Vasospasm Following Aneurysmal Subarachnoid Hemorrhage

Majority of morbidity and mortality due to aneurysmal subarachnoid hemorrhage (aSAH) is secondary to cerebral ischemia. Classically, the angiographic arterial narrowing following aSAH has been termed as angiographic vasospasm, which may or may not lead to clinical manifestations and cerebral ischemia, in which case it would be called symptomatic vasospasm. This concept has recently been questioned. Not always angiographic vasospasm leads to cerebral ischemia, which, in turn, may occur in a territory different from the one irrigated by the narrowed artery or even in the absence of any angiographic vasospasm, i.e., cerebral ischemia that occurs late (days after aSAH) cannot be attributed solely to the arterial narrowing seen on angiography [1]. Currently, the term “delayed cerebral ischemia” (DCI) has been proposed to replace the previously used “symptomatic vasospasm.” The clinician should be able to recognize and differentiate the radiological vasospasm from the clinical worsening secondary to DCI, whose etiology is multifactorial and includes angiographic arterial narrowing (Fig. 29.1). Alternative mechanisms have been proposed and include microvascular spasm and failure of cerebral blood flow (CBF) autoregulation, microthrombosis and microembolism, cortical spreading depolarization and ischemia, and delayed neuronal apoptosis resulting from acute brain injury. A more extensive review of the pathophysiology of DCI is out of the scope of this review. These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.