癫(癎)与睡眠关系的研究进展

目前研究[1]认为,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行为可能是癫(癎)发作的表现,也可能是睡眠行为异常.睡眠障碍影响对癫(癎)发作的控制,而癫(癎)发作又可能以睡眠异常为唯一表现.为此,对癫(癎)与睡眠之间的关系综述如下.     

睡眠脑电图在小儿癫癎中的诊断价值

目的 探讨睡眠EEG对癫癎的诊断价值、优点及诊断中的注意事项。方法 分析应用日本光电4418型EEG仪监测136例癫癎患者睡眠EEG。结果 正常28例(20.6％),非特异性异常12例(8.8％),癎样放电96例(70.6％)。结论睡眠EEG可反映睡眠结构和异常放电的发作情况;同时EEG可观察临床发作的全过程及发作时EEG的演变过程,能更明确局限性癫癎的诊断及定位,也可为全身性发作者寻找致癎灶。     

睡眠性癫癎患者动态脑电图的研究

目的探讨睡眠性癫疒间患者的24h动态脑电图(AEEG)的表现及其诊断价值。方法对91例仅于睡眠中发作癫疒间的患者进行AEEG检查,并对检查结果进行分析。结果AEEG发现疒间性放电71例(78.0%),其中4例出现于清醒状态,41例出现于睡眠状态,26例清醒和睡眠时均有放电;在67例睡眠时有疒间性放电的患者中,34例仅出现在浅睡期,33例整个睡眠中均出现疒间性放电。清醒时有癫疒间波的患者癫疒间发作频率明显高于无异常放电患者和仅睡眠时有疒间性放电的患者(均P<0.05)。结论睡眠中癫疒间发作患者于睡眠中疒间性放电出现率明显高于白天清醒时。AEEG容易发现睡眠性癫疒间患者的发作期和发作间歇期以及自然睡眠状态下的疒间样波。     

睡眠剥夺对癫(癎)发作的影响机制

睡眠剥夺可以改变大脑皮质的兴奋性,造成皮质兴奋和抑制失衡现象.对于几乎所有类型的癫癎,睡眠剥夺是一种强有力的癎性发作激活剂,可有效地激活全面性和部分性发作间期放电,特别是对特发性全面性癫癎[1].现从神经递质和神经肤机制探讨睡眠剥夺对癫癎发作的影响机制.     

睡眠性癫痫52例临床分析

睡眠性癫痫５２例临床分析孙剑，王焕林睡眠性癫痫指仅在或基本上在睡眠中发作［１］而在觉醒状态无发作的一种癫痫发作类型。本组收集分析了５２例临床资料，现报告如下；临床资料一般资料：本组共５２例，其中男３３例，女１９例。年龄７～７５岁（２３．５２±１３．５...     

240例睡眠/清醒不同发作时间癫痫患者24小时动态脑电图分析

目的:了解睡眠/清醒不同发作时间癫痫患者24小时动态脑电图特点。方法:回顾性分析240例癫痫患者的24小时动态脑电图资料。结果:仅于睡眠中发作的癫痫患者AEEG上仅在睡眠中放电的比例高于清醒期和睡眠/ 清醒均发作患者,额叶癫痫患者于睡眠中发作者以及AEEG上单纯夜间放电者均明显多于颞叶癫痫患者,差异具有显著性(P<0.01)。结论:额叶癫痫患者及临床上仅于睡眠中发作患者睡眠中放电明显高于其他癫痫患者,对此类睡眠中高发人群进行AEEG检查有助于提高诊断率。     

睡眠中癫(癎)性电持续状态的研究进展

睡眠中癫癎性电持续状态(ESES)是脑电图异常的一种表现,多见于3-14岁儿童,在慢波睡眠期脑电图出现广泛的1.5-2.5Hz棘慢波持续或接近持续的发放,该现象可持续数月或数年,可伴或不伴临床发作.因为ESES与多种癫癎发作有关,且影响儿童神经心理功能,临床严重程度各不相同[1],越来越多的学者开始对其进行深人研究.     

64例常规清醒脑电图未见癎样放电的小儿癫癎夜间自然睡眠脑电图分析

脑电图(electroencephalography,EEG)是诊断癫癎(epi-lepsy,EP)最重要的辅助检查方法,对发作性症状的诊断有很大价值,有助于明确癫癎的诊断及分型和确定特殊综合征。理论上任何一种癫癎发作都能用EEG记录到发作或发     

癫痫患者的睡眠障碍

目的：探讨癫痫患者的睡眠障碍。方法：对１０例有睡眠障碍主诉的癫痫病人进行夜间多导生理描记仪（ＰＳＧ）测试,所有病人均在抗痫药物治疗前进行检查。结果：本组病人的ＰＳＧ测试睡眠效率减低,多显示浅睡期延长;２例病人的夜间睡眠障碍与睡眠中周期性肢体活动增多有关;２例与夜间鼾声有关;但均未见呼吸暂停或呼吸不足表现。结论：癫痫患者可伴随不同程度的睡眠障碍,这可能与睡眠中周期性肢体活动,夜间打鼾,痫样放电或抗痫     

剥夺睡眠脑电图在癫诊断中的应用

目的 分析睡眠脑电图(EEG)在癫诊断中的价值及适应证.方法 对200例癫病人的睡眠及清醒脑电图进行研究.结果 脑电图有异常爆发活动(PA)者80例,PA只在睡眠中出现者30例,样放电检出率由清醒的25%提高到睡眠的40%.结论 睡眠脑电图对提高样放电的检出率和进一步明确癫发作类型有重要意义.     

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.     

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.     

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.     

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.     

Human sleep spindle characteristics after sleep deprivation

OBJECTIVE: Sleep spindles (12-15 Hz oscillations) are one of the hallmarks of the electroencephalogram (EEG) during human non-rapid eye movement (non-REM) sleep. The effect of a 40 h sleep deprivation (SD) on spindle characteristics along the antero-posterior axis was investigated. METHODS: EEGs during non-REM sleep in healthy young volunteers were analyzed with a new method for instantaneous spectral analysis, based on the fast time frequency transform (FTFT), which yields high-resolution spindle parameters in the combined time and frequency domain. RESULTS: FTFT revealed that after SD, mean spindle amplitude was enhanced, while spindle density was reduced. The reduction in spindle density was most prominent in the frontal derivation (Fz), while spindle amplitude was increased in all derivations except in Fz. Mean spindle frequency and its variability within a spindle were reduced after SD. When analyzed per 0.25 Hz frequency bin, amplitude was increased in the lower spindle frequency range (12-13.75 Hz), whereas density was reduced in the high spindle frequency range (13.5-14.75 Hz). CONCLUSIONS: The observed reduction in spindle density after SD confirms the inverse homeostatic relationship between sleep spindles and slow waves whereas the increase in spindle amplitude and the reduction in intra-spindle frequency variability support the hypothesis of a higher level of synchronization in thalamocortical cells when homeostatic sleep pressure is enhanced.     

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.     

Light sleep and sleep time misperception – Relationship to alpha–delta sleep

ObjectiveWe investigated the association of alpha–delta sleep (A–DS) with: (1) perception of light sleep and (2) discrepancy between subjective and objective sleep duration.MethodsWe analyzed data from 5764 individuals who underwent polysomnography (PSG) and replied questions about quantity and quality of sleep, including sleep depth. The difference between objectively recorded sleep time and subjectively estimated sleep time was calculated. Alpha–delta sleep (A–DS) was visually scored in a scale from 1 to 4, based on the density and overnight duration of alpha activity and confirmed using spectral array of the electroencephalographic activity.ResultsA–DS scores 1–4 occurred in, respectively, 37.9%; 31.3%; 20.5%; and 6.2% of the cases. ANOVA showed significant difference of light sleep sensation (p < 0.001) and sleep time underestimation (p < 0.001) among the four A–DS categories. Regression to explain both light sleep and sleep time underestimation, controlling for confounders, confirmed A–DS as a significant regressor.ConclusionsThis study of a large prospective sample provides evidence for the association of alpha–delta sleep with subjective sensation of light sleep and with sleep time underestimation.SignificanceAlpha–delta sleep may be a marker of the physiological disorder underlying light sleep and sleep state misperception.