右佐匹克隆治疗适应性失眠患者的有效性及对睡眠结构的影响

目的 使用临床评估量表和多导睡眠检测技术研究镇静催眠药物右佐匹克隆治疗适应性失眠患者的有效性及其对睡眠结构的影响.方法 采用治疗前后自身对照设计,比较适应性失眠患者使用右佐匹克隆治疗前后的睡眠结构变化及评估其药物疗效.纳入对象为上海长征医院神经内科睡眠障碍门诊中符合诊断标准的患者共32例,其中女性20例,男性12例,平均年龄36.2岁.患者接受连续3d药物治疗(每次3 mg右佐匹克隆),观察指标为服药前及服药第3天睡眠相关的主观与客观检查(量表评估和多导睡眠图检查),记录并分析患者的总卧床时间、总睡眠时间、觉醒时间、入睡潜伏期、睡眠效率、非快速眼动(NREM)睡眠各期时间百分比、快速眼动(REM)睡眠时间百分比等,并使用失眠严重程度指数量表( ISI)和MMSE评价患者的失眠严重程度和药物对于患者日间认知功能的影响.结果 右佐匹克隆能够缩短入睡潜伏期[治疗前( 52.92±11.71) min,治疗后(28.2±10.11)min;t=-4.376,P＜0.01]、延长总睡眠时间[治疗前(365.22±30.13) min,治疗后(429.18±26.93)min;t=4.102,P＜0.01]、减少觉醒次数[治疗前(5.00±1.92)次,治疗后(2.73±0.91)次;t=-4.592,P＜0.01]、提高睡眠效率(治疗前72.69％±6.32％,治疗后82.67％±4.16％;t=3.371,P＜0.01)、缩短觉醒时间[治疗前(88.51±17.48) min,治疗后(65.93±21.10) min;t=-5.863,P＜0.01]、降低NREM 1期时间百分比(治疗前12.54％±2.10％,治疗后7.30％±2.90％;t=-3.155,P＜0.01)、增加慢波睡眠时间百分比(治疗前8.03％±5.37％,治疗后9.31％±5.29％;t=4.228,P＜0.01),而对NREM 2期睡眠时间百分比、REM睡眠时间百分比无明显影响.右佐匹克隆能够提高患者对睡眠质量的主观评价(ISI评分降低,t=-2.551,P＜0.05),且服药后对患者次日清晨的认知功能无明显影响(MMSE评分未见降低).结论 右佐匹克隆能够正性调节急性失眠患者的睡眠结构,提高患者的主观睡眠质量,对日间认知功能无明显影响,安全性好.     

经颅直流电刺激联合认知行为治疗对产后抑郁症的作用

目的:探索经颅直流电刺激(tDCS)联合认知行为治疗(CBT)对轻中度产后抑郁症(PPD)的作用。方法:采用随机数字表法将62例PPD患者随机分为对照组(CBT+伪tDCS)和观察组(CBT+tDCS),疗程4周。治疗前、治疗后第2、4周时采用9条目患者健康问卷(PHQ-9)、7条目焦虑问卷(GAD-7)评估患者的抑郁、焦虑情况;采用匹兹堡睡眠质量指数(PSQI)评估患者睡眠状况。结果:治疗前两组PHQ-9、GAD-7及PSQI评分比较差异无统计学意义;治疗后两组PHQ-9、GAD-7及PSQI评分明显降低(P0.05或P0.01);且观察组各项评分明显低于对照组(P均0.05)。结论:CBT能够改善轻中度PPD患者抑郁焦虑情绪及睡眠质量;tDCS联合CBT作用更佳。     

精神障碍患者自杀意念与失眠关系研究

目的探讨精神障碍患者中自杀意念与失眠的关系。方法选取559例住院精神障碍患者,采用Beck自杀意念量表评估自杀情况,以ICD-10中失眠症诊断标准诊断失眠症,采用匹茨堡睡眠质量指数量表(Pittsburgh sleep quality index,PSQI)评估睡眠质量。分析有无自杀意念精神障碍患者失眠症发生情况,及失眠和自杀意念的相关性。结果受试者中32例有自杀意念。自杀意念组与非自杀意念组失眠症的发生率差异有统计学意义(31.3%vs.10.1%,χ~2=13.55,P0.01);自杀意念组PSQI评分高于非自杀意念组(9.16±4.75 vs.5.56±3.71,t=5.24,P0.01)。多因素logistics回归分析示PSQI评分与自杀意念相关联(OR=1.21,95%CI:1.12~1.32,P0.01)。结论精神障碍患者自杀意念与失眠相关。     

盐酸氟西汀联合利培酮治疗难治性抑郁症的效果及对患者睡眠质量的影响

目的探讨盐酸氟西汀联合利培酮治疗难治性抑郁症临床效果及对患者睡眠质量的影响,为难治性抑郁症的治疗提供参考。方法选取2015年1月-2016年10月就诊于新疆维吾尔自治区人民医院符合《国际疾病分类(第10版)》(ICD-10)诊断标准的92例难治性抑郁症患者,采用随机数字表法分为盐酸氟西汀组(对照组)和盐酸氟西汀联合利培酮组(观察组)各46例,疗程8周。于治疗前和治疗8周后,采用汉密尔顿抑郁量表17项版(HAMD-17)评定疗效,采用匹兹堡睡眠指数量表(PSQI)评定睡眠质量,采用自制不良反应记录表记录药物治疗过程中不良反应发生情况。结果治疗8周后,观察组总有效率高于对照组(93.5%vs.78.3%,χ~2=4.39,P0.05),观察组HAMD-17评分低于对照组[(13.2±2.8)分vs.(16.3±3.4)分,t=4.77,P0.01],PSQI评分较对照组低[(10.2±1.2)分vs.(12.1±1.4)分,t=6.99,P0.01]。两组不良反应发生率比较差异无统计学意义(6.5%vs.13.0%,χ~2=0.49,P=0.48)。结论单用盐酸氟西汀与盐酸氟西汀联合利培酮均可改善难治性抑郁症患者的临床症状及睡眠质量,但联合用药较单用盐酸氟西汀效果更好,二者安全性相当。     

认知-行为疗法及结合药物治疗原发性失眠的对照研究

目的了解认知-行为疗法在原发性失眠患者中的治疗作用。方法 99例原发性失眠患者随机分成3组:认知行为治疗组、药物治疗组和联合治疗组。分别使用匹兹堡睡眠质量指数(PSQI)评价认知-行为疗法、药物疗法(唑吡坦10mg)及认知-行为疗法结合药物递减疗法(联合治疗)治疗原发性失眠症患者99例的疗效。结果联合治疗组及药物治疗组在治疗第1周较认知-行为治疗组PSQI值明显下降(P0.01);联合治疗组与药物治疗组PSQI相比差异无统计学意义(P0.05);治疗第6周3组PSQI差异无统计学意义(P0.05);治疗3个月时联合治疗组与认知-行为治疗组较药物治疗组PSQI明显下降(P0.01),联合治疗组与认知-行为治疗组PSQI差异无统计学意义(P0.05)。联合治疗组不同时间点PSQI比较差异有统计学意义(P0.01);药物治疗组治疗第1周及治疗第6周与治疗前PSQI比较明显下降(P0.01),治疗第6周与治疗3个月时PSQI比较差异无统计学意义(P0.05);单纯认知行为治疗组在治疗前与治疗第1周PSQI比较差异无统计学意义(P0.05),与治疗第6周及3个月PSQI明显下降(P0.01)。结论认知-行为疗法结合非苯二氮卓艹类安眠药物治疗失眠,起效快,与认知-行为疗法治疗同样具有显著稳定持久的远期效果。     

失眠症患者的睡眠行为、应付方式及心理控制源的调查研究

目的　探讨失眠症患者的睡眠行为、应付方式及其心理控制源。方法　采用睡眠行为特征量表、应付方式问卷及内在-外在心理控制源量表对68例失眠症患者(失眠症组)和68名睡眠正常者(对照组)进行了测评,并将测评结果加以比较。结果　①失眠症组对睡眠的不合理信念、非功能性睡眠行为和夜间焦虑3个因子评分均明显高于对照组(t=6 07、7 99、17 98,P<0 01),而睡眠效率则明显低于对照组(t=15. 65,P<0.01);②失眠症组解决问题评分明显低于对照组(t=4 .41,P<0 .01),而自责评分则明显高于对照组(t=3 .13,P<0 .01);③失眠症组I-E量表评分明显高于对照组(t=19. 21,P<0. 01)。结论　失眠症患者存在对睡眠的不合理信念、非功能性睡眠行为和夜间焦虑;解决问题能力低,心理控制源为外控。     

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.     

慢性失眠患者血清神经营养因子改变及其与睡眠质量和认知功能的关系

目的探讨慢性失眠患者血清脑源性神经营养因子(BDNF)和胶质源性神经营养因子(GDNF)水平的变化及其与睡眠质量和认知功能间的关系。方法纳入2017年5月至2018年7月安徽医科大学附属巢湖医院睡眠障碍科就诊的慢性失眠患者57例,以同期本院健康体检中心的30名健康体检者作为对照。采用匹兹堡睡眠质量指数(PSQI)评估受试者的失眠程度(部分慢性失眠患者接受整夜多导睡眠监测),采用蒙特利尔认知评估量表(MoCA)评估总体认知功能,采用九盒迷宫评估特殊记忆功能,ELISA检测受试者的血清BDNF和GDNF水平。结果慢性失眠患者的PSQI得分显著高于对照组[慢性失眠组(14.0±2.2)分,对照组(3.9±1.1)分;t=28.093,P<0.01],MoCA评分显著低于对照组[慢性失眠组(24.5±3.6)分,对照组(26.5±0.9)分;t=-2.985,P<0.01],同时物体工作[慢性失眠组1.0(0,1.0),对照组0(0,0.3)]、空间工作[慢性失眠组3.0(2.0,4.0),对照组1.0(1.0,2.0)]、物体再认记忆[慢性失眠组0(0,0),对照组0(0,0)]错误数高于对照组(Z=-2.896、-5.007、-2.306,均P<0.05)。慢性失眠患者血清BDNF[慢性失眠组(19.48±7.50)ng/ml,对照组(46.49±13.33)ng/ml]和GDNF[慢性失眠组(32.76±14.04)pg/ml,对照组(59.63±20.30)pg/ml]水平显著低于对照组(t=-10.274、-7.240,均P<0.01),与PSQI得分呈负相关(r=-0.293、-0.320,均P<0.05),与MoCA评分呈正相关(r=0.331、0.295,均P<0.05)。BDNF还与病程和空间工作记忆错误数呈负相关(r=-0.319、-0.393,均P<0.05),GDNF与多导睡眠监测中总睡眠时间呈正相关(r=0.520,P<0.05)。结论慢性失眠患者的血清BDNF和GDNF水平较正常人降低,并与其睡眠质量和认知功能损害相关。     

认知行为治疗联合药物治疗与单纯药物治疗强迫障碍患者的随机对照研究北大核心CSCD

目的比较单用SSRIs与SSRIs合并认知行为治疗（cognitivebehavioraltherapy,CBT）强迫障碍患者的临床疗效。方法选取符合DSM—IV中强迫障碍诊断标准的门诊患者共80例,采用随机数字表法分为单用SSRIs治疗组f简称药物治疗组,n=40）和SSRIs合并CBT组（简称联合治疗组,n=401,分别于0、4、8、12、24、36、48周末采用Y—BOCS、HAMA等对患者进行盲法评定比较药物治疗和联合治疗的临床治疗效果,采用Logistic回归分析治疗效果的影响因素。结果4周末联合治疗组[（20．0±6．4）分与（23．6±6．0）分]及药物治疗组[（20．8±7．0）分与（23．7±6．3）分]Y．BOCS总分均低于基线（t=4．05,P=0．000;t=3．46,P=0．001）。2组患者Y—BOCS总分（F=3．986～7．104,P=0．009-0．049）和Y—BOCS强迫行为因子分（辟5．370～5．895,P=O．017～0．023）自8周末开始至48周末组问差异有统计学意义;2组患者Y—BOCS强迫思维因子分在48周末差异有统计学意义（F=5．523,P=0．021）。Logistic回归分析显示,联合CBT、Y-BOCS总分4周末治疗是否有效对患者48周末的疗效有正性预测作用（OR=8．61、9．25,均P〈0．05）。结论药物联合CBT能有效缓解强迫障碍患者症状,且优于单纯药物治疗,尤其对强迫行为的改善更为突出,且接受CBT、4周末起效的患者在后续的治疗中能获得更好地改善。     

曲唑酮片联合唑吡坦治疗失眠对SDRS PSQI评分及PSG指标的影响

目的 分析曲唑酮片联合唑吡坦治疗失眠对睡眠障碍评定量表(SDRS)、匹兹堡睡眠质量指数(PSQI)及多导睡眠图(PSG)的影响.方法 纳入120例于2018-05—2021-10于郑州大学第二附属医院接受治疗的失眠患者,A组40例施予曲唑酮片治疗,B组40例施予唑吡坦治疗,C组40例施予曲唑酮片联合唑吡坦治疗,对比3组SDRS、PSQI评分及PSG各指标.结果 治疗后7 d、14 d、28 d,C组SDRS评分分别为(14.04±5.57)分、(10.15±4.32)分、(7.82±3.62)分,均较A组(18.73±6.41、12.15±5.53、11.37±4.55)、B组(18.32±5.92、12.42±4.37、11.23±4.65)低,差异均有统计学意义(P<0.05);C组PSQI评分分别为(12.29±1.29)分、(12.35±1.04)分、(7.14±0.63)分,均较A组(15.83±1.34、14.32±1.27、12.29±1.29)、B组(15.84±1.43、14.45±1.15、12.35±1.04)低,差异均有统计学意义(P<0.05);C组中PSG睡眠效率、睡眠总时间、醒觉时间、入睡时间(82.53±6.74、389.24±33.34、80.27±32.63、29.24±4.77)各项指标优于A组(74.18±6.83、333.61±34.69、120.53±33.48、36.08±4.17)、B组(73.84±7.03、334.63±35.75、120.63±34.15、35.93±3.84),差异均有统计学意义(P<0.05).结论 失眠患者给予曲唑酮片联合唑吡坦治疗效果显著,有助于改善患者的SDRS、PSQI评分及PSG指标.     

Randomized clinical trial of supervised tapering and cognitive behavior therapy to facilitate benzodiazepine discontinuation in older adults with chronic insomnia

OBJECTIVE: This study evaluated the effectiveness of a supervised benzodiazepine taper, singly and combined with cognitive behavior therapy, for benzodiazepine discontinuation in older adults with chronic insomnia. METHOD: Seventy-six older adult outpatients (38 women, 38 men; mean age of 62.5 years) with chronic insomnia and prolonged use (mean duration of 19.3 years) of benzodiazepine medication for sleep were randomly assigned for a 10-week intervention consisting of a supervised benzodiazepine withdrawal program (N=25), cognitive behavior therapy for insomnia (N=24), or supervised withdrawal plus cognitive behavior therapy (N=27). Follow-up assessments were conducted at 3 and 12 months. The main outcome measures were benzodiazepine use, sleep parameters, and anxiety and depressive symptoms. RESULTS: All three interventions produced significant reductions in both the quantity (90% reduction) and frequency (80% reduction) of benzodiazepine use, and 63% of the patients were drug-free within an average of 7 weeks. More patients who received medication taper plus cognitive behavior therapy (85%) were benzodiazepine-free after the initial intervention, compared to those who received medication taper alone (48%) and cognitive behavior therapy alone (54%). The patients in the two groups that received cognitive behavior therapy perceived greater subjective sleep improvements than those who received medication taper alone. Polysomnographic data showed an increase in the amount of time spent in stages 3 and 4 sleep and REM sleep and a decrease in total sleep time across all three conditions from baseline to posttreatment. Initial benzodiazepine reductions were well maintained up to the 12-month follow-up, and sleep improvements became more noticeable over this period. No significant withdrawal symptoms or adverse events were associated with benzodiazepine tapering. CONCLUSIONS: A structured, time-limited intervention is effective in assisting chronic users of benzodiazepine medication to discontinue or reduce their use of medication. The addition of cognitive behavior therapy alleviates insomnia, but sleep improvements may become noticeable only after several months of benzodiazepine abstinence.     

失眠症患者心理社会因素分析

目的:探讨失眠症患者的应付方式,心理健康状况和社会支持状况.方法:采用应付方式问卷(CSQ)、症状自评量表(SCL-90)和社会支持量表(SSS)对失眠症患者和正常对照者各88例进行测评.结果:失眠症组自责、幻想和退避分量表的得分显著高于对照组,求助分量表的得分显著低于对照组(P＜0.01);失眠症组SCL-90总分及躯体化、抑郁、焦虑、睡眠障碍各因子分与对照组比较,有显著差异(P＜0.01).失眠症组社会支持总分、客观支持和对社会支持的利用度评分显著低于正常对照组(P＜0.05).失眠症组自责与躯体化症状、焦虑、抑郁等因子及总分呈显著正相关,而求助与焦虑、抑郁、偏执和总分呈显著负相关(P＜0.05).结论:失眠症患者多采用不成熟的应付方式,且有较多的心身症状,应付方式和身心健康有相关性.失眠症患者缺乏社会支持.     

“Non nocere: but we both care”: Commentary on “Non nocere if you really care” by Dr Kripke, MD

Chronic primary insomnia is a recurrent condition that negatively effects the daily functioning of patients, diminishing the quality of their lives. It is associated with, and in some situations, is a risk factor in both psychiatric (depression) and physical (cardiovascular) illness. Treatment effectiveness has been shown in the short term for both drug (benzodiazepine and benzodiazepine agonists) and behavioral treatment. Expert opinion has strongly advised against long-term drug treatment because of concerns about residual sedative effects, memory impairment, falls, respiratory depression, rebound insomnia, medication abuse, dose escalation, dependency and withdrawal difficulties, and an increased risk of death possibly associated with the current hypnotic medications. Many of these concerns could be made against using these agents at all. Worries about these potential problems are challenged by the widespread clinical practice of using hypnotic drugs long-term without any of these difficulties developing and with patients who feel their sleep and daily function function is improved with the nightly use of their sleeping pill. The ability to mount a randomized, placebo-controlled, parallel group, double-blind trial of hypnotic medication in primary insomnia may not be possible. We may have to develop large systematic clinical databases, a number of case series in effect, to monitor both emergent symptoms and possible clinical effectiveness. There is the additional concern that there is a reluctance to examine the long-term drug treatment of insomnia. This reluctance may reflect a negative moral judgement about treating primary insomnia with drugs, a sort of ««pharmacological Calvinism»», rather than just a data based judiciousness.     

Hypnotic medication in the treatment of chronic insomnia: non nocere! Doesn't anyone care?

Chronic primary insomnia is a recurrent condition that negatively effects the daily functioning of patients, diminishing the quality of their lives. It is associated with, and in some situations, is a risk factor in both psychiatric (depression) and physical (cardiovascular) illness. Treatment effectiveness has been shown in the short term for both drug (benzodiazepine and benzodiazepine agonists) and behavioral treatment. Expert opinion has strongly advised against long-term drug treatment because of concerns about residual sedative effects, memory impairment, falls, respiratory depression, rebound insomnia, medication abuse, dose escalation, dependency and withdrawal difficulties, and an increased risk of death possibly associated with the current hypnotic medications. Many of these concerns could be made against using these agents at all. Worries about these potential problems are challenged by the widespread clinical practice of using hypnotic drugs long-term without any of these difficulties developing and with patients who feel their sleep and daily function function is improved with the nightly use of their sleeping pill. The ability to mount a randomized, placebo-controlled, parallel group, double-blind trial of hypnotic medication in primary insomnia may not be possible. We may have to develop large systematic clinical databases, a number of case series in effect, to monitor both emergent symptoms and possible clinical effectiveness. There is the additional concern that there is a reluctance to examine the long-term drug treatment of insomnia. This reluctance may reflect a negative moral judgement about treating primary insomnia with drugs, a sort of , rather than just a data based judiciousness.     

Double-blind, comparative study of cyamemazine vs. bromazepam in the benzodiazepine withdrawal syndrome

Cyamemazine is an anxiolytic antipsychotic, which reduces ethanol withdrawal symptoms. Here, we investigated if cyamemazine can be also effective as substitute drug to facilitate benzodiazepine withdrawal. A total of 168 patients treated with benzodiazepines for at least 3 months and with a <18 score in the Hamilton Anxiety Rating Scale (HARS) were included in the study. Previous benzodiazepine treatment was withdrawn, and patients were randomized to a 4-week treatment with cyamemazine (25-50 mg q.d.) or bromazepam (3-6 mg q.d.), followed by 2 weeks of placebo. The primary efficacy variable was the maximal anxiety rebound as measured with the HARS during the 42 days of treatment. No statistically significant differences between treatment groups were found for the extent or incidence of rebound anxiety. Considering all dropout patients as withdrawal failures, after 6 months of follow-up, 56/84 patients in the cyamemazine group (66.7%) and 55/84 patients in the bromazepam group (65.5%) were successfully withdrawn. 28 patients in the cyamemazine group and 18 in the bromazepam group had an adverse event, including anxiety, insomnia, dry mouth and somnolence. No extra-pyramidal symptoms were reported. In conclusion, cyamemazine was comparable to bromazepam in ensuring successful benzodiazepine withdrawal and in controlling the acute benzodiazepine withdrawal syndrome. Cyamemazine may be useful to facilitate benzodiazepine withdrawal in those patients where bromazepam substitution is not appropriate.     

Family studies in insomnia

OBJECTIVE: Several predisposing factors to insomnia have been hypothesized, including a familial component; however, few studies have focused on this topic. The aim of this study is to evaluate the prevalence of insomnia among first-degree relatives of chronic insomniacs and to compare the symptoms between sporadic and familial insomnia. METHODS: Two hundred fifty-six consecutive chronic insomniacs completed a clinical interview, psychometric questionnaires, a questionnaire on the family history of insomnia and, when indicated, a polysomnography. A control group was performed to estimate a base-rate incidence of insomnia in their families. RESULTS: Patients with primary (n=77) and psychiatric (n=104) insomnia were definitely included. Of those with primary insomnia, 72.7% reported familial insomnia compared with 24.1% in the noninsomnia control group. Among the psychiatric insomniacs, 43.3% reported familial insomnia. The mother was the relative most frequently affected. Comparisons between the family prevalence rates of insomnia assessed by the probands and by first-degree relatives show high concordance. A tendency to a younger age at onset was observed in familial and primary insomnia. CONCLUSION: This study reports a significant increase of familial aggregation of insomnia, warranting further genetic studies in primary insomnia with early age at onset.     

Comparative meta-analysis of pharmacotherapy and behavior therapy for persistent insomnia.

OBJECTIVE: Although four meta-analytic reviews support the efficacy of pharmacotherapy and behavior therapy for the treatment of insomnia, no meta-analysis has evaluated whether these treatment modalities yield comparable outcomes during acute treatment. The authors conducted a quantitative review of the literature on the outcome of the two treatments to compare the short-term efficacy of pharmacotherapy and behavioral therapy in primary insomnia. METHOD: They identified studies from 1966 through 2000 using MEDLINE, psycINFO, and bibliographies. Investigations were limited to studies using prospective measures and within-subject designs to assess the efficacy of benzodiazepines or benzodiazepine receptor agonists or behavioral treatments for primary insomnia. Benzodiazepine receptor agonists included zolpidem, zopiclone, and zaleplon. Behavioral treatments included stimulus control and sleep restriction therapies. Twenty-one studies summarizing outcomes for 470 subjects met inclusion criteria. RESULTS: Weighted effect sizes for subjective measures of sleep latency, number of awakenings, wake time after sleep onset, total sleep time, and sleep quality before and after treatment were moderate to large. There were no differences in magnitude between pharmacological and behavioral treatments in any measures except latency to sleep onset. Behavior therapy resulted in a greater reduction in sleep latency than pharmacotherapy. CONCLUSIONS: Overall, behavior therapy and pharmacotherapy produce similar short-term treatment outcomes in primary insomnia.     

Psychophysiological insomnia: combined effects of pharmacotherapy and relaxation-based treatments

Objective: To compare treatment outcomes associated with combined pharmacologic and non-pharmacologic treatments for psychophysiological insomnia.Background: Treatments for insomnia have included a variety of pharmacotherapy and cognitive–behavioral interventions, although few studies have investigated the combined efficacy of drug and non-drug therapy.Methods: Forty-one patients with primary insomnia were randomly assigned to one of three treatment groups: (i) estazolam + muscle relaxation, (ii) estazolam + guided imagery, and (iii) estazolam + sleep education. After 4 weeks of active treatment, subjects were withdrawn from medication and followed for an additional 6 months.Results: Significant improvements were observed in self-report measures of total sleep time, sleep efficiency, and wakefulness after sleep onset in the combined drug and relaxation groups, compared to a significant improvement in total sleep time only in the educational control group. At follow-up, all three groups showed significant improvements across the major sleep measures. Positive changes were also observed in quality of life measures, including mood state and self- ratings of daytime arousal.Conclusions: These findings provide support for the value of combined pharmacotherapy and relaxation training in the treatment of psychophysiological insomnia.