Pathogenesis of cerebral vasospasm following aneurysmal subarachnoid hemorrhage: putative mechanisms and novel approaches

Journal of Neuroscience Research
Angelos G KoliasAntonio Belli

Abstract

Cerebral vasospasm is a potentially incapacitating or lethal complication in patients with aneurysmal subarachnoid hemorrhage (SAH). The development of effective preventative and therapeutic interventions has been largely hindered by the fact that the underlying pathogenic mechanisms of cerebral vasospasm remain poorly understood. However, intensive research during the last 3 decades has identified certain mechanisms that possibly play a role in its development. Experimental data suggest that calcium-dependent and -independent vasoconstriction is taking place during vasospasm. It appears that the breakdown products of blood in the subarachnoid space are involved, through direct and/or indirect pathways, in the development of vasospasm after SAH. Free radicals reactions, an imbalance between vasoconstrictor and vasodilator substances (endothelium derived substances, e.g., nitric oxide, endothelin; arachidonic acid metabolites, e.g., prostaglandins, prostacyclin), inflammatory processes, an upheaval of neuronal mechanisms that regulate vascular tone, endothelial proliferation, and apoptosis have all been put forward as causative and/or pathogenic factors. Translational research in the field of vasospasm has traditionally aimed to...Continue Reading

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