Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “SLEEP DEPRIVATION”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 901 records · Page 50Linked to original sources
PubMed1988

The effects of acute sleep deprivation during residency training.

Verbal and symbol concentration, learning, problem solving, clear thinking, manual skills, and memory were tested in 42 surgical residents to assess the effects of acute sleep deprivation on specific neuropsychological parameters. A series of eight neuropsychological tests--digit symbols, digit vigilance, story memory, trail making, PASAT, Raven matrices, delayed story, and pegboard--and a questionnaire on mood states were completed by the residents both when fatigued (less than 4 hours of sleep: mean, 2.0 +/- 1.5 hours) and when rested (more than 4 hours of sleep: mean, 6.5 +/- 1.0 hours), with at least 7 days between tests. In order to eliminate the effects of learning from the first test series, randomization of residents was performed so that one half were first evaluated when rested and one half when fatigued. ANOVA, multiple regression analysis, and the Student t test were used to assess differences. In the acute sleep-deprived state, residents were less vigorous and more fatigued, depressed, tense, confused, and angry (p less than 0.05) than they were in rested state. Despite these changes in mood, however, the responses on all of the functional tests were no different statistically in those who were rested and those who were fatigued (even in those with less than 2 hours' sleep). We conclude that acute sleep deprivation of less than 4 hours alters mood state but does not change performance in test situations in which concentration, clear thinking, and problem solving are important.

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↗
PubMed2006

Comparison of the sleep pattern throughout a protocol of chronic sleep restriction induced by two methods of paradoxical sleep deprivation.

The purpose of the present study was to evaluate the sleep homeostasis of rats submitted to a protocol of chronic sleep restriction by two methods and to evaluate the sleep characteristics during the recovery period. The sleep restriction protocol was accomplished by sleep depriving rats for 18 h everyday for 21 days, using the single platform method (SPM) or the modified multiple platform method (MMPM) of paradoxical sleep (PS) deprivation. Rats were allowed to sleep for 6 h (from 10:00 to 16:00; starting 3 h after lights on) in their individual home-cages, during which their sleep was recorded. At the end of the sleep restriction protocol, rats were recorded in their home-cages for 4 days, where they could sleep freely. Both methods used to induce chronic sleep restriction were effective, in sofar as they resulted in augmented sleep time during the 6h-sleep period, with very few bouts of wakening. Although comparison between the methods did not reveal differences, sleep restriction under MMPM produced a more consistent daily rebound, mainly of paradoxical sleep, with longer episodes. These results showed distinct sleep recovery patterns, suggesting a possible role of the waking experiences (i.e. immobilization stress, social interaction) acting on sleep consolidation.

Animals↗
PubMed2005

Sleep deprivation suppresses neurogenesis in the adult hippocampus of rats.

We reported previously that 96 h of sleep deprivation (SD) reduced cell proliferation in the dentate gyrus (DG) of the hippocampus in adult rats. We now report that SD reduces the number of new cells expressing a mature neuronal marker, neuronal nuclear antigen (NeuN). Rats were sleep-deprived for 96 h, using an intermittent treadmill system. Total sleep time was reduced to 6.9% by this method in SD animals, but total treadmill movement was equated in SD and treadmill control (CT) groups. Rats were allowed to survive for 3 weeks after 5-bromo-2-deoxyuridine (BrdU) injection. The phenotype of BrdU-positive cells in the DG was assessed by immunofluorescence and confocal microscopy. After 3 weeks the number of BrdU-positive cells was reduced by 39.6% in the SD group compared with the CT. The percentage of cells that co-localized BrdU and NeuN was also lower in the SD group (SD: 46.6 +/- 1.8% vs. CT: 71.9 +/- 2.1, P < 0.001). The percentages of BrdU-labeled cells co-expressing markers of immature neuronal (DCX) or glial (S100-beta) cells were not different in SD and CT groups. Thus, SD reduces neurogenesis in the DG by affecting both total proliferation and the percentage of cells expressing a mature neuronal phenotype. We hypothesize that sleep provides anabolic or signaling support for proliferation and cell fate determination.

Animals↗
PubMed1996

Sleep deprivation reduces the citalopram-induced inhibition of serotoninergic neuronal firing in the nucleus raphe dorsalis of the rat.

Sleep deprivation (SD) for one night induces mood improvement in depressed patients. However, relapse often occurs on the day after deprivation subsequently to a sleep episode. In light of the possible involvement of central serotonin (5-hydroxytryptamine, 5-HT) neurotransmission in both depression and sleep mechanisms, we presently investigated, in the rat, the effects of SD and recovery sleep on the electrophysiological response of 5-HT neurons in the nucleus raphe dorsalis (NRD) to an acute challenge with the 5-HT reuptake blocker citalopram. In all rats, citalopram induced a dose-dependent inhibition of the firing of NRD neurons recorded under chloral hydrate anaesthesia. After SD, achieved by placing rats in a slowly rotating cylinder for 24 h, the inhibitory action of citalopram was significantly reduced (with a concomitant 53% increase in its ED50 value). After a recovery period of 4 h, a normal susceptibility of the firing to citalopram was restored. The decreased sensitivity of 5-HT neuronal firing to the inhibitory effect of citalopram after SD probably results in an enhancement of 5-HT neurotransmission. Such an adaptive phenomenon (similar to that reported after chronic antidepressant treatment), and its normalization after recovery sleep, parallel the mood improvement effect of SD and the subsequent relapse observed in depressed patients. These data suggest that the associated changes in 5-HT autocontrol of the firing of NRD serotoninergic neurons are relevant to the antidepressant action of SD.

Animals↗
PubMed1996

[Subjective diurnal fatigue and sleep deprivation response].

29 major depressive patients, the majority suffering from a melancholic subtype and typical diurnal variation of mood, rated subjective tiredness on a 100 mm analogous scale before and after total sleep deprivation (TSD). In study A every four hours during the day before and after TSD and every 2 hours during the TSD-night ratings were performed, in study B at 8.00 a.m. before and after TSD. The mean response rate was 55.2% in the 2 studies. In study A subsequent responders were less tired during the afternoon before TSD. Responding patients were more alert the morning after sleep deprivation than non-responders. A higher inter-individually variability of tiredness ratings in responders before and after sleep deprivation was found in study B, assuming an arousing property and a greater variability in subjective arousal at least during the morning hours. In summary the determination of the subjective arousal level may help to predict response.

Adult↗
PubMedDate not supplied

Age-dependent changes in recovery sleep after 48 hours of sleep deprivation in rats.

To characterize possible changes in homeostatic regulation of sleep with aging, we have examined sleep stages during recovery sleep after 48 h of sleep deprivation in young (3 months), middle aged (12 months), and old (24 months) rats. It was found that young and middle aged, in contrast to old rats, had large (21-24%) increases in total sleep time during recovery sleep; the old rats experienced a quantitatively small (8%) but significant rise in total sleep. NREM sleep increased significantly during the recovery period in young and middle aged, but not older rats. High voltage NREM sleep (HS2) declined by 30% during recovery in the young animals, but remained unchanged compared to baseline in the middle aged and old animals. The young and middle aged rats had increases in REM sleep during recovery compared to their baseline by 96% and 93%, respectively, which was significantly greater than a 65% increase during recovery in the old rats. Increases in total sleep and REM sleep during recovery were largely confined to the first 6 h in young and middle aged rats, but maxima for the old rats occurred in the second 6 h.

Aging↗
PubMed1995

Sleep deprivation in the rat: XX. Differences in wake and sleep temperatures during recovery.

We examined the relationship between wake and sleep peritoneal temperature (T(ip)) during recovery from short-term (five rats, 5 days of deprivation) and long-term (nine rats, 14-21 days) total sleep deprivation (TSD). Mammalian body temperature normally declines in the passage from wakefulness to sleep. Recovery from TSD featured reductions of the typical wake-sleep T(ip) differences. Previous studies from our laboratory have shown that chronic TSD in the rat produces a progressive rise in energy production and an initial rise in wake T(ip), followed by a later fall in T(ip) to below baseline that becomes more acute as death becomes imminent. During recovery from both short-term TSD (wherein pre-recovery wake T(ip) was still above baseline) and long-term TSD (wherein pre-recovery wake T(ip) had fallen to below baseline), wake T(ip) and energy production quickly returned towards baseline. On the first recovery day, both short- and long-term TSD rats showed mean non-rapid eye movement (NREM) and paradoxical sleep (PS) T(ip) values that were slightly, although not significantly, above mean wake T(ip). In short-term TSD rats, wake-NREM and wake-PS T(ip) differences were reduced from baseline significantly (p < 0.0025) on the first recovery day and nonsignificantly on the remaining three recovery days. In long-term TSD rats, wake-NREM and wake-PS T(ip) differences were significantly (p < 0.001) reduced from baseline on the first four recovery day block. On the last four recovery day block, wake-sleep T(ip) differences tended to return toward baseline. Hypothalamic wake-sleep temperature differences in long-term TSD rats showed similar reductions during recovery. The reduction of wake-sleep temperature differences in recovery does not support either energy reduction or cooling functions for sleep.

Animals↗
PubMed1991

Sleep deprivation reduces LH secretion in men independently of melatonin.

Melatonin affects gonadal function in non-primate mammals. Confirmatory data in man are not available. We assessed melatonin's acute effects on luteinizing hormone secretion in 17 normal men. We studied these men in conditions of sleep in the dark, and sleep deprivation in bright light, dim light, and bright light combined with a physiologically relevant infusion of melatonin, while measuring blood levels of immunoreactive LH every 20 min for 7 h. We compared overnight LH secretion, and LH pulse frequency, amplitude, length, interval and area under the curve using a modification of the PULSAR peak identification program, among the four treatments. Areas under the curve for peaks in all three conditions of sleep deprivation were lower than in normal sleep. The presence or absence of melatonin had no additional effect. We conclude that acute suppression of melatonin does not affect LH pulse parameters in normal man, but that sleep deprivation may reduce the amount of LH secreted per pulse.

Adult↗
PubMed1991

Effects of partial sleep deprivation on the diurnal variation of mood and motor activity in major depression.

Partial sleep deprivation (PSD), keeping a subject awake from 2 AM to 9 PM produces an acute mood improvement in 60% of patients with major depression. We sought to characterize the timing, subcomponent mood, and motor activity changes of this response. Thirty-seven subjects with major depression were rated with the 6-item Hamilton Depression Scale (HAM-6) at 1 PM and completed the Profile of Mood States (POMS) every 2 hr on the day before and day of PSD. Locomotor activity was monitored continuously during the trial with an automated device. Bipolar I patients responded more frequently than other groups. Positive mood responders had greater improvement than nonresponders in POMS subscales of depression, tension, confusion, and anger. The mood improvement increased steadily during the day, peaked in late afternoon, and declined thereafter. Responders showed significantly higher levels of locomotor activity on the baseline pre-PSD day than did nonresponders. All subjects increased motor activity following sleep deprivation, however.

Adult↗
PubMed1987

Effect of interrupted sleep patterns and partial sleep deprivation on DST and mood in psychiatric house officers.

To gain further insight into clinical associations seen in depression, the authors investigated the effect of interrupted night-time sleep on the HPA axis and mood in 20 psychiatric house officers taking overnight call. Specific interest was in whether multiple awakenings could induce a positive DST. No statistically significant association emerged between number of nocturnal awakenings, number of hours of sleep deprivation or temporal occurrence of sleep deprivation and cortisol, DST or mood. The results suggest that cortisol and DST changes are not likely to be causally linked to, or epiphenomenon of disrupted sleep. The implications of these findings for major depression are discussed.

Adult↗
PubMed2000

Effects of a new slow release formulation of caffeine on EEG, psychomotor and cognitive functions in sleep-deprived subjects.

Caffeine is a widely-consumed psychoactive substance whose stimulant effects on mood, attention and performance are largely recognised. The central nervous system pharmacodynamic profile of a single oral dose of a new slow release (SR) caffeine formulation (600 mg) was assessed in a randomised, double-blind, crossover, placebo-controlled study. Twelve young, health, male, sleep-deprived (for 36 h) subjects were studied using EEG and various measures of psychomotor and cognitive functions, including critical flicker fusion (CFF), choice reaction task (CRT), tracking, continuous performance task (CPT), Stroop test, body sway and subjective evaluation (Stanford Sleepiness Scale). Caffeine significantly ( < 0/05) antagonised the detrimental effects of sleep-deprivation on EEG (i.e. produced a significant decrease in delta and theta relative power and a significant increase in alpha and beta (12-40 Hz) relative power) and psychomotor performance (significant increase in speed of reaction on the CRT and Stroop tests, significant decrease in body sway, significant increase in accuracy of the CPT and significant reduction in subjective sedation) compared to placebo. The effect peaked 4 h after dosing and was maintained until the end of sleep deprivation (i.e. 24 h after dosing). In conclusion, the present results demonstrate that a single dose of caffeine SR possesses alerting effects which are able to reverse the deleterious effect of 36 h sleep deprivation for at least 24 h. Copyright 2000 John Wiley & Sons, Ltd.

Journal Article↗