NREM-REM Cycles Research Articles

Slow wave sleep (SWS) distribution across night sleep episode in the elderly.

Slow wave sleep (SWS) distribution across night sleep was shown to be different between infants and young adults. The present research aimed at studying the SWS distribution across night sleep in elderly subjects. Nine healthy elderly subjects, 61-71 years old, were submitted to nocturnal polygraphic sleep recording. Eleven young subjects, 21-23 years old, were the control group. Recordings were visually analyzed according to Rechtschaffen and Kales rules; the method proposed by Webb and Dreblow was used for scoring SWS. An NREM-REM cycle was defined as a sequence of NREM and REM sleep not interrupted by a waking period longer than 15 minutes. SWS percentage was calculated for each successive NREM episode. No significant association between SWS percentage and cycle rank was shown in elderly subjects, whereas a significant association was observed in the young ones. This kind of SWS distribution could be interpreted as reflecting the restructuring of internal organization of sleep in the elderly.

Effects of time of night and sleep stage on perception of sleep in subjects with sleep state misperception

Although previous studies have documented that some persons who complain of poor sleep report having been awake when questioned following an awakening from Stage 2 sleep induced by an auditory stimulus, such observations have been confined to the first NREM-REM cycle. We have examined the possibility that the perception of having been awake or asleep may differ across the night. Eight subjects with sleep state misperception were awakened by a 500-Hz tone of progressive amplitude at five time points and were then asked to report whether they believed themselves to have been awake or asleep. This procedure was carried out on an early night during the first sleep cycle, and on a late night during the third sleep cycle, in random sequence. During the early Stage 2 trial, subjects were more likely to report having been awake, whereas in the late Stage 2 trial, they were more likely to report that they had been asleep. Conversely, in the REM sleep trial on the early night, subjects were more likely to report that they had been asleep. On the late night they were more likely to report that they had been awake, a change which was paralleled by a significant drop in scores on the Foulkes Dream Complexity Scale. Calculation of the duration of uninterrupted sleep prior to the trials suggests that this may have been a factor in the Stage 2, but not the REM, findings. There were no significant differences between the early and late REM trials in the frequency of dream reports, quality of dreams, or fragmentation of REM. These data indicate that subjects with sleep state misperception may experience REM sleep very differently in the first and third NREM-REM cycles.

Cyclic Alternating Pattern as a Provocative Factor in Nocturnal Paroxysmal Dystonia

We made a polygraphic study of 6 patients with nocturnal paroxysmal dystonia (NPD) in which the cyclic alternating pattern (CAP) parameters were compared with those of a group of age- and sex-matched controls. All patients met the requirements for NPD diagnosis, characterized by generalized stereotyped movements (dystonic-dyskinetic), with a 1-min centered duration but with no clear evidence of epileptic abnormalities in the waking EEG and during nocturnal recordings. Besides the major events, the NPD polysomnograms also showed shorter, repeated episodes of shorter duration (generally <20 s) consisting of abrupt movements involving one or more body segments. Overall, the motor events in patients with NPD were closely related to periods of unstable non-REM (NREM) sleep, as evidenced by the sequences of CAP, and began during an A phase. According to the conventional scoring parameters, NPD and controls differed only in sleep latency (+14 min in the NPD patients: p < 0.04). However, the architecture of sleep in the group with NPD was characterized by prolonged and irregular NREM/REM cycles. In addition, the NPD recordings showed significantly higher values of CAP rate (p < 0.0001). When major motor attacks were suppressed by medication, sleep was characterized by a decrease in the excessive amounts of CAP rate and by a more regular architecture. The modulatory role of CAP on nocturnal motor events is reported.

The diurnal distribution of sleep propensity: experimental data about the interaction of the propensities for slow-wave sleep and REM sleep.

The aim of the present study was to assess the diurnal variation of sleep propensity by evaluating the temporal distribution of sleep onset latency (SOL) and REM- and slow-wave sleep (SWS) parameters in systematically scheduled daytime naps for 12 young males. To reduce the effect of prior SWS on subsequent REM sleep, a double-nap technique was used, i.e. two adjacent naps A and B, which were separated by a 10-min break. Nap duration was adjusted in such a way that nap A allowed 30 min of sleep and nap B one complete NREM-REM cycle. EEG slow wave activity (SWA, power density from 0.5-4 Hz) was estimated from nap A and REM sleep parameters from nap B. The time span between 08.00 hours and 24.00 hours was covered by nine double-naps at 2 h intervals. The order of the nap sessions was systematically varied within and across subjects. For each subject, the time between successive double-nap recordings was at least three days. SOL was shortest in the time interval 12.00 hours to 16.00 hours and significantly longer between 20.00 hours and 24.00 hours. REM sleep duration and the percentage of sleep onset REM episodes decreased continuously from 08.00 hours to the interval 18.00-20.00 hours and increased thereafter, with a time course inversely related to the one of body temperature, which was also measured continuously. SWA showed a steady, threefold increase from 08.00 hours to 24.00 hours. The study offers new data on the diurnal variation of sleep propensity which seems to be a composite function of the drives for SWS and REM sleep.

Dreaming in the Late Morning: Summation of REM and Diurnal Cortical Activation

Since the discovery that the characteristics of dreaming sleep are far stronger in Stage 1 rapid eye movement (REM) sleep than in any other biological state, investigators have attempted to determine the relative responsibility of the tonic versus the phasic properties of REM sleep for the different characteristics of dreaming–features such as the amount of information in the dream report, the brightness and clarity of the visual images, shifts in thematic continuity, and incongruities of image and meaning. The present experiment is designed to identify dream characteristics that are specifically associated with tonic changes in level of cortical activation within sleep. It samples reports of imagery and thought during spontaneous variations within one phase of the 24-h diurnal rhythm and across the REM-NREM (non-REM) sleep cycle in order to identify the independent and joint contributions of the two cycles to imagery and thought. The rising phase of the diurnal cycle in the late night and morning was estimated from clock time during the late night and early morning and was varied by delaying the sleep onset and waking time of the subjects. Considered together with other studies, the results suggest that the major determinant of vivid visual imagery and enhanced cognitive activity during sleep is a pattern of subcortical and cortical activation that is common to both the REM phase of the REM-NREM cycle and the activated phase of the 24-h diurnal wake-sleep cycle.

A 20-h recovery sleep after prolonged sleep restriction: some effects of competing in a world record-setting cinemarathon.

The recovery sleep of a 21-year-old normal woman was assessed after she had endured 11(1/2) days of sleep restriction in a world record-setting film-viewing marathon. An exceptional sleep debt was observed as indicated by an instanteous sleep onset, a high sleep efficiency, and a total sleep duration of over 20 hours. Other striking features of this recovery sleep were very short latencies to stages 3 and 4 sleep, return of Stage 4 sleep after 14.5 h, REM and SWS sleep rebound, and a linear increase in REM sleep efficiency across 14 consecutive REM-NREM episodes. Seven of nine home dreams reported after this recording contained competition themes, but none relating to the marathon films. Comparisons of the present results with those from subjects in previous record-setting events suggest possible explanations for the extremely long recovery sleep. Results also suggest that analyses of multiple consecutive sleep cycles may provide novel ways of assessing hypotheses about regulation of the REM-NREM cycle.

The time course of σ activity and slow-wave activity during NREMS in cortical and thalamic EEG of the cat during baseline and after 12 hours of wakefulness

The extrapolation from recent neurophysiological findings concerning the dependency of spindle and slow-wave oscillations of thalamocortical neurons on membrane potential to macroscopic EEG events, predicts a reciprocal relation between spindle activity and slow-wave activity (SWA) in thalamic and cortical EEG during non-rapid-eye-movement sleep (NREMS). To test this hypothesis, the EEG recorded in 8 cats, from the nucleus centralis lateralis of the thalamus and from the skull during a 12-h baseline dark period and during a 12-h recovery dark period, following a 12-h sleep deprivation, were analyzed. Per 12-h epoch, sleep-wake behaviour was determined and spectral power density was computed in the slow-wave frequency range (0.5–4.0 Hz) and in the spindle frequency region (σ activity: 11.0–14.5 Hz). To analyze the development of EEG power densities in the course of NREMS and during the transition from NREMS to REMS, the last epoch of wakefulness and the first 15 epochs of NREMS, as well as the last epochs of NREMS and the first epoch of REMS were selected from the NREM-REM cycles. For each animal the values were averaged over 4-h intervals. In the cortical EEG, SWA was minimal at NREMS onset and increased progressively in the course of NREMS. SWA declined sharply prior to REMS, σ Activity increased gradually towards a uniform level after NREMS onset. During the transition to REMS, σ activity initially increased and then decreased rapidly. in the thalamic EEG, the time course of SWA paralleled that of the cortex. However, the development of σ activity during the first part of NREMS differed: in the thalamic EEG, σ activity was maximal during the beginning of NREMS and slightly decreased thereafter. After sleep deprivation, SWA within NREMS was markedly enhanced in both the cortical and the thalamic EEG. Sigma activity was attenuated in the thalamic EEG, whereas in the cortical EEG it was temporarily elevated. The present data show that, in the thalamic EEG, an inverse relation exists between spindle and slow-wave activity during baseline NREMS. This relation is preserved after sleep deprivation. In the cortical EEG, a reciprocal relation between spindling and SWA is less evident.

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.

Aging of core and optional sleep

Two consecutive 24-hr ambulatory recordings of 14 healthy elderly persons (7 women, 7 men, ages 88–102) and of 19 healthy young adults (10 women, 9 men, ages 25–35) were evaluated. In addition to the classical sleep parameter analysis, sleep structure was also analyzed in terms of a proposed distinction between “core” and “optional” sleep (Horne 1989). Core sleep is the essential part of the sleep and is mainly slow wave sleep. This type of sleep is composed of stages 3 and 4 on non-REM sleep (NREM 3–4). Core sleep is obtained during the first three sleep cycles and the remainder of the night sleep is considered optional sleep. Optional sleep is more altered than core sleep. However, in both optional and core sleep, NREM sleep and REM are reduced. There is also an increase in drowsiness and in the time spent awake after sleep onset; however, the extent of these effects are more obvious in elderly men. Aging effects of slow wave sleep probably represent an amplification of the changes as observed in awake electroencephalic (EEG) patterns in healthy seniors. The decrease in slow wave sleep (stages NREM 3–4) is gender related and prevails in elderly men. REM sleep diminishes with increasing age. In the elderly, most REM sleep occurs at the beginning of the night. This contrasts to younger persons where the duration of REM sleep is longer at the end of the night. Furthermore, a decrease in REM sleep latency is particularly obvious in elderly men and probably secondary to the curtailment of slow wave sleep. The ultradian NREM-REM cycle rhythm (as defined by the periodic occurrence of REM sleep) shows a monophasic trend suggesting a diminished adaptive function of aged sleep. The informative value of true, continuous ambulatory recordings in the assessment of sleep-wakefulness patterns in normal and pathological aging is stressed.

Time course of EEG power density during long sleep in humans

In nine subjects sleep was recorded under base-line conditions with a habitual bedtime (prior wakefulness 16 h; lights off at 2300 h) and during recovery from sleep deprivation with a phase-advanced bedtime (prior wakefulness 36 h; lights off at 1900 h). The duration of phase-advanced recovery sleep was greater than 12 h in all subjects. Spectral analysis of the sleep electroencephalogram (EEG) revealed that slow-wave activity (SWA; 0.75-4.5 Hz) in non-rapid-eye-movement (NREM) sleep was significantly enhanced during the first two NREM-REM sleep cycles of displaced recovery sleep. The sleep stages 3 and 4 (slow-wave sleep) and SWA decreased monotonically over the first three and four NREM-REM cycles of, respectively, base-line and recovery sleep. The time course of SWA in base-line and recovery sleep could be adequately described by an exponentially declining function with a horizontal asymptote. The results are in accordance with the two-process model of sleep regulation in which it is assumed that SWA rises as a function of the duration of prior wakefulness and decreases exponentially as a function of prior sleep. We conclude that the present data do not provide evidence for a 12.5-h sleep-dependent rhythm of deep NREM sleep.

All night spectral analysis of EEG sleep in young adult and middle-aged male subjects

The sleep EEGs of 9 young adult males (age 20–28 years) and 8 middle-aged males (42–56 years) were analyzed by visual scoring and spectral analysis. In the middle-aged subjects power density in the delta, theta and sigma frequencies were attenuated as compared to the young subjects. In both age groups power density in the delta and theta frequencies declined from NREM period 1 to 3. In the sigma frequencies, however, no systematic changes in power density were observed over the sleep episode. In both age groups the decay of EEG power (0.75–7.0 Hz) over successive NREM-REM cycles and the time course of EEG power during NREM sleep was analyzed. The decay rate of both EEG power density over successive NREM-REM cycles and EEG power density during NREM sleep was smaller in the middle-aged subjects than in the young subjects. It is concluded that the age-related differences in human sleep EEG power spectra are not identical to the changes in EEG power spectra observed in the course of the sleep episode. Therefore age-related differences in EEG power spectra cannot be completely explained by assuming a reduced need for sleep in older subjects. The smaller decay rate of EEG power during NREM sleep in the middle-aged subjects is interpreted as a reduced sleep efficiency. The results are discussed in the frame work of the two-process model of sleep regulation.

Effects of sleep interruption on REM-NREM cycle in nocturnal human sleep

Forty-four normal male students, aged 18–23 years were studied. After adaptation and baseline night (BN), 3 or 4 consecutive nights were interrupted by a forced awakening (10–90 min) once a night (ENs). Subjects (Ss) were awakened after they had slept for the first sleep cycle plus 20 min of NREM sleep in the 2nd cycle. The REM latencies following return to sleep showed a bimodal distribution separated by 25–30 min. The ENs were divided into 2 clusters: SOREMP (sleep onset REM period) and non-SOREMP nights. After interruption, the 2nd and the 3rd REM durations increased on non-SOREMP nights compared to SOREMP nights. We plotted, separately for SOREMP nights, the fluctuation of REM episode probability (FRP) at successive points in time. We examined the correspondence of FRPs derived from the sleep-independent, the sleep-dependent, and the reset hypotheses, with FRP of intact BN. On both SOREMP and non-SOREMP nights, none of the 3 models corresponded with BN. Thus, we suggest that, for both SOREMP and non-SOREMP nights, intervening wakefulness cancels the pre-awakening REM rhythm, and a new REM rhythm starts with or without SOREMP. We discuss factors influencing the rate of SOREMP occurrence (SOREMP %), such as circadian effect, individual differences, length of interruption, and pre-awakening NREM duration.

Acute changes in sleep-related hormone secretion of depressed patients following oral imipramine

Tricyclic antidepressants have acute effects on hormone secretion when given either orally or parenterally in the morning. These drugs also have acute effects on the sleep electroencephalogram (EEG) when given immediately before sleep onset. In particular, imipramine significantly delays the REM-nREM cycle and increases the amount of delta wave activity. This study shows that an oral dose of 50 mg imipramine given at bedtime to depressed patients has little effect on the secretion of prolactin and melatonin, but acutely advances the secretion of growth hormone and cortisol. This suggests that sleep and hormone secretion may only be temporally related, as they can be dissociated pharmacologically.

Perception of waking and sleeping: possible implications for the evaluation of insomnia.

Perception of awakening, its connection to electroencephalogram (EEG), and its significance for morning recall were studied in insomniacs and normals. Fourteen insomniacs and 14 age- and sex-matched controls kept a sleep log for 1 week and slept once in the laboratory (standard polygraphy). In addition, actual perception of awakening was measured by a behavioral device. Results suggest that physiological arousal is necessary, but not sufficient, for perception of awakening. Many arousals that are not perceived occur during the first REM-NREM cycle. Insomniacs nearly exclusively perceive those arousals occurring after consolidated sleep (at least 15 min) and at the beginning of interrupted sleep intervals. It is suggested that insomniacs perceive these intervals as continuous wakefulness and have difficulty in perceiving short-lasting sleep, whereas controls often do not perceive wakefulness at all. The latter may be a sleep-protecting mechanism. Number and correlation suggest that recalled awakenings are exactly those perceived. The connection between physiological and experimental subjective data is discussed.

Sleep and Affective Disorders: A Minireview

The most predictable electroencephalographic sleep changes of major depression are a shortened first NREM sleep period, a prolonged first REM period (with increased density of rapid eye movements), sleep continuity disturbance, and diminished slow wave sleep (with shifting of delta activity from the first to the second NREM sleep period). The more rapid appearance of the first REM sleep period occurs in relation to sleep onset but not apparently in relation to clock time. The changes occurring in the first NREM-REM cycle of the night appear to be relatively specific to major (particularly endogenous) depression. Depressed men appear to have diminished nocturnal penile tumescence compared with healthy controls, but depressed patients generally do not have a higher incidence of sleep apnea or nocturnal myoclonus. The sleep physiologic changes of depression appear to persist into clinical remission, suggesting that they are trait-like. Published studies appear to support the conclusion that there is a close link between the regulation of sleep and the regulation of mood in affective illness.

Response of polygraphic sleep to phenytoin treatment for epilepsy. A longitudinal study of immediate, short- and long-term effects.

Report on a prospective longitudinal study of alterations in polygraphic sleep by phenytoin monotherapy for epilepsy. A first dose of 100mg already caused abbreviation of sleep latency and an increase of slow-wave sleep in the first NREM-REM cycle. In the course of adjustments to steady state, an increase of Stage 3 + 4 sleep in the later REM cycles developed, such that the percentage of slow-wave sleep for the whole night was also augmented, whereas the percentage of light sleep decreased. Sleep structure was affected particularly in the third NREM-REM cycle. With continuing therapy, however, these effects were reversed. The only permanent effect was an abbreviated sleep latency. There were only minimal differences in the response of generalized and of localization-related epilepsies. Serum drug levels had only a very limited influence, seizure control and length of follow-up had no influence on the results. As a collateral finding, a delayed further decrease of epileptic discharges during sleep was observed under long-term conditions in patients who were seizure-free and had been so since adjustment to the steady state.

Sleep research in affective illness: state of the art circa 1987.

Future sleep research in affective illness will probably continue the current evolution beyond cross-sectional to longitudinal studies, and beyond a largely descriptive emphasis to the testing of specific hypotheses and predictions derived from models of the pathophysiology of depression. These models are and will be variously neurochemical, chronobiological, genetic, and developmental in nature. Adequate testing of these models and predictions from them will require the use of pharmacologic and naturalistic probes and the use of sophisticated CNS imaging techniques. These probes will help further characterize the physiology of depression under conditions of disequilibrium or perturbation, such as following sleep deprivation, REM deprivation, phase advancement of the major sleep period, or the administration of antidepressant drugs with specific monoaminergic activity. Concurrently, if one is to understand further whether the sleep abnormalities of depression are part of a larger circadian rhythm disturbance, investigations will necessarily include 24-h measures of sleep-wake activity, psychomotor activity, and probably core body temperature rhythm under constant routine conditions. A complementary point of view would suggest that more intensive investigative efforts be focused on the first 100 min of sleep at night, since it is the first NREM-REM cycle that seems to show the greatest and most specific deviation in depressed patients from normal controls. Efforts to characterize further this part of the 24-h cycle, with respect to age- and gender-related variance as well as responses to physiologic, hormonal, pharmacologic, and naturalistic probes, are strongly warranted.

Commentary on the mutual interaction model of McCarley and Massaquoi for REM-NREM cycle.

McCarley and Massaquoi successfully simulated human REM-NREM cycle characteristics by extending the McCarley-Hobson model with two sets of assumptions, one creating limit cycle behavior, the other introducing two sources of circadian variation. We argue that the limit cycle assumptions, due to freedom in choosing parameter values, suffice to explain variation in REM across the night. Nonmonotonic circadian variation in REM latency requires a circadian cycle dependence only of initial conditions at sleep onset.

Changes in the interhemispheric correlation during sleep in normal subjects

The correlation coefficients between left and right activity in the various frequency bands of the EEG signal were computed during sleep for 11 normal adults. The values of the correlation during REM sleep were compared with those for NREM sleep. This comparison was performed ‘locally,’ i.e., during each period of the REM-NREM cycle, as well as over the whole night. For 9 out of the 11 examined subjects, both a visual comparison with the hypnogram and a statistical analysis showed the existence of cyclic variations during the night in the delta and/or sigma correlation coefficient. These variations lasted for the whole night and were synchronized with the REM-NREM cycle. A possible connection between these results and data on the interhemispheric relationship given by amplitude analysis is briefly discussed.

Distribution of REM latencies and other sleep phenomena in depression as explained by a single ultradian rhythm disturbance.

The McCarley-Hobson model, describing the alternation of NREM and REM sleep in the cat, was applied to human electroencephalographic data. The influence of initial conditions on oscillatory behavior was especially emphasized. It appears that the distribution of REM latency in depression, the abnormal accumulation of REM sleep, the variability of NREM-REM cycle duration, the frequent stage shifts, and frequent awakenings can be explained in this model by means of a decrease in the initial value of a single variable, which may be regarded as representing the strength of REM inhibition. The observation of slow wave sleep deficiency in depression may well be another reflection of this parameter.