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PubMed1984

Clinical and biological correlates of sleep deprivation in depression.

Sleep deprivation is reported to have therapeutic effectiveness in depressive illness. Furthermore, the response to sleep deprivation has important research implications. Recent conceptual advances, resulting in increased understanding of the role of abnormal biological rhythms and neurotransmitter function of the pathophysiology of affective disorder, highlight the future role of sleep deprivation in the research and treatment of these disorders.

Bipolar Disorder↗
PubMed2000

Altered brain response to verbal learning following sleep deprivation.

The effects of sleep deprivation on the neural substrates of cognition are poorly understood. Here we used functional magnetic resonance imaging to measure the effects of 35 hours of sleep deprivation on cerebral activation during verbal learning in normal young volunteers. On the basis of a previous hypothesis, we predicted that the prefrontal cortex (PFC) would be less responsive to cognitive demands following sleep deprivation. Contrary to our expectations, however, the PFC was more responsive after one night of sleep deprivation than after normal sleep. Increased subjective sleepiness in sleep-deprived subjects correlated significantly with activation of the PFC. The temporal lobe was activated after normal sleep but not after sleep deprivation; in contrast, the parietal lobes were not activated after normal sleep but were activated after sleep deprivation. Although sleep deprivation significantly impaired free recall compared with the rested state, better free recall in sleep-deprived subjects was associated with greater parietal lobe activation. These findings show that there are dynamic, compensatory changes in cerebral activation during verbal learning after sleep deprivation and implicate the PFC and parietal lobes in this compensation.

Adult↗
PubMed1998

Sleep deprivation induces brain region-specific decreases in glutathione levels.

Rats were deprived of sleep for 96 h by the platform technique and total glutathione (GSHtau) levels were measured in seven different brain areas. Glutathione levels were found to be significantly reduced in the hypothalamus of sleep-deprived animals when compared with large platform (-18%) or home cage (-31%) controls. Deprived rats also had reduced GSHtau levels in thalamus compared with home cage controls only. Glutathione levels did not differ among the three groups in any of the other brain areas examined. These results indicate that specific brain areas may be differentially susceptible to oxidative stress after sleep deprivation. The apparent vulnerability of the hypothalamus to these effects may contribute to some of the functional effects of sleep deprivation.

Animals↗
PubMed2003

Simulation study of rested versus sleep-deprived anesthesiologists.

BACKGROUND: Sleep deprivation causes physiologic and subjective sleepiness. Studies of fatigue effects on anesthesiologist performance have given equivocal results. The authors used a realistic simulation environment to study the effects of sleep deprivation on psychomotor and clinical performance, subjective and objective sleepiness, and mood. METHODS: Twelve anesthesia residents performed a 4-h anesthetic on a simulated patient the morning after two conditions of prior sleep: sleep-extended (EXT), in which subjects were allowed to arrive at work at 10:00 AM for 4 consecutive days, thus allowing an increase in nocturnal sleep time, and total sleep deprivation (DEP), in which subjects were awake at least 25 h. Psychomotor testing was performed at specified periods throughout the night in the DEP condition and at matched times during the simulation session in both conditions. Three types of vigilance probes were presented to subjects at random intervals as well as two clinical events. Task analysis and scoring of alertness were performed retrospectively from videotape. RESULTS: In the EXT condition, subjects increased their sleep by more than 2 h from baseline (P = 0.0001). Psychomotor tests revealed progressive impairment of alertness, mood, and performance in the DEP condition over the course of the night and when compared with EXT during the experimental day. DEP subjects showed longer response latency to vigilance probes, although this was statistically significant for only one probe type. Task analysis showed no difference between conditions except that subjects "slept" more in the DEP condition. There was no significant difference in the cases' clinical management between sleep conditions. Subjects in the DEP condition had lower alertness scores (P = 0.02), and subjects in the EXT condition showed little video evidence of sleepiness. CONCLUSIONS: Psychomotor performance and mood were impaired while subjective sleepiness and sleepy behaviors increased during simulated patient care in the DEP condition. Clinical performance between conditions was similar.

Adult↗
PubMed1992

Biperiden administration during REM sleep deprivation diminished the frequency of REM sleep attempts.

Sixteen subjects were assigned to a group using either placebo or biperiden, with eight subjects in each group. Both groups were studied for one acclimatization night, one baseline night, four nights of rapid eye movement (REM) sleep deprivation and two recovery nights. All the subjects received either placebo or 4 mg biperiden 1 hour before sleep during the four nights of REM sleep deprivation. During the baseline and the recovery nights both groups received placebo capsules. The results showed that REM sleep time during the REM sleep deprivation was reduced by 70-75% below the baseline night in both groups. The number of attempts to enter REM sleep was significantly reduced by biperiden as compared to placebo for each of the four REM sleep deprivation nights. Because the total sleep time in the biperiden group was reduced, the number of REM sleep attempts was corrected by the total sleep time. The adjusted number of REM sleep attempts was also significantly reduced in the biperiden group. REM sleep latency showed a reduction in the placebo group, whereas in the biperiden group REM sleep latency was unchanged throughout the deprivation nights. In the recovery night REM sleep time was increased in both groups, with no differences between the groups. The REM sleep latency showed a reduction in the first recovery night in both groups that persisted through the second recovery night. The above findings support the role of biperiden as a REM sleep suppressive drug.

Adult↗
PubMed1996

Total sleep deprivation and the thyroid axis: effects of sleep and waking activity.

BACKGROUND: Circadian and sleep components modulate anterior pituitary release of thyrotropin (TSH), the chemical substance regulating the thyroid hormones, thyroxine (T4), and triiodothyronine (T3). The present study examined TSH, T4, and T3 concentrations across the wake-sleep boundary time (2300-0130 hours) before, during, and after a 64-h sleep deprivation paradigm. Additionally, adrenocorticotropic hormone (ACTH) and cortisol were measured as an index of hypothalamic-pituitary-adrenal axis activation. Activity levels and ratings of effort required to perform cognitive tasks were also incorporated to evaluate physical and cognitive load, respectively, across the study period. Assessing the combined effects of activity and sleep deprivation on thyroid hormone economy is relevant to the relationship of high physical and/or cognitive performance demands during sleep deprivation inherent in extended military operations and space exploration. METHODS: There were 12 healthy subjects who were monitored during a 2-d baseline period, 3 d of total sleep deprivation, and 2 nights of recovery sleep. Serum samples were collected at 2300 hours and 0130 hours across the entire study period, and measured for TSH, T4, T3, and glucocorticoids. RESULTS: Change scores evaluated at the wake-sleep boundary time demonstrated significant inhibitory effects of sleep on thyroid hormone measures. As expected, sleep deprivation was associated with elevated TSH. However, sleep deprivation also significantly increased circulating levels of T3 at 2300 hours and T4 concentration change scores (2300-0130 hours). Glucocorticoid levels did not track thyroid hormone changes. Physical activity remained constant while subjective ratings of effort to perform cognitive tasks increased significantly during sleep deprivation. CONCLUSION: Compared to sleep deprivation studies under constant conditions reporting no change in peripheral T4 and T3 levels, the present study suggests activity level, including cognitive effort to perform, during total sleep deprivation may produce substantive changes in the thyroid axis.

Adult↗
PubMed1992

Sleep deprivation in narcoleptic subjects: effect on sleep stages and EEG power density.

Sleep of 8 narcoleptic and 8 control subjects was recorded under baseline (i.e., prior wakefulness 16 h) and after 24 h without sleep. During both baseline and recovery total sleep time and stage 2 non-REM sleep were significantly decreased in narcoleptic subjects. Slow wave activity (i.e., EEG power density in the range of 0.75-4.5 Hz) decayed exponentially during baseline and after sleep deprivation in both narcoleptic and control subjects. During both baseline and recovery EEG power density in delta and sigma frequencies in non-REM sleep was enhanced in narcoleptic subjects relative to controls. In REM sleep differences in the same direction were present in delta and beta frequencies. After sleep deprivation EEG power density in non-REM sleep was elevated in delta and some higher frequencies in both patients and controls, but the response to sleep deprivation was stronger in narcoleptic subjects. These data show that in narcoleptic subjects regulatory processes underlying non-REM sleep homeostasis are operative and indicate that the response to sleep deprivation is stronger than in control subjects.

Adolescent↗
PubMed2006

Changes in brain gene expression after long-term sleep deprivation.

Long-term sleep deprivation in rats produces dramatic physiological changes including increase in energy expenditure, decrease in body weight, and death after 2-3 weeks. Despite several studies, the sleep deprivation syndrome remains largely unexplained. Here, to elucidate how prolonged sleep loss affects brain cells we used microarrays and screened the expression of > 26 000 transcripts in the cerebral cortex. Rats were sleep deprived using the disk-over-water method for 1 week. Seventy-five transcripts showed increased expression in these animals relative to controls that had been spontaneously awake or sleep deprived for a few hours. Most of them were induced as a result of chronic sleep loss and not non-specific effects of the disk stimulation. They include transcripts coding for several immunoglobulins, stress response proteins (macrophage inhibitor factor-related protein 14, heat-shock protein 27, alpha-B-crystallin), minoxidil sulfotransferase, globins and cortistatin. Twenty-eight transcripts decreased their expression in long-term sleep-deprived rats. Sixteen of them were specifically decreased as a result of chronic sleep loss, including those coding for type I procollagen and dihydrolipoamide acetyltransferase. We also compared sleeping rats to short-term and long-term sleep-deprived rats, and found that acute and chronic sleep loss led to some differences at the molecular level. Several plasticity-related genes were strongly induced after acute sleep deprivation only, and several glial genes were down-regulated in both sleep deprivation conditions, but to a different extent. These findings suggest that sustained sleep loss may trigger a generalized inflammatory and stress response in the brain.

Animals↗
PubMed2006

Effects of two nights sleep deprivation and two nights recovery sleep on response inhibition.

This study examined the effects of two nights of total sleep deprivation (TSD) and two nights of recovery sleep on response inhibition. Thirty-eight young, healthy adults performed a Go-NoGo task at 14 : 00 after: (1) a normal night of sleep; (2) each of two consecutive nights of TSD; and (3) each of two consecutive nights of recovery sleep; they also performed the task at 05 : 00 during the first night of sleep deprivation. We hypothesized that TSD would lead to an impaired ability to withhold a response that would be reversed with recovery sleep. Subjects did experience a significant increase in false positive responses throughout all of TSD, errors of omission (i.e. missed 'go' targets) were not significant until after the second night of TSD. Both components (withholding a response and automatic responding) of the task returned to baseline levels after one night of recovery sleep. These data suggest that individuals experience difficulty in withholding an inappropriate response during TSD, even when they are able to attend to the incoming stimuli and respond accurately to appropriate stimuli.

Adult↗
PubMed2002

Stress response genes protect against lethal effects of sleep deprivation in Drosophila.

Sleep is controlled by two processes: a homeostatic drive that increases during waking and dissipates during sleep, and a circadian pacemaker that controls its timing. Although these two systems can operate independently, recent studies indicate a more intimate relationship. To study the interaction between homeostatic and circadian processes in Drosophila, we examined homeostasis in the canonical loss-of-function clock mutants period (per(01)), timeless (tim(01)), clock (Clk(jrk)) and cycle (cyc(01)). cyc(01) mutants showed a disproportionately large sleep rebound and died after 10 hours of sleep deprivation, although they were more resistant than other clock mutants to various stressors. Unlike other clock mutants, cyc(01) flies showed a reduced expression of heat-shock genes after sleep loss. However, activating heat-shock genes before sleep deprivation rescued cyc(01) flies from its lethal effects. Consistent with the protective effect of heat-shock genes, was the observation that flies carrying a mutation for the heat-shock protein Hsp83 (Hsp83(08445)) showed exaggerated homeostatic response and died after sleep deprivation. These data represent the first step in identifying the molecular mechanisms that constitute the sleep homeostat.

ARNTL Transcription Factors↗
PubMed1971

Anemia in sleep-deprived rats receiving anticoagulants.

Independent groups of rats were deprived of sleep and treated with the anticoagulant drugs phenylindanedione or dicoumarol for 1 to 8 days. These animals developed an extremely severe anemia which was accelerated by p-chlorophenylalanine. The red cell count and amount of hemoglobin decreased to half of normal values. No decrease occurred in animals subjected to any one single treatment. Histological examination indicated hemolysis, hypoplasia of hemopoietic organs, slight hemorrhage, but no evidence of stress. The severity of the anemia was inversely related to the amount of sleep permitted during sleep deprivation. This new syndrome demonstrates marked effects of sleep deprivation on both maturation and destruction of red blood cells. Depletion of serotonin by injection of parachlorophenylalanine blocked the increase in amount of brain waves of the type commonly seen in slow wave sleep but did not eliminate the production of these waves. This result is at variance with the theory that serotonin is the neurochemical responsible for the "priming" of slow wave sleep.

Anemia↗
PubMed1992

Effects of selective sleep deprivation on ventilation during recovery sleep in normal humans.

To assess the effects of selective sleep loss on ventilation during recovery sleep, we deprived 10 healthy young adult humans of rapid-eye-movement (REM) sleep for 48 h and compared ventilation measured during the recovery night with that measured during the baseline night. At a later date we repeated the study using awakenings during non-rapid-eye-movement (NREM) sleep at the same frequency as in REM sleep deprivation. Neither intervention produced significant changes in average minute ventilation during presleep wakefulness, NREM sleep, or the first REM sleep period. By contrast, both interventions resulted in an increased frequency of breaths, in which ventilation was reduced below the range for tonic REM sleep, and in an increased number of longer episodes, in which ventilation was reduced during the first REM sleep period on the recovery night. The changes after REM sleep deprivation were largely due to an increase in the duration of the REM sleep period with an increase in the total phasic activity and, to a lesser extent, to changes in the relationship between ventilatory components and phasic eye movements. The changes in ventilation after partial NREM sleep deprivation were associated with more pronounced changes in the relationship between specific ventilatory components and eye movement density, whereas no change was observed in the composition of the first REM sleep period. These findings demonstrate that sleep deprivation leads to changes in ventilation during subsequent REM sleep.

Adult↗
PubMed2005

Partial sleep deprivation therapy combined with sertraline affects subjective sleep quality in major depressive disorder.

BACKGROUND AND PURPOSE: Earlier studies have shown an association between mood disorders and sleep regulation. Total or partial sleep deprivation was demonstrated to have rapid antidepressive effects in depression. Depressive symptoms recur after one night of recovery sleep, but relapse is less when patients are receiving medication. In this study, we examined the subjective sleep quality changes with the antidepressive therapy using partial sleep deprivation plus sertraline and sertraline monotherapy in patients with major depressive disorder. PATIENTS AND METHODS: Thirteen patients received six partial sleep deprivation therapies in addition to sertraline; the sleep schedule on deprivation nights started at 11:00 p.m. and ended at 3:00 a.m. Eleven patients were treated with sertraline monotherapy as a control group. Six nights of partial sleep deprivation were completed in the first two weeks. Subjective sleep quality was evaluated with the Pittsburgh Sleep Quality Index (PSQI); depression and the accompanying anxiety were also assessed at baseline and at the end of the fourth week. RESULTS: The late partial sleep deprivation (LPSD) group showed less increase in estimated sleep duration and less significant improvement in subjective sleep quality than the control group. Although decreased sleep latency and increased sleep efficiency are associated with the sleep deprivation, contrary results were found in our study. CONCLUSIONS: In conclusion, changes in subjective sleep quality could occur relative to the combined partial sleep deprivation therapy and to pharmacotherapy and must be differentiated from the rapid effects of sleep deprivation therapy and objective polysomnographic measures.

Adult↗
PubMedDate not supplied

Functional consequences of sustained sleep deprivation in the rat.

Sleep deprivation disrupts vital biological processes that are necessary for cognitive ability and physical health, but the physiological changes that underlie these outward effects are largely unknown. The purpose of the present studies in the laboratory rat is to prolong sleep deprivation to delineate the pathophysiology and to determine its mediation. In the rat, the course of prolonged sleep deprivation has a syndromic nature and eventuates in a life-threatening state. An early and central symptom of sleep deprivation is a progressive increase in peripheral energy expenditure to nearly double normal levels. An attempt to alleviate this negative energy balance by feeding rats a balanced diet that is high in its efficiency of utilization prolongs survival and attenuates or delays development of malnutrition-like symptoms, indicating that several symptoms can be manipulated to some extent by energy and nutrient consumption. Most changes in neuroendocrine parameters appear to be responses to metabolic demands, such as increased plasma catecholamines indicating sympathetic activation. Plasma total thyroid hormones, however, decline to severely low levels; a metabolic complication that is associated with other sleep deprivation-induced symptoms, such as a decline in body temperature to hypothermic levels despite increased energy expenditure. Metabolic mapping of the brain revealed a dissociation between the energy metabolism of the brain and that of the body. Sleep deprivation's effects on cerebral structures are heterogeneous and unidirectional toward decreased functional activity. The hypometabolic brain structures are concentrated in the hypothalamus, thalamus and limbic systems, whereas few regions in the rest of the brain and none in the medulla, are affected. Correspondence can be found between some of the affected cerebral structures and several of the peripheral symptoms, such as hyperphagia and possible heat retention problems. The factor predisposing to mortality is a decreased resistance to infection. Lethal opportunistic organisms are permitted to infect the bloodstream, which presumably results in a cascade of toxic-like reactions. Host defense is thus the first system to fail. There is neither fever nor marked tissue inflammatory reactions typical of infectious disease states, suggesting that sleep deprivation is immunosuppressive. Each of the four abnormalities identified--(1) a deep negative energy balance and associated malnutrition; (2) heterogeneous decreases in cerebral function; (3) low thyroid hormone concentrations; and (4) decrease resistance to infection--can be viewed as having an early origin during the sleep deprivation process to signify the foremost pathogenic situation to which the other abnormalities might be secondarily related.(ABSTRACT TRUNCATED AT 400 WORDS)

Adaptation, Physiological↗
PubMed2003

Utility of dextroamphetamine for attenuating the impact of sleep deprivation in pilots.

INTRODUCTION: Dextroamphetamine (Dexedrine) is an effective fatigue countermeasure for use in military subject pilots who are deprived of sleep. Anecdotal reports have indicated Dexedrine (Dex) is effective in "real world" sustained operations, and controlled laboratory tests have yielded positive results as well. The aim of this study was to substantiate the efficacy of Dex for sustaining the alertness and performance of pilots during periods of sleep deprivation by showing the robust effects of the medication and its consistent effects across several research efforts. METHODS: In the present report, selected data from several controlled aviation studies were reviewed and combined to corroborate the efficacy of Dex as a fatigue countermeasure. RESULTS: The results showed Dex to be effective for maintaining flight skills, psychological mood, and physiological activation (measured via electroencephalograph data) in sleep-deprived pilots. The positive benefits of the medication were not offset by marked disruptions in recovery sleep, although some negative effects were observed (sleep was lighter for several hours following drug administration). CONCLUSIONS: Dex is a viable remedy for fatigue in aviation sustained operations. However, Dex is not a substitute for proper crew-rest scheduling because there is no replacement for adequate restful sleep.

Adult↗
PubMed2006

Frontal lobe metabolic decreases with sleep deprivation not totally reversed by recovery sleep.

We studied the effects of total sleep deprivation and recovery sleep in normal subjects using position emission tomography with 18F-deoxyglycose. Sleep deprivation resulted in a significant decrease in relative metabolism of the frontal cortex, thalamus, and striatum. Recovery sleep was found to have only a partial restorative effect on frontal lobe function with minimal reversal of subcortical deficits. Sleep may be especially important for maintenance of frontal lobe activity.

Adult↗
PubMed1997

Recovery sleep and performance following sleep deprivation with dextroamphetamine.

Twelve subjects were studied to determine the after-effects of using three 10-mg doses of dextroamphetamine to sustain alertness during sleep deprivation. Sleep architecture during recovery sleep was evaluated by comparing post-deprivation sleep after placebo. Performance and mood recovery were assessed by comparing volunteers who received dextroamphetamine first (during sleep deprivation) to those who received placebo first. Stages 1 and 2 sleep, movement time, REM latency, and sleep latency increased on the night after sleep deprivation with dextroamphetamine vs. placebo. Stage 4 was unaffected. Comparisons to baseline revealed more stage 1 during baseline than during either post-deprivation sleep period and more stage 2 during baseline than during sleep following placebo. Stage 4 sleep was lower during baseline and after dextroamphetamine than after placebo. Sleep onset was slowest on the baseline night. Next-day performance and mood were not different as a function of whether subjects received dextroamphetamine or placebo during deprivation. These data suggest dextroamphetamine alters post-deprivation sleep architecture when used to sustain alertness during acute sleep loss, but next-day performance and subjective mood ratings are not substantially affected. A recovery sleep period of only 8 h appears to be adequate to regain baseline performance levels after short-term sleep deprivation.

Adult↗