PubMed Health⌕ Search

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 415 records · Page 23Linked to original sources
PubMed1986

Sleep regulation in rats: effects of sleep deprivation, light, and circadian phase.

Sleep states and electroencephalographic (EEG) parameters were determined in unrestrained rats that had been implanted with electrodes under deep pentobarbital sodium anesthesia. Two base-line days with a light-dark cycle (LD) and 2 days under continuous darkness (DD) were followed by 24 h of sleep deprivation (SD) ending in the middle of the circadian activity period and by 2 recovery days in DD. In the base-line LD rest period, the amount of rapid-eye-movement sleep (REMS) and the EEG amplitude of non-REMS (NREMS) were lower than in the corresponding DD period. SD caused an immediate enhancement of REMS, NREMS, the slow-wave sleep (SWS) fraction of NREMS, and NREMS EEG amplitude. Although REMS, NREMS, and SWS showed a second peak at habitual light onset, they did not exceed base line. Subsequently, all parameters exhibited a marked negative rebound. We conclude that REMS and the EEG amplitude of NREMS are suppressed by light, amplitude and frequency parameters of NREMS are differently affected by light as well as by SD, and the short duration of the SD-induced increase of SWS may reflect a circadian influence on sleep homeostasis.

Animals↗
PubMed1999

Effects of method, duration, and sleep stage on rebounds from sleep deprivation in the rat.

Total sleep deprivation (TSD) of rats for 24 hours or less by continually enforced locomotion has consistently produced subsequent rebounds of slow-wave or high-amplitude EEG activity in NREM sleep, which has contributed to the widely held view that this EEG activity reflects particularly "intense" or restorative sleep. These rebounds usually have been accompanied by substantial rebounds of REM sleep. In contrast, chronic TSD (2 weeks or longer) by the disk-over-water (DOW) method has produced only huge, long-lasting rebounds of REM sleep with no rebound of high-amplitude NREM sleep. To evaluate whether the different rebounds result from different methods or from different lengths of deprivation, rats were subjected to 24-hour TSD by the DOW method. Rebounds included increases in high-amplitude and slow-wave activity; i.e., the methods produced similar rebound patterns following short-term TSD. (Chronic TSD by continually enforced locomotion would be strategically difficult and severely confounded with motor fatigue.) Rats subjected to DOW-TSD for 4 days, well before the development of severe TSD symptoms, showed primarily REM sleep rebounds. Rats subjected to 1 day of selective REM sleep deprivation, but not their closely yoked control rats, showed large, significant REM sleep rebounds, which evidently were not induced by the stress of the deprivation method per se. The combined findings prompted reexamination of published evidence relevant to "sleep intensity," including "negative rebounds," rebounds in other species, the effects of stress and fatigue, depth of sleep indicators, and extended sleep. The review points out pitfalls in the designation of any specific pattern as intense sleep.

Animals↗
PubMed1991

A review of studies concerning effects of sleep deprivation and fatigue on residents' performance.

Possible effects of sleep deprivation and fatigue on the performance and well-being of residents have received little scientific examination until recently. This article is a review of the studies on this topic published since 1970. All those studies that dealt with residents' moods and attitudes demonstrated deleterious effects of sleep deprivation and fatigue. The implications of this finding for patient care deserve exploration. Residents' acuity on performance tests requiring prolonged vigilance tended to deteriorate with acute sleep loss, while their performances on most brief psychomotor tests measuring manual dexterity, reaction times, and short-term recall were not adversely affected. The data presently available suggest that sleep-deprived or fatigued house officers can compensate for sleep loss in crises or other novel situations. However, sleep-deprived residents may be more prone to errors on routine, repetitive tasks and tasks that require sustained vigilance, which form a substantial portion of residents' workload. The authors concur with the recommendation of the Executive Council of the Association of American Medical Colleges that the total working hours for residents should not exceed 80 hours per week averaged over four weeks.

Affect↗
PubMed2001

Sleep deprivation elevates plasma corticosterone levels in neonatal rats.

Plasma corticosterone (CORT) levels were measured after short periods of sleep deprivation in rats at postnatal days 12, 16, 20, and 24. There was an age-dependent increase in basal CORT levels and sleep deprivation significantly elevated CORT at all ages compared to non-sleep deprived controls. The levels of CORT after sleep deprivation in P16, P20 and P24 animals were similar, resulting in an age-dependent decrease of the magnitude of the response. Sleep deprived P12 animals had lower levels of CORT. However, the observed response to sleep deprivation suggests that sleep loss is a significant stressor at this age. These observations suggest that younger animals are more sensitive to the effects of mild sleep deprivation than older ones.

Aging↗
PubMed1985

Antidepressant effects of sleep deprivation in bright and dim light.

In order to test whether exposure to bright artificial light at night is a necessary condition for the antidepressant response to sleep deprivation therapy, five patients were totally sleep-deprived on two separate nights, once in very bright light and once in nearly total darkness. During the day after the sleep-deprivation night patients were found to have responded equally well to sleep deprivation in both conditions. During the sleep-deprivation night, however, antidepressant responses may have been greater in the bright light condition. Thus, light at night is not necessary for the antidepressant response to sleep deprivation, but we cannot rule out the possibility that the effects of light exposure and sleep deprivation are additive or that exposure to light at some time after sleep deprivation begins (including during the following day) is necessary for the response.

Adult↗
PubMed1988

Central responses to cholinergic drugs of REM sleep deprived rats.

The present work studied the effects of REM sleep deprivation on the responses to cholinomimetic drugs in rats. Cataleptic behavior induced by pilocarpine, oxotremorine and eserine was not modified by previous REM sleep deprivation. On the other hand, the intensity of oxotremorine- and eserine-induced tremors, but not that of pilocarpine, was clearly augmented in the REMd rats and latency to the first tremor was shorter. REM sleep deprivation also potentiated the convulsions induced by nicotine. Two hypothetical mechanisms through which REM sleep deprivation could lead to the described hyperresponsiveness to cholinomimetic drugs are discussed.

Animals↗
PubMed2003

[Inhibition and working memory: effect of acute sleep deprivation on a random letter generation task].

The literature contains inconsistent data on the effects of acute sleep deprivation on the superior cognitive functions. The primary purpose of this study is to determine the effectiveness of inhibition, one of the functions of the working memory executive centre (EC), over an extended, 36-hour waking period. Inhibition is a cognitive mechanism whereby individuals ignore non-relevant information recorded in their working memory. We also tested the effects of a 36-hour period of acute sleep deprivation on simple reaction time. Twelve young, healthy volunteers (M = 21.5 years, sigma = 2.3) performed a random generation task involving letters and a simple reaction time psychomotor test over four sessions held at 10-hour intervals. Each participant was assigned a "constant routine." Participants were kept awake in a prone position within a room whose environment was held strictly constant (light, noise, temperature, meals, etc.). This control procedure provided assurance that any variation in participant performance was solely caused by sleep deprivation. The random generation task, nearly two minutes in length, consisted in verbally producing a sequence of 100 letters in a random fashion (i.e. by inhibiting, for example, alphabetical order) and by keeping to a set rhythm. Our assumption was that capacity for inhibition diminished as the number of hours of sleep deprivation increased. The simple reaction test, 10 minutes in length, involved pressing a button as swiftly as possible to cause a black square to disappear from a screen. In this case our assumption was that acute sleep deprivation alters simple reaction time. Analysis of variance (ANOVA) through repeated measures using the "sessions" factor as an intra-subject variable showed no significant changes in randomization indices of the random generation task, contrary to analysis of average simple reaction times. Participants' reaction times deteriorated over the first two minutes of the test during the night they were deprived of sleep. It would seem that the contradictory results of previous studies of the effects of acute sleep deprivation on the inhibition function would be due to errors in factor identification. In conclusion, the inhibition function, as measured during the performance of a brief task, seems to remain intact during an extended, 36-hour waking period. Simple reaction time assessed by means of a brief psychomotor test is affected during a night of sleep deprivation. The working-memory inhibition executive function shows greater resistance to acute sleep deprivation than does psychomotor reaction time for the performance of short tasks.

Adolescent↗
PubMed2006

Serotonin turnover in discrete regions of young rat brain after 24 h REM sleep deprivation.

The present study has attempted to elucidate the alteration of serotonin turnover after 24 h REM sleep deprivation in different regions in brain of young rat. Sleep deprivation was induced by the inverted flower pot technique. Results of this study show increased serotonin turnover after 24 h REM sleep deprivation in all the brain regions except in the hypothalamus. The decreased 5-HT ratio shows increased serotonin in the hypothalamus after 24 h sleep deprivation. This study indicates increased activity of serotonergic neurons in the hypothalamus after 24 h sleep deprivation. This also indicates that the hypothalamus plays a role in the immediate compensatory mechanism during 24 h REM sleep deprivation in young rats.

Animals↗
PubMed1996

Effect of sleep deprivation on driving safety in housestaff.

Sleep deprivation is known to affect driving safety. Housestaff (HS) are routinely sleep-deprived when on call. We hypothesized that this would affect their driving. We therefore administered questionnaires regarding driving to 70 pediatric HS, who were on call every fourth night, and to 85 faculty members (FAC), who were rarely disturbed at night. HS were questioned about events during their residency, and FAC were questioned about events during the preceding three years. There was an 87% response rate for each group. HS slept 2.7 +/- 0.9 (SD) hours when on call vs 7.2 +/- 0.8 hours when not on call (p < 0.001). 44% of HS had fallen asleep when stopped at a light, vs 12.5% FAC (p < 0.001). 23% of HS had fallen asleep while driving vs. 8% FAC (ns). A total of 49% of HS had fallen asleep at the wheel; 90% of these events occurred post-call. In contrast, only 13% of FAC had fallen asleep at the wheel (p < 0.001). HS had received a total of 25 traffic citations for moving violations vs. 15 for FAC and were involved in 20 motor vehicle accidents vs. 11 for FAC. One traffic citation clearly resulted from HS falling asleep at the wheel vs. none for FAC. We conclude that HS frequently fall asleep when driving post-call. We speculate that current HS work schedules may place some HS at risk for injury to themselves and others. Further study, using prospectively objective measures is indicated.

Accidents, Traffic↗
PubMed2006

Sleep deprivation in rats produces attentional impairments on a 5-choice serial reaction time task.

STUDY OBJECTIVES: To develop a rodent model of the attentional dysfunction caused by sleep loss. DESIGN: The attentional performance of rats was assessed after 4, 7, and 10 hours of total sleep deprivation on a 5-choice serial reaction time task, in which rats detect and respond to brief visual stimuli. SETTING: The rats were housed, sleep deprived, and behaviorally tested in a controlled laboratory setting. PARTICIPANTS: Ten male Long-Evans rats were used in the study. INTERVENTIONS: Rats were trained to criteria and subsequently tested in daily sessions of 100 trials at approximately 4:00 PM (lights on 8:00 AM-8:00 PM). Attentional performance was measured after 4, 7, 10 hours of total sleep deprivation induced by gentle handling. RESULTS: Sleep deprivation produced a monotonic increase in response latencies across the 4-hour, 7-hour, and 10-hour deprivations. Sleep deprivation also led to increased omission errors, but the overall number of perseverative and premature responses was unchanged. Subgroups of rats were differentially affected in the number of omission errors and perseverative responses. CONCLUSIONS: The effects of sleep deprivation on rats are compatible with a range of human findings on the effects of sleepiness on selective attention, psychomotor vigilance, and behavioral control. Rats also exhibited differential susceptibility to the effects of sleep deprivation, consistent with 'trait-like' susceptibility that has been found in humans. These findings indicate the feasibility of using the 5-choice serial reaction time task as an animal model for investigating the direct links between homeostatic sleep mechanisms and resulting attentional impairments within a single animal subject.

Animals↗
PubMed1980

Partial sleep deprivation as therapy for depression.

We investigated the influence of partial sleep deprivation on depressive symptoms in 30 patients with endogenous depression. The patients were awakened during the second half of the night and remained awake until the following evening. Antidepressant pharmacotherapy was not interrupted. Partial sleep deprivation significantly reduced the depression symptoms (mean value, 30.1%). The interindividual variations were considerable; deterioration was rare, and in 75% of the cases improvement occurred. Execution is simple, less stressful for the patient than total sleep deprivation, and can be carried out at home. Partial sleep deprivation has no contraindications except in the case of severe physical illness. The duration of the therapeutic effect is varied; repetition is possible. We discuss chronobiological hypothesis to explain the effect of sleep deprivation.

Aged↗
PubMed1990

Changes in pontine unit activity with REM sleep deprivation.

Short term rapid eye movement (REM) sleep deprivation produced a decrease in walking discharge rates of presumably noradrenergic pontine 'REM sleep-off' cells and an increase in waking discharge rates of pontine 'REM sleep-on' cells. These changes can be viewed as a correlate of increased REM sleep pressure. Slowing of REM sleep-off cells in waking is hypothesized to counteract the functional effects of REM sleep loss on noradrenergic receptor sensitivity. This slowing and the resulting reduction in norepinephrine release may contribute to the loss of vigilance seen with sleep deprivation.

Action Potentials↗
PubMed2000

Neural basis of alertness and cognitive performance impairments during sleepiness. I. Effects of 24 h of sleep deprivation on waking human regional brain activity.

The negative effects of sleep deprivation on alertness and cognitive performance suggest decreases in brain activity and function, primarily in the thalamus, a subcortical structure involved in alertness and attention, and in the prefrontal cortex, a region subserving alertness, attention, and higher-order cognitive processes. To test this hypothesis, 17 normal subjects were scanned for quantifiable brain activity changes during 85 h of sleep deprivation using positron emission tomography (PET) and (18)Fluorine-2-deoxyglucose ((18)FDG), a marker for regional cerebral metabolic rate for glucose (CMRglu) and neuronal synaptic activity. Subjects were scanned prior to and at 24-h intervals during the sleep deprivation period, for a total of four scans per subject. During each 30 min (18)FDG uptake, subjects performed a sleep deprivation-sensitive Serial Addition/Subtraction task. Polysomnographic monitoring confirmed that subjects were awake. Twenty-four hours of sleep deprivation, reported here, resulted in a significant decrease in global CMRglu, and significant decreases in absolute regional CMRglu in several cortical and subcortical structures. No areas of the brain evidenced a significant increase in absolute regional CMRglu. Significant decreases in relative regional CMRglu, reflecting regional brain reductions greater than the global decrease, occurred predominantly in the thalamus and prefrontal and posterior parietal cortices. Alertness and cognitive performance declined in association with these brain deactivations. This study provides evidence that short-term sleep deprivation produces global decreases in brain activity, with larger reductions in activity in the distributed cortico-thalamic network mediating attention and higher-order cognitive processes, and is complementary to studies demonstrating deactivation of these cortical regions during NREM and REM sleep.

Adult↗
PubMed1998

Effect of sleep deprivation on serum influenza-specific IgG.

Intra-pulmonary protection against influenza virus in immune mice, largely dependent upon serum lgG, is reported to be suppressed by 7 hours of sleep deprivation following viral challenge. This implies that sleep deprivation may accelerate the catabolism of influenza-specific antibodies. To determine the effects of sleep deprivation on the catabolism of serum antibodies, BALB/c mice were passively immunized intravenously with lgG anti-influenza monoclonalantibodies and catabolism kinetics monitored for 6 days. Mice were then sleep-deprived for either 9 hours (one episode) or for 9 hours followed by 6 hours on the consecutive day (two episodes) and the serum titer of influenza-specific monoclonal antibodies monitored for an additional 8 days via ELISA. One episode of sleep-deprivation had only minor effects on lgG catabolism; however, two episodes of sleep-deprivation caused significant changes in the kinetics of lgG catabolism, resulting in elevated lgG levels (p = 0.02) for 2 days post-sleep deprivation. Elevation of serum influenza-specific lgG (p = 0.005) was also seen in actively immune mice following two episodes of sleep-deprivation. Serum chemistries ruled out dehydration as a cause of the increased antibody levels; however, some anomalies were noted: total protein and albumin were elevated, although not significantly, and P and Ca were decreased. Thus, our data do not support the hypothesis that sleep-deprivation lowers existing serum antibody titers by accelerating antibody catabolism.

Animals↗
PubMed1988

The timing and duration of sleep in partial sleep deprivation therapy of depression.

The antidepressant response to partial sleep deprivation early in the night (PSD-E) was compared with the response to partial sleep deprivation late in the night (PSD-L) in 16 drug-free depressed inpatients using a balanced order crossover design. PSD-L had a significantly greater antidepressant effect that PSD-E. The response to PSD-L was sustained and enhanced by a second night of treatment. Patients had significantly shorter sleep durations and reduced REM sleep on PSD-L that did not occur in the PSD-E situation. There was a significant negative correlation between response to PSD and sleep duration, and in particular, REM sleep duration, in the late sleep deprivation situation. Thus, the amount and timing of sleep appear to be factors in the response to PSD, but additional studies are needed to evaluate the relative importance of these parameters.

Adult↗
PubMed2000

Sleep after immobilization stress and sleep deprivation: common features and theoretical integration.

The goal of the present paper is to elucidate and to resolve contradictions in the relationships among different forms of stress, sleep deprivation, and paradoxical sleep (PS) functions. Acute immobilization stress and the stress of learned helplessness are accompanied by an increase of PS, whereas the stress of defense behavior and the stress of self-stimulation cause PS reduction. Recovery sleep after total sleep deprivation performed on the rotating platform is marked by a dramatic rebound of PS although NREM (non-rapid eye movement) sleep deprivation is more prominent than PS deprivation. This PS rebound leads to a quick reversal of the pathology caused by prolonged sleep deprivation. The search activity (SA) concept presents an explanation for these contradictions. SA increases body resistance to stress and diseases, whereas renunciation of search (giving up, helplessness) decreases body resistance. PS and dreams contain covert SA, which compensates for the lack of the overt SA in the preceding period of wakefulness. The requirement for PS increases after giving up and decreases after active defense behavior and self-stimulation. Immobilization stress prevents SA in waking behavior and increases the need in PS. Sleep deprivation on the rotating platform, like immobilization stress, prevents SA, produces conditions for learned helplessness and, suppresses PS. Such a combination increases PS pressure and decreases body resistance.

Animals↗
PubMed1988

The effect of sleep deprivation on the rate of focal interictal epileptiform discharges.

Eight men with complex partial seizures who had frequent focal interictal epileptiform discharges (FIEDs) during routine EEGs were selected for all-night EEG recording before, and after 36 h of sleep deprivation. After sleep deprivation 6 of 8 patients showed increased FIEDs. The pooled mean number of FIEDs was greatest during light non-REM stages of sleep, especially stage II. Thus sleep deprivation is an effective activation method in medicated patients with complex partial seizures. However, a significant activation requires recording stage II sleep after sleep deprivation.

Adult↗