以火针疗法为主治疗急性脑梗死近期临床疗效观察

目的探讨以火针疗法为主治疗急性脑梗死近期临床疗效观察。方法对我院2007年8月至2009年8月急性急性脑梗死患者56例随机分为2组,对照组为28例,采用常规西药治疗,治疗组为28例在常规西药治疗下采用火针疗法治疗,比较2组的总体治疗疗效、治疗前后的神经功能缺损评分和病残程度分级。结果治疗组治疗后总有效率92.9%,对照组治疗后总有效率82.1%,(P<0.01)差异具有统计学意义。治疗组神经功能缺损评分与对照组相比(t=1.690,P<0.05),差异具有统计学意义。治疗组病残程度分级与对照组相比(t=1.915,P<0.05),差异具有统计学意义。结论以火针疗法为主治疗急性脑梗死近期相比常规治疗,疗效更明显,值得临床推广。     

氧自由基水平检测与小儿病毒性脑炎颅内高压的关系探讨

目的探讨黄芪、硫酸镁配合甘露醇治疗急性颅内高压的作用机制。方法将102例急性病毒性脑炎患儿随机分为观察组与对照组。对照组只应用传统的甘露醇治疗,观察组在甘露醇治疗基础上加用黄芪注射液及硫酸镁,治疗后分别检测其SOD及LPO的含量,然后通过统计学t检验与卡方检验进行差异显著性比较。结果观察组有效29例(56.9%),显效22例(43.1%),总有效率100%。对照组有效20例(39.2%),显效12例(23.5%),无效19例(37.2%),总有效率62.7%。与对照组相比,观察组患者治疗后SOD活性明显升高,LPO明显水平明显降低(P<0.01)。结论清除氧自由基对降低由小儿病毒性脑炎引起的颅内高压有重要作用。     

依达拉奉联合降纤酶治疗急性脑梗死临床疗效观察

目的探讨依达拉奉联合降纤酶治疗急性脑梗死的预后和影响。方法将60例急性脑梗死患者分为治疗组(32例),对照组(28例),2组均给予常规治疗,治疗组在常规治疗的基础上加用依达拉奉和降纤酶治疗,疗程5d。常规治疗包括控制血压、血糖、使用银杏达莫、奥扎格雷钠、小剂量阿司匹林、辛伐他汀及输液治疗,脑水肿时给予20%甘露醇或甘油果糖。结果治疗组与对照组治疗前后神经功能缺损恢复情况比较,差异有显著性(P<0.01)。结论依达拉奉联合降纤酶治疗显著改善急性脑梗死的预后,值得临床推广使用。     

辛伐他汀联用阿司匹林治疗扩张型心肌病的临床分析

目的评价辛伐他汀及联用阿司匹林对扩张型心肌病患者栓塞事件及死亡率的影响。方法将27例扩张型心肌病患者分为辛伐他汀及联用阿司匹林组27例和对照组26例,追踪观察两组的栓塞事件发生率、死亡率及总有效率。结果辛伐他汀及联用阿司匹林组栓塞事件发生率明显低于对照组(P<0.05);两组治疗总有效率及死亡率相比差异无统计学意义(P>0.05)。治疗前、后未发现皮肤黏膜淤斑及内脏出血情况、过敏反应等不良反应。结论扩张型心肌病患者应用应用辛伐他汀及联用阿司匹林抗血小板治疗,可降低患者的栓塞事件发生,但并不增加患者治疗总有效率及减少死亡率。     

60例脑梗死偏瘫患者综合征康复治疗疗效对比分析

目的探讨脑梗死偏瘫患者综合征康复治疗的疗效。方法脑梗死偏瘫患者122例随机分成康复组60例和对照组62例,对照组只进行药物治疗,康复组除进行药物治疗外,还给予康复治疗措施,观察两组治疗30d、90d后肢体运动功能及日常生活自理能力的变化。结果经过综合性康复治疗90d后,康复组总有效率93.33%,对照组为67.74%。两组比较有显著性差异(P<0.05)。30d、90d后神经功能缺损评分减少程度康复组与对照组相比有显著性差异(P<0.05);FMA提高程度康复组与治疗组相比有高度显著性差异(P<0.01)。结论综合性康复治疗可以显著改善恢复期脑梗死偏瘫患者肢体功能,明显提高其生活质量。     

长春西汀与巴曲酶联合治疗急性脑梗死的疗效观察

目的观察联合应用长春西汀与巴曲酶治疗急性脑梗死的疗效。方法选择60例急性脑梗死患者随机分为:治疗组(30例),用长春西汀20mg,每日1次静滴,共2周,巴曲酶10U,每日1次静漓,连用3d;对照组(30例),用ATP40mg,CoA100U,每日1次静滴,共2周,巴曲酶10U,每日1次静漓,连用3d。观察两组治疗前后神经功能缺损评分,血液流变学的变化。结果治疗组显效率(90%)明显高于对照组(50%),两组比较差异有显著性(P<0.01);治疗组治疗后神经功能缺损积分减少及生活能力等级较治疗前有显著提高(均P<0.01),与对照组相比差异也有显著性(P<0.05);治疗组治疗后血液粘度及血小板聚集率均有明显下降(均P<0.01),且较对照组尤为明显(P<0.05);而血浆粘度和纤维蛋白原亦有显著性下降(P<0.01),但两组之间差异无显著性。结论长春西汀与巴曲酶联合应用治疗急性脑梗死较单用巴曲酶效果更好。     

小剂量螺内酯联合美托洛尔治疗慢性心力衰竭患者的临床效果观察

目的探讨小剂量螺内酯联合美托洛尔治疗慢性心力衰竭患者的临床效果。方法将84例慢性心力衰竭患者随机分为对照组(常规治疗组)和观察组(小剂量螺内酯联合美托洛尔组),各42例,比较2组患者的治疗总有效率、不良反应发生率、心功能改善情况及血清NT-proBNP水平。结果观察组的治疗总有效率高于对照组,不良反应发生率低于对照组,心功能好于对照组,血清NT-proBNP水平低于对照组,差异显著性或有非常显著性,P<0.05或P<0.01。结论小剂量螺内酯联合美托洛尔治疗慢性心力衰竭患者的临床效果佳,优势明显,值得推广应用。     

依达拉奉治疗急性脑梗死的疗效观察

目的观察依达拉奉治疗急性脑梗死的临床效果。方法采用随机分组对照试验,选择136例急性脑梗死患者,分为观察组(68例)和对照组(68例)。2组均给予拜阿司匹林、复方甘露醇作为基础治疗,观察组应用依达拉奉,对照组应用脉络宁,分别比较2组7d和14d的疗效。结果依达拉奉组治疗14d后神经功能缺损评分显著优于对照组(P<0.01);依达拉奉组临床有效率为88.24%,显著高于对照组的54.41%(P<0.05)。结论依达拉奉治疗急性脑梗死有确切疗效。     

盐酸法舒地尔联合奥扎格雷钠治疗急性脑梗死106例疗效观察

目的探讨盐酸法舒地尔联合奥扎格雷钠治疗急性脑梗死的临床疗效。方法选择2007年5月至2009年5月在我院就诊的106例急性脑梗死患者,随机分为治疗组和对照组,治疗组用盐酸法舒地尔与奥扎格雷钠联合治疗,对照组单用奥扎格雷钠治疗,比较2组疗效和不良反应。结果治疗组总有效率为88.7%,对照组总有效率为64.2%,2组比较差异有统计学意义(P<0.05),治疗组疗效优于对照组;治疗组患者有8例出现不良反应,不良反应发生率为15.1%;对照组有5例患者出现不良反应,不良反应发生率为9.4%,差异并无统计学意义(P>0.05)。结论盐酸法舒地尔联合奥扎格雷钠治疗急性脑梗死效果显著,值得在临床推广应用。     

灯盏花素治疗中心性渗出性视网膜炎62例疗效分析

目的探讨灯盏花素治疗中心性渗出性视网膜炎的临床效果。方法将我院收治的62例中心性渗出性脉络膜视网膜炎患者,随机分为对照组和观察组,对照组采用复方丹参注射液治疗,观察组采用灯盏花素治疗,比较2组治疗效果及不良反应发生情况。结果对照组总有效率60%。观察组总有效率95%。2组总有效率经统计学分析,差异有统计学意义(P<0.05)。2组治疗过程中均未见明显不良反应发生。观察组视力改善情况明显优于对照组,差异有统计学意义(P<0.05)。结论采用灯盏花素治疗中心性渗出性视网膜炎,总有效率优于复方丹参治疗,视力提高优于复方丹参组,治疗过程中未见明显不良反应发生,使用方便,值得临床推广应用。     

自由基清除剂在治疗急性脑梗塞中的临床分析

目的观察自由基清除剂依达拉奉治疗急性脑梗塞的临床效果及安全性。方法选择急性脑梗塞患者68例,随机分为依达拉奉治疗组和对照组。两组在常规治疗基础上,治疗组静脉滴注依达拉奉30mg/次,2次/天,共14天,治疗前后定期对患者进行改良爱丁堡-斯堪的那维亚量表(SSS)及日常生活能力(ADL)的评定。结果治疗7d及14d后治疗组SSS评分及ADL评定与对照组比较差异有显著性(P<0.05或0.01)。治疗组治疗前后SSS评分及ADL评定差异有高度显著性(P<0.01)。治疗组无不良反应。结论依达拉奉治疗急性脑梗塞是有效安全的。     

小剂量低分子肝素防治脑梗死进展60例临床观察

目的观察小剂量低分子肝素防治急性进展性脑梗死的临床疗效并探讨其机制。方法将120例急性进展性脑梗死患者(起病6～48h内)随机分为两组,治疗组(60例)于常规治疗基础上小剂量低分子肝素治疗和对照组(60例)仅行常规治疗,分别于治疗4周前后作实验室检查及脑卒中患者临床神经功能缺损程度评分,并进行统计分析,比较两组的疗效。结果治疗组在临床神经功能缺损程度评分及疗效方面均较对照组改善明显(P<0.05)。结论低分子肝素治疗进展型脑梗死疗效显著,应用方便,安全可靠,值得临床推广应用。     

川芎嗪注射液对急性脑梗死患者血管性血友病因子和超敏C反应蛋白的影响

目的:研究川芎嗪注射液对急性脑梗死患者血管性血友病因子(vWF)及超敏C反应蛋白(hs-CRP)的影响并探讨其作用机制。方法:120例急性脑梗死患者随机分成两组,对照组:川芎嗪注射液10 mL,1次/天,连续14天,静脉滴注);治疗组:银杏达莫20 mL,1次/天,连续14天,静脉滴注。检测治疗前和治疗后第14天患者血浆vWF及血清hs-CRP浓度的变化,测定治疗前、治疗第30天的NIHSS评分,判定两组的疗效。结果:在治疗第14天,川芎嗪注射液组的vWF浓度明显低于对照组(P<0.01)。治疗第14天时,与对照组相比,川芎嗪注射液组hs-CRP浓度下降明显(P<0.01)。川芎嗪注射液组治疗的有效率及显效率明显高于对照组(P<0.05)。结论川芎嗪注射液能够直接降低血清vWF和hs-CRP的浓度,这可能是其治疗脑梗死的机制之一。     

脑梗死部分诱发因素的研讨

目的研讨脑梗死的发病危险因素。方法对研究组(脑梗死组)、健康对照组人群分别测定血压、血糖、血脂等指标,并通过t检验,与病例研究方法进行2组间各指标的比较。结果血脂、心电、血压、血糖、2组间比较有显著差异,均是P<0.01。其相对危险度OR,低HDL血症(22.91)>心电异常(12.51)>高血压(3.39)>高LDL血症(2.74)>高血糖(2.39)。且低HDL血症(男19.10,女4.73)、高血压(男2.71,女1.74),患者患脑梗死的危险性,不同性别间差异显著。结论血脂紊乱、心脏病、高血压、糖尿病是脑梗死的主要危险因素。     

Neuroprotective Properties of Picroside II in a Rat Model of Focal Cerebral Ischemia

The aim of this study was to explore the effect of picroside II on neuronal apoptosis and the expression of caspase-3 and poly ADP-ribose polymerase (PARP) following middle cerebral artery occlusion/reperfusion in male Wistar rats. Picroside II (10 mg/kg) was administered intravenously into the tail vein of the animals. The neurological function deficits were evaluated with the Bederson's test and the cerebral infarction volume was visualized with tetrazolium chloride (TTC) staining. The apoptotic cells were counted by in situ terminal deoxynucleotidyl transferase-mediated biotinylated deoxyuridine triphosphate nick end labeling (TUNEL) assay. The immunohistochemistry stain and enzyme linked immunosorbent assay (ELISA) was used to determine the expressions of caspase-3 and PARP in brain tissue. The results indicated that rats in the control group showed neurological function deficit and cerebral infarction in ischemic hemisphere after two hours ischemia followed by 22 hours reperfusion. Caspase-3 and PARP expressions were also profound in the cortex, the striatum and the hippocampus, along with increased apoptotic cells in this group. Bederson's score, infarction volume, and expressions of caspase-3 and PARP, as well as apoptosis in the treatment group were, however, significantly decreased compared to those in the control group indicating that intravenous treatment with picroside II might be beneficial to inhibit neuronal apoptosis and, thus, to improve the neurological function of rats upon cerebral ischemia reperfusion injury.     

急性脑卒中与便秘57例分析

目的探讨急性脑卒中与便秘的关系。方法57例脑卒中患者分成动脉粥样硬化血栓性脑梗死(ATI)组23例;腔隙性梗死(LI)组23例;脑出血(ICH)组11例,观察各组便秘发生率并进行比较。结果脑卒中者第1周便秘发生率50.88%,显著高于正常老年人对照组(P<0.05)。基底节区脑卒中者便秘发生率57.1%,明显高于非基底节卒中者(P<0.05)。结论脑卒中患者急性期常发生便秘,基底节区脑卒中者便秘发生率较非基底节区脑卒中者高。     

西医结合中医治疗急性脑梗死临床研究

目的观察中西医结合治疗急性脑梗死的临床疗效。方法233例急性脑梗死患者随机分为两组,对照组116例采用中医辨证治疗,治疗组117例在此基础上结合西医治疗。采用神经功能缺损评分量表(CSS)进行疗效评价。结果以90d为试验终点时间。治疗组总有效率74.11%(83/112例),优于对照组的60.36%(67/111例)。经统计学处理差异均有显著性,治疗组优于对照组(P<0.05)。结论中医辨证结合西医治疗急性脑梗死有较为明显的疗效优势。     

低分子肝素和阿司匹林治疗急性脑梗死的疗效分析

目的探讨低分子肝素和阿司匹林对急性脑梗死的疗效。方法随机将358例发病48h内入院的急性脑梗死患者分为3组,分别给予低分子肝素、阿司匹林和低分子肝素与阿司匹林两者联合进行治疗。治疗30d按照脑卒中患者临床神经功能缺损程度评分标准评价疗效,最后统计3组的治疗总有效率。结果 3组的总有效率分别为60.8%、38.3%和66.1%。低分子肝素治疗组效果明显优于阿司匹林治疗组(P<0.01),与联合治疗组疗效相当(P>0.05),但不良反应少于联合治疗组。结论低分子肝素皮下注射作为对超过溶栓治疗时间窗的急性脑梗死患者的另一治疗手段,安全有效。     

Hemodynamics and Tissue Optical Properties in Bimodal Infarctions Induced by Middle Cerebral Artery Occlusion

Various infarct sizes induced by middle cerebral artery occlusion (MCAO) generate inconsistent outcomes for stroke preclinical study. Monitoring cerebral hemodynamics may help to verify the outcome of MCAO. The aim of this study was to investigate the changes in brain tissue optical properties by frequency-domain near-infrared spectroscopy (FD-NIRS), and establish the relationship between cerebral hemodynamics and infarct variation in MCAO model. The rats were undergone transient MCAO using intraluminal filament. The optical properties and hemodynamics were measured by placing the FD-NIRS probes on the scalp of the head before, during, and at various time-courses after MCAO. Bimodal infarction severities were observed after the same 90-min MCAO condition. Significant decreases in concentrations of oxygenated hemoglobin ([HbO]) and total hemoglobin ([HbT]), tissue oxygenation saturation (StO₂), absorption coefficient (μa) at 830 nm, and reduced scattering coefficient (μs’) at both 690 and 830 nm were detected during the occlusion in the severe infarction but not the mild one. Of note, the significant increases in [HbO], [HbT], StO₂, and μa at both 690 and 830 nm were found on day 3; and increases in μs’ at both 690 and 830 nm were found on day 2 and day 3 after MCAO, respectively. The interhemispheric correlation coefficient (IHCC) was computed from low-frequency hemodynamic oscillation of both hemispheres. Lower IHCCs standing for interhemispheric desynchronizations were found in both mild and severe infarction during occlusion, and only in severe infarction after reperfusion. Our finding supports that sequential FD-NIRS parameters may associated with the severity of the infarction in MCAO model, and the consequent pathologies such as vascular dysfunction and brain edema. Further study is required to validate the potential use of FD-NIRS as a monitor for MCAO verification.     

2-Decenoic Acid Ethyl Ester, a Compound That Elicits Neurotrophin-like Intracellular Signals, Facilitating Functional Recovery from Cerebral Infarction in Mice

In our previous study, we found that trans-2-decenoic acid ethyl ester (DAEE), a derivative of a medium-chain fatty acid, elicits neurotrophin-like signals including the activation of extracellular signal-regulated kinases 1 and 2 (ERK1/2) in cultured mouse cortical neurons. Here, we examined the efficacy of intraperitoneal administration of DAEE on the treatment of a mouse model of the cerebral infarction caused by unilateral permanent middle cerebral artery occlusion (PMCAO). DAEE-treatment (100 μg/kg body weight injected at 0.5, 24, 48, 72 h after PMCAO) significantly restored the mice from PMCAO-induced neurological deficits including motor paralysis when evaluated 48, 72, and 96 h after the PMCAO. Furthermore, DAEE facilitated the phosphorylation of ERK1/2 on the infarction side of the brain when analyzed by Western immunoblot analysis, and it enhanced the number of phosphorylated ERK1/2-positive cells in the border areas between the infarction and non-infarction regions of the cerebral cortex, as estimated immunohistochemically. As the infarct volume remained unchanged after DAEE-treatment, it is more likely that DAEE improved the neurological condition through enhanced neuronal functions of the remaining neurons in the damaged areas rather than by maintaining neuronal survival. These results suggest that DAEE has a neuro-protective effect on cerebral infarction.