Presentation
Found collapsed, aphasic and unable to move
Patient Data
Large right sided intracerebral hematoma. It involves both deep and lobar structures (parietal lobe, thalamus, corpus callosum). Its epicenter is within the right parietal white matter. There is subarachnoid extension but no ventricular hemorrhage. The hematoma is irregular but there are no finger-like projections.
There is significant mass effect relating to the hematoma and perihaematomal white matter edema 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.
Case Discussion
Large right intracerebral hemorrhage. It involves both the deep and lobar structures, causes significant mass effect and extends into the subarachnoid space.
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 right parietal white matter, so this hemorrhage would be classified as "uncertain but probably lobar".
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PATHOLOGY
The patient died one day after the ICH and underwent a post mortem. This showed an acute, extensive right intracerebral hemorrhage with subarachnoid hemorrhage. There is extensive small vessel disease in the form of lipohyalinosis and arteriolosclerosis with several lacunar infarcts. There is no amyloid angiopathy on immunohistochemistry
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