Vasospasm: Effect on Cerebral Perfusion and Threshold of Injury

In those who survive the initial impact of aneurysmal subarachnoid hemorrhage (aSAH), delayed ischemic neurological deficit (DIND) is the leading cause of morbidity and mortality. Despite therapeutic advances leading to decreased case fatality rate of 0.9% per year from 1960 to 1992, mainly attributed to improved prevention of rebleeding, the 30-day case fatality rate has remained static, and advances in treating DIND is the Holy Grail in aSAH research. The exact pathogenesis of DIND is incompletely understood. Angiographic visualization of proximal arterial vasoconstriction was the first laboratory finding to be associated with DIND reported by Ecker and Riemenschneider. The axiom that aSAH produces proximal arterial narrowing and subsequent ischemia causing infarction and poor outcome has thus become the research and clinical focus in the treatment of aSAH. This article, based on a presentation given at the 2012 Princeton Conference, discusses the significance of delayed vasospasm in the pathogenesis of DIND by attempting to answer the following questions. What is the threshold of vasoconstriction that causes brain injury and how frequently is it reached in the setting of aSAH-induced vasospasm? What causes vasospasm, and is it a necessary and sufficient condition for DIND?