Intracranial saccular aneurysms have been a well-known clinical and pathological entity for over two centuries. The pathophysiological events that lead to aneurysm formation and rupture are, however, poorly understood. Besides an HLA-associated genetic factor, the most widely accepted risk factors are arterial hypertension, female gender, and increasing age. Some aneurysm patients have a deficient formation of Type III collagen. This seems to interfere with the mechanical integrity of the cerebral arterial wall encouraging aneurysm formation. While some of the risk factors may be involved in the process of aneurysm formation, others may be of importance in the actual aneurysm rupture. Medical and surgical developments have only had a slight impact on mortality rates from aneurysm rupture. The principal cause of death and disability is cerebral arterial spasm. Considerable effort has been expended in investigating the etiology of this phenomenon. Previous studies have failed to yield conclusive evidence of the causative agent(s) or the nature of cerebral artery narrowing. The time course of vasospasm after the onset of subarachnoid hemorrhage is consistent with an immune-mediated response, and more recent observations suggest that immunological processes including activation of the complement system may be involved. Missed minor bleeding episodes may thus be a risk factor for aneurysm patients in respect to the development of cerebral vasospasm.
