佐匹克隆与阿普唑仑治疗伴睡眠障碍老年期痴呆患者的多导睡眠图观察

目的:观察佐匹克隆与阿普唑仑对照治疗伴睡眠障碍的老年期痴呆患者的临床疗效与不良反应。方法:将72例老年期痴呆睡眠障碍的患者以随机数字表法分为2组,研究组39例,每晚睡前15 min口服佐匹克隆片7.5 mg/d;对照组33例,每晚睡前15 min口服阿普唑仑片0.4 mg/d,两组疗程均为3周;采用多导睡眠图评价疗效,不良反应量表(TESS)评价不良反应。结果:研究组与对照组治疗后各睡眠参数较治疗前均有好转(P0.01);两组间比较差异无统计学意义(P0.05)。治疗过程中佐匹克隆组除口腔苦味感外的不良反应发生率(20.51%)低于对照组(60.61%,χ2=11.39,P0.01),佐匹克隆组口腔苦味感发生率(100%)高于阿普唑伦组(3.03%,P0.01)。结论:佐匹克隆与阿普唑仑能够缩短伴睡眠障碍的老年期痴呆患者入睡时间,提高睡眠的质量,疗效相当。但佐匹克隆除口腔苦味感明显外,其他不良反应较少。     

右佐匹克隆替换对长期服用苯二氮(卓)类药的慢性精神分裂症患者睡眠的影响

目的:探讨右佐匹克隆替换对长期服用苯二氮(卓)类药的慢性精神分裂症患者睡眠的影响.方法:采用开放式设计,依照医师和患者协商结果将80例长期服用苯二氮(卓)类药的慢性精神分裂症住院患者分成右佐匹克隆组(41例,在1周内逐渐换用右佐匹克隆3 mg/d)和对照组(39例,服用的苯二氮(卓)类药品及剂量不变);观察4周.替换前后分别给予匹兹堡睡眠质量指数量表(PSQI)、阳性和阴性症状量表(PANSS)及治疗中出现的症状量表(TESS)评定及比较. 结果:替换前后两组间PSQI评分差异无统计学意义;替换后右佐匹克隆组PSQI总分及睡眠质量、入睡时间、睡眠时间和日间功能障碍评分明显低于替换前(F =31.69,7.03,4.79,10.58;P＜0.05或P＜0.01);替换前后两组PANSS评分比较差异无统计学意义;右佐匹克隆组药物不良反应发生率(6.25％)低于对照组(23.75％),差异有统计学意义(P＜0.05). 结论:应用右佐匹克隆替换,可改善长期服用的苯二氮(卓)类药慢性精神分裂症患者的睡眠质量和日间功能;安全可行.     

右佐匹克隆对抑郁症伴失眠患者日间功能的影响

目的:探讨右佐匹克隆对抑郁症伴失眠患者日间功能的影响. 方法:将抑郁症伴失眠患者127例随机分为右佐匹克隆组66例和阿普唑仑组61例,分别给予右佐匹克隆和阿普唑仑观察2周.2周后采用日间功能障碍量表评定疗效及治疗中出现的症状量表(TESS)评定不良反应. 结果:治疗2周,日间功能障碍评定量表中除困倦项两组差异无统计学意义外(t=0.84,P＞0.05),其他项如白天乏力、打盹、精神差、反应迟钝、共济失调、判断力下降、意识模糊、精神紊乱上差异均有统计学意义(t分别=2.89,3.43,6.61,10.03,3.09,9.57,11.14,4.49;P均＜0.01).两组不良反应仅在嗜睡和头昏上差异有统计学意义(x2 =6.67,3.89;P ＜0.01或P＜0.05). 结论:右佐匹克隆对抑郁症伴失眠患者日间功能的影响以及不良反应显著低于阿普唑仑.     

右佐匹克隆片联合奥氮平对精神分裂症患者睡眠的影响

目的探讨右佐匹克隆片联合奥氮平对精神分裂症患者睡眠的影响。方法选取于笔者医院就诊的有睡眠障碍的精神分裂症患者60例为患者组,按照随机数字表法分为联合组和单药组,各30例。单药组给予右佐匹克隆片3mg/d,睡前30min服用,联合组在次基础上给予奥氮平2.5mg/d,睡前30min服用。连续服用4周。观察患者治疗前和治疗4周后多导睡眠图(PSG)监测描记结果,并与60名健康自愿者进行对比。结果患者组睡眠总时间、REM睡眠时间、S2时间及SWS时间均短于正常组,觉醒时间、S1时间均长于正常组(P0.05);治疗后两组睡眠总时间、REM睡眠时间、S2时间及SWS时间均增长,联合组增长程度高于单药组,两组觉醒时间、S2时间均缩短,联合组缩短程度高于单药组(P0.05);联合组总有效率高于单药组(P0.05);联合组体重增加率高于单药组,差异有统计学意义(P0.05)。结论右佐匹克隆片联合奥氮平治疗精神分裂症效果显著,能增加患者睡眠总时间,改善睡眠质量,且安全性较高,值得临床作进一步推广。     

银丹心脑通软胶囊联合佐匹克隆治疗老年慢性失眠的临床疗效

目的 观察银丹心脑通软胶囊和佐匹克隆联用治疗老年慢性失眠的临床疗效,以期为老年慢性失眠的临床治疗提供一种安全有效的措施. 方法 将成都军区昆明总医院自2010年1月至2011年8月收治的92例老年慢性失眠患者按随机数字表法分为银丹心脑通软胶囊组(30例)、佐匹克隆组(31例)和联合治疗组(3l例),并给予相应处理,疗程共持续4周.分别在治疗前、治疗后2周、治疗后4周时采用匹兹堡睡眠质量指数(PSQI)、多导睡眠图检查对患者的睡眠质量进行评价. 结果 治疗2周后3组PSQI均较治疗前有改善,特别是治疗4周后3组PSQI均较治疗前有明显改善,其中联合治疗组PSQI明显优于佐匹克隆组和银丹心脑通软胶囊组,比较差异均有统计学意义(P＜0.05).治疗2周后3组患者中有NREM睡眠期S3期、S4期的例数明显上升,尤其是在治疗4周后,3组患者中有NREM睡眠期S3期、S4期的例数更进一步上升,其中联合治疗组治疗效果最好,大部分患者基本能恢复睡眠连续性.治疗4周后3组治疗措施均能使患者的总睡眠时间较治疗前明显延长,且REM睡眠期、NREM睡眠期S3期、S4期(慢波睡眠期)所占比例也较治疗前明显提高,NREM睡眠期S1期、S2期(浅睡眠期)所占比例较治疗前明显缩短,差异均有统计学意义(P＜0.05),其中联合治疗组的总睡眠时间、REM睡眠期、NREM睡眠期S3期、S4期较佐匹克隆组和银丹心脑通软胶囊组明显升高,NREM睡眠期S1期、S2期所占比例明显降低.另外,银丹心脑通软胶囊单独使用同样可以改善患者睡眠质量,只是起效较慢. 结论 银丹心脑通软胶囊和佐匹克隆联用是一种可供选择的较好的治疗老年慢性失眠的方案.     

右佐匹克隆治疗卒中后失眠症的效果分析

目的分析右佐匹克隆治疗卒中后失眠症的临床有效性。方法我院2015-01—2016-06收治的卒中后失眠症患者56例,根据随机数字表法分为2组各28例。所有患者用药前1周停用各种催眠、镇静药物,作为洗脱期。阿普唑仑组给予阿普唑仑治疗,每晚睡前40min服用0.4mg,1周后可根据情况调整为0.8mg,治疗4周。右佐匹克隆组给予右佐匹克隆治疗,每晚睡前40min服用2mg,1周后可根据情况调整为1mg或3mg,治疗4周。2组治疗期间均给予复方丹参片、尼莫地平、阿司匹林肠溶片等治疗,合并高血压者可给予硝苯地平缓释片治疗。对比2组治疗前后睡眠质量指数、神经功能缺损情况,以及总有效率、药物不良反应发生率,比较2组治疗前后SCL-90量表中各项心理指标。结果右佐匹克隆组失眠症总有效率明显高于阿普唑仑组,差异有统计学意义(P0.05)。右佐匹克隆组药物不良反应发生率明显低于阿普唑仑组(P0.05)。2组治疗前睡眠质量指数、神经功能缺损情况无显著差异(P0.05);经治疗,右佐匹克隆组睡眠质量指数、神经功能缺损情况均明显优于阿普唑仑组(P0.05)。2组治疗前SCL-90量表中各项心理指标无显著差异(P0.05);经治疗,右佐匹克隆组SCL-90量表中各项心理指标均明显优于阿普唑仑组(P0.05)。结论右佐匹克隆治疗卒中后失眠症的临床有效性高,可快速发挥药效,有效改善患者神经功能及焦虑、抑郁、恐惧等各种不良心理状态,提升睡眠质量,且不良反应更少,安全性高,值得临床推广。     

右佐匹克隆与阿普唑仑辅助治疗抑郁症睡眠障碍对照研究

目的探讨右佐匹克隆辅助治疗抑郁症睡眠障碍的疗效及安全性。方法选取符合《中国精神障碍分类与诊断标准第3版》（CCMD-3）抑郁症诊断标准的门诊或住院抑郁症伴失眠患者,按随机数字表分为右佐匹克隆组和阿普唑仑组,二组均观察2周。两组患者均在治疗前、治疗后第2周末采用匹兹堡睡眠质量指数（Pittsburgh Sleep Quality Index,PSQI）评定;在治疗前、治疗后第2周末采用汉密尔顿抑郁量1表-24（Hamihon Depression Rating Scale,HAMD-24）评定;在治疗后第1、2周末采用副反应量表（Treatment Emergent Symptom Scale,TESS）评定。以PSQi的减分率判定疗效。结果右佐匹克隆组和阿普唑仑组治疗后PSQI评分经t检验（t=-3．58,P〉0．05）差异无统计学意义;但两组各因子分比较,治疗后日间功能障碍因子分右佐匹克隆组显著低于阿普唑仑组（t=5．18,P〈0．05）。右佐匹克隆组嗜睡、头昏各1例,阿普唑仑组嗜睡10例、头昏6例,两组经x。检验差异均有统计学意义（X^2=6．67、3．89,P〈0．01或0．05）;结论右佐匹克隆辅助治疗抑郁症睡眠障碍疗效显著,与阿普唑仑相比疗效没有差异。对日间功能的影响显著低于阿普唑仑,不良反应发生率少于阿普唑仑。     

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.     

右佐匹克隆联合米氮平对慢性失眠障碍的疗效分析

目的探讨右佐匹克隆联合米氮平对慢性失眠障碍患者的临床疗效。方法按随机数字法将82例慢性失眠患者分成研究组42例,对照组40例,对照组给予口服右佐匹克隆(1.5～3mg/d),研究组在对照组的基础上联合口服米氮平(15～30mg/d)治疗,在治疗前,治疗后1、2、4周分别对两组研究对象进行匹兹堡睡眠指数(PSQI)、不良反应量表(TESS)的评定;并以PSQI量表减分率进行有效率评定。同时在治疗前、治疗后4周对两组研究对象进行整夜睡眠呼吸监测(PSG),通过PSG睡眠指标观察对比两组治疗前后的变化。结果治疗后两组PSQI总分较治疗前均逐步下降,治疗4周后研究组有效率92.9%,对照组80%,差异具有统计学意义(χ2=11.296,P=0.010);研究组PSQI总分明显低于对照组,差异有统计学意义(P0. 05)。经治疗两组均出现TST延长,ATA、AT明显减少,SL明显缩短,SE明显提高,REM潜伏期缩短,REM、N2时间延长,与治疗前差异均有统计学意义(P0. 05);其中研究组对比治疗前还有N3时间及比例的明显增加,差异有统计学意义(P0. 05);治疗后研究组在TST、N2、N3时间及N3比例的增加,SL、ATA、AT的减少,SE的提高方面均较对照组明显,差异具有统计学意义(P0. 05)。结论右佐匹克隆联合米氮平对慢性失眠的治疗较单一使用右佐匹克隆疗效要好;安全性高,能加深睡眠,减少觉醒。     

脑电生物反馈辅助治疗老年失眠症的疗效观察

目的 研究脑电生物反馈疗法辅助治疗老年失眠症的效果.方法 将67例老年失眠症患者随机分为研究组（34例,使用右佐匹克隆合并脑电生物反馈治疗8周）和对照组（33例,单用右佐匹克隆治疗8周）.采用多导睡眠（PSG）监测技术和匹兹堡睡眠质量指数量表（PSQI）评定疗效.结果 治疗后第8周末,两组多导睡眠脑电图中实际睡眠总时间、睡眠效率、睡眠维持率、睡眠潜伏期、REM（快速眼动）潜伏期、REM睡眠比例、夜间觉醒次数、觉醒总时间较治疗前显著改善（P＜0.05）;且研究组睡眠脑电图各项数据与对照组比较差异有统计学意义（P＜0.05）.两组PSQI评分均低于各自治疗前（P＜0.05）,研究组PSQI评分显著低于对照组（P＜0.05）.结论 脑电生物反馈疗法辅助治疗老年失眠症有较好的效果.     

An evaluation of the efficacy and safety of eszopiclone over 12 months in patients with chronic primary insomnia

BACKGROUND AND PURPOSE: A double-blind placebo-controlled study of eszopiclone found significant, sustained improvement in sleep and daytime function. The 6-month open-label extension phase is described herein. PATIENTS AND METHODS: Adults (21-64) with primary insomnia who reported sleep duration <6.5 h/night or sleep latency >30 min/night were included. Patient-reported endpoints included sleep and daytime function. Safety and compliance were assessed at monthly clinic visits. The final double-blind month was used as the baseline for efficacy analyses of the open-label period. RESULTS: Patients who were initially randomized to double-blind placebo and then switched to open-label eszopiclone (n=111) significantly reported the following: (1) decreased sleep latency, wake time after sleep onset, and number of awakenings; (2) increased total sleep time and sleep quality; and (3) improved ratings of daytime ability to function, alertness and sense of physical well-being compared to baseline (P5% of patients. CONCLUSIONS: The significant improvements in sleep and daytime function were evident in those switched from double-blind placebo to 6 months of open-label eszopiclone therapy and were sustained during the 6 months of open-label treatment for those receiving prior double-blind eszopiclone. During 12 months of nightly treatment, eszopiclone 3mg was well tolerated; tolerance was not observed.     

A pilot study evaluating acute use of eszopiclone in patients with mild to moderate obstructive sleep apnea syndrome

OBJECTIVE: To evaluate the effects of eszopiclone on measures of respiration and sleep using polysomnography in patients with mild to moderate obstructive sleep apnea syndrome (OSAS). METHODS: This double-blind, randomized crossover study included patients (35-64 years) with mild-to-moderate OSAS [apnea and hypopnea index (AHI) range 10 and 40]. Patients received either eszopiclone 3mg or placebo for two consecutive nights, with a 5-7 day washout between treatments. Continuous positive airway pressure (CPAP) was not allowed on nights in the sleep laboratory. RESULTS: The primary endpoint, mean total AHI, was not significantly different from placebo (16.5 with placebo and 16.7 with eszopiclone; 90% confidence interval (CI) -1.7, 1.9). No significant differences in total arousals, respiratory arousals, duration of apnea and hypopnea episodes, or oxygen saturation were noted. Significant differences in spontaneous arousals (13.6 versus 11.4 for placebo and eszopiclone, respectively; 90% CI -3.7, -0.7), sleep efficiency (85.1% and 88.4%; p=0.0075), wake time after sleep onset (61.8 and 48.1 min; p=0.0125), and wake time during sleep (55.9 and 43.2 min; p=0.013) were noted after eszopiclone treatment. Eszopiclone was well tolerated. CONCLUSIONS: In this pilot study, eszopiclone did not worsen AHI, and it improved sleep maintenance and efficiency. Further study is warranted to determine whether eszopiclone could improve CPAP compliance or next-day function in patients with OSAS.     

右旋佐匹克隆治疗失眠症随机双盲对照研究

目的：评价右旋佐匹克隆治疗失眠症患者的疗效和安全性。方法：257例失眠症患者随机分为研究组（131例）和对照组（126例）。研究组给予右旋佐匹克隆和佐匹克隆模拟剂,对照组给予佐匹克隆及右旋佐匹克隆模拟剂,治疗2周。采用睡眠障碍量表（SDRS）评定疗效。基线和终点时进行血生化、血常规、尿常规以及心电图检查,以评价安全性。结果：两组的SDRS评分在治疗2周末较基线均明显下降（P〈0．01）,而两组间比较差异无统计学意义（P〉0．05）。治疗2周,研究组和对照组在有效率（71．0％,69．8％）方面相当（P〉0．05）,1周后随访,两组的症状反跳率（2．0％,3．1％）无显著差异。研究中未出现严重不良事件,两组间不良事件的总发生率差异无统计学意义（P〉0．05）。结论：右旋佐匹克隆治疗失眠安全有效。     

失眠伴抑郁与单纯失眠患者失眠认知行为治疗的疗效分析

目的分析失眠认知行为疗法(cognitive behavioral therapy on insomnia,CBT-i)对失眠伴抑郁患者以及单纯失眠患者的疗效。方法71例符合失眠症诊断的患者,根据贝克抑郁量表(Beck Depression Inventory,BDI)得分分为单纯失眠组(<14分,33例)和失眠伴抑郁组(≥14分,38例)。2组患者每天填写睡眠日记,并给予8周标准的CBT-i治疗,在治疗前(基线)、治疗第4周、治疗第8周、治疗结束后4周(第3个月)、治疗结束后16周(第6个月)采用匹兹堡睡眠质量指数(Pittsburgh Sleep Quality Index,PSQI)、失眠严重程度指数(Insomnia Severity Index,ISI)、BDI、贝克焦虑量表(Beck Anxiety Inventory,BAI)、SF-36健康调查简表对2组患者睡眠质量、抑郁焦虑程度、个人健康状况等进行评估,采用独立样本t检验进行组间比较,采用重复测量方差分析进行各时间点组内比较。结果与基线时比较,单纯失眠组和失眠伴抑郁组第8周、第3个月和6个月随访时入睡潜伏期、睡眠效率、PSQI、ISI、BDI、BAI、SF-36组内比较差异均有统计学意义。失眠伴抑郁组较单纯失眠组在基线、第8周、第3个月和6个月随访时BAI(t=-6.340、-3.301、-3.511、-2.982)、SF-36(t=4.162、3.195、2.022、3.629)评分差异有统计学意义(P<0.01或0.05),2组ISI评分在第6个月随访时差异有统计学意义[(7.3±4.6)分与(4.7±3.4)分,t=-2.044,P=0.048]。2组入睡潜伏期和睡眠效率以及PSQI的评分在第8周、第3个月和6个月随访时与基线的变化量差异均无统计学意义;而2组BAI、BDI评分在第8周与第3个月和6个月随访时与基线的变化量差异有统计学意义。结论CBT-i对失眠伴抑郁患者和单纯失眠患者均有效,且可以缓解失眠伴抑郁患者的抑郁症状以及改善患者生活质量。     

帕金森病患者睡眠障碍的多导睡眠图、多次睡眠潜伏期试验分析

目的 使用多导睡眠图、多次睡眠潜伏期试验客观分析帕金森病(PD)患者睡眠障碍特征.方法 对26例临床确诊的PD患者(PD组)和31名无明显中枢神经系统疾病的对照者(对照组)行全夜可移动视频多导睡眠监测及次日多次睡眠潜伏期试验,分析比较2组患者睡眠结构及平均睡眠潜伏期、入睡期快速眼球运动(REM)睡眠(SOREMPs)、睡眠发作(Sas)情况.结果 PD组N2睡眠期百分比(32.8%±13.1%)、REM睡眠期百分比(8.6%±5.3%)、平均睡眠潜伏期[(9.6±4.4)min]较对照组[40.2%±9.1%、11.5%±5.1%、(15.7±3.1)min]明显降低(t=-2.515、-2.054、-6.164,P＜0.05),PD组醒觉指数[(41.8±32.1)次/h]较对照组[(28.6±11.0)次/h]明显升高(t=2.151,P＜0.05).PD患者中出现日间过度瞌睡(EDS)7例(7/26,26.9%),明显高于对照组(1/31,3.2%;×2=4.764,P＜0.05).多元逐步线性回归分析显示校正睡眠效率、呼吸暂停低通气指数、醒觉指数,PD患者平均睡眠潜伏期的缩短与年龄(β=-0.328)、左旋多巴等效剂量(β=-0.008)的增加呈线性相关(t=-2.829、-2.352,均P＜0.05).PD组有5例(5/26,19.2%)出现SOREMPs,3例(11.5%)出现Sas,而对照组均无出现SOREMPs和Sas.结论 PD患者睡眠结构改变和EDS较常见,虽然PD患者中Sas不多见,但临床医师需提高警惕.     

Betahistine in the treatment of Ménière’s disease

Eszopiclone is the S-isomer of racemic zopiclone, a cyclopyrrolone with sedative-hypnotic activity that has been available in Europe, Canada, and Latin America since 1987. Eszopiclone acts by binding to the GABA_A receptor. In contrast to the benzodiazepine (BZD) hypnotics, eszopiclone has more selectivity for certain subunits of the GABA_A receptor. Oral eszopiclone is rapidly absorbed and extensively distributed to body tissues including the brain. Peak plasma concentrations are attained 1.0–1.6 hours after a 3 mg dose, while the mean elimination half-life is 6 hours. The half-life increases with age to about 9.0 hours in patients 65 years or older. Eszopiclone’s pharmacokinetic (PK) profile is not substantially modified in patients suffering from renal failure or mild-to-moderate hepatic impairment, although patients with severe hepatic insufficiency should have a reduced dose. The subjective perception of improved sleep following eszopiclone 2 or 3 mg treatment has been demonstrated in randomized, double-blind, placebo-controlled studies of up to 6 months’ duration. In these studies the drug significantly reduced sleep onset latency (SOL), the number of awakenings, and wake time after sleep onset (WASO) whereas total sleep time (TST) and quality of sleep were increased in non-elderly and elderly subjects. Sleep laboratory studies of the effects of eszopiclone have confirmed the drug’s clinical efficacy in subjects with chronic primary insomnia. Eszopiclone, unlike BZD hypnotics, does not significantly alter values corresponding to slow wave sleep (SWS or stages 3 and 4) and rapid eye movement (REM) sleep. Rebound insomnia following withdrawal of eszopiclone has been examined in only one study. Discontinuation of the active treatment with 2 mg was followed by rebound insomnia in non-elderly subjects. Three-mg doses of eszopiclone administered for a period of up to 12 months was associated with a sustained beneficial effect on sleep induction and maintenance, with no occurrence of tolerance. The most common side-effects were unpleasant or bitter taste, headache, dyspepsia, pain, diarrhea, dry mouth, upper respiratory infection, urinary tract infection, dizziness, and accidental injury. New adverse events (withdrawal symptoms) including anxiety, abnormal dreams, hyperesthesia, nausea, and upset stomach were recorded in one study on the days following eszopiclone 2 or 3 mg discontinuation. Although dependence and abuse potential have not been formally assessed, unpublished data show that eszopiclone at doses of 6 and 12 mg produces euphoria effects similar to those of diazepam 20 mg in BZD drug addicts. In conclusion, available evidence tends to indicate that eszopiclone is effective and safe for the treatment of chronic primary insomnia in non-elderly and elderly subjects. Tolerance did not occur during active drug administration for a 12-month period. Thus eszopiclone can be efficacious not only during short- and intermediate-term administration but also in patients requiring prolonged regular drug usage.     

帕金森病患者记忆监测与情景记忆的相关研究

目的 研究帕金森病患者( Parkinson's disease,PD)对情景记忆监测情况,并进一步探讨PD患者情景记忆障碍的可能机制.方法 建立情景记忆知晓感(feeling of knowing-episodic memory,FOK-EM)判断的试验范式,对25例PD患者和25名年龄及教育程度相匹配的健康对照(HC)者进行研究.结果 与HC组的FOK-EM的回忆率(39.67％±6.11％)、再认率(58.42％±7.50％)以及FOK判断准确率(0.61 ±0.22)比较,PD患者组FOK-EM的回忆率(19.33％±5.10％)、再认率(45.93％±7.82％)以及FOK判断准确率(-0.18±0.46)显著降低,差异均有统计学意义(t=-4.833,P＜0.01;t=-2.497,P＜0.05;t=-5.986,P＜0.01);FOK-EM的肯定判断/正确再认成绩(20.47％±10.78％)以及肯定判断/错误再认成绩(即高估,29.53％±5.62％)与HC组的肯定判断/正确再认成绩(39.47％±9.47％)以及肯定判断/错误再认成绩(即高估,13.90％±5.50％)之间差异有统计学意义(t =3.564,P＜0.05;t=2.306,P＜0.05),且Stroop效应与FOK-EM的肯定判断/错误再认成绩呈正相关(r =0.640,P＜0.01).结论 PD患者的情景记忆监测受损,表现为对自身再认能力的高估.这种记忆监测受损与执行功能的损害相关,提示此机制可能是导致PD患者情景记忆障碍的重要因素.     

Eszopiclone co-administered with fluoxetine in patients with insomnia coexisting with major depressive disorder.

BACKGROUND: Insomnia and major depressive disorder (MDD) can coexist. This study evaluated the effect of adding eszopiclone to fluoxetine. METHODS: Patients who met DSM-IV criteria for both MDD and insomnia (n = 545) received morning fluoxetine and were randomized to nightly eszopiclone 3 mg (ESZ+FLX) or placebo (PBO+FLX) for 8 weeks. Subjective sleep and daytime function were assessed weekly. Depression was assessed with the 17-item Hamilton Rating Scale for Depression (HAM-D-17) and the Clinical Global Impression Improvement (CGI-I) and Severity items (CGI-S). RESULTS: Patients in the ESZ+FLX group had significantly decreased sleep latency, wake time after sleep onset (WASO), increased total sleep time (TST), sleep quality, and depth of sleep at all double-blind time points (all p < .05). Eszopiclone co-therapy also resulted in: significantly greater changes in HAM-D-17 scores at Week 4 (p = .01) with progressive improvement at Week 8 (p = .002); significantly improved CGI-I and CGI-S scores at all time points beyond Week 1 (p < .05); and significantly more responders (59% vs. 48%; p = .009) and remitters (42% vs. 33%; p = .03) at Week 8. Treatment was well tolerated, with similar adverse event and dropout rates. CONCLUSIONS: In this study, eszopiclone/fluoxetine co-therapy was relatively well tolerated and associated with rapid, substantial, and sustained sleep improvement, a faster onset of antidepressant response on the basis of CGI, and a greater magnitude of the antidepressant effect.     

Treatment of insomnia in Parkinson's disease: A controlled trial of eszopiclone and placebo

Parkinson's disease (PD) is a common neurodegenerative disease affecting up to 1 million individuals in the United States. Sleep disturbances, typically in sleep maintenance, are found in up to 88% of these individuals and are associated with a variety of poor outcomes. Despite being common and important, there are few data to guide clinical care. We conducted a 6‐week, randomized, controlled trial of eszopiclone and placebo in 30 patients with PD and insomnia. Patients with other primary sleep disorders (PSG defined) were excluded. The primary outcome was total sleep time (TST), and secondary measures included wake after sleep onset (WASO), number of awakenings, and quality of sleep, among others. The groups did not significantly differ on TST, but significant differences, favoring eszopiclone, did emerge in number of awakenings (P = 0.035), quality of sleep (P = 0.018), and in physician‐rated CGI improvement (P = 0.035). There was also a trend toward significance in WASO (P = 0.071). There were no significant differences between groups in measures of daytime functioning. The drug was well tolerated, with 33% of patients on eszopiclone and 27% of patients on placebo reporting adverse events. Although modest in size, this is the first controlled study of the treatment of insomnia in patients with PD. Eszopiclone did not increase TST significantly but was superior to placebo in improving quality of sleep and some measures of sleep maintenance, which is the most common sleep difficulty experienced by patients with PD. Definitive trials of the treatment of sleep disorders in this population are warranted. © 2010 Movement Disorder Society