Abstract
A histological study of the cerebral arteries was made on 30 patients (15 male, 15 female, average age 56) who died from subarachnoideal hemorrhages as a result of the rupture of berry aneurysms in the Willis' circle. Particular attention was paid to the small-sized arteries less than 300μm in diameter which are located in the cerebral cortex, medulla, putamen, pallidum, cerebellum, mid brain and pons.
For comparison, vascular alteration were observed in 12 patients (10 male, 2 female, average age 60) with cerebral hemorrhages of hypertensive nature, and 10 patients (6 male, 4 female, average age 67) with cerebral infarction. Most arteries examined in the above mentioned three groups showed considerable changes in the intima, media and adventitia in variable extent. In the patients with subarchnoideal hemorrhages and with cerebral hemorrhages, commonly seen were plasma imbibition, focal aneurysmal dilatation due to partial defect in the media, marked dilatation with attenuated wall and fibrous sclerosis with distension-all of which showed irregular asymmetrical contours. In comparison with cerebral hemorrhages, the arteries of the patients with subarachnoideal hemorrhages were consistently characterized with plasma imbibition into the media and partial medial defect, especially in the subarachnoideal branches.
Thus it can be postulated that small-sized arteries of the patients with subarachnoideal hemorrhages were exposed to repeated circulatory dysfunction which caused recurrent and aggravated hemodynamic abnormalities, resulting in plasma imbibition into the media and damage of smooth muscle cells of the media. It is possible to assume that irregular asymmetrical shaped arteries were due to repeated abnormal arterial movement. Berry aneurysms may occur in such sites of locus minoris by abnormal pressure as in the arteries of the Willis' circle.
The author believes that the rupture of the berry aneurysms as a cause of a subarachnoideal hemorrhage is one of the final events on the continuation of repeated burdens to subarachnoideal arteries, while various mural alterations of these arteries take place as a result of dysfunction of arterial wall movement over a long period.
