gms | German Medical Science

62. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC)
Joint Meeting mit der Polnischen Gesellschaft für Neurochirurgen (PNCH)

Deutsche Gesellschaft für Neurochirurgie (DGNC) e. V.

07. - 11. Mai 2011, Hamburg

Molsidome treatment for the prophylaxis of DIND and delayed brain infarction following subarachnoid hemorrhage

Meeting Abstract

Suche in Medline nach

  • A. Ehlert - Klinik für Neurochirurgie, Asklepios Klinik St. Georg, Hamburg
  • V. Hesselmann - Institut für klinische Radiologie, Universitätsklinikum Münster
  • C. Schmidt - Klinik für Anaesthesiologie, Universitätsklinikum Münster

Deutsche Gesellschaft für Neurochirurgie. Polnische Gesellschaft für Neurochirurgen. 62. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC), Joint Meeting mit der Polnischen Gesellschaft für Neurochirurgen (PNCH). Hamburg, 07.-11.05.2011. Düsseldorf: German Medical Science GMS Publishing House; 2011. DocP 047

doi: 10.3205/11dgnc268, urn:nbn:de:0183-11dgnc2682

Veröffentlicht: 28. April 2011

© 2011 Ehlert et al.
Dieser Artikel ist ein Open Access-Artikel und steht unter den Creative Commons Lizenzbedingungen ( Er darf vervielfältigt, verbreitet und öffentlich zugänglich gemacht werden, vorausgesetzt dass Autor und Quelle genannt werden.



Objective: The delayed cerebral vasospasm (CVS) in micro- and macrocirculation is an important reason for delayed neurological deficits (DIND) and brain infarction in patients after aneurysmal subarachnoid hemorrhage (SAH). The risk for CVS correlates to the clot volume. Molsidomine, is a well-known NO-donor, and this represents the first usage in the context of CVS after SAH for prophylaxis of DIND and CVS-related cerebral infarctions. We proved the pharmocotherapeutic effects of molsidomine in delayed vasospasm-associated DIND and brain infarctions as well as outcome in patients with subarachnoid hemorrhage after aneurysmal rupture. The idea was based firstly on the physiological crucial role of NO in the micro- and macrocirculation of the brain and secondly on an argued NO depletion after SAH.

Methods: Considering therapy failures under continuous nimodipin therapy and after having shown CVS in the TCD (mean flow > 120 cm/sec) or angiographically, molsidomine was used in addition to standard therapy in the highest possible dosage to maintain a MAP > 65 mmHg. A HHH-therapy was not desired. 27 SAH patients were treated with molsidomine and were compared with 52 SAH patients in the ICU under standard nimodipine therapy with or without CVS. A CCT at the beginning and after treatment were analyzed independently by two experienced neuroradiologists and screened for associated brain infarcts. At least 3 months after discharge, a modified NIH-SS and a modified Rankin Scale (mRS) for clinical follow-up were assessed.

Results: 3/27 patients treated with high-dose molsidomine and 26/52 patients not being treated with molsidomine developed vasospasm-associated brain infarctions. As shown by follow-up at least 3 months after discharge, we found a formidable clinical benefit measured by mNIH-SS and modified Rankin Scale (mRS) especially in patients with higher Hunt and Hess (H&H) grades (molsidomine mean mNIH 4.58 and mRS 1.85 compared to patients treated solely with nimodipine mNIH 10.26 and mRS 3.83). We did not see any serious adverse effects except some episodes of hypotension. There was a trend in TCD-values towards normal velocities.

Conclusions: Treatment of SAH-survivors with molsidomine showed an impressive improvement in clinical condition and long-term outcome in the follow-up and patients evolved substantially less vasospasm-related brain infarctions at the rate of 1:4 in favor of molsidomine patients, which is probably due to an improvement in microcirculation.