Presentation
Fall, headache
Patient Data
The images are degraded by patient positioning. There is a small ovoid acute hemorrhage in the right frontal lobe. This involves the subcortical white matter as well as the cortex. There is no subarachnoid, subdural or extradural hemorrhage. No significant mass effect.
Tiny subcortical hemorrhage in the left frontal white matter.
Moderate periventricular low attenuation in keeping with small vessel change. Mild central and moderate cortical cerebral volume loss.
Case Discussion
Small right frontal lobar hemorrhage without involvement of the cortical surface or extension into the subarachnoid space. Background changes of small vessel disease and moderate atrophy. The location of the hemorrhage is not typical for a traumatic ICH and likely represents a primary ICH.
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.
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PATHOLOGY: Post mortem showed extensive beta amyloid in the neocortex and hippocampus which is predominantly parenchymal in keeping with Alzheimer disease (Braak and Braak stage 2) with very little vascular amyloid (cerebral amyloid angiopathy). Background small vessel disease is present but mild. No tumor or vascular malformation. The cause of the hemorrhage is unclear.
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