The effects of sleep deprivation and sleep on depressive mood and subjective arousal.
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Adult↗
Biomedical subjects
D G Beersma
Publications and source records attributed to D G Beersma.
Effects of SWS deprivation on subsequent EEG power density and spontaneous sleep duration.
In order to test predictions of the 2-process model of sleep regulation, the effects of slow wave sleep (SWS) deprivation by acoustic stimulation during the first part of the sleep period on EEG power density and sleep duration were investigated in 2 experiments. In the first experiment, 8 subjects were deprived of SWS during the first 5 h of a baseline nocturnal sleep period without awakening. Compared to the same interval of undisturbed sleep, power densities in the delta frequencies were attenuated. In the hour following SWS deprivation, power densities in the delta and theta frequencies were considerably enhanced in comparison with the same interval of undisturbed sleep. No change in sleep duration was observed. In the second experiment, 8 subjects were sleep deprived for 1 night and recovery sleep was initiated at 11 a.m. on 2 occasions. In 1 condition subjects were deprived of SWS during the first 3 h of recovery sleep. In the other condition recovery sleep was not experimentally disturbed. During undisturbed recovery sleep, power densities in the delta and theta frequencies were higher than during baseline sleep. During SWS deprivation, power densities in this frequency range were lower than during undisturbed recovery sleep. In the hour following SWS deprivation, power densities were enhanced relative to the same interval of undisturbed recovery sleep. Again, SWS deprivation did not cause an increase of sleep duration. The observed changes in EEG power density support the hypothesis that this EEG parameter reflects the homeostatic process S.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Observed behavior as a predictor of the response to sleep deprivation in depressed patients.
Total sleep deprivation (TSD) in depressive patients is known to produce sudden changes in mood, but the factors involved in these mood changes are poorly understood. In this study the role of psychomotor activation was investigated by examining the relationships between baseline measures of activation and subsequent clinical response to TSD. Two methods were used to assess the degree of activation: global judgment (clinical ratings) and direct observation and registration of behavior (ethological methods). Behavioral and global assessments took place 1 day before TSD during a medication-free psychiatric interview. The amount of looking displayed during the interview was negatively correlated with the subsequent clinical response to TSD, while body- and object-touching hand movements showed a positive correlation. During switches from speaking turn and at the start of the patients' speaking turn, responders to TSD showed more hand movements than nonresponders. No relation was found between clinical ratings of the degree of psychomotor activation and the TSD response. Our data suggest that the clinical response to TSD may be predicted and therefore possibly mediated by dimensions of activation. For the detection of these dimensions, behavioral observation appears to be more suitable than global clinical judgment.
Adult↗
Sex differences in the sleep EEG of young adults: visual scoring and spectral analysis.
Baseline sleep of 13 men (mean age of 23.5 years) and 15 women (21.9 years) was analyzed. Visual scoring of the electroencephalograms (EEGs) revealed no significant differences between the sexes in the amounts of slow-wave sleep and rapid-eye-movement (REM) sleep. Spectral analysis, however, detected significantly higher power densities during non-REM sleep over a wide frequency range (0.25-11.0 Hz) in the female versus male subjects. Also, during REM sleep, power densities were higher in the females. Analysis of the time course of EEG power density during sleep revealed that the differences between males and females persisted throughout the sleep episode. Comparison of these differences with published data on the effects of sleep deprivation on EEG power spectra did not suggest a common mechanism underlying sleep deprivation effects and the sex difference in sleep EEGs. It is concluded that sex differences in EEG power spectra are not likely to be caused by sex differences in sleep regulatory mechanisms but may, for instance, be caused by sex differences in skull characteristics.
Adult↗
Bright morning light advances the human circadian system without affecting NREM sleep homeostasis.
Eight male subjects were exposed to either bright light or dim light between 0600 and 0900 h for 3 consecutive days each. Relative to the dim light condition, the bright light treatment advanced the evening rise in plasma melatonin and the time of sleep termination (sleep onset was held constant) for an average approximately 1 h. The magnitude of the advance of the plasma melatonin rise was dependent on its phase in dim light. The reduction in sleep duration was at the expense of rapid-eye-movement (REM) sleep. Spectral analysis of the sleep electroencephalogram (EEG) revealed that the advance of the circadian pacemaker did not affect EEG power densities between 0.25 and 15.0 Hz during either non-REM or REM sleep. The data show that shifting the human circadian pacemaker by 1 h does not affect non-REM sleep homeostasis. These findings are in accordance with the predictions of the two-process model of sleep regulation.
Adult↗
Prediction of clinical change by ethological methods.
The aim of this paper is to show that ethology may contribute to the search for early indicators of clinical changes in depression. Three studies are presented. One study deals with the prediction of treatment outcome over 10 weeks and the other two with the prediction of the acute clinical response to total sleep deprivation (TSD). In each study a number of behaviours were observed, as displayed during a baseline psychiatric interview by the patients as well as the psychiatrist. In this report, the predictive potency of directly observed behaviours is compared to the predictive value of global clinical measures of psychomotor activation. The behaviours of the patients were interpreted as "relational" and "nonrelational" behaviours. The relational behaviours (i.e., variation in looking, yes-nodding, gesturing) occurred less, the nonrelational behaviours (i.e., intensive body touching, head movements) occurred more in responders than in nonresponders to 10 weeks of treatment. Also in the TSD studies body touching was positively related to improvement. Global clinical assessment of psychomotor activation could not be related to outcome. The advantages of the observational methods are discussed.
Behavior↗
On the contribution of sleep wake physiology to the explanation and the treatment of depression.
Physiological exploration has disclosed profound disturbances in the regulation of sleep in depression. The finding that depression can be relieved or intensified by manipulation of sleep has inspired the investigation of the possible pathogenetic significance of these dysregulations. Three hypotheses play a leading role in this context: the "phase-advance", the "S-deficiency" and the "acetylcholine-monoamine imbalance" hypothesis. They explain the therapeutic effects of a variety of sleep wake manipulations as consequences of the normalization of depressogenic sleep regulation disturbances. The issue discussed in this paper is whether these claims are valid. To what extent can the hypotheses explain the existing sleep physiological disturbance in depression as well as the results of therapeutic interventions in sleep? The empirical data provide firm evidence for the importance of particularly the timing of sleep in relation to the course of depression, both in respect to the spontaneous and the experimentally induced fluctuations of the clinical state. Without considerable extensions none of the hypotheses provide an adequate explanation of these facts.
Acetylcholine↗
Reduction of human sleep duration after bright light exposure in the morning.
In 8 subjects the spontaneous termination of sleep was determined after repetitive exposure to either bright or dim light, between 6.00 and 9.00 h, on 3 days preceding sleep assessment. Sleep duration was significantly shorter following bright light than following dim light. During sleep the time course of EEG energy was not affected by the light treatment. Analysis of the time course of body temperature during sleep indicated an earlier rise of body temperature following the bright light treatment. In terms of the two-process model of sleep regulation this can be interpreted as a direct effect of light on the circadian phase of the wake up threshold.
Adult↗
Quantitative analysis of the effects of slow wave sleep deprivation during the first 3 h of sleep on subsequent EEG power density.
The relation between EEG power density during slow wave sleep (SWS) deprivation and power density during subsequent sleep was investigated. Nine young male adults slept in the laboratory for 3 consecutive nights. Spectral analysis of the EEG on the 2nd (baseline) night revealed an exponential decline in mean EEG power density (0.25-15.0 Hz) over successive nonrapid eye movement--rapid eye movement sleep cycles. During the first 3 h of the 3rd night the subjects were deprived of SWS by means of acoustic stimuli, which did not induce wakefulness. During SWS deprivation an attenuation of EEG power densities was observed in the delta frequencies, as well as in the theta band. In the hours of sleep following SWS deprivation both the power densities in the frequency range from 1 to 7 Hz and the amount of SWS were enhanced, relative to the same period of the baseline night. Both the amount of EEG energy accumulating subsequent to SWS deprivation and its time course could be predicted accurately from the EEG energy deficit caused by SWS deprivation. The data show that the level of integral EEG power density during a certain period after sleep onset depends on the amount of EEG energy accumulated during the preceding sleep rather than on the time elapsed since sleep onset. In terms of the two-process model of sleep regulation (Borbély 1982; Daan et al. 1984) this finding indicates that EEG power density reflects the rate of decay of the regulating variable, S, rather than S itself, as was originally postulated.
Acoustic Stimulation↗
EEG power density during nap sleep: reflection of an hourglass measuring the duration of prior wakefulness.
The relation between the duration of prior wakefulness and EEG power density during sleep in humans was assessed by means of a study of naps. The duration of prior wakefulness was varied from 2 to 20 hr by scheduling naps at 1000 hr, 1200 hr, 1400 hr, 1600 hr, 1800 hr, 2000 hr, and 0400 hr. In contrast to sleep latencies, which exhibited a minimum in the afternoon, EEG power densities in the delta and theta frequencies were a monotonic function of the duration of prior wakefulness. The data support the hypothesis that EEG power density during non-rapid eye movement sleep is only determined by the prior history of sleep and wakefulness and is not determined by clock-like mechanisms.
Adult↗
The mathematical structure of the human sleep-wake cycle.
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Circadian Rhythm↗
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.
Animals↗
Sleep disorders in depression.
Recently some hypotheses explaining sleep disturbances in depression have been proposed. One hypothesis assumes an advanced phase position of the circadian pacemaker controlling a.o. REM sleep (REMS) production. In another a deficiency of process S is proposed. In this paper the sleep of depressed patients and healthy subjects is compared with respect to REMS production and EEG power density (a possible reflection of process S). Data were derived from the literature and from own experiments. The results provide support only for the S deficiency hypothesis.
Adult↗
Depression: the chronophysiological approach.
The author discusses the different clinical phenomena which stimulate a chronophysiological approach; he illustrates in particular the role of sleep in depression. He then discusses the alternation between sleep and wakefulness and describes a model that has been proposed to explain its regulation.
Affect↗
Observed behaviors during clinical interviews predict improvement in depression.
A considerable percentage of depressed patients does not respond to antidepressive treatment. Early indicators of prognosis are needed. The aims of this study are to examine a) whether the interpersonal behavior of patients and psychiatrist, as assessed by means of direct observation of behavior during a baseline clinical interview, might have predictive value with respect to therapeutic outcome, and b) which predictive potency might have measures of psychomotor activation. The relational behaviors (i.e. looking, yes-nodding, gesturing) occur less in patients who will improve, whereas the non-relational behaviors (i.e. intensive body touching, head movements) occur more in these patients. Global clinical assessment of psychomotor activation could not be related to outcome.
Adult↗
On the explanation of short REM latencies in depression.
Sleep in depression is characterized by the occurrence of episodes of rapid eye movement (REM) sleep at sleep onset. The empirical foundations of three hypotheses about the origin of this phenomenon are examined: A circadian rhythm hypothesis stating that sleep onset REM episodes (SOREMs) are the result of an abnormal phase-position of the REM sleep production cycle. A REM sleep-slow wave sleep interaction hypothesis that attributes SOREMs to a low non-REM sleep propensity. A circadian amplitude hypothesis, in which a flattening of the circadian arousal cycle is thought to be causally related to SOREMs. None of the hypotheses are found to be supported by firm empirical evidence.
Circadian Rhythm↗
The timing of sleep in depression: theoretical considerations.
Endogenously depressed subjects frequently show severe sleep problems. In this article sleep time in depression is discussed in relation to a recently developed model for sleep timing in healthy subjects. In terms of the model, two parameter sets survive a qualitative comparison with the empirical data. These are a deficient increase of sleep need (process S) and, alternatively, an increased amplitude of random fluctuations in the wake threshold (process C). Distinct predictions based on these alternatives are discussed.
Circadian Rhythm↗
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.
Biological Clocks↗