Pathophysiological basis of cerebral vasospasm following aneurysmal subarachnoid haemorrhage

Subarachnoid haemorrhage (SAH) following rupture of an intracranial aneurysm is associated with a greater than 35% mortality within the first 3 months. Delayed ischaemia due to cerebral vasospasm (CVSP) occurs in approximately one-third of all patients with this disease and accounts for over 20% of its overall morbidity and mortality. Although the clinical and experimental features of CVSP have been widely documented, the pathophysiology remains controversial. Its basis, however, is almost certainly multifactorial. The cerebrovascular microenvironment is significantly altered a consequence of haemorrhage into the subarachnoid space. Important putative factors implicated in this change include oxyhaemoglobin, endothelin, oxygen- derived free radicals, and neurovascular nitric oxide, arachidonic acid and carbon monoxide systems. In addition, distinct histological changes related to the overall physiological response occur in cerebral vessels undergoing spasm, The present work aims to detail and unify our current understanding of the biological mechanisms underlying this devastating condition.