Delayed cerebral ischemia after subarachnoid hemorrhage: from vascular spasm to cortical spreading depolarizations.

Non-traumatic subarachnoid hemorrhage (SAH) represents about 5 to 6% of the overall incidence of stroke and is associated with high morbidity and mortality. Despite the substantial research and clinical efforts, delayed cerebral ischemia (DCI) is still the major complication after SAH and represents an important factor for severe neurological deficits. Cerebral vasospasm (VSP) has been recognised for a long time as an important underlying pathophysiologic cause of DCI, but it is now clearer that the mechanisms underlying DCI are multifactorial. Among other pathomechanisms proposed, ischemia-producing cortical spreading depolarizations (CSDs) are likely to be involved in DCI development. Understanding the plethora of different pathophysiological derangements after SAH is very important for the development of new therapies, in order to abolish secondary ischemic brain injuries early-on and improve patients' outcome. In this review, we strive to summarise the mechanisms and therapeutic developments of DCI.