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1.
目的 观察尤瑞克林治疗短暂性缺血发作(TIA)的临床疗效.方法 选择50例TIA患者,随机分为对照组(n=24) 与治疗组(n=26),对照组给予常规治疗,治疗组则在常规治疗的基础上加用尤瑞克林,观察两组用药后TIA发作情况、病情进展情况以及安全性.结果 两组临床疗效比较,差异有显著统计学意义(P<0.05);治疗组较对照组的有效率明显提高(分别为96.2%和75.0%, P<0.05).结论 尤瑞克林治疗TIA疗效确切.  相似文献   

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目的观察尤瑞克林联合依达拉奉治疗进展性脑梗死的临床疗效。方法进展性脑梗死85例随机分为尤瑞克林联合依达拉奉治疗组(n=45例)和对照组(n=40例),2组均给予抗凝、抗血小板、活血化瘀、神经康复等治疗。治疗组同时给予0.9%生理盐水100mL+0.15PNAU尤瑞克林静滴,1次/d,连用7~14d,给予依达拉奉针30mg+糖水或盐水100mL静滴,2次/d,连用2周,于治疗前后评定神经功能缺损程度(NIHSS)、日常生活活动能力(ADL)和临床疗效。结果治疗后2组患者的神经功能缺损、日常生活活动能力均有改善,与对照组相比差异有统计学意义(P<0.01)。治疗组临床有效率91.11%,近期治愈率55.55%,显著高于对照组(P<0.01),且无明显不良反应。结论尤瑞克林联合依达拉奉治疗进展性脑梗死疗效较好,且无明显不良反应,值得进一步观察探讨。  相似文献   

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尤瑞克林治疗急性脑梗死临床疗效观察   总被引:1,自引:1,他引:0  
目的探讨尤瑞克林治疗急性脑梗死的临床疗效。方法将62例急性脑梗死患者随机分为对照组和尤瑞克林治疗组,两组均给予抗血小板聚集、控制血压等常规治疗,治疗组加用尤瑞克林治疗,共静脉滴注14d,观察两组患者治疗前及治疗后14d神经功能缺损程度、临床疗效及生化指标变化。结果治疗组患者神经功能恢复明显优于对照组,两组治疗后神经功能评分比较,差异有统计学意义(P=0.025),两组临床疗效差异有统计学意义(P=0.021),治疗组治疗前后实验室指标无明显变化(P0.05)。结论尤瑞克林能有效治疗急性脑梗死。  相似文献   

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目的探讨依达拉奉联合尤瑞克林治疗急性脑梗死的临床疗效。方法在嵩县人民医院神经内科2014-07—2016?10诊治的急性脑梗死患者中抽取72例为研究对象,随机分为2组,治疗组(n=36)采取依达拉奉联合尤瑞克林治疗,对照组(n=36)应用常规综合治疗,对比2组临床疗效、神经功能变化。结果治疗组总有效率94.4%,高于对照组的77.8%(P0.05);治疗前,2组NIHSS评分对比差异无统计学意义(P0.05);治疗后,治疗组NIHSS评分明显低于对照组(P0.01);治疗组生活质量评分(90.1±1.4)分,高于对照组的(76.3±4.7)分,差异有统计学意义(P0.01)。结论依达拉奉联合尤瑞克林治疗急性脑梗死的临床疗效确切,可有效改善其神经功能。  相似文献   

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尤瑞克林在急性脑梗死治疗中的应用   总被引:3,自引:0,他引:3  
目的 评价尤瑞克林治疗急性脑梗死的临床疗效和安全性.方法 126例急性脑梗死患者随机分为治疗组(n=68)和对照组(n=58),在对症治疗的基础上,对照组给予脑复康,治疗组给予尤瑞克林,两组疗程均为14 d.评定患者治疗前后神经功能缺损程度(NIHSS)及残障水平(mRS),监测用药期间血压变化,并随访90 dmRS.结果 治疗后,两组患者NIHSS和mRS评分均降低(全部P<0.01),治疗组NIHSS、mRS以及总有效率均优于对照组(全部P<0.05);治疗组90 d mRS与治疗结束相比显著降低,与对照组90 d mRS相比也显著降低(全部P<0.01);血压无明显波动(P>0.05).结论 尤瑞克林能够安全有效地治疗急性脑梗死,改善患者的远期预后.  相似文献   

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目的观察尤瑞克林改善前循环急性脑梗死患者侧支循环的效果。方法采用抽签法将确诊91例急性前循环脑梗死患者进行分组,对照组给予抗血小板和脑保护等神经内科常规治疗,观察组在此基础上静滴尤瑞克注射液,连续治疗14d后观察神经功能改善情况、综合疗效和后侧支循环开放率。结果治疗14d末2组NIHSS评分均降低,观察组降低幅度明显高于对照组,差异有统计学意义(P0.05);观察组总有效率91.30%,明显高于对照组的75.56%,差异有统计学意义(P0.05);观察组软脑膜侧支循环开放率71.74%(33/46),明显高于对照组的51.11%(23/45),差异有统计学意义(P0.05)。结论尤瑞克林改善前循环急性脑梗死患者侧支循环的效果确切,能够有效提高侧支循环开放率和改善预后,在提高患者生活质量方面具有重要意义。  相似文献   

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尤瑞克林治疗急性脑梗死的临床疗效观察   总被引:3,自引:0,他引:3  
目的观察尤瑞克林治疗急性脑梗死患者的临床疗效。方法采用尤瑞克林静脉滴注治疗急性脑梗死100例,用脑卒中评分(NIHSS)量表评定临床神经功能缺损,临床总有效率等指标,分析其与同期未应用尤瑞克林治疗的对照组之间临床疗效的差异。同时分析尤瑞克林治疗不同年龄段患者疗效的区别。在发病3个月时,随访Barthel指数(BI)分值,以了解尤瑞克林治疗缺血性卒中对恢复期疗效的影响。结果缺血性卒中患者尤瑞克林治疗后患者临床症状、NIH评分改善(P0.05),临床有效率更高(P0.05)。对于≥65岁患者,尤瑞克林治疗后可改善患者NIH评分,但总有效率的改善无统计学差异(P0.05)。在发病3个月时,电话随访Barthel指数分值,尤瑞克林组和对照组无统计学差别。结论尤瑞克林治疗急性期脑梗死安全,有效。  相似文献   

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尤瑞克林联合依达拉奉治疗急性后循环脑梗死疗效观察   总被引:1,自引:0,他引:1  
目的观察尤瑞克林联合依达拉奉注射液治疗急性后循环脑梗死的疗效。方法将95例急性后循环脑梗死患者随机分为治疗组(尤瑞克林联合依达拉奉)45例和对照组(单用依达拉奉)40例,分别于入院时和治疗后14 d、28 d进行临床神经功能缺损程度(NIHSS)评分,治疗后90 d进行Barthel指数评分;分别在治疗前后测血液流变学并行经颅多普勒(TCD)检查。结果 2组治疗后14 d及28 d神经功能缺损评分均有明显改善,但治疗组与对照组的NIHSS、Barthel指数、血液流变学、TCD变化等比较差异均有统计学意义(P<0.05或P<0.01)。结论尤瑞克林联合依达拉奉可增加急性后循环脑梗死患者的脑血流,改善微循环,并有助于急性后循环脑梗死患者的神经功能恢复。  相似文献   

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目的观察重组组织型纤溶酶原激活剂(rt-PA)联合丁苯肽或尤瑞克林治疗急性脑梗死的疗效和安全性,对比丁苯肽与尤瑞克林治疗急性脑梗死的疗效。方法 75例符合溶栓条件的急性脑梗死患者随机分为对照组(予rt-PA治疗)和丁苯肽组(予rt-PA联合丁苯肽治疗)及尤瑞克林组(予rt-PA联合尤瑞克林治疗)各25例,于治疗前及治疗后7d、14d、1个月采用NIHSS评分进行疗效评定。结果 3组治疗后NIHSS评分均较治疗前降低(P0.01),治疗后14d、1个月丁苯肽组及尤瑞克林组的NIHSS评分较对照组低(P0.05);丁苯肽组及尤瑞克林组NIHSS评分治疗后比较差异无统计学意义(P0.05)。结论rt-PA联合丁苯肽或尤瑞克林较单用rt-PA能更显著改善急性脑梗死患者神经功能缺损症状,丁苯肽与尤瑞克林在改善脑梗死患者神经功能缺损症状方面疗效相当。  相似文献   

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目的观察丁苯酞软胶囊联合尤瑞克林治疗急性脑梗死的疗效。方法选取我院收治的急性脑梗死患者80例为研究对象,根据随机数表法分为对照组和观察组各40例,对照组静滴尤瑞克林,观察组在此基础上口服丁苯酞软胶囊,观察2组治疗效果。结果观察组总有效率(90.0%)明显高于对照组(67.5%),有显著性差异(P0.05);2组治疗前血浆各项血管内皮功能指标无明显差异(P0.05),治疗后观察组血浆内皮素-1、血浆一氧化氮水平明显优于对照组(P0.05);2组治疗前ADL评分与神经功能评分无明显差异(P0.05),治疗后观察组均明显优于对照组(P0.05);2组不良反应率比较差异无统计学意义(P0.05)。结论丁苯酞软胶囊联合尤瑞克林治疗急性脑梗死的临床疗效确切,可有效改善患者预后,不良反应少,值得临床推广。  相似文献   

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Fine structural characteristics of synapses in the spiral organ of Corti were examined, with reference to differences between inner and outer haircell systems, and to location of neurons of origin of efferent axons. Surgical interruption of crossed olivocochlear bundle, of vestibular nerve, of facial nerve, and excision of superior cervical ganglia were used to determine the pathways of efferent axons. Interruption of the vestibular nerve near the brainstem results in degeneration of all efferent terminals on outer hair cells. Mid-line lesions at, and caudal to, the facial colliculus result in degeneration of about half of these efferent terminals. Efferent synaptic bulbs to the inner hair-cell system are small, of the order of one micron, and form type 2 junctions with afferent dendrites. They tend to have more large dense-core vesicles (about 80 nm) than the large efferent terminals of the outer hair-cell system, and appear to be the terminals of axons in the habenula perforata, which exhibit varicosities laden with large dense core vesicles. The varicosities are unaffected by excision of the superior cervical ganglia. So far as our material can reveal, it appears that the varicosities in the habenula perforata do not survive vestibular root interruption, nor do the efferent processes in the internal spiral bundle or at the base of inner hair cells. Most interestingly, the afferent processes of the inner hair-cell system, as identified for example by their relation to pre-synaptic bodies in the inner hair cells, are subject to a trans-synaptic reaction after severance of the vestibular root. They undergo a dramatic cytological transformation, characterized by increase of volume, engorgement with microtubules, microfilaments, microvesicles of various sizes, and clusters of lysosomes. Thus, both the efferent and afferent terminals of the inner hair-cell system show marked cytological differences from the corresponding terminals of the outer hair cell system.  相似文献   

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Tubocurarine (Tc) effect on membrane currents elicited by acetylcholine (ACh) was studied in isolated superior cervical ganglion neurons of rat using patch-clamp method in the whole-cell recording mode. The "use-dependent" block of ACh current by Tc was revealed in the experiments with ACh applications, indicating that Tc blocked the channels opened by ACh. Mean lifetime of Tc-open channel complex, tau, was found to be 9.8 +/- 0.5 s (n = 7) at -50 mV and 20-24 degrees C. tau exponentially increased with membrane hyperpolarization (e-fold change in tau corresponded to the membrane potential shift by 61 mV). Inhibition of the ACh-induced current by Tc (3-30 microM/1) was completely abolished by membrane depolarization to the level of 80-100 mV. Inhibition of ACh-induced current was augmented at increased ACh doses. It is concluded that the open channel block produced by Tc is likely to be the only mechanism for Tc action on nicotinic acetylcholine receptors in superior cervical ganglion neurons of rat.  相似文献   

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Background Dementia occurs in the majority of patients with Parkinson’s disease (PD). Late onset of PD has been reported to be associated with a higher risk for dementia. However, age at onset (AAO) and age at baseline assessment are often correlated. The aim of this study was to explore whether AAO of PD symptoms is a risk factor for dementia independent of the general effect of age. Methods Two community-based studies of PD in New York (n = 281) and Rogaland county, Norway (n = 227) and two population-based groups of healthy elderly from New York (n = 180) and Odense, Denmark (n = 2414) were followed prospectively for 3–4 years and assessed for dementia according to DSM-IIIR. All PD and control cases underwent neurological examination and were followed with neurological and neuropsychological assessments. We used Cox proportional hazards regression based on three different time scales to explore the effect of AAO of PD on risk of dementia, adjusting for age at baseline and other demographic and clinical variables. Findings In both PD groups and in the pooled analyses, there was a significant effect of age at baseline assessment on the time to develop dementia, but there was no effect of AAO independent of age itself. Consistent with these results, there was no increased relative effect of age on the time to develop dementia in PD cases compared with controls. Interpretation This study shows that it is the general effect of age, rather than AAO that is associated with incident dementia in subjects with PD. Received in revised form: 22 December 2005  相似文献   

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After a hopeful beginning, the social process of the reintegration of those with severe mental illness has come to a standstill. I am led to wonder whether "the community" really wants to live together with people suffering from severe mental illness, and if so, how closely? As long as the medical treatment of mental illness provided by the general practitioners is fundamentally deficient, as they are not able to prescribe the necessary interventions--such as out-patient psychiatric nursing, and service providers in the out-patient sector are content with offering increasingly intensive forms of care for the less seriously ill at the cost of the Social Welfare System--the reintegration of those with serious mental illness remains an illusion--which is mainly to the benefit of providers of residential care in homes and hostels.  相似文献   

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