阿立哌唑治疗首发精神分裂症的随访对照研究

目的：探讨阿立哌唑与利培酮治疗首发精神分裂症的疗效和安全性。方法：将148例首发精神分裂症患者随机分为阿立哌唑组75例和利培酮组73例。以阳性与阴性症状量表（PANSS）减分率评定疗效同时评定社会功能缺陷筛选表（SDSS）和治疗中出现的症状量表（TESS）,以SDSS评定社会功能,用TESS评定不良反应。结果：阿立哌唑组与利培酮组在痊愈率、显效率、PANSS评分与SDSS评分差异无统计学意义（P均〉0.05）。阿立哌唑组在体质量增加、内分泌失调与锥体外系方面少于利培酮组,而在兴奋激越与恶心呕吐多于利培酮组,差异均具有统计学意义（P均〈0.05）。结论：阿立哌唑与利培酮治疗首发精神分裂症长期疗效均好,阿立哌唑不良反应较少,依从性高。     

3种抗精神病药对精神分裂症认知功能的影响

目的:探讨阿立哌唑、利培酮和氯丙嗪对首发精神分裂症患者认知功能的影响。方法:56例首发精神分裂症患者分为阿立哌唑组(n=18)、利培酮组(n=24)和氯丙嗪组(n=14),在治疗前和治疗6周进行阳性与阴性症状量表(PANSS)评分,威斯康星卡片分类测验(WCST)、连线测验(A和B)、韦氏成人智力量表(WAIS)中的数字符号和数字广度(顺、逆)测验等神经心理测验。结果:治疗6周后,3组PANSS评分均明显下降,3组之间差异无显著性。阿立哌唑组和利培酮组各项认知功能指标均有不同程度的改善,而氯丙嗪组只有2项(WCST中持续反应数和数字广度测验)较治疗前显著好转。连线测验B阿立哌唑组显著优于利培酮组,其余各指标两组间差异无显著性。阿立哌唑组除WCST中持续反应数、完成分类数和数字广度测验外,其余各指标均显著优于氯丙嗪组;利培酮组除WCST中持续反应数外,其余各指标均显著优于氯丙嗪组。结论:阿立哌唑和利培酮对首发精神分裂症患者认知功能的改善作用相当,均显著优于氯丙嗪。     

阿立哌唑联合艾司西酞普兰对首发精神分裂症患者认知功能及社会功能的疗效

目的探讨阿立哌唑联合艾司西酞普兰对首发精神分裂症患者认知功能及社会功能的临床效果。方法将140例首发精神分裂症患者随机分为观察组和对照组,各70例,对照组给予阿立哌唑治疗,观察组给予艾司西酞普兰联合阿立哌唑治疗。治疗前及治疗6个月后,采用阳性和阴性症状量表(PANSS)、威斯康星卡片分类测验(WCST)、社会功能缺陷筛选量表(SDSS)评估患者临床症状、认知功能、社会功能。结果治疗前两组患者上述量表评分组间无明显差异(P0.05);治疗6个月后观察组PANSS各项评分明显低于对照组,WCST量表中的完成分类数、正确应答数、概念化水平百分比评分明显高于对照组,持续性错误数明显低于对照组,SDSS量表中的社会性退缩、家庭外活动、家庭内活动、家庭职能、个人生活自理、对外界兴趣评分均明显低于对照组,上述差异均有统计学意义(P0.05)。结论阿立哌唑联合艾司西酞普兰能更有效地缓解首发精神分裂症患者精神病性症状,改善其认知功能与社会功能。     

阿立哌唑与利培酮对血清催乳素及体质量的影响

目的:比较阿立哌唑与利培酮治疗女性首发精神分裂症的疗效及对血清催乳素(PRL)水平及体质量的影响. 方法:70例女性首发精神分裂症患者分为阿立哌唑组和利培酮组,每组35例.分别给予阿立哌唑和利培酮治疗8周.以阳性与阴性症状量表(PANSS)及治疗中出现的症状量表(TESS)评估疗效和不良反应,同时检测两组的血清PRL水平. 结果:两组间PANSS各项评分及临床有效率差异无显著性(P>0.05);阿立哌唑组在PRL水平改变及体质量增加方面优于利培酮组(P<0.05或P<0.01),泌乳、月经紊乱明显少于利培酮组. 结论:两药治疗女性精神分裂症均有较好疗效,以阿立哌唑对内分泌影响较小,更适合于女性患者.     

阿立哌唑与利培酮治疗精神分裂症的对照研究

目的评价阿立哌唑与利培酮治疗精神分裂症的疗效及安全性。方法阿立哌唑组50例,剂量范围10~30mg/d;利培酮组48例,剂量范围4~6mg/d,两组均以PANSS、CGI量表及TESS、RSESE量表评定观察6周。结果阿立哌唑组治疗精神分裂症与利培酮组相比总体疗效相当。阿立哌唑组PANSS-阴性因子项目减分在第4周末(t=1.89,P<0.05)及6周末(t=2.27,P<0.05)优于利培酮组。阿立哌唑组的药物不良反应小。结论阿立哌唑是有效且安全的非典型抗精神病药,对精神分裂症阴性阳性症状均有效。     

阿立哌唑与利培酮治疗精神分裂症对照研究

目的:探讨阿立哌唑与利培酮治疗首发精神分裂症的临床疗效及安全性。方法:将首发精神分裂症患者100例随机分为阿立哌唑组与利培酮组,疗程8周。采用阳性与阴性症状量表(PANSS)及副反应量表(TESS)评定疗效与不良反应。结果:阿立哌唑组与利培酮组的有效率分别为84.1%和88.9%,两组间治疗前后PANSS评分差异均无显著性(P>0.05),而不良反应发生率阿立哌唑组显著低于利培酮组(P<0.05)。结论:阿立哌唑与利培酮对精神分裂症疗效相当,不良反应发生率低,是一种安全有效的抗精神病药物。     

阿立哌唑与利培酮治疗精神分裂症的随机双盲多中心对照研究

目的 评价阿立哌唑治疗精神分裂症的疗效及安全性.方法 采用随机双盲多中心对照研究方法.240例精神分裂症患者随机分为:阿立哌唑组120例,剂量10～30 mg/d;利培酮组120例,剂量2～6 mg/d.疗程6周.以阳性和阴性症状量表(PANSS)总分变化和有效率为疗效指标.结果 治疗第6周末,阿立哌唑组PANSS总分从基线的85.12分降至52.26分,平均减分32.86分;利培酮组从基线的86.89分降至50.30分,平均减分36.58分;两组的差异无统计学意义(F=1.61,P=0.206).阿立哌唑组有效率为64.3%,利培酮组为68.9%,两组的差异没有统计学意义(X2=1.00,P=0.316).阿立哌唑组和利培酮组相关不良事件发生率分别为65.0%和73.3%.阿立哌唑组对体质量(F=4.535,P=0.034)和血清催乳素(F=33.576,P=0.000)的影响较利培酮组小.结论 阿立哌唑治疗精神分裂症的疗效与利培酮相当,不良反应相似;但阿立哌唑较少引起患者体质量增加,对血清催乳素水平无影响.     

阿立哌唑联合认知干预对精神分裂症患者认知功能的影响

目的探讨阿立哌唑联合认知干预对精神分裂症患者认知功能的影响。方法将92例精神分裂症患者随机分为阿立哌唑联合认知干预组(研究组,n=46)和阿立哌唑组(对照组,n=46),疗程12周,采用PANSS评估患者的精神症状,WCST、CPT、TMT、CF、HVLT-R及WMS-Ⅲ评估患者的认知功能,TESS评估患者的不良反应。结果治疗12周末两组PANSS各项评分较治疗前均显著降低(P0.01),而研究组阴性症状分、一般症状分及总分较对照组显著降低(P0.05或0.01),阳性症状分较对照组则无明显变化(P0.05)。两组WCST、CPT、TMT、CF、HVLT-R及WMS-Ⅲ评分较治疗前均明显改善(P0.01),且研究组较对照组改善更加明显(P0.05或0.01)。两组患者TESS量表总分差异无统计学意义(P0.05)。结论阿立哌唑联合认知干预对改善精神分裂症患者的认知功能可能优于单用阿立哌唑治疗。     

阿立哌唑与利培酮治疗精神分裂症对照研究

目的:以利培酮为对照,探讨阿立哌唑治疗精神分裂症的疗效和安全性。方法:将60例精神分裂症患者随机分为两组,分别给予阿立哌唑和利培酮治疗8周。采用阳性与阴性症状量表(PANSS)及副反应量表(TESS)评定疗效及不良反应。结果:治疗8周后阿立哌唑组和利培酮组的疗效相当,有效率差异无显著性(P>0.05)。利培酮组的锥体外系反应(EPS)发生明显高于阿立哌唑组(P<0.05)。结论:阿立哌唑治疗精神分裂症疗效肯定,不良反应小,患者依从性好。     

阿立哌唑与利培酮对血清催乳素水平的影响

目的:比较阿立哌唑与利培酮对精神分裂症患者血清催乳素(PRL)的影响及其与临床疗效的关系。方法:选取70例精神分裂症患者,随机分为阿立哌唑组36例,利培酮组34例,分别给予阿立哌唑和利培酮治疗8周,在治疗前及治疗1、2、4、6、8周末采用阳性与阴性症状量表(PANSS)对两组进行评定。并于治疗前、中、后采用放射免疫法测查PRL水平。结果:两组PANSS减分率分别为阿立哌唑组(44.9±15.0)%、利培酮组(51.3±14.3)%,临床有效率分别为89.7%、92.1%,治疗前后阿立哌唑组PRL水平比较差异无显著性(P>0.05),利培酮组PRL明显增高(P<0.05)。阿立哌唑组治疗前后PRL水平的差值与PANSS减分率经相关分析差异有显著性(r=0.50,P<0.05),而利培酮组差异则无显著性(r=0.20,P>0.05)。出现月经紊乱或泌乳阿立哌唑组(1/14,7.1%)较利培酮组(7/18,38.9%)明显为少(χ2=4.23,P<0.05)。结论:2药对精神分裂症均有较好疗效,阿立哌唑与利培酮对PRL影响不同,与疗效关系不明显。     

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.