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Lobar intracerebral hemorrhage

Case contributed by Mark Rodrigues
Diagnosis certain

Presentation

Chest pain and right sided paresthesia

Patient Data

Age: 85 years
Gender: Female

Small ovoid acute hemorrhage in the left temporal periventricular and subcortical white matter.  This does not involve the cerebral cortex and there is no subarachnoid, ventricular or subdural extension. No finger-like projections arising from the hematoma.

There is mild localized mass effect on the adjacent left lateral ventricle.

Mild periventricular low attenuation in keeping with small vessel change and mild generalized cerebral volume loss.

3 Month follow up MRI

mri

Slit-like signal drop out on the SWI images in the left temporal periventricular and subcortical white matter consistent with a resolved hematoma. No other macrohaemorrhages and no superficial siderosis. There are several microbleeds in the right cerebellar hemisphere. Symmetrical signal dropout in the basal ganglia in keeping with mineralization.

Multiple enlarged perivascular spaces in the basal ganglia and centrum semiovale, mild periventricular and pontine hyperintensities in keeping with small vessel disease, and moderate generalized cerebral volume loss.

Case Discussion

Left temporal lobar hemorrhage without involvement of the cortex or extension into the subarachnoid space. Background changes of small vessel disease (enlarged perivascular spaces and white matter hyperintensities) and moderate 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 Edinburgh CT and genetic diagnostic criteria for lobar intracerebral hemorrhage associated with cerebral amyloid angiopathy uses 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. This patient shows no subarachnoid hemorrhage, no finger-like projections and no APOE e4 allele and is therefore low risk for CAA-associated ICH on the Edinburgh criteria.

 The modified Boston criteria for cerebral amyloid angiopathy use MRI features to classify patients as probable, possible or neither probable/possible CAA. This patient has a single lobar macrohaemorrhage and multiple cerebellar microbleeds and so is probable for CAA on the modified Boston criteria.

 Post mortem showed a left parietotemporal hematoma which is predomintanly in white matter but does involve the cortex.  There is severe small vessel disease throughout the cerebrum, cerebellum, and brainstem.  Immunohistochemistry showed no cerebral amyloid angiopathy.

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