Hemodynamic mechanisms underlying cerebral aneurysm pathogenesis

Abstract

Intracranial aneurysms and associated subarachnoid hemorrhage (SAH) are predominant cerebrovascular disorders that present a significant public health risk through high rates of morbidity and mortality. Unruptured aneurysms that become large enough compress cerebral tissue and manifest various neurological signs. But the largest danger presented by these cerebrovascular lesions is from the increased likelihood that the vessel will rupture, causing a SAH, a condition that creates higher risk of cerebral ischemia through reduced cerebral blood flow and vasospasm. The specific pathophysiological mechanisms that cause these lesions are not fully understood. The current literature focuses on understanding the effects of and links between hemodynamic forces, vascular remodeling and inflammation, and genetics in aneurysm formation, development, and rupture. The present study represents a survey of the complete hemodynamic pathogenesis of aneurysmal SAH detailing the many factors and their connections that contribute to the pathophysiology of this disorder.