CEREBRAL VASCULAR LESIONS IN AUTOPSY CASES OF APOPLECTIC CEREBRAL HEMORRHAGE, WITH SPECIAL REFERENCE TO THE MORPHOGENESIS OF THE SO-CALLED ANGIONECROSIS

Abstract

In 20 autopsy cases of apoplectic cerebral hemorrhage, the cerebral vascular lesions were investigated morphologically. 1) In 18 of them was found the so-called angionecrosis, which closely resembled, histologically and histochemically, the experimental fibrinoid degeneration in arterial walls of rabbits (in Arthus phenomenon), dogs (by bilateral nephrectomy), rats (by DOCA administration) and rabbits (by Goldblatt's procedure). Because fibrinoid substance of the angionecrotic lesions inhibits transintimal perfusion, the vascular walls underwent histolysis, resulting in rupture. 2) In apoplectic cerebral hemorrhage, hemorrhage by rupture owing to fibrinoid degeneration (angionecrosis) of medium-sized (150360μ in diameter) and small-sized (50150μ) arteries played a decisive role. Fibrinoid degeneration of minute vessels (arterioles in diameter less than 50μ and capillaries) occurred, in most cases, secondarily as a result of massive hemorrhage. 3) Almost in all the medium-sized arteries in which fibrinoid degeneration (angionecrosis) developed, preceded old arteriosclerotic changes as well as fresh arteriosclerotic changes such as the intimal edema (blood plasma infiltration) were observed. This was also the case with some of the small-sized arteries with angionecrosis. 4) Angionecrosis may be understood as acute and severe development of arteriosclerosis or its acute exacerbation. 5) Fibrinoid substance of angionecrosis (fibrinoid degeneration), which is the direct cause of apoplectic cerebral hemorrhage is derived from the permeation of blood plasma and fibrin into arterial walls as the result of abnormal or increased vascular permeability due to various causes. As such causes can de considered a) direct action of hypertension, b) disturbed nourishment (hypoxidosis) of arterial walls due to decreased transintimal perfusion caused by hypertension, arteriosclerosis, vascular spasms and vascular aging, and c) change in nature of blood and tissue fluid due to failure of renal function and others.