Assessment #1 case-set #2 case #11

Normal

Small area of encepholmalacia along the R frontal parietal paranchyma

No evidence of hemorrhage. No midline shift.

Evidence of small vessel disease.

If concern for acute stroke, consider MRI for further evaluation

Age indeterminate infarction of the right thalamus.

mild ventriculomegaly

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Macro CT old brain. Macro CT stroke disclaimer.

Faint hypoattenuation within b/l parietal white matter favored chronic vessel given ex vacuo dilation. If concern for acute ischemia, PRES, or embolic stroke, could further eval with MRI.

Age indeterminate, remote favored lacunar infarct in the R thalamus.

left occipital?

Low attenuation of subcortical parenchyma in right frontal and left aprieto occipital lobes, suggestive of prior ischemic event or watershed ischemia. Prior right thalamic stroke. Mild hydrocephalus.

Left occipital hypodensity.
Chronic small vessel disease.

right cerebellum and frontal

Several regions of hypodensity in b/l cerebral cortices, likely 2/2 prior stroke.

hypoattenuation and loss of g/w diff in superior r frontal lobe concerning for acute/early subac infarct. rec mri for further evaluation.

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Multiple low dense white matter ares

Dense left vertebral artery at the foramen magnum concerning for vertebral occlusion. Old left occipital infarct.

There is hypodensity and reduction in gray-white differentiation in the cortical/superior region of the right frontal lobe, representative of an acute infarct. In addition, there is a questionable hypodensity in the right cerebellum that is likely infarct but could represent an additional infarct. No visible intracranial hemorrhage. No hydrocephalus or mass effect.

Paranasal sinuses and mastoid air cells are clear. Calvarium is intact.

Age indeterminant infarcts of the left cerebellum, likely BL thalami, and occipital lobe, as well as the high right parietal lobe. MRI can delineate chronicity. No large territory infarct, hemorrhage, or mass effect.

mild dilation of the lateral and 3rd ventricles concerning for hydrocephalus. calcification at the cerebral aqueduct.

Multiple areas of hypoattenuation with loss of gray-white differentiation in a watershed territory of distribution including between the right ACA and MCA territories, the left cerebellar peduncle, the left MCA and PCA territories, and the right cerebellar hemisphere. Constellation of findings is concerning for acute/early subacute infarcts in a watershed type of distribution. No evidence of hemorrhagic transformation or significant mass effect.

White matter edema involving the bilateral parieto-occipital regions and high right frontal lobe. This appearance may indicate posterior reversible encephalopathy syndrome (PRES). Brain MRI could further assess for associated ischemia. Remote appearing right thalamic infarct.

Hypoattenuation of the bilateral posterior circulation, which may be compatible with PRES. Recommend MRI.

Enlarged ventricular system.

right MCA and right PCA loss of gray-white differentiation concerning for ischemia.

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Hypodensity in the bilateral occipital lobe concerning for acute ischemic infarct.

Multifocal loss of gray-white diff involving right cerebellum, bilateral deep gray nuclei, high frontal. Rec MRI

Bilateral right frontal and left parietal white matter hypodensities without mass effect, likely encephalomalacia. Remote right cerebellar infarct. Left basal ganglia hypodensity, may represent age indeterminate infarct. Rec MRI brain for further evaluation.

No acute intracranial hemorrhage or large vascular territory ischemia. Apparent enlargement of the ventricular system without evidence of obstruction. Hypodensity within the R basal ganglia is technically age indeterminant in the absence of prior imaging, favored to be remote–if clinical concern for acute ischemia MRI could better evaluate. Patchy white matter disease/loss of grey/white differentiation likely the sequela of chronic small vessel disease.

left pca territory infarct, mri; also maybe right

Hypodense regoion in the right frontal lobe region, concerning for ischemia. No hemorrhage or midline shift. The lateral ventricles are enlarged.

PCA territory infarct

posterior hypo

Multifocal bilateral regions of hypoattenuation concerning for acute/early subacute infarcts, possibly of cardioembolic origin.

Hypodensity within the right frontoparietal and occipital white matter with additional hypodensities and loss of grey white differentiation in the posterior left occipital and parietal lobes. This is concerning for age indeterminate infarcts in a watershed distribution, concerning for a central cardioembolic source. Recommend MRI wo contrast for further evaluation. Microvascular white matter disease and global cerebral atrophy with ex vacuo diliation of the ventricles. Remote left cerebellar infarct.

Areas of hypodensity and loss of grey-white differentiation along the high right parietal lobe concerning for ischemia in an MCA territory distribution. Consider MRI for further evaluation.

Hypoattenuating regions in the right medial frontoparietal region (ACA territory) and left occipital lobe (PCA territory) concerning for acute ischemia. Recommend MRI for further evaluation. Question gyriform areas of hyperattenuation adjacent to both areas of ischemia. Left vert is hyperattenuating but may reflect athero.

areas of hypodensity in the bilateral occipitaoparietal lobes with loss of grey white differentiation which could represent acute ischemia or PRES. Consider MRI brain for further evalutation.
Ventriculomegaly without direct comparison images, which makes it difficult to exclude hydrocephalus.
no hemorrhage, mass effect, or midline shift.

Multiple ill defined areas of hypodensity in the right centrum semiovale, left posterior limb of internal capsule, and left occipital lobe, concerning for watershed or embolic strokes. No herniation or significant mass effect.

-hypodensities concerning for bilateral watershed infarcts
-right thalamus lacunar infarct, age indeterminant
-hyperdensities along the sulci of the left parietal and right frontal lobes and could present petechial hemorrhage.
-no hydrocephalus or mass effect

Bilateral occipital, posterior limb internal capsule, and high right frontal, concerning for acute/subacute (recent) stroke.

Enlarged ventricular system for the degree of volume loss. In the absence of priors, this is concerning for hydrocephalus.

Hypodense lesions at right paramedian gyrus and left occipital lope concerning for stroke

Hypoattenuating lesions of the right thalamus, right posterior limb of the internal capsule, right temporal lobe, right corona radiata, and bilateral occipital lobes, concerning for multifocal infarcts and PRESS.

Hypoattenuating collections along the bilateral frontal convexities, concerning for chronic subdural hematomas. No mass effect. No hydrocephalus. No midline shift.

Vascular calcifications. Age advanced global cerebral volume loss with ex vacuo dilatation of the ventricles. Leukoaraiosis.

Subtle areas of hypoattenuation along the high right frontopareital , left parietal, and right temporoparietal white matter, as well as the right cerebellar hemisphere. These areas could represent infarcts which are age indeterminate in the absence of prior imaging. Recommend MRI for further evaluation.

Communicating hydrocephalus
Age indeterminate right ACA/MCA watershed

Multiple foci of hypoattenuation within bihemispheric white matter consistent with vasogenic edema. Recommend MRI for further characterization.

Multiple areas of hypoattenuation within the right ACA territory, left MCA/PCA watershed terriotry, and left basal ganglia likely representing age indeterminant infarcts. No acute hemorrhage or mass lesion. No significant hydrocephalus. Generalized cerebral volume loss with ex vacuo dilation.

Areas of hypoattenuation and loss of gray white differentiation in the bilateral occipital lobes, bilateral thalami, and extending along the right centrum semiovale. This pattern is concerning for basilar/PCA pathology. Recommend CTA head/neck for further evaluation and neuro consultation. NO acute hemorrhage or significant mass effect.

Loss of gray-white differentiation with local sulcal effacement in the watershed territory of the left MCA/PCA concerning for acute infarct. MRI can further evaluate.

Hypodensity in the left occipital lobe, in a watershed area between MCA and PCA. Findings concerning for ischemia. Mild hydrocephalus of the lateral and third ventricles. No mass effect or midline shift.

Loss of gray white diff in bilateral posterior occipital lobes and right frontal lobe.

concern for ischemia

Vasogenic edema and relative hyperattenuation in the occipital and parietal lobes. This is concerning got Posterior Reversible Encephalopy Syndrome in the appropriate clinical setting.

Hypoattenuation within the right superior frontal lobe and left parieto-occipital lobes likely representing acute ischemia. Additional hypoattenuation within the right cerebellum which may represent ischemia vs remote infarct. No mass effect or midline shift. No acute hemorrhage. Consider further evaluation with MRI and echo given likihood of cardioembolic etiology.

watershed ischemia

acute ischemic infarct of the right ACA territory with mild adjacent cytotoxic edema.

focal hypoattenuation in the left posterior lobe with surrounding edema. additional high frontal right paramidline focus of hypoattenuation. No signficant mass effect or midline shift. Questioned adjacent subarachnoid hemorrhage along the sulci abutting these regions of hypoattenuation. Relatively preserved gray-white.

These findings may represent multifocal acute/subacute infarct. Alternatively, multifocal metastatis vs infection is another consideration. Recommend MRI brain w/wo to further characterize.

FINDINGS:

Small acute intraparenchymal hemorrhage within the left superior posterior parietal lobe with surrounding vasogenic edema. Area of hypoattenuation in the right superior parietal lobe. No mass effect. The mastoid air cells and paranasal sinuses are clear.

IMPRESSION:

1. Acute intraparenchymal hemorrhage in the left superior posterior parietal lobe.
2. Hypoattenuation in the right superior parietal lobe concerning for chronic microvascular ischemia.

Posterior predominant white matter hypoattenuation involving the bilateral parieto-occipital regions and cerebellum in a pattern most suggestive of posterior reversible encephalopathy syndrome (PRES). Recommend brain MRI for further evaluation.
Lacunar infarct in the right thalamus.
No loss of gray-white differentiation to suggest associated ischemia, though MRI is more sensitive. No acute hemorrhage, mass effect, or hydrocephalus.

Acute infarcts in right MCA and left PCA territories. Subtle intraparenchymal hemorrhage in the right MCA infarct.

R cerebellar, BL occipital, BL basal ganglia, BL parietal hypodensities rep age ind infarcts in absence of prior imaging for comparison. mri to further eval.

Trace scattered parenchymal hemorrhages in the bl cerebral hemispheres. no mass effect. no hydrocephalus.

scatter foci of intraparenchymal hemorrhage
hypoattenuation of the rightfrontoparietal region in addition to the bilateral occiptal lobes of unknown age

left frontal subdural hemorrhage. no mass effect or hydrocephalus.

Right subdural hematoma.

loss of grey white/hypodensities multiple vasc territories as below;

RIGHT corona radiata,bilat parietooccipital lobes, left internal capsule, right thalamus, right frontal, left temporal. concern for embolic stroke.

recommend mri. no herniation or hydro

Symmetric vasogenic edema within the bilateral parietoccpital lobes, concerning for PRES.

multifocal areas of hypoattenuation with the right frontal and left parietal lobe white matter likely representing vasogenic edema. possible etiologies include subacute infarct, underlying mass lesion, infection, and inflammary. MRI with and without could further eval.

area of hypodensity in the posterior, medial parietal and occipital lobes in L PCA distribution, concerning for ischemia. minimal mass effect with sulfcal effacement, no hemorrhage, no herniation, no hydrocephalus. small hypodensity in right thalamus, may represent prior lacunar infarct

Findings concerning for bilateral PCA and right MCA territory infarction. No acute intracranial hemorrhage. Mild local mass effects. Reccomend CTA and MRi for further evaluation.

R ACA infarct

Symmetric Areas of hypoattenuation in the posterior parietal and occipital lobes as well as the cerebellum concerning for vasogenic edema as can be seen with PRES. Recommend brain MRI for further evaluation.

There is mild local effacement without herniation.

No intracranial hemorrhage or hydrocephalus.

Areas of hypodensity primarily affecting the white matter in the high parietal- occipital regions bialterally favoring vasogenic edema and most consistent with PRESS. Consider MRI w/ and w/o contrast for further evaluation. Brain mass or infection would also be a consideration.

White matter lesion with adjacent vase genie edema

Vasogenic edema in the bilateral occipital lobes and in the right superior frontal lobe.

foci of hypoattenuation at the G-W junction within the bilateral high parietal and right high frontal lobes, which is concerning for multiple masses, favoring metastatic process, though bilateral watershed territory vascular compromise cannot be excluded. scattered edema surrounding these regions with hyperattenuating foci, may represent hemorrhage vs calficiation of tumors.

no hydrocephalus

multifocal of vasogenic edema, sugg of underlying mass lesions. rec mri.

Posterior predominant white matter hypoattenuation within the high right frontal, left greater than right parieto-occipito regions, and right greater than left cerebellar hemispheres concerning for PRES. Recommend brain MRI for further evaluation.
Remote appearing lacunar infarcts verses dilated perivascular spaces in the bilateral thalami.
Intracranial atherosclerosis.

Multiple areas of ischemia in different vascular territories. Subarachnoid hemorrhage.

Loss of grey-white differentiation within the ACA/MCA and MCA/PCA watershed zones and within the ACA territory of the right frontoparietal and left parietal lobes. Findings are concerning for global ischemia, possibly as a result of hypoxia and/or embolic cause for ischemia. Recommend MRI brain without contrast for further evaluation.

Small volume subarachnoid hemorrhage within bilateral cerebral convexities.

No significant mass effect or herniation.

No hydrocephalus.

Intracranial atherosclerosis with global parenchymal volume loss and ex-vacuo ventricular enlargement.

Incidental bilateral proptosis.

Hypoattenuating regions in the Left greater than right posterior parietal lobes, and superior right frontal lobe concerning for vasogenic edema due to PRESS vs mass/neoplasm. Regions or corresponding hyperattenuation could indicate trace intraparenchymal hemorrhage. No associated mass effect, hydrocephalus, or midline shift. No acute osseous or soft tissue abnormalities.
Recommend MR brain for further evaluation.

Hypodense foci within the bilateral occipital lobes, the right parietal/frontal lobe, right thalamus, and the right cerebellum. No significant edema, sulcal effacement, or concerns for acute hydrocephalus. Global volume loss and likely ex vacuo dilatation of the ventricles. Microvascular changes.

Trace subarachnoid hemorrhage layering within the high left occipital sulci.

Recommend CT Code stroke if within TPA window and follow up MRI.

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loss of gray white matter differential of the left parafalcine occipital lobe. Small foci of high attenuation within the left parafalcine occipital lobe may represent small area of intraparenchymal hemorrhage. Recommend MRI for further evaluation.

Multifocal white matter hypoattenuation involving the paramedian posterior left frontal lobe, left parietal lobe, bilateral occipital lobes, and right cerebellar hemisphere with some regions of gray-white differentiation loss. Differential considerations include multifocal acute/early subacute ischemia (likely central embolic in etiology given bilateral distribution across multiple vascular territories) versus entities such as PRES given the predominantly posterior circulation and watershed territory distribution of findings. MRI brain is recommended for further evaluation.

There is associated sulcal effacement most prominently in the bilateral occipital regions with some scattered cortical-based curvilinear hyperdensity raising suspicion for petechial hemorrhagic conversion and/or cortical laminar necrosis. No large space-occupying intracranial hemorrhage. No hydrocephalus, midline shift, or herniation.

An additional focus of hypoattenuation is identified in the right thalamus, raising concern for age-indeterminate ischemic change, which can also be further evaluated with MRI.

Dense atherosclerotic calcifications along the proximal intradural portion of the left vertebral artery and bilateral carotid siphons.

Hypoattenuating region in the left posterior parietal lobe with overlying area of hyperattenuation at the cortex, suggestive of subarachnoid hemorrhage. Rounding of the 3rd ventricle suggestive of hydrocephalus.