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Updated: May 25, 2026

A Volumetric Method for Quantification of Cerebral Vasospasm in a Murine Model of Subarachnoid Hemorrhage
Published on: July 28, 2018
Novel treatments for vasospasm after subarachnoid hemorrhage
Carl Muroi1, Martin Seule, Kenichi Mishima
1Neurocritical Care Unit, University Hospital Zurich, Zurich, Switzerland.
Insights
Treatment for cerebral vasospasm (CVS) after subarachnoid hemorrhage is evolving. Current evidence suggests CVS is not the only cause of poor outcomes, and novel treatments are under investigation.
Area of Science:
- Neurocritical Care
- Cerebrovascular Diseases
- Neurosurgery
Background:
- Cerebral vasospasm (CVS) following aneurysmal subarachnoid hemorrhage (aSAH) presents significant challenges in neurocritical care.
- The understanding of delayed cerebral ischemia (DCI) and poor outcomes is expanding beyond CVS.
Purpose of the Study:
- To review recent advancements and novel treatment strategies for CVS.
- To discuss emerging factors contributing to DCI and poor outcomes after aSAH.
Main Methods:
- Literature review of recent studies on CVS treatment.
- Analysis of clinical trial results for novel therapeutic agents.
Main Results:
- Treatment solely targeting CVS is considered outdated.
- Early brain injury, cortical spreading depolarization, inflammation, and microthrombosis are implicated in DCI.
- An endothelin-1 antagonist trial reduced CVS but did not improve outcomes.
- Induced hypertension is recommended for DCI; endovascular intervention is for refractory CVS.
- Magnesium sulfate and statins are in Phase III trials; other factors lack dedicated trials.
Conclusions:
- Recent updates provide some revised recommendations for CVS management.
- Novel treatment modalities are under investigation, but none have demonstrated convincing efficacy yet.
Purpose Of Review:
Cerebral vasospasm (CVS) after aneurysmal subarachnoid hemorrhage remains a considerable challenge in neurocritical care medicine. This review aims to cover the recent novel aspects and results in CVS treatment.
Recent Findings:
On the basis of the recent literature, treatment focusing on CVS alone is outdated. A considerable amount of evidence suggests CVS not to be the sole cause of delayed cerebral ischemia (DCI) and poor outcome. Early brain injury, cortical spreading depolarization, inflammation and microthrombosis have recently been discussed as additional factors. The results of a well designed phase III trial, using an endothelin-1 antagonist, indicated a decrease in the occurrence of CVS but did not change the clinical outcome significantly. Induced hypertension is currently recommended for treating suspected DCI, whereas hemodilution and hypervolemia are not. Endovascular intervention is only recommended in case of refractory symptomatic CVS. A couple of newer treatment strategies are under evaluation. Phase III trials are underway for magnesium sulfate and statins. Clinical trials aiming specifically at recently discussed factors other than CVS have not been reported.
Summary:
Reviewing the recent literature, there have been some updates on recommendations and newer treatment modalities are under evaluation. However, a novel treatment with convincing evidence has not been reported so far.
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