Biomedical subjects

D J Dijk

Publications and source records attributed to D J Dijk.

At least 73 records · Page 4Linked to original sources

PubMed1994

Dynamics of slow-wave activity and spindle frequency activity in the human sleep EEG: effect of midazolam and zopiclone.

Electroencephalographic slow-wave activity (SWA; power density in the 0.75 to 4.5 Hz band) and spindle frequency activity (SFA; 11.25 to 15.0 Hz) exhibit a typical time course and a distinct mutual relationship during sleep. Because benzodiazepines (BDZ) suppress SWA and enhance SFA, we investigated the effect of two BDZ-receptor agonists on the dynamics of these EEG parameters. A single dose of midazolam (15 mg), zopiclone (7.5 mg), or placebo was administered before bedtime to healthy young men. Although the two drugs reduced SWA and enhanced SFA, their time course across and within sleep cycles as well as their mutual relationship were little affected. The results constitute further evidence that hypnotics acting as BDZ-receptor agonists do not substantially interfere with the homeostatic aspect of sleep regulation.

Adult↗

PubMed1993

Dynamics of electroencephalographic sleep spindles and slow wave activity in men: effect of sleep deprivation.

Recent developments in the understanding of the neurophysiological mechanisms underlying electroencephalographic (EEG) slow waves and sleep spindles imply an inverse relationship between these two EEG activities. The interrelationship between slow wave activity (0.75-4.5 Hz) and sleep-spindle activity (12-15 Hz) in electroencephalograms recorded in nine male subjects, during nocturnal baseline sleep and during recovery sleep from 40 h of wakefulness, was analyzed by power spectral analysis based on the fast Fourier transform and by transient patterns detection algorithms. Both techniques revealed that spindle activity was highest in sleep stage 2, increased over consecutive non-rapid-eye-movement sleep (non-REM sleep) episodes and was suppressed during recovery sleep. In contrast, slow wave activity decreased over consecutive non-REM sleep episodes and was enhanced during recovery sleep. Analysis of the dynamics of spindle and slow-wave activity within non-REM sleep episodes demonstrated that in the initial 20% of these episodes both spindle activity and slow wave activity increased, whereafter slow wave activity continued to increase but the average amplitude of spindles and total spindle activity, but not spindle density, decreased. At the end of non-REM sleep episodes the reverse pattern was observed. Sleep deprivation induced a more rapid rise of both spindle and slow wave activity in the very beginning of sleep. These data demonstrate that when averaged per sleep episode or non-REM sleep episode an inverse relationship between SWA and spindle activity exists but that in the initial and final part of non-REM sleep episodes the association between these two activities is positive. This biphasic relationship is discussed with reference to the hypothesis that the transition from sleep spindles to slow waves is dependent on a progressive hyperpolarization of thalamo-cortical neurons.

Adult↗

PubMed1993

A model of human sleep homeostasis based on EEG slow-wave activity: quantitative comparison of data and simulations.

EEG slow-wave activity (SWA; spectral power in the 0.75-4.5 Hz band) is a function of the duration of prior waking and, thereby, an indicator of sleep homeostasis. We present a model that accounts for both the declining trend of SWA during sleep and for its variation within the successive nonrapid eye movement (non-REM) sleep episodes. The values of the model parameters were estimated by an optimization procedure in which empirical SWA of baseline nights (16 subjects, 26 nights) served as a reference. A sensitivity analysis revealed the model to be quite robust to small changes (+/- 5%) of the parameter values. The estimated parameter values were used to simulate data sets from three different experimental protocols (sleep in the evening or sleep in the morning after prolonged waking, or extended sleep initiated at the habitual bedtime; n = 8 or 9). The timing of the REM trigger parameter was derived from the empirical data. A close fit was obtained between the simulated and empirical SWA data, and even the occasional late SWA peaks during extended sleep could be reproduced. Minor discrepancies suggest indirect or direct circadian influences on SWA. The simulations demonstrate that the concept of sleep homeostasis as proposed in the two-process model of sleep regulation can be refined to account in quantitative terms for empirical data and to predict the changes induced by the prolongation of waking or sleep.

Adult↗

PubMed1993

Repeated partial sleep deprivation progressively changes in EEG during sleep and wakefulness.

The effect of repeated partial sleep deprivation on sleep stages and electroencephalogram (EEG) power spectra during sleep and wakefulness was investigated in nine healthy young subjects. Three baseline nights of 8 hours (2300-0700 hours) were followed by four nights with 4 hours of sleep (2300-0300 hours) and three recovery nights of 8 hours (2300-0700 hours). Sleep restriction curtailed sleep stages 1 and 2 as well as rapid eye movement (REM) sleep, but left slow wave sleep largely unaffected. In the first two recovery nights, total sleep time and REM sleep were enhanced, and sleep latency was shortened. Slow wave sleep was increased only in the first recovery night. In accordance with the prediction of the two-process model of sleep regulation, slow wave activity (SWA; spectral power density in the 0.75-4.5-Hz range) in nonrapid eye movement (NREM) sleep increased by approximately 20% in the first night following sleep restriction, remained at this level in the subsequent 3 nights and decreased immediately after the first recovery night. In contrast to these immediate changes, progressive and more persistent changes were seen in the EEG activity of higher frequencies. Thus, activity in the upper delta band tended to gradually increase from night to night during the sleep restriction period, whereas after an initial increase, activity in the theta-alpha band changed in the opposite direction. The progressive changes were also present in the EEG spectra of REM sleep and wakefulness. Because the time course of these changes paralleled the cumulative deficit in REM sleep, they may represent a correlate of REM sleep pressure.

Adult↗

PubMed1993

Circadian sleep regulation in the absence of light perception: chronic non-24-hour circadian rhythm sleep disorder in a blind man with a regular 24-hour sleep-wake schedule.

Sleep disturbances and the failure to entrain circadian rhythms to the 24-hour day have been reported in the majority of totally blind subjects. The present case study of a totally blind man with a well-documented recurring sleep disturbance was designed to investigate the mutual relationship between sleep and the circadian timing system. The 63-year-old subject, a high school teacher with a regular work schedule, had suffered from cyclically recurring insomnia for the past 28 years. Analysis of a sleep log that he had kept for the past 15 years suggested that his circadian rhythms were not entrained to the 24-hour day. During a 3-month inpatient study, the period of the endogenous circadian pacemaker was assessed by analysis of ambulatory core body temperature, urinary excretion and a series of estimates of the phase of core body temperature cycles and plasma cortisol levels during constant routines. All circadian markers revealed periods in the range of 24.22-24.27 hours, with no evidence for a modulation of the observed periods by the sleep-wake cycle. During this 3-month inpatient study, a complete cycle of the subject's sleep disturbance and remission was polysomnographically documented while the subject lived on a regular 24-hour schedule. Because the subject's circadian rhythms were free-running and his sleep times were fixed, sleep occurred at virtually all circadian phases. Analysis of sleep latency, REM sleep latency, sleep duration, wake in sleep episode and REM sleep during sleep episode revealed a strong modulation by circadian phase. These findings in this blind man suggest that: 1) the period of his cyclically recurring sleep disturbance is directly related to the nonentrained period of an endogenous circadian pacemaker that drives circadian variation in core body temperature, urinary excretion, plasma cortisol and sleep propensity; 2) both his sleep structure and the severity of his daily sleep disruption are directly related to circadian phase and 3) his circadian pacemaker, which has an endogenous period that deviates only 0.2-0.3 hours from 24 hours, cannot be entrained by periodic daily exposure to nonphotic time cues, including a very regular 24-hour sleep-wake schedule.

Blindness↗

PubMed1992

Short-term memory, alertness and performance: a reappraisal of their relationship to body temperature.

Previous studies have led to the beliefs: (1) that short-term memory is best during the night when the body temperature is at its nadir, and (2) that the circadian rhythms of short-term memory and subjective alertness are driven by oscillators independent from each other and from the body temperature cycle. Unfortunately, these conclusions, which would have major implications for understanding the organization of the human circadian timing system, are largely based on field and laboratory studies, which in many cases sampled data infrequently and/or limited data collection to normal waking hours. In order to investigate these points further, we have monitored behavioural variables in two different protocols under controlled laboratory conditions: (1) during a period of 36-60 h of sustained wakefulness; and (2) during forced desynchrony between the body temperature and sleep/wake cycles, allowing testing of non-sleep-deprived subjects at all circadian phases. Contrary to earlier findings, we report here that the circadian rhythm of short-term memory varies in parallel with the circadian rhythms of subjective alertness, calculation performance, and core body temperature under both these experimental conditions. These results challenge the notion that short-term memory is inversely linked to the body temperature cycle and suggest that the human circadian pacemaker, which drives the body temperature cycle, is the primary determinant of endogenous circadian variations in subjective alertness and calculation performance as well as in the immediate recall of meaningful material.

Adolescent↗

PubMed1992

Circadian and sleep/wake dependent aspects of subjective alertness and cognitive performance.

Circadian and sleep/wake dependent processes underlying variations in subjective alertness and cognitive performance were assessed in a constant routine protocol and in a protocol in which the sleep/wake cycle was uncoupled from the output of the endogenous circadian pacemaker. In the latter protocol, the contribution of a sleep/wake dependent process and a circadian process to alertness and performance were separated by folding the data at either the period of the sleep/wake cycle or at the period of the endogenous circadian body temperature rhythm. This analysis revealed that prior wakefulness within a range of 0-18 h significantly reduced alertness and performance and that the circadian rhythm of core body temperature paralleled the circadian rhythm of alertness and performance. During the first 16 h of the constant routine protocol, which coincided with the subjects' habitual period of wakefulness, alertness and performance remained at a stable level. The latter finding was explained by assuming that during our usual waking day the circadian system counteracts the detrimental effects of increasing duration of prior wakefulness.

Adolescent↗

PubMed1992

The effects of ethanol on human sleep EEG power spectra differ from those of benzodiazepine receptor agonists.

A single dose of ethanol (0.60 g/kg of body weight) was administered to eight young healthy male subjects 35 minutes before bedtime. Compared to the average value of two baseline nights, subjective sleep and polysomnographically determined sleep parameters were not significantly affected. In the first 2 hours of sleep after ethanol intake, the combined value of wakefulness, stage 1, and movement time was reduced. In this interval, visually scored stage 4 sleep was increased, and electroencephalographic (EEG) power density in nonrapid-eye-movement (nonREM) sleep was enhanced in the lowest delta frequencies and reduced in the beta range. Computed for the entire sleep episode, power density in REM sleep was enhanced in some theta frequencies. In the sleep episode initiated 24 hours after ethanol intake, power density in nonREM and REM sleep was enhanced in delta and theta frequencies, and the subjectively perceived number of awakenings was reduced. The effects of ethanol on EEG power spectra during sleep differ from those published for benzodiazepine and nonbenzodiazepine hypnotics. This indicates that the effects of ethanol on the human sleep EEG are not mediated by the benzodiazepine receptor.

Adult↗

PubMed1992

Dynamics of EEG slow-wave activity and core body temperature in human sleep after exposure to bright light.

In seven subjects sleep was recorded after a single 3-hour (2100-0000 hours) exposure to either bright light (BL, approx. 2,500 lux) or dim light (DL, approx. 6 lux) in a crossover design. The latency to sleep onset was increased after BL. Whereas rectal temperature before onset and during the first 4 hours of sleep was higher after BL than after DL, the time course of electroencephalographic (EEG) slow-wave activity (SWA, EEG power density in the range of 0.75-4.5 Hz) in nonrapid eye movement sleep (NREMS) differed only slightly between the conditions. After BL, SWA tended to be lower than after DL in the first NREMS-REMS cycle and was higher in the fourth cycle at the time when the rectal temperature did not differ. The differences in SWA may have been due to a minor sleep-disturbing aftereffect of BL, which was followed by a rebound. The data are not in support of a close relationship between SWA and core body temperature.

Adult↗

PubMed1991

Effect of a single 3-hour exposure to bright light on core body temperature and sleep in humans.

Seven human subjects were exposed to bright light (BL, approx. 2500 lux) and dim light (DL, approx. 6 lux) during 3 h prior to nocturnal sleep, in a cross-over design. At the end of the BL exposure period core body temperature was significantly higher than at the end of the DL exposure period. The difference in core body temperature persisted during the first 4 h of sleep. The latency to sleep onset was increased after BL exposure. Rapid-eye movement sleep (REMS) and slow-wave sleep (SWS; stage 3 + 4 of non-REMS) were not significantly changed. Eight subjects were exposed to BL from 20.30 to 23.30 h while their eyes were covered or uncovered. During BL exposure with uncovered eyes, core body temperature decreased significantly less than during exposure with covered eyes. We conclude that bright light immediately affects core body temperature and that this effect is mediated via the eyes.

Adult↗

PubMed1991

Effect of clomipramine on sleep and EEG power spectra in the diurnal rodent Eutamias sibiricus.

Sleep was recorded in the diurnal rodent Eutamias sibiricus, chronically implanted with EEG and EMG electrodes. The tricyclic antidepressant drug clomipramine suppressed the duration of REM sleep and EEG power density in the frequencies between 1.5 and 13.5 Hz in nonREM sleep. During the administration of clomipramine, 24 h of sleep deprivation by forced locomotion significantly reduced the duration of waking and increased the duration of nonREM sleep. During the first 2 h of recovery sleep, EEG power density of the frequencies between 2.5 and 6 Hz was enhanced. These effects of sleep deprivation were to a large extent similar to those of sleep deprivation under drug free conditions. It is concluded that clomipramine affects the EEG in nonREM sleep but does not interfere substantially with nonREM sleep regulatory processes, which are activated by sleep deprivation.

Animals↗

PubMed1991

Effect of zolpidem on sleep and sleep EEG spectra in healthy young men.

A single 10 mg dose of zolpidem, an imidazopyridine hypnotic, was administered to young, healthy male volunteers prior to bedtime. The drug reduced REM sleep but did not significantly affect other sleep stages and subjective sleep parameters. All-night spectral analysis of the EEG revealed that power density in nonREM sleep was reduced in the low-frequency range (1.25-2.5 Hz; 5.25-10.0 Hz) and increased in the spindle frequency range (12.25-13.0 Hz). Significant changes in the EEG spectrum were present in the first 4 h of sleep. The pattern of the spectral changes was similar to those induced by other hypnotics that bind to the GABAA/benzodiazepine receptor complex. There were no residual effects of zolpidem on psychomotor performance in the morning, on the self-rated state in the morning and at noon, and on sleep and EEG parameters in the subsequent drug-free night.

Adult↗

PubMed1991

EEG power density during recovery sleep in the morning.

Sleep was recorded under baseline conditions (waking prior to sleep 16 h; lights off 23.00 h) and during recovery sleep in the morning (waking prior to sleep 24 h; lights off 07.00 h). Slow-wave activity (SWA; EEG power density in the range of 0.75-4.5 Hz) declined progressively over consecutive nonREM-REM cycles in both conditions despite the different circadian phase at which sleep occurred. SWA in nonREM sleep in the first 5 h of sleep was significantly higher in recovery than in baseline. Also SWA within the first 20 min of nonREM-episodes 2 and 3 was significantly higher in recovery sleep, and a tendency in the same direction was seen for nonREM-episode 1. These data show that homeostatic processes are expressed in the EEG also when sleep is initiated at a circadian phase where REM sleep propensity is high. However, comparison of the power spectrum in the first cycle of day-time recovery sleep with published data on recovery sleep at various circadian phases suggests that circadian factors influence the EEG spectra.

Adult↗

PubMed1991

Sleep extension in humans: sleep stages, EEG power spectra and body temperature.

In eight male subjects the electroencephalogram (EEG) and core body temperature (Tcore) were recorded during long sleep episodes from 0000 to 1,500 hr. EEGs were visually scored and subjected to spectral analysis by fast Fourier transform. Slow-wave sleep [SWS, i.e. stages 3 + 4 of non-rapid eye movement (NREM) sleep and slow wave activity (SWA, mean EEG power density in the range of 0.75-4.5 Hz)] in NREM sleep attained highest values in the first 3 hr of sleep and lowest values in the morning hours when rapid eye movement (REM) sleep was at its maximum. Wakefulness was significantly enhanced in the last 3 hr of the recording period. Occasional NREM episodes containing SWS were observed in the late morning and early afternoon. However, no significant increase in SWS or SWA in the last 3 hr of the sleep episode over any of the preceding 3-hr intervals was present and SWA in this interval was significantly below the values observed at the beginning of sleep. The duration of NREM episodes varied significantly over the sleep episode. Analysis of the dynamics of SWA within NREM episodes revealed that SWA gradually rose during the episode. Consequently, SWA averaged per episode was positively correlated with episode duration. Tcore dropped in the initial part of sleep, rose during the morning hours and reached values in the afternoon that were higher than at the beginning of sleep. Thus the time course of Tcore dissociated from the time course of SWA. This indicates that SWA in NREM sleep is not directly related to the variation in core body temperature.

Adult↗

PubMed1991

Sleep deprivation in rats: effects on EEG power spectra, vigilance states, and cortical temperature.

Vigilance states, electroencephalogram (EEG) power spectra (0.25-25.0 Hz), and cortical temperature (TCRT) of 10 rats were obtained during a baseline day, a 24-h sleep deprivation (SD) period, and 2 days of recovery (recoveries 1 and 2). EEG power density in waking gradually increased in most frequencies during the SD period. Non-rapid-eye-movement (NREM) sleep was enhanced on both recovery days, and rapid-eye-movement sleep was enhanced only on recovery 1. In the initial 4 h of recovery 1, EEG slow-wave activity (SWA; mean power density 0.75-4.0 Hz) in NREM sleep was elevated relative to baseline, and the number of brief awakenings (nBA) was reduced. In the dark period of recovery 1 and the light period of recovery 2, SWA was below baseline, and nBA was increased. During the entire recovery period, SWA and nBA, both expressed as deviation from baseline values, were negatively correlated. During the SD period, TCRT was above baseline, and in the initial 16 h of recovery 1 it was below baseline. Whereas TCRT was negatively correlated with NREM sleep, no significant correlation was found between TCRT and SWA within NREM sleep. It is concluded that SD causes a short-lasting intensification of sleep, as indicated by the enhanced SWA and the reduced nBA, and a long-lasting increase in sleep duration. The different time courses of SWA and TCRT suggest that variations in NREM sleep intensity are not directly related to changes in TCRT.

Animals↗

PubMed1991

Effects on night-time motor activity and performance in the morning after midazolam intake during the night.

The hypnotic action and residual effects of a single night-time dose of midazolam (Ro 21-3981, Dormicum, 7.5 mg; CAS 59467-70-8) were investigated in young, healthy adults. The subjects went to bed at the habitual time and were awakened 3 h later for drug or placebo intake. Then they were allowed to continue their sleep. Motor activity was continuously recorded by a wrist-worn activity monitor. In comparison to placebo, prolonged night-time immobility periods were more frequent after midazolam. Sleep tended to be perceived as more quiet and as less interrupted by awakenings. 15 min after awakening in the morning, the subjects felt more relaxed after midazolam than after placebo. Performance assessed 2 h after awakening by a psychomotor test showed no decrement. The results show that a 7.5-mg dose of midazolam taken in the first half of the night has a significant hypnotic action without impairing psychomotor performance in the morning.

Adult↗

PubMed1990

Effect of partial sleep deprivation on sleep stages and EEG power spectra: evidence for non-REM and REM sleep homeostasis.

The effect of repeated partial sleep deprivation on sleep stages and sleep EEG parameters was investigated in young subjects. After 2 baseline nights (B1, B2) of 7.5 h, sleep was restricted for 2 nights (D1, D2) to the first 4 h of the habitual bedtime period. Two recovery nights (R1, R2) with 7.5 h sleep followed. During the deprivation nights, stages 1 and 2 and REM sleep were reduced, while slow wave sleep (SWS; stages 3 and 4) was not significantly affected. However, the time integral of EEG power density in the range of 0.75-4.5 Hz (slow wave energy) was reduced. In the recovery period, SWS showed an enhancement in R1, and REM sleep showed a rebound in R1 and R2. An increase of REM sleep in the early part of the sleep period was evident in R1. Sleep latency was reduced in D2, R1 and R2. In accordance with the 2-process model of sleep regulation, EEG power density in non-REM sleep in the range of 0.75-4.5 Hz (slow wave activity) was only slightly higher in D2 and R1 than in baseline. An enhancement of slow wave activity in REM sleep was present in D2. Power density in the frequency range of 13-16 Hz was reduced in non-REM sleep (R1), SWS (R2) and stage 2 (R1). The results show (1) that the moderate reduction of slow wave energy in the deprivation nights induces only a minor enhancement of slow wave activity during recovery sleep; and (2) that a REM sleep deficit gives rise to an immediate rebound when 'slow wave pressure' is low.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1990

REM sleep deprivation during 5 hours leads to an immediate REM sleep rebound and to suppression of non-REM sleep intensity.

Nine healthy male subjects were deprived of REM sleep during the first 5 h after sleep onset. Afterwards recovery sleep was undisturbed. During the deprivation period the non-REM EEG power spectrum was reduced when compared to baseline for the frequencies up to 7 Hz, despite the fact that non-REM sleep was not experimentally disturbed. During the recovery interval a significant rebound of REM sleep was observed, which was only accompanied by a very slight increase of power in the lower non-REM EEG frequencies. In order to control for intermittent wakefulness, the same subjects were subjected to non-REM sleep interruption during the first 5 h after sleep onset 2 weeks later. Again subsequent recovery sleep was undisturbed. The interventions resulted in a similar amount of wakefulness in both conditions. During the intervention period, the non-REM EEG power spectrum was only marginally reduced in the delta frequency range. REM sleep duration was only slightly reduced. During the recovery interval, however, a substantial increase in EEG power in the delta frequency range was noted, without notable changes in REM time. It is concluded that an increased pressure for REM sleep results in longer REM episodes and a reduced intensity of non-REM sleep.

Adult↗