Sleep Recordings in the Laboratory and Home: A Comparative Analysis

All-night sleep recordings were obtained for 8 subjects who slept for 3 consecutive nights in a standard sleep laboratory and for 3 consecutive nights at home. The order of recording locations was counterbalanced across subjects. No first night effects were found in either location. Subjects' sleep in the two locations was highly correlated, with nonsignificant correlations occurring on only four variables (Number of Stage 1 Arousals, Minutes of Stage 1 Sleep, Latency to First REM, and number of REM periods). Significant differences between mean values were found on four variables: Minutes of Stage 3 Sleep, Percent of Stage 2 Sleep, Percent of Stage 3 Sleep, and Number of REM periods. Variances on Total Sleep Time and Latency to Sleep Onset were greater in the laboratory than at home. Generalizability theory was used to generate estimates of the degree to which each experimental factor (subjects, occasions, and raters) influenced observed score variance in each location. There was less between and within-subject variability at home on Total Sleep Time, Latency to Sleep Onset, and Stages 1 and 2 Sleep. Minutes Awake after Sleep Onset, Number of Arousals, and REM Sleep were less variable in the laboratory than at home. Taken together, these data suggest strong relationships between estimates of sleep parameters obtained in the two locations. But recordings in different locations may yield different values on some variables for groups of persons and for some individuals within those groups.     

Sleepiness and REM Sleep Recurrence: The Effects of Stage 2 and REM Sleep Awakenings

Determinants of daytime sleepiness include sleep length, sleep continuity, and circadian factors. Sleep stage composition has not been seen as influencing subsequent daytime functioning; however, earlier studies did not focus explicitly on sleepiness. The present experiment studied the effects of selective sleep-stage restriction on an objective measure of sleep tendency, and explored the relationship between sleepiness and subsequent REM recurrence during REM deprivation. Daytime sleep latency was measured by a modified Multiple Sleep Latency Test prior to and following two nights of awakenings from either REM or Stage 2 sleep in 16 normal young adults. Sleep latency following these awakenings was also measured. REM sleep and Stage 2 awakenings produced comparable levels of sleepiness, both during the Awakening Nights and subsequent daytime Multiple Sleep Latency Testing. Pooling the groups, daytime and nocturnal sleepiness measures were correlated within individuals. In the REM-Awakening Group, Pre-Awakening daytime sleepiness was associated with the tendency for REM sleep to recur following experimental awakenings. Comparable levels of sleepiness may result from nonspecific processes such as sleep curtailment and fragmentation, or alternatively from separate REM and Stage 2 mechanisms. The relationship between REM sleep and sleepiness is discussed in the context of both state and trait models.     

Effects of otolithic vestibular stimulation on sleep

This study evaluated the effects of otolithic vestibular stimulation in the form of a linearly accelerated parallel swing on nighttime sleep parameters and daytime sleep tendency in eight normal subjects. The protocol consisted of one adaptation night following by two motion nights, one adaptation night followed by two stationary nights, and two Multiple Sleep Latency Tests (MSLT), one motion and one stationary. On the motion nights, there was a decrease in stage 2 percentage as well as a facilitative effect on sleep latency on the last night. In addition, an increase in the number of rapid eye movements (REMs) per night was found without a significant alteration of REM sleep amount or latency. No significant differences were found between the motion and stationary MSLT days.     

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.     

Night-time sleep and daytime sleepiness in narcolepsy

This report describes night-time sleep and daytime sleepiness in a large (N=530) sample of patients meeting the International Classification of Sleep Disorders criteria for diagnosis of narcolepsy. Sleep data were obtained from polysomnographic recordings on two consecutive nights. Sleepiness was assessed using the Multiple Sleep Latency Test, the Maintenance of Wakefulness Test and the Epworth Sleepiness Scale. Analysis revealed that sleep was mild to moderately disturbed on both recording nights. A first-night effect was suggested by decreased REM latency and increased percentage REM and slow-wave sleep on the second night. Sleepiness and sleep disturbance varied across patient subgroups created based on patient ethnicity and on the presence/absence of cataplexy, sleep apnoea, and periodic limb movements. Covariation of sleep and sleepiness measures across patients was significant but weak. Strong association was found between subgroup means of sleep and sleep disturbance measures. The findings reported here show that sleepiness and sleep disturbance vary across patient subgroups and that sleep disturbance is related to, although unable to account, for the pathological sleepiness of narcolepsy.     

Sleep During and After Gradual Sleep Reduction

To determine: 1) the minimum amounts of sleep subjects would tolerate, 2) the changes in EEG sleep measures, and 3) whether subjects would revert to baseline sleep after study termination, 4 couples gradually reduced their sleep. Three couples reduced their TST in 30-min steps from a baseline of 8 hrs and one couple from a baseline of 6.5 hrs. Subjective estimates of sleep time, sleep quality, and mood were collected daily. Home EEG sleep recordings were obtained 3 nights a week. Two of the 8-hr sleepers reduced their sleep to 5.5 hrs, 2 to 5.0 hrs, and 2 reached 4.5 hrs. These 6 subjects continued sleeping 1 to 2.5 hrs below baseline amounts a year after reduction terminated. The 6.5-hr baseline couple reached 5.0 hrs and returned to 6.5 hrs TST during follow-up. Stages W, 2, and REM decreased significantly in absolute amounts. Percentage of stages W and 2 also decreased significantly. REM percent remained constant. Stage 3 was constant while stage 4 increased in both absolute and relative amounts. REM cycle length remained constant. Stage 4 rebound on 7-hr nights was not observed during times of greatest sleep reduction. Occurrences of stage REM within 10 min of stage 1 onset were observed in 2 subjects when their TST was below 6.5 hrs. Our results are consistent with other studies of shortened sleep, indicating that TST is the major determinant of sleep-stage characteristics.     

Effect of 64 hours of sleep deprivation upon sleep in geriatric normals and insomniacs

Fifty-eight geriatric normal and chronic insomniac sleepers were screened with sleep recordings to define groups of 12 Normal (Sleep Efficiency greater than 85%) and Insomniac (Sleep Efficiency less than 80%) sleepers. All subjects then had 4 baseline sleep nights, 64 hours of total sleep loss, and 4 recovery nights. Insomniacs, had lower sleep efficiencies and less REM than Normals during baseline. Sleep efficiency was high (97%) in both groups on the first recovery night but decreased toward baseline values in both groups between the second (Normal) and fourth (Insomniac) recovery night. The groups had relatively little slow wave sleep, but had a significant increase on the first recovery night. Five Normals and one Insomniac had REM latency of less than 15 min on their first recovery night. This REM latency was found to be significantly correlated with the amount of slow wave sleep on baseline. Decreased REM latency in initial recovery sleep was interpreted as evidence of decreased pressure for slow wave sleep in aging.     

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.     

The Effects of Distorted Visual Input on Sleep

An experiment in which 3 subjects wore prism lenses, which rotated the visual environment through 90 degrees and reversed right-left the visual field, was carried out to investigate whether visual distortion would affect sleep. An initial 2 laboratory adaptation nights, 6 pre-experimental days wearing heavy spectacles of plain glass that restricted the visual field but did not distort it, followed by 6 experimental days wearing distorting prisms, and then 6 post-experimental days with no spectacles, were consecutive. All-night sleep recordings were performed. Sleep parameters remained within normal limits during the 18-day period and there was no change in % REM sleep, or eye movement profusion, despite the fact that performance tasks confirmed that learning to cope with the disorted visual world took place. The latency to the first REM period, the % of stages 3 and 4 sleep, and the amount of REM sleep in the first 2 hrs of sleep were unaffected. There was a tendency toward greater intra-sleep restlessness. Results did not confirm the report of Zimmerman, Stoyva, and Metealf (1970). The results should not, however, be taken as providing positive evidence against links between learning, cerebral protein synthesis, and REM sleep.     

Reliability of Sleep Measures

The reliability of sleep measures was calculated over two nights (and within the nights) for 20 young adult males. Percent time in stages 1, 2, 3, and 4, percent movement time, number of movements, and number of stage changes were significantly correlated between Ss over nights. The percent REM time and REM cycle duration were not significantly correlated over nights. Within Ss, the length of the REM period had a significant negative correlation with the length of the preceding NREM period but not with the following NREM period. These data raise questions as to the use of the standard sleep measures as reliable human traits in young male adults.     

Sleep misperception,EEG characteristics and Autonomic Nervous System activity in primary insomnia: A retrospective study on polysomnographic data

Misperception of Sleep Onset Latency, often found in Primary Insomnia, has been cited to be influenced by hyperarousal, reflected in EEG- and ECG-related indices. The aim of this retrospective study was to examine the association between Central Nervous System (i.e. EEG) and Autonomic Nervous System activity in the Sleep Onset Period and the first NREM sleep cycle in Primary Insomnia (n = 17) and healthy controls (n = 11). Furthermore, the study examined the influence of elevated EEG and Autonomic Nervous System activity on Stage2 sleep-protective mechanisms (K-complexes and sleep spindles). Confirming previous findings, the Primary Insomnia-group overestimated Sleep Onset Latency and this overestimation was correlated with elevated EEG activity. A higher amount of beta EEG activity during the Sleep Onset Period was correlated with the appearance of K-complexes immediately followed by a sleep spindle in the Primary Insomnia-group. This can be interpreted as an extra attempt to protect sleep continuity or as a failure of the sleep-protective role of the K-complex by fast EEG frequencies following within one second. The strong association found between K-alpha (K-complex within one second followed by 8–12 Hz EEG activity) in Stage2 sleep and a lower parasympathetic Autonomic Nervous System dominance (less high frequency HR) in Slow-wave sleep, further assumes a state of hyperarousal continuing through sleep in Primary Insomnia.     

Sleep spindle activity changes in patients with affective disorders

Various polysomnographic sleep patterns are associated with affective disorders, but very little is known about sleep spindle characteristics in adult depression. In primary endogenous depressive male patients (unipolar, UP, and bipolar, BP) with comparable depression scores and in normal control subjects recorded during 3 consecutive nights, no night effect was observed on the sleep variables investigated except for REM latencies of stages 1 and 2. Stage 2 duration and variables related to sleep spindle characteristics (the number and the density of spindles of 1/2 s; the number and the density of full spindles of stage 2 over the 3 nights) were significantly lower in depressed patients than in control subjects, the mean number of spindles being lower in UP than in BP patients. Sleep spindle measures were clearly negatively correlated with age in the overall group (i.e., depressed plus control subjects). They were also negatively correlated with the REM latencies of stages 1 and 2 in BP depressed patients, whereas this relation was not observed in UP patients.     

THE DISPLACEMENT OF STAGES 4 AND REM SLEEP WITHIN A FULL NIGHT OF SLEEP

Stage 4 typically occurs dominantly in the first third of a normal night of sleep and REM sleep occurs dominantly in the last third of the night. In this experiment conditions were imposed to prevent these stages from occurring at their usual peak periods. Stage 4 sleep was permitted to occur only during the last two hours of sleep and REM was permitted to occur only during the first two hours of sleep. The results show that each stage can be partially displaced to the peak period of the other, but that stage 4 sleep is elicited more readily late in the sleep period than is REM early during the night.     

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.     

Interaction of REM Deprivation and Stage 4 Deprivation With Total Sleep Loss: Experiment 2

To determine whether prior deprivation of stage REM or stage 4 sleep would potentiate the effects of total sleep loss, 7 young adult males were denied REM sleep and 7 were denied stage 4 sleep for 3 nights before 1 night of total sleep loss. Measures of autonomic and EEG activity, mood, anxiety, Rorschach CET and on several performance tasks were obtained during baseline, following stage deprivation, total sleep loss, and during recovery. There were no marked changes in any area following 3 nights of stage REM and stage 4 deprivation. The changes following total sleep loss were similar for both groups. Prior deprivation of stage REM or stage 4 did not potentiate sleep loss effects. Ss who had no stage deprivation prior to 1 night of sleep loss had more impairment following sleep loss than did the Ss of this study.     

Long-term extension to sleep -Are we really chronically sleep deprived?

During 26 consecutive nights, electroencephalographic recordings and/or actigraphs were used to monitor the nighttime sleep of 10 asymptomatic healthy sleepers (mean age = 23.6 years). The schedule comprised: 7 nights of base line sleep, 14 nights of extended sleep (up to 10 hr/night), and 5 nights of recovery sleep. During extended sleep, subject1, slept significantly longer (approximately 1 hr), but sleep latency and interim wakefulness deteriorated. Extended sleep produced no improvements to sell-rated mood or subjective sleepiness. Vigilance tests showed a small but significant reduction in reaction time following extended compared with both baseline and recovery nights. Ability to detect target tones did not change significantly. Multiple Sleep Latency Test scores during extended sleep showed small (about 1 min) reductions. These findings give little support to the view of chronic sleep deprivation in the average 7.5-hr sleeper.     

A Dose-Response Study of Sleep Loss and Spontaneous Sleep Termination

Recent concepts of sleep/wake regulation have emphasized circadian influences and largely disregarded homeostatic ones. The present experiment was designed to study sleep loss homeostasis while minimizing confounding circadian influences. Eight male subjects participated in the study. Night sleep was curtailed across four conditions to yield 0, 2, 4, or 8 hrs of sleep. The effects were studied on subsequent day sleep begun at 1100h and spontaneously terminated. Total sleep time (TST), Stage 2 (S2), and Stages 3+4 (SWS) showed very strong dose-dependent increases with increasing loss. REM sleep did not respond. After maximum sleep loss TST and S2 doubled whereas SWS increased fivefold. Sleep did not terminate until the prior loss of SWS had been recovered. The total SWS recovery approximately matched the loss. TST, S2, and REM failed to recover more than limited amounts of the loss. The results show that homeostatic influences on sleep may be much larger than usually acknowledged and that SWS closely, although not perfectly, reflects the “active component’ of sleep homeostasis.     

Sleep in infant monkeys: Normal values and behavioral correlates

Measures of all night sleep physiology (EEG, EOG, EMG, heart rate (HR), body temperature (BT)) were recorded from 8 totally unrestrained infant M. nemestrina monkeys (mean age 26.1 weeks) for a total of 31 nights. Objective measurements of daytime behaviors were obtained in 7 of the infants. Mean sleep latency for the group was 35 min; individual sleep latency was related to maternal dominance. Mean total sleep time was 558 min, and mean sleep stage values for the group were drowsy, 16 min, Stage 2, 302 min, Stage 3–4, 150 min, and REM, 90 min. Mean interREM interval was 59.2 min. Infants exhibiting more locomotive behavior also had more Stage 3–4 sleep. Lower HR values were often found during deep slow wave sleep, but most nocturnal HR and BT variability did not appear closely associated with sleep patterns per se. Higher nocturnal body temperature and heart rate values were found in those infants engaging in greater amounts of play behavior and receiving more punishment from adults. Our findings are considered in terms of developing a biobehavioral developmental profile for the monkey infant.     

QUANTIFICATION OF THE REM SLEEP CYCLE AS A RHYTHM

The goal of this study was to develop an objective quantitative method for representing the temporal organization of sleep in terms of the period and rhythmicity of REM sleep occurrences. Data on normative human sleep, already scored for stage REM and not stage REM, were subjected to a “binary autocorrelation.” The mean period over 92 nights of sleep for 10 Ss was 101.5 min and quite stable. Data is also presented on variability of the rhythm in terms of an “index of rhythmicity.” Measures of temporal organization may prove to be as significant for sleep research as amount of the various sleep stages.     

Performance and Sleepiness as a Function of Frequency and Placement of Sleep Disruption

Eight normal young adult sleepers spent 4 nonconsecutive weeks in the laboratory. Each week consisted of a baseline night followed by 2 consecutive nights of disrupted sleep, followed by 2 recovery nights. Disruption conditions included: a) brief awakening after each minute of accumulated sleep, b) brief awakening after each 10 min of accumulated sleep, c) 2.5 hrs of normal sleep followed by a brief awakening at each sleep onset, and d) total sleep deprivation. Morning testing revealed that all disruption conditions decreased sleep latency in a morning nap test. Performance after 1-min disruptions approximated that seen after total sleep loss. Performance decrements were less in the 10-min condition and least in the 2.5-hr sleep condition. Performance under baseline and total sleep loss conditions was used to predict performance during the sleep deprivation condition using four sleep stage rules. Total time asleep and total time asleep minus stage 1 predicted performance poorly. Total SWS plus REM predicted performance best but could not differentiate the 10-min and 2.5-hr conditions. Therefore, it was concluded that the data were most parsimoniously explained by the Sleep Continuity Theory—i.e., that periods of uninterrupted sleep in excess of 10 min are required for sleep to be restorative.