抑郁症的多导睡眠脑电图研究

目的探讨抑郁症患者的多导睡眠图异常改变，与正常对照组之间的差异。方法采用多导睡眠仪（PSG）对20例抑郁症患者进行整夜睡眠描记，并与对照组比较。结果抑郁症组与正常组比较：睡眠潜伏期延长，慢波睡眠减少，维持率低；REM潜伏期缩短，密度增加。结论我们认为抑郁症患者存在入睡困难、易醒、早醒及浅睡为主的睡眠障碍，多导睡眠图特征性变化是以快动眼睡眠过度活跃为特征，表现为REM潜伏期（RL）缩短，REM密度增加，原因可能与5-羟色胺／去甲肾上腺素（5-HT/NE）能神经传递减少及／或胆碱能传递增加有关。笔者认为抑郁症患者REM睡眠的特征性改变对抑郁症的诊断及鉴别诊断有一定临床意义。     

脑梗死和失眠症患者的多导睡眠图对照研究

为探讨脑梗死和失眠症患者睡眠参数改变的生物学特点,对30例脑梗死和30例失眠症患者及22名正常人,采用多导睡眠图进行通宵睡眠描记,对照分析相关睡眠参数。结果,脑梗死组和失眠症组均有睡眠潜伏期延长,夜间觉醒次数多,总睡眠时间减少,深睡眠和REM睡眠及REM活动度降低的特点(P<0.05～0.01),脑梗死组和失眠症组有关睡眠参数比较也具有差异性(P<0.05～0.01)。提示,脑梗死组和失眠症组两者睡眠参数皆有特征性改变,这些改变特点是脑梗死和失眠症睡眠障碍的病理生理学基础。     

抑郁症患者睡眠生理的特征改变

目的:探讨抑郁症患者睡眠生理结构的变化,并与正常人比较。方法:抑郁症组为2002-01/2004-12广州市精神病医院门诊抑郁症患者42例,正常对照组为广州市精神病医院部分职工和广州医学院部分学生,共选择30人。使用英国Oxford工厂生产的Medilog多导睡眠图记录仪进行多导睡眠图检查,记录整夜的脑电图信号。主要观察①睡眠进程:包括总记录时间,睡眠总时间,睡眠潜伏期,快速眼动睡眠潜伏等。②睡眠结构:包括各阶段(非快速眼动S1、S2、S3、S4、快速眼动)睡眠的时间和百分比,快速眼动活动度、密度和强度,睡后觉醒的次数、时间和百分比。③睡眠片断的平均时程。对此项检查获患者及家属全面知情同意。结果:抑郁症组及正常对照组均完成多导睡眠图的检查,全部进入结果分析。①睡眠进程分析:总记录时间两组无差异,抑郁症组睡眠总时间比正常对照组少,睡眠潜伏期比正常对照组长,快速眼动睡眠潜伏期比正常对照组短,差异均有显著性(P<0.05),抑郁症组睡眠效率和维持率低。②睡眠结构分析:抑郁症组非快速眼动S1时间比正常对照组长,但无统计学意义;非快速眼动S2时间比正常对照组短,[(212.72±22.9),(224.63±8.1)min,F=9.388,P=0.004];而非快速眼动(S3+S4)时间比正常组短,但无统计学意义,不少患者的整个慢波睡眠(S3+S4)缺失。抑郁症组快速眼动活动度、密度和强度均显著高于正常对照组,睡后觉醒时间长。③抑郁症组睡眠片断的平均时程低于正常对照组(81.90±7.2),(96.73±8.6)min,P=0.818。结论:抑郁症组睡眠潜伏期长、睡后觉醒时间长,睡眠效率和维持率低,快速眼动潜伏期缩短,S1睡眠延长,S3,S4睡眠缩短,部分患者的整个慢波睡眠(S3+S4)缺失。提示抑郁症患者与正常人有不同的睡眠模式,其睡眠障碍模式以快速眼动睡眠过度活跃为特征。     

多道睡眠图指标评估脑卒中后抑郁的价值

目的探讨多道睡眠图 ( polysomnograph,PSG)指标对脑卒中后抑郁 (post-stroke depression,PSD)的诊断价值. 方法 30例研究对象分为 3组进行多道睡眠图检查并分析其结果病例组为 10例 PSD患者,根据 DSM-Ⅳ诊断标准确诊;对照组为 10例脑卒中后无抑郁的患者;正常组为年龄、性别匹配的健康者. 结果与对照组、正常组比较,病例组睡眠结构发生明显变化,表现为睡眠潜伏期延长,快速动眼睡眠与非快速动眼睡眠( REM-NREM)周期次数增加;快速动眼睡眠( rapid eye movements,REM)潜伏期缩短; REM活动度、强度、密度增加; S1阶段睡眠增加, S2和 S3+ 4阶段睡眠减少.总睡眠时间、慢波睡眠时间比正常组少,但与对照组之间无差异. 3组之间觉醒时间、睡眠效率无明显差异. 结论 PSD患者存在 PSG指标变化,这些改变可能有助于 PSD的诊断参考.     

多道睡眠图指标评估脑卒中后抑郁的价值

目的：探讨多道睡眠图(polysomnograph，PSG)指标对脑卒中后抑郁(post-stroke depression，PSD)的诊断价值。方法：30例研究对象分为3组进行多道睡眠图检查并分析其结果：病例组为10例PSD患者，根据DSM-Ⅳ诊断标准确诊；对照组为10例脑卒中后无抑郁的患者；正常组为年龄、性别匹配的健康者。结果：与对照组、正常组比较，病例组睡眠结构发生明显变化，表现为睡眠潜伏期延长，快速动眼睡眠与非快速动眼睡眠(REM-NREM)周期次数增加；快速动眼睡眠(rapid eye movements，REM)潜伏期缩短；REM活动度、强度、密度增加；S1阶段睡眠增加，S2和S3 4阶段睡眠减少。总睡眠时间、慢波睡眠时间比正常组少，但与对照组之间无差异；3组之间觉醒时间、睡眠效率无明显差异。结论：PSD患者存在PSG指标变化，这些改变可能有助于PSD的诊断参考。     

发作性睡病的临床监测与特征分析

目的探讨多导睡眠图(ploysomnography;PSG)、多次睡眠潜伏期试验(multiplesleeplatencytest;MSLT)在发作性睡病(Narcolepsy;NC)和嗜睡症(lethargy;IH)患者诊断、鉴别诊断中的价值。方法对35例发作性睡病(NC)和30例嗜睡症(IH)进行整夜多导睡眠图(PSG)描记和多次睡眠潜伏期试验(MSLT),分析其睡眠参数异同。结果MSLT结果显示:NC组睡眠潜伏期和快动眼睡眠(REM)潜伏期显著缩短,入睡次数和REM睡眠出现次数明显多于IH组和对照组(P<0.01),睡眠潜伏期<5分钟和ROREMPs≥2次30例(85.7%),与IH组比较差异有统计学意义(P<0.01);整夜PSG结果显示:NC组总睡眠时间和深睡眠(SWS)百分比及REM潜伏期显著低于IH组和对照组,而S1阶段睡眠显著高于IH组,两组比较,差异具有统计学决心义(P<0.01)。结论NC患者具有明显的睡眠潜伏期缩短和反常的REM睡眠特征,MSLT、PSG对NC和IH的诊断和鉴别诊断具有重要参考价值。     

脑卒中后抑郁状态与抑郁症患者的多导睡眠图对照研究

目的探讨脑卒中后抑郁状态(PSD)患者的睡眠图异常改变及与抑郁症之间的差异。方法采用多导睡眠图对62例脑卒中和30例抑郁症患者进行整夜睡眠描记,并与对照组比较。结果PSD组与对照组和非抑郁组比较多项睡眠指标均有显著性差异(P<0.05～0.01);PSD组的REM睡眠时间和密度明显低于抑郁症组,差异有显著性(P<0.01)。结论PSD状态病人除具有睡眠障碍在多导睡眠图改变外,REM睡眠时间和密度是一个较为特征性的改变,PSD的发生可能与脑内5-羟色胺(5-TH)递质改变有关。     

脑卒中后抑郁患者的睡眠脑电图研究

目的：探讨脑卒中后抑郁状态患者的睡眠脑电图异常改变及与抑郁症患者之间的差异。方法：采用多导睡眠图对32例脑卒中抑郁患者和30例抑郁症患者进行睡眠描记，并与对照组比较。结果：PSD组的REM睡眠时间和密度明显低于抑郁症组，差异有显著性。结论：PSD患者REM睡眠时间和密度是一个较为特征性的改变，提示卒中后抑郁的发生可能与脑内5-羟色胺递质改变有关。     

低频脉冲电刺激治疗失眠症的临床研究

目的 观察低频脉冲电刺激治疗失眠症患者多导睡眠图的变化特点,探讨低周波治疗失眠症的机制.方法 将80例患者随机分为低频脉冲电刺激组(低频脉冲电刺激)和药物对照组(口服艾司唑仑片),每组患者40例.分别于治疗前和治疗3个疗程后检测2组患者睡眠指标的改善情况.结果 疗程结束后,低频脉冲电刺激组有效率为87.5%,药物对照组有效率为65.O%,差异有统计学意义(P＜0.05).2组患者经治疗后,低周波治疗组S2期睡lilac间明显减少(P＜0.01)且S3+S4期睡眠时间明显增多(P＜0.01),药物对照组REM睡眠时间明显延长(P＜0.05).结论 低频脉冲电刺激治疗失眠症的疗效优于口服艾司唑仑,可更好地帮助患者维持正常生理性睡眠.     

低频脉冲电刺激治疗失眠症的临床研究

目的 观察低频脉冲电刺激治疗失眠症患者多导睡眠图的变化特点,探讨低周波治疗失眠症的机制.方法 将80例患者随机分为低频脉冲电刺激组(低频脉冲电刺激)和药物对照组(口服艾司唑仑片),每组患者40例.分别于治疗前和治疗3个疗程后检测2组患者睡眠指标的改善情况.结果 疗程结束后,低频脉冲电刺激组有效率为87.5%,药物对照组有效率为65.O%,差异有统计学意义(P＜0.05).2组患者经治疗后,低周波治疗组S2期睡lilac间明显减少(P＜0.01)且S3+S4期睡眠时间明显增多(P＜0.01),药物对照组REM睡眠时间明显延长(P＜0.05).结论 低频脉冲电刺激治疗失眠症的疗效优于口服艾司唑仑,可更好地帮助患者维持正常生理性睡眠.     

Nocturnal Sleep Recording with Cassette EEG in Chronic Headaches

Many headache patients complain of poor sleep, and sleep disturbance has been shown to play a role in chronic pain. We recorded nocturnal sleep with a 4-channel cassette EEG monitoring device in 10 common migraine patients, 10 individuals with muscle contraction (tension) headache, and 10 chronic tension-vascular headache sufferers. Migraine patients had essentially normal sleep, although rapid eye movement (REM) sleep and REM latency were increased. Patients with tension headache had reduced sleep time and sleep efficiency, decreased sleep latency but frequent awakenings, increased nocturnal movements, and marked reduction in slow wave sleep, without change in REM sleep or latency. Mixed-element headaches with both tension and vascular features were associated with reduced sleep, increased awakening, diminished slow wave sleep, and REM sleep that was decreased in amount and reduced in latency. The findings suggest that patients with intermittent migraine may have minimal sleep disturbance, while chronic headache may be worsened by chronically poor sleep. Muscle contraction headache may be associated with frequent awakenings and decreased slow wave sleep similar to the sleep changes of fibrositis, while chronic tension-vascular headache may have a depressive substrate. Four-channel sleep recording may miss contributory sleep apnea, but nonetheless cassette EEG may facilitate outpatient evaluation of refractory headaches.     

The role of emotional brain processing during sleep in depression

ACCESSIBLE SUMMARY: ? Explores current research illuminating the physiological mechanisms contributing the relationship of sleep dysfunction and depression. ? Investigates the crucial role of sleep in the affective modulation of brain functioning. ? Describes the relationship between emotional brain processing during rapid eye movement and depression. ? Points to the use of multi-therapeutic approaches for treatment with emphasis on positive behavioural imagery therapies. ABSTRACT: This review synthesizes some of the most current investigative research to illuminate the physiological mechanisms contributing to the relationship between sleep dysfunction and depression. Major depression has consistently been linked to sleep abnormalities and insomnia is a robust risk factor in the initiating and development of depression. Recent neurobiological findings indicate the crucial role of sleep in the affective modulation of brain functioning. Studies have demonstrated that sleep in major depression is characterized by a reduction in slow wave sleep, interruptions in sleep continuity, longer periods of rapid eye movement (REM) sleep including a shortening of REM latency (i.e. the time between sleep onset and the occurrence of the first REM period), as well as an increase in REM density. The failure of sleep dependant emotional brain processing in REM sleep that seems to occur in depression, support the development and fostering of clinical depression. How depression likely interplays with these sleep processes points to the use of multi-therapeutic approaches for treatment with emphasis on positive behavioural imagery therapies.     

松郁安神方对PCPA致失眠大鼠睡眠时相的影响

目的:观察松郁安神方对失眠大鼠睡眠时相的影响.方法:采用腹腔注射对氯苯丙氨酸(Para-chlorophenylalanine,PCPA)建立失眠大鼠模型,用松郁安神方进行干预,通过动物睡眠生物解析系统,记录脑电(Electroencephalogram,EEG)和肌电(Electromyogram,EMG),分析睡眠...     

gamma-aminobutyric Acid(A) (GABA(A)) agonist 4,5,6, 7-tetrahydroisoxazolo[4,5-c]pyridin-3-ol persistently increases sleep maintenance and intensity during chronic administration to rats

Many hypnotics, such as benzodiazepines, are agonistic modulators of gamma-aminobutyric acid(A) (GABA(A)) receptors. Such compounds increase the ability to fall and stay asleep, but inhibit rapid-eye movement (REM) sleep and deep non-REM sleep. However, tolerance to their hypnotic action may develop rapidly. Previous findings in rats and humans demonstrate that the gamma-aminobutyric acid(A) agonist 4, 5,6,7-tetrahydroisoxazolo[4,5-c]pyridin-3-ol (THIP) promotes deep non-REM sleep and increases non-REM sleep continuity. To investigate the effects of repeated administration, we assessed sleep in rats before, during, and after chronic dosing of THIP (3 mg/kg, once daily for 5 days; n = 9) or of placebo (n = 8). The substances were administered i.p. at the onset of darkness. The electroencephalogram (EEG) and electromyogram were recorded during the first 6 h after injection. During baseline recording, the placebo and the THIP group exhibited similar sleep patterns. After the first THIP injection, rats displayed more non-REM sleep, longer non-REM episodes, and higher levels of slow wave activity in the EEG within non-REM sleep than the placebo group rats. The effects were sustained during all treatment days. REM sleep was not affected. After drug withdrawal, the sleep patterns of the THIP and the placebo group were practically identical again. These observations suggest that THIP does not rapidly produce tolerance toward its sleep effects and abrupt drug withdrawal may not be associated with sleep disturbances. These findings confirm and extend the existing information suggesting that THIP may be promising for treatment of insomnia.     

抑郁症状与睡眠脑电图参数的相关分析

目的调查抑郁症状与睡眠脑电图参数的相关性。方法对停用精神药物3d的18例病人估价其汉密顿抑郁量表(HAMD)总分/诸因子分与14项睡眠脑电图参数的相关性。结果(1)焦虑/躯体化因子与快波睡眠百分率呈显著负相关性(r=-0.5097,df=16,P<0.05);(2)绝望感因子与慢波睡眠2相百分率呈显著正相关性(r=0.4874,df=16,P<0.05);(3)绝望感因子与快波睡眠活动量及强度分别呈显著负相关性(r分别为-0.5067和-0.5657,df=16,P均<0.05)。结论慢波睡眠2相百分率、快波睡眠活动量及强度可作为绝望感因子的生物学标记。     

Polysomnographic findings in nights preceding a migraine attack

Sleep recordings were performed in eight patients to analyse sleep alterations preceding migraine attacks. Polysomnographic recordings from nights before an attack were compared with nights without following migraine. We analysed standard sleep parameters and electroencephalogram (EEG) power spectra. The main findings preceding migraine attacks were a significant decrease in the number of arousals, a decrease in rapid eye movement (REM) density, a significant decrease of beta power in the slow wave sleep, and a decrease of alpha power during the first REM period. The results suggest a decrease in cortical activation during sleep preceding migraine attacks. According to the models of sleep regulation, alterations in the function of aminergic or cholinergic brainstem nuclei have to be discussed.     

Sleep and Brain Development: The Critical Role of Sleep in Fetal and Early Neonatal Brain Development

Sleep and sleep cycles begin at around 26 to 28 weeks' gestational age. They were originally recognized by observing infant behaviors. This observation of behaviors and changes in physiology has now added electoenchephalography (EEG) and continuous electoenchephalography (aEEG) to the studies of sleep and sleep cycles. Sleep partitions from indeterminate sleep EEG patterns to quiet sleep or non–rapid eye movement (REM) sleep, REM sleep, and quiet awake intervals. The REM sleep follows the quiet or slow wave sleep in the cycles. Sleep and sleep cycles are essential for the development of the neurosensory and motor systems in the fetus and neonate. They are essential for the creation of memory and long-term memory circuits, and they are essential for the maintenance of brain plasticity over the lifetime of the individual. The importance of sleep and preservation of sleep cycles in infants has been known for more than 40 years. They are critical for the fetus in utero and the preterm infant in the newborn intensive care unit (NICU). The infants' state and sleep-wake cycles have been studied as part of developmental care since the 1980s. A major part of the implementation of developmentally appropriate care involves using the infant state and cues to plan care and interventions. This is also essential for the preservation of sleep and sleep cycles that are essential for early neurosensory development. Interference with sleep and disruption of sleep cycles can significantly interfere with the early processes of sensory development. Parents are playing an increasingly important role in supporting early development.     

Heart rate variability during sleep and sleep apnoea in a population based study of 387 women

Increased sympathetic activity during sleep has been suggested as a link between obstructive sleep apnoea syndrome and cardiovascular disease. Heart rate variability (HRV) is a measure of autonomic effect on the heart. Different parameters have been associated with sympathetic and parasympathetic activity. We have studied HRV in different sleep stages and related the HRV‐pattern to sleep apnoea in a population‐based sample of 387 women. We investigated the HRV‐parameters standard deviation of all R‐R intervals (SDNN), root of the averaged square of successive differences (RMSSD), low frequency component (LF), high frequency component (HF), ratio of low frequency component to high frequency component LF/HF and VSAI [variation in sympathetic activity between rapid eye movement (REM) and slow wave sleep, defined as LF_REM?LF_SWS]. The HRV‐parameters were compared with the results of a full‐night polysomnography. Hourly incidence of obstructive episodes was used for classifying the subjects into four apnoea‐hypopnoea index (AHI)‐groups (<5, ≥5 and <15, 15–30 and >30 events). Individual sleep stages were analysed by pooling all recordings. Women with high AHI had higher heart rate and LF/HF ratio. In subjects with AHI >30, LF/HF ratio however dropped to same level as with AHI <5. Subjects with high AHI had low VSAI. Levels of SDNN, LF and LF/HF ratio during REM and light sleep were similar to wakefulness. In slow wave sleep the parameters decreased. In conclusion, moderately increased prevalence of obstructive apnoeas was associated with signs of higher sympathetic activity. High AHI was however associated with a HRV‐pattern suggestive of depressed sympathetic drive and lowered ability to increase it during REM.