Assessment #1 case-set #3 case #9

Parenchymal volume loss, with nonspecific periventricular white matter hypodensities. Mild hydrocephalus

Hydrocephalus. No evidence of ischemia or hemorrhage. No fracture or soft tissue injury.

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generalized cerebral atrophy with ex vacuo dilatation. no acute intracranial abnormality.

Soft tissue contusion with subcutaneous emphysema along the left parietooccipital bone without underlying calvarial fracture.
Chronic age related changes.

Global enlargement of the ventricular system with enlargement of the Sylvian fissures. Findings may be seen in NPH in the appropriate clinical setting. Macro CT old brain.

Normal pressure hydrocephalus

Cerebral atrophy

nph, encephalomalacia

hydrocephalus with age related cortical atrophy

NPH?

No acute intracranial hemorrhage
No large vessel territory infarct
Prominent periventricular white matter disease with ex-vacuo dilatation of the ventricles, these findings are nonspecific but may be seen in NPH.

age indeterminate lacunar infarct anterior limb of the internal capsule on the left.

Enlarged ventricles. Posterior head contusion.

moderate cerebral atrophy with prominent sulci. enlargement of the lateral ventricles, likely related to cerebral atrophy. scattered hypodense areas in the right inferior frontal lobe and bilateral basal ganglia likely represent prior infarcts. moderate area of encephalomalacia in the right temporal lobe likely represents sequelae from prior infarct. no hemorrhage, herniation

Dilated ventricles, cortical volume loss. Possible normal pressure hydrocephalus.

Soft tissue contusion/laceration along the posterior calvarium. No clear underlying fracture. Macro old brain.

FINDINGS:

Cerebral atrophy out of proportion to age. Associated enlargement of the lateral and third ventricles. No evidence of hemorrhage or acute ischemia. No skull fractures. The mastoid air cells and paranasal sinuses are clear.

IMPRESSION:

Cerebral atrophy with associated hydrocephalus ex vacuo. No acute findings.

There is moderate to severe diffuse brain parenchymal volume loss with proportional ventricular dilation. There is also hypodensity adjacent to the bilateral lateral ventricles representing chronic microvascular atherosclerosis. No visible acute infarct or hemorrhage. No mass effect or hydrocephalus.

There is soft tissue swelling and subcutaneous emphysema outside the the posterior skull. Calvarium is intact.

Posterior scalp soft tissue laceration.

No acute intracranial abnormality.

Age advanced volume loss.

Remote infarct in left caudate/ant IC.
LAceration of left occiptal scalp without inderlying calv fx. No acute hemmorage or ischemia.

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enlarged ventricles concerning for normal pressure hydrocephalus. consult neurosurg.

adsf

no acute intracranial abnomrality

diffuse vol loss with ex vacuo

likely remote lacunar infarcts, consider MRI for further eval if acute concern.

acute hemorrhage centered in the pons, given location etiology is favored to be hypertensive.

Dilated lateral and 3rd ventricles beyond the expected degree of exvacuo dilation in the setting of cerebral and cerebellar volume loss which could suggest normal pressure hydrocephalus. No evidence of mass effect or herniation. No hemorrhage or large territory ischemia.

hydroceophalus acute extraaxial obstructive hydrocephalus

Left thalamic hypoattenuation concerning for age indeterminant infarct. Rec MRI wwo for further eval.
Patchy white matter disease.
Vascular calcs.
Volume loss + ex vacuo dilation.

-Left parietal laceration and fracture without subjacent fracture
-No acute hemorrhage
-Bilateral age indeterminant basal ganglia lucanar infarcts, MRI could further eval
-white matter disease and ex vacuo dilation of the ventricles

diffuse global cerebral and cerebellar atrophy with ventriculomegaly which is favored to be ex vacuo in nature as it is proportional to the degree of sulcal enlargement. However, in the absennse of direct comparison imaging, NPH could have a similar appearance.
periventricular hypoattenuations which likely relate to chronic small vessel disease.
no hemorhhage, mass effect, hydrocephalus, or midline shift.

1. Likely nondisplaced central occipital bone fracture. No associated intracranial hemorrhage.
2. Left insular and right external capsule loss of grey white differentiation which may represent subacute/early ischemia. Consider MRI if clinically indicated as this is more sensitive and specific for ischemia.
2. Occipital contusion.
3. Age advanced global cerebral volume loss with ex vacuo dilation.
4. Ischemic periventricular white matter disease.

Area of asymmetric hypoattenuation in the anterior limb of the left internal capsule and lentiform nucleus of the basal ganglia concerning for age indeterminate infarct. Recommend brain MRI for further evaluation.

Tiny locule of gas in the left orbit but no fx identified.
Macro old brain. Age advanced volume loss.

rt mca

Global hydrocephalus and greater than expected parenchymal volume loss.

Findings concerning for NPH including ventriculomegaly, marked enlargement of the sylvian fissures and rounding of the temporal horns.

Hydrocephalus with diffuse ventriculomegaly, disproportional enlargement of the sylvian fissures, and acute callosal angle. These findings raise concern for NPH, especially given clinical context of recent fall. No mass effect. No hemorrhage. Consider LP for diagnostic and possibly therapeutic purposes.

Age indeterminate infarct of the left cerebellar hemisphere. Recommend MRI for further evaluation.

Left posterior scalp hematoma/contusion without subjacent fracture.

Chronic small vessel disease. Global cerebral volume loss out of proportion to patient’s age with ex vacuo dilatation of the ventricles.

PRES Duret
Occ contusion

No acute hemorrhage, no large vascular territory infarct. But CT rel insensitive for ischemia in first 24-48 hrs, consider MRI if clinical concern.

global ventriculomegaly which may represent ex vacuo ventricular dilation secondary cerebral volume loss. There is periventricular white matter attenuation and clinical history of falls. Normal pressure hydrocephalus should be considered. No evidence of large vascular territory infarct.

Hypoattenuation of the lateral aspect of the left cerebellar hemisphere, which may represent acute/subacute infarct. recommend MRI to further eval.

remote lacunar infarct vs dilated perivasc space left anterior limb internal capsule.
macro CT old brain galore.

Left cerebellar infarct in the PICA territory.
Diffuse atrophy.

soft tissue laceration and hematoma of the occipital scalp.
communicating hydrocephalus
moderate amount of brain volume loss and probably sequela of chronic microvascular ischemia.

Diffuse cortical atrophy consistent with age-related degenerative changes and associated hydrocephalus ex-vacuo.

Hydrocephalus with periventricular white matter hypoattenuation which may reflect transependymal flow or chronic microvascular disease. If clinical history of multiple, recurrent falls, findings could be seen with NPH. MRI could further evaluate.

Age indeterminate, although remote favored lacunar infarcts in the b/l basal ganglia. MRI could further evaluate.

hydrocephalus ex-vacuo concerning for NPH. no evidence of herniation

subdural hematoma, Occipital skull fracture with soft tissue hematoma

-Hyperattentuation in the interpenduncular fossa, favored trace layering SAH
-Occipital scalp hematoma with locules of soft tissue gas. No underlying calvarial fracture.
-Age advanced cerebral atrophy, global ventriculomegaly, periventricular white matter hypoattenuation and acute pericallosal angle, findings suggestive of NPH.
-No evidence of acute large vascular territory ischemia, mass effect, or hemorrhage.

Questionable pontine hemorrhage

hydrocephalus. hyperdense focus about the ventral medulla.

Hydrocephalus. Blood in interpeduncular fossa

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Subarachnoid hemorrhage in pre-pontine cistern. Global atrophy, compensatory ventricular enlargement, and chronic microvascular ischemic changes.

Age indeterminate left anterior limb internal capsule hypodensity. Stroke disclaimer. Generalized parenchymal volume loss with ex vacuo ventricular dilatation. Hyperattenuating focus within the interpeduncular cistern, concerning for acute subarachnoid hemorrhage. L occipital horn layering intraventricular hemorrhage.

Small volume subarachnoid hemorrhage layering in the interpeduncular fossa.
Chronic ischemic microvascular disease. Remote lacunar infarcts.
Global cerebral volume loss with ex-vacuo dilatation of the ventricles.
Hypodensity in the left cerebellar hemisphere may reflect artifact or acute ischemic stroke.

acute small volume subarach hem layering in the interpeduncualr fossa.

posterior parietooccipital soft tissue contusion/hematoma with scattered air

Age indeterminate bilateral basal ganglia lacunar. Stroke disclaimer.
Interpenduncular subarachnoid?

Small volume subarachnoid hemorrhage withing the interpeduncular fossa.
Left occipital-parietal scalp contusion/hematoma/laceration. No underlying calvarial fracture.
No mass effect, intraventricular extension, or hydrocephalus.
Macro CT old brain.

Small volume subarachnoid hemorrhage layering dependently in the interpeduncular fossa, possibly small volume in a gyriform fashion in the sylvian fissures? Left occipital scalp laceration/hematoma without underlying calvarial fracture. CT old brain, Hydro ex vacuo.

Acute SAH in the interpeduncular fossa. Left occipital soft tissue hematoma/laceration without subadjacent calvarial fracture. Diffuse cerebral volume loss with ex vacuo dilatation of the ventricles. Presumed chronic ischemic white matter disease. Remote infarct in the left anterior limb of the internal capsule.

small volume sah over interpedunicular fossa.
generalized enlargement of ventricles, maybe exvacuo given diffuse cerebral atrophy however developing hydro not excluded
no herniation

Acute subarachnoid hemorrhage in the interpeduncular fossa. No intraparenchymal hemorrhage. No mass effect or hydrocephalus. L occipital contusion/laceration with subcutaneous gas in the soft tissues. Diffuse cerebral volume loss with scattered areas of subcortical and periventricular white matter hypoattenuation which though nonspecific likely represents sequela of chronic microvascular ischemia in this age group.

Left parieto-occipital scalp hematoma with subcutaneous gas and without underlying calvarial fracture.
Small subarachnoid hemorrhage layering in the interpeduncular cistern. Moderate global volume loss with expansion of the ventricles and sulci.

interpedu

small SAH

left occipoparietal scalp contusion with no underlying fracture.

Small amount of subarachnoid blood seen layering in interpeduncular cistern.

Scattered age indeterminant foci of hypo attenuation in bilateral, left greater than right basal ganglia. Likely chronic infarcts.

Age related chronic small vessel and ex vacuum dilation.

dilation of the lateral ventricles
small SAH in the interpeduncular fossa

Small volume SAH in the interpeduncular groove. Recommend CTA of head/neck for further evaluation.
Small area of hypoattenuation in the left putamen, age indeterminate infarct vs dilated perivascular space in the absence of priors.
Global cerebral volume loss with ex vacuo dilatation of the ventricular system. Periventricular hypoattenuation as can be seen with chronic small vessel disease. Intracranial atherosclerosis.

Small volume subarachnoid hemorrhage layering in the interpeduncular fossa. Left occipital region scalp contusion without underlying fracture. Periventricular and subcortical white matter hypoattenuations consistent with chronic small vessel disease. Exvacuo dilation of the ventricles due to global volume loss. Atherosclerosis. Possible ischemia vs artifact in the left cerebellar hemisphere. If there is clinical concern for acute ischemia, recommend MR brain for further evaluation.

Small focus of subarachnoid hemorrhage layering in the interpeduncular fossa. No hydrocephalus or appreciable mass effect.

Senescent changes of the brain with scattered white matter hypoattenuation, generalized cerebral volume loss and associated ex vacuo dilatation of the ventricular system.

Small amount of acute subarachnoid hemorrhage layering in the interpeduncular fossa.
Macro old brain.
No acute ischemia.
No acute calvarial fx.

Small amount of subarachnoid hemorrhage layering in the interpeduncular cistern, with 3rd and lateral ventricle enlargement and periventricular edema. Small soft tissue swelling/hematoma overlying left occipital lobe.

Left occipital scalp hematoma and laceration. No underlying calvarial fracture.

Small volume acute SAH layering in the interpeduncular fossa.

Pan enlargment of the ventricles which are out of proportion for global cerbral volume loss an may realte a component of early hydrocephalous or chronic NPH.

Subarachnoid hemorrhage in the interpeduncular fossa.

Hypodense attenuation within the left frontal lobe and subinsular ribbon, which may represent early infarct. Recommend MRI for further characterization.

Scattered hypodense lesions within the high right frontal cortex, left cingulate gyrus, left thalamus, and bilateral basal ganglia are favored to reflect age-indeterminate infarcts which could be assessed on MRI.

Trace subarachnoid hemorrhage layering over the interpeduncular fossa and the left anterior cerebellum.

Symmetric cerebral volume loss with ex vacuo dilatation of the ventricles and patchy microvascular changes.

Small volume SAH layering in the interpeduncular fossa. No mass effect. Posterior scalp contusion without fracture. Global cerebral atrophy with dilation of ventricles.

L basal ganglia likely remote infarct. Small interpeduncular cistern hemorrhage with hydrocephalus.