With rupture of the aneurysm, blood under high pressure is forced into the subarachnoid space and the resulting clinical events assume one of three patterns: (1) the patient is stricken with an excruciating generalized headache and vomiting and falls unconscious almost immediately; (2) severe generalized headache develops in the same instantaneous manner but the patient remains relatively lucid with varying degrees of stiff neck—the most common syndrome; (3) rarely, consciousness is lost so quickly that there is no preceding complaint. If the hemorrhage is massive, death may ensue in a matter of minutes or hours, so that ruptured aneurysm must be considered in the differential diagnosis of sudden death. A considerable proportion of such patients probably never reach a hospital. Decerebrate rigidity and brief clonic jerking of the limbs may occur at the onset of the hemorrhage, always in association with unconsciousness. Persistent deep coma is accompanied by irregular respirations, attacks of extensor rigidity, and finally respiratory arrest and circulatory collapse. In these rapidly evolving cases, the subarachnoid blood has greatly increased the intracranial pressure to a level that approaches arterial pressure and caused a marked reduction in cerebral perfusion. In some instances, the hemorrhage has dissected intracerebrally and entered the brain or ventricular system.
Rupture of the aneurysm usually occurs while the patient is active rather than during sleep, and in a few instances, during sexual intercourse, straining at stool, lifting heavy objects, or other sustained exertion (see “Headaches Related to Sexual Activity” in Chap. 9). A momentary Valsalva maneuver, as in coughing or sneezing, has generally not caused aneurysmal rupture (it may cause arterial dissection). In patients who survive the initial rupture, the most feared complication is rerupture, an event that may occur at any time from minutes up to 2 or 3 weeks.
In less-severe cases, consciousness, if lost, is regained within minutes or hours, but a residuum of drowsiness, confusion, and amnesia accompanied by severe headache and stiff neck persists for at least several days. Because the hemorrhage in most cases is confined to the subarachnoid space, there are few if any focal neurologic signs. That is to say, hemiparesis, hemianopia, and aphasia are absent. On occasion, a jet of blood emanating from an aneurysm ruptures into the adjacent brain or insular cistern and produces a hemiparesis or other focal syndrome. This may be more common when the aneurysm has bled in the past, after which it adheres to the brain, thus predisposing to intracerebral hemorrhage at the time of subsequent rupture. There is, however, a transient focal acute syndrome that occasionally occurs in the territory of the aneurysm-bearing artery. The pathogenesis of such manifestations is not fully understood, but a transitory fall in pressure in the circulation distal to the aneurysm or some form of acute transient vasospasm has been postulated. An entirely separate problem of delayed vasospasm is responsible for focal signs that emerge after several days as discussed below. Transient deficits when they do occur constitute reliable indicators of the site of the ruptured aneurysm (see below).
Convulsive seizures, usually brief and generalized, occur in 10 to 25 percent of cases according to Hart and associates (1981) (but far less often in our experience) in relation to acute bleeding or rebleeding. These early seizures do not correlate with the location of the aneurysm and do not appear to alter the prognosis.