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Updated: May 8, 2026

A Volumetric Method for Quantification of Cerebral Vasospasm in a Murine Model of Subarachnoid Hemorrhage
Published on: July 28, 2018
Treatment modality and vasospasm after aneurysmal subarachnoid hemorrhage
Bradley A Gross1, Pui Man Rosalind Lai1, Kai U Frerichs1
1Department of Neurological Surgery, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, USA.
Objective:
Vasospasm is the leading source of neurological morbidity after aneurysmal subarachnoid hemorrhage. Our objective was to evaluate the impact of treatment modality on vasospasm, delayed cerebral infarction, and clinical deterioration caused by delayed cerebral ischemia (CD-DCI).
Methods:
We reviewed an institutional cohort, comparing rates of vasospasm, delayed cerebral infarction, and CD-DCI between patients managed with only microsurgical clipping and those treated with only endovascular coiling within 72 hours of rupture. Age, sex, smoking status, Hunt-Hess grade, and Fisher grade were adjusted for in a multivariate regression model.
Results:
Two hundred three patients were treated with clipping and 52 with coiling. There was no significant difference in patient age, sex, smoking status, aneurysm location, and presenting clinical (Hunt-Hess) and radiographic (Fisher) grade between these two groups. Sixty-percent of patients had moderate or severe vasospasm after clipping compared with 38% after coiling (Multivariate odds ratio [OR] 2.32, 95% confidence interval [95% CI] 1.21-4.47, P = 0.01). Clipping was associated with a greater number of territories with vasospasm (mean of 3.1 vs. 2.3, P = 0.03 after multivariate analysis). Delayed radiographic cerebral infarction was more common in the clipping group (17% vs. 6%, multivariate OR 3.66, 95% CI 1.06-12.71, P = 0.04). For CD-DCI, a trend was seen as 16% of patients treated with clipping had CD-DCI compared with 6% of patients treated with coiling (multivariate OR 3.11, 95% CI 0.89-10.86, P = 0.07).
Conclusion:
We demonstrate significantly lower rates of vasospasm and delayed infarction after endovascular coiling of ruptured aneurysms.
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