动脉瘤性蛛网膜下腔出血后脑血管痉挛的诊治分析

目的：探讨脑血管造影（DSA）、颅脑CT、经颅多普勒（TCD）的临床诊断价值,以及动脉瘤夹闭或血管内栓塞术、持续腰大池引流的临床治疗效果。方法61例动脉瘤性蛛网膜下腔出血患者分为观察组和对照组,对照组给予动脉瘤夹闭或血管内栓塞术,观察组在此基础上术后第2天行腰大池持续引流,观察2组患者的临床疗效,并比较术后第1、5、10天M C A血流速度、脑脊液压力、红细胞计数的变化。结果观察组总有效率达90·32％,对照组为76·67％,观察组临床疗效优于对照组,差异有统计学意义（P＜0·05）;术后第5、10天观察组大脑中动脉血流速度明显比对照组低,差异有统计学意义（P＜0·05）;术后第5、10天观察组脑脊液压力、红细胞计数均明显比对照组低,差异有统计学意义（P＜0·05）。结论 DSA、颅脑C T扫描、T CD可以明确诊断动脉瘤性蛛网膜下腔出血后脑血管痉挛,并能够评价血管痉挛的程度;采取动脉瘤夹闭或血管内栓塞术、持续腰大池引流治疗动脉瘤性蛛网膜下腔出血后脑血管痉挛有满意效果。     

动脉瘤性蛛网膜下腔出血后抗血管痉挛的药物治疗

正蛛网膜下腔出血(su[barachnoid hemorrhage,SAH)的年发病率为9/10万1],占所有脑卒中的[2]2]3%。颅内动脉瘤破裂是自发性SAH的主要原因[,而动脉瘤破裂后脑血管痉挛(cerebral vasospasm,[3,4C]VS)是导致SAH患者死亡、严重残疾的主要因素。因此,动脉瘤破裂出血后抗CVS的治疗尤为重要。本文总结动脉瘤性SAH后CVS药物治疗现状及最新进展,以提高对CVS的认识,并为临床治疗提供参考。     

动脉瘤性蛛网膜下腔出血后脑血管痉挛的治疗及临床分析

目的探讨颅内动脉瘤性蛛网膜下腔出血后脑血管痉挛的治疗方法。方法对动脉瘤性蛛网膜下腔出血71例患者的临床资料进行回顾性分析。结果71例均在出血后早期（72h内）行动脉瘤栓塞术或开颅动脉瘤夹闭术。术后均予尼莫地平,脑脊液引流,3-H疗法等治疗,共发生症状性血管痉挛22例,12例恢复良好,9例中重度残疾,1例死亡。结论尽早行开颅动脉瘤夹闭术或动脉瘤栓塞术,术后予尼莫地平、脑脊液引流、3-H疗法等是治疗和预防动脉瘤破裂后脑血管痉挛的有效方法。     

硫酸镁对颅内动脉瘤性蛛网膜下腔出血后脑血管痉挛的治疗作用

目的观察硫酸镁对动脉瘤性蛛网膜下腔出血后症状性脑血管痉挛和神经功能预后的治疗作用。方法39例动脉瘤性蛛网膜下腔出血患者在发病48 h内,随机分到生理盐水组(A组)、硫酸镁治疗1组(B组)、硫酸镁治疗2组(C组),B组首次静脉推注25％硫酸镁10 mL后,继以每日25％硫酸镁40 mL静脉滴注,C组首次静脉推注25％硫酸镁20 mL后,继以每日25％硫酸镁80 mL静脉滴注,A组输入等量生理盐水,均连续输入14 d并每日检测血清Mg2+浓度、血压及TCD检测大脑中动脉平均血流速度。6个月后随访并记录患者Glasgow Outcome Scall-Extended、Modified Rankin Scall用以评价患者神经功能预后情况。结果17例患者发生症状性脑血管痉挛,A组7例,B组5例、C组5例;17例症状性脑血管痉挛患者的6个月GOSE评分,A组1／7例,B组3／5例、C组3／5例患者神经功能恢复良好;39例患者中硫酸镁治疗组患者6个月后GOSE、Modified Rankin Scale评分与生理盐水组比较,神经功能预后有改善倾向。然而,这些疗效评分差异均没有达到统计学意义(P>0．05)。结论硫酸镁治疗安全且血清Mg2+水平较容易维持,硫酸镁有减少症状性脑血管痉挛发生和改善患者神经功能预后的趋势,但由于样本例数较少,其治疗作用仍有待于进一步研究证实。     

动脉瘤性蛛网膜下腔出血后脑血管痉挛与血浆花生四烯酸代谢产物的关系

目的探讨动脉瘤性蛛网膜下腔出血(aSAH)病人血浆花生四烯酸代谢产物的含量与脑血管痉挛(CVS)发生、发展之间的关系。方法选取34例aSAH病人作为研究组,在aSAH后第1、3、7、14天抽取外周静脉血测定血栓素B2(TXB2)和6-酮-前列腺素F1α(6-Keto-PGF1α)的含量。另选取同时期健康成人6例作为对照组,进行对比研究。结果研究组发生CVS 23例,其中表现为迟发性缺血性神经功能障碍(DIND)的症状性CVS 10例,无症状性CVS(无DIND)13例。与对照组相比,研究组各时间点血TXB2含量均明显升高,而血6-Keto-PGF1α含量变化无显著性差异;与无CVS病人相比,CVS病人血TXB2含量在各时间点均明显升高,而血6-Keto-PGF1α含量仅在第7天时明显降低;与无DIND病人相比,DIND病人血6-Keto-PGF1α含量在第1、3、14天明显降低,而血TXB2含量仅在第3天时明显升高。结论 aSAH后CVS、DIND的发生、发展与血TXB2、6-Keto-PGF1α含量变化可能存在相关性。     

蛛网膜下腔出血后脑血管痉挛的治疗

自发性蛛网膜下腔出血(spontaneous subarachnoid hemor- rhage,sSAH)是临床常见的一种神经外科急症,约80%～95%的sSAH患者是颅内动脉瘤源性蛛网膜下腔出血(aneu- rysmal SAH,aSAH)。aSAH患者常易并发脑血管痉挛(cerebral vasospasm,CV),严重影响预后。CV是一种持续性的对血管舒张药物无反应的血管收缩状态。依据患者神经系统症状的有无可将其分为无症状性脑     

动脉瘤破裂性蛛网膜下腔出血后脑血管痉挛治疗新进展

脑血管痉挛（CVS）会引起脑血管的收缩,从而扰乱血管错综复杂的调控系统。它是蛛网膜下腔出血后残疾和死亡的主要原因之一,也是造成迟发性脑缺血及神经功能障碍的驱动因素。目前临床上对于CVS的治疗选择还很少,药物疗法主要有诱发性升压疗法、钙通道阻滞剂、血管扩张剂、磷酸二酯酶抑制剂、他汀类药物、抗痉挛剂、促红细胞生成剂、内皮素受体拮抗剂等。非药物疗法主要有血管扩张剂的血管内干预、机械血管成形术等。CVS的发病机制至今尚未完全阐明,尚无一种有效的治疗方法可以用来治疗CVS。随着人们对其潜在发病机制认识和理解的扩大,可能会找到好的治疗靶点。在蛛网膜下腔出血后,神经炎症和微凝块的形成是引起血管痉挛和迟发性脑缺血的新兴机制。迄今为止最有希望的疗法是调节一氧化氮或内皮素通路,并通过抑制痉挛的作用获益。钙通道阻滞剂的进一步研究也在进行中,以更好地了解有关血管痉挛的作用机制。尼莫地平能使蛛网膜下腔出血患者的血管舒张,改善神经系统症状,可以在一定程度上防止迟发性脑缺血,但对蛛网膜下腔出血后的死亡率影响不大。因此,针对不同机制的联合治疗可能是更理想的方法。该文对近年来有关CVS的治疗方法进行综述。国际神经病学神经外科学杂志, 2023, 50(3): 60-65]     

蛛网膜下腔出血后脑血管痉挛的研究进展

脑血管痉挛（ＣＶＳ）也称颅内动脉痉挛,为脑底大动脉的一支或多支由于动脉壁平滑肌的收缩或血管损伤引起其管腔形态学变化,从而在动脉造影时表现的管腔狭窄。严重者可造成脑缺血和脑梗塞,引起迟发性神经功能障碍。动脉瘤破裂性蛛网膜下腔出血（ＳＡＨ）常引起ＣＶＳ,...     

动脉瘤性蛛网膜下腔出血后脑血管痉挛的脑血流动力学改变

目的探讨动脉瘤性蛛网膜下腔出血（aSAH）后脑血管痉挛（CVS）的血流动力学改变。方法对337例（382枚动脉瘤）aSAH患者临床资料进行回顾性分析,均经数字减影血管造影（DSA）和／或CT血管造影（CTA）检查证实为动脉瘤（An）,其中动脉瘤颈夹闭术297例,瘤颈夹闭及载瘤动脉塑形术29例,动脉瘤孤立术8例及包裹术3例。术后给予尼莫地平持续泵入扩血管、脑脊液引流、3H疗法等治疗,并于SAH1—3d．4～7d,8～14d、15～20d进行床边经颅超声多普勒（TCD）检测,主要观察MCA平均血流速度（VmMcA）、计算Lindegaard指数,即同侧MCA与颅外段ICAVm之比（LI）,观察CVS及颅内压（ICP）等脑血流动力学变化。结果SAH患者不同程度的存在CVS,25％的患者1—3d就出现CVS,8～14d达高峰;Hunt-Hess分级与CVS的变化成正相关;102例患者（102／337,30．3％）出现不同程度的颅内压增高;17例（17／337,5％）出现延迟性缺血性神经功能障碍（DIND）,颅内压增高且有CVS者预后较差。结论TCD可以床边、动态监测aSAH患者的脑血流动力学改变,具有无创、简单易行的特点。TCD检测的脑血流速度、Lindegaard指数和频谱形态相结合对临床和血管造影诊断CVS有价值。     

刺五加防治蛛网膜下腔出血后脑血管痉挛

目的 观察刺五加注射液防治蛛网膜下腔出血（ＳＡＨ）后脑血管痉挛（ＣＶＳ）的疗效。方法 将ＳＡＨ患者４４例,随机分为刺五加组（２０例）和ＳＡＨ对照组（２４例）,２组均于发病４８小时内接受治疗,ＳＡＨ对照组用脱不、止血等常规疗法,刺五加组在常规疗法基础上加用刺五加注射液１００毫升,静脉滴注,每日一次,共７日。结果 一个月内,刺五加组的ＣＶＳ发生率、死亡率明显低于ＳＡＨ对照组（Ｐ〈０．０５）,再出血发生率２组比较无明显差异（Ｐ〉０．０５）。发病第１４天时,刺五加组患者的病情级别明显低于ＳＡＨ对照组（Ｐ〈０．０５）。结论 刺五加注射液防治ＳＡＨ后ＣＶＳ疗效确切,并能促进神经功能的尽快恢复,且无增加再出血的危险。     

Treatment Options for Cerebral Vasospasm in Aneurysmal Subarachnoid Hemorrhage

Cerebral vasospasm occurs frequently after aneurysmal subarachnoid and contributes to delayed cerebral ischemia. In this article we address systematic problems with the literature on vasospasm and then review both established and experimental treatment options.     

Intraarterial Nimodipine Infusion to Treat Symptomatic Cerebral Vasospasm after Aneurysmal Subarachnoid Hemorrhage

Objective

Cerebral vasospasm leading to cerebral ischemic infarction is a major cause of morbidity and mortality in the patients who suffer with aneurysmal subarachnoid hemorrhage. Despite adequate treatment, some patients deteriorate and they develop symptomatic vasospasm. The objective of the present study was to investigate the efficacy and clinical outcome of intraarterial nimodipine infusion on symptomatic vasospasm that is refractory to hemodynamic therapy.

Methods

We retrospectively reviewed the procedure reports, the clinical charts and the transcranial doppler, computed tomography and digital subtraction angiography results for the patients who underwent endovascular treatment for symptomatic cerebral vasospasm due to aneurysmal SAH. During the 36 months between Jan. 2005 and Dec. 2007, 19 patients were identified who had undergone a total of 53 procedures. We assessed the difference in the arterial vessel diameter, the blood flow velocity and the clinical outcome before and after these procedures.

Results

Vascular dilatation was observed in 42 of 53 procedures. The velocities of the affected vessels before and after procedures were available in 33 of 53 procedures. Twenty-nine procedures exhibited a mean decrease of 84.1 cm/s. We observed clinical improvement and an improved level of consciousness with an improved GCS score after 23 procedures.

Conclusion

Based on our results, the use of intraarterial nimodipine is effective and safe in selected cases of vasospasm following aneurysmal SAH. Prospective, randomized studies are needed to confirm these results.     

Hyperacute Vasospasm After Aneurysmal Subarachnoid Hemorrhage

Background

Cerebral vasospasm after aneurysmal subarachnoid hemorrhage typically occurs 3–14 days after aneurysm rupture. We describe a series of patients who developed vasospasm within minutes of aneurysm rupture. This phenomenon, which we term, “hyperacute vasospasm,” has been reported in animal models of SAH, but hitherto has been poorly described in humans.

Methods

Eleven patients were identified from an institutional registry who had aneurysmal rupture during catheter cerebral angiography between 1997 and 2009. We quantified the degree of vasoconstriction using vascular diameter index (VDI). The change in VDI (delta VDI or DVDI) was calculated by determining the difference in VDI before and after the procedure. We also examined the relationship between hyperacute vasospasm and delayed cerebral ischemia.

Results

Ten of eleven (91 %) patients with intraoperative aneurysm rupture had cerebral vasoconstriction within minutes of intra-procedural aneurysmal rupture. Six of eleven patients (55 %) with hyperacute vasospasm developed delayed cerebral infarction.

Conclusions

Hyperacute vasospasm is likely common in patients with intraoperative aneurysm rupture and may be an unrecognized element of the natural history of aneurysmal subarachnoid hemorrhage. In this limited series, there was an association between hyperacute vasospasm and delayed cerebral infarction.

     

Intra-arterial Dantrolene for Refractory Cerebral Vasospasm After Aneurysmal Subarachnoid Hemorrhage

Background

Intravenous dantrolene has been used to prevent and treat cerebral vasospasm. We report a case of refractory cerebral vasospasm treated with intra-arterial dantrolene after aneurysmal subarachnoid hemorrhage.

Methods

A 56-year-old woman suffered a diffuse subarachnoid hemorrhage from a ruptured anterior communicating artery aneurysm which was successfully treated with coil embolization. She subsequently developed bilateral severe angiographic vasospasm which was treated with intra-arterial vasodilators. However, owing to the recurrence of vasospasm, intra-arterial dantrolene followed by balloon angioplasty was used.

Results

There was moderate improvement of the severe vasospasm in bilateral A1 segments of the anterior cerebral arteries after microcatheter-based intra-arterial infusion of 30?ml (1?mg/ml) dantrolene. Patient??s hemodynamic parameters were monitored during and after the procedure and no significant changes were seen after dantrolene infusion. A follow up cerebral angiogram after 1?day demonstrated the persistence of therapeutic effect.

Conclusion

Intra-arterial dantrolene induced a sustained improvement in cerebral vasospasm secondary to ruptured aneurysm. No significant side effects were observed during or after the infusion of the drug.     

动脉瘤性SAH迟发性脑血管痉挛的多元因素分析

目的 探讨动脉瘤性蛛网膜下腔出血（SAH）继发脑血管痉挛的相关因素。方法 回顾性分析本院收治的54例动脉瘤性SAH病人的临床资料，判定脑血管痉挛程度，统计分析其相关因素。结果Fisher分级Ⅲ-Ⅳ级患者脑血管痉挛发生率（7014％，19／27）明显高于Fisher分级Ⅰ-Ⅱ级者（4414％，12／27）（P〈0．01）；Hunt—Hess分级Ⅲ-Ⅴ级患者脑血管痉挛发生率（75．0％，21／28）明显高于Hunt—Hess分级Ⅰ-Ⅱ级者（38．5％，10／26）（P〈0．05）；3d后手术患者的脑血管痉挛发生率（70．0％，21／30）明显高于3d内手术患者（41．7％，10／24）（P〈0．05）。结论SAH的Fisher分级〉Ⅱ级和Hunt—Hess分级〉Ⅱ级是颅内动脉瘤继发脑血管痉挛的危险因素。早期手术能降低脑血管痉挛的发生率。     

Intravenous Magnesium Infusion for the Prevention of Symptomatic Cerebral Vasospasm after Aneurysmal Subarachnoid Hemorrhage

Objective

The study examined the difference in the incidence of symptomatic cerebral vasospasm with magnesium supplementation in aneurysmal subarachnoid hemorrhage (SAH) in a Korean population.

Methods

This retrospective analysis was performed in 157 patients diagnosed with aneurysmal SAH from January 2007 to December 2011 at a single center. Seventy patients (44.6%) received a combination treatment of nimodipine with magnesium and 87 patients (55.4%) received only nimodipine. A matched case-control study using propensity scores was conducted and 41 subjects were selected from each group. A dosage of 64 mmol/day of magnesium was administrated.

Results

The infusion of magnesium did not reduce the incidence of symptomatic cerebral vasospasm (n=7, 17.1%, p=0.29) compared with simple nimodipine injection (n=11, 26.8%). The ratios of good clinical outcome (modified Rankin scale 0-2) at 6 months were similar, being 78% in the combination treatment group and 80.5% in the nimodipine only group (p=0.79). The proportions of delayed cerebral infarction was not significantly lower in patients with combination treatment (n=2, 4.9% vs. n=3, 7.3%; p=0.64). There was no difference in the serum magnesium concentrations between the patients with symptomatic vasospasm and without vasospasm who had magnesium supplementation. No major complications associated with intravenous magnesium infusion were observed.

Conclusion

Magnesium supplementation (64 mmol/day) may not be beneficial for the reduction of the incidence of symptomatic cerebral vasospasm in patients with aneurysmal SAH.     

Serum Glucose and Potassium Ratio as Risk Factors for Cerebral Vasospasm after Aneurysmal Subarachnoid Hemorrhage

Objective: Cerebral vasospasm is associated with poor prognosis in patients with aneurysmal subarachnoid hemorrhage (SAH), and biomarkers for predicting poor prognosis have not yet been established. We attempted to clarify the relationship between serum glucose/potassium ratio and cerebral vasospasm in patients with aneurysmal SAH. Methods: We studied 333 of 535 aneurysmal SAH patients treated between 2006 and 2016 (123 males, 210 females; mean age 59.7 years; range 24-93). We retrospectively analyzed the relationship between cerebral vasospasm grade and clinical risk factors, including serum glucose/potassium ratio. Results: Postoperative angiography revealed cerebral vasospasm in 112 patients (33.6%). Significant correlations existed between the ischemic complication due to cerebral vasospasm and glucose/potassium ratio (P < .0001), glucose (P = .016), and potassium (P = .0017). Serum glucose/potassium ratio was elevated in the cerebral vasospasm grade dependent manner (Spearman's r = 0.1207, P = .0279). According to the Glasgow Outcome Scale (GOS) score at discharge, 185 patients (55.5%) had a poor outcome (GOS scores 1-3). Serum glucose/potassium ratio was significantly correlated between poor outcome (GOS scores 1-3) and age (P < .0001), serum glucose/potassium ratio (P < .0001), glucose (P < .0001), potassium (P = .0004), white blood cell count (P = .0012), and cerebral infarction due to cerebral vasospasm (P < .0001). Multivariate logistic regression analyzes showed significant correlations between cerebral infarction due to cerebral vasospasm and serum glucose/potassium ratio (P = .018), glucose (P = .027), and potassium (P = .052). Conclusions: Serum glucose/potassium ratio in cases of aneurysmal SAH was significantly associated with cerebral infarction due to cerebral vasospasm and GOS at discharge. Therefore, this factor was useful to predict prognosis in patients with cerebral vasospasm and aneurysmal SAH.