Inflammation and Cerebral Aneurysms

Abstract

Cerebral aneurysms (CAs) occur in up to 5% of the population in the US, and up to 7% of all strokes are caused by CA rupture. Little is known about the pathophysiology of cerebral aneurysm formation, though inflammatory cells such as macrophages and neutrophils have been found in the walls of CAs. After many studies of both human specimens and experimentally induced animal models of aneurysms, the predominant model for CA formation and progression is as follows: (1) endothelial damage and degeneration of the elastic lamina, (2) inflammatory cell recruitment and infiltration, (3) and chronic remodeling of vascular wall. Endothelial damage can be caused by changes in hemodynamic stress, which results in the upregulation of proinflammatory cytokine secretion followed by the recruitment of various inflammatory cells. This recruitment and subsequent infiltration induces smooth muscle cell proliferation, apoptosis, and remodeling of the artery wall. These complex events are thought to lead to aneurysm rupture. This review will focus on the role of the immune system in the formation and progression of saccular CA and the ways in which the immune response may be modulated to treat aneurysms and prevent rupture.