剥夺睡眠对颞叶癫痫的检测

目的对常规脑电图正常的颞叶癫痢病人进行剥夺睡眠诱发。方法常规脑电图检查每人2次以上正常者，再进行剥夺睡眠诱发试验。结果颞区以癫痫综合波出现为主，单侧多于双侧，左侧多于右侧，以灶性阵发。癫痫波出现时间在思睡期-睡眠I期、睡眠Ⅱ期以后癫痫波逐渐减少至消失。结论剥夺睡眠诱发对癫痫尤其是颞叶癫痫及常规脑电图正常的癫痫者是一种非常有效的检测方法，还可对将要减药或停药的癫痫病人进行监测。     

睡眠剥夺的动物实验研究

本文就睡眠剥夺对机体生理、行为、学习、记忆以及早期即刻基因表达的影响作一综述     

全部睡眠剥夺对健康男性青年情绪的影响

目的 探讨长时间睡眠剥夺（SD）对情绪的影响。方法 挑选身体健康男性青年志愿者30名,剥夺全部睡眠52h。采用情绪状态问卷、贝克焦虑问卷、考虑自评量表、状态焦虑问卷和自评抑郁量表,分别在SD前（基础值）、SD期间（1次／6h,共8次）及一夜恢复性睡眠后评定受试者的情绪状态。结果 与基础值比较,随SD时间的延长,疲惫－惰性、焦虑、抑郁、困惑-迷茫等消极情绪的因子分逐渐增加（P＜0．05－0．001）,并与SD时间呈正相关;而有力－好动积极情绪因子分逐渐下降（P＜0．001）,与SD时间呈负相关（r＝－0．846,P＜0．001）。一夜恢复性睡眠后,疲惫－惰性和有力－好动因子分与基础值的差异仍有显著性（P＜0．05－0．01）,余均恢复到基础水平。结论 长时间的SD可导致情绪逐渐恶化。;一夜的恢复性睡眠对情绪的改善有一定效果。     

睡眠剥夺与应激

睡眠是人类不可缺少的生理过程.随着生活节奏的加快,出现睡眠障碍的患者越来越多,严重的影响了生活质量及健康.睡眠剥夺(SD)是采用人工技术减少正常睡眠量,造成睡眠障碍,以此作为对睡眠功能及睡眠障碍机制研究的窗口.     

睡眠剥夺与脑内的基因表达

睡眠十分重要，并且有着非常精细的自稳调节，研究发现觉醒时间的延长总是伴随着睡眠时间和（或）强度补偿性地增加。睡眠的自稳调节现象表明一旦剥夺睡眠，脑的生理、生化或分子学过程便会发生显著变化，揭示这些变化可以为我们了解睡眠功能提供重要线索。     

剥夺睡眠与睡眠诱发试验脑电图对不同类型癫痫的作用

目的：探讨诱发试验脑电图与不同类型癫痫的关系及临床意义。方法：对９８例临床确诊的癫痫患者分别进行常规脑电图检查和剥压睡眠诱发及睡眠诱发脑电图试验,比较三次结果的异常率和棘波出现率。结果：睡眠与剥夺睡眠诱发试验均可提高脑电图的异常率和棘波出现率,均可提高全身性强直阵挛发作、复杂部分性发作和失神发作等类型癫痫的棘波出现率,录夺睡眠诱发还可提高简单部分发作棘波的出现率,而对多种类并存者和不能分类者均无意义。结论：诱发试验提高棘波出现率不仅与诱发方法有关,而且与癫痫的发作类型有关。     

睡眠剥夺在抑郁症临床中的应用

睡眠剥夺在抑郁症临床中的应用杨理荣国外有关睡眠剥夺的研究文献较多，这一工作开展也较普遍，但国内很少有临床应用的报道。现对睡眠剥夺的有关资料作一介绍。一、睡眠剥夺的治疗机制睡眠剥夺主要用于抑郁症的治疗。有关治疗机制也象抑郁症的病理机制一样，还远未被认识...     

睡眠剥夺诱发精神分裂症一例

患者　男 ,2 3岁 ,农民 ,内向性格。于 2 0 0 3年 2月 5日在外地某歌厅打工从事倒班工作 ,因不能适应睡眠节律和相位的改变 ,遂于 5天内持续服用大剂量咖啡 (共 2 0袋 ) ,每天服 4袋。致使 5天内不能进入睡眠状态 ,每天只睡几十分钟。 5天后患者迅速出现精神异常 ,表现为言语增多 ,语无伦次 ,打骂他人等 ,在当地某精神病医院诊断为精神分裂症 ,予氟哌啶醇 2 4mg/d等治疗 ,2 0余天未见好转。于 2 0 0 3年3月 7日来我院。患者表现兴奋 ,话多 ,夸大 ,多疑 ,思维散漫 ,言语结构松散 ,缺乏逻辑性 ,情感不协调 ,智能正常 ,有攻击行为 ,无自知力。…     

睡眠剥夺对抑郁模型大鼠及正常大鼠行为的影响

目的 分析睡眠剥夺对抑郁模型大鼠及正常大鼠行为的不同影响.方法 实验动物为2～3月龄Sprague Dawley(SD)雄性大鼠,取24只随机分为:(A)正常对照组、(B)正常+大平台对照组、(C)正常+睡眠剥夺组,每组8只.另48只大鼠用21 d慢性不预见性应激制造抑郁模型.将造模成功者随机分为:(D)抑郁+睡眠剥夺组、(E)抑郁+大平台对照组.前三组在第0天和第3天检测大鼠自发活动.后两组在第0天、第21天和第24天检测大鼠自发活动.观察快眼动睡眠剥夺作用下正常大鼠和抑郁模型大鼠自发活动总路程、中央路程和休息时间的变化.结果 抑郁模型大鼠睡眠剥夺后与抑郁+大平台组大鼠相比较,总路程和休息时间显著增加,差异具有统计学意义(P＜0.05),中央路程之间差异无统计学意义(P＞0.05).抑郁模型大鼠睡眠剥夺后与睡眠剥夺前相比,总路程、中央路程均显著增加,差异具有统计学意义(P＜0.05);慢性应激抑郁模型大鼠在大平台水环境处理前后自发活动无明显变化,差异无统计学意义(P＞0.05).正常大鼠睡眠剥夺后与正常+大平台对照组比,自发活动总路程增加,差异具有统计学意义(P＜0.05),自发活动中央路程及休息时间无明显变化,差异无统计学意义(P＞0.05);正常大鼠经大平台水环境处理后,自发活动总路程、自发活动中央路程及自发活动休息时间均较正常对照组无明显变化,差异无统计学意义(P＞0.05).结论 睡眠剥夺后正常大鼠出现焦虑样行为改变,而对抑郁模型大鼠可以缓解其抑郁样行为.     

睡眠剥夺对大鼠脑损害的生化研究

目的 探讨睡眠剥夺(SD)的脑损害机制。方法 采用小平台水环境法建立睡眠SD模型，将30只Sprague-Dawley大鼠随机分为睡眠剥夺1天、3天和5天组(SDld、SD3d、SD5d)，大平台组(TC)和正常对照组(NC)，每组6只。测定脑组织一氧化氮(N0)含量和超氧化物歧化酶(SOD)活性，测定血清髓鞘碱性蛋白(MBP)、皮质醇、白细胞介素—1β(IL-1β)和白细胞介素—2(IL—2)含量。结果 (1)N0含量：SD各组及TC组鼠额叶、海马和中脑的N0含量均高于NC组(F＝10．97，7．96，5．23，P＜0．01)，且随SD时间的延长而升高；仅下丘脑N0含量差异未达显著性(F＝1．64，P＞0．05)。(2)SOD活性：SD各组及TC组鼠额叶、海马、中脑和下丘脑SOD活性均高于NC组(F＝10．44，16．15，28．94，12．75，P＜0．01);其中在海马、中脑和下丘脑SOD活性均以SD3组为最高。(3)血清皮质醇、IL-1β、IL—2和MBP含量：SD各组均高于NC组(F＝8．60，3．62，3．84，2．83，P＜0．01和P＜0．05)，且各项指标含量均随SD时间的延长而逐渐升高。TC组仅皮质醇的含量与NC组的差异有显著性。结论 睡眠剥夺的脑损害可能与N0、氧自由基、皮质醇及细胞因子等生化因素有关。     

DST in healthy volunteers and after sleep deprivation

The dexamethasone suppression test (DST) was performed in 46 healthy volunteers and repeated in nine of them following total sleep deprivation (TSD). While only 2 postdexamethasone cortisol values were insufficiently suppressed (greater than 5 micrograms %) in control DSTs, 5 postdexamethasone cortisol values were above 5 micrograms % following TSD. The mean postdexamethasone value was increased from 1.55 +/- 1.06 to 4.47 +/- 5.86 micrograms % following TSD at 8.00 h. The authors conclude that sleep deprivation as a therapeutic approach and prolonged sleeplessness may bias DST results.     

Effects of different sleep deprivation protocols on sleep perception in healthy volunteers

Objectives

To investigate whether different protocols of sleep deprivation modify sleep perception.

Methods

The effects of total sleep deprivation (TD) and selective rapid eye movement (REM) sleep deprivation (RD) on sleep perception were analyzed in normal volunteers. Thirty-one healthy males with normal sleep were randomized to one of three conditions: (i) normal uninterrupted sleep; (ii) four nights of RD; or (iii) two nights of TD. Morning perception of total sleep time was evaluated for each condition. Sleep perception was estimated using total sleep time (in hours) as perceived by the volunteer divided by the total sleep time (in hours) measured by polysomnography (PSG). The final value of this calculation was defined as the perception index (PI).

Results

There were no significant differences among the three groups of volunteers in the total sleep time measured by PSG or in the perception of total sleep time at baseline condition. Volunteers submitted to RD exhibited lower sleep PI scores as compared with controls during the sleep deprivation period (P < 0.05). Both RD and TD groups showed PI similar to controls during the recovery period.

Conclusion

Selective REM sleep deprivation reduced the ability of healthy young volunteers to perceive their total sleep time when compared with time measured by PSG. The data reinforce the influence of sleep deprivation on sleep perception.     

睡眠剥夺对健康青年男性工作记忆的影响及莫达非尼的干预作用

目的 探讨不同时间睡眠剥夺对健康青年男性工作记忆的影响,以及莫达非尼对睡眠剥夺的对抗作用. 方法 10名健康男性青年志愿者进行间隔1周的3次36 h睡眠剥夺,第一次不服药,为剥夺组,后2次志愿者交叉服用莫达非尼和安慰剂(于睡眠剥夺14 h和24h 2次服用1.每次服药后3 h进行工作记忆任务测试(倒数n项测验),剥夺组也在同样的时间进行测试.把睡眠剥夺前清醒时设为正常对照组.并进行测试. 结果 剥夺组的1-back任务的第2次测试平均反应时间较第1次测试明显延长,2-back任务的第2次测试平均反应时间、错误率较第1次测试明显增高,差异均有统计学意义(P＜0.05).剥夺组的l-back任务的第2次测试错误率与平均反应时间均比正常对照组明显增高,2-back任务的两次测试平均反应时间和错误率较正常对照组明显增高,差异均有统计学意义(P＜0.05).莫达非尼组的1-back任务的第2次测试平均反应时间较剥夺组明显降低,2-back任务的两次测试平均反应时间和错误率较剥夺组明显降低,差异均有统计学意义(P＜0.05). 结论 睡眠剥夺后工作记忆受到损害,并随着剥夺时间延长,受损加重.莫达非尼对睡眠剥夺后的工作记忆损害有明显的改善作用.     

Altered insula-prefrontal functional connectivity correlates to decreased vigilant attention after total sleep deprivation

BackgroundSleep deprivation can robustly affect vigilant attention. The insula is a key hub of the salience network that mediates shifting attention between endogenous and exogenous states. However, little is known regarding the involvement of insular functional connectivity in impaired vigilant attention after total sleep deprivation (TSD). The purpose of this study is to explore the alterations in insular functional connectivity and its association with vigilant attention performance following TSD.MethodsTwenty-six adult men were enrolled in the study. Participants underwent two counterbalanced resting-state functional magnetic resonance imaging (rs-fMRI) scans, once in rested wakefulness (RW) and once after 36 h of TSD. Seed-based functional connectivity analysis was performed using rs-fMRI data for the left and right insula. The vigilant attention was measured using a psychomotor vigilance test (PVT). Furthermore, Pearson correlation analysis was conducted to investigate the relationship between altered insular functional connectivity and PVT performance.ResultsCompared to RW, enhanced functional connectivity was observed between the insula and prefrontal cortex and anterior cingulate cortex, while reduced functional connectivity was observed between the insula and temporal, parietal, and occipital regions following TSD. Moreover, altered insular functional connectivity with the prefrontal cortex, ie superior frontal gyrus and middle frontal gyrus, and inferior temporal gyrus was correlated with PVT performance after TSD.ConclusionOur results suggest that insular coupling with the prefrontal cortex and inferior temporal gyrus may act as neural indicators for vigilant attention impairment, which further reveals the critical role of the salience network in cognitive decline following TSD.     

Effect of sleep deprivation on sleep and EEG power spectra in the rat

EEG power spectra of the rat were computed for consecutive 4-s epochs of the daily light period and matched with the scores of the vigilance states. Sleep was characterized by a progressive decline of low frequency spectral values (i.e. slow wave activity) in non-rapid eye movement (non-REM) sleep, and a progressive increase in the amount of REM sleep. During recovery from 24-h total sleep deprivation (TSD) the following changes were observed: an increase of slow wave activity in non REM sleep with a persisting declining trend; an enhancement of theta activity (7.25-10.0 Hz) both in REM sleep and waking; a decrease of non-REM sleep and an increase of REM sleep. In addition, a slow wave EEG pattern prevailed in the awake and behaving animal during the initial recovery period. In selective sleep deprivation paradigms, either REM sleep or slow wave activity in non-REM sleep was prevented during a 2-h period following upon 24-h TSD. During both procedures, non-REM sleep spectra in the lowest frequency band showed no increase. There was no evidence for a further enhancement of slow wave activity after its selective deprivation. The results indicate that: (1) slow wave activity in non-REM sleep and theta activity in REM sleep may reflect sleep intensity; and (2) REM sleep and active waking, the two states with dominant theta activity, may be functionally related.     

大鼠睡眠剥夺方法的研究进展

目前睡眠的功能并不十分清楚．睡眠研究方法的不足很大程度上制约了睡眠研究及其理论的发展。睡眠剥夺是目前一种很有发展潜力的研究睡眠的手段．它对人们研究睡眠各期的功能有很强的启发性。在睡眠剥夺研究中．要想得到可靠的实验结果．需要有效专一地消除睡眠，因而，消除睡眠的睡眠剥夺方法在研究中有着很重要的意义。本文将几种常用的大鼠睡眠剥夺方法予以综述．     

功能磁共振成像研究睡眠剥夺36小时对健康男性工作记忆的影响

目的 利用功能磁共振成像(functional magnetic resonance imaging,fMRI)技术研究睡眠剥夺36 h对健康男性工作记忆的影响及可能机制.方法 10名健康男性受试者连续36 h睡眠剥夺,睡眠剥夺前后分别接受工作记忆任务测试,同时进行fMRI扫描.fMRI扫描采用2项工作记忆任务,收集获得的行为学结果和fMRI图像,用SPM2软件进行图像分析.比较睡眠剥夺前后工作记忆任务测试及fMRI扫描结果.结果 剥夺后LTR任务的反应时间为(866±102)ms,比剥夺前[(754±91)ms]明显延长(t=2.59,P<0.01),准确率为84.78%±8.71%,比剥夺前(95.31%±3.56%)明显降低(t=3.52,P<0.01);剥夺后PLUS任务的反应时间为(848±94)ms,比剥夺前[(756±79),ms]明显延长(t=2.37,P<0.05),准确率为84.22%±9.66%,比剥夺前(95.70%±4.72%)明显降低(t=3.38,P<0.01);剥夺前在额顶叶、前扣带回和丘脑等工作记忆相关性脑区被激活.PLUS任务较LTR任务激活脑区范围更广,强度更显著.剥夺后顶叶激活降低,前额叶和丘脑的激活增强.结论 睡眠剥夺能够导致工作记忆能力受损.fMRI显示睡眠剥夺后完成工作记忆任务时,在相应脑区顶叶激活降低,前额叶和丘脑激活增强,这可能是睡眠剥夺导致认知功能损害的机制之一.     

Maintenance of therapeutic effects of total sleep deprivation by limitation of subsequent sleep A PILOT STUDY

In a previous study it was shown that in endogenous depression repeated sleep deprivation (SD) during clomipramine treatment resulted in rapid improvement after each SD. However, except after the first night, relapses were observed after all sleep nights following SD (the “recovery nights”). The present pilot study had a therapeutic aim, namely to prevent these relapses. We were interested in whether limitation of sleep during the recovery nights might prevent these relapses and whether different amounts of sleep would have different effects on the course of mood after recovery sleep. Ten endogenously depressed patients were treated with clomipramine and with three SD's. Five patients slept for approximately 2 h, and the other five for about 5 h during the second and third recovery nights. On average, no relapse was shown by these patients and, in fact, there was some additional improvement after these nights, in contrast to the findings in the previous study, where patients were allowed unlimited sleep.     

The timing and duration of sleep in partial sleep deprivation therapy of depression

The antidepressant response to partial sleep deprivation early in the night (PSD-E) was compared with the response to partial sleep deprivation late in the night (PSD-L) in 16 drug-free depressed inpatients using a balanced order crossover design. PSD-L had a significantly greater antidepressant effect that PSD-E. The response to PSD-L was sustained and enhanced by a second night of treatment. Patients had significantly shorter sleep durations and reduced REM sleep on PSD-L that did not occur in the PSD-E situation. There was a significant negative correlation between response to PSD and sleep duration, and in particular, REM sleep duration, in the late sleep deprivation situation. Thus, the amount and timing of sleep appear to be factors in the response to PSD, but additional studies are needed to evaluate the relative importance of these parameters.