Neuroprotection in subarachnoid hemorrhage

Abstract

Despite advances in aneurysm ablation and the initial management of patients presenting with aneurysmal subarachnoid hemorrhage, delayed cerebral ischemia remains a significant source of morbidity. Traditionally, delayed cerebral ischemia was thought to be a result of vasospasm of the proximal intracranial vessels, and clinical trials have relied largely on radiographic evidence of vasospasm as a surrogate for functional outcome. However, a number of trials have demonstrated a dissociation between angiographic vasospasm and outcome, and more recent data suggest that other mechanisms of injury, such as microvascular dysfunction and complex neuronal-glial interactions, may influence the development of delayed ischemic deficit after aneurysmal subarachnoid hemorrhage. Our evolving understanding of the pathophysiology of delayed cerebral ischemia may offer the opportunity to test new therapeutic strategies in this area and improve clinical trial design.

Figure 1

Following SAH, mediators of inflammation, including endothelin may initiate mass neuronal depolarization. In the presence of decreased availability of nitric oxide, an inverse coupling between neuronal and astroglial interaction with cerebral blood flow may resulting in spreading ischemia.