Theories Of Saccular Aneurysm Etiology

Controversy continues over the etiology of intracranial saccular aneurysms. The leading theories can be divided into 2 groups. The first group argues that congenital or early developmental factors are responsible for aneurysmal formation. The second favors acquired, or postnatal, changes in the intracerebral vasculature. These views are certainly not mutually exclusive, and it is likely that multiple factors are responsible for aneurysmal formation.

One of the earliest theories of congenital origin of aneurysms is known as the medial defect theory, which states that congenital defects of the vascular media (defects of Forbus) are the starting points for the formation of aneurysms. Studies by Forbus demonstrated that the media at the apex of cerebral arterial bifurcations is often absent (12). However, autopsy studies suggested that such bifurcation medial defects are common and can occur in 80% of the population, including those without aneurysms (24) . It was argued that these areas are relatively weak and are susceptible to the hemodynamic stress of blood flow. Forbus likens aneurysmal formation to the formation of "false diverticulum" in areas of inherent weakness in intestinal walls (areas where large vessels enter). Just as false diverticula develop over time with peristaltic intestinal movements, cerebral aneurysms form over time at medial defects under the effects of blood pulsation. Without the media for support, the IEL is easily damaged and becomes the nidus for aneurysmal growth.

However, some observations argue against congenital medial defects as the origin of aneurysms. Medial defects increase in frequency with age (24), which indicates that these defects are not all congenital. They are more common in the posterior circulation, which does not coincide with the most common locations of saccular aneurysms (25). They are also located in extracranial arteries, where aneurysms are uncommon (21,26). Medial defects are common at the lateral angles of bifurcations, yet saccular aneurysms do not typically form there (17,20,26,27). Interestingly, studies of early aneurysmal formation suggest that the initial mural thinning or microevagination often occurs adjacent to the apical raphe and not at the raphe itself (21,28,29).

Stehbens disputes the idea that the medial defect is a defect at all and argues instead for a functional role (30). The term "medial defect" suggests that some sort of deficiency exists. He suggests that a better term would be "medial raphe" to emphasize the possible functional role of the lack of media at the apical bifurcation. He argues that the media of adjoining walls will pull in opposite directions during vasoconstriction and suggests that the apex acts as an anchor for the muscle. In support of this theory, it has been shown that the apex is composed of collagen fibrils that anchor the smooth muscle of the media and provide more stability for the vessel wall (31). Thus, the apex of the bifurcation might not be an area of weakness, even without media. Furthermore, animal models of cerebral aneurysms and autopsy studies both suggest that the early development of aneurysms occurs at sites other than medial defects (32,33).

The medial defect theory is not the only congenital theory that has been proposed. In 1933, Drennan proposed that aneurysms originate from remnants of embryonic vessels. If they existed, such remnants would certainly be an inherent weakness in the vessel wall, which would be susceptible to hemodynamic stress (34). However, no evidence of such remnants has been revealed, despite multiple studies of the histology of normal arterial bifurcations (28). Bremer hypothesized that vessels of the primitive capillary plexus might have failed to atrophy, providing a focus for vessel wall dilatation and aneurysmal formation (35). However, vessels do not commonly exit from the apex of an aneurysm.

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