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Double Direct Injection of Blood into the Cisterna Magna as a Model of Subarachnoid Hemorrhage
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The role of spreading depolarization in subarachnoid hemorrhage

R Sánchez-Porras1, Z Zheng, E Santos

  • 1Department of Neurosurgery, Heidelberg University Hospital, Heidelberg, Germany.

European Journal of Neurology
|April 5, 2013
PubMed

Insights

Delayed cerebral ischaemia (DCI) after subarachnoid hemorrhage (SAH) is a major cause of death. Spreading depolarization (SD) is emerging as a key factor in DCI, prompting further research into its role and potential treatments.

Area of Science:

  • Neuroscience
  • Neurology
  • Critical Care Medicine

Background:

  • Subarachnoid hemorrhage (SAH) is a severe neurological condition with high mortality and morbidity.
  • Delayed cerebral ischaemia (DCI) is the primary cause of poor outcomes following SAH.
  • The traditional understanding of DCI, primarily attributed to vasospasm, is evolving due to emerging evidence of multifactorial causes.

Purpose of the Study:

  • To investigate the role of spreading depolarization (SD) as a potential pathophysiological mechanism contributing to DCI after SAH.
  • To explore the relationship between SD, cortical spreading ischaemia, and hemodynamic responses in the context of DCI.
  • To highlight the need for further research into SD to develop novel diagnostic and therapeutic strategies for DCI.

Main Methods:

  • Review of current literature on SAH, DCI, vasospasm, and spreading depolarization.
  • Analysis of emerging evidence implicating SD in the pathophysiology of DCI.
  • Discussion of the potential link between SD, cortical spreading ischaemia, and inverse hemodynamic responses.

Main Results:

  • Spreading depolarization (SD) is increasingly recognized as a significant factor in the development of DCI post-SAH.
  • Cortical spreading ischaemia, potentially driven by SD and inverse hemodynamic responses, offers a new perspective on DCI etiology.
  • The established role of vasospasm in DCI is being re-evaluated in light of these new findings.

Conclusions:

  • DCI following SAH is likely multifactorial, with SD emerging as a critical pathophysiological mechanism.
  • Further intensive research into SD is crucial for understanding its contribution to DCI.
  • Elucidating the role of SD could lead to innovative diagnostic tools and treatments to improve patient outcomes after SAH.

Keywords:
delayed cerebral ischaemiaspreading depolarizationspreading ischaemiasubarachnoid hemorrhage

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