Piracetam in acute stroke: a systematic review

We studied whether the administration of piracetam in acute, presumed ischemic stroke affects case fatality and functional outcome. The Cochrane Stroke Group strategy was used to evaluate all randomized controlled trials of patients with presumed ischemic stroke examined within 48 h; death and (when available) functional outcome were used as end points. Three studies were included; the most recent one contributed more than 97% of the data. There were 501 patients treated with piracetam and 501 controls. Piracetam was associated with a nonsignificant 31% increase in the odds of death (95% CI –5% to 81%). This result was due almost completely to the effect of the larger trial, which, however, reported that the difference in case fatality rate between piracetam and control disappeared after correcting for the imbalance in stroke severity between the two groups. Data on functional outcome were available only for the largest study, and no difference was reported. Data obtained from the manufacturer suggested a nonsignificant trend (–10%) towards reduction in dependency with piracetam (CI –33% to 20%); the proportions of patients dead or dependent in the two groups were the same. Relevant adverse effects were not reported. The evidence from this review does not support routine administration of piracetam in patients with acute ischemic stroke; however, since a possible beneficial effect cannot completely be ruled out, further controlled trials are warranted. Received: 31 August 1999/Received in revised form: 3 November 1999/Accepted: 25 November 1999     

短暂性脑缺血发作对后继脑梗死影响的研究

目的:评价短暂性脑缺血发作(T IA)对后继脑梗死是否有保护作用。方法:选择2000~2005年我院老年神经病科及神经内科既往有同侧T IA的脑梗死患者98例,并对有同侧T IA的脑梗死患者根据T IA发作持续时间分为<10m in(26例)、10~20m in(38例)及>20m in(34例),并选择同期住院无T IA的脑梗死患者102例进行病例对照观察。在入院及病程一月时采用改良的爱丁堡-斯堪的那维亚卒中量表进行神经功能缺损评分,病程一月时进行预后评分。结果:两组患者年龄及其他危险因素包括高血压病、糖尿病、高脂血症及冠心病无差异(P>0.05);入院及病程一月时,无T IA的脑梗死患者其神经功能缺损评分及近期预后与T IA持续时间在10~20m in的脑梗死患者有显著性差异(P<0.05),但与T IA持续时间<10m in及>20m in的脑梗死患者无差异(P>0.05),且T IA持续时间在10~20m in之间与<10m in、>20m in比较有显著性差异(P<0.05)。结论:T IA对后继脑梗死有保护作用。     

他汀类与抗血小板药联合用药对缺血性脑血管病患者颈动脉粥样硬化的干预作用

目的:探讨缺血性脑血管病患者联合应用他汀类及抗血小板药对颈动脉粥样硬化和脑血管事件的干预作用。方法:选择146例缺血性脑血管病合并颈动脉粥样硬化患者,将其随机分为治疗组和对照组。治疗组74例,应用氟伐他汀(每晚40mg)和拜阿斯匹灵(100mg/d),对照组72例,仅给拜阿斯匹灵(100mg/d)。共随访2年,分别在治疗前,治疗后6月、12月、18月、24月检测血脂,颈动脉内-中膜厚度,颈动脉斑块积分。结果:治疗组平均颈动脉内-中膜厚度和颈动脉斑块积分,治疗前分别为(1.22±0.19)mm和4.4±2.5,治疗后分别为(0.87±0.15)mm和2.8±1.1,治疗前后比较差异具有显著性(P<0.01)。随访结束时,治疗组缺血性脑血管病复发率9.5%,与对照组复发率(26.3%)相比明显下降。结论:联合应用他汀类及抗血小板药能延缓和逆转缺血性脑血管病患者颈动脉粥样硬化的进展,对缺血性脑血管病的复发有很好的预防作用,且不增加脑出血发生率。     

丹参注射液对急性肾衰竭兔心肌缺血的保护作用

目的探讨丹参注射液对急性肾衰竭(ARF)家兔心肌缺血的保护作用。方法取家兔28只，随机分为3组，对照组8只，模型组12只，丹参组8只。麻醉后对照组和模型组给予0.9%氯化钠注射液耳缘静脉注射，丹参组给予丹参注射液耳缘静脉注射。均为0.5 mL·kg^-1，每6 h重复1次，共4次。第1次给药后0.5 h，对照组给予0.9%氯化钠注射液双侧后肢肌内加压注射，10 mL·kg^-1，模型组和丹参组制备家兔ARF模型，即给予50%甘油溶液双侧后肢肌内加压注射，10 mL·kg^-1。检测各组家兔不同时相血小板聚集功能、前列环素(PGI2)、血栓素A2(TXA2)、内皮素(ET)等指标及心肌组织形态学变化。结果与对照组比较，模型组肌内注射给药后2，24 h血小板聚集性、TXA2 、ET均明显升高(均P＜0.01)，6-酮-前列腺素F1a(6-Keto-PGF1a)明显降低(P＜0.01)，心肌组织出现严重的缺血性损害;丹参组则无明显变化。与模型组比较，丹参组家兔肌内注射给药后2，24 h，血小板聚集性、TXA2、ET明显降低(均P＜0.01)，6-Keto-PGF1a明显升高(P＜0.01)，心肌组织缺血性损害明显减轻。结论ARF时，家兔血小板聚集性改变和血管活性物质与氧自由基的增高可能是造成心肌组织缺血性损害的直接原因之一。丹参可通过抑制血小板聚集功能，降低TXA2、ET等明显减轻ARF家兔心肌组织缺血性损伤。     

针刺为主治疗缺血性视乳头病变临床观察

目的:观察针刺与西药治疗缺血性视乳头病变的疗效差异.方法:31例患者以针刺治疗为主,辅以穴位注射.对于发病2周之内者,局部配合球后注射.记录治疗前后视力、视野的变化.结果:治疗前后视力、视野比较,差异均有极显著性意义(P<0.001).结论:该疗法是改善缺血性视乳头病变患者视功能的有效方法.     

2015—2019年江西省缺血性脑卒中患者特征及住院费用分析

目的 了解江西省2015—2019年缺血性脑卒中住院患者特征及住院费用情况，为缺血性脑卒中防控提供数据支持。方法 收集来自江西省卫生健康委员会DRGs管理系统中2015—2019年全省228家医院（69家三级综合医院，159家二级综合医院），总计381 416例出院主诊断疾病编码为I63（采用国际疾病分类第十版ICD - 10）的缺血性脑卒中患者住院信息。对住院患者特征及费用进行描述性分析。结果 2015—2019年江西省缺血性脑卒中患者,男性占比大于女性，近5年住院率由119.09/10万升高至206.61/10万。缺血性脑卒中患者最常见的共病及并发症为高血压、糖尿病、动脉粥样硬化。缺血性脑卒中次均住院费用为7 067.2(6 846.1)元，5年间，次均住院费用由7 384.0（7 353.6）元降低至6 816.9（6 769.1）元，差异具有统计学意义（H = 12.155，P＜0.002），总费用中药费占比最高，但未见明显变化趋势（H = 7.425，P = 0.063）。结论 2015—2019年江西省缺血性脑卒中住院患者住院率增长较快，高血压、糖尿病、动脉粥样硬化为3个最常见的共病,次均住院费用呈下降趋势，但住院费用负担仍较重。     

Pathogenesis of acute stroke and the role of inflammasomes

Inflammation is an innate immune response to infection or tissue damage that is designed to limit harm to the host, but contributes significantly to ischemic brain injury following stroke. The inflammatory response is initiated by the detection of acute damage via extracellular and intracellular pattern recognition receptors, which respond to conserved microbial structures, termed pathogen-associated molecular patterns or host-derived danger signals termed damage-associated molecular patterns. Multi-protein complexes known as inflammasomes (e.g. containing NLRP1, NLRP2, NLRP3, NLRP6, NLRP7, NLRP12, NLRC4, AIM2 and/or Pyrin), then process these signals to trigger an effector response. Briefly, signaling through NLRP1 and NLRP3 inflammasomes produces cleaved caspase-1, which cleaves both pro-IL-1β and pro-IL-18 into their biologically active mature pro-inflammatory cytokines that are released into the extracellular environment. This review will describe the molecular structure, cellular signaling pathways and current evidence for inflammasome activation following cerebral ischemia, and the potential for future treatments for stroke that may involve targeting inflammasome formation or its products in the ischemic brain.