This is the fourth most frequent cerebrovascular disorder—following embolism, atherothrombosis including lacunes, and primary intracerebral hemorrhage, but one that is often disastrous. Saccular aneurysms are also called “berry” aneurysms because they take the form of small, thin-walled blisters protruding from arteries of the circle of Willis or its major branches. Their rupture causes a flooding of the subarachnoid space with blood under high pressure. As a rule, the aneurysms are located at vessel bifurcations and branchings (Fig. 33-25) and are generally presumed to result from developmental defects in the media and elastica of the arteries. An alternate theory holds that the aneurysmal process is initiated by focal destruction of the internal elastic membrane, which is produced by hemodynamic forces at the apices of bifurcations (Ferguson). As a result of the local weakness in the vessel wall, the intima bulges outward, covered only by adventitia; the sac then gradually enlarges and may finally rupture. Cerebral aneurysms vary in size from 2 mm to 2 or 3 cm in diameter, averaging 7.5 mm (Wiebers et al, 1981 and 1987). Those that rupture usually have a diameter of 10 mm or more, but rupture also occurs, albeit less often, in those of smaller size. Aneurysms vary greatly in form. Some are round and connected to the parent artery by a narrow stalk; others are broad-based without a stalk; and still others take the form of narrow cylinders. The site of rupture is usually at the dome of the aneurysm, which may have one or more secondary sacculations. A review of the subject by Schievink gives further details of this extensively studied subject.
The incidence of unruptured aneurysms in routine autopsies is almost 2 percent—excluding minor vessel outpouchings of 3 mm or less. Moreover, aneurysms are multiple in 20 percent of patients. In the past, it was estimated that 400,000 Americans harbored unruptured aneurysms and that there were 26,000 aneurysmal subarachnoid hemorrhages per year (Sahs et al, 1981 and 1984). Rupture of saccular aneurysms in childhood is rare, and they are seldom found at routine postmortem examination in this age group; beyond childhood, they gradually increase in frequency to reach their peak incidence between ages 35 and 65 years. Therefore aneurysms cannot be regarded as typical congenital anomalies; rather, they appear to develop over the years on the basis of either a developmental or acquired arterial defect. There is an increased incidence of polycystic kidneys, fibromuscular dysplasia of the extracranial arteries, moyamoya, arteriovenous malformations of the brain, and coarctation of the aorta among persons with saccular aneurysms and vice versa. An accompanying saccular aneurysm is found in approximately 5 percent of cases of cerebral arteriovenous malformation, usually on the main feeding artery of the malformation.