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Intravenous but not oral application of nimodipine reduces peak systolic flow velocities in vasospastic cerebral arteries following aneurysmatic subarachnoid hemorrhage

J Wessig, J Wessig, S Zimmermann, M Rosenkranz, W Niesen · Klinische Neurophysiologie · 2006 · Heft 03

Dokument
1072694
CareLit-ID
Jahr
2006
Publikation
PDF
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Metadaten
DOI
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Bibliografische Angaben

Zeitschrift
Klinische Neurophysiologie
Autor:innen
J Wessig, J Wessig, S Zimmermann, M Rosenkranz, W Niesen
Ausgabe
Heft 03 / 2006
Seiten
–
Erschienen: 2006-03-24 00:00:00
ISSN
1434-0275

Zusammenfassung

Background: Cerebral vasospasm is a major complication of aneurysmal subarachnoid hemorrhage (SAH) and may cause delayed ischemic neurological deficits (DIND). Nimodipine improves the clinical outcome following SAH. A spasmolytic effect of systemic nimodipine administation, however, has not yet been reported. Methods: We prospectively monitored 20 patients with aneurysmal SAH for the occurrence and severity of cerebral vasospasm by use of transcranial Doppler and duplex ultrasound. All subjects received oral applications of nimodipine. Upon development of vasospasm, the oral medication was replaced by intravenou…

Schlagworte

Klinische Neurophysiologie