The Pathophysiology of Delayed Cerebral Ischemia

Subarachnoid hemorrhage (SAH) affects 30,000 people in the Unites States alone each year. Delayed cerebral ischemia occurs days after subarachnoid hemorrhage and represents a potentially treatable cause of morbidity for approximately one-third of those who survive the initial hemorrhage. While vasospasm has been traditionally linked to the development of cerebral ischemia several days after subarachnoid hemorrhage, emerging evidence reveals that delayed cerebral ischemia is part of a much more complicated post-subarachnoid hemorrhage syndrome. The development of delayed cerebral ischemia involves early arteriolar vasospasm with microthrombosis, perfusion mismatch and neurovascular uncoupling, spreading depolarizations, and inflammatory responses that begin at the time of the hemorrhage and evolve over time, culminating in cortical infarction. Large-vessel vasospasm is likely a late contributor to ongoing injury, and effective treatment for delayed cerebral ischemia will require improved detection of critical early pathophysiologic changes as well as therapeutic options that target multiple related pathways.