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Year : 2011  |  Volume : 59  |  Issue : 6  |  Page : 810--816

Intraarterial nimodipine for the treatment of symptomatic vasospasm after aneurysmal subarachnoid hemorrhage: A preliminary study

1 Department of Neurosurgery, Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland; Department of Neurosurgery, Geisinger Medical Center, Danville, PA, USA
2 Department of Diagnostic Imaging, Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland
3 Department of Neurosurgery, Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland; Department of Neurosurgery, Utrecht Medical Center, Utrecht, The Netherlands

Correspondence Address:
Amir R Dehdashti
Department of Neurosurgery, Geisinger Medical Center, 100 North Academy Avenue, Danville, 17821 PA, USA

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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0028-3886.91356

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Objective: Despite dramatic advances in all medical era, cerebral vasospasm is still the major complication in patients with subarachnoid hemorrhage (SAH). The purpose of this study was to assess the influence of intraarterial (IA) nimodipine in the treatment of symptomatic vasospasm and in preventing neurological disabilities. Materials and Methods: We retrospectively reviewed 10 patients of SAH who received IA nimodipine in 15 procedures. The decision to perform angiography and endovascular treatment was based on the neurological examination, brain computed tomography (CT) and CT-angiography. The procedure reports, anesthesia records, neurological examination before and after the procedure, brain imaging and short- and long-term outcome were studied. Results: The average dose of nimodipine was 2 mg. The median change in mean arterial pressure at 10 min was -10 mmHg. No significant change of heart rate was observed at 10 min. There was radiological improvement in 80% of the procedures. Neurological improvement was noted after eight out of 12 procedures when nimodipine was used as the sole treatment and after 10 out of 15, overall. Six patients clinically improved after the treatment and had good outcome. In one patient, an embolus caused fatal anterior and middle cerebral arteries infarction. There was no other neurological deficit or radiological abnormality due to the nimodipine treatment itself. Conclusion: Low-dose IA nimodipine is a valid adjunct for the endovascular treatment of cerebral vasospasm. Beneficial effects are achieved in some patients, prompting a prospective control study.


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Online since 20th March '04
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