Ehlert Angelika, Schmidt Christoph, Wölfer Johannes, Manthei Gerd, Jacobs Andreas H, Brüning Roland, Heindel Walter, Ringelstein E Bernd, Stummer Walter, Pluta Ryszard M, Hesselmann Volker
Department of Neurosurgery, Asklepios Hospital St. Georg, Hamburg;
Departments of 2 Anästhesiology, Intensive Care and Pain Medicine.
J Neurosurg. 2016 Jan;124(1):51-8. doi: 10.3171/2014.12.JNS13846. Epub 2015 Jul 10.
OBJECT Delayed ischemic neurological deficits (DINDs) and cerebral vasospasm (CVS) are responsible fora poor outcome in patients with aneurysmal subarachnoid hemorrhage (SAH), most likely because of a decreased availability of nitric oxide (NO) in the cerebral microcirculation. In this study, the authors examined the effects of treatment with the NO donor molsidomine with regard to decreasing the incidence of spasm-related delayed brain infarctions and improving clinical outcome in patients with SAH. METHODS Seventy-four patients with spontaneous aneurysmal SAH were included in this post hoc analysis. Twenty-nine patients with SAH and proven CVS received molsidomine in addition to oral or intravenous nimodipine. Control groups consisted of 25 SAH patients with proven vasospasm and 20 SAH patients without. These patients received nimodipine therapy alone. Cranial computed tomography (CCT) before and after treatment was analyzed for CVS-related infarcts. A modified National Institutes of Health Stroke Scale (mNIHSS) and the modified Rankin Scale (mRS) were used to assess outcomes at a 3-month clinical follow-up. RESULTS Four of the 29 (13.8%) patients receiving molsidomine plus nimodipine and 22 of the 45 (48%) patients receiving nimodipine therapy alone developed vasospasm-associated brain infarcts (p < 0.01). Follow-up revealed a median mNIHSS score of 3.0 and a median mRS score of 2.5 in the molsidomine group compared with scores of 11.5 and 5.0, respectively, in the nimodipine group with CVS (p < 0.001). One patient in the molsidomine treatment group died, and 12 patients in the standard care group died (p < 0.01). CONCLUSIONS In this post hoc analysis, patients with CVS who were treated with intravenous molsidomine had a significant improvement in clinical outcome and less cerebral infarction. Molsidomine offers a promising therapeutic option in patients with severe SAH and CVS and should be assessed in a prospective study.
迟发性缺血性神经功能缺损(DINDs)和脑血管痉挛(CVS)是导致动脉瘤性蛛网膜下腔出血(SAH)患者预后不良的原因,最可能是由于脑微循环中一氧化氮(NO)的可用性降低。在本研究中,作者研究了使用NO供体吗多明治疗对降低SAH患者痉挛相关迟发性脑梗死的发生率及改善临床预后的影响。方法:本事后分析纳入了74例自发性动脉瘤性SAH患者。29例确诊为CVS的SAH患者除口服或静脉注射尼莫地平外,还接受了吗多明治疗。对照组包括25例确诊为血管痉挛的SAH患者和20例未发生血管痉挛的SAH患者。这些患者仅接受尼莫地平治疗。分析治疗前后的头颅计算机断层扫描(CCT)以评估与CVS相关的梗死灶。在3个月的临床随访中,使用改良的美国国立卫生研究院卒中量表(mNIHSS)和改良的Rankin量表(mRS)评估预后。结果:29例接受吗多明加尼莫地平治疗的患者中有4例(13.8%)发生了血管痉挛相关的脑梗死,45例仅接受尼莫地平治疗的患者中有22例(48%)发生了血管痉挛相关的脑梗死(p<0.01)。随访显示,吗多明组的mNIHSS评分中位数为3.0,mRS评分中位数为2.5,而CVS的尼莫地平组评分分别为11.5和5.0(p<0.001)。吗多明治疗组有1例患者死亡,标准治疗组有12例患者死亡(p<0.01)。结论:在本事后分析中,静脉注射吗多明治疗的CVS患者临床预后有显著改善,脑梗死较少。吗多明为重症SAH和CVS患者提供了一种有前景的治疗选择,应在前瞻性研究中进行评估。