自由基清除剂联合巴曲酶治疗椎基底动脉系统进展型卒中

目的 评价新型自由基清除剂依达拉奉联合巴曲酶治疗椎基底动脉系统进展型卒中的有效性和安全性.方法 选择发病72h内的椎基底动脉系统进展型卒中患者76例,随机分为联合组和巴曲酶组,2组均采用巴曲酶注射液(10BU、5BU、5BU)静滴,隔日1次,共3次.联合组加用依达拉奉注射液30mg静滴,2次/d,共14d;巴曲酶组用等量生理盐水代替依达拉奉.2组病人分别在治疗前后定期进行神经功能缺损评分(NDS)并进行比较.结果 联合组临床显效率(63.16%)明显优于巴曲酶组(39.47%)(P＜0.01);2组均无明显不良反应.结论 依达拉奉联合巴曲酶治疗椎基底动脉系统进展型卒中安全有效.     

依达拉奉和巴曲酶联合治疗急性进展型脑梗死的疗效观察

目的 观察依达拉奉和巴曲酶联合治疗急性进展型脑梗死的疗效.方法 将80例急性进展型脑梗死患者随机分为联合治疗组和对照组各40例.联合治疗组使用依达拉奉30 mg静脉滴注,每天2次,连用10 d;同时在第1 d、3 d、5 d静脉滴注巴曲酶,剂量分别是10 BU、5 BU、5 BU.对照组则单用巴曲酶,用法同联合治疗组.两组治疗前后均进行神经功能缺损程度评分(NDS)及凝血指标检查.结果 联合治疗组的总有效率(95%)明显高于对照组(75%)(P＜0.05).治疗后两组的血纤维蛋白原水平均明显降低(均P＜0.05),血小板数、出凝血时间、凝血酶原时间差异无统计学意义.联合治疗组有1例出现皮下出血.结论 依达拉奉联合巴曲酶治疗急性进展型脑梗死效果显著,无明显不良反应.     

依达拉奉联合巴曲酶治疗进展性脑梗死疗效观察

目的 观察依达拉奉联合巴曲酶治疗进展性脑梗死的临床疗效及安全性.方法 选择发病72h内的进展性脑梗死患者76例,随机分为联合组和巴曲酶组,2组均采用巴曲酶注射液(10BU、5BU、5BU)静滴,隔日1次,共3次;联合组加用依达拉奉注射液30mg静滴,2次/d,共14d.2组病人分别在治疗前后进行神经功能缺损评分(NDS),并进行比较.结果 联合组临床显效率(68.42%)明显优于巴曲酶组(42.11%),2组均无明显不良反应.结论 依达拉奉联合巴曲酶治疗进展性脑梗死安全有效.     

巴曲酶联合依达拉奉治疗急性脑梗死疗效及安全性

目的 观察巴曲酶联合依达拉奉对急性脑梗死的临床疗效及安全性.方法 选择本院75例急性脑梗死患者为观察对象,符合国家脑血管病诊断标准,并经CT或磁共振成像(MRI)证实,除外禁忌证.按入院顺序随机分为依达拉奉组(A组)、巴曲酶组(B组)和依达拉奉+巴曲酶联用组(C组)各25例.在急性脑梗死常规治疗基础上,A组依达拉奉30 mg加生理盐水100 mL静滴,2次/d,疗程14 d;B组巴曲酶,第1天生理盐水100 mL+巴曲酶10 BU静滴,第3天和第5天分别以生理盐水100 mL+巴曲酶5 BU静滴,半小时内滴完.共三次20 BU.C组依达拉奉、巴曲酶,剂量及用法同A、B组.3周后观察神经功能缺损评分情况,按缺损分值的减少判定疗效.用药期间监测肝肾功能、出凝血时间,观察并记录药物不良反应.结果 治疗后 A、B、C 3组总有效率分别为84%、80%和92%.各组治疗前后自身比较差异均有统计学意义(P＜0.05),组间比较,A、B 2组间无显著差异(P＞0.05),C组则明显优于A、B组(P＜0.05).病人顺应性良好,无严重不良反应.结论 巴曲酶联用依达拉奉治疗急性脑梗死疗效肯定,安全性好.     

巴曲酶联合依达拉奉治疗急性脑梗死的疗效观察

目的 研究巴曲酶、依达拉奉联合应用治疗急性脑梗死的临床疗效.方法 选择78例急性脑梗死患者,随机分为治疗组39例和对照组39例.治疗组巴曲酶、依达拉奉联合应用,对照组应用复方丹参、曲克芦丁,2组其他内科治疗相同.于治疗前、治疗后3、7、21d分别进行神经功能缺损程度评分及观察凝血酶原时间(PT)、部分凝血酶原时间(APTT)、凝血酶时间(TT)、纤维蛋白原(Fib)含量变化及国际标准化比值(INR).结果 治疗组Fib较稳定下降,临床疗效显著提高.显效率66.7%,总有效率89.7%,较对照组46.2%、71.8%有显著差异(P＜0.01).结论 巴曲酶与依达拉奉联合应用治疗急性脑梗死可提高临床疗效,用药安全,未见严重不良反应.     

巴曲酶联合依达拉奉治疗急性脑梗死疗效观察

目的评价巴曲酶联合依达拉奉治疗急性脑梗死的临床疗效和安全性。方法采用随机对照试验,选择192例急性脑梗死,随机分为2组,治疗组给予巴曲酶、依达拉奉,对照组给予基本治疗,均于治疗前与治疗后21 d评价神经功能。结果治疗组21 d后总有效率95.2%,明显优于对照组62.5%。神经功能缺损评分与对照组比较差异有统计学意义(P0.05)。结论巴曲酶联合依达拉奉在治疗急性脑梗死方面有明显疗效,能明显减轻神经功能损伤。     

依达拉奉与巴曲酶联用治疗脑梗死的疗效评价

目的研究依达拉奉与巴曲酶联用在脑梗死治疗中的疗效。方法120例脑梗死的患者分为联用组(巴曲酶加依达拉奉),依达拉奉组,巴曲酶组和对照组,每组30例。观察治疗后神经功能改善情况及血浆纤维蛋白原(F IB)的变化。结果联用组治疗后各时期ESS评分均显著高于对照组(P<0.05),21d及90d显著高于巴曲酶组和依达拉奉组(P<0.05);联用组的显效率在90d显著高于其它各组(P<0.05),21d后有效率显著高于其它组(P<0.05);联用组及巴曲酶组治疗后血浆纤维蛋白原含量显著降低(P<0.01)。结论依达拉奉与巴曲酶联用能显著提高脑梗死患者的疗效。     

依达拉奉联合纳络酮治疗急性脑梗死的疗效

目的 探讨依达拉奉联合纳络酮治疗急性脑梗死的疗效.方法 120例进展型脑梗死随机分为纳络酮组(对照组)和依达拉奉联合纳络酮治疗组(治疗组).分别对两组治疗前、治疗14 d后的神经功能缺损及临床疗效进行评价.结果 两组治疗后14 d的神经功能缺损较治疗前均有显著改善P＜0.01,治疗组与对照组比较有显著性差异P＜0.01.治疗14 d后临床疗效评价治疗组总有效率(85%)较对照组(71.67%)有显著性差异P＜0.01.结论 依达拉奉联合纳络酮治疗急性脑梗死能保护脑细胞,有效改善神经功能.     

依达拉奉治疗脑出血的疗效观察

目的观察依达拉奉治疗脑出血的疗效。方法122例脑出血患者随机分为依达拉奉组(61例)和常规治疗组(61例),两组均予常规治疗,在此基础上,依达拉奉组给予依达拉奉30 mg加入生理盐水100 ml静脉滴注,每日2次,共14 d。分别于治疗前、治疗后3 d、7 d、14 d检测血清S-100β蛋白(S-100β)、神经元特异性烯醇化酶(NSE)浓度;治疗前、治疗后7 d、14 d、28 d进行神经功能缺损程度评分(NDS);治疗前、治疗后7 d、21 d行头部CT检查,计算血肿和水肿体积;治疗后28 d和90 d进行疗效及Barthel指数(BI)的评价。结果与治疗前相比,治疗后各时间点两组血清S-100β及NSE水平、NDS、血肿及水肿体积较治疗前显著改善(均P<0.01);依达拉奉组较常规治疗组改善更明显(均P<0.01);依达拉奉组总有效率(86.89%)和显效率(21.34%)显著优于常规治疗组(63.93%,9.84%)(均P<0.01)。结论依达拉奉通过减少神经细胞损伤促进神经功能的恢复,治疗脑出血具有较好的近期和远期疗效。     

依达拉奉对急性脑梗死患者血清血管内皮生长因子和肿瘤坏死因子水平的影响

目的 探讨依达拉奉对急性脑梗死患者血清血管内皮生长因子(VEGF)和肿瘤坏死因子(TNF)-α水平的影响.方法 84例急性脑梗死患者随机分为依达拉奉组和对照组;在脑梗死常规治疗的基础上,依达拉奉组加用依达拉奉60 mg/d静脉滴注14 d.治疗前、治疗后14 d及28 d应用改良爱丁堡斯堪的那维亚量表( SSS)对患者进行临床神经功能缺损程度评分;应用酶联免疫吸附测定法检测患者发病3d、7d及14 d血清VEGF及TNF-α水平.结果 两组患者治疗14 d及28 d时SSS评分均较治疗前明显降低(P＜0.05 ～0.01),依达拉奉组各时间点SSS评分明显低于对照组(均P＜0.05).两组血清VEGF及TNF-α水平发病后各时间点较正常值明显增高,发病第7d时明显高于第3d和第14 d(均P＜0.05);依达拉奉组各时间点血清VEGF水平明显低于对照组(均P＜0.01);两组各时间点血清TNF-α水平差异无统计学意义.结论 依达拉奉可明显降低急性脑梗死患者血清VEGF水平,减轻脑梗死后自由基导致的脑损害.     

Denervation study of synapses of organ of corti of old world monkeys

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.     

Mechanism of action of tubocurarine on nicotinic cholinoreceptors of neurons of the sympathetic ganglia of rats

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.     

The effect of age of onset of PD on risk of dementia

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     

Limits of deinstitutionalization--perspectives of relatives of psychiatric patients

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.     

Summary of Legislation of 1933 of interest to the Department of Mental Hygiene

Psychiatric Quarterly -