Abstract
A complete serial section of the occluded arterial segments from twenty-one cases of thrombosis of the large branches of circle of Willis was made. Twenty-three thrombi were found in these cases and all the thrombi were precipitated on the atherosclerotic or fibrosed arterial wall.
Fifteen cases out of 18 cases of which blood pressure was examined during life showed persistent hypertension and 11 cases out of 18 cases showed hypercholesteremia (>200mg/dl) before the onset of cerebral thrombosis.
The characteristics of thrombosed arterial wall were as follows: intimal hemorrhage in 17 cases, superficial edema of fibrous cap in 2 cases, rupture of the atheroma in 1 case, superficial foam cell accumulation in 1 case and intimal thickening or atheroma in 2 cases.
Many intramural capillaries were present in the atheroma or thickened intima in 13 cases with intimal hemorrhage. It was considered that intimal hemorrhage was resulted from the rupture of these capillaries, not from the backflow of blood through intimal defects, and that these capillaries were derived from the main arterial lumens. In most cases with hypertension the capillary wall were thickened and occasionally showed fibrinoid necrosis associated with hemorrhage and infiltration of hemosiderin-laden macrophages.
Only one thrombus was developed over the break of the atheroma, from which many foam cells, cholesterin crystals and a little fatty gruel were escaped into the arterial lunina.
Two cases showed no intramural hemorrhage, rupture of the intima nor other specific findings except atherosclerotic change of the arterial wall. Clinically these two cases had severe persistent high blood pressure.
From the obervations in these series it appears that intimal hemorrhage from the rupture of intimal capillaries derived from the arterial lumens is the main cause of cerebral thrombosis and that persistent hypertension is the imminent danger of rupture of the intimal capillaries.
