睡眠知觉障碍者的睡眠生理及其人格特征

目的:比较睡眠知觉障碍者与原发性失眠症患者、睡眠正常者的睡眠生理、睡眠感觉和人格差异。方法:于2003-01/2004-01选择到北京市第二医院睡眠障碍治疗中心门诊就诊的睡眠知觉障碍者12例,以年龄、性别、受教育程度、工作性质(脑力和体力)为参照配对,选择12例原发性失眠症门诊患者和12例睡眠正常者,构成3组观察对象。用夜间多导睡眠图检测观察对象的客观睡眠指标,记录睡眠潜伏期、睡眠总时间、睡眠效率、醒觉时间和睡眠结构。同时让观察对象回忆自己昨晚大约用多长时间入睡,总共睡眠时间,即睡眠潜伏期和主观睡眠总时间的判断,以作为主观睡眠指标。白天进行明尼苏达多相人格测验量表测量,评估观察对象的疑病、抑郁、癔病、精神病态、性度、偏执、精神衰弱、精神分裂、轻躁狂、社会内向性共10个临床量表因子分。结果:3组观察对象都完成了实验调查的全部过程,均进入结果分析。①睡眠知觉障碍者的客观睡眠指标中睡眠潜伏期、睡眠总时间、睡眠效率、醒觉时间和睡眠结构与睡眠正常者比较差异均无显著性;睡眠知觉障碍者的主观睡眠潜伏期和睡眠总时间与客观多导睡眠记录差值很大,显著大于睡眠正常者和原发性失眠症患者(P<0.05)。②睡眠知觉障碍者的明尼苏达多相人格测验量表的精神病态和轻躁狂因子分显著高于原发性失眠症和睡眠正常者(P<0.01)。结论:睡眠知觉障碍者的客观睡眠状态与睡眠正常者基本相同,主观睡眠与睡眠正常者和原发性失眠症比较存在很大异常。睡眠知觉障碍者的人格特征既有别于睡眠正常者也不同于原发性失眠症患者,并可能对其异常的主观睡眠行为产生影响。     

音乐治疗对失眠症患者睡眠状况及多导睡眠图的影响

目的:探讨音乐治疗对失眠症患者睡眠状况及多导睡眠图的影响.方法:将60例失眠症患者按随机数字表法分为实验组与对照组各30例,均口服安神丸治疗,实验组在此基础上联合音乐治疗,观察8周.治疗前后采用多导睡眠仪监测两组睡眠状况及多导睡眠图的变化.结果:治疗后两组睡眠总时间均较治疗前显著延长,睡眠潜伏期、醒觉时间均较治疗前显著缩短(P＜0.05或0.01).实验组睡眠总时间、睡眠潜伏期、睡眠效率、快速眼球运动睡眠时间较对照组改善更为显著(P＜0.05或0.01).结论:音乐治疗对失眠症患者具有辅助治疗作用,对其夜间多导睡眠脑电参数有不同程度的影响,有利于改善失眠症状,提高睡眠质量.     

对失眠症患者实施睡眠护理干预的研究

目的探讨护理干预对失眠症病人睡眠的影响.方法对55例失眠症病人实施睡眠卫生教育,进行干预前后的主-客观评价,并与对照组比较.结果失眠症组有明显的睡眠潜伏期延长,总睡眠时间减少;睡眠干预配合组睡眠潜伏期和总睡眠时间明显好于不配合组,两组差异有统计学意义(P<0.05).结论对失眠症病人实施睡眠护理干预,可取得明显效果,方法简便易行,值得推广.     

不宁腿综合征多导睡眠图监测情况分析

目的探讨不宁腿综合征（restless legs syndrome,RLS）夜间视频多导睡眠图与患者睡眠质量主观感受的差异,分析RLS患者伴发焦虑-抑郁状态。方法 26例RLS患者为RLS组,24例体检健康者为对照组,分析2组视频多导睡眠图结果,应用汉密尔顿焦虑抑郁量表及匹兹堡睡眠质量问卷评价RLS患者的焦虑-抑郁状态及主观睡眠情况。结果与对照组比较,RLS组总睡眠时间、睡眠效率、睡眠维持率、快速眼动睡眠次数降低（P〈0.05）,睡眠潜伏期、快速眼动睡眠潜伏期、醒起时间、≥5min的醒觉次数、非快速眼动睡眠Ⅰ期和Ⅱ期所占睡眠比例延长或增高（P〈0.05）。结论多导睡眠监测可客观评定患者睡眠质量,对RLS诊断有一定价值。     

慢性失眠症患者对睡眠的主观评估特征

目的:探讨慢性失眠症患者对睡眠后主观评估的特点。方法:2000-10/2003-09对新乡医学院第二附属医院收治的37例慢性失眠症患者和30名健康成人分别进行多导睡眠图和睡眠自评量表主客观评估。结果:失眠症患者不但有睡眠量的减少,同时存在有睡眠时间的判断错误,其中对睡眠潜伏期、总睡眠时间、总觉醒时间及快速动眼睡眠时间这4个睡眠参数主客观评价分别为(67.43±29.32,37.83±13.73);(155.19±40.70,295.54±59.71);(208.84±56.67,110.86±20.77);(52.27±16.84,37.81±12.26)min,与对照组比较和自身比较差异有显著性意义(P<0.001)。女性在各项指标主观评估上明显差于男性,女性和男性对4个参数的评估分别为(83.31±22.05,50.61±12.70);(136.47±36.95,184.89±25.65);(273.84±63.88,135.50±24.29);(78.68±22.00,26.28±6.34)min(P<0.01)。结论:慢性失眠症有着过分夸张症状的特征,女性比男性更明显。     

中医香囊对老年失眠患者睡眠时间及睡眠深度的影响

目的:探讨中医香囊对老年失眠患者睡眠时间及睡眠深度的影响。方法:选取2019年6月至2020年6月东莞市东坑医院收治的护理院入住的失眠症老年患者60例作为研究对象,使用中医香囊进行治疗。采用国际通用SPIEGEL量表比较治疗前后失眠症老年患者的入睡时间、总睡眠时间、夜醒次数、睡眠深度、夜间做梦情况、醒后情况。结果:治疗后,失眠症老年人的入睡时间、总睡眠时间、夜醒次数、睡眠深度、夜间做梦情况、醒后情况评分均明显降低,且治疗总有效率达76.67%。结论:采用中医香囊治疗老年失眠症,能够有效改善老年失眠的睡眠状况,延长其睡眠时间及睡眠深度,提高睡眠质量。     

慢性失眠症患者对睡眠的主观评估特征

目的：探讨慢性失眠症患者对睡眠后主观评估的特点。方法：2000—10／2003—09对新乡医学院第二附属医院收治的37例慢性失眠症患者和30名健康成人分别进行多导睡眠图和睡眠自评量表主客观评估。结果：失眠症患者不但有睡眠量的减少，同时存在有睡眠时间的判断错误，其中对睡眠潜伏期、总睡眠时间、总觉醒时间及快速动眼睡眠时间这4个睡眠参数主客观评价分别为(67．43&;#177;29．32，37．83&;#177;13．73)；(155．19&;#177;40．70，295．54&;#177;59．71)：(208．84&;#177;56．67，110．86&;#177;20．77)：(52．27&;#177;16．84，37．81&;#177;12．26)min，与对照组比较和自身比较差异有显著性意义(P&;lt;0．001)。女性在各项指标主观评估上明显差于男性，女性和男性对4个参数的评估分别为(83．31&;#177;22．05，50．61&;#177;12．70)；(136．47&;#177;36．95，184．89&;#177;25．65)；(273．84&;#177;63．88，135．50&;#177;24．29)；(78．68&;#177;22．00，26．28&;#177;6．34)min(P&;lt;0．01)。结论：慢性失眠症有着过分夸张症状的特征，女性比男性更明显。     

原发性失眠主客观睡眠质量与日间功能损害的关系

目的探讨原发性失眠患者日间功能损害及其影响因素。方法选取2010年3月-12月符合美国《精神障碍诊断与统计手册》第4版诊断标准的原发性失眠者62例,另选择性别、年龄匹配的健康睡眠者53例。失眠组和对照组均采用匹茨堡睡眠质量指数量表(PSQI)评估1个月的主观睡眠质量,多导睡眠监测(PSG)评估客观睡眠质量,并通过"主观睡眠时间/客观睡眠时间×100%"计算睡眠知觉,PSG监测后受试者完成一系列日间功能评定,包括Epworth嗜睡量表(ESS)评价嗜睡程度、Flinders疲劳量表(FFS)评价疲劳程度、贝克抑郁量表(BDI)和状态-特质焦虑量表(STAI)评估情绪状态。结果①与对照组相比,失眠组主客观睡眠质量均较差;PSQI分数更高[(14.37±2.44)、(2.74±1.79)分,P<0.001)];睡眠知觉差[(49.76±33.29)、(99.36±12.79)分,P<0.001)]。②失眠组FSS、BDI、SAI、TAI分数明显高于对照组,ESS分数低于对照组(P值均<0.05)。③PSQI总分与ESS呈负相关(r=0.17,P<0.01),与FSS、BDI、SAI、TAI分数呈正相关(r=0.54,r=0.66,r=0.70,r=0.87)(P值均<0.01)。客观睡眠时间与ESS(r=0.01,P=0.138)、FSS(r=0.02,P=0.019)、BDI(r=0.03,P=0.022)、SAI(r=0.03,P=0.086)、TAI(r=0.04,P=0.015)分数均无明显相关性。结论原发性失眠者主观睡眠质量与多项日间功能损害相关,这为有效的治疗失眠和改善日间症状提供理论依据。     

亚健康失眠者睡眠结构特征分析

目的:探讨亚健康失眠者的睡眠结构特征表现.方法:应用微动敏感床垫睡眠监测系统检测亚健康失眠者的睡眠结构情况.结果:168例(男94例,女74例)亚健康失眠者均存在有睡眠结构不同方面的异常,其中浅睡期、深睡期和非快速眼动期异常例数的比例均在70%以上.量化分析睡眠结构检测结果,除了睡眠总时间外其他指标的总体均数均有异常.与42例睡眠正常者(男23例,女19例)比较,两者在入睡潜伏期、浅睡期、深睡期、快速眼动期及醒觉总时间之间差异均有非常显著性(P<0.01).结论:亚健康失眠者的睡眠结构存在有不同方面的异常,其特征以入睡困难、睡眠表浅、易醒等为主要表现.     

腺样体肥大儿童睡眠特征分析及护理

目的研究腺样体肥大对儿童睡眠结构的影响,以便有针对性地指导护理。方法通过多导睡眠图分析47例腺样体肥大儿童睡眠结构,并与同龄组儿童睡眠结构正常值进行比较。结果腺样体肥大组的睡眠结构存在如下异常:与同龄组正常儿童相比,S1期、Delta期、NREM期所占比例增加,S2期、REM期所占比例减少;总醒觉时间,NREM醒觉次数明显高于REM醒觉次数;REM潜伏期比正常值延长约2倍,睡眠效率低于正常值。结论腺样体肥大主要引起睡眠结构紊乱、醒觉次数增加、REM睡眠剥夺睡眠片段、睡眠效率低,但Delta期睡眠时间增加。针对睡眠和围手术期的护理干预有助于该病患儿的康复。     

Genes for normal sleep and sleep disorders

Sleep and wakefulness are complex behaviors that are influenced by many genetic and environmental factors, which are beginning to be discovered. The contribution of genetic components to sleep disorders is also increasingly recognized as important. Point mutations in the prion protein, period 2, and the prepro‐hypocretin/orexin gene have been found as the cause of a few sleep disorders but the possibility that other gene defects may contribute to the pathophysiology of major sleep disorders is worth in‐depth investigations. However, single gene disorders are rare and most common disorders are complex in terms of their genetic susceptibility, environmental effects, gene‐gene, and gene‐environment interactions. We review here the current progress in the genetics of normal and pathological sleep.     

Genes for normal sleep and sleep disorders

Sleep and wakefulness are complex behaviors that are influenced by many genetic and environmental factors, which are beginning to be discovered. The contribution of genetic components to sleep disorders is also increasingly recognized as important. Point mutations in the prion protein, period 2, and the prepro-hypocretin/orexin gene have been found as the cause of a few sleep disorders but the possibility that other gene defects may contribute to the pathophysiology of major sleep disorders is worth in-depth investigations. However, single gene disorders are rare and most common disorders are complex in terms of their genetic susceptibility, environmental effects, gene-gene, and gene-environment interactions. We review here the current progress in the genetics of normal and pathological sleep.     

BDNF in sleep,insomnia, and sleep deprivation

The protein brain-derived neurotrophic factor (BDNF) is a member of the neurotrophin family of growth factors involved in plasticity of neurons in several brain regions. There are numerous evidence that BDNF expression is decreased by experiencing psychological stress and that, accordingly, a lack of neurotrophic support causes major depression. Furthermore, disruption in sleep homeostatic processes results in higher stress vulnerability and is often associated with stress-related mental disorders. Recently, we reported, for the first time, a relationship between BDNF and insomnia and sleep deprivation (SD). Using a biphasic stress model as explanation approach, we discuss here the hypothesis that chronic stress might induce a deregulation of the hypothalamic-pituitary-adrenal system. In the long-term it leads to sleep disturbance and depression as well as decreased BDNF levels, whereas acute stress like SD can be used as therapeutic intervention in some insomniac or depressed patients as compensatory process to normalize BDNF levels. Indeed, partial SD (PSD) induced a fast increase in BDNF serum levels within hours after PSD which is similar to effects seen after ketamine infusion, another fast-acting antidepressant intervention, while traditional antidepressants are characterized by a major delay until treatment response as well as delayed BDNF level increase.

• Key messages

• Brain-derived neurotrophic factor (BDNF) plays a key role in the pathophysiology of stress-related mood disorders.

• The interplay of stress and sleep impacts on BDNF level.

• Partial sleep deprivation (PSD) shows a fast action on BDNF level increase.