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Updated: Jun 8, 2026

Double Direct Injection of Blood into the Cisterna Magna as a Model of Subarachnoid Hemorrhage
Published on: August 30, 2020
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.
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.
Abstract:
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.
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