Site Specificity of Cerebral Arteriosclerosis Involved by Hypertension; Cerebral Hemorrhage and Binswanger's Disease

Abstract

We studied electron microscopically vascular lesions of lenticulostriate artery and subcortical artery of the front lobs in autopsied brains with hypertensive disorders such as cerebral hemorrhage, 15 cases, cerebral thrombosis or infarction, 5 cases and Binswanger's disease, 6 cases. Diffuse medial cell damage (exhausted degeneration) is an essential alteration regardless association of atherosclerotic intimal thickening. Small arteries, 100-200μ in diameter distributed in subcortical white matter in patients with Binswanger's disease were mostly patent regardless atherosclerosis, and were involved by severe medial cell damage (moth-eaten atrophy and cell necrosis). Those arteries seem to be insufficient on responce to vascular autoregulation mechanism by vascular autonervus and/or vasoactive agents, PGI₂ and TXA₂. Thus, dysfunctional ischemia may occur as a progression mechanism of angiopathic dementia.