唑吡坦治疗失眠症双盲研究

目的：比较国产唑吡坦片和进口唑吡坦片治疗失眠症的疗效和不良反应。方法：对32例失眠症患者随机分为两组,分别服用国产或进口唑吡坦。采用睡眠障碍量表（SDRS）、汉密尔顿焦虑量表（HAMA）、临床总体印象量表（CGI）和副反应量表（TESS）评定疗效和不良反应。结果：SDRS评定国产唑吡坦组减分率为49．7％,与进口唑吡坦组49．8％相近,主要不良反应为头痛、口干、便秘和出汗等,病人均能耐受。结论：国产唑吡坦治疗失眠症的疗效和进口唑吡坦相当。     

唑吡坦治疗老年原发性失眠的开放性前瞻性多中心自身对照研究

目的 评价唑吡坦5 mg每日1次治疗老年原发性失眠的疗效和安全性.方法 采用开放性、前瞻性、固定剂量、多中心、自身对照的研究方法.115例符合美国精神障碍诊断和统计手册第4版原发性失眠诊断标准的老年门诊患者每日1次服用固定剂量唑吡坦5 mg,疗程3周.以治疗第1周末匹兹堡睡眠质量指数评分(PSQI)相对于基线的差值作为研究的主要疗效评价指标,次要疗效指标包括:治疗第3周末PSQI评分相对于基线的差值,治疗第1周末和第3周末主观睡眠有效参数评分(睡眠潜伏期、总的睡眠时间、睡眠质量)相对于基线的差值,治疗第3周末17项汉密尔顿抑郁量表(HAMD-17)评分和汉密尔顿焦虑量表(HAMA)评分相对于基线的差值.结果 治疗第1周末,PSQI量表总分较基线下降2.8分,差异有统计学意义(P＜0.01);治疗第3周末,PSQI评分较基线下降3.2分,差异有统计学意义(P＜0.01);治疗第1周末和第3周末主观睡眠有效参数均有明显改善:睡眠潜伏期缩短(P＜0.01),睡眠时间延长(P＜0.01),日间功能提高(P＜0.01);治疗第3周末,患者的HAMD-17和HAMA评分较基线均有降低(P＜0.01);不良事件的发生率为19.1%,主要为头晕、头痛、困倦、恶心、乏力等,程度为轻、中度.结论 每日1次服用固定剂量唑吡坦5 mg治疗老年原发性失眠安全有效.     

唑吡坦对失眠症患者睡眠影响的多导睡眠图研究

目的 应用多导睡眠图(PSG)探讨唑吡坦对失眠症患者睡眠脑电活动的影响.方法 对27例符合国际疾病分类标准第10版(ICD-10)非器质性失眠症诊断标准的患者连续进行3晚PSG描记,其中第3晚睡前予10 mg唑吡坦,观察用药后PSG的变化.正常对照组33名,作1夜适应和1夜基础PSG监测.结果 与基线睡眠比较,患者服用唑吡坦后睡眠效率提高[(91%±4%)vs(87%±8%),P＜0.05],觉醒时间减少[(24±6)min vs(39±16)min,P＜0.01],S1减少[(18%±6%)vs(30%±18%),P＜0.01],S2增加[(60%±5%)vs(44%±18%),P＜0.01],睡眠潜伏期缩短[(36±18)min vs(22±11)min,P＜0.01].结论 唑吡坦对失眠症患者夜间多导睡眠图脑电有影响.     

θ爆发刺激治疗卒中相关失眠的疗效分析

目的 观察连续性θ爆发刺激(cTBS)治疗卒中相关失眠的疗效。方法 纳入亚急性期脑梗死患者60例，采用匹兹堡睡眠质量指数(PSQI)进行测评，以PSQI量表总分>7分作为判断睡眠障碍的标准。随机分为药物治疗组、联合治疗组，各30例。药物治疗组给予唑吡坦10 mg口服、联合治疗组给予唑吡坦5 mg口服+cTBS模式刺激右侧背外侧前额叶和顶枕区域，分别比较两组患者抗失眠药物停药时间和2周停药率、PSQI减分率、NIHSS评分、HAMD和HAMA评分的变化，以观察cTBS治疗卒中相关失眠的临床疗效。结果 联合治疗组平均停药时间短于药物治疗组，2周停药率均高于药物治疗组(P<0.05);两组患者NIHSS评分、HAMD及HAMA评分随治疗时间呈现好转趋势，同一随访时间组间比较无明显差异。由于两组患者HAMD、HAMA评分交互P有统计学意义，说明随着时间的变化，两组间的HAMD、HAMA评分会出现差异。结论 cTBS对于卒中相关失眠的治疗具有明显作用，且一定程度上改善了患者的焦虑抑郁状态。     

曲唑酮治疗苯二氮类药物依赖和戒断反应的临床对照研究

目的探讨曲唑酮对苯二氮类药物依赖性失眠的疗效和安全性。方法共40例苯二氮类药物依赖性失眠患者,分为苯二氮类联合曲唑酮组(曲唑酮组)和苯二氮类联合安慰剂组(对照组),逐渐减半苯二氮类药物剂量,治疗3个月后根据Holtzman-Gellert戒断症状评分法、汉密尔顿焦虑量表(HAMA)和多导睡眠图监测结果评价曲唑酮戒断疗效,副反应量表(TESS)评价药物不良反应。结果与对照组比较,曲唑酮组患者自治疗后7d戒断症状评分开始降低(P=0.000),自治疗后15dHAMA评分开始降低(P=0.000);与治疗前比较,经曲唑酮治疗后两项评分均降低(P=0.000)。与对照组比较,曲唑酮组患者治疗后7d总睡眠时间和慢波睡眠时间延长、睡眠效率提高、睡眠潜伏期缩短(均P=0.000);与治疗前相比,经曲唑酮治疗后总睡眠时间和慢波睡眠时间延长、睡眠效率提高、睡眠潜伏期缩短(均P=0.000)。未见明显不良反应,两组患者治疗前后TESS评分差异无统计学意义(P>0.05)。结论曲唑酮治疗苯二氮类药物依赖和戒断反应疗效显著,且安全性良好。     

心理应激性失眠患者主客观睡眠特征分析

目的:探讨心理应激性失眠患者的主、客观睡眠特征及其差异,为心理应激性失眠的治疗提供依据。方法:采用匹兹堡睡眠质量指数量表(PSQI)及睡眠自评量表(SRSS)对43例心理应激性失眠患者的主观睡眠质量进行评估,同时通过多导睡眠监测(PSG)对患者的客观睡眠质量进行评定。结果:心理应激性失眠患者PSQI和SRSS分别为(14.0±3.2)分和(32.4±5.0)分,均显著高于我国常模7分和(22.1±5.5)分。与PSG睡眠参数常模比较,总睡眠时间(TST)、睡眠潜伏期(SL)、各睡眠时相、睡眠结构短觉醒次数均在正常范围内,但长觉醒次数(9.7±4.7)次较常模5次明显增多;主观SL(55.7±52.7)min,较客观SL(18.8±20.0)min显著为长(t=-4.619,P=0.001);主观TST(306.3±113.1)min,较客观TST(376.8±46.7)min显著为短(t=-3.764,P<0.001)。结论:心理应激性失眠患者存在睡眠状态感知不良,具有高估SL,低估TST的特点。     

失眠症患者睡眠质量的主观评估与多导睡眠图参数对比分析

目的 探讨失眠症患者对睡眠质量的主观评估,并通过对多导睡眠图(PSG)睡眠参数的定量分析,对失眠症患者的睡眠状况进行客观评估,进一步将二者进行对比分析.方法 对失眠症患者和健康人各100例运用匹兹堡睡眠质量指数问卷(PSQI)进行评定,并分别进行多导睡眠图的整夜睡眠描记,次日晨起后询问夜间睡眠情况.结果 失眠症组PSQI各成分得分及总分均高于对照组,差异有统计学意义(P＜0.01).与对照组相比,失眠症组的睡眠潜伏期(min)延长(失眠症组43.69±11.54,对照组16.01±10.44)、总睡眠时间(min)减少(失眠症组314.65±91.89,对照组446.41±77.81)、睡眠效率降低(失眠症组64.51%±18.59%,对照组91.32%±3.58%)、快眼动睡眠时间(min)减少(失眠症组33.26±15.61,对照组93.21±21.63),差异有统计学意义(P＜0.01).失眠症组对总睡眠时间的评估较PSG检测值显著减低、对睡眠潜伏期的评估较PSG检测值显著增高,自我评估与实际睡眠情况不一致.结论 失眠症患者睡眠质量较差.失眠症患者的PSG各睡眠参数有特征性的改变,利用PSG检查发现失眠症患者对失眠情况的主客观评估不一致,存在过高估价睡眠潜伏期和过低估价睡眠时间的倾向.     

超低频经颅磁刺激治疗缺血性脑卒中患者失眠的 临床疗效

目的 观察超低频经颅磁刺激（ILF-TMS）治疗缺血性脑卒中后失眠的临床疗效。方法 选 取60例缺血性脑卒中后失眠患者，按照随机数字表法将其分为常规治疗组（30例）和ILF-TMS治疗组（30 例）， 两组患者均口服酒石酸唑吡坦片，每晚睡前口服5 mg。ILF-TMS 治疗组在此基础上加用ILF-TMS 治疗， 常规治疗组每日接受伪ILF-TMS治疗，患者治疗前和治疗后（10 d 后）均给予匹兹堡睡眠质量指数（PSQI） 和多导睡眠图（PSG）相关参数评价睡眠情况，PSG 评价参数主要包括总睡眠时间（TST）、睡眠潜伏期（SL） 以及睡眠NREM（S1、S2、S3 +S4 ）、REM 的睡眠结构比。结果 治疗前两组患者PSQI、TST、SL、S1、S2、 S3+S4、REM 评分比较，差异无统计学意义（P＞ 0.05）。常规治疗组患者10 d 后PQSI评分较前明显降低 ［（18.03±1.37）分比（12.60±2.43）分］；TST 较前明显延长［（251.42±42.42）min 比（288.80±40.32）min］； SL 较治疗前有显著缩短［（39.60±17.62）min 比（34.40±14.89）min］，差异均有统计学意义（P ＜ 0.05），睡 眠结构S1、S2、S3+S4、REM 较治疗前均无明显变化。ILF-TMS 治疗组患者10 d 后PQSI评分较前明显降 低［（18.17±1.29）分比（10.40±2.13）分］；TST较前明显延长［（241.50±51.75）min 比（353.45±52.20）min］； SL 较治疗前有显著缩短［（40.80±17.47）min 比（26.60±13.22）min］，差异均有统计学意义（P ＜ 0.05），而 睡眠结构S1、S2、S3+S4、REM 较治疗前均无明显变化。与常规治疗组比较，ILF-TMS 治疗组患者治疗后 PSQI评分更低，TST更长，SL更短，差异均有统计学意义（P＜ 0.05）。结论 ILF-TMS 可以改善缺血性脑 卒中后失眠症状，短期（10 d）ILF-TMS 治疗尚不能改善缺血性脑卒中后失眠患者的睡眠结构。     

酒石酸唑吡坦片治疗急性脑卒中后失眠的临床疗效

目的分析酒石酸唑吡坦片在急性脑卒中后失眠治疗中的应用价值。方法选取我院2014-07—2016-08收治的急性脑卒中后失眠的90例患者,随机分为2组,对照组44例给予常规治疗,观察组46例给予酒石酸唑吡坦片治疗,比较2组患者治疗效果及不良反应。结果对照组治疗总有效率70.45%,观察组93.48%,差异有统计学意义(P0.05);治疗后,观察组阿森斯失眠量表评分、MESSS评分均显著低于对照组,Barthel指数显著高于对照组(P0.05)。对照组无不良反应,观察组不良反应发生率为4.35%,2组比较差异无统计学意义(P0.05)。结论将酒石酸唑吡坦片用于急性脑卒中后失眠的临床治疗,可有效改善患者失眠症状,提高患者的日常生活能力,且不会增加不良反应的发生风险,值得临床推广。     

米氮平治疗抑郁症患者的早期睡眠多导图改变

目的 通过睡眠多导图(PSG)客观评价米氮平治疗早期抑郁症伴失眠患者睡眠结构的影响及改善睡眠的疗效.方法 入组25例抑郁症伴失眠患者,在进行基线量表评估和PSG监测后开始服药,米氮平起始剂量每天15 mg,3 d后增至每天30 mg,睡前1 h服用;7 d后再次进行量表评估和PSG监测;观察治疗后失眠、焦虑抑郁症状、PSG的变化.结果 25例抑郁症伴失眠患者在米氮平治疗7 d后分别进行量表评分,显示各量表减分值分别为Athens失眠量表(7.92±3.86,t=10.255,P=0.000)、汉密尔顿抑郁量表(9.80±4.41,t=12.132,P=0.000)、汉密尔顿焦虑量表(6.84±5.57,t=6.137,P=0.000);PSG结果显示治疗总睡眠时间(min)延长(402.46±80.75,t=-2.990,P=0.006)、睡眠觉醒时间(min)缩短(80.38±48.02,t=2.972,P=0.007)、睡眠效率明显提高(76.17%±10.65%,t=-2.750,P=0.011),深睡眠比例显著增加(19.66%±11.43%,t=3.236,P=0.004),而入睡潜伏期和睡眠中清醒次数、快速眼动睡眠潜伏期、比例及出现次数无差异.结论 单一使用米氮平治疗抑郁症伴失眠患者起效快,同时能增加总睡眠时间、缩短睡眠觉醒时间、提高睡眠效率、增加深睡眠比例等,达到有效改善失眠.     

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.