度洛西汀与西酞普兰治疗抑郁症的临床对照研究

目的探讨度洛西汀与西酞普兰治疗抑郁症的疗效与不良反应。方法将符合中国精神障碍分类与诊断标准第三版(CCMD-3)的住院及门诊46例抑郁症患者,随机分为度洛西汀组22例和西酞普兰组24例,共治疗8周。采用汉密尔顿抑郁量表(HAMD)、汉密尔顿焦虑量表(HAMA)和治疗中出现的症状量表(TESS)评定疗效及不良反应。结果治疗第1周末度洛西汀组HAMD评分较西酞普兰组下降明显(P0.05),提示度洛西汀起效快于西酞普兰;治疗6周末度洛西汀组有效率为95.45%,西酞普兰组为91.66%,两组疗效相当(χ2=0.247,P0.05);两组不良反应均较轻微。结论度洛西汀和西酞普兰均为治疗抑郁症安全有效的药物,但度洛西汀较西酞普兰起效快,可作为临床治疗抑郁症理想药物的选择。     

度洛西汀与西酞普兰治疗老年抑郁症对照研究

目的探讨度洛西汀与西酞普兰治疗老年抑郁症的疗效及安全性。方法 58例老年抑郁症患者随机分为度洛西汀组（n=29）和西酞普兰组（n=29）。治疗8周后用汉密顿抑郁量表（HAMD）和副反应量表（TESS）评定疗效及不良反应。结果两组疗效相仿（P〉0.05）;两组不良反应差异无统计学意义（P〉0.05）。结论度洛西汀治疗老年抑郁症是安全有效的。     

西酞普兰治疗脑卒中后抑郁临床研究

目的比较西酞普兰与氟西汀治疗脑卒中后抑郁的疗效与不良反应。方法56例脑卒中后抑郁患者随机分为西酞普兰组和氟西汀组,治疗6周。治疗前后用汉密顿抑郁量表(HAMD)、汉密顿焦虑量表(HAMA)、疾病严重程度量表(CGI-SI)和副反应量表(TESS)评定疗效和不良反应。结果西酞普兰与氟西汀疗效相当,显效率82.1%;西酞普兰较氟西汀起效快,治疗1、2周末两组HAMD评分比较差异有显著性。两组TESS评分差异无显著性。结论西酞普兰治疗脑卒中后抑郁安全、有效。     

西酞普兰治疗脑卒中后抑郁临床分析

目的探讨西酞普兰治疗脑卒中后抑郁的疗效和安全性。方法将符合脑卒中诊断标准同时符合CCMD-3抑郁症诊断标准的66例患者随机分为2组,分别给予西酞普兰和阿米替林治疗。治疗时间为6周,采用汉密顿抑郁量表(HAMD)、副反应量表(TESS)于治疗前和治疗1、2、4、6周分别评定疗效和不良反应。结果 2组治疗各周末评分HAMD均较前下降(P<0.05),但治疗1周末,西酞普兰组HAMD评分下降较阿米替林组显著(P<0.01),治疗6周末2组HAMD分值下降差异无统计学意义(P>0.05)。西酞普兰组不良反应较阿米替林组少而轻。结论西酞普兰治疗脑卒中后抑郁疗效与阿米替林相当,但起效快,不良反应少,安全性高。     

路优泰与西酞普兰治疗老年抑郁症的疗效观察

目的探讨路优泰治疗老年抑郁症患者的疗效和安全性。方法将60例老年抑郁症患者随机分为路优泰组与西酞普兰组，共治疗6周。采用汉密顿抑郁量表（HAMD）、汉密顿焦虑量表（HAMA）和治疗中出现的症状量表（TESS）评定疗效和不良反应。结果路优泰与西酞普兰治疗老年抑郁症的有效率分别为83．3％及86．7％，两药疗效相当；前者的不良反应较少而轻。结论路优泰治疗老年抑郁症疗效确切，安全性良好。     

奥氮平对伴有焦虑的抑郁症的治疗作用

目的:观察西酞普兰合并小剂量奥氮平治疗伴有焦虑的抑郁症患者的临床疗效和安全性。方法:将68例伴有焦虑的抑郁症患者随机分为两组,研究组给予西酞普兰合并奥氮平治疗,对照组给予西酞普兰治疗,疗程均为8周。采用汉密尔顿抑郁量表(HAMD)及汉密尔顿焦虑量表(HAMA)评定临床疗效,治疗中出现的症状量表(TESS)评定不良反应。结果:治疗8周末两组HAMD及HAMA评分均显著性下降(P均<0.01)。研究组起效较快,显效率高于对照组(P<0.05),两组不良反应均较轻微。结论:西酞普兰合并奥氮平对伴有焦虑的抑郁症起效快,疗效肯定,安全性高,依从性好。     

草酸艾司西酞普兰联合度洛西汀对抑郁伴焦虑的疗效及安全性

目的:观察草酸艾司西酞普兰联合度洛西汀对抑郁伴焦虑患者的疗效及安全性。方法:204例抑郁伴焦虑患者随机分为观察组及对照组各102例,两组均给予草酸艾司西酞普兰,观察组在此基础上联用度洛西汀,进行6周治疗。采用汉密尔顿抑郁量表(HAMD)和汉密尔顿焦虑量表(HAMA)于治疗前后评分,比较两组临床疗效并观察不良反应。结果:两组HAMA、HAMD评分治疗后均显著降低(F=17.219~23.585,P均0.05);观察组在治疗1周和2周时HAMA、HAMD评分均显著低于对照组(HAMA:t=3.959,t=2.836;HAMD:t=4.602,t=4.278;P0.05)。两组总有效率分别为91.2%和89.2%(P0.05)。两组不良反应发生率分别为9.8%和7.8%(P0.05)。结论:草酸艾司西酞普兰联合度洛西汀治疗抑郁伴焦虑起效快、疗效佳、安全性高。     

舒必利联合西酞普兰治疗老年抑郁症伴躯体症状疗效分析

目的探讨舒必利联合西酞普兰治疗老年抑郁症伴躯体症状的疗效。方法老年抑郁症患者随机数字表法分为2组,观察组:西酞普兰+舒必利组;对照组:西酞普兰组,评估比较2组疗效。结果经治疗8周后,观察组汉密顿抑郁量表(HAMD)、临床疗效总评量表(CGI)及老年抑郁量表(GDS)评分均显著低于对照组(P0.05);而2组TESS量表评分比较差异无统计学意义(t=0.323;P=0.748)。治疗8周后,观察组躯体症状发生率显著低于对照组,差异有统计学意义(11.63%.5/43vs 28.89,13/45;χ2=4.026,P=0.045)。结论舒必利联合西酞普兰治疗老年抑郁症伴躯体症状临床疗效佳,改善躯体症状明显,值得临床应用。     

艾司西酞普兰与舍曲林治疗伴焦虑症状抑郁症患者疗效比较

目的:比较艾司西酞普兰与舍曲林治疗伴焦虑症状的抑郁症疗效和安全性. 方法:76例符合入组标准的患者随机分为艾司西酞普兰组和盐酸舍曲林组各38例,疗程6周.用汉密尔顿抑郁量表(HAMD-17)、汉密尔顿焦虑量表(HAMA)评定疗效,采用治疗中出现的症状量表(TESS)评定安全性.结果:两组HAMD、HAMA评分均较治疗前显著降低(P＜0.01),以艾司西酞普兰组HAMD、HAMA评分在治疗1周时降分显著低于盐酸舍曲林组(t=-2.839,-2.862;P ＜0.01),其余各周差异无统计学意义(P＞0.05).艾司西酞普兰组与舍曲林组不良反应发生率分别为39.5％和42.1％ (P＞0.05).结论:艾司西酞普兰与舍曲林治疗伴焦虑症状的抑郁症疗效相当,但艾司西酞普兰起效更快.     

西酞普兰与奎硫平治疗伴躯体症状抑郁症观察

目的:探讨西酞普兰联合奎硫平治疗伴有躯体不适主诉的抑郁症患者的疗效与安全性。方法:收集伴有躯体不适主诉的抑郁症患者68例,随机分成合用组(西酞普兰加用奎硫平)和单用组(单用西酞普兰),以汉密尔顿抑郁量表(HAMD)、汉密尔顿焦虑量表(HAMA)、临床疗效总评量表(CGI)、副反应量表(TESS)在治疗1、2、4、6周时各评定1次。结果:治疗6周末,两组HAMD和HAMA评分均显著低于治疗前。治疗第4、6周末两组间HAMD、HAMA评分差异有极显著性(P<0.01及0.05)。合用组有效率86%,显著优于单用组的有效率62%。结论:西酞普兰联合奎硫平治疗伴躯体症状的抑郁症疗效好,安全性高。     

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 1935 of interest to the department of Mental Hygiene

Psychiatric Quarterly -