Mechanisms of early brain injury after subarachnoid hemorrhage

J Cereb Blood Flow Metab. 2006 Nov;26(11):1341-53. doi: 10.1038/sj.jcbfm.9600283. Epub 2006 Feb 15.


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.

Publication types

  • Review

MeSH terms

  • Animals
  • Apoptosis / genetics
  • Apoptosis / physiology
  • Brain Edema / etiology
  • Brain Edema / pathology
  • Brain Injuries / etiology*
  • Brain Injuries / pathology
  • Brain Injuries / physiopathology
  • Caspases / metabolism
  • Genes, p53 / physiology
  • Humans
  • Mitochondria / physiology
  • Necrosis
  • Subarachnoid Hemorrhage / complications*
  • Subarachnoid Hemorrhage / pathology
  • Subarachnoid Hemorrhage / physiopathology


  • Caspases