舒血宁注射液对缺血性脑卒中患者神经功能及血液流变学的影响

缺血性脑卒中发作时,脑组织由于长时间缺血缺氧而处于无氧代谢状态,进而导致能量衰竭和酸中毒,引起脑组织和神经功能损伤.因此,对缺血性脑卒中患者除采取溶栓治疗改善脑部供血供氧外,对其神经功能修复也至为重要.此文主要观察舒血宁注射液(博安兄弟制药有限公司生产,其主要成分为银杏内酯A、总黄酮醇苷,每5 mL中含17.5 mg有效成分)对缺血性脑卒中患者的疗效、神经功能改善及血液流变学的作用,期望为临床治疗缺血性脑卒中积累经验.     

高压氧对新生儿缺氧缺血性脑病血液流变学的影响

目的探讨高压氧对新生儿缺氧缺血性脑病血液流变学的影响。方法选取我院2015-06—2016-04诊治的缺氧缺血性脑病新生儿62例为研究对象,随机抽签分组,对照组(n=31)应用常规综合性治疗,治疗组(n=31)在常规综合性治疗基础上加用高压氧治疗,对比2组治疗效果、住院时间及治疗前后的血液流变学指标变化。结果治疗前,2组血浆黏度、红细胞比积、全血黏度、血小板聚集指数组对比差异均无统计学意义(均P0.05);治疗后治疗组均明显低于对照组(均P0.01)。治疗组总有效率96.8%,高于对照组的64.5%(P0.01)。治疗组住院时间(14.9±3.6)d,低于对照组的(22.6±4.4)d(P0.01)。结论高压氧可明显改善新生儿的血液流变学指标,并消除其临床症状,缩短住院时间,疗效肯定,可作为新生儿缺氧缺血性脑病的理想治疗手段。     

神经节苷脂钠对重症缺血性脑卒中患者血液流变学及预后的影响

目的评价神经节苷脂钠注射液对重症缺血性脑卒中患者血液流变学及预后的影响。方法选取我院收治的90例重症缺血性脑卒中患者为研究对象,按照随机平行分组法随机分为治疗组与对照组各45例,2组均给予常规降压、降脂、溶栓、抗凝等治疗,治疗组在此基础上加用神经节苷脂钠注射液100mg+生理盐水250mL静滴,1次/d。疗程8周。比较2组治疗前后血液流变学及神经功能变化。结果治疗组全血比黏度、血浆比黏度、血小板聚集率及纤维蛋白原改善程度均明显优于对照组(P0.05),治疗组愈显率明显高于对照组(P0.05)。结论神经节苷脂钠注射液可有效改善重症缺血性脑卒中患者血液流变学及神经功能预后。     

动脉粥样硬化性缺血性脑卒中血液流变学及相关危险因素

目的 探讨动脉粥样硬化性缺血性脑卒中的血液流变学变化.方法 采用中勤世帝R80-A锥板式全自动血液流变分析仪,对90例动脉粥样硬化性缺血性脑卒中患者和80例健康体检对照者进行血液流变学指标进行测定.结果 缺血性脑组卒中患者的全血高、中、低切黏度、血浆黏度、红细胞比积、红细胞聚集指数、红细胞变形指数、纤维蛋白原均高于正常对照组,2组进行比较差别有统计学意义(P＜0.01).结论 动脉粥样硬化性缺血性脑卒中患者的血液流变学指标有明显改变,改善血液的粘稠度,预防危险因素,可有效降低脑卒中的发生.     

纤溶酶对急性缺血性脑卒中患者血液流变学的影响

目的 观察纤溶酶对急性缺血性脑卒中患者血液流变学的影响.方法 本试验采用前瞻性开放性病例对照研究,将121 例急性缺血性脑卒中患者随机分为治疗组和对照组,对照组(50 例) 采用常规治疗,治疗组(71 例)在常规治疗的基础上加用纤溶酶(200IU 1次/d) 静滴,于治疗前及治疗10 d 后评定患者神经功能缺损程度,检测血液流变学指标.结果 常规治疗与纤溶酶治疗均对神经功能缺失有一定改善,治疗组有效率87.32%,对照组72.0%,2 组疗效差异有统计学意义(P<0.05) .常规组与纤溶酶组对血液流变学各项指标均有改善,纤溶酶组更加显著.结论 纤溶酶有改善急性缺血性脑卒中患者血液流变学指标的作用,同时又对促进急性缺血性脑卒中患者神经功能的恢复具有良好作用.     

尤瑞克林对进展性脑梗死患者血液流变学及神经功能恢复的影响

目的探讨尤瑞克林治疗进展性脑梗死的临床疗效及对脑血液流变学和神经功能恢复的影响。方法选取经颅脑CT或MRI确诊的进展性脑梗死患者110例,随机分为观察组和对照组。对照组给予常规治疗,观察组在常规治疗基础上加尤瑞克林静滴治疗。均连续治疗2周,观察临床疗效,NIHSS评分及检测血浆黏度、全血高切/低切黏度、纤维蛋白原及红细胞压积等变化。结果观察组临床疗效显著优于对照组(P0.05);治疗后,2组NIHSS评分显著降低,且观察组NIHSS评分降低幅度显著大于对照组(P0.05);治疗后,血浆黏度、全血高切/低切黏度、纤维蛋白原及红细胞压积水平均显著降低,且观察组各项水平降低幅度显著大于对照组(P0.05)。结论尤瑞克林治疗进展性脑梗死患者能改善脑血液流变学指标,恢复神经功能,具有较好疗效。     

脑卒中后抑郁对神经功能恢复的影响

目的通过比较脑卒中病人出院时的治疗效果,评价脑卒中后抑郁对病人神经功能恢复的影响。方法根据焦虑/抑郁情绪测定量表测定得分将211例脑卒中病人分成抑郁组及非抑郁组,比较2组病人的治疗效果并评价其神经功能恢复情况。结果本组211例脑梗死病人发生抑郁症状59例（59/211）,发生率27.96%。出院时疗效对比：抑郁组治愈9例（15.3%）,非抑郁组50例（32.9%）;抑郁组好转32例（54.2%）,非抑郁组73例（48.0%）;抑郁组未愈18例（30.5%）,非抑郁组29例（19.1%）。2组总有效率分别为69.5%、80.9%,差异具有统计学意义（P〈0.05）,结果显示抑郁组神经功能恢复程度显著差于非抑郁组。结论脑卒中后发生抑郁将严重影响脑卒中病人神经功能的恢复进程,临床医生需给予足够重视。     

灯盏花素对急性缺血性脑卒中患者血清hs-CRP及神经功能恢复的影响

目的探讨灯盏花素对急性缺血性脑卒中患者临床疗效、神经功能恢复和血清高敏C反应蛋白(hs-CRP)的影响及安全性。方法 83例AIS患者随机分对照组40例和试验组43例,对照组给予常规降血压、抗血小板、降血脂、控制血糖等治疗;试验组在对照组的基础上加用盏花素注射液40mL+0.9%NS 250mL ivggt 2周,后改口服灯盏花素片40mg tid,连用6周。治疗2个月后采用卒中量表(NIHSS)及致残量表(mRS)比较2组治疗前后神经功能恢复情况及不良反应。同时比较2组治疗前后血清hs-CRP变化。结果治疗2个月后2组患者NIHSS评分及血清hs-CRP较入组时均明显下降(P0.05),且试验组下降更为显著(P0.05);试验组和对照组总有效率为分别为45.0%和23.3%,试验组显著高于对照组(P0.05)。结论灯盏花素可显著改善AIS患者神经功能,降低全身炎症反应和致残率。     

休闲娱乐康复对脑卒中患者抑郁及神经功能康复的影响

目的探讨休闲娱乐康复对脑卒中患者抑郁及神经功能康复的影响。方法将60例缺血性脑卒中抑郁患者随机分为康复组和对照组各30例。两组均按康复科常规进行药物治疗和运动治疗、作业治疗及理疗等，康复组另给予休闲娱乐康复治疗。两组患者治疗前后分别采用改丁堡-斯堪的那维亚评分标准（MESSS）评定其神经功能缺陷程度，采用汉密尔顿抑郁量表（HAMI））进行程度评分，采用Fug—Meyer评分（FMA）及Barthel指数（BI）评定其步行、平衡能力及ADI。水平。结果两组分别经3个月的治疗后，其MESSS、HAMD、FMA及BI评分等均较治疗前有明显改善；治疗后两组间比较，康复组各项指标改善程度均明显优于对照组，差异均有统计学意义（P〈0．05）。结论休闲娱乐康复不仅有助于改善脑卒中后抑郁，而且有利于患者神经功能的康复，提高其日常生活能力。     

氢溴酸西酞普兰对缺血性脑卒中后抑郁患者的情绪、认知功能和神经功能的影响

目的 探讨氢溴酸西酞普兰联合奥扎格雷钠对缺血性脑卒中后抑郁患者的情绪、认知功能和神经功能的影响.方法 选取我科2017年7月～2019年7月期间收治的119例缺血性脑卒中后抑郁患者作为研究对象,采用随机数字表法分为2组,均给予奥扎格雷钠作为基础治疗,对照组59例增加氟西汀治疗,观察组60例增加氢溴酸西酞普兰治疗,16周...     

神经血管单元在脑缺血治疗中的作用和意义

脑卒中是当前威胁人类健康的三大主要疾病之一,具有高发病、高病残及高病死的特点,其中缺血性卒中发生率占60%～80%。世界卫生组织(WHO)调查结果显示,中国缺血和(或)出血性卒中发病率居世界首位,约高于美国1倍。全国第3次死因回顾抽样调查资料表明,目前脑卒中已上升为中国的首位死因。近20年的流行病学研究结果显示,脑卒中病死率逾150万例/年,并呈逐年增长趋势,严重威胁着国民的生命和健康生活质量,长期     

Emerging strategies for nerve repair and regeneration in ischemic stroke: neural stem cell therapy

Ischemic stroke is a major cause of mortality and disability worldwide, with limited treatment options available in clinical practice. The emergence of stem cell therapy has provided new hope to the field of stroke treatment via the restoration of brain neuron function. Exogenous neural stem cells are beneficial not only in cell replacement but also through the bystander effect. Neural stem cells regulate multiple physiological responses, including nerve repair, endogenous regeneration, immune f...     

The stroke prognosis instrument II (SPI-II) : A clinical prediction instrument for patients with transient ischemia and nondisabling ischemic stroke

BACKGROUND AND PURPOSE: In 1991 we developed the Stroke Prognosis Instrument (SPI-I) to stratify patients with transient ischemic attack or ischemic stroke by prognosis for stroke or death in 2 years. In this article we validate and improve SPI-I (creating SPI-II). METHODS: To validate SPI-I, we applied it to 4 test cohorts and calculated pooled outcome rates. To create SPI-II, we incorporated new predictive variables identified in 1 of the test cohorts and validated it in the other 3 cohorts. RESULTS: For SPI-I, pooled rates (all 4 test cohorts) of stroke or death within 2 years in risk groups I, II, and III were 9%, 17%, and 24%, respectively (P<0.01, log-rank test). SPI-II was created by adding congestive heart failure and prior stroke to SPI-I. Each patient's risk group was determined by the total score for 7 factors: congestive heart failure (3 points); diabetes (3 points); prior stroke (3 points); age >70 years (2 points); stroke for the index event (not transient ischemic attack) (2 points); hypertension (1 point); and coronary artery disease (1 point). Risk groups I, II, and III comprised patients with 0 to 3, 4 to 7, and 8 to 15 points, respectively. For SPI-I, pooled rates (3 cohorts excluding the SPI-II development cohort) of stroke or death within 2 years in risk groups I, II, and III were 9%, 17%, and 23%, respectively. For SPI-II, pooled rates were 10%, 19%, and 31%, respectively. In receiver operator characteristic analysis, the area under the curve was 0.59 (95% CI, 0.57 to 0.60) for SPI-I and 0.63 (95% CI, 0.62 to 0.65) for SPI-II, confirming the better performance of the latter. CONCLUSIONS: Compared with SPI-I, SPI-II achieves greater discrimination in outcome rates among risk groups. SPI-II is ready for use in research design and may have a role in patient counseling.     

操作性肌电反馈联合常规康复治疗对脑梗死患者血清BDNF表达及运动功能的影响

目的 观察操作性肌电反馈联合常规康复治疗对脑梗死患者血清中脑源性神经营养因子(BDNF)表达及肢体运动功能的影响.方法 将73例脑梗死患者随机分为治疗组(n=38)和对照组(n=35),两组常规的药物治疗及康复治疗相同,治疗组在常规治疗基础上辅以操作性肌电生物反馈治疗,共8周.分别于治疗前、治疗8周后检测患者血中BDNF水平,采用美国国立卫生研究院卒中量表(NIHSS)和简化Fugl-Meyer运动功能评分(FMA)分别评估神经功能缺损程度及肢体运动功能水平.结果 两组患者治疗后NIHSS评分均低于治疗前,血中BDNF表达及FMA评分均较治疗前增加(均P<0.01),但治疗组的改善优于对照组(P<0.05).治疗组患者治疗前后的NIHSS评分变化值和FMA评分变化值与血中BDNF水平变化均呈正相关(r=0.405,0.672;P<0.05).结论 操作性肌电生物反馈疗法联合常规康复治疗可上调脑梗死患者BDNF表达,促进其功能康复.     

A comparison of three platelet function tests in ischemic stroke patients with antiplatelet therapy

Predicting the effectiveness of antiplatelet drugs is critical to precision antiplatelet therapy. However, there is a lack of an acceptable method, although there are a variety of methods for detecting platelet function. In this study, we compared three major platelet function tests to assess their performance and found better methods for platelet function evaluation after aspirin or clopidogrel treatment in ischemic stroke patients by comparative study. A total of 249 ischemic stroke patients were enrolled who were treated with aspirin or clopidogrel or both. Three platelet function tests including light transmittance aggregometry (LTA), thromboelastography (TEG), platelet function analyzer (PFA) were performed as well as CYP2C19 genotype determination. Correlation analyses and kappa statistics were used. All three methods were effective in evaluating aspirin function. However, only LTA and TEG had good correlation and consistency (r = -0.37, kappa = 0.634). TEG-ADP was the least sensitive for clopidogrel, as the platelet inhibition ratio did not differ between the clopidogrel-user group and the control (P = 0.074), while LTA and PFA were sensitive (P ＜ 0.001). Correlations between platelet assays were poor for clopidogrel (the absolute value of r range from 0.13 to 0.35) and so was the agreement (Kappa from 0.232 to 0.314). LTA and PFA have a good correlation with CYP2C19 genotyping (P = 0.034 and 0.014). In conclusion, all three tests were able to evaluate aspirin effect, LTA-AA and TEG-AA had a good correlation. TEG perform badly for clopidogrel effect detection. The fair-to-modest agreement among assays indicated further study was indispensable.     

Neuroprotective therapy for the treatment of acute ischemic stroke]

Following cerebral ischemia, various biochemical reactions are provoked in a stepwise manner leading neuronal cells to ischemic death. The prevention of these biochemical reactions may exert neuroprotective actions and consequently reduce the magnitude of ischemic cerebral injury. On the basis of such a view, numerous neuroprotective drugs have been developed during the last decade. Quite a few drugs were found effective in reducing the infarct volume in experimental studies, and more than 15 of them were subjected to clinical phase III trials to see a therapeutic effectiveness. However, the results of phase III trials were disappointing in the majority drugs. Only three drugs, nicaravene, ebselen and edaravone, all radical scavengers, were judged effective by small-sized trials with a wide therapeutic window, 48-72 hours after stroke, in Japan. The fact suggests that a one-point prevention of biochemical reactions by single drug is unable to rescue ischemic neuronal cells. Ischemic insult causes damages of vascular wall including the endothelium which play an important role in the development of hemorrhagic changes or cerebral edema. Vascular protection is considered as important as neuroprotection in treatment of clinical stroke. Mild hypothermia has neuroprotective and vascular protective actions and hence may be more effective than neuroprotective drugs for the treatment of stroke. The prevention of fever, which often occurs in severe stroke, may exert the similar effect as hypothermia in neuroprotection. Neuroprotective therapy in the future should proceed toward the simultaneous protections of neurons and vessels using combination of multiple drugs.     

Immunomodulators and microRNAs as neurorestorative therapy for ischemic stroke

Most of all strokes are ischemic due to occlusion of a vessel, and comprise two main types, thrombotic and embolic. Inflammation and immune response play an important role in the outcome of ischemic stroke. Pharmaceutical and cell-based therapies with immunomodulatory properties could be of benefit in treating ischemic stroke. Possible changes in microRNAs brought about by immunomodulatory treatments may be important. The pharmaceutical studies described in this review have identified several differentially regulat-ed miRNAs associated with disregulation of mRNA targets or the upregulation of several neuroprotective genes, thereby highlighting the potential neuroprotective roles of specific miRNAs such as miR-762, -1892,-200a, -145. MiR-124, -711, -145 are the strongly associated miRNAs predicted to mediate anti-inflamma-tory pathways and microglia/macrophage M2-like activation phenotype. The cell-based therapy studies reviewed have mainly utilized mesenchymal stem cells or human umbilical cord blood cells and shown to improve functional and neurological outcomes in stroke animals. MiR-145 and miR-133b were implicated in nerve cell remodeling and functional recovery after stroke. Human umbilical cord blood cells decreased proinflammatory factors and promoted M2 macrophage polarization in stroke diabetic animals.