Intracranial aneurysms
| Intracranial aneurysms |
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Overview
The catastrophic potential of intracranial aneurysms, arteriovenous malformations (AVMs), and arteriovenous fistulas (AVFs) and the complexity of their pathogenesis have made them the subject of intense interest and study over the past 80 years. Advances in the ability to treat these lesions have been paralleled by rigorous research on their pathophysiology. An increase in the longevity of the population over the past century and improvements in imaging techniques contribute to more frequent encounters with these lesions by neurosurgeons and interventionists. Despite numerous clinical and laboratory research projects studying the pathophysiology of these lesions, much remains to be learned. In this chapter, we will discuss the pathophysiology of various types of intracranial aneurysms, as well as AVMs and AVFs.
Berry Aneurysms
Berry aneurysms arise at vessel bifurcations or curves. These aneurysms occur mostly between the ages of 40 and 70 years. The pathogenesis of berry aneurysms is multifactorial. Compelling evidence suggests that hemodynamic factors as well as degenerative histological changes in the parent vessel wall contribute to aneurysm formation. Early in the process of berry aneurysm formation, destruction and eventual loss of the media occur (1). The internal elastic layer becomes disrupted and is eventually lost.
The mechanisms by which these changes occur are not well understood but have been attributed in part to atherosclerotic changes. This weakening in the vessel wall sets the stage for hemodynamic forces to cause saccular dilation (2). Reduced peripheral resistance in the intracranial circulation, along with more rapid blood flow, may be associated with an augmented pulse pressure, which can lead to saccular dilation (1). Recent studies have demonstrated that hemodynamic stress in vascular walls can result in alterations in extracellular matrix organization (3). Turbulent flow in aneurysmal sacs damages the endothelium and results in laminar necrosis of the wall and expansion of the aneurysm. If a small aneurysm does not rupture, partial healing occurs through mural thrombus formation followed by organization of the thrombus with scarring of the wall, invasion of fibroblasts, collagen formation, platelet aggregation, and deposition of fibrous material. Repeat hemorrhages can occur in the wall, leading to repetitive cycles of abnormal healing and aneurysm growth. Giant aneurysms are believed to form by these mechanisms (4).
Several risk factors and associated conditions have been linked with intracranial aneurysm growth and rupture. Smoking has been associated with larger berry aneurysm size and multiple aneurysms (5-7). Alcohol abuse has been associated with aneurysm rupture (7). The role of hypertension in aneurysm formation has been controversial in the literature. Hypertension as a direct cause of aneurysms has never been established; however, it is believed that hypertension may exacerbate a rupture when it occurs and may contribute to aneurysm growth. Several conditions have been associated with a greater propensity for berry aneurysms. These conditions include coarctation of the aorta, polycystic kidney disease, and various connective tissue disorders such as Ehlers-Danlos syndrome (1).