BACKGROUND:The impact of prolonged work cycles among senior doctors remains disputed. We evaluated the effects of overnight duty on awake activity and sleep quality in senior doctors in emergency medical specialties. METHODS:Thirty-six healthy doctors were monitored during a 2-week period including three separate 84 h on-call cycles. An on-call cycle consisted of the night and the day before night duty; the night duty itself and the subsequent 2 days and nights after night duty. The first day after night duty could either be worked or not. Actigraphy was used to measure physical activity and to evaluate sleep duration and quality. A standardized questionnaire was used to assess daytime performance and night sleep quality. RESULTS:Night actigraphy demonstrated that on-call work induced a significant reduction in sleep duration that was not recovered during the subsequent two nights. Sleep during the night duty itself was fragmented and of poor quality. Awake activity was significantly impaired on the day after night duty. Although subjectively night sleep quality did not differ between the nights before and after night duty, all subjective daytime parameters were impaired the day after night duty, and mood, fatigue and concentration remained altered on the second day. Working the day after night duty impaired objective measurements of daytime activity and sleep quality during the subsequent two nights. CONCLUSIONS:On-call night work in acute specialties induces sleep debt associated with prolonged impairment of awake activity, sleep quality and performance. Not working the following day after an on-call night allows partial recovery of sleep quality to begin.

The effects of hypnotics on descriptive and functional aspects of electrophysiological sleep parameters are assessed in this report. Because of the arbitrary definition of some of the criteria underlying the conventional sleep stage scoring procedure, computer-aided methods of EEG analysis have become increasingly important for recording and interpreting pharmacological effects on sleep. Of particular interest are the changes of EEG slow-wave activity, since this parameter varies as a function of prior sleep and waking. Several types of interaction between hypnotics and sleep regulation are discussed, some recent pharmacological developments are highlighted, and some common problems in clinical trials are specified.

The present studies evaluated to what extent duration (all-night or 4-hour exposures) and timing of nocturnal bright light (BL) (beginning or end of the night) modulate effects on vigilance. The results showed that all-night BL exposure is able to alleviate the nocturnal decrements in alertness and performance. However, under certain circumstances, this continuous BL exposure may induce adverse effects on mood and finally reveal to be counterproductive. Shorter BL exposure (4 h) during nighttime helps improve mood and performance, although the effects of short BL pulses were less efficacious than all-night BL exposure. The latter part of the night appears the best time for using the alerting effect of BL. The immediate alerting effect of BL seems to be mediated by a global activation of the central nervous system.

Objectives: Spectral power of 40 all-night sleep EEGs (Cz-Pz bipolar lead) recorded in 20 healthy young subjects was calculated after normalization on 30-s consecutive epochs by means of an autocorrelation method based on a 15-order autoregressive model.Methods: The spectral parameters were calculated for the 7 main EEG bands: slow delta (0.7-2 Hz); fast delta (2-4 Hz); theta (4-8 Hz); alpha (8-12 Hz); sigma (12-16 Hz); beta1 (16-35 Hz); and beta 2 (>35 Hz).Results: Strong negative correlations were found between power in the fast delta and either the alpha or the beta bands and between slow delta and theta bands, whereas the two delta bands showed little correlation with each other.Conclusion: The possibility that theses different relationships of slow and fast delta components with other frequency bands might reflect the neocortical or the thalamocortical origin of the delta waves is discussed. (C) 2000 Elsevier Science Ireland Ltd. All rights reserved.

The effects of zopiclone on the rest/activity rhythm were investigated after a westward flight with a 5-h phase delay (Grenoble-Martinique). The rest/activity rhythm was recorded continuously with an actigraph monitor during a 6-day baseline episode in Grenoble and a 6-day sojourn in Martinique. Rectal temperature was recorded before the flight on day 2 and after the flight on days 2 and 5. Subjective jet-lag score was assessed before the flight on days 1 and 2 and in Martinique on days 1, 2, 5 and 6. Zopiclone (7.5 mg) or placebo were administered double blind 30 min prior to bedtime during the first 4 post-flight days (D1–D4). Under zopiclone treatment, sleep was less fragmented on the first post-flight night and the curtailment of sleep duration observed on D2 and D3 under placebo was prevented. During daytime, subjects tended to be more active than with placebo. By contrast, subjective jet-lag scores did not differ between both groups. Zopiclone seemed to accelerate the readjustment of the rest/activity rhythm and the normalisation of the phase relationship between sleep and the temperature rhythm. Zopiclone probably exerts its ”resetting” effects on jet-lag desynchronosis by facilitating sleep induction rather than via a chronobiotic action.

Eight young adults were exposed to either 36 hours of moderate bright light (BL; 1,000-2,000 lux) or a light/dark cycle (L/D <50 lux) during constant routine. Sleep was recorded on the two subsequent recovery sleeps (R1 and R2) and compared to baseline. After the BL exposure, the rebound of stage 4 sleep and slow wave activity (SWA) were split over R1 and R2, whereas after the L/D cycle, the stage 4 sleep debt was almost completely compensated for during R1. During R1, stage 2 sleep and wakefulness accumulated faster in the BL condition than in the L/D condition. An elevation of the temperature level was also found during R1 of the BL condition. No differences between light conditions were found in urinary levels of melatonin or cortisol secreted during R1 or R2. Homeostasic process does not appear to be affected by the BL condition. A modification in the sleep-wake balance and a change in the temporal relationship between the circadian system and the sleep-wake cycle are discussed.

Poor sleepers are a valid model for studying sleep/wake regulation in insomnia. The respective influence of the homeostatic and circadian components of this regulation was studied using various protocols (habitual sleep, recovery after sleep deprivation, bedrest, sleep latency in MSLT and RTSW procedures, and circadian rhythms of body temperature and alertness during a 24-hour constant routine). Poor sleepers were compared to age matched good sleepers studied using similar procedures. The main results are reviewed. Our findings do not support a deficiency in the homeostatic component of sleep/wake regulation. An abnormality in the relationship between the sleep/wake cycle and temperature rhythm cannot be excluded, although most of our results are consistent with the hyperarousal hypothesis.

The 24-hour motor activity pattern was evaluated in 26 inpatients with major depression at treatment onset and after 4 weeks of antidepressant therapy. Clinical state, depression, and psychomotor retardation, as well as motor activity level and circadian rhythm, were simultaneously assessed. Treatment responders and nonresponders were also considered. Diurnal hypoactivity and reduced 24-hour rhythm amplitude were found at treatment onset. Activity level increased significantly on discharge. The rest-activity cycle for each depressed patient fit a cosine function of 24-hour periodicity. Data tended to show no phase shift but a large intragroup phase variability. Preliminary findings of a negative correlation between basic activity level and clinical improvement, and a trend toward responders having a lower activity level than nonresponders, suggest that activity could be used to predict therapeutic response.

We have studied the effects of two anxiolytic drugs frequently prescribed in alcohol withdrawal, diazepam and tetrabamate, on sleep polygraphy of alcohol‐dependent patients hospitalized for alcohol detoxification. Twenty‐three inpatients (16 M and 7F) fulfilling the DSM 3R alcohol‐dependence criteria were included. Twelve patients were treated with tetrabamate and the other 11 with diazepam. Sleep polygraphy was carried out on average 15 days after alcohol withdrawal. The sleep of tetrabamate‐treated patients differs from that of diazepam‐treated patients in having a much longer duration of stage 4, at the expense mainly of stage 2. The two groups of patients had a greater total sleep time and duration of delta sleep than comparable untreated patients. These results suggest that the delta sleep deficit of abstinent alcoholics is paradoxically corrected by anxiolytic treatment. Tetrabamate seems to induce the production of delta waves during the sleep of abstinent alcoholics.

Bien que l'alcool facilite objectivement l'apparition du sommeil, il altère notablement sa structure: fragmentation, particulièrement en fin de nuit, augmentation de la quantité de sommeil lent profond en début de nuit et diminution de la quantité et de la densité en mouvements oculaires du sommeil paradoxal. Cet effet hypnotique de l'alcool explique peut-être son utilisation abusive chez certains sujets insatisfaits de leur sommeil. Chez l'alcoolique, le sevrage d'alcool provoque l'effet inverse de la prise aiguë d'alcool: allongement de la latence d'endormissement, diminution de la quantité de sommeil lent profond, augmentation de celle du sommeil paradoxal, qui présente par ailleurs l'anomalie d'une persistance du tonus musculaire. À distance du sevrage, le sommeil reste perturbé. L'alcool modifie la fonction ventilatoire au cours du sommeil, favorisant l'apparition d'épisodes hypoxémiques ou apnéiques. Cet effet persiste après sevrage chez les alcooliques. Les troubles du sommeil rencontrés dans l'alcoolisme peuvent se comprendre, au moins en partie, comme l'expression d'un trouble des rythmes biologiques, tels qu'une diminution de l'amplitude et une avance de phase. Ainsi les caractéristiques chronobiologiques de l'alcoolique rappellent celles du déprimé ou du sujet âgé.

Alcohol reduces sleep latency but notably alters sleep structure: sleep is fragmented, particularly at the end of the night. Slow wave sleep duration is enhanced in the first part of the night and REM sleep duration and density are diminished. Alcohol withdrawal provokes inverse effects in alcoholic patients: sleep onset is delayed, slow wave sleep durations diminished and REM sleep duration is enhanced. REM sleep is associated with motor inhibition failure. Sleep remains disturbed in long term evaluations. Alcohol promotes the occurrence of sleep apneas and hypopneas. This effect persists in alcoholics after alcohol withdrawal. Sleep disturbances in alcoholism can be partly understood as the expression of amplitude diminution and phase advance of biological rhythms. Thus, the chronobiologic characteristics of alcoholics resemble those of depressives or the elderly.

The aim of the present study was to assess the stimulating effects of bright light (BL) on subjective and objective alertness. Eight subjects were exposed to either bright light or dim light (DL) during a 24-h constant routine (0900-0900). Bright light failed to modify either the 24-h course or the level of body temperature. Compared to DL, BL delayed the circadian trough of motor activity by 2 h. During the night, relative to the dim-light condition, BL significantly increased subjective and objective (EEG test) alertness and improved performances. Thus, BL exposure partly counteracted the effects of sleep deprivation and/or the circadian trough on alertness and performances. During the day, BL only improved the mood and motivation levels. However, the time course of mood and motivation was not affected by the BL exposure, a nocturnal circadian trough occurring at 0630 in both light conditions.

Using 24 h constant conditions, time course of body temperature, plasma cortisol and wrist motility was measured in response to a 3 day morning 2 h bright light pulse. This protocol demonstrated that a 2000 lux illumination was sufficient to elicit a shift of about 2 h of temperature minimum and cortisol peak. In reference session, actimetric recordings showed a circadian time course, closely in relation with core temperature. Bright light pulse resulted in a decrease of amplitude and a disappearance of circadian pattern of actimetry.

SLEEP and body temperature characteristics were studied in man in baseline (B), 24 h-constant routine (CR) and recovery (R) after the CR. The sleep advanced and deepened the trough of the minimum temperature when compared with CR. No relevant difference in minimum body temperature, or in the slope of temperature decrease was found, however, between B and R sleeping nights. No correlation was found between the amount of slow wave sleep and body cooling. The results do not support a homeostatic role of slow wave sleep in brain and/or body cooling.

ALLILAIRE, J. F.; DANTCHEV, N.; RAOUX, N.; BENOIT, O.; WIDLOCHER, D. Author Information