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BioMed Research International
Volume 2014 (2014), Article ID 970741, 11 pages
Clinical Study

Continuous Selective Intra-Arterial Application of Nimodipine in Refractory Cerebral Vasospasm due to Aneurysmal Subarachnoid Hemorrhage

1Department of Neurosurgery, Academic Teaching Hospital Munich-Bogenhausen, Technical University of Munich, Englschalkinger Straße 77, 81925 Munich, Germany
2Department of Neurosurgery, Charité University Hospital, Augustenburger Platz 1, 13353 Berlin, Germany
3Department of Radiology, Academic Teaching Hospital Munich-Bogenhausen, Technical University of Munich, Englschalkinger Straße 77, 81925 Munich, Germany
4Department of Neurosurgery, Academic Teaching Hospital Munich-Schwabing, Ludwig Maximilian University of Munich, Kölner Platz 1, 80804 Munich, Germany

Received 13 September 2013; Revised 8 December 2013; Accepted 11 December 2013; Published 16 January 2014

Academic Editor: Robert M. Starke

Copyright © 2014 Stephanie Ott et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Background. Cerebral vasospasm is one of the leading courses for disability in aneurysmal subarachnoid hemorrhage. Effective treatment of vasospasm is therefore one of the main priorities for these patients. We report about a case series of continuous intra-arterial infusion of the calcium channel antagonist nimodipine for 1–5 days on the intensive care unit. Methods. In thirty patients with aneurysmal subarachnoid hemorrhage and refractory vasospasm continuous infusion of nimodipine was started on the neurosurgical intensive care unit. The effect of nimodipine on brain perfusion, cerebral blood flow, brain tissue oxygenation, and blood flow velocity in cerebral arteries was monitored. Results. Based on Hunt & Hess grades on admission, 83% survived in a good clinical condition and 23% recovered without an apparent neurological deficit. Persistent ischemic areas were seen in 100% of patients with GOS 1–3 and in 69% of GOS 4-5 patients. Regional cerebral blood flow and computed tomography perfusion scanning showed adequate correlation with nimodipine application and angiographic vasospasm. Transcranial Doppler turned out to be unreliable with interexaminer variance and failure of detecting vasospasm or missing the improvement. Conclusion. Local continuous intra-arterial nimodipine treatment for refractory cerebral vasospasm after aSAH can be recommended as a low-risk treatment in addition to established endovascular therapies.