Cerebral amyloid angiopathy-associated lobar intracerebral hemorrhage

Case contributed by Mark Rodrigues
Diagnosis certain


Acute onset left sided weakness with slurred speech

Patient Data

Age: 85 years
Gender: Female

Right frontal lobar hemorrhage involving cortex and subcortical white matter. There is adjacent subarachnoid but no intraventricular or subdural hemorrhage. The hematoma has an irregular lobulated contour with finger-like projections (best seen on the sagittal plane - see stack key images).

The hematoma and perihaematomal edema result in some midline shift and partial effacement of the right lateral ventricle.

Moderate periventricular low attenuation in keeping with small vessel change. Marked cortical atrophy.

Case Discussion

Right frontal lobar hemorrhage with the involvement of the cortex and extension into the subarachnoid. The hematoma contains multiple finger-like projections.

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 Edinburgh CT and genetic diagnostic criteria for lobar intracerebral hemorrhage associated with cerebral amyloid angiopathy use CT features (presence of subarachnoid hemorrhage, finger-like projections arising from the ICH) and APOE e4 genotype (if available) to classify a patient as high, intermediate or low risk of CAA-associated ICH. The CT shows subarachnoid hemorrhage and finger-like projections from the hematoma. The patient also possessed at least one APOE e4 allele. Therefore they are high risk for CAA-associated ICH on the Edinburgh CT and genetic diagnostic criteria for lobar intracerebral hemorrhage associated with cerebral amyloid angiopathy.


PATHOLOGY: Postmortem performed 1 month after the ICH showed a large right cerebral hematoma in the posterior frontal lobe with extension into the subarachnoid space. Immunohistochemistry showed vascular deposits mostly in the leptomeningal vessels and parenchyma (Braak and Braak stage 3). Mild small vessel disease throughout the white matter but no lacunar infarcts.


The overall appearances are more consistent with cerebral amyloid angiopathy-associated hemorrhage.

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