阿立哌唑与利培酮治疗门诊首发精神分裂症病人的对照研究

目的以利培酮为对照,研究阿立哌唑口腔崩解片治疗门诊首发精神分裂症的疗效和安全性。方法将70例符合CCMD-3精神分裂症诊断标准的病人随机分为阿立哌唑组（36例）和利培酮组（34例）,分别进行8周治疗。采用CGI-SI、PANSS评定疗效,TESS、实验室检查评定不良反应。结果治疗第2周末,阿立哌唑组与利培酮组PANSS及CGI-SI评分与治疗前比较有显著性下降（P〈0．05）,治疗第4周末起PANSS评分均有极显著改善（P〈0．01）。治疗有效率分别为88．89％和91．18％,两组间比较无差异（P〉0．05）。两组不良反应总评分无显著性差异,但锥体外系、体重增加和内分泌方面不良反应利培酮组明显高于阿立哌唑组,有显著性差异（P〈0．05）。结论阿立哌唑治疗门诊首发精神分裂症病人疗效肯定,安全性高,值得临床推广。     

氟西汀合并小剂量阿立哌唑治疗脑卒中后抑郁临床观察

目的观察氟西汀合并小剂量阿立哌唑治疗脑卒中后抑郁的临床疗效和不良反应。方法70例脑卒中后抑郁患肯随机分成氟西汀组和氟四汀合并小剂量阿立哌唑组（治疗组）,疗程8周。于治疗的、治疗后第1、2、4、6、8周末分别采用汉密尔顿抑郁量表（HAMD）和副反应量表（TESS）评定疗效和不良反应。结果治疗第8周末,氟西汀合并小剂量阿立哌唑组与氟西汀组显效率分别为85．71％、68．57％,差异有统计学意义（P〈0．05）;氟西汀合并小剂量阿立哌唑组在第1周末起效,氟西汀组在治疗后第2周末起效;2组治疗后第1、2、4周末HAMD评分比较差异均有统计学意义（P〈0．05）,不良反应均较轻。结论氟西汀合并小剂量阿立哌唑治疗脑卒中后抑郁起效快,疗效好,不良反应轻,安全性高,依从性好。     

阿立哌唑对男性精神分裂症患者泌乳素及血糖、体重的影响

目的探讨阿立哌唑对男性精神分裂症患者泌乳素及血糖、体重的影响。方法将83例男性精神分裂症患者随机分为研究组（41例,阿立哌唑治疗）和对照组（42例,利培酮治疗）,共治疗12周,基线时、治疗后第4周末、治疗后第8周末及治疗后第12周末应用阳性与阴性症状量表（PANSS）和副反应量表（TESS）分别评定疗效及安全性,并进行泌乳素、血糖、体重、BMI的测定。结果研究组和对照组在治疗后第4周末、第8周末及第12周末的PANSS各因子分及总分均低于基线时,差异均具有显著性意义（P〈0．05）。在治疗各阶段,研究组的泌乳素、血糖、体重、BMI水平较基线时均无显著性改变（P〉0．05）,而在对照组中,治疗后各阶段的泌乳素、血糖、体重、BMI的水平较基线时均有不同程度的增加,且差异均具有显著性意义（P〈0．05）。研究组的不良反应与对照组相当,均未见严重不良反应。结论阿立哌唑可有效改善男性精神分裂症患者的精神症状,且对泌乳素及血糖、体重无明显影响。     

阿立哌唑合并帕罗西汀治疗男性精神分裂症阴性症状的临床研究

目的对比阿立哌唑合并帕罗西汀与单用阿立哌唑治疗男性以阴性症状为主的精神分裂症的疗效和安全性。方法将符合入组标准的60例男性精神分裂症患者随机分为阿立哌唑合并帕罗西汀组（研究组）和阿立哌唑纽（对照组）,观察8周。共完成研究60例,研究组30例,对照组30例,采用阳性和阴性综合征量表（PNASS）分别评定基线和治疗后组内组间总分、各分量表分的变化以及不良反应。结果治疗后第4、8周末,两组患者的PANSS总分及阴性症状分均较治疗前显著降低（P〈0．05,P〈0．01）,治疗后第8周末,研究组PANSS总分及阴性症状分显著低于对照组（P〈0．05）。研究组总有效率为80％,对照组总有效率为47％,两组有效率比较差异有统计学意义（P〈0．05）。两组不良反应均轻微。结论阿立哌唑合并帕罗西汀能明显改善精神分裂症患者的阴性症状,且副反应较少。     

西酞普兰合并阿立哌唑治疗老年抑郁症的对照研究

目的探讨西酞普兰合并阿立哌唑治疗老年抑郁症的疗效。方法将60例老年抑郁症患者随机分成西酞普兰组（单用组）和西酞普兰合并阿立哌唑组（合用组）。共观察6周。于治疗前、后1、2、4、6周末采用汉密尔顿抑郁量表（HAMD），不良反应量表（TESS）评定疗效及不良反应。结果治疗第6周末，西酞普兰合用阿立哌唑组疗效显著，合用组与单用组的有效率分别为83．3％和60％，有显著性差异（X^2=4．021，P〈0．05）；合用组在1周末起效，单用组在2周末起效；两组治疗后1、2、4周HAMD评分有显著性差异（P〈0．05）；TESS评分无明显差异（P〉0．05）。结论西酞普兰合并阿立哌唑治疗老年抑郁症起效快，克服了抗抑郁药起效慢的特点。     

阿立哌唑与喹硫平治疗精神分裂症的疗效观察

目的比较阿立哌唑与喹硫平治疗精神分裂症的疗效及安全性。方法将80例精神分裂症患者随机分为阿立哌唑组和喹硫平组各加例，共治疗8周，在治疗前及治疗后1、2、4、6、8周末分别采用PANSS、TESS进行评定。结果两组治疗前后的PANSS评分比较，有极显著性差异（P〈0．001），两组间比较无统计学差异（P〉0．05）。临床有效率阿立哌唑92．50％，奎硫平90．00％；两组比较无差异（P〉0．05）。两组均在第1周末起效，第2周末效果显著。两组TESS评定无差异。结论两药对精神分裂症均有较好的疗效，且起效快、不良反小。     

阿立哌唑治疗精神分裂症血药浓度与临床疗效的相关性研究

目的探讨阿立哌唑在精神分裂症患者中的血药浓度与临床疗效的关系。方法采用高效液相色谱的方法测定52例精神分裂症患者体内阿立哌唑的血浆药物浓度,采用阳性和阴性综合征量表（PANSS）评定疗效。结果治疗后第1、2、3、4周末与治疗前比较PANSS量表总分及各因子分均显著降低（P〈0．05）。阿立哌唑在治疗后第3周末达到稳态血药浓度,治疗后第3周末有效率为71．2％。治疗后第1、2、3、4周末血药浓度与对应周的剂量呈正相关（P〈0．05）;治疗后第1、2、3、4周末血药浓度与对应周的PANSS量表评分无相关性（P〉0．05）;治疗后第3周末将阿立哌唑血药浓度分成低浓度组（≤76μg／L）、中浓度组（76～116μg／L）、高浓度组（〉116μg／L）3组,中、低浓度组PANSS评分大于高浓度组,但3组差异无统计学意义（P〉0．05）。结论阿立哌唑治疗精神分裂症的血药浓度与其临床疗效之间无相关性。     

阿立哌唑与奋乃静治疗女性精神分裂症对照性研究

目的比较阿立哌唑与奋乃静治疗女性精神分裂症疗效和安全性。方法将83例女性精神分裂症住院患者随机分为阿立哌唑组（研究组）41例和奋乃静组（对照组）42例。以阳性和阴性综合征量表（PANSS）评定疗效,治疗中需处理的不良反应症状量表（TESS）评定不良反应。结果治疗后第2、4、8周末两组PANSS总分及各因子分与治疗前比较均显著下降（P〈0．05,P〈0．01）。治疗后第8周末研究组PANSS量表阴性症状分显著低于对照组（P〈0．05）。两组不良反应均较轻微,不良反应发生率在两组之间无统计学差异（P〉0．05）。结论阿立哌唑治疗女性精神分裂症安全有效。     

阿立哌唑与氯氮平治疗精神分裂症的疗效比较

目的探讨阿立哌唑治疗精神分裂症的疗效及安全性。方法按照CCMD-3诊断标准选择100例住院精神分裂症患者，并随机分为阿立哌唑组（47例）及氯氮平组（43例）分别进行治疗。疗程为8周。结果在治疗第8周末，两组的显效率分别为72．34％及69．77％（P〉0．05）；两组的PANSS总分的减分率分别为69．3％及67．8％（P〉0．05）；两组治疗前后的PANSS总分及各分量表分同组比较有显著性差异（P〈0．01），两组间比较除治疗末PANSS的阴性症状分阿立哌唑组较低，且有显著性差异（P〈0．01）外，其它均无显著性差异（P〉0．05）。其次，阿立哌唑组不良反应为焦虑、头痛、失眠、胃肠道反应等，未发现有明显的体重增加、锥体外系反应。结论阿立哌唑治疗精神分裂症的阳性及阴性症状有较好疗效，不良反应较微，安全性良好。     

阿立哌唑及氟哌啶醇治疗儿童青少年抽动障碍的开放性对照研究

目的 比较非典型抗精神病药物阿立哌唑与经典抗精神病药物氟哌啶醇治疗儿童青少年抽动障碍的疗效及耐受性.方法 对48例符合〈中国精神障碍分类与诊断标准（第3版）〉（CCMD-3）抽动障碍诊断标准的儿童青少年抽动障碍患者按2：1比例随机分配入阿立哌唑或氟哌啶醇治疗组,分别治疗8周,治疗前后分别使用耶鲁抽动症严重程度量表（YGTSS）评定疗效,使用副反应量表（TESS）评定不良反应.结果 两组患者治疗后的YGTSS总分均较治疗前下降,差异有统计学意义（P〈0.001）,但在治疗终点时两组间YGTSS总分差异无统计学意义（P＞0.05）;阿立哌唑组的睡眠过度、锥体外系症状及头痛三种不良反应发生率低于氟哌啶醇组（P〈0.05）.结论 阿立哌唑及氟哌啶醇对儿童青少年抽动障碍疗效相当,但阿立哌唑的耐受性优于氟哌啶醇.     

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.