acute infarct or intracranial hemorrhage is identified. There is\nno mass effect, mass, or midline shift. No abnormal enhancement is\nappreciated. Ventricles are normal in size and configuration. The ventricles\nare midline. Cisterns are patent. No regions of abnormal signal intensity\nareas seen within the brain parenchyma. The paranasal sinuses demonstrate\nscattered areas of mucosal thickening with moderate sinus disease in the left\nfrontal and left sphenoid sinuses as well as obstruction of the\nfrontoethmoidal recesses bilaterally. Incidentally noted is a T1 hyperintense\n0.8 AP x 1.6 TV x 2.1 cm size cm lesion within the left parotid gland.\n\nMRI orbits:  The globes and extraocular muscles are normal bilaterally. The\nintraconal fat is preserved. There is no abnormal enhancement or enhanced mass\nin the orbits. The optic chiasm, nerves and tracts have size and signal\nintensity without abnormal enhancement. There is no extrinsic mass compressing\nthe optic chiasm or optic nerves. The cavernous sinuses appear unremarkable as\nimaged, with less apparent soft tissue in the left cavernous sinus which was\npreviously described. The interpeduncular fossa and superior orbital fissures\nare unremarkable.  The included portions of the intracranial compartment\nappear unremarkable as visualized.",
            "output": "1. Paranasal sinus disease as detailed above.\n2. Left parotid gland 2.1 cm cyst, which may be a manifestation of the\npatient's known HIV.\n3. Otherwise unremarkable MRI of the brain and orbits, without abnormal\nenhancement."
        },
        {
            "input": "There is enlargement and abnormal enhancement involving the inferior orbital\nnerve along its visualized course along the left orbital floor posteriorly to\nthe pterygopalatine fossa.  There is abnormal enlargement of the foramen\nrotundum on the left when compared to the right (07:20).  Enhancement is less\nobvious given artifact from adjacent sphenoid sinus, regardless, the finding\nis worrisome for perineural tumor extension.  Evaluation for interval changes\nalso difficult given lack of high-resolution on the prior exam.\n\nIn addition, there is abnormal enhancement and enlargement of the mandibular\ndivision of the trigeminal nerve at the level of the foramen ovale.  Abnormal\nenhancement is also seen to involve Meckel's cave on the left (12:5). \nFindings are worrisome for all perineural tumor spread.  There is no apparent\ninvolvement of the cisternal portion of the trigeminal nerve.\n\nIn addition, there is a T2 hyperintense enhancing nodule overlying the left\nmasseter (11:2 and 13:15) which measures 1.1 x 0.8 cm which was not clearly\npresent on most recent prior exam.  There had however been abnormal enhancing\ntissue in this region on older prior exams including exam from ___. \nIn addition, linear enhancement is seen along the course of the left facial\nnerve at its intra parotid course suspicious for perineural tumor spread.\n\nScattered subcortical and periventricular FLAIR hyperintense foci in the\nsubcortical white matter are visualized without associated enhancement.  These\nare nonspecific, commonly due to chronic small vessel disease.  Scattered\nopacified mastoid air cells are noted.",
            "output": "1. Evidence of perineural tumor spread along the left infraorbital nerve,\nextending in a retrograde fashion along the second division of the trigeminal\nnerve to the level of Meckel's cave.\n2. Additional involvement of the third division of the left trigeminal nerve\nfrom Meckel's cave through foramen ovale.\n3. Abnormal enhancement overlying the left masseter, new since prior and not\nas extensive as on previous exams from ___.  Linear enhancement\nextending back along the course of the left facial nerve also worrisome for\nperineural tumor spread."
        },
        {
            "input": "MRI BRAIN: Re-identified is diffuse asymmetric enlargement of the V3 division\nof the trigeminal nerve at the level of foramen ovale with extension\nproximally to Meckel's cave with extension distally, no longer well seen as\nthe nerve reaches the level of the pterygoid musculature.  There is no\ndefinite involvement more proximally to the cisternal segment of the\ntrigeminal nerve.  This is increased as compared to the prior study (13:21,\nsee 13:24 on the ___ examination) and Meckel's cave involvement was\nnot seen on prior examination.\n\nThere is also asymmetric enlargement of left foramen rotundum with prominent\nasymmetric enlargement and enhancement along the course of the left\ninfraorbital nerve, which has increased as compared to the prior study (13:9).\n\nEnhancing nodule overlying the left masseter measuring roughly 13 x 8 mm is\nslightly increased as compared to the prior study (1500:38), with a linear\ncomponent extending superiorly and posteriorly along the surface of the\nmasseter along the expected course of the facial nerve.  The interval increase\nin size is most notable on the coronal orbit images (13:16, 8:16, see 13:16 on\nthe ___ examination).  These areas of enhancement demonstrate slowed\ndiffusion.\n\nNo new enhancing lesion is seen.\n\nThere is no evidence of hemorrhage, edema,other masses,mass effect,midline\nshift or infarction.   There is mild prominence of the ventricles and sulci\nsuggestive of involutional change.  Scattered areas of periventricular and\nsubcortical white matter T2/FLAIR hyperintensities are unchanged, likely\nreflecting the sequela of chronic small vessel ischemic disease.  The\nprincipal intracranial vascular flow voids are preserved.  There is minimal\nfluid signal within the bilateral mastoid air cells.  There is trace mucosal\nwall thickening in the bilateral ethmoid air cells.  The remainder of the\nvisualized paranasal sinuses are grossly clear.\n\nMRI ORBITS: The bony orbits and preseptal soft tissues are preserved.  The\nglobes are intact and normal in appearance. The optic nerves and complex are\nnormal, without edema or abnormal enhancement. The extraocular muscles are\nuniform in size and normal in signal. The lacrimal apparatus is normal.\nRetrobulbar soft tissues are otherwise unremarkable.",
            "output": "1. Interval increase in degree of asymmetric expansion and enhancement along\nthe course of the left infraorbital nerve, V3 division of the left trigeminal\nnerve, as well as nodular and linear enhancing lesion overlying the left\nmasseter along the expected course of the left facial nerve, as described in\ndetail above, all consistent with increasing perineural tumor spread.  There\nis new involvement of the left Meckel's cave, not seen on prior examination. \nAs described above, no evidence of extension into the trigeminal cisternal\nsegment.\n2. No new enhancing mass.\n3. Otherwise no acute intracranial abnormality including hemorrhage, infarct,\nor other enhancing lesion.\n4. Otherwise unremarkable MR examination of the orbits."
        },
        {
            "input": "MR HEAD:\n\nLeptomeningeal slow diffusion, high signal on T2/FLAIR images, and contrast\nenhancement within overlying the bilateral superior temporal gyri and left\noccipital lobe appear similar to the ___ MR head.\n\nThere is a focus of enhancement within the fundus of the left IAC.  Given the\nsuspected enlargement of the tympanic segment of the left facial nerve, this\nmay reflect perineural spread rather than an additional site of leptomeningeal\ndisease.  There is no abnormal enhancement of the cisternal segment of the\nleft seventh and eighth nerve complex or definite abnormal enhancement within\nthe membranous labyrinth.\n\nThere is abnormal enhancement within the left Meckel's cave and marked\nthickening of the V2 and V3 segments of the left trigeminal nerve.  The left\nV2 segment appears significantly worse from ___.  The degree of\nperineural spread on the left V2 and V3 segments is extensive and appears\nsignificantly worse from ___.  There is additional perineural\nspread in the left vidian nerve.  Possible perineural spread on the left V1 is\ndifficult to exclude due to the degree of motion artifact.\n\nThere is likely an old infarct within the uncus of the right temporal lobe\n(series 8, image 12).  Small foci of hyperintense signal on T2/FLAIR within\nthe subcortical and periventricular white matter could reflect the sequela of\nmild chronic small vessel disease and/or treatment related change.\nThere is no acute infarct, mass effect, or hydrocephalus.\n\nMR ORBITS:\nThe degree of perineural spread associated with the V2 segment of the left\ntrigeminal nerve appears significantly worse.  Possible perineural spread on\nleft V1 is difficult to exclude due to degree of motion artifact.\n\nThere is significant interval enlargement, likely of buccal branches of the\nleft facial nerve, consistent with additional perineural spread.  The left\nparotid duct appears normal.\n\nThe globes and optic nerves appear normal in signal intensity.  The optic\nchiasm appears normal.  The extraocular muscles and lacrimal glands appear\nsymmetric.  There is no evidence for a mass or abnormal enhancement within the\nnasolacrimal ducts.",
            "output": "1. Extensive perineural spread on the V2 and V3 segments of the left\ntrigeminal nerve, and left facial nerve with significant interval progression\nfrom the ___ MRI.  Abnormal enhancement within the fundus of the\nleft IAC most likely reflects facial cisternal perineural spread, given the\nprobable signal abnormality and expansion of the labyrinthine segment,\ngeniculate ganglion, and tympanic segment.  Possible perineural spread on the\nleft V1 segment is difficult to exclude due to the degree of motion artifact.\n2. No evidence for nasolacrimal duct or lacrimal mass.  No evidence for\nparanasal sinus mass.\n3. Stable appearance of the known intracranial neoplastic leptomeningeal\ndisease burden from ___."
        },
        {
            "input": "There remains thickening of the left inferior orbital nerve and the\nsurrounding soft tissues anterior to the medial aspect of the left orbit.  The\ncavernous sinuses remain symmetric.  There is no intraconal or extraconal mass\nlesion identified otherwise.  The infratemporal fossa appears symmetric in\nappearance.  The pituitary gland and suprasellar region are unremarkable. \nMucosal thickening is identified in the maxillary sinuses slightly increased\nfrom the prior study.",
            "output": "Unchanged appearance of the left inferior orbital nerve which appears\nthickened compared to the right side with subtle soft tissue changes in the\nmedial aspect of the left orbit.  No significant new abnormalities are seen."
        },
        {
            "input": "Again noted is a enhancing 8 mm ill-defined focus of the left medial temporal\nlobe (series 12, image 15).  No additional lesions are noted.\n\nThe globes and optic nerves are unremarkable. The extraocular muscles and\nintraorbital fat are also unremarkable. The optic chiasm demonstrates normal\nsignal.  There is no mass or mass effect on the optic chiasm. The infundibulum\nis midline. The pituitary gland is unremarkable.",
            "output": "1. The orbits, optic nerves and chiasm are unremarkable. The pituitary gland\nand infundibulum are also unremarkable.\n2. Unchanged size of a nonspecific and ill-defined 8 mm enhancing focus of the\nleft medial temporal lobe. Followup with MRI with and without contrast is\nadvised to document stability or resolution of this lesion."
        },
        {
            "input": "Stable bithalamic abnormalities, left greater than right without significant\nenhancement.  Ventricles are prominent but unchanged. There presumed chronic\nsmall vessel ischemic changes in the white matter.  No significant enhancement\nis noted.\n\n\n\nMR Perfusion:  No convincing increased perfusion.\n\n\n\nMRS:   Increase choline decrease NAA compatible with neoplasm.\n\n\n\nIntracranial flow voids are maintained. Visualized paranasal sinuses and\nmastoid air cells are clear.",
            "output": "Stable bialamic abnormalities."
        },
        {
            "input": "There is mild persistent filling at the base of the previously coiled left\nsupraclinoid/para clinoid ICA aneurysm. Mild dilation of the right\nsupraclinoid ICA is unchanged. No additional lesions are seen.",
            "output": "Stable minimal residual filling at the base of the previously coiled left\nsupraclinoid ICA aneurysm.  Bulbous appearance to the right supraclinoid ICA\nis unchanged."
        },
        {
            "input": "Evaluation the intracranial vascular demonstrates unchanged coiled left\nsupraclinoid internal carotid artery aneurysm with minimal residual filling.\nBulbous appearance of right supraclinoid ICA aneurysm is unchanged. No other\naneurysm or vascular malformation were hemodynamically significant stenosis\nwithin the vasculature of the neck.\n\nEnhancing foci are seen within the left frontal and temporal lobe in\nassociation with marked T2 and diffusion signal abnormality seen on most\nrecent outside facility MRI dated ___.  Compared to the MRA from ___, these are less prominent. Overall findings concerning for\ninflammatory process favoring etiologies such as acute disseminating\nencephalomyelitis (ADEM) or vasculitis, less likely neoplasm.\n\nOrbits and paranasal sinuses are unremarkable.",
            "output": "1.  Enhancing foci within left frontal and temporal lobe in association with\nmarked T2 signal abnormality seen on most recent outside facility MRI --\noverall findings concerning for inflammatory process such as acute\ndisseminating encephalomyelitis (ADEM), or vasculitis as described above.\n2.  Unchanged appearance of coiled left supraclinoid internal carotid artery\naneurysm with minimal residual filling."
        },
        {
            "input": "There has been interval improvement in previously noted left frontal and\ntemporal lobe enhancing T2/FLAIR hyperintense lesions.  On today's study,\nthere is only residual abnormal T2/FLAIR signal and minimal enhancement noted\nin the previously seen left temporal lobe lesion. There are no new regions of\nabnormal signal or enhancement\n\nThere is no evidence of infarction, hemorrhage, abnormal 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. The orbits are unremarkable, the paranasal\nsinuses and mastoid air cells are clear\n\nMRA:  There is an unchanged coiled left supraclinoid internal carotid artery\naneurysm noted. There is aright again noted to be minimal residual filling in\nthe base of the aneurysm. This is unchanged. There is no other aneurysm or\nvascular malformation noted.",
            "output": "1.  Interval improvement in previously seen left frontal and temporal lobe\nenhancing lesions. Only minimal signal abnormality and enhancement noted in\nleft temporal lobe. No new lesions are seen. The differential diagnosis for\nthis process includes a demyelinating process such as ADEM versus vasculitis.\n\n2.  Status post left supraclinoid aneurysm coiling. There is unchanged minimal\nresidual filling noted at the base of the aneurysm"
        },
        {
            "input": "There is no evidence of hemorrhage, edema, masses, mass effect, or acute\ninfarct. There are foci of FLAIR hyperintensity in the left temporal lobe and\nleft frontal cortex with resolution of previously seen enhancement in the left\ntemporal region. These foci could be related to areas of ischemia. There is no\nabnormal parenchymal vascular or meningeal enhancement seen following contrast\nadministration.\n\nMRA of the head shows extent assisted embolization of the left supraclinoid\ncarotid aneurysm. There is no residual filling of the aneurysm identified.\nThere is flow signal identified within the stent which extends from the\ncavernous sinus to the subsequent r region. Flow signal is normally maintained\nwithin both middle cerebral arteries and the main arteries of the anterior and\nposterior circulation. No vascular occlusion seen.",
            "output": "No evidence of residual filling of the stent assisted coiling of the left\nsupraclinoid carotid aneurysm. Flow signal is seen within the stent.  No\nvascular occlusion.\nFoci of marrow abnormalities in the left temporal lobe and left frontal cortex\ncould be related to prior infarcts.  They are better visualized on the current\nstudy likely related to evolution."
        },
        {
            "input": "Again post embolization changes seen in the right posterior communicating\nartery region. There is no residual aneurysm filling identified. Minimal\nnarrowing of the right supraclinoid internal carotid arteries again seen.\nThere is no vascular occlusion or significant stenosis seen in the arteries of\nthe anterior or posterior circulation.  No other definite aneurysms greater\nthan 3 mm in size identified.",
            "output": "There is no evidence of recanalization of previously coiled right posterior\ncommunicating artery aneurysm."
        },
        {
            "input": "Please note the study is in degraded by motion.\n\nMRI:  A 1.4 x 0.7 cm (11:19) nonenhancing heterogeneously T2 hyperintense\nlesion with peripheral rim of T2 hypointensity,  T1 hyperintense component\ncentrally is seen along the posterior falx which demonstrates GRE\nsusceptibility (11:19; 06:19; 10:19) most consistent with falx ossification. \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. On T2 weighted imaging the\nmajor intracranial vascular flow voids are preserved.  No abnormal areas of\nrestricted diffusion.\n\nMRV:  No evidence of dural sinus venous thrombosis.  A dominant right\ntransverse and sigmoid sinuses noted.",
            "output": "1.  Study is mildly degraded by motion.\n2. No acute intracranial abnormality.\n3. No evidence of venous sinus thrombosis.\n4. 1.4 cm posterior falx ossification, which can be a normal variant, but can\nalso be seen in setting of hyperthyroidism or chronic renal failure. \nRecommend clinical correlation.\n\nRECOMMENDATION(S):  1.4 cm posterior falx ossification, which can be a normal\nvariant, but can also be seen in setting of hyperthyroidism or chronic renal\nfailure.  Recommend clinical correlation."
        },
        {
            "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.\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.  No abnormal vascular structures are\nidentified.",
            "output": "No significant abnormalities are seen on MRI of the brain without gadolinium.\nNo significant abnormalities are seen on MRA of the head."
        },
        {
            "input": "The small protuberance seen at the junction of P1 and P2 segment on the left\non previous CT angiography is at the site where posterior communicating artery\nmeets the posterior cerebral artery and is consistent with an infundibulum\n(3:88).  This is also better visualized on the reformatted images (10: ___.\n\nNo vascular occlusion or stenosis seen.  No other aneurysms are identified.",
            "output": "The small protuberance at the P1 and P2 junction on the left seen previously\nis confirmed to be an infundibulum as it is at the site of PCOM meeting the\nposterior cerebral artery.  No discrete aneurysm is identified."
        },
        {
            "input": "Study is moderately degraded by motion.  Within these confines:\n\n  MRI BRAIN:\nThere is no evidence of hemorrhage, edema, mass effect,midline shift or\ninfarction.   There is prominence of the ventricles and sulci suggestive of\ninvolutional changes.  Periventricular and subcortical T2 and FLAIR\nhyperintensities are noted which may represent small vessel ischemic changes. \nThickening of the pituitary stalk up to approximately 5 mm is grossly\nunchanged compared to ___ prior exam (see 17:76 on current study\nand 9:82 on ___ prior exam).  There is no definite new abnormal\nenhancement after contrast administration.\n\nMRI ORBITS:\nThe bony orbits and preseptal soft tissues are grossly preserved.  The globes\nare intact and grossly preserved in appearance. The optic nerves and complex\nare grossly preserved, without edema or abnormal enhancement. The extraocular\nmuscles are grossly uniform in size and preserved in signal. The lacrimal\napparatus is grossly preserved. Retrobulbar soft tissues are grossly\npreserved.\n\n OTHER:\nMucosal thickening of all the paranasal sinuses present.",
            "output": "1.  Study is moderately degraded by motion.\n2. No acute intracranial abnormality, without definite evidence of acute\ninfarct.\n3. Grossly stable pituitary stalk thickening.  Differential considerations\nagain include lymphoma, lymphocytic hypophysitis, neurosarcoidosis, and\nmetastatic lesion.\n4. Within limits of study, no definite evidence of new intracranial enhancing\nmass.\n5.  Within limits of study, no definite evidence of orbital mass, optic nerve\nlesion or abnormal enhancement.\n6.  Paranasal sinus disease , as described."
        },
        {
            "input": "MRI BRAIN: There are several FLAIR hyperintense and predominantly\nperiventricular and deep white matter lesions, some of which along the corpus\ncallosum and radiating perpendicularly from it, suggestive of a demyelinating\nprocess such as multiple sclerosis.  Some of these lesions demonstrate\nhyperintensity on DWI sequence but without definitive ADC correlate to suggest\nrestricted diffusion.\nAnother FLAIR hyperintense lesion is seen in the right middle cerebellar\npeduncle which demonstrates mild enhancement after contrast administration\n(series 13, image 11).\n\nThere is no evidence of hemorrhage, edema, masses, mass effect, midline\nshiftorinfarction.\n\nThe ventricles and sulci are normal in caliber and configuration.\n\nThere is mild mucosal thickening along the ethmoid air cells and left\nmaxillary sinus.\n\n\nMRI ORBITS: Limited evaluation of the orbits due to motion artifact.\nAllowing for this limitation, the optic nerves appears grossly symmetric\nwithout abnormal enhancement.  The bony orbits and preseptal soft tissues are\nnormal. The globes are intact and normal in appearance. The extraocular\nmuscles are uniform in size and normal in signal. The lacrimal apparatus is\nnormal. Retrobulbar soft tissues are normal.",
            "output": "1. Several FLAIR hyperintense and predominantly periventricular and deep white\nmatter lesions, some of which along the corpus callosum or radiating\nperpendicularly from it.  Additional lesion in the left middle cerebellar\npeduncle demonstrating mild enhancement after contrast administration. \nFindings suggestive of an underlying demyelinating process such as multiple\nsclerosis.\n2. Limited evaluation of the orbits due to motion artifact.  Allowing for this\nlimitation, no evidence of optic neuritis."
        },
        {
            "input": "MRI head: There is no intra or extra-axial mass, acute hemorrhage or infarct.\nSulci, ventricles and cisterns are within expected limits. Arising from the\nleft ICA terminus is a greater than 2 cm enhancing flow void compatible with\naneurysm, better evaluated on MRA portion of the exam described below. There\nare punctate periventricular and subcortical T2/FLAIR nonspecific white matter\nhyperintensities, which may be seen in setting of chronic microangiopathy. The\nparanasal sinuses are clear. The orbits are unremarkable. The mastoid air\ncells are clear. The dural venous sinuses are patent. No abnormal enhancement.\n\nMRA head:  A 2.4 x 1.6 x 1.5 cm (TRV, SI, AP) aneurysm arises from the\napproximate location of the left ICA terminus. Decreased flow related signal\nin the left A1 segment compared to the contralateral side is noted, which may\nbe secondary to slow flow. The A2 segments are trifurcated. Fetal type origin\nof the right posterior cerebral artery is noted. The left vertebral artery is\ndominant. Otherwise, the remainder of the intracranial circulation\ndemonstrates no stenosis or occlusion. No other aneurysms within the confines\nof MRI technique.",
            "output": "1. No intra or extra-axial mass, acute hemorrhage or infarct.\n2. A 2.4 cm left ICA terminus aneurysm as described above. Neurosurgery\nconsultation is recommended. Comparison with prior imaging if available is\nalso recommended.\n\nNOTIFICATION:   The findings were discussed by Dr. ___ with Dr.\n___ on the telephone on ___ at 8:54 AM, 20 min after the\ndiscovery of the findings."
        },
        {
            "input": "There has been expected interval maturation of the patient's right\ntemporal/parietal parenchymal hematoma, which has better defined T1\nhyperintense borders today and measures 33 x 32 x 52 mm (transverse x\ncraniocaudad x AP).  There has been interval decrease in adjacent vasogenic\nedema and mass effect with better definition of adjacent sulci, slight\ndecrease in adjacent increased FLAIR signal and less effacement of the right\nlateral ventricle.\n\nThe adjacent intraventricular hemorrhage has also improved.\n\nA faint region of susceptibility artifact within the right parietal lobe is\nbetter defined today compared to prior. This is nonspecific and may represent\nsequela of a remote small hemorrhage.\n\nThere is no definite enhancement and no enlarged vessels to suggest underlying\nmass or AVM.\n\nThere is no new hemorrhage and there is no evidence of interval infarct. \n\n Mild symmetric age-related prominence of the ventricles, cisterns and sulci\nis otherwise age appropriate.  Extracranial soft tissue and osseous structures\nare otherwise unremarkable.",
            "output": "Interval expected maturation of the patient's right\ntemporal/parietal hematoma with no evidence of underlying mass or AVM. \nContinued followup is advised as an underlying lesion could still be obscured\nby residual hematoma."
        },
        {
            "input": "MRI head: There is an intraparenchymal hematoma centered within the left post\ncentral gyrus which measures 1.5 cm AP x 3.5 cm transverse (series 8, image\n19). There is surrounding T2/FLAIR signal hyperintensity compatible with mild\nedema.  Question presence of a small amount of adjacent subarachnoid\nhemorrhage.  There is minimal enhancement at the superior medial margin of\nhematoma (series series 10, image 89) .  The ventricles are stable in size.\n\nThere is an additional focus of gradient signal hypointensity within the right\nbasal ganglia (series 7, image 12) , which corresponds to area of mild\nhyperintensity on prior CT (series 2B, image 18) . There is an associated\nenhancing venous structure immediately adjacent (series 10, image 120- 146). \nWithin the left thalamus there are additional similar enhancing vessels. (See\nseries 10, images 97-115). These vessels within bilateral thalami line are\nhyperintense on FLAIR imaging (see series 8 images. ___.\n\nThere are normal otherwise vascular flow voids. There is no evidence of acute\ninfarct based on diffusion-weighted imaging. The brain parenchymal volume is\nwithin normal limits. There are scattered punctate foci of T2/FLAIR signal\nhyperintensity within the subcortical white matter of the bilateral cerebral\nhemispheres which is greater than expected for age.\n\nThere is suggestion additional deviated within the left cerebellum (see series\n1000, image 29 series 10 images. 800).\n\nThe orbits, paranasal sinuses, and mastoid air cells are unremarkable.\n\nMRA head: There is no evidence of aneurysm or occlusion within the\nintracranial vasculature. The anterior cerebral arteries, middle cerebral\narteries, and posterior cerebral arteries appear normal. Anterior\ncommunicating and bilateral posterior communicating arteries are seen.",
            "output": "1. Intraparenchymal hematoma with surrounding edema and minimal subarachnoid\nhemorrhage centered within the left post central gyrus.  Recommend clinical\ncorrelation and followup imaging to resolution.\n2. Minimal nodular enhancement along lateral margin of left post central gyrus\nhematoma may represent small vessels of an AVM, with other etiology, including\nseptic embolus, not excluded on the basis of this examination. Recommend\nclinical correlation for findings. If clinically indicated, consider cerebral\nangiogram for further evaluation of possible DVA.\n3. Developmental venous anomaly within the right basal ganglia with additional\nfocus of possible hemorrhage, as described above, which could represent an\nassociated cavernous malformation with hemorrhage.\n4. Suggestion of additional left thalamic and left cerebellar DVA's as\ndescribed. Recommend clinical correlation.\n5. No definite evidence of acute infarct.\n\nRECOMMENDATION(S):\n1. Followup MRI exam after resolution of hematoma is recommended for further\nevaluation.\n2. Recommend clinical correlation for findings. If clinically indicated,\nconsider cerebral angiogram for further evaluation of possible AVM."
        },
        {
            "input": "There is an unchanged intraparenchymal hematoma in the left postcentral gyrus,\nmeasuring approximately 17 x 34 mm in transverse dimension (image 70, series\n11), unchanged bilateral developmental venous anomaly seen in the thalamic\nregion. The previously described left cerebellar developmental venous anomaly\nis not clearly identified. The arterial spin labeled sequence is notable for\nincreased perfusion in posterior thalamic region (image 15, series 10).  The\ntractography color maps demonstrate mild deviation towards the midline of the\nmajor corticospinal,  association and commissural tracts in the area of the\nleft precentral gyrus hematoma.\n\nThe functional MRI demonstrates BOLD activation areas during the movement of\nthe hands, feet and tongue.  Cortical BOLD signal is identified in the left\nprecentral gyrus adjacent to the intraparenchymal hematoma (image 22, series\n22). During the tongue movement the BOLD activity appears both cerebral\nhemispheres with slightly stronger signal on the left anterior to the left\npostcentral gyrus hematoma\n\nThe language paradigm demonstrates the propagation of activation in the\nconvexity with the majority of left post central gyrus intraparenchymal\nhematoma the BOLD activity on the left cerebral hemisphere, likely related\nwith dominance, there is mild BOLD activation areas adjacent to the left.",
            "output": "1. Unchanged left post central gyrus intraparenchymal hematoma as described in\ndetail above.\n\n2.  On the ASL sequence, there is increased profusion in the thalamus\nbilaterally, there is a bilateral developmental venous anomaly as described\nabove.\n\n3. The language paradigm demonstrates the propagation of activation in the\nconvexity with the majority of the BOLD activity on the left cerebral\nhemisphere, likely related with dominance, with a small area of activation\nadjacent to the left postcentral gyrus intraparenchymal hematoma."
        },
        {
            "input": "MRI head:  The examination is slightly limited by patient motion artifact on\nall sequences.\n\nThere is no intra or extra-axial mass effect or acute hemorrhage. There is a\nsubtle diffusion-weighted hyperintense 6 mm focus, in the left centrum\nsemiovale just superior to the posterior limb of the left internal capsule,\nwith suggestion of corresponding very subtle asymmetric FLAIR hyperintense\nsignal extending along the cortical spinal tract to the level of the cerebral\npeduncle (series 11, image 10 through 13). There is no associated ADC\nhypointensity.  The findings would suggest a subacute infarct with subtle\nWallerian degeneration.\n\nSulci, ventricles and cisterns are within expected limits given the degree of\nage-appropriate global cerebral volume loss. The major intracranial flow voids\nare preserved. There are superimposed periventricular and subcortical white\nmatter T2/FLAIR hyperintensities, which are nonspecific, but commonly seen in\nthe setting of small vessel ischemic disease.\n\nThe patient is status post right lens replacement. Otherwise, the orbits are\nunremarkable. The paranasal sinuses are essentially clear. The mastoid air\ncells are clear.\n\nMRA head: The examination is limited secondary to patient motion artifact\ndespite multiple acquisitions.\n\nIncidental note is made of a fenestrated right A1 segment (series 1400, image\n13).\n\nThere is apparent paucity of flow related signal in the in the superior\ndivision of the left MCA and distal branches as well as of the proximal M2\ninferior division without evidence of focal occlusion. This may be secondary\nto slow flow from atherosclerotic disease and stenosis.\n\nThere is a 2 mm outpouching at the expected origin of the left PCA and SCA\nwhich is connected to the SCA and a diminutive left P1 segment. The left\nposterior communicating artery is prominent. The combination of findings\nsuggest an infundibular origin of the left PCA and SCA with a superimposed\nfetal type origin of the left PCA.\n\nThere is focal narrowing of the right P1 segment as well as long segment\nnarrowing of the right P2 segment (series 1402 on image 27), compatible with\natherosclerotic disease.\n\nScattered areas of focal narrowing seen the proximal and 2 branches of the\nMCAs bilaterally, some of which is likely due to atherosclerotic narrowing.\nRemainder of the intracranial ICA, ACA, right MCA and posterior circulation is\nunremarkable allowing for artifact.",
            "output": "1. The study is motion limited.\n2. Findings compatible with 6 mm focus of subacute infarct in the left centrum\nsemiovale in close association with the posterior limb of the left internal\ncapsule with suggestion of Wallerian degeneration along the cortical spinal\ntract to the level of the left cerebral peduncle.\n3. Superimposed white matter changes compatible with small vessel ischemic\ndisease in a patient of this age.\n4. Although there is no evidence of large vessel occlusion, there is paucity\nof flow related signal in the distal left MCA distribution, which may\nrepresent slow flow in the setting of atherosclerotic disease.  Narrowing of\nthe right P1 and P2 segments are noted, as well as scattered areas of\nnarrowing along the M2 segments of the MCAs also compatible atherosclerotic\ndisease.  CTA of the head may yield additional information if desired.\n5. There is a 2 mm likely infundibular origin of the left PCA and SCA with\nsuperimposed fetal type origin of the left PCA.  This may be further evaluated\nwith CTA of the head as clinically indicated.\n\nNOTIFICATION:   The findings were discussed by Dr. ___ with Dr.\n___ on the telephone on ___ at 3:10 ___, the time of\ndiscovery of the findings."
        },
        {
            "input": "The intracranial vertebral and internal carotid arteries and their major\nbranches appear normal without evidence of stenosis, occlusion, or aneurysm\nformation.  Bilateral A-comm, PCOM are present.  Note is made of a dominant\nleft vertebral artery.",
            "output": "Normal brain MRA."
        },
        {
            "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.\n\nVisualized paranasal sinuses and mastoid air cells are clear.  There is a left\nmaxillary sinus retention cyst.\n\nMRA of the circle of ___ demonstrates no evidence for aneurysm or high\ngrade stenosis.  There is stable left superior hypophyseal artery aneurysm.\nThere is a stable appearing right para ophthalmic aneurysm. There is partial\nfilling measuring 6 mm within the interstices of the previously coiled left\nsupraclinoid ICA aneurysm as well as slight flow related enhancement the base\nof the aneurysm.",
            "output": "Flow related enhancement within the interstices and at the base of the\npreviously coiled aneurysm suggestive of partial recanalization.\n\nNormal MRA of the brain"
        },
        {
            "input": "MRI BRAIN: There is no evidence of infarction or edema.  There is no enhancing\nmass or abnormal enhancement.  The ventricles are normal in size. There is no\nmidline shift.  The dural venous sinuses appear patent on post-contrast MP\nrage images.  There is opacification of the right maxillary sinus with\nprobable mucosal retention cyst.  There is an additional anterior small\nenhancing mucosal retention cyst (17:5) there is mild mucosal thickening of\nthe left frontal, bilateral ethmoid air cells.\n\nMRI ORBITS: There is faint enhancement surrounding the left optic nerve\n(15:13).  The apparent asymmetric size of the optic nerves is likely related\nto differences in course of the optic nerves.  There is no enlargement of the\nleft optic nerve.  There is no orbital abscess. The globes and extraocular\nmuscles appear unremarkable.  The preseptal soft tissues appear unremarkable.",
            "output": "1. Faint enhancement surrounding the left optic nerve, which is normal in\nsize.  Finding is nonspecific, but given the clinical presentation, finding\nmay be related to infectious or inflammatory process, suggest perineuritis. \nNo evidence of orbital abscess.  Clinical correlation and attention on\nfollow-up imaging is recommended, as clinically warranted.\n2. Right maxillary sinus mucosal retention cysts or polyps.\n\nNOTIFICATION:  The findings were discussed with ___, M.D. by ___\n___, M.D. on the telephone on ___ at 11:28 am, 2 minutes after\ndiscovery of the findings."
        },
        {
            "input": "Confluent areas of T2 and FLAIR hyperintensity are present within the\nperiventricular, subcortical and deep white matter as well as within the pons.\nThere are scattered white matter foci of T2 and FLAIR hyperintensity\nsuperimposed on the more confluent regions of signal abnormality. In addition,\nthere is a focal area of T2 and FLAIR hyperintensity within the right frontal\nlobe which extends to the cortex.\n\nThere is no acute infarct or intracranial hemorrhage. The ventricles, cerebral\nsulci and cisterns are mildly prominent, reflecting a mild degree of cerebral\natrophy. Flow voids for the major intracranial vessels are preserved.\n\nThe visualized orbits and soft tissues are unremarkable.\n\nMRA head: The major intracranial vessels are patent without evidence of\nstenosis or occlusion. Infundibular origin of the left posterior communicating\nartery is noted. No aneurysm or arterial venous malformation is detected.",
            "output": "Confluent regions of T2/FLAIR hyperintensity in the periventricular white\nmatter and a focal FLAIR hyperintense right frontal lobe lesion extending to\nthe cortex. This may represent an infiltrating neoplasm such as gliomatosis\ncerebri.  The right frontal lobe lesion is less likely to reflect infarct\ngiven the fast diffusion. It is also unlikely to be the result of seizure\ngiven the deep white matter component of the lesion, and is unlikely to\nrepresent a prior contusion given name lack of atrophy. Further\ncharacterization with postcontrast images is recommended."
        },
        {
            "input": "There is late subacute infarct in a left MCA/ACA/PCA distribution,\nparticularly posteriorly.  These show mostly increased signal on the ADC map\nwith linear regions of decreased signal peripherally all suggestive of\nmaturing subacute infarcts.  They are hyperintense on FLAIR and there is no\nassociated mass effect, also compatible with late subacute infarct.  There is\nno evidence of hemorrhage and no mass effect.",
            "output": "Late subacute left MCA/ACA/PCA watershed infarcts."
        },
        {
            "input": "Normal flow signal is noted in the petrous, cavernous, and supraclinoid\nportions of the internal carotid arteries. The anterior and middle cerebral\narteries are normal. The anterior 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\nposterior communicating arteries are identified.\n\nNo arterial stenosis, saccular aneurysm, or AVM is identified. Flow is\nsymmetric. There is no evidence of vasculitis.  No vascular lesion is\nidentified in the region of the left posterior fossa mass seen on MRI from ___.",
            "output": "Normal MRA of the head."
        },
        {
            "input": "MRI HEAD:  Well-circumscribed enhancing left temporoparietal lesion, with\nextensive surrounding edema pattern and sulcal effacement is essentially\nunchanged in size when compared to the most recent prior exam, measuring\napproximate 3.2 x 3.1 cm, in its greatest ___. Please note, this region\nof measurement differs from the technique used on the prior exam. No new\nenhancing lesions are noted. Multiple punctate foci of gradient echo\nsusceptibility artifact within the lesion appears slightly more prominent when\ncompared to the prior exam, which may be secondary to use of the 3 Tesla\nmagnet on today's exam compared 1.5 T on the prior exam versus increased\ninterval hemorrhage. Focus of gradient echo susceptibility artifact of the\nposterior right occipital/parietal lobe is stable. Increase foci of\ndiffusion-weighted abnormality along the posterior aspects of the lesion (is\n602, image 15 and 16), when compared to prior exam, also likely secondary to\ntechnical factors.\n\nPrior cerebellar infarcts are again seen left and right cerebellum, unchanged\nfrom prior exam.\n\nThere are superimposed periventricular and subcortical white matter T2/FLAIR\nhyperintensities, which are nonspecific, but commonly seen in setting of small\nvessel ischemic disease. Sulci, ventricles and cisterns are within expected\nlimits, given the mass effect from the left temporoparietal mass. The major\nflow voids are preserved. The paranasal sinuses are clear. The orbits are\nunremarkable. The mastoid air cells are also clear.\n\nThere is decreased blood flow and blood volume to the left temporal parietal,\nwith no change in mean transit time consistent with nonviable brain tissue,\nlikely expected sequela from prior treatment.\n\nASL perfusion: Decreased blood flow to the left temporoparietal lobe in the\nregion of the known tumor is noted.\n\nSpectroscopy:  Decreased NAA and increased lactate in the center and posterior\naspect of the left temporal parietal tumor is noted, consistent with necrosis;\nsome of the regions with increased lactate also demonstrate mild increased\ncholine. At the tumor margins, there is increased Choline relative to NAA,\nwithout associated increased lactate.",
            "output": "1.  Increased lactate with areas of mildly elevated choline within the tumor\nconsistent with necrosis. However, there are more peripheral regions of mildly\nincreased choline cut associated increased lactate, which may represent\nregions of residual tumor.\n\n2.  No increase perfusion to the left temporoparietal lesion.\n\n3. No new lesions. Unchanged appearance of enhancing left temporal parietal\nlobe lesion with surrounding edema."
        },
        {
            "input": "MRI HEAD: Well-circumscribed enhancing left temporoparietal lesion, with\nworsened extensive surrounding edema and sulcal effacement is slightly\nincreased in size from prior allowing for difference in slice selection, now\nmeasuring 4.2 x 3.9 cm, versus 3.9 x 3.8 cm (series 18 image 15).  The lesion\nshows peripheral enhancement and absence of central enhancement which may be\nrelated to necrosis.  Overall the volume of enhancing tissue appears slightly\nincreased from prior.  A central and posterior area of slow diffusion within\nthe lesion (series 400 image 17) is significantly more prominent from the\nprevious exam.  No new enhancing lesions are noted. Multiple punctate foci of\ngradient echo susceptibility artifact within the lesion are unchanged, as is a\nright occipital lobe focus (series 8 image 9).\n\nFoci of encephalomalacia in the left and right cerebellum from prior infarcts\nare unchanged. There are superimposed periventricular and subcortical white\nmatter T2/FLAIR hyperintensities, which are nonspecific, but commonly seen in\nsetting of small vessel ischemic disease. Sulci, ventricles and cisterns are\nwithin expected limits, given the mass effect from the left temporoparietal\nmass. The major flow voids are preserved. The paranasal sinuses are clear. The\norbits are unremarkable. The mastoid air cells are also clear.\n\nDSC PERFUSION: No increased perfusion is identified in the lesion.\n\nSPECTROSCOPY:  Increased choline-to-NAA ratio as well as substantially\nelevated and dominant lactate peak is seen in the voxels involving the center\nand posterior aspect of the lesion (voxels 19 and 20).  This pattern is\nsuggestive of regions of necrosis and viable tumor within these voxels, not\nsignificantly changed from prior spectroscopy exam.",
            "output": "1.  Compared with the previous exam there has been interval increase in size\nof a necrotic left temporoparietal lesion with more extensive surrounding\nFLAIR hyperintensity and a more prominent area of slow diffusion centrally and\nposteriorly.  These findings may be related to treatment effect, tumor growth\nor a combination of these factors. The etiology of the observed change is\nunclear as some imaging characteristics - more prominently the lack of\nincreased perfusion - are suggestive of radiation necrosis; while some others\n- such as the spectroscopy findings - are indicative of tumor growth.\n\n2.  No new lesions are identified."
        },
        {
            "input": "Limited examination secondary to incomplete performance of dedicated\ncontrast-enhanced brain MRI, due to patient refusal to complete the\nexamination.\n\nThere is redemonstration of a left periatrial lesion which again demonstrates\nrestricted diffusion. There is persistent restricted diffusion within the\nsplenium of the corpus callosum.  Increased signal intensity involving the\nleft frontoparietal lobe and extending into the left occipital and temporal\nlobe is noted in the ADC map. There is also increased signal intensity in the\ncontralateral cerebral hemisphere seen in the ADC map.  Increased signal\nintensity within the left cerebellum is consistent with focal encephalomalacia\nfrom prior infarctions.",
            "output": "Limited examination secondary to incomplete performance of dedicated\ncontrast-enhanced brain MRI, due to patient refusal to complete the\nexamination.\n\nRedemonstration of an incompletely assessed left periatrial lesion showing\ninternal restricted diffusion.\n\nRedemonstration of an incompletely assessed lesion in the splenium of the\ncorpus callosum showing internal restricted diffusion.\n\nRECOMMENDATION(S):  Completion of dedicated contrast-enhanced brain MRI is\nrecommended for thorough assessment of disease."
        },
        {
            "input": "There is a hypoplastic A1 segment of the left ACA.  Incidentally noted is\nfenestration of the anterior communicating artery comlex, an anatomic variant.\nThe middle cerebral arteries are unremarkable.\n\nThe posterior communicating arteries are not identified.  Incidentally noted\nis an infundibular origin of the left AICA.  The left vertebral artery is\nsmall in caliber, immediately distal to the origin of its ___ branch.  There\nis no evidence of significant stenosis or aneurysm larger than 2 mm.",
            "output": "Unremarkable brain MRA with incidental fenestration of the ACom complex, but\nno evidence of aneurysm larger than 2mm, significant mural irregularity or\nflow-limiting stenosis."
        },
        {
            "input": "In comparison with the most recent examination, no significant changes are\ndemonstrated in the left frontal lobe heterogeneous enhancing lesion, with\npattern of enhancement extending to the right frontal ventricular subependymal\nregion, grossly this lesion measures approximately 38 x 36 mm in transverse\ndimension, similar pattern of vasogenic edema is again seen, causing narrowing\nof the right frontal ventricular body and effacement of the sulci.  There is\nno evidence of new areas with abnormal enhancement since the most recent exam.\nOn the ASL sequence, there is no evidence of increased perfusion.  The\ntractography demonstrates deviation of the commissural, corticospinal and\nassociation tracts.\n\nThe functional language paradigm demonstrates the majority of the activation\non the right cerebral hemisphere (image 42, series 22), the BOLD signal\nintensity on the left cerebral hemisphere is less avid in comparison with the\nright, however it is possible to see BOLD activation in the Broca's area as\ndemonstrated on the image 43, series 22 which apparently is situated at\napproximately 15 mm from the mass lesion in coronal projection (image 23,\nseries 23).\nThe functional paradigm during movement of the tongue demonstrates expected\nactivation areas bilaterally and on the left at more than 2 cm from the mass\nlesion (image 34, series 31).\n\nThe functional MRI demonstrates the expected BOLD activation areas for the\nmovement of the hands and feet, with no significant BOLD signal adjacent to\nthe mass lesion.",
            "output": "1.  Unchanged left frontal lobe heterogeneous enhancing lesion with associated\nvasogenic edema, there is no evidence of new lesions in this short interval.\n\n2.  The functional MRI demonstrates the majority of the BOLD activation for\nthe language in the right cerebral hemisphere, and less avid signal on the\nleft cerebral hemisphere in the expected location for the Broca's area at\napproximately 15 mm from the mass lesion.\n\n3.  There is no evidence of increased profusion on the ASL sequence.\n\n4.  The tractography demonstrates deviation of the association, corticospinal\ncommissural tracts towards the midline, likely related with vasogenic edema."
        },
        {
            "input": "BRAIN MRI:  There is no acute infarction, edema, mass effect, or evidence for\nblood products in the brain parenchyma.  T2 weighted and FLAIR images\ndemonstrate multiple 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 a patient of this\nage. Mild prominence of the ventricles and sylvian fissures is compatible with\nmild age-related parenchymal volume loss. In addition, all components of the\nleft lateral ventricle larger than the right, indicating congenital or\ndevelopmental etiology.\n\nBRAIN MRA:  Concurrent contrast-enhanced neck MRA is reported separately.  The\nexam is limited by motion artifact.\n\nMost caudal aspect of the posterior fossa is not included on the images. V4\nsegment of the non dominant right vertebral artery is hypoplastic, as also\nseen on the neck MRA. Right ___ is not identified in the field of view\nof the current brain MRA, and is also not included in the field of view of the\ncontrast enhanced neck MRA. Arterial branches are present in the right ___\nterritory. Left ___ is large, but is not clear whether it supplies branches\nto the right ___ territory. AICA is not visualized on either side.\nIntracranial left vertebral artery, basilar artery, proximal superior\ncerebellar arteries, and proximal posterior cerebral arteries are patent.\nApparent irregularity of the distal P1 and proximal P2 segment of the left\nposterior cerebral artery is most likely related to artifact on the source\ndata.\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 acute intracranial abnormalities.\n2. Moderately extensive supratentorial white matter signal abnormalities,\nnonspecific but likely sequela of chronic small vessel ischemic disease in a\npatient of this age.\n3. Technically limited brain MRA with motion artifact and incomplete inclusion\nof the proximal intracranial vertebral arteries.  Right ___ is not\nvisualized, though arterial branches are seen in the right ___ territory.\nMild irregularity of the left posterior cerebral artery, without significant\nnarrowing, is most likely artifactual, though atherosclerotic plaque is not\nexcluded."
        },
        {
            "input": "MRA head:  The major intracranial arteries appear normal with no evidence of\nstenosis, occlusion, or aneurysm formation.  The left vertebral artery is\ndominant.\n\nMRI head: Accounting for differences in modality, there has been no\nsignificant interval change in left vertex subdural hematoma.  There is\nincreased T2/FLAIR signal also noted in the frontal parietal sulci which\ndemonstrate abnormal enhancement on post-contrast images. Differential\ndiagnosis for this finding include subarachnoid hemorrhage versus meningitis.\n\nThere is no evidence of infarction, mass effect, or midline shift.   The\nventricles and sulci are mildly dilated likely reflecting age-related\nparenchymal volume loss. There are additional scattered foci of T2/FLAIR\nsignal hyperintensity in the periventricular, subcortical, and deep white\nmatter which is nonspecific but likely on the basis of chronic small vessel\nischemic disease.\n\nMajor vascular flow voids are preserved. Patient is status post bilateral lens\nreplacement. The paranasal sinuses and mastoid air cells are grossly clear.",
            "output": "1. No significant interval difference in left vertex subdural hematoma\naccounting for differences in modality.\n\n2.  Increased FLAIR signal in the sulci of the left frontal and parietal lobe\nwith corresponding post-contrast enhancement. This finding could be seen with\nsubarachnoid hemorrhage which is considered more likely given patient's\nclinical history and the concomitant presence of a subdural hematoma. However,\nan infectious process, such as meningitis, could also have this appearance."
        },
        {
            "input": "MRA 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.",
            "output": "No significant abnormalities are seen on MRA of the head."
        },
        {
            "input": "MRA:\nThe major intracranial arteries appear normal without evidence of stenosis,\nocclusion, or aneurysm formation greater than 3 mm. The left vertebral artery\nis dominant.  The right posterior inferior cerebellar artery is not well\nseen-? diminutive.  Left posterior inferior cerebellar artery is tortuous in\ncourse.\n\nMR BRAIN: There is no evidence of hemorrhage, edema,  mass effect, or\ninfarction.\nProminent ventricles and sulci are compatible with mil diffuse parenchymal\nvolume loss.\nScattered T2/FLAIR hyperintensities are noted in the periventricular and\nsubcortical white matter which are nonspecific but likely reflect sequelae of\nchronic small vessel ischemic disease.\nThe paranasal sinuses and mastoid air cells are clear. The globes are\nunremarkable.",
            "output": "1. No evidence of infarction or other acute intracranial process. Probable\nchronic small vessel ischemic disease.\n\n2.  Patent major intracranial arteries as described above."
        },
        {
            "input": "MRI HEAD: There is no evidence of   mass,  hemorrhage or infarction. Sulci,\nventricles and cisterns are within expected limits. The major intracranial\nflow voids are preserved. Mucous retention cysts in the maxillary sinuses,\ngreater on the left are noted. The remainder the paranasal sinuses are\nessentially clear. The orbits are unremarkable. The mastoid air cells are\nclear. No evidence of abnormal enhancement. The dural venous sinuses are\npatent. Again noted is a T1 hypointense T2 hypointense nodule without\nenhancement within the right transverse sinus compatible with arachnoid\ngranulation.  There is a hypoplastic left transverse sinus.\n\nHEAD MRV: Lack of flow related signal in the left transverse sinus is seen on\nphase contrast MR of the, in combination with findings on postcontrast MP rage\nis compatible with hypoplastic left transverse sinus. In addition, CTV\nperformed earlier in the day also supports this finding. Otherwise, normal\nflow related signal is seen in the remainder of the dural venous sinuses.",
            "output": "1. No evidence of  infarction or  hemorrhage.  No intracranial mass.\n2. No evidence of venous  sinus  thrombosis. Hypoplastic left transverse sinus\nagain identified.\n3. Small arachnoid granulation in the right transverse sinus, unchanged from\nCTV performed earlier in the day, allowing for technical differences."
        },
        {
            "input": "MRI head:  There is no intra or extra-axial mass, acute hemorrhage or infarct.\nSulci, ventricles and cisterns are within expected limits given the degree of\nage-appropriate global cerebral volume loss. Bilateral cerebellar hemispheric\nencephalomalacia is noted, presumably from prior infarct. No abnormal\nenhancement. The major intracranial flow voids are preserved. The dural venous\nsinuses are patent. There are confluent periventricular and subcortical\nT2/FLAIR white matter hyperintensities, which are nonspecific, but commonly\nseen in setting of small vessel ischemic disease in a patient of this age,\ncorresponding to diffuse hypointensity seen on earlier CT examination.\n\nOther: On both MPRAGE and T1 sagittal sequences, there is a large left\nparacentral disc protrusion which contacts and effaces the left ventral aspect\nof the cord at C3-4 (series 1002b, image 4 and series 3, image 12). This\nresults in moderate spinal canal narrowing. In addition, there is associated\nlinear enhancement at this level (series 1002b, image 7) likely venous in\nnature.\n\nMRA head: Mild atherosclerotic narrowing of the right internal carotid artery.\nOtherwise, the major intracranial arteries appear normal with no evidence of\nstenosis, occlusion, or aneurysm formation. The right vertebral artery is\ndominant.",
            "output": "1. No evidence of intracranial metastatic disease.\n2. No intracranial hemorrhage or infarct.  White matter changes compatible\nwith small vessel ischemic disease.\n3. Bilateral cerebellar hemisphere encephalomalacia.\n4. Essentially unremarkable MRA of the head.\n5. On MPRAGE in T1 sagittal sequences, there is a large left paracentral disc\nprotrusion at C3-4 which results in moderate spinal canal narrowing and\neffacement of the ventral aspect of the cord.  This may be further evaluated\nwith dedicated MRI of the cervical spine as clinically indicated."
        }
    ]
}