Pathology of stroke

Abstract

Large cerebral infarctions were caused by atherosclerosis with or without thrombosis in the proximal circumflex (cortical) cerebral arteries. Hypertension, hypercholesterolemia, hypoxidosis, and vasospasm were considered to induce endothelial cell injuries, which might be the primary events not only in atherosclerosis, but also in arteriosclerosis and arteriosis formation. Morphogenesis of atherosclerosis and causes of associated thrombosis were also discussed. Small cerebral infarcts were produced not only by arteriosclerosis, arteriosis, and atherosclerosis, but also by arterionecrosis-derived microaneurysms occluded by thrombi in the distal penetrating (perforating) cerebral arteries. Pathogenesis and morphogenesis of the arterial lesions were discussed. Recent increase of the arterionecrosis occluded by thrombosis in the pathogenesis of small infarcts (lacunes) was noted. The direct cause of hypertensive cerebral hemorrhage was the rupture of arterionecrosis-derived microaneurysms in the distal penetrating cerebral arteries. The primary change of the arterionecrosis was the medial muscle cell necrosis, the causes of which were considered to be hypertension, aging, poor diet low in cholesterol, vasospasm, and the congenitally poor wall structure of the arteries. The development and healing of experimental arterionecrosis in hypertensive rats were also reported.