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Volume 72, Issue 4, Pages 347-353 (October 2009)


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Near-complete resolution of angiographic cerebral vasospasm after extreme elevation of mean arterial pressure: case report

Wilson Z. Ray, MDaCorresponding Author Informationemail address, Christopher J. Moran, MDabc, Colin P. Derdeyn, MDabc, Michael N. Diringer, MDab, Ralph G. Dacey Jr., MDa, Gregory J. Zipfel, MDabemail address

Received 16 July 2008; accepted 9 October 2008. published online 15 January 2009.

Abstract 

Background

Cerebral vasospasm is a widespread and potentially treatable complication after aneurysmal SAH. Aggressive treatment often includes hemodynamic augmentation, although the exact mechanism by which such therapy leads to improved cerebral blood flow and reduced neurologic deficits is incompletely established. This case report is only the second to provide compelling evidence that hypertension can lead to direct dilation of vasospastic arteries, thereby providing valuable insight into its potential mechanism.

Case Description

We present a patient with SAH from a ruptured anterior communicating artery aneurysm who developed marked decline in mental status on posthemorrhage day 11, consistent with symptomatic cerebral vasospasm.

A diagnostic cerebral angiogram was performed demonstrating extensive and diffuse cerebral vasospasm. After receiving a nonselective slow infusion of verapamil, the patient developed an episode of extreme hypertension. Repeat angiography immediately after hypertensive crisis revealed near-complete resolution of the previously noted cerebral vasospasm. Rapid improvement in the patient's neurologic status ensued.

Conclusion

The present case illustrates that extreme hypertension can lead to direct dilation of vasospastic arteries and suggests that hypertensive-type hemodynamic therapy may act not only through increasing the pressure gradient across vasospastic arteries but also via direct induction of arterial vasodilation.

a Department of Neurological Surgery, Washington University School of Medicine, Campus Box 8057, St Louis, MO 63110, USA

b Department of Neurology, Washington University School of Medicine, Campus Box 8057, St Louis, MO 63110, USA

c Interventional Neuroradiology Service, Mallinckrodt Institute of Radiology, Washington University School of Medicine, St Louis, MO 63110, USA

Corresponding Author InformationCorresponding author. Tel.: +1 314 362 3577; fax: +1 314 362 2107.

PII: S0090-3019(08)00883-5

doi:10.1016/j.surneu.2008.10.006


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