中风后抑郁多导睡眠脑电图研究

目的探讨脑卒中后抑郁（PSD）患者的多导睡眠图异常改变，与正常对照组及抑郁症组之间的差异。方法采用多导睡眠仪（PSG）对20例PSD患者和20例抑郁症患者进行整夜睡眠描记，并与对照组比较。结果PSD组与正常组比较：睡眠潜伏期延长，醒觉时间增加，睡眠效率及维持率低，慢波睡眠减少，有显著性差异。REM睡眠时间及活动度明显减少，有极显著性差异；REM周期数减少，有显著性差异；REM潜伏期、密度、强度无差异。结论我们认为PSD患者多导睡眠图特征性变化是REM睡眠时间减少，原因可能与脑损害后大量兴奋性氨基酸等神经毒性物质释放和脑内5-HT含量减少有关。因其合并脑器质性损害等因素影响所以不能与原发性抑郁症一样以REM潜伏期（RL）缩短、REM密度增加作为PSD的诊断依据。     

文拉法辛对抑郁症患者睡眠的影响

目的 探讨文拉法辛对抑郁症患者多导睡眠图及主观睡眠质量的影响.方法 对20名抑郁症患者及30名正常对照者进行多导睡眠图检测,并应用匹兹堡睡眠质量指数(PSQI)和汉密尔顿抑郁量表(HAMD)睡眠障碍因子分评定抑郁症患者的主观睡眠质量.比较治疗前后多导睡眠图指标和主观睡眠质量的变化.结果 与对照组比较,病例组显示多导睡眠图指标异常.病例组经过文拉法辛治疗后与治疗前比较,多导睡眠图显示觉醒次数和觉睡比增加、睡眠效率降低、睡眠阶段S1百分比增加、快眼动(REM)睡眠时间及百分比减少、REM睡眠潜伏期延长、REM活动度及强度降低,但PSQI和HAMD睡眠障碍因子分均明显降低.结论 文拉法辛能抑制抑郁症患者的REM睡眠,并加重睡眠维持障碍,导致浅睡眠增加,但能够明显改善患者的主观睡眠质量.     

阿戈美拉汀对甲基苯丙胺依赖者脱毒后睡眠障碍的干预研究

目的:观察阿戈美拉汀对甲基苯丙胺依赖者脱毒后睡眠障碍的临床疗效。方法:选取91例甲基苯丙胺依赖者,脱毒后随机分为治疗组与对照组,治疗组给予阿戈美拉汀治疗,对照组给予安慰剂治疗。对所有人员采用匹兹堡睡眠质量指数量表进行评价并应用整夜多导睡眠监测。结果:(1)治疗4周后,治疗组匹兹堡睡眠质量指数量表评分显著提高,明显高于对照组(P<0. 01)。(2)治疗4周后,治疗组的觉醒次数、觉醒时间、睡眠潜伏期、N1比例、N2比例、N3比例、觉醒睡眠比显著改善,与治疗前相比,差异有显著性意义(P<0.01),改善明显优于对照组(P<0.01);REM潜伏期、REM睡眠时间、REM活动度、REM密度、REM强度和入组时无明显改善(P>0.05)。而对照组仅在总睡眠时间较入组时延长(P<0. 01)、睡眠潜伏期低于入组时(P<0. 01),睡眠效率高于入组时(P<0. 01);其余指标和入组时相比无明显改善(P>0.05)。结论:阿戈美拉汀可以显著改善甲基苯丙胺依赖者的睡眠质量。     

阻塞性睡眠呼吸暂停低通气综合征患者术后脑电图的分析

目的分析阻塞性睡眠呼吸暂停低通气综合征(OSAHS)患者手术前、后脑电图变化。方法对32例OSAHS患者施行改良UPPP手术,应用多导睡眠呼吸监测(PSG)进行睡眠监测,分析比较手术前、后睡眠结构参数变化和睡眠各期所占百分比。结果手术后深睡眠S3～S4、REM睡眠明显增加,分别为(15.43±10.06)%和(18.506±8.54)%,REM睡眠潜伏期降低为(71.13±55.43)min,睡眠效率为(92.61±10.82)%,上述参数与对照组相比有显著性差异(P<0.01或P<0.05)。两组总睡眠时间、睡眠潜伏期无显著性差异(P>0.05)。结论 UPPP手术治疗能改善OSAHS患者睡眠结构紊乱,值得临床推广。     

对精神分裂症患者作多导睡眠图分析

目的 为了解精神分裂症患者的睡眠生理变化。方法对28例精神分裂症患者及19例正常对照者进行全依多层睡眠图(PSG)检测。结果①与对照组比较,病例组醒觉时间、Ⅰ期睡眠(S_1)、觉睡比及醒觉次数增多(P<0.05～0.01);睡眠效率、睡眠维持率、Ⅲ Ⅳ期深睡眠(S_3S_4),快速眼动期(REM)周期数减少(P<0.05～0.01);REM睡眠缩短(P<0.05),REM潜伏期延长(P<0.05)。与对照组同性别间比较发现,病例组男性睡眠参数改变较女性尤为明显。②从28例精神分裂患者中检出2例阻塞性呼吸睡眠暂停综合征患者(占7.1％)。③病例组年龄与S_(34)期睡眠呈负相关(γ=-0.39,P>0.05);BPRS与REM睡眠呈负相关(γ=0.37,P<0.05)。结论 精神分裂症患存在着睡眠学的异常变化,且男性较女性更易受到影响。     

无抽搐电休克治疗对男性抑郁症病人多导睡眠图的影响

目的:探讨无抽搐电休克(MECT)治疗对抑郁症病人睡眠脑电活动的影响。方法:应用多导睡眠图(PSG)对12例男性首发抑郁症病人在MECT治疗前后进行整夜PSG记录,观察MECT治疗前后PSG的变化。结果:与正常对照组比较,病人组睡眠总时间减少、睡眠潜伏期延迟、觉醒增加、快动眼睡眠(REM)时间增多、REM潜伏期缩短、S1和S2增加以及慢波睡眠减少。病人组经过MECT治疗后PSG显示睡眠总时间增加[治疗前:(342±s51)min,治疗后:(437±25)min,t值11.840,P<0.01],睡眠潜伏期缩短[治疗前:(68±12)min,治疗后:(56±7)min,t值4.249,P<0.01],觉醒时间减少[治疗前:(163±43)min,治疗后:(30±7)min,t值10.409,P<0.01],REM睡眠时间减少[治疗前:(164±19)min,治疗后:(120±5)min,t值9.333,P<0.01],S1减少[治疗前:(46±15)min,治疗后:(39±11)min,t值5.071,P<0.01],慢波睡眠增加[治疗前:(34±19)min,治疗后:(99±7)min,t值-13.146,P<0.01]。REM潜伏期和S2未见明显变化(P>0.05)。结论:MECT有改善睡眠的作用。这可能是MECT起到治疗抑郁症的重要机制之一。     

氯丙米嗪治疗强迫障碍前后多导睡眠图及血小板五羟色胺的研究

目的　观察用氯丙米嗪 (LPM)前后患者的临床症状变化和睡眠图指标变化的关系 ,探索强迫障碍的多导睡眠图模式。方法　对 4 0例强迫障碍患者的多导睡眠图和血小板五羟色胺 (5 -HT)含量进行检测 ,采用LPM 15 0～ 30 0mg·d-1治疗 4 2d后 ,评价临床疗效 ,并再次检测患者的多导睡眠图和血小板 5 -HT。结果　患者多导睡眠图存在有睡眠纺槌指数 (SS)增高 ;快眼动 (REM)睡眠潜伏期缩短 (RL) ,REM活动度、强度、密度及第一次REM睡眠时间 (FRT)及其百分比 (FRT % )增高 ;患者的血小板 5 -HT含量明显高于正常人等改变。在治疗后RL明显延长 ,其余指标明显下降。 5 -HT含量变化与SS、FRT及FRT %呈正相关 ,此外Y -BOCS总分与RL呈负相关。结论　SS和REM睡眠指标的改变可能代表了强迫障碍的某些生物学特征 ,RL改变则反映了强迫症状的程度。     

帕罗西汀联合小剂量奥氮平对抑郁症伴失眠患者睡眠进程和睡眠结构的影响

目的:探讨帕罗西汀联合小剂量奥氮平对抑郁症伴失眠患者睡眠进程和睡眠结构的影响。方法:84例抑郁症伴失眠患者随机均分为对照组和观察组。对照组患者给予帕罗西汀片20 mg,每日早晨口服1次;观察组患者在对照组治疗的基础上加用奥氮平片2.5 mg,每日睡前口服1次。观察两组患者治疗前和治疗3、6个月后的睡眠质量[匹兹堡睡眠质量指数(PSQI)]、抑郁情绪评分[汉密顿抑郁量表(HAMD)]、睡眠进程[睡眠潜伏期(SL)、觉醒次数(AT)、实际睡眠总时间(TST)、睡眠效率(SE)、快速眼球运动睡眠(REM)潜伏期(RL)]和睡眠结构[睡眠阶段1(S1)、2(S2)、3(S3)和REM占睡眠时间的比例],并记录不良反应发生情况。结果:治疗后,两组患者PSQI、HAMD评分均显著低于同组治疗前,且随时间延长逐渐降低,观察组低于对照组;观察组患者TST显著高于治疗前和对照组,S1占睡眠比例显著低于同组治疗前;两组患者SE、S3和REM占睡眠比例均显著高于同组治疗前,且观察组高于对照组,SL、AT、RL、S2占睡眠比例均显著低于同组治疗前,且观察组低于对照组,差异均有统计学意义(P<0.05)。两组患者治疗期间未见明显不良反应发生。结论:帕罗西汀联合小剂量奥氮平能显著改善患者抑郁情绪,优化睡眠进程和睡眠结构,提高睡眠质量。     

度洛西汀对抑郁症多导睡眠图及主观睡眠质量的影响

目的研究度洛西汀对阻滞性和非阻滞性抑郁症患者多导睡眠图(PSG)和主观睡眠质量的影响。方法将符合中国精神障碍分类与诊断标准第3版(CCMD-3)中抑郁发作标准纳入观察的抑郁症患者32例按汉密尔顿抑郁量表(HAMD)阻滞因子的得分,分为阻滞组16例和非阻滞性组16例,两组均采用度洛西汀治疗,疗程4周。治疗前后采用PSG测定睡眠特点,匹兹堡睡眠质量指数(PSQI)评定主观睡眠质量,HAMD减分率评定疗效。结果阻滞组治疗前和治疗后PSQI评分与非阻滞组相比无显著差异(P>0.05);两组治疗后PSQI评分均显著低于治疗前(P<0.05)。阻滞组和非阻滞组治疗后觉醒次数和觉睡比增加,睡眠效率降低,S1百分比增加,SWS时间延长,快速眼动(REM)睡眠百分比及睡眠时间减少,REM睡眠潜伏期延长,REM活动度和强度及密度均降低,与治疗前比较均有显著性差异(P<0.05);治疗后阻滞组REM睡眠百分比及睡眠时间高于非阻滞组(P<0.01),余各指标治疗后两组间比较无明显差异(P>0.05)。相关分析显示,阻滞组和非阻滞组PSQI的变化率与所有PSG指标变化率均无显著相关性(P>0.05)。结论度洛西汀能延长阻滞性和非阻滞性抑郁症患者慢波睡眠,度洛西汀治疗后PSG和主观睡眠质量变化间可能并不存在相关性。     

抑郁症病人睡眠结构特征与前瞻性记忆的相关性研究

目的探讨抑郁症病人睡眠结构特征及其与前瞻性记忆的相关性。方法选取 2017年 1月至 2020年 1月安徽省精神卫生中心 113例住院抑郁症病人作为抑郁组,同期该中心公开招募 47例健康者作为对照组,两组对象均行多导睡眠监测,评估汉密尔顿抑郁量表( HAMD)、汉密尔顿焦虑量表( HAMA)、基于事件的前瞻性记忆( EBPM)和基于时间的前瞻性记忆( TBPM),分析抑郁症病人睡眠结构与 EBPM和 TBPM的关系。结果相比于对照组,抑郁组快速眼动睡眠( REM)潜伏期( 235.52±83.65)min和卧床时间 507.00(49.25)min较对照组 REM潜伏期( 137.78±56.23)min和卧床时间 483.80(54.50)min长( P<0.05);抑郁组 EBPM评分 2.00(5.00)分和 TBPM评分 2.00(4.00)分较对照组的 EBPM 6.00(5.00)分和 TBPM 5.00(5.00)分少( P<0.05)。相关性分析显示,抑郁组 N2潜伏期与 TBPM呈正相关［ β=0.041,95%CI:(0.008,0.074)］,REM持续时间与 TBPM呈正相关［ β=0.024,95%CI:(0.010,0.039)］。模型加入性别、年龄、文化、体质量指数( BMI)、 HAMD、HAMA、病程等混杂因素后,多因素线性回归分析结果显示,抑郁组 REM持续时间仍与 TBPM呈正相关［ β=0.017,95%CI:(0.003,0.031)］;而 N2潜伏期与 TBPM的关联差异无统计学意义( P>0.05)。结论抑郁症病人存在睡眠结构异常和前瞻性记忆损害, TBPM与 REM持续时间呈正相关,且这种关联不受病人性别、年龄、文化、体质量指数、抑郁程度、焦虑程度和病程等的影响。     

The Effect of Baclofen on Alterations in the Sleep Patterns Induced by Different Stressors in Rats

We have previously reported that sleep patterns are significantly affected by both physical and psychological stress induced by a communication box ; however, the mechanism by which stress alters sleep patterns was not established. In the present study, we investigated the role of γ-aminobutyric acid (GABA), acting through the GABA_B receptor, on stress-induced changes in sleep patterns. Our results show that physical stress increased the total wakefulness time by increasing sleep latency and inhibiting both rapid eye movement (REM) and non rapid eye movement (NREM) sleep during a 6 h sleep–recording period. The GABA_B agonist baclofen (20 pmol/2 μl) attenuated the effects of physical stress on sleep latency, total wakefulness, and NREM sleep, but not total REM sleep. In contrast, psychological stress enhanced total REM sleep and shortened REM sleep latency without altering other sleep patterns. The effect of psychological stress on total REM sleep was also reversed by baclofen. These results suggest that GABA via GABA_B receptors may play a role in the regulation of specific sleep patterns by both physical and psychological stress.     

焦虑障碍患者的客观睡眠与临床特征相关性研究

目的 探讨焦虑障碍患者睡眠状况的一般特点以及与临床症状之间的关系.方法 运用病例对照研究方法分析32例焦虑障碍患者和30例健康对照人群的整夜多导睡眠图差异,并与临床症状进行相关分析.结果 与正常对照组比较,焦虑障碍患者表现为睡眠效率下降(P<0.05),睡眠潜伏期时间延长(P<0.05),非快动眼睡眠阶段百分比增加(P<0.01),快动眼睡眠阶段时限减少(P<0.01),以及快动眼睡眠阶段百分比下降(P<0.01).非快眼动睡眠第Ⅱ期睡眠百分比与汉密尔顿焦虑量表总分成正相关(r=0.356,P<0.05),与精神焦虑因子分成正相关(r=0.448,P<0.05).结论 焦虑障碍存在多项客观睡眠指标异常,且临床焦虑症状程度与客观睡眠指标具有相关性.因此,进一步结合神经生化、神经影像学等深入研究,对于探讨该病的病理机制具有一定价值.     

Effects of short-acting hypnotics on sleep latency in rats placed on grid suspended over water

The present study was performed to develop a new sleep disturbance model for evaluating hypnotic potencies by placing rats on a grid suspended over water up to 1 cm under the grid surface. When rats were placed on the grid, significant increases in sleep latency and amount of wakefulness were observed compared with those of rats placed on sawdust. However, the amounts of non-rapid eye movement (non-REM) sleep and rapid eye movement (REM) sleep of rats placed on the grid were significantly decreased compared with those of rats placed on sawdust. Four short-acting hypnotics (triazolam, zopiclone, brotizolam, lormetazepam) caused significant decreases in sleep latency, and the effects of hypnotics in rats placed on the grid were more potent than those in rats placed on sawdust. In conclusion, the present model can serve as a new sleep disturbance model and may also be useful for evaluating the sleep-inducing effects of short-acting hypnotics.     

Conventional and spectral power analysis of all-night sleep EEG after subchronic treatment with paroxetine in healthy male volunteers

Paroxetine is a selective and potent serotonin reuptake inhibitor with reported antidepressant properties. Since changes in the regular sleeping pattern were described as side effects under treatment with paroxetine, the impact of the drug on the sleep architecture is of major interest. The present study addressed the question of subchronic effects of paroxetine medication (30 mg/day) in eight healthy male volunteers in a double blind, placebo-controlled crossover-design. Conventional sleep EEG parameters and additionally computed spectral power analysis based on FFT of 20-s time epochs in the delta, theta, alpha, beta and gamma frequency range for different sleep stages after 4 weeks of treatment were investigated. Subchronic paroxetine administration in healthy subjects led to a prolonged REM latency and a decrease in the number of REM phases, whereas sleep efficiency, total sleep time, sleep onset latency, number of awakenings, and awake during sleep period time were not altered by paroxetine medication. Moreover, we could not detect any alterations of the spectral power values in certain frequency bands during NREM or REM sleep following subchronic paroxetine medication.     

颞叶癫痫患者的睡眠特征研究

目的 通过多导睡眠监测（PSG）研究颞叶癫痫（TLE）患者发作间期的睡眠特征。方法 选取 25 例 TLE 患者为 TLE 组，健康志愿者 18 例为对照组，对 2 组受试者分别进行 PSG，监测指标包括总卧床时间（TIB）、总睡眠时 间（TST）、睡眠效率（SE）、睡眠潜伏期（SL）、快速动眼睡眠期潜伏期（REML）、入睡后觉醒时间（WASO）、非快速动眼 睡眠（NREM）1、2、3 期以及快速动眼睡眠期（REM）时间占总睡眠期时间的百分比（以 N1%、N2%、N3%、REM%表 示）、呼吸暂停低通气指数（AHI）、低通气指数、平均血氧饱和度（SpO2）及最低 SpO2、觉醒指数、每小时周期性肢体运 动指数（PLMs/h）、每小时 REM 期 PLMs、总睡眠期转换次数（SSS）、每小时睡眠期转换次数（SSS/H）、NREM1、2、3 期 以及 REM、清醒期转换次数（以 N1、N2、N3、REM、W 表示）、N1、N2、N3、REM、清醒期转换次数占总睡眠期转换次数 百分比（以 N1/SSS、N2/SSS、N3/SSS、REM/SSS、W/SSS 表示）等睡眠指标。结果 与对照组相比，TLE 组 WASO 延长， 平均 SpO2降低，PLMs 增多，REM 期 PLMs 增多，SSS、SSS/H 及 N2 增多（P＜0.05）。结论 TLE 患者存在睡眠障碍， 主要表现为睡眠结构明显紊乱，睡眠相关呼吸、运动事件增多。     

Cholinergic modulation of respiratory brain-stem neurons and its function in sleep-wake state determination

1. Shifts in behavioural state are controlled by reciprocal changes in discharge of cholinergic and aminergic groups of brain-stem/pontine neurons. During rapid eye movement (REM) sleep, cholinergic neurons are most active and aminergic neurons are least active. 2. Significant changes occur in the central control of breathing during REM sleep; respiration rate increases in frequency and variability, brain-stem respiratory neuron discharge is generally enhanced and the outputs of some respiratory motor neuron pools are depressed. 3. Hypoglossal motor neurons (HM) control tongue movement and their depression during REM sleep has been implicated in obstructive sleep apnoea. The cellular basis of HM depression has been investigated in vitro and may be due to enhanced activation of cholinergic receptors or decreased activation of aminergic receptors. 4. In vitro preparations that show respiratory rhythmogenesis possess advantages for the investigation of the neurochemical basis of state-dependent changes in respiration. Cholinergic changes in respiratory modulation of HM recorded in rhythmic brain-stem slices from mice depend on the site of activation of cholinergic receptors.     

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.     

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.