¹Department of Physiology, Loma Linda University Medical School, Loma Linda, California, USA

Correspondence: Dr J Zhang, Division of Neurosurgery, Loma Linda University Medical Centre, 11234 Anderson Street, Room 2562B Loma Linda, California 92354, USA. E-mail: johnzhang3910@yahoo.com

Received 1 November 2005; Revised 15 December 2005; Accepted 30 December 2005; Published online 15 February 2006.

Abstract

Apoptosis is the term given to programmed cell death, which has been widely connected to a number of intracranial pathologies including stroke, Alzheimer's disease, and more recently subarachnoid hemorrhage (SAH). Subarachnoid hemorrhage is a disease, without any form of effective treatment, that affects mainly the young and middle aged and as a result is responsible for severe disability in otherwise healthy and productive individuals. Despite intense research efforts in the field, we currently possess a very limited understanding of the underlying mechanisms that result in injury after SAH. However, a number of studies have recently indicated that apoptosis may be a major player in the pathogenesis of secondary brain injury after SAH. As a result, the apoptotic cascades present a number of potential therapeutic opportunities that may ameliorate secondary brain injury after SAH. Experimental data suggest that these cascades occur very early after the initial insult and may be related directly to physiologic sequela commonly associated with SAH. It is imperative, therefore, to obtain a thorough understanding of the early events that occur after SAH, which will enable future therapies to be developed.