Cerebral amyloid angiopathy-associated lobar intracerebral hemorrhage
Presentation
Sudden onset right side weakness plus vomiting
Patient Data
Large left frontal lobar hemorrhage involving cortex, subcortical white matter and periventricular white matter. There is subarachnoid and intraventricular hemorrhage. The hematoma has multiple finger-like projections.
Mass effect from the hematoma and perihaematomal edema resulting in midline shift, obstructive hydrocephalus of the lateral ventricles and partial effacement of the suprasellar cistern.
Moderate periventricular low attenuation may represent small vessel change and/or transependymal CSF spread. Mild atrophy.
Case Discussion
Large left frontal lobar hemorrhage with the involvement of the cortex, extension into the subarachnoid and intraventricular spaces. 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 initial CT shows subarachnoid hemorrhage and finger-like projections from the hematoma. The patient did not possess 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 8 days after the ICH showed an extensive left cerebral hematoma with subarachnoid hemorrhage. Immunohistochemistry showed extensive parenchymal (Braak and Braak stage 5) and widespread vascular depositions (cerebral amyloid angiopathy). Extensive small vessel disease throughout the white matter with several lacunar infarcts.
This case highlights that the small vessel diseases underlying lobar ICH is often mixed. The hemorrhage may have been related to arteriolosclerosis/lipohyalinosis or cerebral amyloid angiopathy.
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