氯氮平联合丙戊酸镁治疗难治性精神分裂症疗效观察

目的 探讨氯氮平联合丙戊酸镁对难治性精神分裂症的治疗效果.方法 对60例难治性精神分裂症住院患者采用氯氮平联合丙戊酸镁治疗8周,以简明精神病评定量表(BPRS)和不良反应症状量表(TESS)进行评定.结果 第8周末,有效率70%,不良反应少且轻.结论 氯氮平联合丙戊酸镁治疗难治性精神分裂症有一定疗效.     

高剂量奥氮平治疗难治性精神分裂症的疗效

目的 探讨高剂量奥氮平治疗难治性精神分裂症的临床疗效,并观察其安全性及不良反应.方法 37例难治性精神分裂症患者被随机分为奥氮平组和氯氮平组,奥氮平组:奥氮平20～40mg/d治疗,氯氮平组:氯氮平200～500mg/d治疗.分别于治疗前、治疗4周、8周、12周应用阳性和阴性症状量表(PANSS)评定临床疗效,采用不良反应量表(TESS)、体格检查、实验室检查、心电图、脑电图评价安全性.结果 奥氮平组和氯氮平组PANSS总分及各因子分在治疗4周、8周、12周均显著下降(F=16.456,31.352,13.434,22.277,16.869,34.232,21.026,47.558;P＜0.001);治疗前,治疗后4周、8周、12周PANSS总分及阳性、阴性、一般精神病理症状分组间差异无统计学意义.奥氮平组和氯氮平组在治疗中均无严重不良反应发生,两组不良反应差异无统计学意义.结论 高剂量奥氮平具有很好的安全性,可代替氯氮平治疗难治性精神分裂症.     

合用阿立哌唑及单用喹硫平治疗精神分裂症对照研究

目的 对比阿立哌唑与喹硫平合用及单用喹硫平治疗精神分裂症的疗效及安全性.方法 将符合入组标准的63例精神分裂症患者随机分为阿立哌唑合并喹硫平组(实验组31例)及单用喹硫平组(对照组32例).两组在基线及6周末,用阳性和阴性症状量袁(PANSS)评定疗效,用副反应量表(TESS)评定不良反应.结果 治疗6周末,组内前后比较PANSS总分及各分量表分均显著降低(P＜0.001),组间比较阴性症状量表分实验组较对照组显著降低(t=2.24,P＜0.05).PANSS量表及分量表分治疗前后实验组阴性症状量表分及总分减分值均高于对照组(t=2.48,2.07;均P＜0.05).两组不良反应发生率无差异(x2=0.38,P＞0.05).结论 合用阿立哌唑能够更明显地改善阴性症状,同时不增加不良反应.     

氨磺必利合并氯氮平治疗难治性精神分裂症的疗效

目的探讨氨磺必利合并氯氮平治疗难治性精神分裂症患者的疗效及安全性。方法将58例原已服用氯氮平治疗的难治性精神分裂症患者合并氨磺必利(300~700)mg/d治疗12周,同时于2周内将氯氮平减量至维持量后不再变化,并于治疗前及治疗后4、8、12周末用阳性与阴性症状量表(PANSS)评定临床疗效,于治疗前及治疗后12周末用副反应量表(TESS)评定副反应。结果患者合并氨磺必利治疗后8周及12周末PANSS总分较合并前有明显下降(t=0.167,P0.05或t=0.3581,P0.01)。合并氨磺必利治疗后12周末TESS评分较合并前亦有明显下降。结论氨磺必利合并氯氮平对难治性精神分裂症患者阳性及阴性症状的疗效明显,副反应轻微。     

奥氮平与氟哌啶醇治疗难治性精神分裂症的对照研究

目的比较奥氮平与氟哌啶醇治疗难治性精神分裂症的临床疗效和不良反应。方法 76例符合入组条件的难治性精神分裂症患者,随机分为两组,分别应用奥氮平和氟哌啶醇治疗12周,应用阳性和阴性症状量表(PANSS)和副反应量表(TESS)评定疗效和不良反应。结果奥氮平组有效率为65.79%,氟哌啶醇组有效率为42.11%,两组在PANSS总分、阴性症状量表分和一般病理症状量表分方面有显著性差异。结论奥氮平治疗难治性精神分裂症的疗效优于氟哌啶醇,且不良反应较少。     

氯氮平,利培酮及合用治疗精神分裂症疗效探讨

目的:比较氯氮平,利培酮和2者合用(合用组)治疗精神分裂症的临床疗效和副作用,方法:将符合入组标准的326例精神分裂症患者随机分为氯氮平组,利吉酮组和合用组,用阳性和阴性症状量表(PANSS)评定其疗效,观察副作用,结果:利培酮和氯氮平疗效相仿,氯氮平和利培酮全用优于单独使用.而且副作用较少.     

奎硫平与氯氮平治疗精神分裂症的对照研究

目的探讨奎硫平和氯氮平治疗精神分裂症的疗效和安全性。方法对62例精神分裂症患者随机分成2组,分别给予奎硫平与氯氮平治疗8周,采用阳性症状与阴性症状量表(PANSS)及副反应量表(TESS)在治疗前与治疗后l、2、4、8周末分别评定疗效和副反应。结果奎硫平组和氯氮平组之间疗效无显著差异。TESS评定奎硫平组副作用少于氯氮平组(P<0.01)。结论奎硫平是一种治疗精神分裂症安全有效的药物。     

丙戊酸镁与碳酸锂治疗躁狂发作对照研究

目的 比较丙戊酸镁与碳酸锂治疗躁狂发作的疗效和不良反应。方法 对90例躁狂发作患者随机均分为丙戊酸镁和碳酸锂组，在治疗前，治疗2、4、6周末分别用Bech-Rafaelsen躁狂量表（BRMS）和临床疗效总评量表（CGI）及副反应量表（TESS）评定疗效和不良反应。结果 丙戊酸镁组治疗2周后BRMS总分，及各因子分比治疗前明显降低，且显著低于碳酸锂组，两组治疗6周BRMS总分各因子分均显著低于治疗前，差异显著。治疗2、4、6周末TESS评分，丙戊酸镁组显著低于碳酸锂组，差异有显著性。结论 丙戊酸镁治疗躁狂发作疗效好，起效快，不良反应小。     

西酞普兰合并氯氮平治疗精神分裂症阴性症状的临床研究

目的:观察西酞普兰合并氯氮平治疗精神分裂症阴性症状的疗效和不良反应。方法:将61例精神分裂症阴性症状患者随机分为研究组(西酞普兰 氯氮平)和对照组(氯氮平 安慰剂),进行双盲研究。在治疗前、治疗后3、6、9、12周末,采用阳性和阴性症状量表(PANSS)和药物治疗不良反应量表(TESS)评定疗效和不良反应。结果:治疗12周末,研究组的显效率高于对照组(56．7％比25．8％,X2= 6．00,P=0．014)。从第3周末起,阴性因子分、一般精神病理分和总分均为研究组小于对照组(P<0．05或P<0．01),但是各时点阳性因子分的组间差异均不显著(P>0．05)。两组的不良反应发生率差异无统计学意义。结论:西酞普兰合并氯氮平治疗精神分裂症阴性症状的疗效比单用氯氮平好,并且不增加不良反应。     

奎硫平合并丙戊酸镁治疗老年精神分裂症急性期的对照研究

目的:观察用奎硫平合并丙戊酸镁与单用奎硫平治疗老年精神分裂症急性期的疗效与安全性。方法:将58例老年精神分裂症患者随机分为研究组(奎硫平合并丙戊酸镁组)29例,对照组(奎硫平组)29例,疗程2周。分别于治疗1周末、2周末,用阳性与阴性症状量表(PANSS)及外显攻击行为量表(MOAS)评定治疗效果;用副反应量表(TESS)评估不良反应。结果:在治疗2周末,两组临床疗效差异无统计学意义(P>0.05)。在治疗1周末、2周末,PANSS量表兴奋激越项目评分研究组与对照组比较均有统计学意义(P<0.05);2周末,PANSS量表总分有统计学意义(P<0.05)。在治疗1周末、2周末MOAS量表与治疗前比较两组均有统计学意义(P<0.01);两组间比较,2周末有统计学意义(P<0.01)。治疗后各组TESS量表评分均无显著性(P>0.05)。结论:奎硫平合并丙戊酸镁治疗老年精神分裂症急性期起效快、疗效佳、安全性好。     

Recovery of responsiveness of cells of lateral geniculate nucleus of rat

1. Recovery of responsiveness of single cells in lateral geniculate nucleus of rat has been determined in both P and I cells. There are three types of recovery curve among P cells; (a) early recovery, (b) early partial recovery followed by depression and then complete recovery, (c) prolonged depression followed by cyclic recovery. Type (c) is by far the commonest recovery curve. In contrast to the spike in a P cell, the synaptic potential recovers to its full amplitude in about 20 msec. All I cells exhibit similar rapid recovery curves after a prolonged depression.2. Conditioning stimuli applied to visual cortex also produce a prolonged depression in most P cells but I cells can be re-excited at short intervals from cortex. Decortication does not prevent the prolonged depression of the multineuronal response produced by optic nerve stimulation.3. A neuronal model is proposed to explain these observations. It is supposed that I cells (interneurones) are innervated by axon collaterals of the P cells (principal cells, projecting to visual cortex) and that the I cells exert an inhibitory influence on the P cells.     

Modes of Inheritance of Errors of Refraction

Eighteen families in which both parents had refractions within the range of +4·0 D to −4·0 D and axial lengths seen in emmetropia (22·3-26·0 mm) showed coefficients of correlation of the order 0·5 indicative of polygenic inheritance. Such coefficients were seen for axial length (0·407) and for the cornea (0·487), but not for the lens (which is known to be yoked to the axial length). No such coefficients were seen in 19 families in which one of the parents had axial length outside the emmetropic range (nine families with long axes and 10 with short axes).

The pattern of polygenic inheritance for emmetropia (completely correlated optical components) and errors of refraction up to 4·0 D (inadequately correlated components: correlation ametropia) follows that seen in stature and other measurable characters. In contrast the high refractive errors with their abnormal axial lengths (component ametropia) are—like the extremes in stature—pathological anomalies with monofactorial inheritance.

     

Level of functioning of siblings and parents of probands of varying degrees of retardation

A further analysis of already published data supports the position that retardates of low ability level less frequently have retarded siblings, retarded parents, and parents low in occupational level than do retardates higher in ability level. The analysis supports the position that there are two types of retarded individuals, persons retarded as a result of gene or chromosomal anomalies, brain injury, etc., who more frequently occur in the lower-level retardate group, and persons whose retardation represents polygenic segregation, who more frequently occur in the higher-level group.     

Analysis of two types of dopaminergic responses of neurons of the spinal ganglia of rats

It was established, in experiments on isolated spinal ganglia of adult rats in concluons of intracellular recording, that dopamine (1 M/liter) elicits depolarized responses in 61% of neurons, hyperpolarized in 20% of neurons, and depolarized-hyperpolarized in 19% of neurons. The depolarized responses are associated with the activation of D₁ dopamine receptors, and are governed by the shift of cAMP-dependent cation (sodium) channels to the conducting state. The hyperpolarized responses are triggered by the activation of D₂ dopamine receptors, which by means of HTP-binding protein convert the potassium channels to the conducting state. The change in the polarization of neurons with the action of dopamine influences their electrical excitability variously.Translated from Fiziologicheskii Zhurnal SSSR imeni I. M. Sechenova, Vol. 76, No. 6, pp. 739–745, June, 1990.