Lobar intracerebral haemorrhage
Found collapsed on floor. GCS 6
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Large left sided intracerebral haematoma. It involves both deep and lobar structures. Its epicentre is within the left frontal white matter. The haemorrhage extends into the intraventricular spaces, but there is no clear subarachnoid or subdural haemorrhage. THe haematoma is irregular but there are no finger-like projections
There is significant mass effect relating to the haematoma and perihaematomal white matter oedema causing midline shift, compression of the ipsilateral lateral ventricle and third ventricle and effacement of ipsilateral cortical sulci. There is dilatation of the temporal horns of the lateral ventricles in keeping with hydrocephalus.
Severe periventricular low attenuation probably in keeping with small vessel disease. Moderate to severe cortical atrophy.
Large left intracerebral haemorrhage. It involves both the deep and lobar structures, causes significant mass effect and extends into the intraventricular spaces. Its size and involvement of the ventricular system, along with the patient's age and decreased GCS on admission are poor prognostic factors on the ICH score.
Identifying whether an ICH is lobar or deep is important as this in part determines the likely underlying aetiology as well as the prognosis (deep ICH are usually related to hypertensive arteriopathy, whereas lobar ICH can be due to hypertensive arteriopathy or cerebral amyloid angiopathy, with a higher recurrent ICH rate). In cases such as this one, establishing whether an ICH is lobar or deep is difficult.
The Cerebral Haemorrhage Anatomical RaTing inStrument (CHARTS) is a recently published research tool which aims to improve observer agreement. The epicentre of this haemorrhage (axial slice with the biggest ICH diameter) is within the left frontal white matter, so this haemorrhage would be classified as "uncertain but probably lobar".
Lobar intracerebral haemorrhage is frequently attributed to small vessel diseases (cerebral amyloid angiopathy or arteriolosclerosis). Differentiating lobar haemorrhage 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 haemorrhage associated with cerebral amyloid angiopathy uses CT features (presence of subarachnoid haemorrhage, 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 no subarachnoid haemorrhage or finger-like projections from the haematoma. The patient did not possess at least one APOE e4 allele. Therefore they are low risk for CAA-associated ICH on the Edinburgh CT and genetic diagnostic criteria for lobar intracerebral haemorrhage associated with cerebral amyloid angiopathy.
PATHOLOGY: Post mortem showed a large left sided cerebral haemorrhage. There is background small vessel disease in the form of lipohyalinosis throughout the cerebrum, cerebellum and brainstem. There is extensive small vessel disease. Immunohistochemistry shows extensive parenchymal amyloid deposition (Braak and Braak stage 3) but very little vascular amyloid. No evidence of vascular malformation or malignancy.
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