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The blood and the vessel

Two articles in this issue of Neurology address the problem of predicting vasospasm after aneurysmal subarachnoid hemorrhage (SAH).1,2 Ischemic brain damage from cerebral vasospasm is a major cause of cognitive and motor deficits after SAH. There is angiographic evidence of vasospasm in two-thirds of cases of SAH, half of which become symptomatic typically 4 to 14 days after the bleeding. When symptoms are focal, recognition of vasospasm as the cause is straightforward. However, vasospasm is often diffuse and only manifested by depressed alertness. In these instances, differentiation of vasospasm from other common complications of SAH (such as hydrocephalus, infection, cerebral edema, aneurysmal rebleeding, and hyponatremia) may be difficult.

The pathophysiology of vasospasm is complex and incompletely elucidated. The presence of oxyhemoglobin in the subarachnoid cisterns seems to be the key promoter of the phenomena that ultimately cause narrowing of the arterial lumen and impaired autoregulation.3 The vascular changes are typically reversible, but when severe, they may cause cerebral infarction. The amount of blood in the subarachnoid space on the initial brain CT scan, young age, and history of smoking are risk factors for vasospasm, but their predictive value is limited. Research on vasospasm has been hampered by lack of …