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An aneurysm is a localized weakening of the wall of a cerebral artery causing dilation, or ballooning of a blood vessel. The cerebral vasculature is a common site for aneurysm formation. The incidence of cerebral aneurysm is 1%–6% and the incidence of aneurysm rupture is 12/100,000. Aneurysm occurs at any age but peaks at ages 40–60. The male-to-female ratio is 2:3. There is a genetic component and the chromosomal loci associated with aneurysms are on chromosomes 1, 2, 7, 11, and 19. Tables 36-1 and 36-2 list the inherited and noninherited risk factors for intracranial aneurysms.
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The incidence of rupture depends on the size of the aneurysm according to Laplace’s Law (P = 2T/r, where P = pressure, T = tension, and r = radius), with 90% rupture of size greater than 12 mm, 5% of size greater than 12–15 mm, and 5% rupture incidence of 15 mm or less.
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Most aneurysms occur at the Circle of Willis: anterior communicating artery and anterior cerebral artery (30%–35%), internal carotid artery and posterior communicating artery (25%), middle cerebral artery (20%), and the basilar artery and posterior circulation (5%–10%).
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Most intracranial aneurysms are asymptomatic. Symptomatic aneurysms are likely due to subarachnoid hemorrhage (SAH) from aneurysm rupture. Twenty-five percent of SAH die before hospitalization. In hospital mortality approaches 50% and most survivors have permanent disability. Alternatively, aneurysms present with symptoms related to pressure on cranial nerves 3, 4, and 6.
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Signs and symptoms result from aneurysm rupture with an abrupt rise in ICP that produces a severe headache with or without loss of consciousness. Described as the “worst headache of my life,” SAH may include nausea, vomiting, and vision impairment. Blood in the CSF produces meningism, which causes photophobia, neck stiffness, and headache.
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There are several classification systems for SAH severity. The Hunt and Hess classification is noted in Table 36-3.
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