Vertebrobasilar Vasospasm after Aneurysmal Subarachnoid Hemorrhage: Review

Abstract

Aneurysmal subarachnoid hemorrhage (SAH) affects 5-10 per 100,000 individuals per year1 and is associated with high rates of morbidity and mortality [1-4]. Main contributor to poor outcomes after SAH are the early cerebral injury (ECI) caused by the immediate increase in intracranial pressure, decreased cerebral perfusion pressure and global ischemia [1,5-9] and delayed cerebral ischemia (DCI) which affects 30% of the SAH survivors leading to neurological deficit, cognitive decline [4,6,913], and death [14]. This ischemia is historically though to results from a long-lasting narrowing of the large-capacity cerebral arteries. Kassell et al. [15] published statistics that roughly hold to this day, whereby 40-70% of aSAH patients having survived the acute phase demonstrated angiographic VS, 20-30% manifested delayed neurologic deficits (DID), and 7% having died as a consequence there of. Another seminal study by Broderick et al. [16] have discerned a mortality rate of 45%, attributed 2 of 36 (6%) total deaths to VS, even though 44% of all patients manifested DCI. In 1994, Dorsch & King [17] published a review based on over 30,000 clinical cases that established an incidence of angiographic vasospasm at 43.3% overall and DID occurring at a rate of 32.5%. Of those who experienced DID, 34% sustained permanent neurological deficits and 30% died, such that VS was considered the cause of death in roughly 10% of aSAH patients.