Abstract
It is well known that so-called vasospasm is one of the most important factors complicating the management of patients with subarachnoid hemorrhage from cerebral aneurysms. Yet, the pathogenesis or even the difinition of it remains obscure, and no satisfactory treatment has been devised to combat its adverse effects. Angiographically demonstrated arterial luminal narrowing has been noted to be reversible and has been attributed entirely to vasospasm. Is angiographic arterial narrowing merely the reduction of the lumen due to presumed change in muscle tone in the vessel wall? In an attempt to elucidate this problem, we have made a prospective and histological study of the intracranial arteries with angiographically demonstrated arterial narrowing in 6 cases. In all of them, the course of vasospasm was investigated by repeated angiographies. At autopsy, main intracranial arteries were carefully dissected free from the base of the brain and processed through graded alcohols. After dehydration the specimens were stored in Tetralin (C12H10) for 2 days. The cleared specimens were examined with a dissecting microscope, comparing them with the angiographic findings. Serial sections were cut and stained for light microscopy. The arterial wall corresponding to the angiographic vasospasm showed various structural changes. We have devided so-called vasospasm into three stages according to the duration of the disease as follows. In acute stages (less than 1 day after the onset), contraction of the medial smooth muscle cells may be the main cause of luminal narrowing. In subacute stages (less than 2 weeks after the onset), the arterial wall demonstrated the reduction in its lumen size with medial thickening, marked corrugation of the internal elastic lamina, intimal edema due to endothelial injuries, and thrombus formation, corresponding with the angiographic vasospasm. In chronic stages (more than 2 weeks after the onset), most cases showed dilatation of the arterial lumen on the angiogram. It was noted that there were necrosis and reduction of the medial smooth muscle cells histologically. In a case which showed progressive angiographic arterial narrowing for more than 2 weeks, the arterial wall showed luminal narrowing with cellulofibrous thickening of the intima and the organization of the thrombus.
The presence of these structural changes following the vasospasm seems to be very important to properly understand this phenomenon. It is clear from our study that the most important thing is to prevent the arteries from spasm from the clinical point of view.
