SEARCH · PubMed Health

Results for “SLEEP DEPRIVATION”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

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

At least 379 records · Page 21Linked to original sources

PubMed1993

Effects of sleep deprivation, lunch, and personality on performance, mood, and cardiovascular function.

The present study examined the effects of sleep deprivation on performance, mood, and cardiovascular functioning in the late morning and early afternoon. The results showed that the sleep-deprived subjects felt less alert and detected fewer targets in a cognitive vigilance task. Selective impairments due to sleep deprivation were also observed in a logical reasoning task. There was little evidence to suggest that consumption of lunch altered these effects of sleep deprivation. However, individual differences in the effects of sleep deprivation were apparent, with trait anxiety being related to the changes in subjective alertness produced by sleep deprivation, and sleep-deprived extraverts showing greater performance impairments than the sleep-deprived introverts.

Adolescent↗

PubMed2004

Sleep deprivation impairs hippocampus-mediated contextual learning but not amygdala-mediated cued learning in rats.

Prolonged sleep deprivation results in cognitive deficits. In rats, for example, sleep deprivation impairs spatial learning and hippocampal long-term potentiation. We tested the effects of sleep deprivation on learning in a Pavlovian fear conditioning paradigm, choosing a sleep deprivation paradigm in which REM sleep was completely prevented and non-REM sleep was strongly decreased. During conditioning, rats were given footshocks, either alone or paired with a tone, and tested 24 h later for freezing responses to the conditioning context, and to the tone in a novel environment. Whereas control animals had robust contextual learning in both background and foreground contextual conditioning paradigms, 72 h of sleep deprivation before conditioning dramatically impaired both types of contextual learning (by more than 50%) without affecting cued learning. Increasing the number of footshocks did not overcome the sleep deprivation-induced deficit. The results provide behavioural evidence that REM/non-REM sleep deprivation has neuroanatomically selective actions, differentially interfering with the neural systems underlying contextual learning (i.e. the hippocampus) and cued learning (i.e. the amygdala), and support the involvement of the hippocampus in both foreground and background contextual conditioning.

Amygdala↗

PubMed2000

Melatonin treatment does not prevent decreases in brain glutathione levels induced by sleep deprivation.

Recent findings from this laboratory revealed that sleep deprivation reduces total glutathione (GSH) levels in hypothalamus, suggesting an increased vulnerability to oxidative damage. Since melatonin has been shown to prevent oxidative damage in other experimental situations, the present study tested the effects of exogenous melatonin on sleep deprivation-induced GSH decreases. Rats were deprived of sleep for 96 h on small platforms, and melatonin (10 mg/kg body weight; i.p.) or vehicle was given twice a day. Hypothalamic GSH levels were significantly reduced in sleep-deprived groups, irrespective of melatonin treatment. Indeed, unexpectedly, melatonin treatment resulted in lower hypothalamic GSH levels in all groups, including cage controls. These results confirm that sleep deprivation reduces hypothalamic GSH and further indicate that melatonin treatment not only is ineffective in reversing this effect but may actually potentiate it.

Animals↗

PubMed1976

Potentiation of ketamine effects on the spiking activity in the lateral geniculate nucleus by rapid eye movement (REM) sleep deprivation.

In cats prepared for chronic recording of sleep, an investigation was made on the effects of an anaesthetic agent, ketamine [cl-581, 2-(O-chlorophenyl)-2-methylaminocyclohexamine HCl] and rapid eye movement (REM) sleep deprivation on spiking activity recorded from lateral geniculate (LGN) nucleus. In normal cats most of the LGN spikes occurring during sleep are found in REM sleep. Follwoing injection of 10 mg/kg of ketamine a substantial increase of slow wave sleep (SWS) spikes occurred. While selective REM sleep deprivation had the same effects, combined influences of ketamine and REM-sleep deprivation led to a marked potentiation of their individual effects probably by simultaneous stimulation of the neurone system which determines the endogenous electrical activity of LGN cells.

Action Potentials↗

PubMed1993

Naps after total sleep deprivation in depressed patients: are they depressiogenic?

Total sleep deprivation (TSD) exerts beneficial but transient effects on mood in approximately 60% of patients with a major depressive disorder. The positive effects of a night of total sleep deprivation are generally reversed after the next night of sleep. Several anecdotal reports and a pilot study by our group indicated that even short naps during the period of sleep deprivation are capable of re-inducing depressive mood in responders to TSD. The present study explored whether the structure of naps at 9 a.m. was crucial for the "depressiogenic" impact of naps on mood. A negative effect on mood was replicated, but this effect was not related to any of the nap sleep variables. The effect of naps on mood was attenuated in the early afternoon. The results support the assumption of a "depressiogenic" effect of naps in patients with major depression after successful TSD.

Depressive Disorder↗

PubMed2001

Effects of pinealectomy on baseline sleep and response to sleep deprivation.

STUDY OBJECTIVES: We have previously reported that older (24 mo.) Fischer rats manifest a diminished post-sleep deprivation increase in NREM and REM sleep. In order to examine whether this decline reflects an age-related change in pineal function, we are now reporting on baseline and recovery sleep parameters in pinealectomized 3-, 12-, and 24-month old rats following 24 hours of sleep deprivation using the disk-over-water method. DESIGN: Three independent age groups; within each group there were sequential measures of sleep under baseline conditions and during recovery from sleep deprivation. SETTING: The Sleep Research Laboratory at the University of Chicago PARTICIPANTS: 56 male Fisher (F344) rats INTERVENTIONS: 24 hours of total sleep deprivation using the disk-over-water method MEASUREMENTS: Sleep staging of EEG and EMG, and power spectral analysis of the EEG RESULTS: Pinealectomized (pinex) rats did not differ from sham-operated (sham) rats in total sleep, REM sleep, super-modal high-amplitude NREM sleep (HS2), a measure of NREM EEG delta power, or circadian rhythm amplitude. In the pinex rats, there was a modest (2.5%) age-independent increase in NREM sleep (p<0.02). The pinex rats of all ages failed to manifest the increase in NREM sleep during recovery seen in the sham-operated animals (p<0.04). CONCLUSIONS: We found no evidence that altered pineal function is responsible for age-related changes in baseline sleep in the rat. These data also suggest that, independent of age, normal pineal function may be relevant to the ability to generate increased NREM sleep in response to prior sleep deprivation.

Animals↗

PubMed1975

A review of REM sleep deprivation.

Studies on the behavioral consequences of rapid eye movement (REM) sleep deprivation in animals and humans are critically reviewed. In animals, converging evidence--some reasonably well controlled--indicates that REM sleep deprivation probably heightens central neural excitability and increased motivational behavior, but has nuclear or inconclusive effects on learning. In humans, evidence indicates that REM sleep deprivation is not dream deprivation and is not harmful to schizophrenic, depressed, or healthy subjects. Controversy continues about whether or not (some) schizophrenic patients respond abnormally to REM sleep deprivation by having no REM rebound. Controlled but unconfirmed work indicates that that endogenous, but not reactive, depressive patients are improved by REM sleep deprivation, a finding consistent with the animal behavioral consequences of the procedure and with the unique REM-depriving properties of efficacious antidepressant drugs.

Adjustment Disorders↗

PubMed1997

How sleep deprivation affects psychological variables related to college students' cognitive performance.

The effects of sleep deprivation on cognitive performance psychological variables related to cognitive performance were studied in 44 college students. Participants completed the Watson-Glaser Critical Thinking Appraisal after either 24 hours of sleep deprivation or approximately 8 hours of sleep. After completing the cognitive task, the participants completed 2 questionnaires, one assessing self-reported effort, concentration, and estimated performance, the other assessing off-task cognitions. As expected, sleep-deprived participants performed significantly worse than the nondeprived participants on the cognitive task. However, the sleep-deprived participants rated their concentration and effort higher than the nondeprived participants did. In addition, the sleep-deprived participants rated their estimated performance significantly higher than the nondeprived participants did. The findings indicate that college students are not aware of the extent to which sleep deprivation negatively affects their ability to complete cognitive tasks.

Adult↗

PubMed2005

Effects of progesterone blockade over cocaine-induced genital reflexes of paradoxical sleep-deprived male rats.

Paradoxical sleep deprivation (PSD) enhances cocaine-induced genital reflexes (penile erection [PE] and ejaculation [EJ]) in male rats and induces a significant increase in progesterone concentration. As progesterone treatment facilitates PE in PSD castrated rats, we may speculate that progesterone appears to be a relevant hormonal factor eliciting genital reflexes in PSD males. In order to expand the latter finding, different doses of antiprogestin mifepristone (vehicle, 2.5, 5, 10, and 20 mg/kg, s.c.) were administered to PSD rats at the end of a 4-day period of PSD 1 h prior to cocaine administration (7 mg/kg, i.p.) and placed in observation cages for the evaluation of genital reflexes. Pretreatment with vehicle induced PE in all rats and this effect was significantly reduced by mifepristone at 5 to 20 mg/kg doses that lowered the proportion to 40% of the rats. The frequency of PE was also significantly reduced for all doses used. There were no significant differences between vehicle and mifepristone in EJ behavior. As for hormone concentrations, mifepristone reduced progesterone concentrations at the 5-20 mg/kg doses compared to vehicle group. At 20 mg/kg, it also elevated testosterone concentrations. In addition, mifepristone administration induced a significant decrease in the duration of PS episodes at all doses. These data suggest that progesterone exerts an essential role in erectile response induced by cocaine in PSD male rats.

Analysis of Variance↗

PubMed2004

Nociceptor and age specific effects of REM sleep deprivation induced hyperalgesia.

REM sleep deprivation (REMSD) has been shown to increase rates of negatively reinforced operant behavior, but not operant responding maintained by positive reinforcement. The reason for this differential effect is currently unknown. We hypothesize that REMSD can increase sensitivity to noxious stimuli. In the present study, we sought to determine if REMSD was associated with a change in response to noxious heat (i.e., altered nociceptive sensitivity). Two groups of rats, aged 6 and 22 months, were subjected to hotplate algesia testing at two different temperatures (44 and 52 degrees C). Initially, baseline numbers of responses and total response time were obtained at 44 degrees C. Animals then were exposed to 48 h of REMSD or control conditions. The frequency and duration of hindpaw responses (licking and guarding) increased for young animals only after REMSD and none of the control conditions. Old rats showed increased duration of nocifensive responding after REMSD and tank control conditions without a change in the number of responses at 44 degrees C. Latency to first nocifensive response was significantly longer in the 44 degrees C hotplate tests, but decreased to levels observed throughout the 52 degrees C hotplate tests following REMSD and TC conditions. These findings suggest that REMSD increases nociceptive sensitivity under conditions of sustained, selective C nociceptor activation (42 degrees C), but not under conditions of phasic A-delta activation (52 degrees C). The findings also indicate that age can be a significant variable in REMSD studies.

Age Factors↗

PubMed1999

Auditory attention and multiattribute decision-making during a 33 h sleep-deprivation period: mean performance and between-subject dispersions.

One purpose of this study was to compare attention in the evening (22:00 h), in the late night (04:00 h), in the morning (10:00 h) and in the afternoon (16:00 h) during a period of complete wakefulness beginning at 08:00 h with a mean daytime performance without sleep deprivation. Another purpose was to investigate sleep deprivation effects on a multi-attribute decision-making task with and without time pressure. Twelve sleep-deprived male students were compared with 12 male non-sleep-deprived students. Both groups were tested five times with an auditory attention and a symbol coding task. Significant declines (p < 0.05) in mean level of performance on the auditory attention task were found at 04:00, 10:00 and 16:00 h for subjects forced to the vigil. However, the effect of the sleep deprivation manifested itself even more in increased between-subject dispersions. There were no differences between time pressure and no time pressure on the decision-making task and no significant differences between sleep-deprived and non-sleep-deprived subjects in decision strategies. In fact, the pattern of decision strategies among the sleep-deprived subject was more similar to a pattern of decision strategies typical for non-stressful conditions than the pattern of decision strategies among the non-sleep-deprived subjects. This result may have been due to the fact that the sleep loss acted as a dearouser. Here too, however, the variances differed significantly among sleep-deprived and non-sleep-deprived subjects, indicating that the sleep-deprived subjects were more variable in their decision strategy pattern than the control group.

Adult↗

PubMed1997

Effects of 72 hours sleep deprivation on wound healing in the rat.

The purpose of this study was to examine effects of sleep deprivation on cellular and biochemical markers of wound healing. Expanded polytetrafluoroethylene tubing inserted in subcutaneous tissue created miniature wounds in the dorsal skin of 12 rats. Seven days later, 6 rats were deprived of sleep by the platform method for 72 hr; control rats remained on usual sleep/wake routines. Numbers of macrophages, granulocytes, fibroblasts, and extent of connective tissue present and total amounts of protein, DNA, and hydroxyproline in the implants were not different between sleep-deprived and control rats. There is no evidence from this study that sleep deprivation impairs cellular and biochemical indicators of tissue repair.

Animals↗

PubMed1978

Analysis of mood change during and following sleep deprivation therapy.

Recent work suggests that depriving endogenous depressives of sleep for 1 night may be followed by an alleviation of their illness. In order to facilitate further study of the mechanisms underlying this effect, hourly self-rated measurements of mood were obtained throughout the sleepless night and the time of onset of any response noted. Of the patients who improved, some did so during the day following sleep deprivation; in others the response did not occur until after the next night's sleep. The two groups of responders differed in terms of self-reported emotional arousal during the course of the sleepless night. The implications of these findings are discussed in relation to further studies of sleep deprivation therapy.

Adult↗

PubMed2003

Effects of tyrosine, phentermine, caffeine D-amphetamine, and placebo on cognitive and motor performance deficits during sleep deprivation.

Cognitive and motor performance are critical in many circumstances and are impaired by sleep deprivation. We administered placebo, tyrosine 150 mg/kg, caffeine 300 mg/70 kg, phentermine 37.5 mg and D-amphetamine 20 mg at 15.30 h following overnight sleep deprivation and compare their effects on cognitive and motor performance in healthy young men. Tests of visual scanning, running memory, logical reasoning, mathematical processing, the Stroop task, four-choice serial reaction time, time wall take, pursuit tracking, visual vigilance, Trails (B) task and long-term memory were evaluated at standardized intervals before, during and after sleep deprivation and drugs. Performance decrements with sleep deprivation occurred in visual scanning, running memory, logical reasoning, mathematical processing, the Stroop test, the time wall test, tracking and visual vigilance. Interestingly, with sleep deprivation some tests improved and others did not deteriorate. Improvements with medication following sleep deprivation were seen in running memory, logical reasoning, mathematical processing, tracking and visual vigilance. Although less effective than D-amphetamine, tyrosine improved performance on several tests. We conclude that all drugs tested improved at least some aspects of cognitive and motor performance after sleep deprivation. As a naturally occurring amino acid, and thus amenable to nutritional strategies, tyrosine may deserve further testing.

Adolescent↗

PubMed1980

Relationship between EEG sleep patterns and clinical improvement in depressed patients treated with sleep deprivation.

The effects of a single night of total sleep deprivation were observed in 16 primary depressed patients. Responders to treatment were rated as significantly more depressed and revealed a more "depressed" EEG sleep pattern prior to sleep deprivation than did nonresponders. Following sleep deprivation, patients who improved experienced a rebound in REM sleep during the second night of recovery sleep.

Adult↗

PubMedDate not supplied

Sleep deprivation affects thermal pain thresholds but not somatosensory thresholds in healthy volunteers.

OBJECTIVE: Sleep disturbances have been thought to augment pain. Sleep deprivation has been proven to produce hyperalgesic effects. It is still unclear whether these changes are truly specific to pain and not related to general changes in somatosensory functions. The aim of the present study was to evaluate the effect of total sleep deprivation on thermal pain thresholds (heat, cold) and pain complaints. Thermal detection thresholds (warmth, cold) were included as covariates to determine the contribution of somatosensory functions to changes in pain processing. METHODS: Twenty healthy volunteers were randomly assigned either to two nights of total sleep deprivation or to two nights of undisturbed night sleep. Sleep deprivation nights were separated by two days with normal night sleep. Heat and cold pain thresholds as well as warmth and cold detection thresholds were measured by use of a peltier thermode in the evening before and the morning after each deprivation or control night. Pain complaints were examined by use of a questionnaire in parallel. RESULTS: During treatment nights, sleep deprivation produced a significant overnight decrease in heat pain thresholds. Cold pain thresholds tended to decrease also during sleep deprivation, whereas the warmth and cold detection thresholds remained unaffected. Accordingly, no substantial contributions of the changes in thermal detection thresholds to the changes in thermal pain thresholds were determined by regression analyses. Pain complaints were not induced by sleep deprivation. CONCLUSIONS: The present findings suggest that sleep deprivation produces hyperalgesic changes that cannot be explained by nonspecific alterations in somatosensory functions.

Adult↗

PubMed2000

Sleep deprivation per se does not decrease the hypercapnic ventilatory response in humans.

Several studies have found that sleep deprivation reduces the hypercapnic ventilatory response (HCVR). Such results may have been affected by uncontrolled activities or environmental influences during the sleep deprivation period. The current study determined the "pure" effect of sleep deprivation on respiratory control under strictly controlled behavioral and environmental conditions. After 2 d of acclimation in the laboratory, 10 subjects maintained wakefulness (confirmed by EEG), a constant semirecumbent posture, ate regular small meals, had constant interaction with experimenters, and stayed in an environment with constant low light (10 lux) and constant room temperature for 41 consecutive hours. Measurements of HCVR, resting ventilation, V O(2) and V CO(2) were performed every 2 h. Comparisons were made of six pairs of measurements, with each pair separated by 24 h of sleep deprivation. None of the respiratory variables changed significantly with 24 h of sleep deprivation. Mean HCVR increased by 17% with sleep deprivation (3.12 versus 3.54 L x min(-1) x mm Hg(-1); not significant). These results show that sleep deprivation per se does not reduce the sensitivity of central chemoreceptors nor change resting ventilation or metabolism. The reduced HCVR after sleep loss found in previous studies may have been affected by uncontrolled activities or environmental influences during sleep deprivation periods.

Adult↗

PubMed1997

Inhibition of brain interleukin-1 attenuates sleep rebound after sleep deprivation in rabbits.

It is hypothesized that interleukin-1 (IL-1) is involved in physiological sleep. If this hypothesis is correct, inhibition of IL-1 should attenuate sleep responses after sleep deprivation. We tested the effect of intracerebroventricular or intravenous injection of an IL-1 inhibitor, an IL-1 receptor fragment (IL-1RF), on sleep rebound after sleep deprivation in rabbits. Six hours of total sleep deprivation significantly increased non-rapid eye movement sleep (NREMS) and enhanced electroencephalogram slow-wave activity during NREMS. Intracerebroventricular treatment with the IL-1RF (50 micrograms) significantly attenuated the sleep responses after sleep deprivation. Furthermore, 1.0 mg/kg i.v. injection of the IL-1RF significantly suppressed spontaneous NREMS in rabbits that were not sleep deprived. However, intravenous administration of the IL-1RF (1.0 mg/kg) failed to attenuate the sleep responses following the 6-h sleep deprivation period. These results support the hypothesis that central pools of IL-1 are important for physiological sleep regulation.

Animals↗