Sleep Stage Deprivation and Total Sleep Loss: Effects On Sleep Behavior

The combined effects of total sleep loss and the deprivation of stage 4 or stage REM were studied in I two separate experiments. Two full nights or sleep loss preceded stage 4 deprivation or stage REM deprivation in Experiment 1 (N=12); 1 full night of sleep loss followed 3 nights or stage 4 deprivation or stage REM deprivation in Experiment 2 (N=I4). Total sleep loss before sleep stage deprivation significantly increased the number of attempts to enter stage 4, but had little influence on stage REM. A significant REM rebound was found in only one of the REM-deprived groups, but there was a significant stage 4 rebound in all groups on the first full recovery night, supporting the hypothesis from other studies that stage 4 has priority over REM in terms of recovery from sleep loss. The results suggested that stages 2, 3, and 4 partially overlap in their recuperative functions.     

Effects of sleep fragmentation on the arousability to resistive loading in NREM and REM sleep in normal men

STUDY OBJECTIVE: In healthy subjects, arousability to inspiratory resistive loading is greater during rapid eye movement (REM) sleep compared with non-REM (NREM) sleep but is poorest in REM sleep in patients with sleep apnea. We therefore examined the hypothesis that sleep fragmentation impairs arousability, especially from REM sleep. DESIGN: Two blocks of 3 polysomnographies (separated by at least 1 week) were performed randomly. An inspiratory-loaded night followed either 2 undisturbed control nights (LN(C)) or 2 acoustically fragmented nights (LN(F)) SETTING: Sleep laboratory. PARTICIPANTS: Sixteen healthy men aged 20 to 29 years. INTERVENTIONS: In both loaded nights, an inspiratory resistive load was added via a valved facemask every 2 minutes during sleep and turned off either when arousal occurred or after 2 minutes. MEASUREMENTS AND RESULTS: During LN(F), arousability remained significantly greater in REM sleep (71% aroused within 2 minutes) compared with stage 2 (29%) or stage 3/4 (16%) sleep. After sleep fragmentation, arousability was decreased in stage 2 sleep (LN(F): 29%; LN(C): 38%; p < .05) and low in early REM sleep, increasing across the night (p < .01). In stage 3/4 sleep, neither an attenuation nor a change across the night was seen after sleep fragmentation. CONCLUSIONS: Mild sleep fragmentation is already sufficient to attenuate arousability in stage 2 sleep and to decrease arousability in early, compared with late, REM sleep. This means that sleep fragmentation affects the arousal response to increasing resistance and that the effects are different in stage 2 and REM sleep. The biologic reason for this increase in the arousal response in REM sleep across the night is not clear.     

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.     

REM sleep modifications following a Morse code learning session in humans

Various experimental data indicate that rapid eye movement (REM) sleep is involved in learning processes. In animals, any complex task in a learning environment leads to an increase of the consecutive total REM sleep time, especially just before learning completion. In humans, the oculomotor activity during REM sleep seems to constitute an interesting marker of learning performance. In this work, we focus on the qualitative analysis of REM sleep characteristics after a Morse code learning session. Eight male subjects were polygraphically recorded during three consecutive nights. A computer aided teaching session was performed just before bedrest onset of the experimental night. The learning performance (percentage of saving) was checked on awakening. The Morse code learning led to some modifications in REM sleep components, particularly increases of REM sleep time and number of REM episodes. We did not observe any significant modification in the total number of REMs in the experimental night. However, the correlative analysis between learning performance and sleep parameters indicates a superior r for the oculomotor activity than for the tonic components. This is consistent with the information processing hypothesis in which the temporal distribution of REMs reflects the subject's ability to increase the signal-noise ratio from environmental information intake.     

Recovery sleep following different visual conditions during total sleep deprivation in man.

The findings of visual impairment during total sleep deprivation were used as a basis for a possible link between vision and sleep. It was proposed that the level of visual load imposed during sleep deprivation was an important variable, and would have a substantial effect upon recovery sleep. Six young male subjects underwent two conditions of 64 h of sleep deprivation on separate occasions. One condition incorporated a high visual load, and the other a low load. Exercise and sound were balanced. All night sleep EEGs were taken for two baseline nights, and also for two recovery nights following each condition. There was a significant increase of stage 4 on all recovery nights and a REM rebound on the second recovery night. SWS, particularly stage 4, TST and REM density, were significantly greater following the high load. Implications of these findings for sleep theories and for sleep deprivation research are discussed.     

REM Sleep Interruption: Experimental Shortening of REM Period Duration

This experiment concerns itself with the extent to which psychological factors can influence normal sleep patterns. After 4 baseline nights of uninterrupted sleep, each of 4 Ss was awakened in the course of 2 nights during every REM period about 10 min following each REM onset. Ss, however, were not REM deprived. The interruption nights were followed by a recovery night of uninterrupted sleep. All nights were consecutive. The results show that during recovery nights all Ss continued to have significantly shorter than normal REM periods by going into NREM sleep at about the time they would have been awakened during the interruption nights. These shortened REM periods occurred even during early morning hours, when REM periods normally become longer. Arguments are advanced that this finding may best be explained in terms of a conditioned avoidance response.     

Sleep disturbances due to exposure to tone pulses throughout the night

Sleep electroencephalograms (EEGs) and subjective reports data were obtained from six subjects (male college students) during 2 nights of baseline observation and 5 experimental nights of exposure to a 90-100 dB, 25 ms, 1,000 c/s tone pulse with various interstimulus intervals. The first of the 5 experimental nights started with an intertone interval of 80 s. On each of the following 4 nights, the intertone interval was fixed at 40-, 10-, 2.5-, or 1-s intervals, respectively. With the intensification of noise stimulus by shortening the intervals of tone pulses, a progressive disruption of nightly EEG sleep patterns was observed as follows: (a) increased frequency of awakenings and sleep stage changes during the night, (b) prolonged sleep latency, and (c) increased percentage of time spent in stage 1 sleep. However, total sleep time, REM latency, inter-REM intervals, and the percentages of time in stages 2, 3, 4, and REM sleep did not change significantly. The degree of subjective sleep disturbance was highly associated with objective measures of nightly EEG sleep patterns.     

The Effects of a Restricted Sleep Regime on the Composition of Sleep and on Performance

This study examined the effects of restricting sleep to the first or second half of the night on the composition of sleep and on performance. Eight young women who regularly slept for 8–8.5 hrs a night had their sleep restricted to the first or second half of the night for two consecutive nights. Performance of a 20-min unprepared simple reaction time task was measured at fixed times of day for the two restricted sleep conditions and for a full night sleep control condition. Restricting sleep to the second half of the night produced higher amounts of REM sleep and Stage 4 sleep and lower amounts of Stage 2 sleep compared to restricting sleep to the first half of the night. Both restricted sleep conditions impaired performance relative to the full night sleep control, and performance was worse after two nights of restricted sleep than after one night of restricted sleep. The results show that the effects of a restricted sleep regime on the composition of sleep are partly a function of the time of night to which sleep is restricted. It is suggested that the performance deficits are due to loss of sleep per se rather than due to any change in the composition of sleep.     

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.     

Performance during frequent sleep disruption

Performance on a simple addition task was measured during three schedules of frequent sleep disruption for 2 nights. Five young adults had their sleep briefly disturbed for 2 nights in 3 separate weeks either every 1 min, every 10 min, or at sleep onset after an undisrupted 2.5-h sleep period. Subjects were required to perform a two-number, two-digit addition problem as rapidly as possible on awakening. Main effects were found for sleep disruption condition and time of night, and a significant interaction between the two was also observed. Latency to response was longest for the 10-min condition on night 1, on night 2, however, response latencies were longest in the 1-min condition. Response latencies were fastest in the 2.5-h condition for both nights of disruption. Arousal thresholds were also gathered across both nights. Arousal thresholds were consistently the highest in the 1- and 10-min conditions for both nights of disruption, reaching maximum threshold levels at the end of night 1. Arousal threshold was significantly positively correlated with response latency. Sleep stages (slow-wave sleep (SWS), SWS + REM (SWSR), and total sleep time minus stage 1 sleep) were poor predictors of performance changes across the 2 disruption nights. The data were best explained by sleep continuity theory, which posits that a period of at least 10 min of uninterrupted sleep is required for restoration to take place.     

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.     

Modification of EEG asymmetry induced by auditory biofeedback loop during REM sleep in man

Several studies have emphasized the relationship between (1) rapid eye movement sleep (REM sleep) and learning, and (2) between REM sleep and asymmetry in EEG activity. Since we have shown that obtaining operant conditioned responses via auditory biofeedback during REM sleep is feasible, we demonstrate here that REM contingent auditory stimulations (white noise stimulation or interruption of a continuous white noise stimulation) lead to differential changes in phasic and tonic components of REM sleep. Whereas during baseline nights a relative right activation is found in the medium bands of EEG frequencies, our procedure seems to induce a systematic interhemispheric change during experimental nights. A new approach to the information processing hypothesis during REM sleep is proposed in terms of functional lateralized modifications of the EEG.     

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.     

Body Movements During Sleep After Sleep Loss

Following 4 baseline nights, 7 Ss were deprived of REM sleep for 3 nights and 7 were deprived of stage 4 sleep. Both groups were then deprived of total sleep for 1 night and then allowed 2 nights of uninterrupted recovery sleep. Compared to baseline nights, on the first recovery night the number of body movements was significantly reduced in all sleep stages and for total sleep. On the second recovery night, the number of movements was back to baseline level. The increased amount of slow-wave sleep (stages 3 and 4) during recovery sleep was not the primary reason for the reduced body motility.     

Effect of a presleep optokinetic stimulation on rapid eye movements during REM sleep

Some evidence supports the view point that phasic motor events of REM sleep show a complementary relation with the corresponding wake motor activities: (a) an inverse relationship between waking saccades and REM sleep eye movements (REMs) has been found with respect to frequency, amplitude, and direction; (b) an increase of middle-ear muscle activity (MEMA) in the 2 h before sleep causes a complementary decrease of MEMA during REM sleep. The present study evaluated this relation with respect to the optokinetic (OKN) system, assessing the role of automatically induced eye movements in affecting direction and frequency of REMs during sleep. Ten subjects were recorded following standard rules in 3 consecutive nights (one adaptation, one baseline, one experimental). In the experimental night subjects underwent 2 h presleep OKN stimulation at 15 degrees /s. The actual mean number of quick phases of nystagmus induced by the OKN stimulation was 12461.4 +/- 1.7 quick phases/s). No significant effect was found with regard to direction or frequency of REMs; the hypothesis that differences in REM direction and frequency could be modulated by the rank order of REM episodes (i.e., as a function of time elapsed from presleep stimulation) also failed to show any effect of a complementary relation between OKN and REMs. The results suggest that the complementary relation between wake and sleep eye movements is specific for the saccadic system, allowing us to exclude a peripheral mechanism, that is, an effect due to fatigue of extraocular muscles.     

Thinking and hallucinating: reciprocal changes in sleep

Internal deliberations (focused thoughts) and endogenous percepts (hallucinations) vary in a reciprocal manner across the states of waking and sleep, paralleling changes in regional brain activation. As subjects go from waking through sleep onset to NREM sleep and then to REM sleep, they report progressively more hallucinoid imagery and progressively less thinking. We have investigated whether this reciprocity in cognition between NREM and REM is maintained throughout the night. To do so, we analyzed 229 REM and 165 NREM reports collected with the Nightcap sleep monitoring system from 16 participants in their homes over 14 nights. The reports were scored for the presence of hallucinations and directed thinking by external judges. As predicted, hallucinations were more frequent in REM than in NREM for each segment of the night, and directed thinking was more frequent in NREM in the first 5 h of the night. Late in the night, directed thinking was equally infrequent in NREM and REM. At the same time, hallucinations increased within both NREM and REM as the night progressed, whereas directed thinking decreased in NREM and remained at a stable, low level in REM. These findings suggest that a reciprocal shift in focused thinking and hallucinating is a general property of cognitive activity across the wake-sleep cycle. Biological evidence supports the hypothesis that these cognitive changes are governed by specific state regulatory and neurocognitive processes at several levels of the brain.     

Effect of sleep disruption on sleep, performance, and mood

Eleven young adult subjects were briefly awakened after each minute of electroencephalographic-defined sleep for 2 consecutive nights after undisturbed laboratory adaptation and baseline nights. Two undisturbed recovery nights followed disruption nights. On disruption nights, subjects were awakened with an audiometer and signaled the awakening by subjective rating of sleep state or button push response. The disruption procedure resulted in severely fragmented sleep with only very small amounts of slow-wave and REM sleep. Total sleep time was reduced by approximately 1 h on each night. Arousal threshold increased 56 dB across the disruption nights. Following disruption, subjects performed more poorly and rated themselves sleepier than on baseline. The level of decline was similar to that seen after periods of total sleep loss of 40-64 h. Recovery sleep was also similar to that seen after total sleep loss. It was concluded that periodic disruption of sleep, perhaps by destroying sleep continuity, quickly results in impaired function. These data may help explain function loss in severe sleep apneics.     

Readaptation to the Sleep Laboratory in Insomniac Subjects

A readaptation effect to the sleep laboratory was demonstrated for insomniac subjects who returned lo the laboratory for a second series of consecutive nights after spending one week at home. This effect was similar to that seen in the initial adaptation period, i.e. REM percentage, REM min. number of REM periods, min stage 4. and percentage stage 4 were decreased on the first night upon returning to the laboratory as compared to subsequent nights. In addition, there was an increase in percentage stage 2, sleep latency, and total wake time on this first laboratory night.     

Variability of sleep parameters across multiple laboratory sessions in healthy young subjects: the "very first night effect"

Many studies have been carried out to assess the variability of sleep parameters. The first night effect is one of the most important factors in this variability and has been extensively studied. However, the readaptation phenomenon when subjects returned to the sleep laboratory after spending a certain period of time at home has been not systematically evaluated. To investigate this phenomenon across multiple sleep laboratory sessions, polysomnographic data from 12 healthy young subjects for 12 nights (three periods each of 4 consecutive nights, with a minimum of 1 month between them) were collected. The first night effect was present only in the first night of the first period ("very first night") and was significant only for REM sleep-related variables. We conclude that the results from the first nights of consecutive periods within a specific protocol with healthy young subjects need not be discarded in subsequent analyses.     

Retrograde effects of triazolam and zolpidem on sleep-dependent motor learning in humans

Drugs that act as allosteric activators at the benzodiazepine site of the gamma-aminobutyric acid (GABA_A) receptor complex are used commonly to treat insomnia but relatively little is known of how such use affects learning and memory. Although anterograde effects on memory acquisition have been shown, possible retrograde effects on consolidation are more relevant when such agents are administered at bedtime. We tested the effects of two GABA_A allosteric activators on sleep-dependent motor skill memory consolidation in 12 healthy male subjects. Subjects slept in a sleep laboratory for four consecutive nights (one accommodation night followed by three experimental nights). Placebo, triazolam 0.375 mg, and zolpidem 10 mg were given to each subject in counterbalanced order on the experimental nights. Polysomnographic (PSG) sleep measurement and sleep-dependent motor learning were assessed at each condition. Triazolam was associated with longer total sleep time and increased Stage 2 sleep. Both zolpidem and triazolam were associated with increased latency to rapid eye movement (REM) sleep. Overnight motor learning correlated with total sleep time in the placebo condition but not in the triazolam or zolpidem conditions. A statistically significant impairment in motor performance occurred overnight in the triazolam condition only. Triazolam, given in sufficient doses to prolong sleep in healthy people, affected overnight motor learning adversely. Zolpidem, in a dose sufficient to prolong REM onset latency but without other effects on PSG-measured sleep, degraded the relationship between total sleep time and overnight motor learning. These data indicate that non-selective or α1-preferring benzodiazepine site allosteric activators can interfere with sleep-dependent memory consolidation.