Cerebral amyloid angiopathy-associated lobar intracerebral hemorrhage

Case contributed by Mark Rodrigues
Diagnosis certain

Presentation

Sudden reduction in mobility with right sided weakness

Patient Data

Age: 80 years
Gender: Male

Acute left parietal hematoma involving the cortex and subcortical white matter. There is no definite subarachnoid hemorrhage, and no subdural, extradural or intraventricular component. The haemtoma has a slightly lobulated contour and fluid level but no finger-like projections.

Mass effect on the adjacent lateral ventricle and overlying cortical sulci.

Severe periventricular low attenuation in keeping with small vessel disease.  Severe generalized cerebral volume loss.

Case Discussion

Left parietal lobar hemorrhage with involvement of the cortex. There is no extension into the subarachnoid space or ventricles. Background changes of severe small vessel disease (periventricular low attenuation) and atrophy.

Lobar intracerebral hemorrhage is frequently attributed to small vessel diseases (cerebral amyloid angiopathy or arteriolosclerosis).  Differentiating lobar hemorrhage due to cerebral amyloid angiopathy and arteriolosclerosis is important due to differences in recurrent ICH and post-stroke dementia risk (higher with CAA-associated ICH).

The initial CT shows no subarachnoid hemorrhage or finger-like projections from the hematoma. The patient possessed at least one APOE e4 allele. Therefore they are intermediate risk for CAA-associated ICH on the Edinburgh CT and genetic diagnostic criteria for lobar intracerebral hemorrhage associated with cerebral amyloid angiopathy.

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PATHOLOGY: Post mortem showed left parietal hematomata with extension into the subarachnoid space. There is small vessel disease throughout the white matter with enlarged perivascular spaces and rarefaction, lipohyalinosis and arteriolosclerosis. Widespread amyloid angiopathy with concentric splitting of some vessels.  There is also extensive parenchymal amyloid. 

 

The pathology demonstrates extensive cerebral amyloid angiopathy and arteriolosclerosis, both of which could result in the hemorrhage.  The distribution of hemorrhage is more suggestive of cerebral amyloid angiopathy

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