Cumulative Effects of Sleep Restriction on Daytime Sleepiness

Sleep and daytime sleepiness were evaluated in 10 young adult subjects to determine whether restricting nocturnal step by a constant amount produces cumulative impairment. Subjects were studied for 12 consecutive days, including 3 baseline days with a 10-hr time in bed, 7 days with sleep restricted to 5 hrs, and 2 recovery days. In 5 subjects, recovery included a 10-hr time in bed; in the remaining subject, recovery induced a 5-hr time in bed with a 1-hr daytime nap. Sleepiness was measured using two self-rating scales and the multiple sleep latency test. During sleep restriction, nocturnal stage 2 and REM sleep were reduced and slow wave sleep was unaffected. Stanford Sleepiness Scales showed an immediate increase in daytime sleepiness that reached a plateau after 4 days. An analog sleepiness rating scale showed increased sleepiness after 2 restricted nights and leveled off after the fourth restricted night. The multiple sleep latency tests showed no effect of sleep restriction until the second day, followed by a progressive increase in sleepiness that persisted through the seventh sleep restriction day. During the recovery period, daytime sleepiness returned to basal values on all three measures following one full night of sleep; with a daytime nap, no further cumulative effects of sleep restriction were seen.     

发作性睡病的临床特征及多次小睡潜伏期试验

目的：探讨发作性睡病的临床特征及多次小睡潜伏期试验(MSLT)在诊断发作性睡病中的作用。方法：对6例发作性睡病的诊断过程进行回顾性分析。结果：6例患者均有白天过度嗜睡．其中4例伴猝倒。首发症状为白天过度嗜睡5例。猝倒1例。以白天过度嗜睡就诊者3例，以猝倒就诊者3例。6例患者进行MSLT检查，所有患者平均睡眠潜伏期都小于5min．其中5例出现≥2次的睡眠始发REM睡眠(SOREMS)。结论：充分认识发作性睡病的临床特征是诊断的关键。对于临床表现不典型的病例，MSLT将有助于诊断。     

帕金森病睡眠障碍患者的血浆orexin A浓度变化及其影响因素分析

目的:探讨帕金森病(PD)睡眠障碍患者的血浆orexin A浓度变化,分析其可能影响因素.方法:采用UPDRS-Ⅲ评分、用药调查表、多项睡眠图(PSG)监测及次日多次睡眠潜伏期试验分别对25例PD患者的疾病严重程度、多巴胺能药物应用、睡眠结构、平均睡眠潜伏期等情况进行评定和计算;使用放射免疫分析法对25例临床确诊的PD患者和20例无明显中枢神经系统(CNS)疾病的对照组进行血浆orexin A浓度测定;分析PD患者血浆orexin A浓度与其睡眠结构、平均睡眠潜伏期、服用多巴胺能药物剂量间的相关性.结果:PD组中25例患者的血浆orexin A浓度[(7.72±3.44) pg/ml]和20例对照组的血浆orexin A浓度[(6.04±3.22) pg/ml]比较差异无统计学意义(t=1.669,P＞0.05);PD伴眼快动睡眠期精神行为障碍(RBD)组12例的血浆orexin A浓度[(6.93±2.67)pg/ml]和PD不伴RBD组的13例血浆orexin A浓度[(8.45±3.99)pg/ml]比较差异无统计学意义(t=-1.108,P＞0.05);PD伴SAHS组12例的血浆orexin A浓度[(7.40±3.56)pg/ml]和PD不伴SAHS组13例的血浆orexin A浓度[(8.01±3.44)pg/ml]比较差异无统计学意义(t=-0.433,P＞0.05);多元逐步线性回归分析显示PD患者的血浆orexin A浓度与平均睡眠潜伏期(β=-0.382,95％ CI:-0.708～-0.056)、左旋多巴日等效剂量(β=-0.011,95％ CI:-0.018～-0.004)呈负相关(t=-2.433、-3.132,P＜0.05).结论:PD患者血浆orexin A浓度变化受多巴胺能药物剂量及日间平均睡眠潜伏期的影响.     

Effects of Sleep Deprivation on Memory and Sleep Latencies in Connection with Repeated Awakenings From Sleep

Twelve subjects were kept awake 64 hrs. During baseline and recovery sleep, subjects were given a simple memory task. The subjects were awakened 3 times each night during slow-wave sleep and shown 4 playing cards. Approximately 90 min later the subjects were again awakened and tested for retention of the previous cards and given 4 new cards to learn. This procedure was repeated 3 times each night and upon awakening the following morning. On the recovery night recall was reduced, slow-wave sleep was lengthened, sleep latency was shortened, and body motility was reduced. It was suggested that the reason for the poorer recall was deeper sleep induced by the sleep deprivation.     

24 hours of sleep deprivation in the rat increases sleepiness and decreases vigilance: introduction of the rat‐psychomotor vigilance task

A novel animal‐analog of the human psychomotor vigilance task (PVT) was validated by subjecting rats to 24 h of sleep deprivation (SD) and examining the effect on performance in the rat‐PVT (rPVT), and a rat multiple sleep latency test (rMSLT). During a three‐phase (separate cohorts) crossover design, vigilance performance in the rPVT was compared with 24 h SD‐induced changes in sleepiness assessed by polysomnographic evaluation and the rMSLT. Twenty‐four hours of SD was produced by brief rotation of activity wheels at regular intervals in which the animals resided throughout the experiment. In the rPVT experiment, exercise controls (EC) experienced the same overall amount of locomotor activity as during SD, but allowed long periods of undisturbed sleep. After 24 h SD response latencies slowed, and lapses increased significantly during rPVT performance when compared with baseline and EC conditions. During the first 3 h of the recovery period following 24 h SD, polysomnographic measures indicated sleepiness. Latency to fall asleep after 24 h SD was assessed six times during the first 3 h after SD. Rats fell asleep significantly faster immediately after SD, than after non‐SD baseline sessions. In conclusion, 24 h of SD in rats increased sleepiness, as indicated by polysomnography and the rMSLT, and impaired vigilance as measured by the rPVT. The rPVT closely resembles the human PVT test widely used in human sleep research and will assist investigation of the neurobiologic mechanisms that produce vigilance impairments after sleep disruption.     

The effect of a REM sleep deprivation procedure on different aspects of memory function in humans

Previous studies have suggested that memory is dependent on the occurrence of REM sleep. Research has mainly focused on two distinct types of memory function, declarative and procedural, and it seems that the latter may more directly depend on REM sleep. Memory consolidation has been more investigated than acquisition, maintenance, and recall, despite the fact that sleep may affect flow of information into/from storage. Moreover, tests have often been limited to stimuli within only one modality (usually visual or verbal). This study aimed to clarify the role of REM sleep in memory by investigating aspects of memory function, processing, and modality in the same experimental setting. Tests of acquisition and consolidation of multiple aspects of memory function within the visual and verbal modalities were administrated to subjects before and after REM sleep deprivation. Results show that test performance was not affected by REM sleep deprivation.     

The dynamics of neurobehavioural recovery following sleep loss

Rate of recovery of daytime performance and sleepiness following moderate and severe sleep deprivation (SD) was examined when recovery opportunity was either augmented or restricted. Thirty healthy non-smokers, aged 18-33 years, participated in one of three conditions: moderate SD with augmented (9-h) recovery opportunities, moderate SD with restricted (6-h) recovery opportunities, or severe SD with augmented recovery opportunities. Each participant attended the laboratory for 8-9 consecutive nights: an adaptation and baseline night (23:00-08:00 hours), one or two night(s) of wakefulness, and five consecutive recovery sleep opportunities (23:00-08:00 hours or 02:00-08:00 hours). On each experimental day, psychomotor vigilance performance (PVT) and subjective sleepiness (SSS) were assessed at two-hourly intervals, and MSLTs were performed at 1000 h. PSG data was collected for each sleep period. For all groups, PVT performance significantly deteriorated during the period of wakefulness, and sleepiness significantly increased. Significant differences were observed between the groups during the recovery phase. Following moderate SD, response speed, lapses and SSS returned to baseline after one 9-h sleep opportunity, while sleep latencies required two 9-h opportunities. When the recovery opportunity was restricted to six hours, neither PVT performance nor sleepiness recovered, but stabilised at below-baseline levels. Following severe SD, sleepiness recovered after one (SSS) or two (physiological) 9-h sleep opportunities, however PVT performance remained significantly below baseline for the entire recovery period. These results suggest that the mechanisms underlying the recovery process may be more complicated than previously thought, and that we may have underestimated the impact of sleep loss and/or the restorative value of subsequent sleep.     

Non-REM sleep as a source of learning deficits induced by REM sleep deprivation.

Procedures that deprive animal subjects of rapid eye movement sleep have often been associated with learning impairments. Previously, the conclusion has been drawn that these learning impairments are due to the absence of some positive function of rapid eye movement sleep. The present research indicates more precisely that typical impairments associated with the deprivation procedures may be due to isolated periods of non-REM sleep, rather than due to the simple absence of rapid eye movement sleep. Mice were tested for acquistion of a complex maze task, and subjected to post-trial rapid eye movement sleep deprivation by the pedestal method. Only animals demonstrating (non-REM) sleep behaviors during deprivation gave evidence of learning deficits.     

Physiological arousal and attention during a week of continuous sleep restriction

Waking brain physiology underlying deficits from continuous sleep restriction (CSR) is not well understood. Fourteen good sleepers participated in a 21-day protocol where they slept their usual amount in a baseline week, had their time in bed restricted by 33% in a CSR week, and slept the desired amount in a recovery week. Participants slept at home, completing diaries and wearing activity monitors to verify compliance. Each day participants completed an RT task and mood and sleepiness ratings every 3 h. Laboratory assessment of electrophysiology and performance took place at the end of baseline, three times throughout the CSR week, and at the beginning of recovery. Participants reported less sleep during CSR which was confirmed by activity monitors. Correspondingly, well-being and neurobehavioural performance was impaired. Quantitative EEG analysis revealed significantly reduced arousal between the 1st and 7th days of restriction and linear effects at anterior sites (Fp2, Fz, F8, T8). At posterior sites (P4, P8), reductions occurred only later in the week between the 4th and 7th nights of restriction. Both the immediate linear decline in arousal and precipitous drop later in the week were apparent at central sites (C4, Cz). Thus, frontal regions were affected immediately, while parietal regions showed maintenance of function until restriction was more severe. The P300 ERP component showed evidence of reduced attention by the 7th day of restriction (at Pz, P4). EEG and ERPs deficits were more robust in the right-hemisphere, which may reflect greater vulnerability to sleep loss in the non-dominant hemisphere.     

Disruptive effects of rapid eye movement sleep deprivation on long-term memory

The fact that sleep is associated with very active endogenous neural (chemical and electrical) processes, suggests that these processes may be involved in the maintenance of long-term memory storage. The present experiments were designed to examine the hypothesis that rapid eye movement (REM) sleep deprivation will produce impairment of long-term memory. Mice deprived of REM sleep for 3, 5 or 7 continuous days, during the interval between a one-trial inhibitory avoidance training experience and a subsequent retention test, displayed a temporary retrograde amnesia when tested 30 min or three hr following termination of REM deprivation. The mice did not recover from the amnesia if electroconvulsive shock was administered immediately following the interval of REM sleep deprivation. In a further study, the generality of these findings was obtained by depriving mice of REM sleep during the interval between a discrimination training experiment in a black-white T-maze and the subsequent retention test.     

Effects of sleep deprivation and exercise on cognitive, motor performance and mood

This study examined the effect of 30 h of sleep deprivation and intermittent physical exercise, on both cognitive and psychomotor function as well subjective ratings of mood. Six subjects with the following physical characteristics participated in the study (Mean +/- S.D.): age 22 +/- 0.3 years, height 180 +/- 5 cm, body mass: 77 +/- 5 kg, VO2peak 44 +/- 5 ml kg(-1) min(-1). Three subjects engaged in normal sedentary activities while three others cycled on a cycle ergometer at 50% VO2peak for 20 min out of every 2 h during 30 h of sleep deprivation. One week later sleep deprivation was repeated with a cross over of subjects. Every 4 h, subjects completed simple and two-choice reaction time tasks at both rest and during exercise, a computerized tracking task, a number cancellation task, and an assessment of subjective mood state as measured by the POMS questionnaire. A 3 x 4 repeated measures ANOVA revealed that resting but not exercising reaction times were significantly slower with sleep deprivation. Sleep deprivation was also associated with significantly greater negative disturbances to subjective vigour, fatigue and depression assessed by the Profile of Mood States questionnaire. Compared to those who have been deprived of sleep alone, individuals that performed 5 h of intermittent moderate exercise during 30 h of sleep deprivation appeared to be more vulnerable to negative mood disturbances and impairment in reaction times. This could result in greater risk of accident due to a reduced capacity to respond quickly.     

短半衰期催眠药对失眠症患者白天多次睡眠潜伏期测定的影响

目的 :探讨两种短半衰期催眠药佐匹克隆和三唑仑对失眠患者白天多次睡眠潜伏期测定 (MSLT)的影响。方法 :按照ICD 10的诊断标准收集 2 2例非器质性失眠症患者 ,随机分为两组 ,在服用 0 5mg三唑仑或 15mg佐匹克隆前后 ,分别进行MSLT检测。结果 :两药均可使白天MSLT的平均睡眠潜伏期和前两次测定的睡眠潜伏期明显缩短 ,使REM睡眠增加。两药对MSLT的影响特点相似。结论 :催眠药物可使失眠患者白天的困倦程度明显增高 ,这可能与药物的受体后效应有关 ,与药物种类的关系不大。     

Fragments of wake-like activity frame down-states of sleep slow oscillations in humans: New vistas for studying homeostatic processes during sleep

During NREM sleep cortical activity corresponding to EEG fast rhythms (FRs > 10 Hz) is interrupted by fragments of neural stillness (down-states), responsible for the negative peak within sleep slow oscillation (SSO). Researchers still debate whether the down-states spontaneously occur or need an initial overshoot in fluctuating activity. Herein, we studied temporally-isolated SSO in healthy subjects in order to identify two distinct EEG markers defining a putative initial up-state: i) a significant positive deflection and ii) an associated FR increase, before the negative peak.     

The effects of sleep deprivation in humans: topographical electroencephalogram changes in non‐rapid eye movement (NREM) sleep versus REM sleep

Studies on homeostatic aspects of sleep regulation have been focussed upon non‐rapid eye movement (NREM) sleep, and direct comparisons with regional changes in rapid eye movement (REM) sleep are sparse. To this end, evaluation of electroencephalogram (EEG) changes in recovery sleep after extended waking is the classical approach for increasing homeostatic need. Here, we studied a large sample of 40 healthy subjects, considering a full‐scalp EEG topography during baseline (BSL) and recovery sleep following 40 h of wakefulness (REC). In NREM sleep, the statistical maps of REC versus BSL differences revealed significant fronto‐central increases of power from 0.5 to 11 Hz and decreases from 13 to 15 Hz. In REM sleep, REC versus BSL differences pointed to significant fronto‐central increases in the 0.5–7 Hz and decreases in the 8–11 Hz bands. Moreover, the 12–15 Hz band showed a fronto‐parietal increase and that at 22–24 Hz exhibited a fronto‐central decrease. Hence, the 1–7 Hz range showed significant increases in both NREM sleep and REM sleep, with similar topography. The parallel change of NREM sleep and REM sleep EEG power is related, as confirmed by a correlational analysis, indicating that the increase in frequency of 2–7 Hz possibly subtends a state‐aspecific homeostatic response. On the contrary, sleep deprivation has opposite effects on alpha and sigma activity in both states. In particular, this analysis points to the presence of state‐specific homeostatic mechanisms for NREM sleep, limited to <2 Hz frequencies. In conclusion, REM sleep and NREM sleep seem to share some homeostatic mechanisms in response to sleep deprivation, as indicated mainly by the similar direction and topography of changes in low‐frequency activity.     

Modafinil, d-amphetamine and placebo during 64 hours of sustained mental work. II. Effects on two nights of recovery sleep

Polysomnograms were obtained from 37 volunteers, before (baseline) and after (two consecutive recovery nights) a 64-h sleep deprivation, with (d-amphetamine or modafinil) or without (placebo) alerting substances. The drugs were administered at 23.00 hours during the first sleep deprivation night (after 17.5 h of wakefulness), to determine whether decrements in cognitive performance would be prevented; at 05.30 hours during the second night of sleep deprivation (after 47.5 h of wakefulness), to see whether performance would be restored; and at 15.30 hours during the third day of continuous work, to study effects on recovery sleep. The second recovery night served to verify whether drug-induced sleep disturbances on the first recovery night would carry over to a second night of sleep. Recovery sleep for the placebo group was as expected: the debt in slow-wave sleep (SWS) and REM sleep was paid back during the first recovery night, the rebound in SWS occurring mainly during the first half of the night, and that of REM sleep being distributed evenly across REM sleep episodes. Recovery sleep for the amphetamine group was also consistent with previously published work: increased sleep latency and intrasleep wakefulness, decreased total sleep time and sleep efficiency, alterations in stage shifts, Stage 1, Stage 2 and SWS, and decreased REM sleep with a longer REM sleep latency. For this group, REM sleep rebound was observed only during the second recovery night. Results for the modafinil group exhibited decreased time in bed and sleep period time, suggesting a reduced requirement for recovery sleep than for the other two groups. This group showed fewer disturbances during the first recovery night than the amphetamine group. In particular, there was no REM sleep deficit, with longer REM sleep episodes and a shorter REM latency, and the REM sleep rebound was limited to the first REM sleep episode. The difference with the amphetamine group was also marked by less NREM sleep and Stage 2 and more SWS episodes. No REM sleep rebound occurred during the second recovery night, which barely differed from placebo. Hence, modafinil allowed for sleep to occur, displayed sleep patterns close to that of the placebo group, and decreased the need for a long recovery sleep usually taken to compensate for the lost sleep due to total sleep deprivation.     

Impacts of shift work on sleep and circadian rhythms

Shift work comprises work schedules that extend beyond the typical “nine-to-five” workday, wherein schedules often comprise early work start, compressed work weeks with 12-hour shifts, and night work. According to recent American and European surveys, between 15 and 30% of adult workers are engaged in some type of shift work, with 19% of the European population reportedly working at least 2 hours between 22:00 and 05:00. The 2005 International Classification of Sleep Disorders estimates that a shift work sleep disorder can be found in 2–5% of workers. This disorder is characterized by excessive sleepiness and/or sleep disruption for at least one month in relation with the atypical work schedule. Individual tolerance to shift work remains a complex problem that is affected by the number of consecutive work hours and shifts, the rest periods, and the predictability of work schedules. Sleepiness usually occurs during night shifts and is maximal at the end of the night. Impaired vigilance and performance occur around times of increased sleepiness and can seriously compromise workers’ health and safety. Indeed, workers suffering from a shift work sleep-wake disorder can fall asleep involuntarily at work or while driving back home after a night shift. Working on atypical shifts has important socioeconomic impacts as it leads to an increased risk of accidents, workers’ impairment and danger to public safety, especially at night. The aim of the present review is to review the circadian and sleep-wake disturbances associated with shift work as well as their medical impacts.     

The effects of 28 hours of sleep deprivation on respiratory sinus arrhythmia during tasks with low and high controlled attention demands

Task performance while sleep deprived may be moderated by the controlled attention required by the task (Pilcher, Band, Odle-Dusseau, & Muth, 2007). This study examined the effects of 28 h of sleep deprivation on respiratory sinus arrhythmia (RSA) during tasks with low and high controlled attention demands. The results showed that RSA increased throughout the night for both task types, but was consistently reduced during the low compared to high controlled attention tasks. The increase in RSA was linear for the high controlled attention tasks but curvilinear for the low ones. Hence, RSA followed a circadian pattern during the low controlled attention tasks but not the high ones. These results suggest that the effects of sleep deprivation on task performance may be moderated by parasympathetic activity and task type, and this has implications for task assignment during sustained operations that cause sleep deprivation.     

Sleep onset rapid-eye-movement episodes in narcolepsy: REM sleep pressure or nonREM-REM sleep dysregulation?

SUMMARY  Thirty-two narcoleptic subjects with excessive daytime sleepiness and cataplexy were recorded for 33 continuous hours. The continuous polysomnographic recording (CPSG) was followed by a standard MSLT at 2-h intervals. There were 64 sleep onset REM episodes (SOREMs) vs 64 sleep onset nonREM episodes (SONREMs) during the CPSG, and 102 SOREMs vs 50 SONREMS during the MSLT. Both sleep onset types peaked at 13–15 h during the CPSG while sleep onsets were evenly distributed during the MSLT. In the latter procedure, the mean sleep latency was significantly shorter with SOREMs occurrence than with SONREMs occurrence. Two factors were extracted in each procedure by means of a Varimax Rotated Factor Analysis. During the CPSG, SOREMs were related to the preceding nocturnal sleep parameters in the first factor, and to the daytime total sleep time and the total number of sleep onsets in the second factor. During the MSLT, SOREMs were related only to the mean sleep latency and the total number of sleep onsets. It was concluded that the occurrence of SOREMs is primarily due to the residual somnolence in narcoleptic subjects. However, their occurrence during the MSLT is largely independent of the prior history of sleep and waking. Thus, we propose a nonREM-REM sleep dysregulation hypothesis to account for the appearance of SOREMs in narcolepsy.     

Potential participation of cystatin C in rapid eye movement sleep (REMS) modulation

It has been hypothesized that proteins modulate rapid eye movement sleep (REMS). Studies have shown an increase in the liberation of proteins in the mesencephalic reticular formation of cats during REMS. It has also been determined that protein-synthesis inhibitors diminish REMS and that protease-inhibitors increase this sleep phase. These and other studies support the importance of “di novo” protein molecules in sleep, and in particular, in REMS regulation. In this context, it is important to determine the role of endogenous proteases and their endogenous inhibitors in sleep regulation. In this study, we found that Cystatin C (CC), an endogenous protease inhibitor, diminishes wakefulness and increases REMS. We have also found an increase in CC expression after REMS deprivation and a tendency to decrease after a 2 h period of REMS rebound. We further showed that REMS deprivation increases the expression of Cathepsin H (CH), a protease inhibited by CC. These results suggest that naturally occurring protease-inhibitors enhance REMS, perhaps by facilitating the availability of proteins.     

Sleep extension versus nap or coffee,within the context of ‘sleep debt’

Though extended night‐time sleep mostly reduces the ‘afternoon dip’, little is known about evening benefits to alertness, or about comparisons with an afternoon nap or caffeine. Twenty healthy carefully screened adults, normal waking alertness levels, underwent four counterbalanced conditions: usual night sleep; night sleep extended<90 min (usual bed‐time); up to 20 min afternoon nap; and 150 mg afternoon caffeine (versus decaffeinated coffee). Sleepiness was measured by afternoon and evening multiple sleep latency test (MSLTs), longer psychomotor vigilance test (PVT) sessions and a subjective sleepiness scale. Sleep was extended by average of 74 min, and all participants could nap 15–20 min. Sleep extension had little effect on PVT determined modest levels of morning sleepiness. Afternoon and evening MSLTs showed all active treatments significantly reduced the ‘dip’, with nap most effective until mid‐evening; next effective was caffeine, then extension. Late evening sleepiness and subsequent sleep did not differ between conditions. Arguably, participants may have experienced some ‘sleep debt’, given they extended sleep and reflected some sleepiness within settings sensitive to sleepiness. Nevertheless, extended sleep seemed largely superfluous and inefficient in reducing modest levels of sleepiness when compared with a timely nap, and even caffeine. Sleep, such as food and fluid intakes, can be taken to excess of real biological needs, and for many healthy adults, there is a level of modest daytime sleepiness, only unmasked by very sensitive laboratory measures. It may reflect a requirement for more sleep or simply be within the bounds of normal acceptability.