Presentation
Found on floor, GCS 10. Not moving right hand side
Patient Data
Large left sided intracerebral hematoma. It involves deep (basal ganglia, midbrain) and frontal lobar white matter. The hemorrhage extends into the intraventricular space.
There is significant mass effect relating to the hematoma causing midline shift, compression of the third ventricle and lateral ventricles, and partial effacement of ipsilateral cortical sulci. The temporal horns of the lateral ventricles are dilated in keeping with hydrocephalus.
Severe periventicular low attenation in keeping with small vessel disease +/- transependymal CSF spread. Moderate cortical atrophy evident near vertex.
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 superior basal ganglia/corona radiata. Its configuration is typical of a deep/basal ganglia 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 one week after the ICH and underwent post mortem. This showed an extensive left sided hematoma involving the basal ganglia, anterior aspect of the thalamic nuclei and the left frontal lobe. There is severe small vessel disease in the form of lipohyalinosis and arteriolosclerosis, with enlarged perivascular spaces. There is no evidence of amyloid angiopathy on immunohistochemistry
The post mortem findings are consistent with a deep ICH secondary to small vessel disease.
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