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

Lewis Z Leng1, Matthew E Fink, Costantino Iadecola

  • 1Department of Neurological Surgery, Weill Cornell Medical College, New York Presbyterian Hospital, New York, NY 10065, USA.

Archives of Neurology
|September 15, 2010
PubMed

Insights

Aneurysmal subarachnoid hemorrhage (SAH) complications like delayed cerebral ischemia (DCI) are multifactorial. Cortical spreading depression is a key factor, requiring further study for new DCI treatments.

Area of Science:

  • Neuroscience
  • Neurology
  • Critical Care Medicine

Background:

  • Aneurysmal subarachnoid hemorrhage (SAH) presents high mortality and morbidity.
  • Delayed cerebral ischemia (DCI) remains a primary cause of poor outcomes post-SAH.
  • Traditional focus on vasospasm for DCI is being re-evaluated.

Purpose of the Study:

  • To explore the multifactorial pathophysiology of DCI after SAH.
  • To investigate the emerging role of cortical spreading depression in DCI.
  • To understand the interplay between DCI, vasospasm, and other microcirculatory changes.

Main Methods:

  • Review of current research on SAH pathophysiology.
  • Analysis of emerging evidence on cortical spreading depression.
  • Correlation of DCI with vasospasm, microemboli, and microcirculatory dysfunction.

Main Results:

  • DCI pathophysiology is complex and not solely due to vasospasm.
  • Cortical spreading depression is increasingly recognized as a significant factor in DCI.
  • Interactions between vasospasm, microcirculation, and DCI are critical.

Conclusions:

  • Understanding the multifactorial nature of DCI is crucial for SAH patient outcomes.
  • Targeting cortical spreading depression may offer novel therapeutic strategies for DCI.
  • Integrated approaches addressing vasospasm, microcirculation, and DCI are needed.

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