无抽搐电休克合并帕罗西汀治疗难治性强迫症的临床观察

目的 探讨无抽搐电休克(MECT)合并帕罗西汀治疗难治性强迫症的疗效和安全性.方法 对62例难治性强迫症患者随机分为研究组和对照组各31例.前者给予无抽搐电休克合并帕罗西汀治疗,后者单用帕罗西汀治疗.观察8周,采用Yale-Brown强迫量表(Y-BOCS)、汉密尔顿抑郁量表(HAMD)评定疗效,用治疗中的症状量表TESS评定安全性.结果 治疗后研究组的显效率为60.0%,对照组的显效率为25.8%,两组比较差异有统计学意义(P＜0.05).两组治疗后Y-BOCS、HAMD评分以研究组下降更明显(P＜0.01),两组TESS评分差异无统计学意义(P＞0.05).结论 无抽搐电休克合并帕罗西汀治疗难治性强迫症可提高疗效,安全性好.     

氯氮平合并拉莫三嗪治疗难治性分裂症的对照研究

目的 评价氯氮平合并拉莫三嗪治疗难治性分裂症的疗效和安全性.方法 68例难治性分裂症患者随机分为研究组和对照组,分别给予氯氮平合并拉莫三嗪、氯氮平治疗,疗程12周,采用阴性和阳性症状量表及副反应量表评定疗效和副反应.结果 对照组显效率为16.7%,有效率为50.0%;研究组显效率40.0%,有效率76.7%,两组显效率和有效率均有显著性差异(P＜0.01),两组副反应比较无差异(P＞0.05).结论 氯氮平合用拉莫三嗪治疗难治性分裂症疗效优于单用氯氮平,副作用少.     

无抽搐电休克对难治性精神分裂症的增效作用

目的:探讨无抽搐电休克治疗(MECT)对难治性精神分裂症的疗效和安全性。方法:76例难治性精神分裂症患者随机分为合用组(药物联合MECT)和单用组(单用药物治疗),每组各38例。合用组自药物治疗3周起增加MECT,疗程12周。采用阳性与阴性症状量表(PANSS)和治疗中出现的症状量表(TESS)评定疗效和不良反应;韦氏记忆量表(WMS)评定MECT对记忆力的影响。结果:合用组总有效率84.2%和显效率55.3%显著高于单用组的60.5%和31.6%(χ2=4.34,5.33;P均<0.05);两组PANSS总分及各因子分均较治疗前有显著下降(P均<0.01),以合用组显著低于单用组(P<0.01或P<0.05);WMS评分与治疗前比较差异无显著性(P>0.05)。两组不良反应发生率和TESS评分差异无显著性(P>0.05)。结论:MECT对难治性精神分裂症有较好的增效作用,不良反应少。     

改良电抽搐治疗难治性精神分裂症的作用

目的:评估氯氮平合并改良电抽搐(MECT)治疗对难治性精神分裂症的临床疗效及安全性。方法:74例难治性精神分裂症患者随机分为两组,联合治疗组37例,在应用氯氮平的基础上联合MECT治疗;单药治疗组37例,仅给予氯氮平治疗;观察12周。分别于治疗前及治疗后4周、8周、12周末采用阳性和阴性症状量表(PANSS),治疗中出现的症状量表(TESS)评定其临床疗效和不良反应;治疗前及治疗结束后ld、1周、2周采用韦氏记忆量表(WMS)评定MECT对记忆的影响。结果:治疗12周后,联合治疗组的PANSS减分率(46.17±16.14)%,临床总有效率为58.7%;单药治疗组的PANSS减分率(32.26±14.27)%,临床总有效率为28.9%,两组差异有显著性(P<0.05或P<0.01)。两组TESS评分差异无显著性(P>0.05)。WMS评分在治疗结束后1d明显降低(P<0.01),但在治疗1周、2周与治疗前差异无显著性(P>0.05)。结论:改良电抽搐治疗联合氯氮平对难治性精神分裂症有效、安全。     

不同频次无抽搐电休克治疗难治性精神分裂症对照观察

目的探讨不同频次无抽搐电休克治疗(MECT)对难治性精神分裂症(TRS)的临床疗效及安全性。方法将80例难治性精神分裂症患者随机分为两组,一组给予1周一次MECT治疗(研究组n=40),另一组给予1周2次MECT治疗(对照组n=40);观察12周,于治疗前及治疗第2周、4周、6周、8周、12周末采用阳性与阴性症状量表(PANSS)评定临床疗效,不良反应量表(TESS)评定不良反应。结果两组PANSS总分均较治疗前有下降(P0.05);对照组治疗第2、4周末PANSS评分较研究组低,差异有统计学意义(P0.05),但治疗12周末PANSS评分对比无明显差异(P0.05);治疗12周末,研究组有效率76.67%,对照组有效率73.33%,两组无显著性差异(P0.05)。两组不良反应发生率差异无统计学意义(P0.05)。结论 MECT对TRS有效,一周两次MECT的疗效和不良反应不优于一周一次。     

氯氮平合并改良电抽搐治疗难治性精神分裂症的对照研究

目的评价氯氮平合并改良电抽搐治疗（MECT）难治性精神分裂症的临床疗效及安全性。方法将94例难治性精神分裂症患者按照就诊顺序分为两组,联合治疗组47例,在应用氯氮平的基础上合并MECT治疗,疗程8周;单药治疗组47例,仅给予氯氮平治疗。采用阳性与阴性症状量表（PANSS）及治疗中出现的症状量表（TESS）评定疗效和不良反应。结果联合治疗组的显效率为51.1%,单药治疗组的显效率为27.7%。联合治疗组不良反应较少。结论氯氮平合并改良电抽搐治疗难治性精神分裂症有效、安全。     

丙戊酸钠辅助治疗难治性精神分裂症的作用

目的：评价氯氮平合并丙戊酸钠治疗难治性精神分裂症的疗效和安全性。方法：62例难治性精神分裂症患者随机分为合用组和单用组，分别给予氯氮平合并丙戊酸钠和氯氮平治疗，疗程12周。采用阳性与阴性症状量表（PANSS）及治疗中出现的症状量表（TESS）评定疗效和不良反应结果：单用组显效率为16．7％，有效率为50．0％；合用组显效率43．3％，有效率73．3％，以合用组疗效显著较好（P〈0．05），两组不良反应差异无显著性（P〉0．05）。结论：氯氮平合用丙戊酸钠治疗难治性精神分裂症疗效优于单用氯氮平，不良反应少。     

利培酮与无抽搐电休克治疗难治性精神分裂症近期疗效对照研究

目的评价利培酮和无抽搐电休克对难治性精神分裂症的疗效和副反应。方法将住院的难治性精神分裂症60例,随机分为两组,分别应用利培酮和无抽搐电休克治疗,观察12周。用PANSS量表评定疗效,用TESS量表评定药物副反应。结果利培酮治疗组(在2周内逐渐停用原有抗精神病药)从治疗第6周起PAN-SS量表总分、PANSS量表一般精神病理分和阳性症状分开始下降,第8周起全面下降,各治疗时段TESS评分不大于3,观察期末评定有效率为56.67%,显效率为13.33%。MECT组(将原有抗精神病药减量至2/3-1/2)自治疗第4周起PANSS量表总分、PANSS量表一般精神病理分和阳性症状分开始下降,观察期末,有效率为63.33%,显效率为20%,但TESS评分较高。结论上述两种方法对难治性精神分裂症均有较理想治疗效果。     

无抽搐电休克合并舍曲林治疗难治性抑郁症的对照研究

目的探讨舍曲林合并无抽搐电休克治疗(modified electroconvulsivetherapy,MECT)难治性抑郁症的临床疗效及安全性。方法将43例难治性抑郁症患者随机分为两组,研究组(2l例)在原用抗抑郁剂舍曲林的基础上加用MECT治疗。对照组(22例)仍使用原有抗抑郁剂舍曲林。所有患者进行汉密尔顿抑郁量表(HAMD)、副反应量表(TESS)评定并作比较。结果研究组显效率为71.43%,明显高于对照组的9.09%(P<0.01)。两组TESS分值无差异。结论抗抑郁剂并用无抽搐电休克治疗难治性抑郁症有效、安全。     

无抽搐电休克联合氯氮平治疗难治性精神分裂症临床观察

目的探讨无抽搐电休克(MECT)联合氯氮平对难治性精神分裂症的临床疗效。方法选取符合《中国精神障碍分类与诊断标准(第3版)》(CCMD-3)难治性精神分裂症断标准的患者91例,采用随机数字表法分为观察组(n=46)和对照组(n=45),给予对照组单纯氯氮平25mg,每天睡前服用,观察组在此基础上接受MECT治疗。于治疗前后采用阳性和阴性症状量表(PANSS)评定临床疗效,采用症状量表(TESS)评定不良反应。结果治疗12周后,观察组和对照组总有效率比较差异有统计学意义(91.3%vs.71.1%,P0.05);观察组治疗后的PANSS总评分为(32.7±3.8)分,不良反应发生率为15.2%,低于对照组的(56.6±4.5)分和37.8%,差异有统计学意义(P0.05)。结论 MECT联合氯氮平对难治性精神分裂症疗效和安全性均优于单用氯氮平。     

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.     

Summary of legislation of 1935 of interest to the department of Mental Hygiene

Psychiatric Quarterly -     

Summary of legislation of 1941 of interest to the Department of Mental Hygiene

Psychiatric Quarterly -     

Asymmetry of on- and off-pathways of blue-sensitive cones of the retina of macaques

Macaque retinal ganglion cells whose receptive-field center recieves input from blue-sensitive cones show an overt asymmetry of the frequency of ON-center and OFF-center varieties, an asymmetry not present in ganglion cells whose center receives input from the other two cone types. A similar asymmetry of ON/OFF responses is found in the local electrotetinogram (d-wave) mediated by signals from blue-sensitive cones. ‘Blue-ON-center’ ganglion cells have larger receptive-field centers and shorter conduction latencies than other opponent-color varieties, suggesting an appreciable degree of receptor convergence and presumably large cell bodies. Intracellular stainings of these neurons with Procion Yellow show that they correspond to diffuse stratified (Parasol) ganglion cells whose flat-topped dendritic arborization stratifies in the sclerad half of the inner plexiform layer. In view of the known characteristics of macaque bipolar cells and of the ON/OFF asymmetry, it is proposed that these ganglion cells are postsynaptic to cone-specific flat bipolars possibly mediating sign-inverting synaptic contacts. The results also indicate a reversal, for the blue-cone pathway, of the ON/OFF lamination of the inner plexiform layer that has recently been described in other species.     

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.