The exact mechanism by which berry aneurysms form remains undetermined, but research indicates that propagation and rupture of the aneurysm are aggravated by hypertension and tachycardia (132). The drug most often associated with acute cerebrovascular events is cocaine. Intracerebral hemorrhages or SAHs are the most frequently observed cerebrovascular complications of this drug (123). Several mechanisms might be responsible for the cerebrovascular complications. Traditional teaching is that hypertension is the likely precursive factor in cocaine-induced aneurysmal rupture, and a sudden rise in systemic arterial pressure might cause hemorrhages, frequently in association with an underlying aneurysm or AVM. Recent reports have indicated that these patients might have underlying vascular malformations (133,134). Rupture of aneurysms and AVMs has been detected in up to half of the patients with hemorrhagic stroke due to cocaine abuse. In addition to stroke, cocaine seems to provoke vascular headache (135). Cocaine abuse appears to be a significant negative factor in the natural history of cerebral aneurysms, especially in young adults (136). Cocaine use predisposed aneurysmal rupture at a significantly earlier age and in much smaller aneurysms, particularly of those located in the anterior circulation (137,138).
Was this article helpful?