Mechanisms of cerebral vasospasm and cerebral ischaemia in subarachnoid haemorrhage

Subarachnoid haemorrhage (SAH) is a cerebrovascular emergency associated with significant morbidity and mortality. SAH is characterized by heterogeneity, interindividual variation and complexity of pathophysiological responses following extravasation of blood from cerebral circulation. The purpose of this review is to integrate previously established pre-existing factors, pathophysiological pathways and to develop a concept map of mechanisms of SAH-induced cerebral vasospasm and delayed cerebral ischaemia using a systematic approach. We conducted an extensive mapping of a hypothesized sequence of pathophysiological events. Documentation of supporting evidence was done alongside a concept map building. After finalizing the model, we conducted an analysis of the consequences and connections of pathophysiological events. We included the findings of experimental research, focusing on pathophysiological processes. We focused on SAH-induced cerebral vasospasm and delayed cerebral ischaemia as a component of cerebral injury and potential systemic consequences. SAH-induced brain injury occurs within 72 h following haemorrhage. Pathophysiology of cerebral vasospasm may include reduction in NO production, direct activation of calcium channels, upregulating genes involved with inflammation and extracellular matrix remodelling, triggering oxidative stress and free radical damage to smooth muscle and lipid peroxidation of cell membranes, cortical spreading depolarizations, sympathetic activation, finally resulting in the failure of cerebral autoregulation, microthrombosis and cerebral ischaemic injury. This cascade of events might explain why medical therapy often fails to reverse resistant cerebral vasospasm and to prevent cerebral ischaemia.