Presentation
Sudden onset left arm and leg weakness. Past history of diabetes, hypertension and aneurysmal subarachnoid hemorrhage
Patient Data
Large right parietal lobar hemorrhage involving cortex, subcortical white matter and periventricular white matter. There is localized subarachnoid hemorrhage plus intraventricular hemorrhage. The hematoma has a lobulated contour without finger-like projections.
Mass effect from the hematoma and perihaematomal edema indents the right lateral ventricle without causing significant midline shift. Hydrocephalus of the lateral and third ventricles presumably related to ventricular blood.
Streak artefact from right MCA aneurysm clip.
Severe periventricular low attenuation in keeping with small vessel change. Marked cortical atrophy evident near vertex. Old small cortical infarcts in the right frontal lobe and both cerebellar hemipsheres.
Case Discussion
Large right parietal lobar hemorrhage with the involvement of the cortex, extension into the subarachnoid and intraventricular spaces. The hematoma contains lobulations without distinct 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 CT shows subarachnoid hemorrhage but no finger-like projections from the hematoma. The patient possessed an 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.
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PATHOLOGY: Postmortem performed 18 months after the ICH showed an old right parietal hematoma extending into the subarachnoid space. There is extensive small vessel disease with multiple lacunar infarcts of varying age, enlarged perivascular spaces in the basal ganglia and white matter rarefaction. Immunohistochemistry showed amyloid plaques in the frontal, parietal and temporal regions but no significant cerebral amyloid angiopathy.
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The pathology is in keeping with a small vessel disease (non-cerebral amyloid angiopathy) related hemorrhage. This case highlights that the Edinburgh criteria are not 100% specific for cerebral amyloid angiopathy associated lobar hemorrhage.
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