Background
A cerebral aneurysm is characterized by an abnormal expansion of the cerebral arterial wall, as shown in Figure 1. It is a serious pathological condition because the rupture of an aneurysm leads to subarachnoid hemorrhage (Krex, Schackert, & Schackert, 2001; van Gijn & Rinkel, 2001). Once the cerebral aneurysm ruptures, it results in excessive bleeding into the subarachnoid space, which is the area between the arachnoid membrane and the pia mater surrounding the brain. Subarachnoid hemorrhage has a very high mortality rate between 32% and 67% (Huang & van Gelder, 2002; Schievink, 1997). Despite the risk of potentially serious consequences of cerebral aneurysm, the mechanism of its pathogenesis including initiation, growth, and rupture is still unclear.
Figure 1. Angiogram of a human internal carotid artery with an aneurysm
According to a previous large-scale survey (Rinkel, Djibuti, Algra, & van Gijn, 1998), between 3.6% and 6% of the population have unruptured cerebral aneurysms. Recent developments in medical imaging techniques, such as computed tomography (CT) and magnetic resonance imaging (MRI), have enabled doctors to increasingly detect cerebral aneurysms before they rupture. Although there are some treatment options that are currently in widespread clinical use, such treatments have been known to have a non-negligible potential for complications (Raaymakers, Rinkel, Limburg, & Algra, 1998). Despite these factors, the risk of cerebral aneurysm rupture has been reported to be only approximately 1.9% annually (Rinkel et al., 1998). For these reasons, it is quite difficult for patients and doctors to make a decision on whether surgery should be performed after an aneurysm is detected. To address this problem, it is necessary to understand how cerebral aneurysms initiate and grow. Thus far, it has been widely accepted that blood flow-induced mechanical forces acting on the vessel wall, i.e., hemodynamics, play a vital role in the pathogenesis of cerebral aneurysms.