Basal ganglia hemorrhage

Case contributed by Mark Rodrigues
Diagnosis certain

Presentation

Worsening headache with right sided weakness. Then collapsed with GCS 5

Patient Data

Age: 70 years
Gender: Male
ct

Large left sided intracerebral hematoma. It involves both deep (basal ganglia and thalamus) and parietal white matter. Its epicenter is within the left basal ganglia. The hemorrhage extends into the intraventricular and subarachnoid spaces.

There is significant mass effect relating to the hematoma causing midline shift, compression of the third ventricle and partial effacement of ipsilateral cortical sulci. The temporal horns of the lateral ventricles are dilated in keeping with hydrocephalus.

CT angiogram shows no aneurysm, arteriovenous malformation. or spot sign.

Case Discussion

Large left intracerebral hemorrhage. It involves both the deep and lobar structures, causing significant mass effect.

Identifying whether an ICH is lobar or deep is important as this in part determines the likely underlying etiology 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, which has a higher recurrent ICH rate). In cases such as this one, establishing whether an ICH is lobar or deep is difficult.

The Cerebral Hemorrhage Anatomical RaTing inStrument (CHARTS) is a recently published research tool which aims to improve observer agreement. The epicenter of this hemorrhage (axial slice with the biggest ICH diameter) is within the left basal ganglia. Its configuration is also typical of a deep hemorrhage. Therefore this hemorrhage would be classified as "uncertain but probably deep". The likely underlying etiology is "hypertensive" arteriopathy (non-amyloid small vessel disease).

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PATHOLOGY

The patient died the same day and underwent a post mortem.  This showed an extensive left sided intracerebral hemorrhage involving the basal ganglia, thalamus and periventricular white matter. 

There is severe small vessel disease in the form of lipohyalinosis and arteriolosclerosis, with enlarged perivascular spaces.  There is minimal amyloid angiopathy on immunohistochemistry

The post mortem findings are consistent with a deep ICH secondary to small vessel disease.

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