特发性过度睡眠

目的探讨特发性过度睡眠患者临床表现以及多导睡眠图特征。方法与结果回顾分析4例特发性过度睡眠患者的临床资料,均以白天过度嗜睡首发,无猝倒、睡眠麻痹、睡前幻觉及睡眠行为障碍,其中2例伴自主神经功能障碍。4例患者Epworth嗜睡量表评分均〉11分;多次小睡潜伏期试验平均睡眠潜伏期明显缩短,未见睡眠起始快速眼动期;例3患者全夜多导睡眠图监测显示睡眠潜伏期明显缩短,总睡眠时间延长,但夜间睡眠结构正常。结论明确诊断特发性过度睡眠需结合患者病史资料、临床表现及实验室检查进行综合考虑,多次小睡潜伏期试验和全夜多导睡眠图监测是鉴别诊断特发性过度睡眠与发作性睡病的有效方法。     

特发性过度睡眠

目的 探讨特发性过度睡眠患者临床表现以及多导睡眠图特征.方法 与结果回顾分析4 例特发性过度睡眠患者的临床资料,均以白天过度嗜睡首发,无猝倒、睡眠麻痹、睡前幻觉及睡眠行为障碍,其中2 例伴自主神经功能障碍.4 例患者Epworth 嗜睡量表评分均＞ 11 分;多次小睡潜伏期试验平均睡眠潜伏期明显缩短,未见睡眠起始快速眼动期;例3 患者全夜多导睡眠图监测显示睡眠潜伏期明显缩短,总睡眠时间延长,但夜间睡眠结构正常.结论 明确诊断特发性过度睡眠需结合患者病史资料、临床表现及实验室检查进行综合考虑,多次小睡潜伏期试验和全夜多导睡眠图监测是鉴别诊断特发性过度睡眠与发作性睡病的有效方法.     

发作性睡病夜间睡眠结构特征的探讨

目的了解发作性睡病患者夜间睡眠结构特点。方法对10例符合发作性睡病国际睡眠疾病分类最低诊断标准的发作性睡病患者和13例正常对照者连续进行两夜夜间多导睡眠图监测,比较两组各项睡眠参数,并分析发作性睡病患者的夜间睡眠结构特点。结果发作性睡病组患者的夜间睡眠潜伏期和快速眼动睡眠潜伏期缩短(P<0．01),在整个睡眠过程中睡眠始发快速眼动时段出现比例明显升高(P<0．01),唤醒指数和睡眠纺锤波密度增高(P<0．05),睡眠转换次数和清醒次数及S1期睡眠比例增加(P<0．01),S2期和S3 S4期比例减少(P<0．01),快速眼动密度增加(P<0．01);全夜快速眼动睡眠时段持续时间无逐渐延长趋势。与对照组受试者睡眠生理参数相比,差异具有显著性意义(P<0．05或P< 0．01)。结论发作性睡病患者夜间睡眠结构的特征为快速眼动活动增强,睡眠维持机制紊乱,中枢唤醒水平降低。     

24例成人发作性睡病伴快速眼动睡眠期行为异常患者临床及多导睡眠图分析

目的探讨发作性睡病(Narcolepsy)合并快速眼动睡眠期行为异常(REM sleep behavior disorder,RBD)患者的临床及多导睡眠图特征,为临床诊断提供客观依据。方法收集本院24例临床诊断为发作性睡病同时合并RBD患者,行多导睡眠监测(polysomnography,PSG)及多次睡眠潜伏期试验(multiple sleep latency test,MSLT),对其临床症状及电生理检查结果进行统计分析。结果临床症状:本组24例均存在白天不能控制的过度嗜睡(100%);临床症状表现形式有睡眠相关性幻觉、睡眠瘫痪、猝倒发作、夜间睡眠中打鼾、憋醒、夜间睡眠中拍打同床人、梦境扮演经历。PSG分析:24例患者中24例N1期睡眠时间增加(100%);18例N2期睡眠时间减少(75%);18例N3期睡眠时间减少或消失(75%);12例REM睡眠时间延长(50%);9例(37.5%)存在呼吸暂停-低通气情况(AHI5次/时);15例(62.5%)存在周期性肢体运动(PMLS指数15次/时);24例伴随下颌肌电持续或间断增高(100%);12例伴随出现肢体或颜面部异常活动(50%)。MSLT分析:24例平均睡眠潜伏时间均小于8 min同时大于或等于两次REM起始睡眠(100%)。结论成人发作性睡病患者常合并睡眠呼吸暂停-低通气综合征,继发性嗜睡症状需与发作性睡病相鉴别;发作性睡病者常合并RBD,异常动作并非每夜都发生,但PSG可发现微小的异常动作或肌电活动,帮助疾病诊断;发作性睡病常合并周期性肢体运动,且分布在REM睡眠期较多时,需注意是否同时存在RBD可能。     

发作性睡病并OSAHS(附1例报道及文献复习)

目的探讨发作性睡病并阻塞性睡眠呼吸暂停低通气综合征(obstructive sleep apnea hypopneasyndrome,OSAHS)的发病机制、临床特点及治疗。方法回顾性分析1例发作性睡病并OSAHS患者的临床表现、多导睡眠图及颅脑MRI检查,并复习相关文献。结果患者有白天过度睡眠、嗜睡猝倒发作、睡眠麻痹和睡眠幻觉,睡眠呼吸监测提示严重呼吸暂停低通气表现,颅脑MRI检查示脑内多发腔隙灶及蛛网膜囊肿。结论发作性睡病与OSAHS可能相互影响,两病共存并非罕见,应避免漏诊。     

发作性睡病36例临床分析

目的探讨发作性睡病的临床特征、诊断、治疗及预后。方法对36例发作性睡病患者进行睡眠脑电图监测,结合临床表现进行诊断,采用哌醋甲酯、氯酯醒、氯丙米嗪治疗,并进行随访。结果36例患者均有过度或发作性的不可抑制的白天睡眠,30例有夜间睡眠紊乱,25例伴猝倒,9例伴睡眠瘫痪,10例出现睡眠幻觉。睡眠脑电图监测显示36例患者平均睡眠潜伏期<5 min,有2次或2次以上直接进入快速眼动相睡眠。随访29例,其中20例采用哌醋甲酯治疗,17例白天过度睡眠得到改善;8例采用氯酯醒或合并氯丙米嗪治疗,5例症状改善;大多数患者出现不同程度的心理和学习问题。结论发作性睡病是慢性神经系统疾病,应根据其典型的临床表现及睡眠脑电监测结果作出早期诊断,对患者应给予长期的药物治疗、心理治疗和教育,以提高患者的生活质量。     

多次睡眠潜伏期试验的检测方法及临床应用进展

应用多导睡眠仪（PSG）进行多次睡眠潜伏期试验（MSLT）是客观评价日间思睡严重程度的 标准工具。分析多次试验的睡眠次数、平均睡眠潜伏期以及快速眼动（REM）睡眠出现的潜伏期与次数， 能将思睡的严重程度用睡眠潜伏期的长短显示出来，更具有客观性和可重复性。目前MSLT在临床已 广泛用于发作性睡病的诊断，特发性睡眠增多和阻塞性睡眠呼吸暂停综合征等日间思睡的严重程度评 估，以及精神振奋剂等药物的疗效评估。现对MSLT的具体检测方法及临床应用作一综述。     

发作性睡病患者自发性体动及体温昼夜特征分析

目的探讨发作性睡病患者自发性体动及深部体温昼夜节律特点。方法共14例发作性睡病患者和14例性别、年龄相匹配的正常对照者,行夜间多导睡眠图监测和次日多次睡眠潜伏期试验(MSLT),体动记录仪连续监测自发性体动1~2周并每日记录睡眠日记,于昼夜20个时间点测量深部体温。结果与对照组相比,发作性睡病组患者夜间卧床时间增加(P=0.008),睡眠效率降低(P=0.001),入睡后觉醒次数增加(P=0.000)、觉醒时间延长(P=0.000),易出现睡眠始发的快速眼动睡眠(SOREMP,P=0.002);MSLT试验中平均睡眠潜伏期缩短(P=0.000),SOREMPs次数增加(P=0.000);夜间总活动量和活动度增加(均P=0.000),白天总活动量和活动度减少(均P=0.000),夜间与白天总活动量和活动度比值升高(均P=0.000)。两组受试者深部体温呈现明显昼夜节律变化,其中值、振幅和峰值相位差异均无统计学意义(P=0.177,0.730,0.488)。结论尽管发作性睡病患者存在明显的睡眠-觉醒节律和自发性体动的昼夜节律紊乱,但其对深部体温的影响并不显著,提示发作性睡病患者体温中枢的调节能力相对保留。     

发作性睡病患者行 PSG和MSLT监测的护理

目的：探讨发作性睡病临床主要表现,以及诊断中常用的标准多导睡眠监测（polysomnography ,PSG）和多次睡眠潜伏试验（multiple sleep latency test ,MSLT）的应用和监测方法。方法回顾分析2012‐07—2014‐03到我科监测治疗的26例发作性睡病患者的临床资料。结果26例均顺利完成监测,其中21例夜间PSG检查中睡眠潜伏期＜10 min;14例快动眼睡眠（REM）始于入睡后＜20 min;白天MSLT中,26例平均睡眠潜伏期＜5 min ,入睡开始阶段出现REM（ROREMPs）≥2次的26例。结论护理人员在对患者进行监测的过程中,应采取适合的心理疏导方式,以消除患者的不良情绪,合理的心理疏导能提高检测结果的准确率,将对发作性睡病的诊断起非常重要的作用。     

乙酰唑胺对呼吸暂停综合征的疗效

对睡眠呼吸暂停综合征(SAS)的治疗药物有多种,但无肯定结果。本文报告对20例SAS患者中短期应用乙酰唑胺(acetazolamide)的疗效及夜间持续睡眠多道生理仪(PSG)监测结果。方法:研究对象为20例男性患者,其中主诉白天过度嗜睡(睡眠呼吸暂停伴过度嗜睡综合征)14例,主诉失眠(睡眠呼吸暂停综合征)6例,平均54.6岁。SAS诊断按Guilleminault等的定义,在7小时夜间睡眠中,在NREM期、REM期出现至少持续10秒钟以上的换气停止(无呼吸)30次以上或每小时呼吸暂停次数(呼吸暂停指数)5次以     

Neuroimaging of sleep and sleep disorders

Herein are presented the results of research in the area of sleep neuroimaging over the past year. Significant work has been performed to clarify the basic mechanisms of sleep in humans. New studies also extend prior observations regarding altered brain activation in response to sleep deprivation by adding information regarding vulnerability to sleep deprivation and regarding the influence of task difficulty on aberrant responses. Studies in sleep disorder medicine have yielded significant findings in insomnia, depression, and restless legs syndrome. Extensive advances have been made in the area of sleep apnea where physiologic challenges have been used to probe brain activity in the pathophysiology of sleep apnea syndrome.     

Neuroimaging of sleep and sleep disorders

Herein are presented the results of research in the area of sleep neuroimaging over the past year. Significant work has been performed to clarify the basic mechanisms of sleep in humans. New studies also extend prior observations regarding altered brain activation in response to sleep deprivation by adding information regarding vulnerability to sleep deprivation and regarding the influence of task difficulty on aberrant responses. Studies in sleep disorder medicine have yielded significant findings in insomnia, depression, and restless legs syndrome. Extensive advances have been made in the area of sleep apnea where physiologic challenges have been used to probe brain activity in the pathophysiology of sleep apnea syndrome.     

Cognitive consequences of sleep and sleep loss

Although we still lack any consensus function(s) for sleep, accumulating evidence suggests it plays an important role in homeostatic restoration, thermoregulation, tissue repair, immune control and memory processing. In the last decade an increasing number of reports continue to support a bidirectional and symbiotic relationship between sleep and memory. Studies using procedural and declarative learning tasks have demonstrated the need for sleep after learning in the offline consolidation of new memories. Furthermore, these consolidation benefits appear to be mediated by an overnight neural reorganization of memory that may result in a more efficient storage of information, affording improved next-day recall. Sleep before learning also appears to be critical for brain functioning. Specifically, one night of sleep deprivation markedly impairs hippocampal function, imposing a deficit in the ability to commit new experiences to memory. Taken together, these observations are of particular ecologic importance from a professional and education perspective when considering that sleep time continues to decrease across all age ranges throughout industrialized nations.     

Metabolic consequences of sleep and sleep loss

Reduced sleep duration and quality appear to be endemic in modern society. Curtailment of the bedtime period to minimum tolerability is thought to be efficient and harmless by many. It has been known for several decades that sleep is a major modulator of hormonal release, glucose regulation and cardiovascular function. In particular, slow wave sleep (SWS), thought to be the most restorative sleep stage, is associated with decreased heart rate, blood pressure, sympathetic nervous activity and cerebral glucose utilization, compared with wakefulness. During SWS, the anabolic growth hormone is released while the stress hormone cortisol is inhibited. In recent years, laboratory and epidemiologic evidence have converged to indicate that sleep loss may be a novel risk factor for obesity and type 2 diabetes. The increased risk of obesity is possibly linked to the effect of sleep loss on hormones that play a major role in the central control of appetite and energy expenditure, such as leptin and ghrelin. Reduced leptin and increased ghrelin levels correlate with increases in subjective hunger when individuals are sleep restricted rather than well rested. Given the evidence, sleep curtailment appears to be an important, yet modifiable, risk factor for the metabolic syndrome, diabetes and obesity. The marked decrease in average sleep duration in the last 50 years coinciding with the increased prevalence of obesity, together with the observed adverse effects of recurrent partial sleep deprivation on metabolism and hormonal processes, may have important implications for public health.     

Neuroimmunologic aspects of sleep and sleep loss

The complex and intimate interactions between the sleep and immune systems have been the focus of study for several years. Immune factors, particularly the interleukins, regulate sleep and in turn are altered by sleep and sleep deprivation. The sleep-wake cycle likewise regulates normal functioning of the immune system. Although a large number of studies have focused on the relationship between the immune system and sleep, relatively few studies have examined the effects of sleep deprivation on immune parameters. Studies of sleep deprivation's effects are important for several reasons. First, in the 21st century, various societal pressures require humans to work longer and sleep less. Sleep deprivation is becoming an occupational hazard in many industries. Second, to garner a greater understanding of the regulatory effects of sleep on the immune system, one must understand the consequences of sleep deprivation on the immune system. Significant detrimental effects on immune functioning can be seen after a few days of total sleep deprivation or even several days of partial sleep deprivation. Interestingly, not all of the changes in immune physiology that occur as a result of sleep deprivation appear to be negative. Numerous medical disorders involving the immune system are associated with changes in the sleep-wake physiology--either being caused by sleep dysfunction or being exacerbated by sleep disruption. These disorders include infectious diseases, fibromyalgia, cancers, and major depressive disorder. In this article, we will describe the relationships between sleep physiology and the immune system, in states of health and disease. Interspersed will be proposals for future research that may illuminate the clinical relevance of the relationships between sleeping, sleep loss and immune function in humans.     

Poor recovery sleep after sleep deprivation in delayed sleep phase syndrome

To clarify disturbances in sleep regulation in patients with delayed sleep phase syndrome (DSPS), we studied three patients with DSPS and seven healthy controls. Sleep propensity and melatonin rhythms after 24-h sleep deprivation were investigated under dim light condition by using the ultra-short sleep-wake schedule. The sleep propensity curves displayed clear differences between DSPS patients and the controls. During the subjective day when melatonin was not produced, recovery sleep after the sleep deprivation did not occur in DSPS patients, while recovery sleep occurred during the subjective day in controls. This suggests that DSPS may involve problems related to the homeostatic regulation of sleep after sleep deprivation.     

癫癎与睡眠及睡眠障碍

睡眠、睡眠障碍与癫癎之间的相互影响是复杂且多方面的。睡眠及睡眠剥夺可能活化癫癎发作或活化脑电图的癫癎样放电,某些类型的癫癎发作可能只发生或主要发生在睡眠中;而癫癎发作本身又可干扰睡眠,改变睡眠模式;睡眠中的同一种异常     

Enhanced slow sleep in extended sleep

The slow wave sleep (0.5-2.5 Hz) of 42 subjects who slept in a laboratory for more than 8 h was examined. Although the amount of slow wave sleep diminished exponentially across the first 11 h of sleep, there is evidence of an increase in amount of slow wave sleep in more extended sleep. This finding complicates the concepts of slow wave sleep as an index of sleep need due to prior wakefulness or an index of a restoration process.     

Clinical effects of sleep fragmentation versus sleep deprivation

Common symptoms associated with sleep fragmentation and sleep deprivation include increased objective sleepiness (as measured by the Multiple Sleep Latency Test); decreased psychomotor performance on a number of tasks including tasks involving short term memory, reaction time, or vigilance; and degraded mood. Differences in degree of sleepiness are more related to the degree of sleep loss or fragmentation rather than to the type of sleep disturbance. Both sleep fragmentation and sleep deprivation can exacerbate sleep pathology by increasing the length and pathophysiology of sleep apnea. The incidence of both fragmenting sleep disorders and chronic partial sleep deprivation is very high in our society, and clinicians must be able to recognize and treat Insufficient Sleep Syndrome even when present with other sleep disorders.