进展性缺血性脑卒中的形成因素

目的了解进展性缺血性脑卒中的形成因素。方法136例缺血性脑卒中患者筛选出进展性脑卒中38例，与98例卒中及60例健康者作对照，比较血液中血管性血友病因子抗原（vWF：Ag）、a颗粒膜蛋白-140（GMP-140）、凝血酶抗凝血酶Ⅲ复合物（TAT）、抗凝血酶Ⅲ（ATⅢ）、组织型纤溶酶原激活物（t—PA）、D二聚体（D—D）、纤溶酶原激活物抑制物-1（PA11）、同型半胱氨酸（HCY）、空腹血糖（FBG）的浓度及收缩压（SBP）、舒张压（DBP）。结果缺血性脑卒中的发生者vWF、GMP-140、TAT、PAI、DD、HCY、FBG明显增加，ATⅢ、t—PA减少（P〈0．05）；而进展性缺血性卒中vWF、TAT、PAI、DD、HCY、FBG进一步增加，ATⅢ、t-PA进一步减少，SBP、DBP明显下降（（P〈0．05），GMP-140上升无显著差异（P〉0．05）。结论进展性缺血性卒中与vWF：Ag、TAT、DD、PAI、HCY、FBG进一步增加，ATⅢ、t—PA进一步减少，SBP、DBP下降（P〈0．05）有关。     

老年人颅脑外伤后缺血性脑卒中发作特点及治疗

目的探讨老年人颅脑外伤后缺血性脑卒中发作特点及个性化治疗方案。方法针对7例颅脑外伤后急性期出现缺血性脑血管病症状的老年患者，通过脑血管造影检查分析其发病原因并根据不同的脑血管特点决定治疗方案。结果大多数患者（6／7）受伤前已存在不同程度的颅内外血管狭窄、血管壁溃疡以及附壁血栓形成等改变，提示脑缺血发作主要与这些病变为基础的脑血流下降、血栓脱落等因素密切相关。而外伤后脑灌注降低、脑血管痉挛是脑缺血发作的诱发因素。结论老年人外伤后的缺血性脑卒中发作主要与原有的脑血管基础疾病有关，预防和治疗老年人外伤后缺血性脑卒中发作，应基于这些病变特征并选择个体化治疗方案。     

A national stroke quality register: 12 years experience from a participating hospital

Registration of all hospitalized stroke patients is practiced in Sweden in order to assess care quality. Data in this register, Riks-Stroke (RS), may be biased due to incomplete registration. The purpose of this paper was to report changes in stroke outcome in relation to fluctuations in registration. Patients registered in RS at a hospital during the period 1994–2005 were analyzed. Case fatality at 28 days, living conditions, and activities of daily living (ADL) performance at 3 months were correlated to the number of patients registered and follow-up frequency. A total of 4994 stroke cases were registered during the period. A high annual registration rate was significantly correlated to a high case fatality ratio. A low annual follow-up rate was associated with a low proportion of patients living in their own home without any need of help. Quality parameters are sensible for selection bias, which make them difficult to compare over time and between hospitals. We suggest that by weighing outcome data against stroke severity, safer conclusions may be drawn. Additionally, hospitals considering setting up quality registers should make every effort to attain complete case ascertainment at all times, including patients managed outside the hospital, in order to avoid selection bias.     

依达拉奉防治缺血性脑损伤研究的新进展

近年来,依达拉奉脑保护作用的研究取得了很大进展,尤以对缺血性脑卒中和新生儿缺血缺氧性脑病的防治研究最为深入,而联合治疗策略也得到了广泛的重视.本文就近5年这些热点研究的新进展进行综述.     

急性缺血性卒中大血管闭塞性质的判断与取栓方式和材料的选择

血管内机械取栓是治疗大血管闭塞性急性缺血性卒中的有效治疗方法。应结合病史、发
病形式及影像学检查等综合判断病变性质；依据病变性质并参考手术路径，个性化选择支架取栓、
抽吸取栓、球囊/支架血管成形术、动脉溶栓任一种或多种方法联合取栓；并依据手术方式选择手
术材料，以快速高效地完成手术。     

急性缺血性卒中患者发生院内消化道出血的危险因素分析

目的 分析急性缺血性卒中患者（acute ischemic stroke，AIS）住院期间消化道出血（gastrointestinal
bleeding，GIB）的发生率、发生时间及危险因素。
方法 本研究纳入首都医科大学附属北京天坛医院急性卒中院内并发症队列（inhospital medical
complication after acute stroke，iMCAS）研究中AIS患者。收集患者临床信息，根据住院期间是否发生
GIB分为GIB组和无GIB组，采用多因素Logistic回归模型，分析AIS患者发生GIB相关危险因素。
结果 共纳入1129例AIS患者，平均年龄58.7±12.5岁，女性230例（20.4%）。47例住院期间发生GIB，
发生率为4.2%，卒中发作至GIB确诊时间为5（3～13）d。合并肝硬化（OR 10.06，95%CI 2.44～41.38）、
高入院NIHSS评分（OR 1.13，95%CI 1.08～1.19）、高白细胞计数（OR 1.25，95%CI 1.13～1.38）、住院时
间长（OR 1.05，95%CI 1.01～1.10）是AIS患者发生消化道出血的独立危险因素。
结论 本单中心研究数据提示合并肝硬化、高入院NI HSS评分、高白细胞计数、住院时间长是AI S患
者住院期间发生GIB的独立危险因素。     

交感神经节与椎旁阻滞联合运用于改善脑中风预后的研究

目的 评价交感神经节与椎旁阻滞联合运用在脑中风康复治疗中的效果。方法 150例中风患者随机分为交感神经节与椎旁阻滞联合运用组（SGB组）和康复训练组（H组）。分别在治疗前、治疗后及随访期间，记录患者的体征、实验室检查及特殊检测结果。使用临床神经功能缺损程度评分标准及修订的巴氏指数（modified Barthel index，MBI）评测。采用t检验和卡方检验分析组间差异。结果 治疗1、3、6个月后，SGB组与H组总疗效均有改善，分别为H组：50％、60％、70％；SGB组：90％、95％、100％，SGB组疗效优于H组。两组比较，自觉症状、神经功能缺损改善程度有明显差异，生活活动能力改善程度差别不大。治疗前、后相比，SGB组收缩压、舒张压、局部皮温、血高切黏度、血低切黏度、PGA有改善，H组改变不明显；两组患者血浆黏度无明显改善。TCD显示，SGB组脑血流改善占85．3％，H组占14．3％。SGB组住院时间短于H组，住院费用不增加。结论 在脑中风康复治疗中，联合运用交感神经节与椎旁阻滞，疗效明显优于常规康复训练。     

Poststroke DNA immunization against neurite growth inhibitors is beneficial to the recovery from local cerebral ischemia in rats

BACKGROUND： Inhibitory signals, i.e. neurite growth inhibitors （NGIs）, presenting on central nervous system （CNS） myelin have been shown to play a crucial role in inhibiting lesioned axonal sprouting and leading to less functional recovery. Vaccines targeting NGIs may provide multifactorial protection against brain insults by overcoming the inhibitory effects of these NGIs and boosting the body＇s immune repair mechanisms. OBJECTIVE： To evaluate the effect of poststroke DNA immunization against NGIs on the rehabilitation for sensorimotor function of rat models of local cerebral ischemia. DESIGN： Completely randomized grouping design, and controlled experiment. SETTING： Brain Injury Research Laboratory, Department of Neurosurgery, National Neuroscience Institute, Singapore. MATERIALS： Sixty adult male Sprague-Dawley rats ranging in age from 45 to 120 days and in weight from 180 to 250 grams were provided by Animal Center of Department of Anatomy, Faculty of Medicine, National University of Singapore. pcDNA3.1（＋）-neurite growth inhibitors （pcDNA-NGIs） a gift was provided by Dr. Xiao from Department of Clinical Research, Singapore General Hospital, Singapore. METHODS： The experiment was carried out at Brain Injury Research Laboratory, Department of Neurosurgery, National Neuroscience Institute, Singapore from August 2003 to April 2005. （1）The involved rats were randomized into 3 groups： pcDNA-NGIs group （group A）, pcDNA3.1 （＋） group （group B） and model group （group C）, with 20 rats in each group. Left focal cerebral ischemia （FCI） was permanently induced through middle cerebral artery occlusion （MCAO） with the assistance of an operating microscope. Successful MCAO was determined by a 20% decrease to baseline in the ipsilateral cerebral blood flow. 100 μg of pcDNA-NGIs eluted in phosphate-buffered saline （PBS） was intramuscularly injected into the tibial muscle once a week after MCAO for 6 weeks in group A. As control, pcDNA3.1 （＋） was also administrated in the same way in group B and nothing was administrated in group C. （2） The modified neurological severity score （mNSS）, a composite of motor, sensory, reflex and balance tests, was used to test the sensorimotor deficit. The mNSS was graded on a scale of 0 - 18, i.e. normal score was 0, maximal deficit score was 18, and 1 point was warded for the inability to perform the tasks or the lack of a tested reflex. （3） The newly generated axons of corticorubral projection were traced by stereotaxic guided injection of 100 g/L biotinylated dextran amine. Rats were sacrificed two weeks after tracing, and cryostat coronal sections of midbrains （30μm） were reacted to BDA according to the manufacturer＇s instruction by the free-floating method. Images were captured on a DM RXA2 LEICA Microscope with a Spot Digital Camera system （Germany）, and the numbers of labeled axons on the denervated side in four standard coronal sections including the red nucleus were manually quantified. MAIN OUTCOME MEASURES： （1） The number of newly generated axons of corticorubral projection. （2）The improvement in sensorimotor deficit. RESULTS： All the involved 60 rats entered the stage of final analysis. （1） The number of newly generated axons of corticorubral projection of rats： Only ipsilateral axons of CRP were noted with little evidence of fibers crossing to the contralateral red nucleus in rats of groups B and C. More BDA-positive fibers crossing the midline and terminating in the contralateral red nucleus in appropriate target areas mirroring the non-differentiated red nucleus were found in rats of group A. Quantitative analysis showed that BDA-labeled axons in the denervated side of rats in group A were more than those in group B （P 〈 0.05）. （2） Improvement in sensorimotor deficit of rats： At 2 weeks after immunization, significant improvement in sensorimotor deficit was found in rats of group A. There were significant differences of improvement in sensorimotor deficit of rats between group A and group B or group C at 12 and 14 weeks after immunization （P 〈 0.05）. CONCLUSION： （1） Poststroke DNA immunization against NGIs leads to increased sensorimotor recovery following FCI and compensatory newly growth of axons from corticorubral projection.