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PubMed2002

Selective REM sleep deprivation during daytime I. Time course of interventions and recovery sleep.

Although repeated selective rapid eye movement (REM) sleep deprivation by awakenings during nighttime has shown that the number of sleep interruptions required to prevent REM sleep increases within and across consecutive nights, the underlying regulatory processes remained unspecified. To assess the role of circadian and homeostatic factors in REM sleep regulation, REM sleep was selectively deprived in healthy young adult males during a daytime sleep episode (7-15 h) after a night without sleep. Circadian REM sleep propensity is known to be high in the early morning. The number of interventions required to prevent REM sleep increased from the first to the third 2-h interval by a factor of two and then leveled off. Only a minor REM sleep rebound (11.6%) occurred in the following undisturbed recovery night. It is concluded that the limited rise of interventions during selective daytime REM sleep deprivation may be due to the declining circadian REM sleep propensity, which may partly offset the homeostatic drive and the sleep-dependent disinhibition of REM sleep.

Adult↗

PubMed1993

Effects of catecholamine depletion on alertness and mood in rested and sleep deprived normal volunteers.

Alpha-methyl-para-tyrosine (AMPT), a tyrosine hydroxylase inhibitor, was used to evaluate the physiologic role of central nervous system catecholamines in modulating alertness and mood. Forty healthy males were randomized to one of four conditions: AMPT in a rested condition; AMPT plus 40.5 hours of total sleep deprivation; placebo plus sleep deprivation; or placebo in a rested condition. Repeated measures of alertness and mood revealed that treatment with AMPT or sleep deprivation increased sleepiness, and combined treatment produced greater sleepiness than either treatment alone. In contrast, although combined treatment with AMPT and sleep deprivation led to large increases in negative mood, neither treatment alone produced consistent mood changes. These findings are consistent with the view that sleep deprivation is associated with decreased functional catecholamine neurotransmission. Furthermore, mood effects following sleep deprivation plus AMPT suggest that catecholamines may be involved in mood changes during sleep deprivation.

Adult↗

PubMed1986

Activation of EEG recordings by graded sleep deprivation.

Part I. The EEG recordings of 434 patients were activated by graded sleep deprivation. In clinically manifest epilepsies with a predominantly negative EEG tracing at rest the incidence of epileptic manifestations increased after sleep deprivation from 18.03% to 59.01%, in clinically suspect epilepsies from 6.4% to 39.0%. In other paroxysmal affections such as febrile convulsions, syncopes and collapses, paroxysms of abdominal pain or headaches, affective paroxysms and nocturnal terrors, the tracing activation by sleep deprivation mostly facilitated differential diagnosis between those affections and epilepsy. In organic cerebral affections with or without epileptic seizures activation by sleep deprivation led to an increase in the occurrence of epileptic manifestations from 11.4% to 50.0% of the recordings. The authors conclude that graded sleep deprivation is a very useful activation method for the diagnosis of epilepsy. Part II. The authors studied the occurrence of generalized 2-5 Hz high-amplitude slow wave episodes in 244 patients before and after sleep deprivation. They found such episodes in the resting recordings of 37 patients and in the post-deprivation recordings of 85 patients. The described episodes were mostly observed during sleepiness and superficial sleep. They were significantly more frequent in children and adolescents than in adults. The occurrence of slow wave episodes was ascertained in epileptic as well as non-epileptic affections such as affective attacks in children, night terrors, paroxysms of abdominal pain or headaches, febrile convulsions and organic brain affections without epileptic seizures. The authors conclude that the above episodes are a non-specific manifestation of increased susceptibility to paroxysmal synchronization of EEG rhythms. Their occurrence in young children can, however, be considered normal.

Adolescent↗

PubMed1995

Dose-dependent caffeine pharmacokinetics during severe sleep deprivation in humans.

Following 49 h of sleep deprivation, 37 healthy males ingested either 2.1, 4.3, or 8.6 mg*kg-1 body weight of caffeine in a randomized double-blind design. Subjects were sleep deprived for additional 12 h and venous blood samples were collected intermittently. Caffeine and primary metabolite concentrations were determined by HPLC. Pharmacokinetics were computed using the Lagran computer program. The ratio of the primary human metabolite, paraxanthine, to caffeine was used to estimate the rate of metabolism. There was a significant (p < 0.05) and disproportional increase in the dose normalized caffeine AUC and a significant decrease in its clearance associated with increasing dose. In addition, the paraxanthine to caffeine ratio significantly decreased with an increase in dose, indicating that the rate of caffeine metabolism decreased. These results demonstrate that under the conditions of severe sleep deprivation caffeine exhibits dose-dependent pharmacokinetics. In addition, these results are consistent with a model of capacity-limited metabolism.

Adolescent↗

PubMed2002

Sleep deprivation does not affect indices of necrosis or apoptosis in rat brain.

Recent indications of oxidative stress in hypothalamus of sleep deprived rats prompted us to address the possibility that sleep deprivation may induce pathological cell loss changes in brain. Indices of necrosis and apoptosis were quantified after 96 h of sleep deprivation induced by the classical platform technique in rats. Binding of the "peripheral-type" benzodiazepine ligand [3H]PK 11195 to reactive astrocytes, a reliable and sensitive index of necrotic changes, was not altered in any of 14 brain regions examined. Likewise, no changes were found in mRNA levels of the apoptosis-related genes bcl-2 and bax in any of 24 brain regions examined. This was corroborated by quantitative TUNEL analyses in hypothalamus, amygdala, and cortex, which also revealed no effects in sleep deprived animals. These results are consistent with other recent evidence that sleep deprivation does not induce necrotic or apoptotic cell loss in brain. This suggests that recent findings of oxidative stress in sleep deprived brains do not result in cell loss. The possibility that sleep deprivation may result in functional deficits, or that structural changes may emerge after repeated episodes of sleep deprivation, remains to be addressed.

Animals↗

PubMed2005

Recovery after prolonged sleep deprivation: residual effects of slow-release caffeine on recovery sleep, sleepiness and cognitive functions.

A long work schedule often results in sleep deprivation, sleepiness, impaired performance and fatigue. We investigated the residual effects of slow-release caffeine (SRC) on sleep, sleepiness and cognitive performance during a 42-hour recovery period following a 64-hour continuous wakefulness period in 16 healthy males, according to a double-blind, randomised, placebo-controlled, crossover study. Three hundred milligrams of SRC or placebo was given twice a day at 21:00 and 9:00 during the first 48 h of wakefulness. Recovery sleep was analysed with electroencephalography (EEG) and wrist actigraphy, daytime sleepiness with continuous EEG, sleep latency tests and actigraphy and cognitive functions with computerized tests from the NATO AGARD STRES battery. Both drug groups exhibited almost the same sleep architecture with a rebound of slow-wave sleep during both recovery nights and of REM sleep during the second night. Wakefulness level and cognitive functions were similarly impaired in both groups on the first day of recovery and partially returned to baseline on the second. To conclude, SRC appears to have no unwanted side-effects on recovery sleep, wakefulness and cognitive performance after a long period of sleep deprivation and might therefore be a useful choice over other psychostimulants for a long work schedule.

Adult↗

PubMed2006

Suppression of hippocampal plasticity-related gene expression by sleep deprivation in rats.

Previous work shows that sleep deprivation impairs hippocampal-dependent learning and long-term potentiation (LTP). Brain-derived neurotrophic factor (BDNF), cAMP response-element-binding (CREB) and calcium-calmodulin-dependent protein kinase II (CAMKII) are critical modulators of hippocampal-dependent learning and LTP. In the present study we compared the effects of short- (8 h) and intermediate-term (48 h) sleep deprivation (SD) on the expression of BDNF and its downstream targets, Synapsin I, CREB and CAMKII in the neocortex and the hippocampus. Rats were sleep deprived using an intermittent treadmill system which equated total movement in the SD and control treadmill animals (CT), but permitted sustained periods of rest in CT animals. Animals were divided into SD (treadmill schedule: 3 s on/12 s off) and two treadmill control groups, CT1 (15 min on/60 min off) and CT2 (30 min on/120 min off - permitting more sustained sleep). Real-time Taqman RT-PCR was used to measure changes in mRNA; BDNF protein levels were determined using ELISA. In the hippocampus, 8 h treatments reduced BDNF, Synapsin I, CREB and CAMKII gene expression in both SD and control groups. Following 48 h of experimental procedures, the expression of all these four molecular markers of plasticity was reduced in SD and CT1 groups compared to the CT2 and cage control groups. In the hippocampus, BDNF protein levels after 8 h and 48 h treatments paralleled the changes in mRNA. In neocortex, neither 8 h nor 48 h SD or control treatments had significant effects on BDNF, Synapsin I and CAMKII mRNA levels. Stepwise regression analysis suggested that loss of REM sleep underlies the effects of SD on hippocampal BDNF, Synapsin I and CREB mRNA levels, whereas loss of NREM sleep underlies the effects on CAMKII mRNA.

Animals↗

PubMed2001

Soluble TNF-alpha receptor 1 and IL-6 plasma levels in humans subjected to the sleep deprivation model of spaceflight.

BACKGROUND: The extent to which sleep loss may predispose astronauts to a state of altered immunity during extended space travel prompts evaluation with ground-based models. OBJECTIVE: We sought to measure plasma levels of selected cytokines and their receptors, including the putative sleep-regulation proteins soluble TNF-alpha receptor (sTNF-alpha R) I and IL-6, in human subjects undergoing 2 types of sleep deprivation during environmental confinement with performance demands. METHODS: Healthy adult men (n = 42) were randomized to schedules that varied in severity of sleep loss: 4 days (88 hours) of partial sleep deprivation (PSD) involving two 2-hour naps per day or 4 days of total sleep deprivation (TSD). Plasma samples were obtained every 6 hours across 5 days and analyzed by using enzyme-linked immunoassays for sTNF-alpha RI, sTNF-alpha RII, IL-6, soluble IL-2 receptor, IL-10, and TNF-alpha. RESULTS: Interactions between the effects of time and sleep deprivation level were detected for sTNF-alpha RI and IL-6 but not for sTNF-alpha RII, soluble IL-2 receptor, IL-10, and TNF-alpha. Relative to the PSD condition, subjects in the TSD condition had elevated plasma levels of sTNF-alpha RI on day 2 (P =.04), day 3 (P =.01), and across days 2 to 4 of sleep loss (P =.01) and elevated levels of IL-6 on day 4 (P =.04). CONCLUSIONS: Total sleep loss produced significant increases in plasma levels of sTNF-alpha RI and IL-6, messengers that connect the nervous, endocrine, and immune systems. These changes appeared to reflect elevations of the homeostatic drive for sleep because they occurred in TSD but not PSD, suggesting that naps may serve as the basis for a countermeasures approach to prolonged spaceflight.

Adult↗

PubMed2003

Enzymes of adenosine metabolism in the brain: diurnal rhythm and the effect of sleep deprivation.

Adenosine plays a role in promoting sleep, an effect that is thought to be mediated in the basal forebrain. Adenosine levels vary in this region with prolonged wakefulness in a unique way. The basis for this is unknown. We examined, in rats, the activity of the major metabolic enzymes for adenosine - adenosine deaminase, adenosine kinase, ecto- and cytosolic 5'-nucleotidase - in sleep/wake regulatory regions as well as cerebral cortex, and how the activity varies across the day and with sleep deprivation. There were robust spatial differences for the activity of adenosine deaminase, adenosine kinase, and cytosolic and ecto-5'-nucleotidase. However, the basal forebrain was not different from other sleep/wake regulatory regions apart from the tuberomammillary nucleus. All adenosine metabolic enzymes exhibited diurnal variations in their activity, albeit not in all brain regions. Activity of adenosine deaminase increased during the active period in the ventrolateral pre-optic area but decreased significantly in the basal forebrain. Enzymatic activity of adenosine kinase and cytosolic-5'-nucleotidase was higher during the active period in all brain regions tested. However, the activity of ecto-5'-nucleotidase was augmented during the active period only in the cerebral cortex. This diurnal variation may play a role in the regulation of adenosine in relationship to sleep and wakefulness across the day. In contrast, we found no changes specifically with sleep deprivation in the activity of any enzyme in any brain region. Thus, changes in adenosine with sleep deprivation are not a consequence of alterations in adenosine enzyme activity.

5'-Nucleotidase↗

PubMed1993

Potentiation of metaphit-induced audiogenic seizures by REM sleep deprivation in rats.

The possibility that REM sleep deprivation (REMD) induced increased susceptibility of rats to the convulsive effects of metaphit was investigated. Metaphit-induced audiogenic seizures were studied in three groups of animals: 1) caged controls; 2) large platform animals; and 3) small platform, REMD animals. After 48 h of confinement to their environments the rats from all three groups were injected with metaphit (10 mg kg-1, IP) and the procedures continued for the next 24 h. Immediately after removal from platforms and at 3-h intervals thereafter all rats were individually subjected to intense sound stimulation. Convulsive responses were recorded and analyzed with respect to incidence, intensity, and duration. The REMD rats were found to be more sensitive to the convulsive effects of metaphit compared to nondeprived rats. This was manifested in significantly shorter latencies to seizures, and significantly higher incidence, severity, and duration of seizures, especially of the most severe seizure component-tonic extensor convulsion. Inducing rats to convulse while they were being REM sleep deprived eliminated the REM sleep rebound observed in REMD rats that did not convulse. The occurrence of spontaneous EEG seizures during the undisturbed recovery period reduced REM sleep rebound. The results demonstrate a reciprocal relation between seizure behavior and REM sleep.

Acoustic Stimulation↗

PubMed1999

Naps and modafinil as countermeasures for the effects of sleep deprivation on cognitive performance.

Disruptions in wake-sleep rhythms, particularly induced by sleep deprivation are limiting factors for military personnel in operations. The role of sleep and naps in the recovery of performance is generally accepted. Pharmacological aids, for example hypnotic or stimulant substances can also be effective countermeasures. Recently, a new stimulant compound, modafinil (MODIODAL) has also proven effective. Considering the excellent results obtained with napping and modafinil, we have studied the combined effect of these two countermeasures on psychomotor performance under conditions simulating an operational situation. Beneficial effects of a few hours' nap on performance were confirmed. Consequently naps should be encouraged, even if limited and diurnal. Modafinil, which combines wakening and stimulating properties without any known side effects, was useful for longer periods of sleep deprivation and when there was no real possibility of sleep recovery. Modafinil did not prevent sleep if sleep opportunities were available. The combination of naps and modafinil demonstrated the best cognitive performance during sleep deprivation.

Adult↗

PubMed1975

An attempt to influence by drugs recovery sleep after sleep deprivation.

Rats were deprived of sleep by placing them for 36 hours in a slowly moving drum. After this procedure, during recovery sleep, the latency of onset of the first rhombencephalic - paradoxical sleep period decreased and the proportion of telencephalic/rhombencephalic - slow wave sleep reversed (during the first hour of recovery sleep). Repeated administration during the deprivation period of physostigmine (0,5 mg/kg i. p. in 30 min intervals 20-30 times) inducing in waking animals in EEG pattern close to that of rhombencephalic sleep, or atropine (1 mg/kg i. p. in 60 min intervals 10-15 times) evoking an activity resembling telencephalic sleep, did not change the above measures of recovery sleep. Pharmacologically induced sleep-like patterns did not substitute for the sleep the rats were deprived off.

Animals↗

PubMed1983

Resident performance and sleep deprivation: a review.

The literature on resident performance and sleep deprivation is reviewed. It is suggested that despite the urgent need for definitive work in the area, current research is sparse and inconclusive. It also is suggested that the research that does exist implies there are potentially severe negative effects from sleep deprivation on physicians-in-training. The present authors believe that justifications for sleep-depriving night call schedules remain untested and that the presence of sleep-depriving night call as part of residency training should be reevaluated.

Clinical Competence↗

PubMed2003

Cognitive deterioration and changes of P300 during total sleep deprivation.

The study was conducted to evaluate the cognitive deteriorations induced by sleep deprivation with the computerized neurocognitive tests and the P300 event-related potential. Thirty healthy college students (22 men, eight women) participated in the present study. Subjects remained awake for 38 h under continuous surveillance. In the morning and the evening of the two study days, the computerized neurocognitive tests and the P300 were performed. In vigilance test and reaction unit test, there were significant cognitive impairments during sleep deprivation. However, in the cognitrone test there was significant functional improvement, which might be due to the practice effect. The P300 latency was significantly prolonged and the amplitudes decreased during sleep deprivation. The cognitive impairment during 38 h of sleep deprivation was mainly in terms of vigilance and reaction time. In contrast, higher complex cognitive function such as fine perceptual analyses, visual discrimination and working memory might be not affected by 38 h of total sleep deprivation. The changes of P300 were significantly correlated with the results of vigilance and reaction unit tests but not with the cognitrone test. Taken together, these results suggest that the P300 changes that occur during sleep deprivation are a reflection of the decrement in vigilance, which prolongs reaction time.

Adult↗

PubMed1978

A review of the biological effects of total sleep deprivation in man.

This biologically oriented review attempts to complement earlier and more psychological performance based reviews of total sleep deprivation. Also, the effects of total sleep deprivation are interpreted, here, from a function of human sleep perspective, rather than from the more usual stress viewpoint. It would appear that total sleep deprivation does not produce any major changes in biochemical and physiological measures of somatic functioning. Such a conclusion would not seem to support an hypothesis that human sleep is for body restitution. Although there are equivocal results amongst several of the more psychophysiological measures, EEG does show a pronounced change. This latter finding, together with many reports of psychological performance detriment, would appear to sustain a CNS or cerebral restitutional role for human sleep. However, before definitive conclusions can be drawn from the biochemical and physiological findings of total sleep deprivation, the following qualifications of experimental methodology are made: (1) Apart from sleep loss, many studies have provided unnatural regimes which may have ameliorated possible effects of total sleep deprivation. (2) Most studies are of relatively short duration and may not have been sufficiently long for effects to develop. (3) Measures are often limited in range and depth of analysis. (4) Subjects are mostly fit, young adult, intelligent males and there is little constitutional variability. (5) Reported changes of statistical significance may be of no physiological significance and changes of possible physiological significance may be obscured by statistical procedures. (6) Intervening behavioural variables, such as novelty and anticipation of the sleep deprivation situation, may confound real effects.

17-Hydroxycorticosteroids↗

PubMed1995

Sleep deprivation and spike-wave discharges in epileptic rats.

The effects of sleep deprivation were studied on the occurrence of spike-wave discharges in the electroencephalogram of rats of the epileptic WAG/Rij strain, a model for absence epilepsy. This was done before, during and after a period of 12 hours of near total sleep deprivation. A substantial increase in the number of spike-wave discharges was found during the first 4 hours of the deprivation period, whereas in the following deprivation hours epileptic activity returned to baseline values. Immediately after termination of deprivation, a decrease in the number of spike-wave discharges parallelled a rebound of rapid eye movement (REM) sleep and deep non-REM sleep. An initial increase in epileptic activity has also been reported during sleep deprivation of humans. This initial increase as well as the epileptogenic effects during the course of the sleep deprivation and during the recovery period after sleep deprivation can be interpreted in terms of changes in sleep-wake states. Although the epilepsy-provoking mechanisms are not yet understood, an explanation is suggested based on changes of transitions between sleep-wake states and shifts in level of synchronization.

Animals↗

PubMed2006

Evolution of sleep quantity, sleep deprivation, mood disturbances, empathy, and burnout among interns.

PURPOSE: To explore the relationships between sleep deprivation and the evolution of mood disturbances, empathy, and burnout among a cohort of interns. METHOD: In 2002-03, 47 interns in the internal medicine resident program at the University of Pennsylvania School of Medicine completed the following instruments at baseline and at year end: sleep quantities, Epworth Sleepiness Scale, the Beck Depression Inventory-Short Form, the Interpersonal Reactivity Index, and the Maslach Burnout Inventory-Human Services Survey. The prevalences of acute and chronic sleep deprivation, subjective sleepiness, burnout, empathy, and depression at the beginning of the year were compared to prevalences at the end of internship. Associations between sleep deprivation and mood, empathy, or burnout were explored. RESULTS: The prevalence of chronic sleep deprivation, depression, burnout, and empathy increased from baseline to year end. Specifically, the prevalence of "high" scores changed for chronic sleep deprivation (9% to 43%, p = .0001). The prevalence of moderate depression increased from 4.3% to 29.8% (p = .0002). Only 4.3% reported a high level of burnout initially compared with 55.3% at year end (p < .0001). Scores that were originally more favorable than general population norms (p < .001) approached norms at the end of the year for empathic concern (p = .15). There was an association between becoming chronically sleep deprived and becoming depressed (OR = 7, p = .014). CONCLUSIONS: Given the association between chronic sleep deprivation and mood disturbances during internship, outcome assessment is warranted to see if duty-hour reform will translate into more hours slept or fewer hours worked, coincident with improved mood.

Analysis of Variance↗

PubMed1991

Sleep continuity and the REM-nonREM cycle in the rat under baseline conditions and after sleep deprivation.

Wakefulness, nonrapid eye movement sleep (nonREMS) and REMS of rats were scored in 4-s epochs during the first 8 h of the 12-h light period of a baseline (BL) day and during recovery (REC) from 24-h sleep deprivation (SD). Vigilance state continuity was investigated by analyzing the distribution of state episodes. After SD, state continuity was enhanced. The reduced occurrence of short wake episodes resulted in a consolidation of sleep states. The distribution of the REM-nonREM cycle length showed a mode at 10-13 min for both BL and REC. The variability of the cycle length was reduced after SD. The mean cycle length was markedly influenced by the criteria of minimum REMS episode duration and maximal allowed REMS episode interruption.

Animals↗