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.     

Increased EEG spectral power density during sleep following short-term sleep deprivation in pigeons (Columba livia): evidence for avian sleep homeostasis

Birds provide a unique opportunity to evaluate current theories for the function of sleep. Like mammalian sleep, avian sleep is composed of two states, slow-wave sleep (SWS) and rapid eye-movement (REM) sleep that apparently evolved independently in mammals and birds. Despite this resemblance, however, it has been unclear whether avian SWS shows a compensatory response to sleep loss (i.e., homeostatic regulation), a fundamental aspect of mammalian sleep potentially linked to the function of SWS. Here, we prevented pigeons (Columba livia) from taking their normal naps during the last 8 h of the day. Although time spent in SWS did not change significantly following short-term sleep deprivation, electroencephalogram (EEG) slow-wave activity (SWA; i.e., 0.78-2.34 Hz power density) during SWS increased significantly during the first 3 h of the recovery night when compared with the undisturbed night, and progressively declined thereafter in a manner comparable to that observed in similarly sleep-deprived mammals. SWA was also elevated during REM sleep on the recovery night, a response that might reflect increased SWS pressure and the concomitant 'spill-over' of SWS-related EEG activity into short episodes of REM sleep. As in rodents, power density during SWS also increased in higher frequencies (9-25 Hz) in response to short-term sleep deprivation. Finally, time spent in REM sleep increased following sleep deprivation. The mammalian-like increase in EEG spectral power density across both low and high frequencies, and the increase in time spent in REM sleep following sleep deprivation suggest that some aspects of avian and mammalian sleep are regulated in a similar manner.     

Sleep deprivation and phasic activity of REM sleep: independence of middle-ear muscle activity from rapid eye movements

In the recovery nights after total and partial sleep deprivation there is a reduction of rapid eye movements during REM sleep as compared to baseline nights; recent evidence provided by a selective SWS deprivation study also shows that the highest percentage of variance of this reduction is explained by SWS rebound. The present study assesses whether the reduction of rapid eye movements (REMs) during the recovery night after total sleep deprivation is paralleled by a decrease of middle-ear muscle activity (MEMA), another phasic muscle activity of REM sleep. Standard polysomnography, MEMA and REMs of nine subjects were recorded for three nights (one adaptation, one baseline, one recovery); baseline and recovery night were separated by a period of 40 hours of continuous wake. Results show that, in the recovery night, sleep deprivation was effective in determining an increase of SWS amount and of the sleep efficiency index, and a decrease of stage 1, stage 2, intra-sleep wake, and NREM latencies, without affecting REM duration and latency. However, MEMA frequency during REM sleep did not diminish during these nights as compared to baseline ones, while there was a clear effect of REM frequency reduction. Results indicate an independence of phasic events of REM sleep, suggesting that the inverse relation between recovery sleep after sleep deprivation and REM frequency is not paralleled by a concomitant variation in MEMA frequency.     

EEG arousals in normal sleep: variations induced by total and selective slow-wave sleep deprivation

STUDY OBJECTIVES: Aim of the present study was to assess changes in arousal rates after selective slow-wave (SWS) and total sleep deprivations. DESIGN: Two-way mixed design comparing the arousal index (Al), as expressed by the number of EEG arousals divided by sleep duration, in totally or selectively sleep deprived subjects. SETTING: Sleep laboratory. PATIENTS OR PARTICIPANTS: Nineteen normal male subjects [mean age=23.3 years (S.E.M.=0.55)]. INTERVENTIONS: Al was measured in baseline nights and after selective SWS (N=10) and total sleep deprivation (N=9). MEASUREMENTS AND RESULTS: During the baseline nights AI values changed across sleep stages as follows: stage 1 > stage 2 and REM > SWS, but did not present any significant variations as a function of time elapsed from sleep onset. The recovery after deprivation showed a reduction in EEG arousals, more pronounced after total sleep deprivation; this decrease affected NREM but not REM sleep. During the baseline nights Al showed a close-to-significance negative correlation with REM duration, while during the recovery nights a significant positive relation with stage 1 duration was found. CONCLUSIONS: The present results suggest that recuperative processes after sleep deprivation are also associated with a higher sleep continuity as defined by the reduction of EEG arousals.     

睡眠剥夺对健康成人睡眠脑电图的变化观察

目的：探索睡眠剥夺对健康成人睡眠脑电图（PSG）的影响.方法：选择34名健康成人志愿者行睡眠剥夺36h,作睡眠剥夺前后的PSG整夜监测.结果：与睡眠剥夺前相比,健康成人PSG表现为睡眠潜伏期缩短（P＜0.05）,NREM中的第1阶段睡眠减少（P＜0.05）,第4阶段（S4）睡眠增多（P＜0.01）.结论：睡眠剥夺后再睡眠,健康成人通过其NREM睡眠阶段中S4的比例作为“补偿”.睡眠剥夺可影响健康成人的脑电生理活动.     

The relationship between frequency of rapid eye movements in REM sleep and SWS rebound

Previous studies have shown a decrease in rapid eye movement (REM) frequency during desynchronized sleep in recovery nights following total or partial sleep deprivation. This effect has been ascribed to an increase in sleep need or sleep depth consequent to sleep length manipulations. The aims of this study were to assess REM frequency variations in the recovery night after two consecutive nights of selective slow-wave sleep (SWS) deprivation, and to evaluate the relationships between REM frequency and SWS amount and auditory arousal thresholds (AAT), as an independent index of sleep depth. Ten normal males slept for six consecutive nights in the laboratory: one adaptation, two baseline, two selective SWS deprivation and one recovery night. SWS deprivation allowed us to set the SWS amount during both deprivation nights close to zero, without any shortening of total sleep time. In the ensuing recovery night a significant SWS rebound was found, accompanied by an increase in AAT. In addition, REM frequency decreased significantly compared with baseline. This effect cannot be attributed to a variation in prior sleep duration, since there was no sleep loss during the selective SWS deprivation nights. Stepwise regression also showed that the decrease in REM frequency is not correlated with the increase in AAT, the traditional index of sleep depth, but is correlated with SWS rebound.     

Sleep deprivation in honey bees

Rest at night in forager honey bees (Apis mellifera) meets essential criteria of sleep. This paper reports the effect of a 12-h total sleep deprivation (SD) by forced activity on the behaviour of these animals. The behaviour of sleep-deprived animals is compared with that of control animals under LD [periodic alternation between light (L) and darkness (D)] 12 : 12 hours. SD for 12 h during the first D period resulted in a significant difference with respect to the parameter 'hourly amount of antennal immobility' between sleep-deprived and control animals during the remaining L and D periods. This difference did not occur in the L period following the deprivation night, but rather it became obvious at the beginning of the following D period. The increase of the amount of antennal immobility in sleep-deprived bees was accompanied by an increase of the duration of episodes of antennal immobility. Moreover, the latency from 'lights off' to the first episode of antennal immobility lasting 20 s or longer ('deep sleep latency') tended to be shorter in sleep-deprived than in control animals. Disturbing the bees during the day (L period) did not result in such differences between disturbed and control animals. Highest reaction thresholds in sleeping honey bees occur during long episodes of antennal immobility. We therefore conclude that honey bees compensate a sleep deficit by intensification (deepening) of the sleep process and thus that sleep in honey bees, like that in other arthropods and mammals, is controlled by regulatory mechanisms.     

Slow Wave Sleep and REM Sleep Awakenings Do Not Affect Sleep Dependent Memory Consolidation

Study Objectives:

The effects of REM sleep and slow wave sleep (SWS) deprivation on sleep-dependent motor and declarative memory consolidation.

Design:

Randomized, within-subject, cross-over study

Setting:

Weekly (women: monthly) sleep laboratory visits, with retest 60 hours later

Participants:

Twelve healthy subjects (6 men) aged between 20 and 30 years

Interventions:

REM sleep deprivation, SWS deprivation, or undisturbed sleep

Measurements and Results:

We deprived subjects once each of REM sleep and SWS, and once let them sleep undisturbed through the night. After each night, we tested declarative and procedural memory consolidation. We tested memory performance by a verbal paired associate task and a sequential finger-tapping task at 21:00 on the study night and again 60 hours later. Although REM sleep and SWS awakenings led to a significant reduction of the respective sleep stages, memory consolidation remained unaffected. We also found a significant correlation between the declarative task and sleep spindles in the undisturbed condition, especially the sleep spindles in the first third of the night.

Conclusion:

We suggest that word-pair learning relies on stage 2 sleep spindles and requires little SWS. Their sleep dependent consolidation is not affected by SWS deprivation. Simple motor tasks may either be consolidated in stage 2 sleep or depend on only small amounts of REM sleep. Their sleep dependent consolidation is not influenced by REM sleep deprivation.

Citation:

Genzel L; Dresler M; Wehrle R; Grözinger M; Steiger A. Slow wave sleep and REM sleep awakenings do not affect sleep dependent memory consolidation. SLEEP 2009;32(3):302–310.     

Sleep in human narcolepsy revisited with special reference to prior wakefulness duration.

Sleep of 11 narcoleptic subjects was recorded on baseline and after 16 and 24 hours of prior wakefulness (16 and 24 hours sleep deprivation). Eleven sex- and age-matched control subjects were recorded for comparisons. All recordings in narcoleptic subjects were characterized by frequent sleep onset rapid eye movement (REM) episodes, increased amounts of wake time after sleep onset and low sleep efficiencies. Mean total sleep time (TST) was significantly decreased in narcoleptic subjects after sleep deprivation (SD). Recovery sleep after 24 hours SD showed reduced nonREM (NREM) sleep stage 2 percentage, whereas percentages of stage 4 and slow-wave sleep (SWS = stages 3 + 4) were significantly increased. The values of REM sleep percentage of TST were remarkably constant throughout and did not differ significantly as a function of experimental conditions, indicating a normal REM sleep pressure in narcolepsy. Sleep stage analysis per sleep cycles revealed significant differences between the two groups. Percentages of stage 4 and SWS were increased during the first cycle of recovery sleep in narcoleptic subjects. Stage 2 was decreased during the third cycle, and SWS decreased rapidly from cycle 1 to cycle 2 and slightly increased thereafter. These results indicate that sleep need is increased in narcolepsy, whereas its decrease over the first NREM-REM cycle is accelerated. We hypothesize that this could reflect an alteration of the homeostatic process of sleep regulation in narcolepsy.     

Zolpidem and sleep deprivation: different effect on EEG power spectra

To study the role of GABA-ergic mechanisms in sleep regulation, the combined action of 40 h sleep deprivation and either 20 mg zolpidem or placebo on the sleep electroencephalogram (EEG) were investigated by quantitative EEG analysis in eight young men who participated in a positron emission tomography study. Compared with baseline, sleep deprivation increased low-frequency (1.25-7.0 Hz) EEG power in non-rapid eye movement (NREM) sleep in the placebo night. After administration of zolpidem, power in the 3.75-10.0 Hz range and 14. 25-16.0 Hz band was reduced. The largest decrease was observed in the theta band. Comparison with placebo revealed that zolpidem attenuated power in the entire 1.75-11.0 Hz range. The plasma concentration of zolpidem at 4.5 h after intake showed a positive correlation with the drug-induced difference in power from placebo in the 14.25-16.0 Hz band. Regional EEG analysis based on bipolar derivations along the antero-posterior axis disclosed, for NREM sleep, a drug-induced posterior shift of power in the frequency range of 7.75-9.75 Hz. Zolpidem did not affect rapid eye movemnt sleep spectra. We conclude that sleep deprivation and agonistic modulation of GABAA receptors have separate and additive effects on power spectra and that their effects are mediated by different neurophysiological mechanisms.     

Slow wave activity and slow oscillations in sleepwalkers and controls: effects of 38 h of sleep deprivation

Sleepwalkers have been shown to have an unusually high number of arousals from slow wave sleep and lower slow wave activity (SWA) power during the night than controls. Because sleep deprivation increases the frequency of slow wave sleep (SWS) arousals in sleepwalkers, it may also affect the expression of the homeostatic process to a greater extent than shown previously. We thus investigated SWA power as well as slow wave oscillation (SWO) density in 10 sleepwalkers and nine controls at baseline and following 38 h of sleep deprivation. There was a significant increase in SWA during participants' recovery sleep, especially during their second non‐rapid eye movement (NREM) period. SWO density was similarly increased during recovery sleep's first two NREM periods. A fronto‐central gradient in SWA and SWO was also present on both nights. However, no group differences were noted on any of the 2 nights on SWA or SWO. This unexpected result may be related to the heterogeneity of sleepwalkers as a population, as well as our small sample size. SWA pressure after extended sleep deprivation may also result in a ceiling effect in both sleepwalkers and controls.     

Effect of sleep deprivation on NREM sleep ERPs and related activity at sleep onset.

This research assessed the impact of one night of sleep deprivation on the amplitudes of NREM-sleep event-related potentials (NREM ERPs) and on the frequency of occurrence of related electroencephalogram activity including sleep spindles, arousals, K-complexes, and vertex sharp waves (VSWs). The NREM ERPs identified included P220, N350, P450, N550 and P900. During a pre-deprivation night, ten subjects took two 20-min naps separated by a 20-min break at their normal bedtime. Brief tones were presented at three intensity levels (60, 75 and 90 dB) with a 5-s interstimulus interval. Following these naps, subjects were kept awake until their normal bedtime the following day. At that time, they repeated the two-nap procedure. The ERPs obtained for each tone and wake/sleep state for pre- and post-deprivation conditions were analyzed using repeated measures statistical procedures. As anticipated, NREM ERP amplitudes recorded both pre- and post-deprivation increased with tone intensity and with approaching sleep. Also, sleep deprivation was associated with more rapid sleep onset, reduced arousability, and greater spindle production. While sleep deprivation had no effect on the amplitude of P220. Post-deprivation amplitudes of N350, N550 and P900 were greater, especially following the 90-dB tone. There was a corresponding increase in VSWs and K-complexes. These findings are inconsistent with the view that NREM ERPs reflect arousal. The underlying mechanism(s) may facilitate initiation and maintenance of sleep.     

Biperiden administration during REM sleep deprivation diminished the frequency of REM sleep attempts.

Sixteen subjects were assigned to a group using either placebo or biperiden, with eight subjects in each group. Both groups were studied for one acclimatization night, one baseline night, four nights of rapid eye movement (REM) sleep deprivation and two recovery nights. All the subjects received either placebo or 4 mg biperiden 1 hour before sleep during the four nights of REM sleep deprivation. During the baseline and the recovery nights both groups received placebo capsules. The results showed that REM sleep time during the REM sleep deprivation was reduced by 70-75% below the baseline night in both groups. The number of attempts to enter REM sleep was significantly reduced by biperiden as compared to placebo for each of the four REM sleep deprivation nights. Because the total sleep time in the biperiden group was reduced, the number of REM sleep attempts was corrected by the total sleep time. The adjusted number of REM sleep attempts was also significantly reduced in the biperiden group. REM sleep latency showed a reduction in the placebo group, whereas in the biperiden group REM sleep latency was unchanged throughout the deprivation nights. In the recovery night REM sleep time was increased in both groups, with no differences between the groups. The REM sleep latency showed a reduction in the first recovery night in both groups that persisted through the second recovery night. The above findings support the role of biperiden as a REM sleep suppressive drug.     

Selective slow-wave sleep deprivation and time-of-night effects on cognitive performance upon awakening

We evaluated the effects of selective slow-wave sleep (SWS) deprivation and time-of-night factors on cognitive performance upon awakening. Ten normal men slept for 6 consecutive nights in the laboratory: 1 adaptation, 2 baseline, 2 selective SWS deprivation, and 1 recovery night. Cognitive performance was assessed by means of a Descending Subtraction Task after 2, 5, and 7.5 h of sleep. There was an almost complete selective SWS suppression during both deprivation nights, and a significant SWS rebound during the recovery sleep. Regarding cognitive performance, a progressive linear decrease of sleep inertia upon successive awakenings was found during all experimental nights except for the recovery night. In addition, a significant decrease of sleep inertia was observed upon the morning awakening of the second deprivation night for the measure of performance speed, and a significant increase of sleep inertia upon the morning awakening of the recovery night for the measure of performance accuracy. The results show that cognitive performance upon awakening is adversely affected by sleep depth and that, during the sleep-wake transition, cognitive performance accuracy is more impaired than performance speed.     

Sleep architecture and NREM alterations in children and adolescents with Asperger syndrome

STUDY OBJECTIVES: To analyze sleep in children with Asperger syndrome (AS) by means of standard sleep questionnaires, to evaluate sleep architecture and NREM sleep alterations by means of cyclic alternating pattern (CAP) and to correlate objective sleep parameters with cognitive behavioral measures. DESIGN: Cross-sectional study involving validated sleep questionnaires, neuropsychological scales, and PSG recording. SETTING: Sleep medicine center. PARTICIPANTS: Eight children with AS, 10 children with autism, and 12 healthy control children. INTERVENTIONS: N/A MEASUREMENTS AND RESULTS: Children with AS had a higher prevalence of problems of initiating sleep and daytime sleepiness. Sleep architecture parameters showed minor differences between the 3 groups. CAP parameters showed an increased percentage of A1 and a decreased percentage of A2 subtypes in subjects with AS vs. controls. All A subtype indexes (number per hour of NREM sleep) were decreased, mostly in sleep stage 2 but not in SWS. With respect to children with autism, subjects with AS showed increased CAP rate in SWS and A1 percentage. In subjects with AS, verbal IQ had a significant positive correlation with total CAP rate and CAP rate in SWS and with global and SWS A1 index. The percentage of A2 negatively correlated with full scale IQ, verbal and performance IQ. CBCL total score correlated positively with CAP rate and A1 index while externalizing score correlated negatively with A3%. CONCLUSIONS: This study shows peculiar CAP modifications in children with AS and represents an attempt to correlate the quantification of sleep EEG oscillations with the degree of mental ability/disability.     

Consolidation of strictly episodic memories mainly requires rapid eye movement sleep

STUDY OBJECTIVES: The aim of this study is to examine the effects of sleep deprivation during the first or second half of the night on episodic memory consolidation. Episodic memory is defined as memory for events located in time and space. It is also characterized by autonoetic consciousness, which gives a subject the conscious sensation of traveling back in time to relive the original event and forward into the future. DESIGN: Consolidation of episodic information was tested after 4-hour retention intervals, which followed learning and occurred during either the early or late half night, respectively dominated by slow wave sleep (SWS) or rapid eye movement (REM) sleep, or corresponding periods of wakefulness. SETTING: Data collection occurred in the sleep laboratory. PARTICIPANTS: Forty-three young healthy subjects: 9 men and 34 women, age ranging from 18 to 26 years (mean 20.18 +/- 1.94 years) were included in this study. INTERVENTIONS: Waking after a 4-hour retention interval filled with early or late sleep, or 4-hour sleep deprivation, during early or late period of night. MEASUREMENTS AND RESULTS: The cognitive task, named the What-Where-When test, was specially designed to assess factual, spatial, and temporal components of episodic memory. This task was associated with the Remember/Know paradigm to assess autonoetic consciousness. We measured performance on immediate free recall, delayed free recall (after a 4-hour interval of wakefulness or sleep), and delayed recognition. We also calculated a forgetting rate for each feature (factual, spatial, and temporal) and, for the recognition task, scores of autonoetic consciousness (R responses). REM-sleep deprivation was associated with significantly lower recall of spatial information compared to SWS deprivation (P < .01) or late sleep (P < .05) conditions. REM-sleep deprivation was also associated with a higher forgetting rate of temporal information as compared to the early sleep condition (P< .01). Finally, REM-sleep deprivation led subjects to give significantly fewer R responses, indicative of true memories, as compared to SWS deprivation (P < .05). CONCLUSIONS: These results suggest that consolidation of truly episodic memories mainly involves REM sleep.     

The impact of slow wave sleep proximity on evoked K-complex generation

During human stage 2 non-rapid eye movement (NREM) sleep, spontaneous K-complexes are more likely to occur prior to transitions to stage 3 or stage 4 sleep (referred to as slow wave sleep or SWS) compared to transitions to REM sleep, suggesting that the K-complex may be the 'forerunner' of SWS. The present study investigated the impact of SWS or REM sleep proximity on the probability of evoking a K-complex (pKC) during stage 2 and on components of the NREM sleep averaged evoked potential. Ten subjects spent three nights in the laboratory. On either the second or third night tones were presented continuously during sleep. Evoked K-complexes and sleep-evoked potentials were assessed for the 10 min of stage 2 prior to SWS (SWS-10) or REM (REM-10) sleep episodes as well as for all of SWS. pKC did not differ between SWS-10 (0.88) and SWS (0.91) but was significantly larger in SWS-10 than REM-10 (0.63). Amplitude effects were seen for the P2, N350, P900 NREM sleep-evoked potential components but not for the K-complex related N550. In each case where amplitude effects were found, SWS-10 was larger than REM-10. No latency differences were seen between conditions for the earlier components (P2, N350) however, both N550 and P900 were significantly shorter during SWS-10 compared to REM-10. These results are consistent with previous spontaneous K-complex studies and are supportive of a relationship between the K-complex and delta activity. They also indicate that stage 2 may consist of a continuum of microstates between SWS and REM sleep that are indicative of different brain stem, diecephalic and cortical patterns of activation.     

Dynamics of slow-wave activity during the NREM sleep of sleepwalkers and control subjects

STUDY OBJECTIVE: To compare the number and distribution of awakenings from slow-wave sleep (SWS) and both the power and dynamics of EEG slow-wave activity (SWA) in sleepwalkers and controls. Somnambulism is considered to be a disorder of arousal from NREM sleep and related to anomalous SWS and SWA. Power spectral analyses have never been used to quantify patients' SWA across sleep cycles. DESIGN: N/A SETTING: N/A PATIENTS: A polysomnographic study was performed on 15 adult sleepwalkers and 15 age- and sex-matched controls. INTERVENTIONS: N/A MEASUREMENTS & RESULTS: Sleepwalkers had a significantly greater number of awakenings from SWS than did control subjects. Controls showed a greater decrease in SWA across NREM cycles. Sleepwalkers had a significantly lower level of SWA during the first NREM period, where most awakenings take place. CONCLUSION: Sleepwalkers appear to suffer from an abnormality in the neural mechanisms responsible for the regulation of SWS.     

The distribution of slow-wave sleep across the night: a comparison for infants, children, and adults.

This study describes the temporal distribution of slow-wave sleep (SWS) (defined as the visually scored stages 3 + 4) across the night for 16 infants aged between 20 weeks and 1 year, 17 children between 1 and 6 years, and 17 adults between 20 and 36 years. In all three groups the amounts of SWS peaked during the first nonrapid eye movement (NREM) episode. SWS decreased across the night for adults and children, but not for infants. In infants the amounts of SWS remained at a fairly constant level from the second cycle onward, although many cycles were observed with zero SWS. The latter was evident from the very low tendency for SWS to appear in consecutive NREM/REM cycles. Rather, SWS was observed in alternate cycles. In children this phenomenon was less prominent but still well visible, and the tendency for SWS to appear in consecutive cycles had increased. In adults SWS occurred predominantly in consecutive cycles. The results suggest that whereas REM recurrence time increases twofold from infancy to adulthood, SWS recurrence time remains of similar length in infants, children, and adults.     

The effects of slow-wave sleep (SWS) deprivation and time of night on behavioral performance upon awakening

The aim of the present study is to evaluate the effects of selective SWS deprivation on the motor and sensory motor performance impairment immediately after awakening from nocturnal sleep at different times of the night. Ten normal males slept for 6 consecutive nights in the laboratory: one adaptation, two baseline, two selective SWS deprivation, and one recovery night. During the last 4 nights performance was assessed four times: (a) before sleep, as a baseline measure; (b) within 30 s from the first nighttime awakening, after 2 h of sleep; (c) within 30 s from the second nighttime awakening, after 5 h of sleep; (d) within 30 s from the final morning awakening. After each awakening, following a 3-min cognitive test, a simple Auditory Reaction Time task (ART, about 5 min) and a Finger Tapping Task (FTT, 3 min) were administered. Median of Reaction Times (RT) and of Intertapping Intervals (ITI), 10% fastest RT, 10% slowest RT, and number of misses were considered as dependent variables. The selective SWS deprivation was very effective: SWS percentage during both the deprivation nights was close to zero. This strong manipulation of SWS amount interacted with time-of-night factors in influencing sleep inertia. The SWS deprivation procedure caused a worsening of behavioral performance during the deprivation nights. as well as upon the final awakening of the recovery night. Behavioral performance slowing upon awakening is accounted for by: (1) a general decrement in overall response speed (median of RT); (2) an "optimum response shift", i.e., a decrease in speed of the fastest responses; (3) an increase of lapsing, with more marked response delays resulting in a further decrease in response speed in the "lapse domain". Finally, our results do not support the existence of a circadian rhythm of sleep inertia linked to body temperature rhythm.