Basal ganglia hemorrhage
Found unresponsive. Vomited. GCS 4
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Large left sided intracerebral hematoma. It involves both deep (basal ganglia) and lobar (frontal lobes) structures. Its epicenter is within the right basal ganglia. The hemorrhage extends into the intraventricular space.
There is significant mass effect relating to the hematoma and perihaematomal white matter edema causing midline shift and displacement of the third ventricle. The lateral ventricles are dilated in keeping with hydrocephalus.
Mild generalized cerebral volume loss. Severe periventricular low attenuation in keeping with small vessel change. Chronic left frontal infarct with coarse calcification in keeping with a previous hemorrhage. Chronic infarcts in the right frontal, both occipital lobes and left cerebellar hemisphere.
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, with 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/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).
PATHOLOGY: Post mortem was performed two days after the hemorrhage. This showed an extensive left sided cerebral hematoma involving the basal ganglia and periventricular white matter. There was severe small vessel disease throughout the white matter in the form of lipohyalinosis and arteriolosclerosis There was extensive amyloid deposition in the brain parenchyma (Alzheimer's pathology) and also the parenchymal and meningeal vessels (amyloid angiopathy).
The appearances strongly suggest a primary hemorrhage secondary to chronic hypertension (lipohyalinosis and arteriolosclerosis) however there is extensive cerebral amyloid angiopathy, and it is not possible to definitively say what the underlying cause is.
- Charidimou A, Schmitt A, Wilson D, Yakushiji Y, Gregoire SM, Fox Z, Jäger HR, Werring DJ. The Cerebral Haemorrhage Anatomical RaTing inStrument (CHARTS): Development and assessment of reliability. (2017) Journal of the neurological sciences. 372: 178-183. doi:10.1016/j.jns.2016.11.021 - Pubmed
- Pantoni L. Cerebral small vessel disease: from pathogenesis and clinical characteristics to therapeutic challenges. (2010) The Lancet. Neurology. 9 (7): 689-701. doi:10.1016/S1474-4422(10)70104-6 - Pubmed