氯丙咪嗪合并利培酮治疗强迫症的对照研究

目的探讨利培酮对于氯丙咪嗪治疗强迫症的增效作用。方法将70例强迫症随机分为2组,氯丙咪嗪同时合并利培酮和单独使用氯丙咪嗪治疗,治疗8周。采用强迫症量表(Y-BOCS)、汉密尔顿焦虑量表(HAMA)、汉密尔顿抑郁量表(HAMD)评定疗效。结果合并利培酮组有31例完成试验,氯丙咪嗪组有32例完成试验。治疗8周后,两组Y-BOCS平均总分有明显下降,合并利培酮组优于氯丙咪嗪组,两组无显著性差异(P<0.05);HAMA、HAMD的评分均显著下降,两组无显著性差异(P>0.05)。结论合并利培酮对于氯丙咪嗪治疗强迫症有增效作用。     

利培酮治疗难治性Tourette综合征对照观察

目的:探讨利培酮治疗难治性Tourette综合征(TS)的疗效和安全性。方法:对141例难治性TS患者,随机分为利培酮组(71例)和对照组(70例),进行8周的利培酮开放、对照研究。利培酮组以利培酮单药治疗,对照组以氟哌啶醇等单一或联合治疗。采用耶鲁抽动症状严重程度量表(YGTSS)Achenbach儿童行为量表(CBCL)、治疗中出现的症状量表(TESS),于治疗前、治疗4、8周对两组进行临床疗效及安全性评估。结果:两组症状均有改善。治疗第4周利培酮组有效率56.3%,明显高于对照组32.9%(χ2=8.212,P<0.01);利培酮组YGTSS总分(39.97±15.62)分较对照组(49.84±13.91)分显著为低(P<0.01)。治疗8周时利培酮组有效率为71.8%,明显高于对照组51.4%(χ2=6.357,P<0.05);利培酮组YGTSS总分(17.20±11.24)分明显低于对照组(24.97±10.74)分(P<0.05);减分率(76.55±14.73)%明显高于对照组(66.86±14.28)%(P<0.01)。治疗4周和8周,两组的CBCL总分均显著减少(P<0.05)。治疗4周和8周,利培酮组TESS分显著低于对照组(P<0.01)。结论:利培酮对难治性TS疗效肯定,不良反应较轻。     

利培酮治疗精神分裂症强迫症状的对照研究

目的探索利培酮合并安慰剂与利培酮合并氯丙咪嗪对精神分裂症强迫症状的疗效。方法将合并有强迫症状的住院精神分裂症病人75例随机分为利培酮合并安慰剂组38例与利培酮合并氯丙咪嗪组37例,进行8周的治疗对照研究,治疗前后用MMOCI、Y-BOCS、PANSS、及TESS进行评定。结果治疗前后比较,两组疗效都显著。利培酮合并安慰剂组对强迫症状的总有效率82.9%,显效率为68.6%,利培酮合并氯丙咪嗪组的总有效率为97.3%,显效率为89.2%,两组疗效比较有显著差异。结论利培酮合并安慰剂治疗精神分裂症的强迫症状有效,但合并氯丙咪嗪治疗疗效更好。     

艾司西酞普兰与氯丙咪嗪治疗惊恐障碍的临床对照研究

目的比较艾司西酞普兰和氯丙咪嗪治疗惊恐障碍的临床疗效和安全性。方法采用随机数字表将68例惊恐障碍患者分为艾司西酞普兰组(n=34)和氯丙咪嗪组(n=34),分别给予艾司西酞普兰和氯丙咪嗪治疗,疗程均为10周,分别于治疗前及治疗后1、2、4、6、8、10周末采用惊恐相关症状量表(PASS)、汉密尔顿焦虑量表(HAMA)及副反应量表(TESS)分别评定疗效及安全性。结果治疗后,两组PASS和HAMA评分均较治疗前下降,差异有统计学意义(P均0.01)。艾司西酞普兰组和氯丙咪嗪组有效率分别为87.5%和81.3%,差异无统计学意义(P0.05)。艾司西酞普兰组和氯丙咪嗪组TESS评分[(2.78±1.03)vs.(4.07±2.89)],差异有统计学意义(P0.05)。结论艾司西酞普兰治疗惊恐障碍疗效与氯丙咪嗪相当,但艾司西酞普兰组不良反应少,安全性好。     

利培酮合并氯丙咪嗪治疗伴强迫症状的分裂症对照研究

目的　了解利培酮合并氯丙咪嗪治疗伴强迫症状的分裂症的疗效和副反应。方法　对伴强迫症状的分裂症随机分为研究组和对照组 ,分别用利酮培合并氯丙咪嗪、氯氮平合并氯丙咪嗪治疗 8周。用PANSS、Y -BOCS评定疗效 ,用TESS评定副反应。结果　研究组治疗后PANSS、Y -BOCS总分和各因子分与治疗前比较均明显下降 (P <0 .0 1) ,与对照组相近 (P >0 .0 5 ) ;两组治疗后分裂症、强迫症状的有效率、显效率、痊愈率、总有效率、总显效率相近 (P >0 .0 5 ) ;研究组治疗后TESS总分显著低于对照组 (P <0 .0 5 )。结论　利培酮合并氯丙咪嗪治疗伴强迫症状的分裂症疗效肯定 ,副反应较轻 ,可作为治疗伴强迫症状的分裂症的一个较好选择     

文拉法辛与氯丙咪嗪治疗强迫症对照研究

目的比较文拉法辛与氯丙咪嗪对强迫症治疗的疗效、不良反应以及治疗过程中的心境变化。方法强迫症共74例。根据入组序号随机分为2组。文拉法辛组38例,给文拉法辛150~225mg/d。氯丙咪嗪组36例,给氯丙咪嗪150~225mg/d。在服用药物期间,每四周进行一次恐怖/强迫量表(MSCPOR)、焦虑量表(SAS)评定。结果文拉法辛组治疗24周,总有效率89.47%,治疗中不良反应不明显,强迫、焦虑、抑郁分数降低明显。氯丙咪嗪组治疗总有效率89.89%,与文拉法辛组相比差异没有显著意义(P>0.05)。氯丙咪嗪治疗过程中出现口干和眩晕较多见,药物不良反应较重。结论文拉法辛治疗强迫症不良反应少于氯丙咪嗪,二药治疗总有效率差异没有显著意义(P>0.05)。     

氯丙咪嗪合并奎硫平治疗强迫症的对照研究

目的探讨氯丙咪嗪合并奎硫平治疗强迫症的疗效和副作用。方法60例强迫症患者随机分为氯丙咪嗪合并奎硫平组和氯丙咪嗪组,治疗8周,采用强迫症量表(YBOCS)、副反应量表(TESS)评定疗效和副作用。结果治疗结束时两组YBOCS的评分均降低,而合并奎硫平组降低更明显(P<0.05)。结论奎硫平可以增加氯丙咪嗪治疗强迫症的疗效,副作用较小。     

舍曲林与氯丙咪嗪治疗少年强迫症的对照研究

目的 探讨舍曲林与氯丙咪嗪治疗少年强迫症的临床疗效及不良反应.方法 将64例少年强迫症患者随机分为舍曲林组和氯丙咪嗪组,疗程均为8周.分别于治疗前和治疗后2、4、6、8周采用Yale-Brown强迫量表(Y-BOCS)、汉密尔顿抑郁量表(HAMD)、汉密尔顿焦虑量表(HAMA)评定疗效,采用副反应量表(TESS)评定不良反应.结果 舍曲林组和氯丙咪嗪组治疗后,Y-BOCS、HAMD、HAMA分值均显著下降,差异无统计学意义.舍曲林不良反应发生率明显少于氯丙咪嗪.结论 舍曲林治疗少年强迫症与氯丙咪嗪疗效相当,不良反应较轻.     

氯丙咪嗪、SSRIs及两者合并治疗强迫症的临床对照研究

目的观察氯丙咪嗪、5-羟色胺再摄取抑制剂(SSRIs)及SSRIs合并小剂量氯丙咪嗪治疗强迫症的远期疗效及其对社会功能的影响。方法分别使用氯丙咪嗪、SSRIs、SSRIs联合小剂量氯丙咪嗪治疗84例门诊强迫症患者,分别在治疗3月末和6月末应用Yale-Brown强迫量表、临床疗效总评(CGI)和Sheehan残疾量表进行疗效评定,并自编问卷了解患者的一般资料。结果与治疗前相比,氯丙咪嗪组(N=31)、SSRIs组(N=22)及SSRIs联合小剂量氯丙咪嗪组(N=31)在3月和6月的Yale-Brown强迫量表、CGI评分均有显著性差异(P<0.01)。治疗前和治疗6月末,三组在Sheehan残疾量表评分均有显著差异。结论氯丙咪嗪和SSRIs对强迫症均有效,长期治疗可改善社会功能,SSRIs联合使用小剂量氯丙咪嗪可能与病情较重的患者有潜在的临床应用价值。     

氯丙咪嗪合并暴露疗法与单用氯丙咪嗪治疗强迫症的对照研究

目的：探讨药物合并行为治疗强迫症的效果。方法：将符合CCMD－2－R强迫症诊断标准的28例病人，随机分成两组，14例在氯丙咪嗪治疗的基础上联用暴露疗法做为研究组，另14例单用氯丙咪嗪 治疗做为对照组，均系统治疗8周，用耶鲁－布朗强迫症量表（Y－BOCS）减分率评定两组治疗的疗效，结果；氯丙咪嗪合并暴露疗法组的疗效优单用氯丙咪嗪组，尤其是在控制强迫行为方面更为突出。结论：氯丙咪嗪合并暴露疗法尤其适用于以强迫行为为主的强迫症病人。     

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.