• Wilson Z Ray, Christopher J Moran, Colin P Derdeyn, Michael N Diringer, Ralph G Dacey, and Gregory J Zipfel.
• Department of Neurological Surgery, Washington University School of Medicine, St Louis, MO 63110, USA. rayz@nsurg.wustl.edu
• Surg Neurol. 2009 Oct 1;72(4):347-53; discussion 353-4.

BackgroundCerebral 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 DescriptionWe 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.ConclusionThe 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.

40 keywords...

hide…