Spreading depolarization: a possible new culprit in the delayed cerebral ischemia of subarachnoid hemorrhage

Arch Neurol. 2011 Jan;68(1):31-6. doi: 10.1001/archneurol.2010.226. Epub 2010 Sep 13.


Aneurysmal subarachnoid hemorrhage (SAH) is a devastating disease with a high mortality and morbidity rate. Gradual improvements have been made in the reduction of mortality rates associated with the disease during the last 30 years. However, delayed cerebral ischemia (DCI), the major delayed complication of SAH, remains a significant contributor to mortality and morbidity despite substantial research and clinical efforts. During the last several years, the predominant role of cerebral vasospasm, the long-accepted etiologic factor behind DCI, has been questioned. It is now becoming increasingly clear that the pathophysiology underlying DCI is multifactorial. Cortical spreading depression is emerging as a likely factor in this complex web of pathologic changes after SAH. Understanding its role after SAH and its relationship with the other pathologic processes such as vasospasm, microcirculatory dysfunction, and microemboli will be vital to the development of new therapeutic approaches to reduce DCI and improve the clinical outcome of the disease.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Animals
  • Brain Ischemia / etiology
  • Brain Ischemia / physiopathology*
  • Cortical Spreading Depression / physiology*
  • Humans
  • Subarachnoid Hemorrhage / complications
  • Subarachnoid Hemorrhage / physiopathology*
  • Time Factors
  • Vasospasm, Intracranial / complications
  • Vasospasm, Intracranial / physiopathology