蛛网膜下腔出血后腰池持续引流防治脑血管痉挛作用的影像学观察

目的　研究实验性蛛网膜下腔出血 (SAH)后腰池持续引流对脑血管痉挛 (CVS)预防和治疗作用的影像学分析。方法　经皮枕大池 2次注血法建立犬SAH动物模型 ,将 30条健康成年狗随机分为对照组、早期腰穿组、晚期腰穿组、早期引流组和晚期引流组 ,早期腰穿组和晚期腰穿组分别于 2次注血后 2h和第 5天开始隔日行腰穿排放血性脑脊液 ,早期引流组和晚期引流组分别于 2次注血后 2h和第5天实施腰椎蛛网膜下腔置管持续引流。脑血管造影确定CVS程度 (%reductionofbasilararterydiamit er,%RBAD)的变化发展。结果　①与早期腰穿组和对照组相比 ,早期引流组CVS发生例数少 ,痉挛时程短 ,痉挛程度轻。②与晚期腰穿组和对照组相比 ,晚期引流组CVS程度轻 ,时程短。③与晚期引流组相比 ,早期引流组CVS例数少 ,痉挛程度轻。结论　SAH后实施腰池持续引流可以防治CVS ,早期引流可以取得更好的效果。     

伴有膜部瘤室间隔缺损的封堵治疗

目的　分析和评价伴有膜部瘤室间隔缺损(VSD)的Amplatzer伞的封堵治疗。方法　2 0 0 3年1月至2 0 0 5年4月我科共对16例VSD患者实施了Amplatzer伞封堵治疗,其中伴有膜部瘤VSD 10例。通过左室造影明确VSD大小,膜部瘤形态及与主动脉右冠瓣距离后,在透视及超声监测下建立股动静脉轨道,经右心系统释放封堵器。结果　左心室造影测量室缺直径为4～11(4.9±1.3)mm ,缺损上缘距主动脉根部距离0 .8 9(3.4±1.6 )mm ,膜部瘤缺损呈管状2例,囊袋状5例,漏斗状3例。膜部瘤出口2个以上4例,单出口6例。9例患者封堵器置入成功,7例采用对称型国产室间隔封堵器。2例采用国产动脉导管未闭封堵器,封堵器均未影响右室流出道。其中1例嵴内型缺损,缺损上缘离主动脉右冠瓣小于1mm ,封堵器堵闭膜部瘤的出口,封堵器左室面未影响右冠瓣而封堵成功。1例因基底部宽15mm ,顶端多出口而堵闭失败,转胸外科修补治疗。左室造影即刻9例无残余分流;1例封堵器周边有流速4 .5cm s的微量分流,术后发生机械性溶血,未经治疗术后2d症状消失,复查超声,残余分流减少,流速减少为2cm s。术后发生传导阻滞者4例,其中一过性束支传导阻滞1例,永久性左束支传导阻滞1例、右束支传导阻滞各2例。余无其他并发症。结论　伴有膜部瘤的VSD在VSD中占有比例较高,是Am     

腰穿置管脑脊液持续引流治疗蛛网膜下腔出血的临床观察

目的探讨腰穿置管脑脊液持续引流治疗蛛网膜下腔出血(SAH)的临床价值。方法引流组28例在内科常规治疗的基础上,用16号硬膜外穿刺针于L3,4间隙穿刺置入硬膜外导管,接一次性输液管及引流袋,持续引流,引流速度1～4(平均3)滴/min,引流量度100～400(平均250)ml/d。引流3～7(平均5、6)d后拔管。对照组32例仅给内科常规治疗。结果引流组在治疗后第3,5,7天脑脊液中红细胞比对照组明显减少(P<0.05,或0.01)。神经功能缺损评分,引流组为8.76±8.24明显优于对照组的15.0±8.53。临床疗效,引流组基本痊愈率(20/28)明显高于对照组(7/32),而病死率引流组为2/28明显低于对照组的7/32;两组基本痊愈率与病死率比较,差异均较显著(P<0.05)。两组并发症相比,引流组也少于对照组。结论持续腰池脑脊液引流治疗SAH,能改善患者预后,是一种治疗SAH的有效,安全和简便的治疗方法。     

腰池持续引流防治蛛网膜下腔出血后脑血管痉挛的作用机制

目的　研究腰池持续引流对蛛网膜下腔出血 (SAH)后脑血管痉挛 (CVS)的防治作用 ,并进一步探讨引流的作用机制。方法　经皮枕大池 2次注血法建立犬SAH动物模型 ,设立引流组和对照组 ,引流组于第 2次注血后即开始腰椎蛛网膜下腔置管持续引流血性脑脊液 ,动态测定两组脑脊液中红细胞 (RBC)、内皮素 1(ET 1)和一氧化氮 (NO)含量 ,脑血管造影确定脑血管痉挛程度 (%reductionofbasilararterydiamiter,%RBAD)。对两组CVS的影像学结果及脑脊液中RBC、ET 1和NO含量进行对比分析。结果　SAH后引流组CVS例数少 ,痉挛程度轻。引流组脑脊液中红细胞清除速率快 ,ET 1含量显著低于对照组 ,NO含量显著高于对照组。结论　SAH后腰池持续引流通过清除蛛网膜下腔致痉挛物质 ,改变脑脊液中ET 1和NO的含量 ,可以预防和缓解血管痉挛。     

实验性脑血管痉挛超微结构与形态定量

实验性脑血管痉挛超微结构与形态定量①１００７００北京北京军区总医院刘芳龄张葆樽郝晓淑田玉旺邢惠清关键词脑缺血，暂时性；显微镜检查，电子中国图书资料分类号Ｒ７４３．３５脑血管痉挛（ＣＶＳ）多发生在脑蛛网膜下腔出血（ＳＡＨ）之后，是ＳＡＨ致死与致残的重要...     

CT灌注与脑血管造影对检测兔蛛网膜下腔出血后迟发性脑血管痉挛的比较研究

目的 比较脑血管造影(DSA)和CT灌注成像对脑血管痉挛后组织缺血的检测能力.材料与方法取健康新西兰大白兔64只,随机平均分成实验组和对照组,每组按术前、术后3天、术后7天及术后14天分为4小组,每小组8只.实验组利用2次开颅视交叉池注血建立动物模型,对照组注射等量的生理盐水.每小组均行DSA及CT灌注成像,然后处死动物行常规HE染色病理切片,观察脑组织存活情况.结果 除3只意外死亡,其余实验动物均顺利完成检查.DSA示实验组术后3天时有2只发生中度脑血管痉挛,第7天时有4只发生重度痉挛,14天时2只发生轻度痉挛,余均未见明显脑血管痉挛;CT灌注发现实验组动物在术后的达峰时间(TTP)均发生了明显改变,3天时为(5.82±1.14)s,7天时达到峰值(7.8±1.16)s,14天时恢复到(5.18±0.17)s.而脑血流量(CBF)和脑血容量(CBV)在3天时开始下降,分别为(101±17)ml·min-1·100 g-1、(1.87±0.30)ml·min-1·100 g-1;7天时均达到最低,分别为(61±19)ml·min-1·100 g-1、(1.37±0.17)ml·min-1·100 g-1;14天时恢复至(80±17)ml·min-1·100 g-1、(2.05±0.24)ml·min-1·100 g-1,而对照组则无明显改变;HE染色示实验组3天时脑组织血管周围明显炎性反应,血管壁增厚,7天时脑组织出现无组织结构的片状坏死,14天时脑胶质细胞肿胀、变性,而对照组则无明显炎性反应和血管壁增厚.结论 CT灌注成像较DSA更能反映脑血管痉挛后组织的微循环状况.     

尼莫地平治疗蛛网膜下腔出血伴脑血管痉挛100例

原发性蛛网膜下腔出血发病急、死亡率高。流入蛛网膜下腔的血液或因直接刺激，或因血细胞破坏，释放大量促血管痉挛物质，引起脑血管痉挛，并发脑梗死，加剧脑水肿，导致病情进一步恶化（1）。因此，较好地防治蛛网膜下腔出血（SAH）并发的脑血管痉挛，成为抢救SAH成功的关键。1991年1月～1996年4月，我们应用尼莫地平治疗SAHIOO例，并与1991年1月以前70例未用尼莫地平治疗的SAH患者的疗效进行对比，发现尼莫地平对蛛网膜下腔出血所致的脑血管痉挛有较好的对抗作用。1临床资料1．五一般情况用尼莫地平组（治疗组）100例与未用尼莫地平…     

罂粟碱对于防治脑动脉瘤术后脑血管痉挛的临床研究

通过采用罂粟碱的不同给药途径研究比较其对脑血管痉挛（CVS）的防治效果。将43例动脉瘤患者随机分成A、B两组，A组术中经置入脑池的硅胶管用罂粟碱溶液持续灌洗；B组术后使用罂粟碱30mg肌肉注射，每日3次，共1周。结果显示，A组防治血管痉挛的效果明显优于B组。提示罂粟碱局部灌洗能有效防治脑动脉瘤术后血管痉挛。     

破裂出血动脉瘤的早期栓塞治疗与脑血管痉挛

目的　分析血管内栓塞治疗急性破裂出血动脉瘤脑血管痉挛的发生及治疗。方法　Hunt HessⅠ～Ⅲ级并在发病后 72h内进行介入治疗的动脉瘤患者 32 9例 ,症状性血管痉挛的诊断根据迟发性神经功能损害 ,并有TCD和 (或 )脑血管造影的证据。结果　共发生症状性血管痉挛 6 2例 (18.2 % ) ,血管痉挛的发生率和Hunt Hess分级及Fisher分级有显著的相关关系 ,6 2例发生症状性脑血管痉挛患者中恢复良好 4 1例 ,中度致残 13例 ,重度致残 6例 ,死亡 2例。结论　GDC栓塞治疗动脉瘤后症状性血管痉挛的发生率并不高于常规手术治疗 ;放置腰椎蛛网膜下腔持续引流可能对降低症状性脑血管痉挛的发生有积极意义。     

自发性蛛网膜下腔出血后脑血管痉挛的研究进展

蛛网膜下腔出血引起的脑血管痉挛是患者死亡和致残的主要原因之一,也是影响患者预后的重要因素,治疗上较棘手。近年来有关脑血管痉挛治疗研究进展较快,为提高对本病的认识,现就蛛网膜下腔出血引起脑血管痉挛的发病机理及治疗进展进行综述。     

蛛网膜下腔出血后脑脊液中内皮素-1和一氧化氮变化与脑血管痉挛的关系

目的　研究实验性蛛网膜下腔出血 (SAH)后脑脊液中内皮素 1(ET 1)和一氧化氮 (NO)浓度的变化与脑血管痉挛 (CVS)的关系。方法　经皮枕大池二次注血法建立犬CVS动物模型 ,放免法测定脑脊液中ET 1浓度 ,镉还原法测定脑脊液中NO浓度 ,脑血管造影确定血管痉挛程度 (%reductionofbasilararterydiamiter,%RBAD)。结果　SAH后脑脊液中ET浓度显著高于注血前正常水平 (P <0 .0 5 ) ,第 7天达到峰值 (2 15± 36 ) μg L后逐渐下降 ;脑脊液中NO浓度显著下降 (P <0 .0 5 ) ,至第 7天达到最低值 (5 .8± 1.35 ) μmol L后逐渐升高。SAH后血管痉挛程度逐渐加重 ,第 7天达到最大痉挛程度 4 8± 10 ,其后逐渐缓解。结论　SAH后脑血管痉挛程度与脑脊液中ET 1和NO含量在时间进程和程度上密切相关 ,SAH后脑脊液中ET 1和NO可能参与了CVS的过程。     

Pre-operative micro-angioplasty of refractory vasospasm secondary to subarachnoid hemorrhage

Summary A patient with subarachnoid hermorrhage secondary to a basilar artery aneurysm developed severe bilateral middle and anterior cerebral artery vasospasm with extensive neurologic deficits. Microangioplasty of the middle cerebral artery segments bilaterally led to reversal of the neurologic deficits, allowing early operative treatment of the aneurysm in a previously inoperable patient.     

血清Hcy与蛛网膜下腔出血后脑血管痉挛的相关性分析

目的 探讨蛛网膜下腔出血（SAH）患者血清同型半胱氨酸（Hcy）水平与脑血管痉挛（CVS）的相关性.方法 186例SAH患者中,将继发CVS的68例作为CVS组,未发生CVS的118例作为对照组,对比分析两组血清Hcy水平,并对Hcy水平与CVS的发生率进行相关性分析.结果 CVS组血清Hcy水平为（32.6±16.8）μmol/L,显著高于对照组的（16.2±17.8）μmol/L（t=6.272,P＜0.05）;血清Hcy水平＞20 μmol/L者在CVS组中占47.1%,显著高于对照组的30.5%（χ^2=5.095,P＜0.05）.随着Hcy水平的升高,CVS的发生率逐渐升高,血清Hcy水平与CVS的发生率呈正相关（r=0.969,P＜0.01）.结论 血清Hcy水平与SAH后CVS相关,Hcy的检测有助于CVS的早期预测和干预.     

血管痉挛对蛛网膜下腔出血后脑血管病理性改变的影响

目的探讨蛛网膜下腔出血(SAH)性脑血管痉挛(CVS)与血管壁病理学改变之间的因果关系。方法采用药理学预阻滞法,通过光镜和电镜对42只猫SAH后CVS的形成及其对血管壁病理性改变的影响作用进行观察。结果预先使用血管外周阻滞剂可以明显地减轻SAH所致的CVS反应程度,并使血管壁发生的病理性改变也随之减轻。结论 CVS是血管壁发生病理性改变的成因,继而又成为影响SAH预后的主要原因之一。预防或阻止CVS的发生,可有效地防止血管壁发生相应的病理学改变。     

Regional cerebral blood flow levels as measured by xenon-CT in vascular territorial low-density areas after subarachnoid hemorrhage are not always ischemic

Introduction The aim of this study was to assess regional cerebral blood flow (rCBV) in areas of CT hypoattenuation appearing in the postoperative period in patients treated for aneurysmal subarachnoid hemorrhage (SAH) using xenon-enhanced CT scanning (Xe-CT).Methods We analyzed 15 patients (5 male and 10 female; mean age 49.7±12.1 years) with SAH on CT performed on admission to hospital and who showed a low-density area within a well-defined vascular territory on CT scans after clipping or coiling of a saccular aneurysm. All zones of hypoattenuation were larger than 1 cm² and showed signs of a mass effect suggesting a subacute phase of evolution. Two aneurysms were detected in two patients. Aneurysms were located in the middle cerebral artery (n=7), in the anterior communicating artery (n=6), in the internal carotid artery (n=3), and in the posterior communicating artery (n=1). Treatments were surgical (n=8), endovascular (n=2) or both (n=1). A total of 36 Xe-CT studies were performed and rCBF values were measured in two different regions of interest (ROI): the low-density area, and an area of normal-appearing brain tissue located symmetrically in the contralateral hemisphere.Results rCBF levels were significantly lower in the low-density area than in the contralateral normal-appearing area (P<0.01). In the low-density areas, irreversible ischemia (CBF <10 ml/100 g per minute) was present in 11/36 lesions (30.6%), ischemic penumbra (CBF 10–20 ml/100 g per minute) and oligemia (CBF 20–34 ml/100 g per minute) in 8/36 lesions (22.2%), relative hyperemia (CBF 34–55 ml/100 g per minute) in 7/36 lesions (19.4%), and absolute hyperemia (CBF >55 ml/100 g per minute) in 2/36 lesions (5.6%).Conclusion Our study confirmed that rCBF is reduced in new low-density lesions related to specific vascular territories. However, only about one-third of the lesions showed rCBF levels consistent with irreversible ischemia and in a relatively high proportion of lesions, rCBF levels indicated penumbral, oligemic and hyperemic areas.     

Perfusion-weighted MRI to evaluate cerebral autoregulation in aneurysmal subarachnoid haemorrhage

Introduction  The aim of this study was to evaluate autoregulatory mechanisms in different vascular territories within the first week after aneurysmal subarachnoid haemorrhage (SAH) by perfusion-weighted magnetic resonance imaging (PW-MRI). For this purpose, regional cerebral blood flow and volume (rCVF and rCBV) were measured in relation to different degrees of angiographically visible cerebral vasospasm (CVS). Materials and methods  In 51 SAH patients, PW-MRI and digital subtraction angiography were performed about 5 days after onset of SAH. Regional CBF and rCBV were analysed in the territories of the anterior cerebral artery (ACA), the middle cerebral artery (MCA) and the basal ganglia of each hemisphere in relationship to the degree of CVS in the particular territory. Correlations between rCBF, rCBV and CVS were analysed. Results  CVS was found in 22 out of 51 patients in at least one territory. In all territories, rCBV decreased with increasing degree of CVS, correlated with a decrease of rCBF. In the ACA territories, SAH patients with severe CVS had significantly lower rCBF compared to healthy subjects and to SAH patients without CVS. In the basal ganglia, rCBF and rCBV of the control group were significantly higher compared to the patients without and with moderate vasospasms. Conclusion  PW-MRI showed simultaneous decrease of rCBF and rCBV in patients with SAH. The fact that rCBV did not increase in territories with CVS to maintain rCBF reveals dysfunctional vascular autoregulation. Vasospasms in the microvasculature are most evident in the basal ganglia, showing decreased rCBV and rCBF even in SAH patients without CVS.     

Global and focal cerebral perfusion after aneurysmal subarachnoid hemorrhage in relation with delayed cerebral ischemia

INTRODUCTION: The pathogenesis of delayed cerebral ischemia (DCI) after subarachnoid hemorrhage (SAH) is unclear. We assessed whether DCI relates to focal or global cerebral perfusion on admission and on follow-up imaging. MATERIALS AND METHODS: Twenty-seven SAH patients underwent computed tomography (CT) perfusion (CTP) on admission and at clinical deterioration or 1 week after admission in clinically stable patients. We compared global and focal (least perfused territory) perfusion in patients with DCI (n = 12), clinically stable patients (n = 7), and patients with non-DCI-related deterioration (n = 8). RESULTS: Global cerebral blood flow (CBF) increased on follow-up: 29% (95% confidence interval (CI) 15% to 43%) in patients with DCI, 12% (95%CI -1% to 25%) in stable patients, and 20% (95%CI 4% to 36%) in patients with non-DCI-related deterioration. Focal CBF decreased in patients with DCI, (-23%; 95%CI -58% to 12%) but increased in patients with non-DCI-related deterioration (23%; 95%CI -26% to 55%) and stable patients (7%; 95%CI -30% to 45%).On follow-up, global CBF was lower in patients with DCI (70.0 ml per 100 g/min) than in clinically stable patients (81.6; difference 11.6; 95%CI 0.8 to 22.5 ml per 100 g/min) but comparable to patients with non-DCI-related deterioration (67.6; difference -2.4; 95%CI -11.9 to 7.2 ml per 100 g/min). Focal CBF was lower in patients with DCI (30.7) than in clinically stable patients (53.6; difference 22.9; 95%CI 5.1 to 40.6 ml per 100 g/min) and patients with non-DCI-related deterioration (46.6; difference 15.9; 95%CI -2.6 to 28.4 ml per 100 g/min) CONCLUSION: Our results suggest that DCI is more likely a focal than a global process.