认知疗法及放松训练对失眠者的睡眠质量评价及疗效观察

目的探讨认知疗法及放松训练对失眠者的睡眠疗效。方法对35例门诊主诉失眠者采用认知疗法及放松训练对其进行治疗，疗程6周。以阿森斯失眠量表（AIS）于治疗前，治疗后第1、2、3、4、6周对主诉失眠者进行睡眠评价及疗效评定。结果35例失眠症者28例（80．00％）完成6周的治疗。并停用了安眠药物。AIS评分从治疗前的（8．9±2．5）分降为第6周的（5．6±1．5）分，治疗后第2周AIS评分下降即有显著性差异（氏0．05），第3周AIS评分下降有非常显著性差异（P〈0．01）。以AIS评分〈6分计算睡眠较满意率．睡眠较满意率从治疗开始时的0．0％上升到治疗后6周的46％。结论认知及放松疗法对于改善失眠者睡眠质量有显著的效果。     

豆腐果苷对骨关节炎大鼠软骨和滑膜组织影响

目的研究豆腐果苷对骨关节炎大鼠软骨结构和滑膜组织的影响。方法碘乙酸钠注射 SD雄性大鼠膝关节造模成功后,随机区组分组法分为三组,即假手术组、模型组、豆腐果苷 50 mg·kg.1·d.1组。豆腐果苷灌胃 21 d后,取大鼠膝关节制成组织切片, HE染色观察膝关节软骨和滑膜病理变化,并进行评分;番红固绿染色观察大鼠膝关节软骨病理变化,并进行 Mankin评分。研究起止时间为 2019年 12月至 2020年 7月。结果相对于假手术组,模型组大鼠膝关节软骨和滑膜均受到不同程度损伤,滑膜病理评分显著升高［( 6.88±0.83)分比( 0.50±0.53)分］(P<0.01)且软骨结构、软骨细胞和番红固绿染色的 Mankin评分也显著升高［分别是( 3.88±0.83)分比( 0.50±0.53)分,(1.75±0.46)分比(0,.25±0.46)分,(2.38±0.74)分比( 0.38±0.52)分］(P<0.01)。然而,连续给予豆腐果苷灌胃 21 d后,相对于模型组,大鼠的关节软骨结构和滑膜组织损伤程度均有显著改善,膝关滑膜病理评分显著降低［(3.50±0.53)分比(6.88±0.83)分］(P<0.01)且软骨结构、软骨细胞和番红固绿染色的 Mankin评分也显著降低［分别为( 1.63±0.52)分,(1.13±0.64)分,(0.88±0.64)分］(P<0.0,5)。结论豆腐果苷可减轻骨关节炎大鼠膝关节软     

神经节苷脂治疗急性脑梗死

目的 :观察神经节苷脂治疗急性脑梗死的疗效。方法 :急性脑梗死 6 0例 ,分为神经节苷脂组及对照组。神经节苷脂组 30例 ,给予 6 0～ 10 0mg加入氯化钠注射液 2 5 0mL ,iv ,gtt× 2wk ;对照组30例 ,给予胞磷胆碱 0 .5～ 0 .75 g或吡拉西坦 4 g ,治疗 2wk ,于治疗前、治疗后 1wk和 2wk对 2组病人进行神经功能缺损程度 (NDS)及日常生活活动量 (ADL)评分 ,并进行比较。结果 :神经节苷脂组与对照组疗效比较经Ridit分析 ,差异有显著意义 (P<0 .0 5 ) ,治疗后wk 1,2NDS和ADL评分与治疗前相比 ,差值分别为 (- 12 .0±s 0 .5 )分 ,(- 3.3±0 .3)分 ;(- 17.4± 0 .7)分 ,(- 4.5 4± 0 .2 5 )分 ;(31.8± 2 .4 )分 ,(2 .1± 0 .6 )分 ;(5 2± 10 )分 ,(6± 6 )分 (P <0 .0 1)。结论 :神经节苷脂治疗急性脑梗死有显著的疗效 ,能促进神经功能的早期恢复 ,提高生活质量     

右佐匹克隆与氯硝西泮辅助治疗精神分裂症睡眠障碍对照研究

目的探讨右佐匹克隆辅助治疗精神分裂症睡眠障碍的疗效及安全性。方法 91例伴睡眠障碍的精神分裂症患者(均统一服用阿立哌唑10～20mg·d~(-1))随机分成2组,分别口服右佐匹克隆3～6mg·d~(-1)(n=45)或氯硝西泮2～4mg·d~(-1)(n=46),采用匹兹堡睡眠质量指数(PSQI)、阳性和阴性症状量表(PANSS)、副反应量表(TESS)评定疗效和安全性;观察3wk。结果 2组各完成43例。治疗3wk后,2组睡眠时间均显著延长,PSQI评分和PANSS评分显著下降(均P<0.01),2组间疗效无显著差异(P>0.05);右佐匹克隆组日间功能障碍的改善显著优于氯硝西泮组[(1.2±0.9)分vs.(1.6±0.7)分,P<0.05];2组TESS评分无显著差异(P>0.05),右佐匹克隆组嗜睡、头昏的发生率显著少于氯硝西泮组(P<0.05)。结论右佐匹克隆辅助治疗精神分裂症睡眠障碍疗效显著,安全性优于氯硝西泮。     

联合治疗方案对原发性失眠病人睡眠质量、抑郁情绪及睡眠结构指标的影响

目的探讨联合治疗方案对原发性失眠病人睡眠质量、负面情绪及睡眠结构指标的影响。方法选取自贡市精神卫生中心 2016年 1月至 2018年 1月收治原发性失眠病人共 160例,以随机数字表法分为对照组( 80例)和观察组( 80例),其中对照组给予唑吡坦 +经颅磁刺激( rTMS)假性刺激治疗,观察组给予唑吡坦 +rTMS真性刺激;比较两组病人近期疗效,治疗前后匹茨堡睡眠质量指数量表( PSQI)评分、简单自测抑郁量表( PHQ?9)评分、多导睡眠监测指标、睡眠结构指标水平及不良反应发生率。结果观察组病人近期治疗总有效率为 96.25%,明显优于对照组的 84.21%(P＜0.05);对照组治疗后 1周、 4周及 8周 PSQI评分分别为( 10.92±2.31)分,(8.49±1.92)分,(7.77±1.38)分;观察组治疗后 1周、 4周及 8周 PSQI评分分别为( 9.38±2.09)分,(7.12±1.60)分,(5.49±1.01)分;对照组治疗后 1周、 4周及 8周 PHQ?9评分分别为( 5.96±1.02)分,(5.48±0.89)分,(5.08±0.71)分;观察组治疗后 1周、 4周及 8周 PHQ?9评分分别为( 5.17±0.89)分,(4.73±0.63)分,(3.84±0.40)分;观察组病人治疗后 PSQI评分、 PHQ?9评分、多导睡眠监测指标及睡眠结构指标水平均显著优于对照组、治疗前( P＜0.05);同时两组病人不良反应发生率比较差异无统计学意义( P＞0.05)。结论联合治疗方案用于原发性失眠病人治疗可有效提高睡眠质量,减轻抑郁情绪,改善睡眠结构,且安全性值得认可。     

安神补脑液联合舍曲林治疗脑梗死后睡眠障碍的疗效观察

目的观察安神补脑液联合舍曲林治疗脑梗死后睡眠障碍的临床疗效。方法选取2015年7月—2016年6月重庆市开州区人民医院收治的112例脑梗死后睡眠障碍患者随机分为对照组和治疗组,每组各56例。对照组患者口服盐酸舍曲林片,1片/次;治疗组在对照组治疗基础上口服安神补脑液,10 m L/次,2次/d。两组疗程均为4周。观察两组的临床疗效,比较两组治疗前后匹兹堡睡眠质量指数(PSQI)、阿森斯失眠量表(AIS)评分、美国国立卫生研究院卒中量表(NIHSS)评分、汉密尔顿抑郁量表(HAMD)评分,睡眠状况相关指标。结果治疗后,对照组和治疗组的总有效率分别为71.43%、91.07%,两组比较差异有统计学意义(P0.05)。治疗后,两组PSQI评分、AIS评分、NIHSS评分、HAMD评分均显著降低,同组治疗前后差异有统计学意义(P0.05);治疗后,治疗组PSQI评分、AIS评分、NIHSS评分、HAMD评分低于对照组,两组比较差异有统计学意义(P0.05)。治疗后,两组睡眠总时间、睡眠效率均较治疗前显著提高,夜间觉醒次数减少,同组治疗前后差异有统计学意义(P0.05);治疗后,治疗组睡眠总时间、睡眠效率高于对照组,夜间觉醒次数少于对照组,两组比较差异有统计学意义(P0.05)。结论安神补脑液联合舍曲林治疗脑梗死后睡眠障碍,临床疗效确切,患者睡眠质量改善明显,具有一定的临床推广应用价值。     

米氮平及曲唑酮辅助治疗镇静催眠药常规治疗无效失眠的对照研究

目的:了解米氮平对失眠的疗效和安全性。方法:对符合CCMD-3失眠症并使用镇静催眠药无效的30例门诊病人加用米氮平治疗,剂量10～30 mg·d~(-1),与曲唑酮对照,曲唑酮剂量25～200 mg·d~(-1),共观察8 wk。疗效在治疗后1,2,4,8 wk用阿森失眠量表评定;不良反应用TESS评定。结果:至wk 8,米氮平组减分值为(8±s 5)分,治愈14例(54％),曲唑酮组减分值为(6±3)分,治愈11例(41％),疗效与曲唑酮组无明显差异(P＞0．05),主要不良反应为头昏、瞌睡、乏力和体重增加等,不良反应除食欲减退较曲唑酮少外(P＜0．01),2组无显著差异:米氮平剂量(22±11)mg·d~(-1),曲唑酮剂量(62±38)mg·d~(-1)。米氮平组4例和曲唑酮组3例脱落。结论:米氮平可辅助治疗镇静催眠药无效的失眠病人,疗效与安全性与加用曲唑酮相似。     

曲唑酮与帕罗西汀治疗焦虑症病人睡眠障碍的比较

目的 :比较曲唑酮和帕罗西汀对焦虑症病人睡眠障碍的疗效。方法 :4 5例焦虑症病人随机分为 2组。曲唑酮组 2 2例 ,给予曲唑酮 5 0～ 10 0mg·d- 1,qn× 8wk。帕罗西汀组 2 3例 ,给予帕罗西汀2 0～ 4 0mg·d- 1,qn× 8wk。结果 :睡眠障碍因子评分 :在 1wk时 ,曲唑酮组 3.0±s 1.7,帕罗西汀组4 .0± 1.6 ;在 2wk时 ,曲唑酮组 1.3± 1.2 ,帕罗西汀组 2 .3± 1.3(均P <0 .0 5 )。总睡眠时间 :2组比较在 1wk时差异有非常显著意义 (P <0 .0 1) ;在 2wk时差异有显著意义 (P <0 .0 5 )。早醒现象 :2组比较在 2 ,4wk时差异均有显著意义 (P <0 .0 5 )。睡眠增多、嗜睡不良反应分别为 0 / 2 3,6 / 2 2 (P <0 .0 5 )。结论 :曲唑酮比帕罗西汀改善睡眠见效早、作用快、作用强 ,睡眠时间长 ,早醒现象轻     

针刺配合推拿治疗失眠症效果观察

目的 观察针刺配合推拿治疗失眠症的效果。方法 选取该院2021年1月至2022年12月收治的失眠症患者100例，随机分为对照组与观察组各50例。对照组每晚睡前半小时口服艾司唑仑1 mg，观察组给予针刺配合推拿治疗，10天为1个疗程。两组均持续治疗两个疗程，比较疗效及治疗前后睡眠质量评分。结果 观察组治疗总有效率98.0%(49/50)高于对照组的84.0%(42/50)，治疗后睡眠质量评分低于对照组，差异均有统计学意义（P <0.05）。结论 针刺配合推拿治疗失眠症，可改善患者失眠症状，提高睡眠质量。     

针灸配合推拿治疗颈源性失眠对患者睡眠质量及生活质量的影响

目的 探究与分析针灸配合推拿治疗颈源性失眠对患者睡眠质量及生活质量的影响.方法 选取本院2014年8月至2016年8月收治的90例颈源性失眠患者,采取随机数字表法分为对照组与观察组,各45例.对照组给予针刺治疗,观察组在对照组基础上加用推拿治疗,对比两组患者睡眠质量及生活质量变化情况.结果 对照组治疗后入睡时间、夜间苏醒、比期望的时间早睡、总睡眠时间、总睡眠质量、白天情绪、白天身体功能及白天思睡评分分别为(1.59±0.28)分、(1.62±0.29)分、(1.59±0.30)分、(1.53±0.12)分、(1.61±0.29)分、(1.72±0.19)分、(1.83±0.39)分、(1.72±0.29)分,观察组分别为(0.98±0.13)分、(1.13±0.65)分、(0.87±0.24)分、(1.12±0.25)分、(0.97±0.10)分、(0.89±0.14)分、(0.92±0.61)分、(1.12±0.59)分,两组治疗后入睡时间、夜间苏醒、比期望的时间早睡、总睡眠时间、总睡眠质量、白天情绪、白天身体功能及白天思睡评分均低于治疗前,观察组治疗后与对照组治疗后相比上述评分降低更加显著,差异具有统计学意义(均P＜ 0.05).对照组躯体功能、角色功能、认知功能、情绪功能及社会功能评分分别为(15.35±1.65)分、(14.80±1.33)分、(14.66±1.70)分、(15.24±1.67)分、(14.37±1.82)分,观察组分别为(18.56±2.12)分、(17.65土1.65)分、(18.60±1.92)分、(17.78土2.54)分、(17.50±1.94)分,两组治疗后躯体功能、角色功能、认知功能、情绪功能及社会功能评分均高于治疗前,观察组治疗后与对照组治疗后相比上述指标改善更加显著,差异具有统计学意义(均P＜ 0.05).结论 针灸配合推拿治疗颈源性失眠能够有效改善患者的睡眠质量,促进提高患者的生活质量.     

Effects on sleep of acetylcholine perfusion of the locus coeruleus of cats

The loci coeruleus of freely moving cats were perfused bilaterally with acetylcholine at a dose of 0.001 μg/μl per min, while the animals were recorded polygraphically. The controls consisted of experiments in which no perfusions were done, and experiments in which the loci coeruleus were perfused bilaterally with saline, 1 μl/min. The acetylcholine produced a sharp inhibition of rapid eye movement (REM) sleep, prolonged the sleep cycle and the REM interval and decreased the number of REM periods and the mean duration of the REM episodes. Total sleep time was increased. This was entirely due to a specific elevation by acetylcholine of deep slow-wave sleep; light slow-wave sleep was not affected. The data support the Hobson-McCarley hypothesis of how the brain controls the REM state, and also suggest that cholinergic stimulation of the locus coeruleus may be important for the shift from REM sleep into slow-wave sleep.     

Influence of loxapine on the sleep-wakefulness cycle of the rat

The sleep-wakefulness cycle was studied in 18 Wistar albino rats under the influence of Loxapine, a neuroleptic derived from oxazepine succinate. One single dose of the drug (0.4–1.6 mg/kg) had a marked effect in depressing the paradoxical sleep (PS), maximal within 30 min and lasting about 24 hr. Frequency and mean duration of PS episodes were differentially affected. Synchronized sleep was only slightly affected by Loxapine whereas no significant changes of wakefulness amount were detected. Chronic administration of the drug induced similar changes which disappeared in about 5 days.     

Acute heroin abstinence in man: IV. Sleep-waking state contingencies

This study investigated the effect of acute heroin withdrawal on the pattern of sleep-waking state sequences. Subjects included drug-dependent patients using pure heroin and drug-free controls. Electrophysiological data were recorded on a 24-hour per day basis for the first 5–7 days of withdrawal. EEG records were scored according to standard criteria. Marked increases in the sequential state changes occurred during withdrawal when progressing from awake-with-alpha, stage I, stage II and rapid eye movement (REM) sleep to the awake state. Heroin withdrawal also caused significant decreases in sequential state changes when proceeding from waking or light sleep states into deeper sleep states or into REM sleep. This study revealed that heroin withdrawal caused more abrupt transitions from quiet awake or sleeping conditions into the awake state and impeded progression into slow wave or REM sleep states.     

美沙酮维持治疗海洛因依赖患者的睡眠特征

目的：分析美沙酮维持治疗（MMT）海洛因依赖患者（HAs）的睡眠特征。方法：采用病例对照研究设计分别从MMT门诊和社区招募603例HAs（病例组）和377例性别年龄匹配的健康居民（对照组）,两组对象完成自编睡眠情况问卷和匹兹堡睡眠质量指数（PSQI）。结果：病例组的睡眠潜伏期[（35.7±34.2）min.vs.（24.5±36.5）min.]和睡眠时间[（9.0±2.3）h vs.（7.8±1.5）h]均长于对照组,而其睡眠效率[（87.5±15.3）%vs.（95.1±17.0）%]低于对照组,同时,病例组PSQI总分及其7个睡眠成份分也均高于对照组[如,PSQI总分：（6.5±3.8）vs.（3.5±2.7）],差异均具有统计学意义（P均≤0.002）;目前无业、服用安眠药、既往吸毒时间≥10年和静脉注射方式吸毒的HAs睡眠问题检出率较高。结论：MMT的HAs入睡潜伏期长和睡眠效率差,睡眠质量各维度均全面下降;无业、安眠药使用和既往的较重的吸毒史可能增加了HAs睡眠问题的发生风险。     

REM期睡眠剥夺和恢复及莫达非尼干预后大鼠海马突触可塑性变化

目的：探讨不同程度快动眼睡眠（REM）期睡眠剥夺和恢复及中枢性兴奋药莫达非尼干预后大鼠海马突触可塑性变化,观察莫达非尼对其的影响作用。方法：成年雄性SD大鼠随机分为对照组和睡眠剥夺组,对照组有空白对照（cage control,CC）和环境对照（tank control,TC）,睡眠剥夺组分非用药组（non-drug group,NDG）和用药组（drug group,DC）,每组分睡眠剥夺1d（SD 1d）、3d（SD 3d）、5d （SD 5d）,剥夺5d后恢复6h（SD 5 d/RS 6h）、12h（SD 5d/RS 12h）共5小组,每小组6只大鼠,采用改良多平台睡眠剥夺法（MMPM）进行REM期睡眠剥夺,运用免疫组织化学和电镜的方法分析大鼠海马CA3区突触素（synapsinⅠ）的表达,观察突触可塑性变化。结果：免疫组化结果显示,CC组和TC组间无显著差异（P＞0．05）；在SD 1 d、SD 3 d、SD 5 d、SD 5 d/RS 6 h、SD 5 d/RS 12h各时间点用药组突触素阳性表达均高于非用药组（P＜0．05）；非用药组和用药组SD1d、SD 3 d、SD 5d、SD 5 d/RS 6h各时间点比CC组均有减少（P＜0．05）,而用药组中的SD 5d/RS 12h组与CC组无显著差异（P＞0．05）。电镜下观察显示,非用药SD 1d组的突触联系、突触前膜囊泡数量均较CC组减少,但用药SD 1 d组较非用药SD 1d组增加。结论：REM期睡眠剥夺能够引起大鼠海马突触素表达减少,影响大鼠海马突触可塑性,而莫达非尼可以显著改善睡眠剥夺后突触素的表达减少,调节大鼠海马突触可塑性。     

Effect of clonidine on sleep patterns in man

Summary Clonidine (300 µg orally) increased in man the total duration of sleep and strikingly reduced the duration of REM sleep. Yohimbine (10 mg per os) did not alter the sleep patterns in man but antagonized the effects of clonidine. These results provide evidence that an sympathomimetic mechanism could suppress REM sleep and increased the total duration of sleep.     

Effects of lithium chloride on sleep patterns in the rat.

Continuous EEG recordings were performed in rats both after saline injections (control days) and after LiCl treatments. LiCl administration was always followed by an initial period of general distress and sleep inhibition during 2 to 3 hr after low toxic doses (1.5 mEq/kg) and a much more longer period (10 hr) after high toxic doses (3 mEq/kg). Once this state was overcome, the pharmacological effect of lithimia seems to potentiate sleep and particularly paradoxical sleep (PS). It appears that this potentiation of PS occurs once lithimia reaches levels used in human therapeutics.     

脑卒中后睡眠结构变化的研究

目的观察脑卒中后患者睡眠结构变化的特点。方法采用多导睡眠图对53例脑卒中后患者进行整夜睡眠描记,并与对照组比较。分析相关睡眠参数。结果脑卒中后与对照组比较多项睡眠指标均有显著性差异(P<0.05);脑卒中后患者睡眠潜伏期延长,总睡眠时间减少,入睡后醒觉次数增多,睡眠效率低,快眼动(REM)睡眠潜伏期缩短,REM睡眠时间和REM活动度减少。结论脑卒中后患者睡眠结构发生改变,睡眠时间减少,睡眠质量差。REM睡眠潜伏期、REM睡眠时间和REM睡眠活动度是评估脑卒中后患者的神经功能缺损康复的客观参数。     

Subjective and polysomnographic effects of milnacipran on sleep in depressed patients

The effects of milnacipran (50 mg bid) on sleep patterns of eight depressed inpatients, treated for 4 weeks, were studied during the initial (days 1-3) and terminal (days 26-28) treatment periods and compared with those obtained from three sleep recordings performed just prior to the initiation of the treatment. The clinical evolution of patients was evaluated weekly using the MADRS depression scale and the Spiegel and Norris sleep scales. Clinical improvement, shown by a mean reduction of 58% in MADRS scale scores, was accompanied by an improvement of disturbed sleep parameters. From the beginning of treatment, there was an increase in the total duration of sleep and stage II sleep, a decrease in sleep latency and an increase in sleep efficiency. Total REM sleep was not modified although, since there was an increase in total sleep time, the percent REM sleep was significantly reduced. REM latency was increased early in the study, an effect classically associated with antidepressant treatment. This study suggests that milnacipran improves disturbed sleep parameters in depressed patients without any additional disturbance at the onset of treatment.     

Effect of temazepam and temazepam-ethanol on sleep

Summary The effects of temazepam 20 mg and temazepam 20 mg plus whisky 100 ml on sleep and performance were investigated in 5 healthy volunteers in comparison with placebo. In the sleep laboratory, after temazepam there was a trend for reduction of sleep latency, stage wake and stage 1 sleep, and for an increase in REM sleep. The addition of alcohol to the regimen reduced the sleep latency still further, and diminished REM sleep. In subjective assessments, temazepam received the highest score for quality of sleep and the temazepam/alcohol combination that for ease of falling asleep. None of the observed changes reached statistical significance. No morning hangover, as measured by effects on wakefulness, performance or affective state, was seen after the combined treatment. Its effect on blood pressure was negligible. It is concluded that the combined administration of temazepam and alcohol in the doses used here does not result in excessive additive, but in moderate pharmacological effects.