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Sample records for sleep sleep deprivation

  1. Sleep Deprivation.

    PubMed

    Abrams, Robert M

    2015-09-01

    Sleep deprivation occurs when inadequate sleep leads to decreased performance, inadequate alertness, and deterioration in health. It is incompletely understood why humans need sleep, although some theories include energy conservation, restoration, and information processing. Sleep deprivation has many deleterious health effects. Residency programs have enacted strict work restrictions because of medically related errors due to sleep deprivation. Because obstetrics is an unpredictable specialty with long irregular hours, enacting a hospitalist program enhances patient safety, decreases malpractice risk, and improves the physician's quality of life by allowing obstetricians to get sufficient rest.

  2. SLEEP DEPRIVATION,

    DTIC Science & Technology

    This report was confined to considering the effects of sleep deprivation , in man, with particular reference to studies of the resulting biochemical...have a limited value when taken separately: the biochemical and physiological changes that occur in response to sleep deprivation may depend...three separate heads: first, the biochemical changes resulting from sleep deprivation ; secondly, the physiological ones; and last, the changes in performance and behaviour. (Author)

  3. Sleep Deprivation and Deficiency

    MedlinePlus

    ... page from the NHLBI on Twitter. What Are Sleep Deprivation and Deficiency? Sleep deprivation (DEP-rih-VA- ... Rate This Content: NEXT >> Updated: June 7, 2017 Sleep Infographic Sleep Disorders & Insufficient Sleep: Improving Health through ...

  4. Sleep deprivation and false memories.

    PubMed

    Frenda, Steven J; Patihis, Lawrence; Loftus, Elizabeth F; Lewis, Holly C; Fenn, Kimberly M

    2014-09-01

    Many studies have investigated factors that affect susceptibility to false memories. However, few have investigated the role of sleep deprivation in the formation of false memories, despite overwhelming evidence that sleep deprivation impairs cognitive function. We examined the relationship between self-reported sleep duration and false memories and the effect of 24 hr of total sleep deprivation on susceptibility to false memories. We found that under certain conditions, sleep deprivation can increase the risk of developing false memories. Specifically, sleep deprivation increased false memories in a misinformation task when participants were sleep deprived during event encoding, but did not have a significant effect when the deprivation occurred after event encoding. These experiments are the first to investigate the effect of sleep deprivation on susceptibility to false memories, which can have dire consequences.

  5. Neurobiological Consequences of Sleep Deprivation

    PubMed Central

    Alkadhi, Karim; Zagaar, Munder; Alhaider, Ibrahim; Salim, Samina; Aleisa, Abdulaziz

    2013-01-01

    Although the physiological function of sleep is not completely understood, it is well documented that it contributes significantly to the process of learning and memory. Ample evidence suggests that adequate sleep is essential for fostering connections among neuronal networks for memory consolidation in the hippocampus. Sleep deprivation studies are extremely valuable in understanding why we sleep and what are the consequences of sleep loss. Experimental sleep deprivation in animals allows us to gain insight into the mechanism of sleep at levels not possible to study in human subjects. Many useful approaches have been utilized to evaluate the effect of sleep loss on cognitive function, each with relative advantages and disadvantages. In this review we discuss sleep and the detrimental effects of sleep deprivation mostly in experimental animals. The negative effects of sleep deprivation on various aspects of brain function including learning and memory, synaptic plasticity and the state of cognition-related signaling molecules are discussed. PMID:24179461

  6. Sleep Deprivation and Neurobehavioral Dynamics

    PubMed Central

    Basner, Mathias; Rao, Hengyi; Goel, Namni; Dinges, David F.

    2013-01-01

    Lifestyles involving sleep deprivation are common, despite mounting evidence that both acute total sleep deprivation and chronically restricted sleep degrade neurobehavioral functions associated with arousal, attention, memory and state stability. Current research suggests dynamic differences in the way the central nervous system responds to acute versus chronic sleep restriction, which is reflected in new models of sleep-wake regulation. Chronic sleep restriction likely induces long-term neuromodulatory changes in brain physiology that could explain why recovery from it may require more time than from acute sleep loss. High intraclass correlations in neurobehavioral responses to sleep loss suggest that these trait-like differences are phenotypic and may include genetic components. Sleep deprivation induces changes in brain metabolism and neural activation that involve distributed networks and connectivity. PMID:23523374

  7. Energy expenditure during sleep, sleep deprivation and sleep following sleep deprivation in adult humans.

    PubMed

    Jung, Christopher M; Melanson, Edward L; Frydendall, Emily J; Perreault, Leigh; Eckel, Robert H; Wright, Kenneth P

    2011-01-01

    Sleep has been proposed to be a physiological adaptation to conserve energy, but little research has examined this proposed function of sleep in humans. We quantified effects of sleep, sleep deprivation and recovery sleep on whole-body total daily energy expenditure (EE) and on EE during the habitual day and nighttime. We also determined effects of sleep stage during baseline and recovery sleep on EE. Seven healthy participants aged 22 ± 5 years (mean ± s.d.) maintained ∼8 h per night sleep schedules for 1 week before the study and consumed a weight-maintenance diet for 3 days prior to and during the laboratory protocol. Following a habituation night, subjects lived in a whole-room indirect calorimeter for 3 days. The first 24 h served as baseline – 16 h wakefulness, 8 h scheduled sleep – and this was followed by 40 h sleep deprivation and 8 h scheduled recovery sleep. Findings show that, compared to baseline, 24 h EE was significantly increased by ∼7% during the first 24 h of sleep deprivation and was significantly decreased by ∼5% during recovery, which included hours awake 25-40 and 8 h recovery sleep. During the night time, EE was significantly increased by ∼32% on the sleep deprivation night and significantly decreased by ∼4% during recovery sleep compared to baseline. Small differences in EE were observed among sleep stages, but wakefulness during the sleep episode was associated with increased energy expenditure. These findings provide support for the hypothesis that sleep conserves energy and that sleep deprivation increases total daily EE in humans.

  8. Energy expenditure during sleep, sleep deprivation and sleep following sleep deprivation in adult humans

    PubMed Central

    Jung, Christopher M; Melanson, Edward L; Frydendall, Emily J; Perreault, Leigh; Eckel, Robert H; Wright, Kenneth P

    2011-01-01

    Sleep has been proposed to be a physiological adaptation to conserve energy, but little research has examined this proposed function of sleep in humans. We quantified effects of sleep, sleep deprivation and recovery sleep on whole-body total daily energy expenditure (EE) and on EE during the habitual day and nighttime. We also determined effects of sleep stage during baseline and recovery sleep on EE. Seven healthy participants aged 22 ± 5 years (mean ± s.d.) maintained ∼8 h per night sleep schedules for 1 week before the study and consumed a weight-maintenance diet for 3 days prior to and during the laboratory protocol. Following a habituation night, subjects lived in a whole-room indirect calorimeter for 3 days. The first 24 h served as baseline – 16 h wakefulness, 8 h scheduled sleep – and this was followed by 40 h sleep deprivation and 8 h scheduled recovery sleep. Findings show that, compared to baseline, 24 h EE was significantly increased by ∼7% during the first 24 h of sleep deprivation and was significantly decreased by ∼5% during recovery, which included hours awake 25–40 and 8 h recovery sleep. During the night time, EE was significantly increased by ∼32% on the sleep deprivation night and significantly decreased by ∼4% during recovery sleep compared to baseline. Small differences in EE were observed among sleep stages, but wakefulness during the sleep episode was associated with increased energy expenditure. These findings provide support for the hypothesis that sleep conserves energy and that sleep deprivation increases total daily EE in humans. PMID:21059762

  9. Sleep Deprivation and Advice Taking

    PubMed Central

    Häusser, Jan Alexander; Leder, Johannes; Ketturat, Charlene; Dresler, Martin; Faber, Nadira Sophie

    2016-01-01

    Judgements and decisions in many political, economic or medical contexts are often made while sleep deprived. Furthermore, in such contexts individuals are required to integrate information provided by – more or less qualified – advisors. We asked if sleep deprivation affects advice taking. We conducted a 2 (sleep deprivation: yes vs. no) ×2 (competency of advisor: medium vs. high) experimental study to examine the effects of sleep deprivation on advice taking in an estimation task. We compared participants with one night of total sleep deprivation to participants with a night of regular sleep. Competency of advisor was manipulated within subjects. We found that sleep deprived participants show increased advice taking. An interaction of condition and competency of advisor and further post-hoc analyses revealed that this effect was more pronounced for the medium competency advisor compared to the high competency advisor. Furthermore, sleep deprived participants benefited more from an advisor of high competency in terms of stronger improvement in judgmental accuracy than well-rested participants. PMID:27109507

  10. PHYSIOLOGICAL RESPONSES OF MEN DURING SLEEP DEPRIVATION,

    DTIC Science & Technology

    The effects of 84 hours of sleep deprivation were examined in a group of six young men and compared with a group of six controls. Subjects were... sleep deprivation , physiological regulating systems are relatively unaffected by sleep loss. (Author)

  11. Neurocognitive Consequences of Sleep Deprivation

    PubMed Central

    Goel, Namni; Rao, Hengyi; Durmer, Jeffrey S.; Dinges, David F.

    2012-01-01

    Sleep deprivation is associated with considerable social, financial, and health-related costs, in large measure because it produces impaired cognitive performance due to increasing sleep propensity and instability of waking neurobehavioral functions. Cognitive functions particularly affected by sleep loss include psychomotor and cognitive speed, vigilant and executive attention, working memory, and higher cognitive abilities. Chronic sleep-restriction experiments—which model the kind of sleep loss experienced by many individuals with sleep fragmentation and premature sleep curtailment due to disorders and lifestyle—demonstrate that cognitive deficits accumulate to severe levels over time without full awareness by the affected individual. Functional neuroimaging has revealed that frequent and progressively longer cognitive lapses, which are a hallmark of sleep deprivation, involve distributed changes in brain regions including frontal and parietal control areas, secondary sensory processing areas, and thalamic areas. There are robust differences among individuals in the degree of their cognitive vulnerability to sleep loss that may involve differences in prefrontal and parietal cortices, and that may have a basis in genes regulating sleep homeostasis and circadian rhythms. Thus, cognitive deficits believed to be a function of the severity of clinical sleep disturbance may be a product of genetic alleles associated with differential cognitive vulnerability to sleep loss. PMID:19742409

  12. BDNF in sleep, insomnia, and sleep deprivation.

    PubMed

    Schmitt, Karen; Holsboer-Trachsler, Edith; Eckert, Anne

    2016-01-01

    The protein brain-derived neurotrophic factor (BDNF) is a member of the neurotrophin family of growth factors involved in plasticity of neurons in several brain regions. There are numerous evidence that BDNF expression is decreased by experiencing psychological stress and that, accordingly, a lack of neurotrophic support causes major depression. Furthermore, disruption in sleep homeostatic processes results in higher stress vulnerability and is often associated with stress-related mental disorders. Recently, we reported, for the first time, a relationship between BDNF and insomnia and sleep deprivation (SD). Using a biphasic stress model as explanation approach, we discuss here the hypothesis that chronic stress might induce a deregulation of the hypothalamic-pituitary-adrenal system. In the long-term it leads to sleep disturbance and depression as well as decreased BDNF levels, whereas acute stress like SD can be used as therapeutic intervention in some insomniac or depressed patients as compensatory process to normalize BDNF levels. Indeed, partial SD (PSD) induced a fast increase in BDNF serum levels within hours after PSD which is similar to effects seen after ketamine infusion, another fast-acting antidepressant intervention, while traditional antidepressants are characterized by a major delay until treatment response as well as delayed BDNF level increase. Key messages Brain-derived neurotrophic factor (BDNF) plays a key role in the pathophysiology of stress-related mood disorders. The interplay of stress and sleep impacts on BDNF level. Partial sleep deprivation (PSD) shows a fast action on BDNF level increase.

  13. Recovery sleep and performance following sleep deprivation with dextroamphetamine.

    PubMed

    Caldwell, J L; Caldwell, J A

    1997-06-01

    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.

  14. Sleep deprivation: consequences for students.

    PubMed

    Marhefka, Julie King

    2011-09-01

    During the adolescent years, a delayed pattern of the sleep-wake cycle occurs. Many parents and health care providers are not aware that once established, these poor sleep habits can continue into adulthood. Early school hours start a pattern of sleep loss that begins a cycle of daytime sleepiness, which may affect mood, behavior, and increase risk for accidents or injury. These sleep-deprived habits established in adolescence can often lead to problems during college years. Sleep hygiene can be initiated to help break the cycle, along with education and implementation of a strict regimen. Monitoring all adolescents and college-aged students for sleep insufficiency is imperative to improve both academic and emotional well-being. Copyright 2011, SLACK Incorporated.

  15. Genetic Dissociation of Daily Sleep and Sleep Following Thermogenetic Sleep Deprivation in Drosophila

    PubMed Central

    Dubowy, Christine; Moravcevic, Katarina; Yue, Zhifeng; Wan, Joy Y.; Van Dongen, Hans P.A.; Sehgal, Amita

    2016-01-01

    Study Objectives: Sleep rebound—the increase in sleep that follows sleep deprivation—is a hallmark of homeostatic sleep regulation that is conserved across the animal kingdom. However, both the mechanisms that underlie sleep rebound and its relationship to habitual daily sleep remain unclear. To address this, we developed an efficient thermogenetic method of inducing sleep deprivation in Drosophila that produces a substantial rebound, and applied the newly developed method to assess sleep rebound in a screen of 1,741 mutated lines. We used data generated by this screen to identify lines with reduced sleep rebound following thermogenetic sleep deprivation, and to probe the relationship between habitual sleep amount and sleep following thermogenetic sleep deprivation in Drosophila. Methods: To develop a thermogenetic method of sleep deprivation suitable for screening, we thermogenetically stimulated different populations of wake-promoting neurons labeled by Gal4 drivers. Sleep rebound following thermogenetically-induced wakefulness varies across the different sets of wake-promoting neurons that were stimulated, from very little to quite substantial. Thermogenetic activation of neurons marked by the c584-Gal4 driver produces both strong sleep loss and a substantial rebound that is more consistent within genotypes than rebound following mechanical or caffeine-induced sleep deprivation. We therefore used this driver to induce sleep deprivation in a screen of 1,741 mutagenized lines generated by the Drosophila Gene Disruption Project. Flies were subjected to 9 h of sleep deprivation during the dark period and released from sleep deprivation 3 h before lights-on. Recovery was measured over the 15 h following sleep deprivation. Following identification of lines with reduced sleep rebound, we characterized baseline sleep and sleep depth before and after sleep deprivation for these hits. Results: We identified two lines that consistently exhibit a blunted increase in the

  16. Genetic Dissociation of Daily Sleep and Sleep Following Thermogenetic Sleep Deprivation in Drosophila.

    PubMed

    Dubowy, Christine; Moravcevic, Katarina; Yue, Zhifeng; Wan, Joy Y; Van Dongen, Hans P A; Sehgal, Amita

    2016-05-01

    Sleep rebound-the increase in sleep that follows sleep deprivation-is a hallmark of homeostatic sleep regulation that is conserved across the animal kingdom. However, both the mechanisms that underlie sleep rebound and its relationship to habitual daily sleep remain unclear. To address this, we developed an efficient thermogenetic method of inducing sleep deprivation in Drosophila that produces a substantial rebound, and applied the newly developed method to assess sleep rebound in a screen of 1,741 mutated lines. We used data generated by this screen to identify lines with reduced sleep rebound following thermogenetic sleep deprivation, and to probe the relationship between habitual sleep amount and sleep following thermogenetic sleep deprivation in Drosophila. To develop a thermogenetic method of sleep deprivation suitable for screening, we thermogenetically stimulated different populations of wake-promoting neurons labeled by Gal4 drivers. Sleep rebound following thermogenetically-induced wakefulness varies across the different sets of wake-promoting neurons that were stimulated, from very little to quite substantial. Thermogenetic activation of neurons marked by the c584-Gal4 driver produces both strong sleep loss and a substantial rebound that is more consistent within genotypes than rebound following mechanical or caffeine-induced sleep deprivation. We therefore used this driver to induce sleep deprivation in a screen of 1,741 mutagenized lines generated by the Drosophila Gene Disruption Project. Flies were subjected to 9 h of sleep deprivation during the dark period and released from sleep deprivation 3 h before lights-on. Recovery was measured over the 15 h following sleep deprivation. Following identification of lines with reduced sleep rebound, we characterized baseline sleep and sleep depth before and after sleep deprivation for these hits. We identified two lines that consistently exhibit a blunted increase in the duration and depth of sleep after

  17. Sleep deprivation increases cigarette smoking.

    PubMed

    Hamidovic, Ajna; de Wit, Harriet

    2009-09-01

    Loss of sleep may impair the ability to abstain from drug use, through any of a number of mechanisms. Sleep loss may increase drug use by impairing attention and inhibitory control, increasing the value of drug rewards over other rewards, or by inducing mood states that facilitate use of a drug. In the present study, we examined whether sleep deprivation (SD) would increase smoking in cigarette smokers, and whether it would do so by impairing attention or inhibitory control. Healthy cigarette smokers (N=14) were tested in a two-session within subject study, after overnight SD or after a normal night's sleep. Subjects were tested in both conditions in randomized order, after abstaining from cigarettes for 48 hours. The procedure was designed to model the human relapse situation. On each 6-h laboratory session after sleep or no sleep, subjects completed mood and craving questionnaires, tasks measuring behavioral inhibition and attention, and a choice procedure in which they chose between money and smoking cigarettes. SD increased self-reported fatigue and decreased arousal, it increased the number of cigarettes subjects chose to smoke, impaired behavioral inhibition and attention. However, the impairments in inhibition or attention were not related to the increase in smoking. It is possible that SD increases smoking because smokers expect that it will reduce sleepiness. Thus, the findings suggest that sleep loss may increase the likelihood of smoking during abstinence not through inhibitory or attentional mechanisms but because of the potential of nicotine to reduce subjective sleepiness.

  18. Sleep deprivation suppresses aggression in Drosophila

    PubMed Central

    Kayser, Matthew S; Mainwaring, Benjamin; Yue, Zhifeng; Sehgal, Amita

    2015-01-01

    Sleep disturbances negatively impact numerous functions and have been linked to aggression and violence. However, a clear effect of sleep deprivation on aggressive behaviors remains unclear. We find that acute sleep deprivation profoundly suppresses aggressive behaviors in the fruit fly, while other social behaviors are unaffected. This suppression is recovered following post-deprivation sleep rebound, and occurs regardless of the approach to achieve sleep loss. Genetic and pharmacologic approaches suggest octopamine signaling transmits changes in aggression upon sleep deprivation, and reduced aggression places sleep-deprived flies at a competitive disadvantage for obtaining a reproductive partner. These findings demonstrate an interaction between two phylogenetically conserved behaviors, and suggest that previous sleep experiences strongly modulate aggression with consequences for reproductive fitness. DOI: http://dx.doi.org/10.7554/eLife.07643.001 PMID:26216041

  19. Sleep deprivation induced anxiety and anaerobic performance.

    PubMed

    Vardar, Selma Arzu; Oztürk, Levent; Kurt, Cem; Bulut, Erdogan; Sut, Necdet; Vardar, Erdal

    2007-01-01

    The aim of this study was to investigate the effects of sleep deprivation induced anxiety on anaerobic performance. Thirteen volunteer male physical education students completed the Turkish version of State Anxiety Inventory and performed Wingate anaerobic test for three times: (1) following a full-night of habitual sleep (baseline measurements), (2) following 30 hours of sleep deprivation, and (3) following partial-night sleep deprivation. Baseline measurements were performed the day before total sleep deprivation. Measurements following partial sleep deprivation were made 2 weeks later than total sleep deprivation measurements. State anxiety was measured prior to each Wingate test. The mean state anxiety following total sleep deprivation was higher than the baseline measurement (44.9 ± 12.9 vs. 27.6 ± 4.2, respectively, p = 0.02) whereas anaerobic performance parameters remained unchanged. Neither anaerobic parameters nor state anxiety levels were affected by one night partial sleep deprivation. Our results suggest that 30 hours continuous wakefulness may increase anxiety level without impairing anaerobic performance, whereas one night of partial sleep deprivation was ineffective on both state anxiety and anaerobic performance. Key pointsShort time total sleep deprivation (30 hours) increases state anxiety without any competition stress.Anaerobic performance parameters such as peak power, mean power and minimum power may not show a distinctive difference from anaerobic performance in a normal sleep day despite the high anxiety level induced by short time sleep deprivation.Partial sleep deprivation does not affect anxiety level and anaerobic performance of the next day.

  20. Vascular compliance limits during sleep deprivation and recovery sleep.

    PubMed

    Phillips, Derrick J; Schei, Jennifer L; Rector, David M

    2013-10-01

    Our previous studies showed that evoked hemodynamic responses are smaller during wake compared to sleep; suggesting neural activity is associated with vascular expansion and decreased compliance. We explored whether prolonged activity during sleep deprivation may exacerbate vascular expansion and blunt hemodynamic responses. Evoked auditory responses were generated with periodic 65 dB speaker clicks over a 72-h period and measured with cortical electrodes. Evoked hemodynamic responses were measured simultaneously with optical techniques using three light-emitting diodes, and a photodiode. Animals were housed in separate 30×30×80 cm enclosures, tethered to a commutator system and maintained on a 12-h light/dark cycle. Food and water were available ad libitum. Seven adult female Sprague-Dawley rats. Following a 24-h baseline recording, sleep deprivation was initiated for 0 to 10 h by gentle handling, followed by a 24-h recovery sleep recording. Evoked electrical and hemodynamic responses were measured before, during, and after sleep deprivation. Following deprivation, evoked hemodynamic amplitudes were blunted. Steady-state oxyhemoglobin concentration increased during deprivation and remained high during the initial recovery period before returning to baseline levels after approximately 9-h. Sleep deprivation resulted in blood vessel expansion and decreased compliance while lower basal neural activity during recovery sleep may allow blood vessel compliance to recover. Chronic sleep restriction or sleep deprivation could push the vasculature to critical levels, limiting blood delivery, and leading to metabolic deficits with the potential for neural trauma.

  1. Vascular Compliance Limits during Sleep Deprivation and Recovery Sleep

    PubMed Central

    Phillips, Derrick J.; Schei, Jennifer L.; Rector, David M.

    2013-01-01

    Study Objectives: Our previous studies showed that evoked hemodynamic responses are smaller during wake compared to sleep; suggesting neural activity is associated with vascular expansion and decreased compliance. We explored whether prolonged activity during sleep deprivation may exacerbate vascular expansion and blunt hemodynamic responses. Design: Evoked auditory responses were generated with periodic 65dB speaker clicks over a 72-h period and measured with cortical electrodes. Evoked hemodynamic responses were measured simultaneously with optical techniques using three light-emitting diodes, and a photodiode. Setting: Animals were housed in separate 30×30×80cm enclosures, tethered to a commutator system and maintained on a 12-h light/dark cycle. Food and water were available ad libitum. Patients or Participants: Seven adult female Sprague-Dawley rats. Interventions: Following a 24-h baseline recording, sleep deprivation was initiated for 0 to 10 h by gentle handling, followed by a 24-h recovery sleep recording. Evoked electrical and hemodynamic responses were measured before, during, and after sleep deprivation. Measurements and Results: Following deprivation, evoked hemodynamic amplitudes were blunted. Steady-state oxyhemoglobin concentration increased during deprivation and remained high during the initial recovery period before returning to baseline levels after approximately 9-h. Conclusions: Sleep deprivation resulted in blood vessel expansion and decreased compliance while lower basal neural activity during recovery sleep may allow blood vessel compliance to recover. Chronic sleep restriction or sleep deprivation could push the vasculature to critical levels, limiting blood delivery, and leading to metabolic deficits with the potential for neural trauma. Citation: Phillips DJ; Schei JL; Rector DM. Vascular compliance limits during sleep deprivation and recovery sleep. SLEEP 2013;36(10):1459-1470. PMID:24082305

  2. Sleep deprivation and antidepressant treatment

    PubMed Central

    Voderholzer, Ulrich

    2003-01-01

    The mood-improving effect of sleep deprivation (SD) in depression is even today still not fully understood. Despite the fact that mood and cognitive functions are lowered by prolonged sleep loss and despite convincing data that insomnia is a strong risk factor for subsequent depression,1 acute SD for one night or even partial SD in the second half of the night improves mood in about 60% of depressed patients the day after.2,3 In this respect, among alt types of antidepressant treatments, SD elicits the fastest results, faster even than electroconvulsive therapy. Many authors correlate the likelihood of responding to SD with clinical variables. A summary of predictors is listed in Table I. PMID:22033748

  3. Sleep deprivation and neurobehavioral functioning in children.

    PubMed

    Maski, Kiran P; Kothare, Sanjeev V

    2013-08-01

    Sleep deprivation can result in significant impairments in daytime neurobehavioral functioning in children. Neural substrates impacted by sleep deprivation include the prefrontal cortex, basal ganglia and amygdala and result in difficulties with executive functioning, reward anticipation and emotional reactivity respectively. In everyday life, such difficulties contribute to academic struggles, challenging behaviors and public health concerns of substance abuse and suicidality. In this article, we aim to review 1) core neural structures impacted by sleep deprivation; 2) neurobehavioral problems associated with sleep deprivation; 3) specific mechanisms that may explain the relationship between sleep disturbances and neurobehavioral dysfunction; and 4) sleep problems reported in common neurodevelopmental disorders including attention deficit hyperactivity disorder (ADHD) and autistic spectrum disorders (ASDs).

  4. Sleep, sleep deprivation, autonomic nervous system and cardiovascular diseases.

    PubMed

    Tobaldini, Eleonora; Costantino, Giorgio; Solbiati, Monica; Cogliati, Chiara; Kara, Tomas; Nobili, Lino; Montano, Nicola

    2017-03-01

    Sleep deprivation (SD) has become a relevant health problem in modern societies. We can be sleep deprived due to lifestyle habits or due to sleep disorders, such as insomnia, obstructive sleep apnea (OSA) and neurological disorders. One of the common element of sleep disorders is the condition of chronic SD, which has complex biological consequences. SD is capable of inducing different biological effects, such as neural autonomic control changes, increased oxidative stress, altered inflammatory and coagulatory responses and accelerated atherosclerosis. All these mechanisms links SD and cardiovascular and metabolic disorders. Epidemiological studies have shown that short sleep duration is associated with increased incidence of cardiovascular diseases, such as coronary artery disease, hypertension, arrhythmias, diabetes and obesity, after adjustment for socioeconomic and demographic risk factors and comorbidities. Thus, an early assessment of a condition of SD and its treatment is clinically relevant to prevent the harmful consequences of a very common condition in adult population. Copyright © 2016 Elsevier Ltd. All rights reserved.

  5. Resident Performance and Sleep Deprivation: A Review.

    ERIC Educational Resources Information Center

    Asken, Michael J.; Raham, David C.

    1983-01-01

    A review of the literature on resident performance and sleep deprivation suggests that current research is sparse and inconclusive, and existing research suggests potentially severe negative effects. It is proposed that justifications for sleep-depriving night call schedules remain untested, and their use as part of residency training should be…

  6. Resident Performance and Sleep Deprivation: A Review.

    ERIC Educational Resources Information Center

    Asken, Michael J.; Raham, David C.

    1983-01-01

    A review of the literature on resident performance and sleep deprivation suggests that current research is sparse and inconclusive, and existing research suggests potentially severe negative effects. It is proposed that justifications for sleep-depriving night call schedules remain untested, and their use as part of residency training should be…

  7. Sleep Deprivation in Humans And Transient Immunodepression

    DTIC Science & Technology

    2003-07-21

    Kripke DF, Gruen W, Mullaney DJ, and Gillin CJ (1992). Automatic sleep /wake identification from wrist activity . Sleep , 15(5), 461-469. Dinges DF...of results to each other. Second, we acquired several repeated performance and subjective measures hourly across a single night of sleep ... Measures Body Temperature. Oral temperature was taken hourly during the night of sleep deprivation to estimate circadian rhythm in body

  8. Health Effects of Sleep Deprivation,

    DTIC Science & Technology

    1990-06-01

    anoxia, shock, hypoglycemia, hypotension, physical exercise, psychological stimuli, and drugs in common use, such as caffeine , nicotine , and alcohol...iiii1i’tl 11,11H1 HEALTH EFFECTS OF SLEEP DEPRIVATION P. Naitoh T. I- Kelly C. Englund Repori No. 89-46 9 - 1 3 92 J20 28 Apmrowd fto P..bII .nO~m dI...mand to IO MMuwM I. AGENCY USE ONLY (Laom b 2 REPORT DATE 3. REPORT TYPE AND DATE COVERED 4 TITLE AND SUBTITLE 5. FUNDING NUMBERS Health Effects of

  9. Sleep deprivation sensitizes human craniofacial muscles.

    PubMed

    Kristiansen, Eva Szuchy; Nielsen, Louise Skou; Christensen, Siv Sofie; Botvid, Sofia Hedvig Christina; Nørgaard Poulsen, Jeppe; Gazerani, Parisa

    2017-06-01

    It is unknown whether and how sleep deprivation influences craniofacial muscle sensitivity in healthy humans. We investigated whether total sleep deprivation (TSD) and one night of recovery sleep (RS) can alter mechanical pain sensitivity in temporal and masseter muscles. Fifteen healthy volunteers participated in three consecutive sessions. Pressure pain thresholds were measured on the temporal and masseter muscles. Both temporal and masseter muscles became sensitized after 24 h of TSD. RS reversed the muscle sensitization.

  10. Sleep deprivation and false confessions

    PubMed Central

    Frenda, Steven J.; Berkowitz, Shari R.; Loftus, Elizabeth F.; Fenn, Kimberly M.

    2016-01-01

    False confession is a major contributor to the problem of wrongful convictions in the United States. Here, we provide direct evidence linking sleep deprivation and false confessions. In a procedure adapted from Kassin and Kiechel [(1996) Psychol Sci 7(3):125–128], participants completed computer tasks across multiple sessions and repeatedly received warnings that pressing the “Escape” key on their keyboard would cause the loss of study data. In their final session, participants either slept all night in laboratory bedrooms or remained awake all night. In the morning, all participants were asked to sign a statement, which summarized their activities in the laboratory and falsely alleged that they pressed the Escape key during an earlier session. After a single request, the odds of signing were 4.5 times higher for the sleep-deprived participants than for the rested participants. These findings have important implications and highlight the need for further research on factors affecting true and false confessions. PMID:26858426

  11. Sleep deprivation increases formation of false memory.

    PubMed

    Lo, June C; Chong, Pearlynne L H; Ganesan, Shankari; Leong, Ruth L F; Chee, Michael W L

    2016-12-01

    Retrieving false information can have serious consequences. Sleep is important for memory, but voluntary sleep curtailment is becoming more rampant. Here, the misinformation paradigm was used to investigate false memory formation after 1 night of total sleep deprivation in healthy young adults (N = 58, mean age ± SD = 22.10 ± 1.60 years; 29 males), and 7 nights of partial sleep deprivation (5 h sleep opportunity) in these young adults and healthy adolescents (N = 54, mean age ± SD = 16.67 ± 1.03 years; 25 males). In both age groups, sleep-deprived individuals were more likely than well-rested persons to incorporate misleading post-event information into their responses during memory retrieval (P < 0.050). These findings reiterate the importance of adequate sleep in optimal cognitive functioning, reveal the vulnerability of adolescents' memory during sleep curtailment, and suggest the need to assess eyewitnesses' sleep history after encountering misleading information. © 2016 The Authors. Journal of Sleep Research published by John Wiley & Sons Ltd on behalf of European Sleep Research Society.

  12. Sleep deprivation and interference by emotional distracters.

    PubMed

    Chuah, Lisa Y M; Dolcos, Florin; Chen, Annette K; Zheng, Hui; Parimal, Sarayu; Chee, Michael W L

    2010-10-01

    We determined if sleep deprivation would amplify the effect of negative emotional distracters on working memory. A crossover design involving 2 functional neuroimaging scans conducted at least one week apart. One scan followed a normal night of sleep and the other followed 24 h of sleep deprivation. Scanning order was counterbalanced across subjects. The study took place in a research laboratory. 24 young, healthy volunteers with no history of any sleep, psychiatric, or neurologic disorders. N/A. Study participants were scanned while performing a delayed-response working memory task. Two distracters were presented during the maintenance phase, and these differed in content: highly arousing, negative emotional scenes; low-arousing, neutral scenes; and digitally scrambled versions of the pictures. Irrespective of whether volunteers were sleep deprived, negative emotional (relative to neutral) distracters elicited greater maintenance-related activity in the amygdala, ventrolateral prefrontal cortex, and fusiform gyri, while concurrently depressing activity in cognitive control regions. Individuals who maintained or increased distracter-related amygdala activation after sleep deprivation showed increased working memory disruptions by negative emotional distracters. These individuals also showed reduced functional connectivity between the amygdala and the ventromedial and dorsolateral prefrontal cortices, regions postulated to mediate cognitive control against emotional distraction. Increased distraction by emotional stimuli following sleep deprivation is accompanied by increases in amygdala activation and reduced functional connectivity between the amygdala and prefrontal cognitive control regions. These findings shed light on the neural basis for interindividual variation in how negative emotional stimuli might distract sleep deprived persons.

  13. Sleep deprivation in the rat: III. Total sleep deprivation.

    PubMed

    Everson, C A; Bergmann, B M; Rechtschaffen, A

    1989-02-01

    Ten rats were subjected to total sleep deprivation (TSD) by the disk apparatus. All TSD rats died or were sacrificed when death seemed imminent within 11-32 days. No anatomical cause of death was identified. All TSD rats showed a debilitated appearance, lesions on their tails and paws, and weight loss in spite of increased food intake. Their yoked control (TSC) rats remained healthy. Since dehydration was ruled out and several measures indicated accelerated use rather than failure to absorb nutrients, the food-weight changes in TSD rats were attributed to increased energy expenditure (EE). The measurement of EE, based upon caloric value of food, weight, and wastes, indicated that all TSD rats increased EE, with mean levels reaching more than twice baseline values.

  14. [Treatment of depression with sleep deprivation and sleep phase advancement].

    PubMed

    Riemann, D; Vollmann, J; Hohagen, F; Lohner, H; König, A; Faller, C; Edali, N; Berger, M

    1995-07-01

    Total sleep deprivation (TSD) exerts beneficial but only transient effects on mood in approximately 60% of the patients with a major depressive disorder (MDD). The positive effect of TSD is generally reversed after the next night of sleep. A pilot study of our group indicated that a consecutive one week phase advance of the sleep phase stabilized mood in more than half of the patients who responded to TSD. However, the majority of patients in our pilot study had been treated concomitantly with antidepressive medication. To exclude a possible synergistic effect of simultaneous antidepressive medication and the sleep-wake manipulation in the present study eleven medicated and sixteen drug-free depressed patients were investigated. In two thirds of the patients relapse into depression after successful TSD could be prevented. This effect seemed to be independent of adjunct antidepressant pharmacotherapy. Ten of these patients were studied polysomnographically prior to and during the treatment. Data analysis revealed that during the advance of the sleep phase no prolonged partial sleep deprivation took place. At the end of the study REM % had even increased and REM latency was still short in spite of clinical improvement, thus contradicting the assumption that REM sleep suppression is a necessary prerequisite for antidepressive therapy. The results support the hypothesis of a "critical phase" in the morning hours during which sleep can reinduce depressive mood and, vice versa, prevention of sleep during this time may act antidepressively.

  15. Increased photosensitivity following short sleep in sleep deprived patients.

    PubMed

    Elmalı, Ayşe Deniz; Kurucu, Hatice; Ertürk Çetin, Özdem; Çokar, Özlem; Matur, Zeliha; Dervent, Ayşin; Benbir Şenel, Gülçin; Gürses, Candan; Demirbilek, Veysi

    2017-06-01

    We aimed to determine the effect of short day-time sleep on photoparoxysmal epileptic activity in sleep-deprived patients. We retrospectively reviewed video-EEG recordings performed between 2003 and 2015. All recordings following at least four hours of sleep deprivation, including intermittent photic stimulation (IPS) both before and after sleep with any form of epileptiform activity were included. The study group was divided into four subgroups: (1) no photoparoxysmal response (PPR) group, with epileptiform activities other than PPRs; (2) increment group, with PPR duration increased by ≥200% after vs. before sleep; (3) no significant change group, with PPR duration increased between 50% and 200% after vs. before sleep; (4) decrement group, with PPR duration increased ≤50% after vs. before sleep. A total number of 5805 EEG recordings from 459 patients was analyzed. Photosensitivity was present in 98 patients (21.4%). The PPRs after sleep were increased in 70% of the photosensitive patients, did not change in 23%, and were decreased in 7%. The increase in duration of PPRs was statistically significant (P<0.001). In our cohort, photosensitivity would have been detected in 67 patients if IPS was applied only before sleep and in 91 patients if IPS was applied only after awakening (P<0.05). This study demonstrates that photosensitivity is enhanced after awakening from a short sleep following sleep deprivation. Thus, we recommend performing IPS after awakening to increase sensitivity to detect photoparoxysmal epileptiform discharges. Copyright © 2017 Elsevier Masson SAS. All rights reserved.

  16. Sleep deprivation affects reactivity to positive but not negative stimuli.

    PubMed

    Pilcher, June J; Callan, Christina; Posey, J Laura

    2015-12-01

    The current study examined the effects of partial and total sleep deprivation on emotional reactivity. Twenty-eight partially sleep-deprived participants and 31 totally sleep-deprived participants rated their valence and arousal responses to positive and negative pictures across four testing sessions during the day following partial sleep deprivation or during the night under total sleep deprivation. The results suggest that valence and arousal ratings decreased under both sleep deprivation conditions. In addition, partial and total sleep deprivation had a greater negative effect on positive events than negative events. These results suggest that sleep-deprived persons are more likely to respond less to positive events than negative events. One explanation for the current findings is that negative events could elicit more attentive behavior and thus stable responding under sleep deprivation conditions. As such, sleep deprivation could impact reactivity to emotional stimuli through automated attentional and self-regulatory processes. Copyright © 2015 Elsevier Inc. All rights reserved.

  17. Sleep Deprivation and Interference by Emotional Distracters

    PubMed Central

    Chuah, Lisa Y.M.; Dolcos, Florin; Chen, Annette K.; Zheng, Hui; Parimal, Sarayu; Chee, Michael W.L.

    2010-01-01

    Study Objectives: We determined if sleep deprivation would amplify the effect of negative emotional distracters on working memory. Design: A crossover design involving 2 functional neuroimaging scans conducted at least one week apart. One scan followed a normal night of sleep and the other followed 24 h of sleep deprivation. Scanning order was counterbalanced across subjects. Setting: The study took place in a research laboratory. Participants: 24 young, healthy volunteers with no history of any sleep, psychiatric, or neurologic disorders. Interventions: N/A Measurements and Results: Study participants were scanned while performing a delayed-response working memory task. Two distracters were presented during the maintenance phase, and these differed in content: highly arousing, negative emotional scenes; low-arousing, neutral scenes; and digitally scrambled versions of the pictures. Irrespective of whether volunteers were sleep deprived, negative emotional (relative to neutral) distracters elicited greater maintenance-related activity in the amygdala, ventrolateral prefrontal cortex, and fusiform gyri, while concurrently depressing activity in cognitive control regions. Individuals who maintained or increased distracter-related amygdala activation after sleep deprivation showed increased working memory disruptions by negative emotional distracters. These individuals also showed reduced functional connectivity between the amygdala and the ventromedial and dorsolateral prefrontal cortices, regions postulated to mediate cognitive control against emtional distraction. Conclusions: Increased distraction by emotional stimuli following sleep deprivation is accompanied by increases in amygdala activation and reduced functional connectivity between the amygdala and prefrontal cognitive control regions. These findings shed light on the neural basis for interindividual variation in how negative emotional stimuli might distract sleep deprived persons. Citation: Chuah LYM

  18. Effects of sleep deprivation on cognition.

    PubMed

    Killgore, William D S

    2010-01-01

    Sleep deprivation is commonplace in modern society, but its far-reaching effects on cognitive performance are only beginning to be understood from a scientific perspective. While there is broad consensus that insufficient sleep leads to a general slowing of response speed and increased variability in performance, particularly for simple measures of alertness, attention and vigilance, there is much less agreement about the effects of sleep deprivation on many higher level cognitive capacities, including perception, memory and executive functions. Central to this debate has been the question of whether sleep deprivation affects nearly all cognitive capacities in a global manner through degraded alertness and attention, or whether sleep loss specifically impairs some aspects of cognition more than others. Neuroimaging evidence has implicated the prefrontal cortex as a brain region that may be particularly susceptible to the effects of sleep loss, but perplexingly, executive function tasks that putatively measure prefrontal functioning have yielded inconsistent findings within the context of sleep deprivation. Whereas many convergent and rule-based reasoning, decision making and planning tasks are relatively unaffected by sleep loss, more creative, divergent and innovative aspects of cognition do appear to be degraded by lack of sleep. Emerging evidence suggests that some aspects of higher level cognitive capacities remain degraded by sleep deprivation despite restoration of alertness and vigilance with stimulant countermeasures, suggesting that sleep loss may affect specific cognitive systems above and beyond the effects produced by global cognitive declines or impaired attentional processes. Finally, the role of emotion as a critical facet of cognition has received increasing attention in recent years and mounting evidence suggests that sleep deprivation may particularly affect cognitive systems that rely on emotional data. Thus, the extent to which sleep deprivation

  19. Circadian Rhythms, Sleep Deprivation, and Human Performance

    PubMed Central

    Goel, Namni; Basner, Mathias; Rao, Hengyi; Dinges, David F.

    2014-01-01

    Much of the current science on, and mathematical modeling of, dynamic changes in human performance within and between days is dominated by the two-process model of sleep–wake regulation, which posits a neurobiological drive for sleep that varies homeostatically (increasing as a saturating exponential during wakefulness and decreasing in a like manner during sleep), and a circadian process that neurobiologically modulates both the homeostatic drive for sleep and waking alertness and performance. Endogenous circadian rhythms in neurobehavioral functions, including physiological alertness and cognitive performance, have been demonstrated using special laboratory protocols that reveal the interaction of the biological clock with the sleep homeostatic drive. Individual differences in circadian rhythms and genetic and other components underlying such differences also influence waking neurobehavioral functions. Both acute total sleep deprivation and chronic sleep restriction increase homeostatic sleep drive and degrade waking neurobehavioral functions as reflected in sleepiness, attention, cognitive speed, and memory. Recent evidence indicating a high degree of stability in neurobehavioral responses to sleep loss suggests that these trait-like individual differences are phenotypic and likely involve genetic components, including circadian genes. Recent experiments have revealed both sleep homeostatic and circadian effects on brain metabolism and neural activation. Investigation of the neural and genetic mechanisms underlying the dynamically complex interaction between sleep homeostasis and circadian systems is beginning. A key goal of this work is to identify biomarkers that accurately predict human performance in situations in which the circadian and sleep homeostatic systems are perturbed. PMID:23899598

  20. Loss of negative priming following sleep deprivation.

    PubMed

    Harrison, Yvonne; Espelid, Erik

    2004-04-01

    It has been argued that one night of sleep loss in young healthy adults produces changes similar to that associated with normal, healthy ageing--in particular, that young sleep-deprived adults perform similarly to 60-year-old sleep-satiated adults on some tasks of frontal lobe function. This proposition was examined using a protocol viewed by many to be a direct probe of nonvolitional attention mechanisms associated with frontal lobe function. A negative priming (NP) procedure was used to compare performance between non-sleep-deprived (NSD) and sleep-deprived (SD, 34 hr) young, healthy adults. This protocol allowed for exploration of two theories of the NP effect based on inhibitory or memorial processes. Under conditions believed to facilitate inhibitory processes a normal NP effect was found for NSD(16 ms) and SD (9 ms) participants. Under conditions believed to rely on memorial processes there was no NP effect following SD, compared with a normal NP effect for NSD participants (11 ms). Distractor interference was also greater following SD. These findings do not suggest a similar pattern of change following sleep loss in healthy young adults to that of normal, healthy, non-sleep-deprived aged groups.

  1. [Sleep deprivation in somnambulism. Effect of arousal, deep sleep and sleep stage changes].

    PubMed

    Mayer, G; Neissner, V; Schwarzmayr, P; Meier-Ewert, K

    1998-06-01

    Diagnosis of parasomnias in the sleep laboratory is difficult since the nocturnal behavior reported by the patients often does not show up in the laboratory. To test the efficacy of sleep deprivation as a tool to provoke somnambulism we investigated ten patients (three women and seven men, mean age 27 +/- 3.4) with somnambulism. Their standard polysomnographies and videomonitored nocturnal behavior was compared to that of sex- and age-matched controls and to polysomnography and behavior after sleep deprivation. Patients with parasomnias and controls did not show significant differences in sleep parameters with the exception of longer arousal duration in controls, which was nonsignificant. In magnetic resonance tomography, patients with parasomnias did not reveal abnormality of the brain that might explain release of nocturnal behavior. Sleep deprivation led to significantly reduced number of arousals, reduced arousal index, significantly prolonged arousal duration and more stage shifts from all sleep stages (nonsignificant). Complex behavior during sleep increased under sleep deprivation, whereas sleepwalking did not increase. The majority of complex behavior during sleep is triggered by stage shifts and not by arousal in the sense of the arousal definition of the American Sleep Disorder Society. Complex behavior in sleep is stereotypical and nonviolent. Its complexity seems to depend on the duration and intensity of arousals. Sleep deprivation can be recommended as an efficacious method of increasing complex behavior in sleep, which is a preliminary stage of sleepwalking. Concerning the underlying pathology it seems to be important to register the quality and duration of stimuli that trigger arousals instead of focusing the number of arousals alone.

  2. Benefits of Sleep Extension on Sustained Attention and Sleep Pressure Before and During Total Sleep Deprivation and Recovery

    PubMed Central

    Arnal, Pierrick J.; Sauvet, Fabien; Leger, Damien; van Beers, Pascal; Bayon, Virginie; Bougard, Clément; Rabat, Arnaud; Millet, Guillaume Y.; Chennaoui, Mounir

    2015-01-01

    Objectives: To investigate the effects of 6 nights of sleep extension on sustained attention and sleep pressure before and during total sleep deprivation and after a subsequent recovery sleep. Design: Subjects participated in two experimental conditions (randomized cross-over design): extended sleep (EXT, 9.8 ± 0.1 h (mean ± SE) time in bed) and habitual sleep (HAB, 8.2 ± 0.1 h time in bed). In each condition, subjects performed two consecutive phases: (1) 6 nights of either EXT or HAB (2) three days in-laboratory: baseline, total sleep deprivation and after 10 h of recovery sleep. Setting: Residential sleep extension and sleep performance laboratory (continuous polysomnographic recording). Participants: 14 healthy men (age range: 26–37 years). Interventions: EXT vs. HAB sleep durations prior to total sleep deprivation. Measurements and Results: Total sleep time and duration of all sleep stages during the 6 nights were significantly higher in EXT than HAB. EXT improved psychomotor vigilance task performance (PVT, both fewer lapses and faster speed) and reduced sleep pressure as evidenced by longer multiple sleep latencies (MSLT) at baseline compared to HAB. EXT limited PVT lapses and the number of involuntary microsleeps during total sleep deprivation. Differences in PVT lapses and speed and MSLT at baseline were maintained after one night of recovery sleep. Conclusion: Six nights of extended sleep improve sustained attention and reduce sleep pressure. Sleep extension also protects against psychomotor vigilance task lapses and microsleep degradation during total sleep deprivation. These beneficial effects persist after one night of recovery sleep. Citation: Arnal PJ, Sauvet F, Leger D, van Beers P, Bayon V, Bougard C, Rabat A, Millet GY, Chennaoui M. Benefits of sleep extension on sustained attention and sleep pressure before and during total sleep deprivation and recovery. SLEEP 2015;38(12):1935–1943. PMID:26194565

  3. Prevention and treatment of sleep deprivation among emergency physicians.

    PubMed

    Nelson, Douglas

    2007-07-01

    Emergency physicians commonly experience sleep deprivation because of the need to work shifts during evening and late night hours. The negative effects of this problem are compounded by job stress and traditional methods of scheduling work shifts. Sleep deprivation may be reduced by schedules designed to lessen interference with normal sleep patterns and circadian rhythms. Pharmacological treatments for sleep deprivation exist in the form of alertness-enhancing agents, caffeine and modafinil. Sleep-promoting agents may also help treat the problem by helping physicians to sleep during daytime hours. Minimizing sleep deprivation may help prevent job burnout and prolong the length of an emergency physician's career.

  4. Degradation of Binocular Coordination during Sleep Deprivation

    PubMed Central

    Tong, Jianliang; Maruta, Jun; Heaton, Kristin J.; Maule, Alexis L.; Rajashekar, Umesh; Spielman, Lisa A.; Ghajar, Jamshid

    2016-01-01

    To aid a clear and unified visual perception while tracking a moving target, both eyes must be coordinated, so the image of the target falls on approximately corresponding areas of the fovea of each eye. The movements of the two eyes are decoupled during sleep, suggesting a role of arousal in regulating binocular coordination. While the absence of visual input during sleep may also contribute to binocular decoupling, sleepiness is a state of reduced arousal that still allows for visual input, providing a context within which the role of arousal in binocular coordination can be studied. We examined the effects of sleep deprivation on binocular coordination using a test paradigm that we previously showed to be sensitive to sleep deprivation. We quantified binocular coordination with the SD of the distance between left and right gaze positions on the screen. We also quantified the stability of conjugate gaze on the target, i.e., gaze–target synchronization, with the SD of the distance between the binocular average gaze and the target. Sleep deprivation degraded the stability of both binocular coordination and gaze–target synchronization, but between these two forms of gaze control the horizontal and vertical components were affected differently, suggesting that disconjugate and conjugate eye movements are under different regulation of attentional arousal. The prominent association found between sleep deprivation and degradation of binocular coordination in the horizontal direction may be used for a fit-for-duty assessment. PMID:27379009

  5. Effects of different sleep deprivation protocols on sleep perception in healthy volunteers.

    PubMed

    Goulart, Leonardo I; Pinto, Luciano R; Perlis, Michael L; Martins, Raquel; Caboclo, Luis Otavio; Tufik, Sergio; Andersen, Monica L

    2014-10-01

    To investigate whether different protocols of sleep deprivation modify sleep perception. The effects of total sleep deprivation (TD) and selective rapid eye movement (REM) sleep deprivation (RD) on sleep perception were analyzed in normal volunteers. Thirty-one healthy males with normal sleep were randomized to one of three conditions: (i) normal uninterrupted sleep; (ii) four nights of RD; or (iii) two nights of TD. Morning perception of total sleep time was evaluated for each condition. Sleep perception was estimated using total sleep time (in hours) as perceived by the volunteer divided by the total sleep time (in hours) measured by polysomnography (PSG). The final value of this calculation was defined as the perception index (PI). There were no significant differences among the three groups of volunteers in the total sleep time measured by PSG or in the perception of total sleep time at baseline condition. Volunteers submitted to RD exhibited lower sleep PI scores as compared with controls during the sleep deprivation period (P <0.05). Both RD and TD groups showed PI similar to controls during the recovery period. Selective REM sleep deprivation reduced the ability of healthy young volunteers to perceive their total sleep time when compared with time measured by PSG. The data reinforce the influence of sleep deprivation on sleep perception. Copyright © 2014 Elsevier B.V. All rights reserved.

  6. The effects of sleep and sleep deprivation on metabolic, endocrine and immune parameters.

    PubMed

    Maurovich-Horvat, E; Pollmächer, T Z; Sonka, K

    2008-01-01

    Sleep curtailment is becoming widespread in modern society. In parallel with this, more and more studies are dealing with the health consequences of sleep deprivation. This short review focuses on the main results of studies examining the effects of sleep and sleep deprivation on metabolism with extra emphasis on appetite regulation, and on the endocrine and immune system.

  7. The role of thyroid hormone in sleep deprivation.

    PubMed

    Pereira, José Carlos; Andersen, Mônica Levy

    2014-03-01

    Sleep deprivation is a stressful condition, as the subject experiences feelings of inadequate well-being and exhibits impairments in his/her functioning. However, in some circumstances sleep deprivation may be crucial for survival of the individual. Most likely, complex neural circuits and hormones play a role in allowing sleep deprivation to occur. For instance, thyroid hormone activity sharply increases when an individual is in a state of sleep deprivation. We believe that this increase is central to sleep deprivation physiology. During sleep deprivation, the hypothalamic-pituitary-thyroid axis initially increases as a consequence of increased release of thyroid stimulating hormone from the pituitary. Subsequently, as sleep deprivation continues, the sympathetic nervous system is recruited through its anatomical connection with the thyroid gland. While thyroid stimulating hormone levels markedly increase during sleep deprivation, it has been suggested that these increases are secondary to sleep deprivation. However, there is little evidence to support this assumption. We believe that the physiology of the thyroid axis during sleep deprivation and the actions of the effector hormone thyroid hormone suggest that thyroid hormone inhibits sleep and not the contrary. To our knowledge, few studies have addressed the possible neural functions that enable sleep deprivation. In this article, we discuss the hypothesis that an augmentation in the thyroid hormone axis is central to a subject's ability to curtail sleep.

  8. Unsupervised online classifier in sleep scoring for sleep deprivation studies.

    PubMed

    Libourel, Paul-Antoine; Corneyllie, Alexandra; Luppi, Pierre-Hervé; Chouvet, Guy; Gervasoni, Damien

    2015-05-01

    This study was designed to evaluate an unsupervised adaptive algorithm for real-time detection of sleep and wake states in rodents. We designed a Bayesian classifier that automatically extracts electroencephalogram (EEG) and electromyogram (EMG) features and categorizes non-overlapping 5-s epochs into one of the three major sleep and wake states without any human supervision. This sleep-scoring algorithm is coupled online with a new device to perform selective paradoxical sleep deprivation (PSD). Controlled laboratory settings for chronic polygraphic sleep recordings and selective PSD. Ten adult Sprague-Dawley rats instrumented for chronic polysomnographic recordings. The performance of the algorithm is evaluated by comparison with the score obtained by a human expert reader. Online detection of PS is then validated with a PSD protocol with duration of 72 hours. Our algorithm gave a high concordance with human scoring with an average κ coefficient > 70%. Notably, the specificity to detect PS reached 92%. Selective PSD using real-time detection of PS strongly reduced PS amounts, leaving only brief PS bouts necessary for the detection of PS in EEG and EMG signals (4.7 ± 0.7% over 72 h, versus 8.9 ± 0.5% in baseline), and was followed by a significant PS rebound (23.3 ± 3.3% over 150 minutes). Our fully unsupervised data-driven algorithm overcomes some limitations of the other automated methods such as the selection of representative descriptors or threshold settings. When used online and coupled with our sleep deprivation device, it represents a better option for selective PSD than other methods like the tedious gentle handling or the platform method. © 2015 Associated Professional Sleep Societies, LLC.

  9. BINOCULAR FUSION TIME IN SLEEP-DEPRIVED SUBJECTS,

    DTIC Science & Technology

    fatigue induced by sleep deprivation on the binocular fusion reflex. Binocular fusion times were measured morning and evening in six subjects during 86...hours of sleep deprivation and in six control subjects. The binocular fusion reflex under the experimental conditions employed appeared to be resistant to fatigue incident to sleep - deprivation . (Author)

  10. Sleep Deprivation and Exercise Tolerance.

    DTIC Science & Technology

    1986-01-01

    thermoneutral environment) is alike unchanged by loss of sleep. 5) Seven subjects were allowed to exercise to thermal comfort in a very cold (OC, 2.5...Subjects selected identical work loads for thermal comfort , and became exhausted/miserable after similar period of exposure. Physiologi- cal response and

  11. Benefits of Sleep Extension on Sustained Attention and Sleep Pressure Before and During Total Sleep Deprivation and Recovery.

    PubMed

    Arnal, Pierrick J; Sauvet, Fabien; Leger, Damien; van Beers, Pascal; Bayon, Virginie; Bougard, Clément; Rabat, Arnaud; Millet, Guillaume Y; Chennaoui, Mounir

    2015-12-01

    To investigate the effects of 6 nights of sleep extension on sustained attention and sleep pressure before and during total sleep deprivation and after a subsequent recovery sleep. Subjects participated in two experimental conditions (randomized cross-over design): extended sleep (EXT, 9.8 ± 0.1 h (mean ± SE) time in bed) and habitual sleep (HAB, 8.2 ± 0.1 h time in bed). In each condition, subjects performed two consecutive phases: (1) 6 nights of either EXT or HAB (2) three days in-laboratory: baseline, total sleep deprivation and after 10 h of recovery sleep. Residential sleep extension and sleep performance laboratory (continuous polysomnographic recording). 14 healthy men (age range: 26-37 years). EXT vs. HAB sleep durations prior to total sleep deprivation. Total sleep time and duration of all sleep stages during the 6 nights were significantly higher in EXT than HAB. EXT improved psychomotor vigilance task performance (PVT, both fewer lapses and faster speed) and reduced sleep pressure as evidenced by longer multiple sleep latencies (MSLT) at baseline compared to HAB. EXT limited PVT lapses and the number of involuntary microsleeps during total sleep deprivation. Differences in PVT lapses and speed and MSLT at baseline were maintained after one night of recovery sleep. Six nights of extended sleep improve sustained attention and reduce sleep pressure. Sleep extension also protects against psychomotor vigilance task lapses and microsleep degradation during total sleep deprivation. These beneficial effects persist after one night of recovery sleep. © 2015 Associated Professional Sleep Societies, LLC.

  12. Sleep

    MedlinePlus

    ... NICHD Research Information Clinical Trials Resources and Publications Sleep: Condition Information Skip sharing on social media links Share this: Page Content What is sleep? Sleep is a period of unconsciousness during which ...

  13. Gene Networks Underlying Chronic Sleep Deprivation in Drosophila

    DTIC Science & Technology

    2014-06-15

    SECURITY CLASSIFICATION OF: Studies of the gene network affected by sleep deprivation and stress in the fruit fly Drosophila have revealed the...Chronic Sleep Deprivation in Drosophila Report Title Studies of the gene network affected by sleep deprivation and stress in the fruit fly Drosophila have...stressed flies , the involvement of axonogenesis as a process regulated by these stressors. This goes beyond the current hypothesis of sleep as functioning

  14. A New Model to Study Sleep Deprivation-Induced Seizure

    PubMed Central

    Lucey, Brendan P.; Leahy, Averi; Rosas, Regine; Shaw, Paul J.

    2015-01-01

    Background and Study Objectives: A relationship between sleep and seizures is well-described in both humans and rodent animal models; however, the mechanism underlying this relationship is unknown. Using Drosophila melanogaster mutants with seizure phenotypes, we demonstrate that seizure activity can be modified by sleep deprivation. Design: Seizure activity was evaluated in an adult bang-sensitive seizure mutant, stress sensitive B (sesB9ed4), and in an adult temperature sensitive seizure mutant seizure (seits1) under baseline and following 12 h of sleep deprivation. The long-term effect of sleep deprivation on young, immature sesB9ed4 flies was also assessed. Setting: Laboratory. Participants: Drosophila melanogaster. Interventions: Sleep deprivation. Measurements and Results: Sleep deprivation increased seizure susceptibility in adult sesB9ed4/+ and seits1 mutant flies. Sleep deprivation also increased seizure susceptibility when sesB was disrupted using RNAi. The effect of sleep deprivation on seizure activity was reduced when sesB9ed4/+ flies were given the anti-seizure drug, valproic acid. In contrast to adult flies, sleep deprivation during early fly development resulted in chronic seizure susceptibility when sesB9ed4/+ became adults. Conclusions: These findings show that Drosophila is a model organism for investigating the relationship between sleep and seizure activity. Citation: Lucey BP, Leahy A, Rosas R, Shaw PJ. A new model to study sleep deprivation-induced seizure. SLEEP 2015;38(5):777–785. PMID:25515102

  15. The effects of rapid eye movement sleep deprivation during late pregnancy on newborns' sleep.

    PubMed

    Aswathy, B S; Kumar, Velayudhan M; Gulia, Kamalesh K

    2017-05-31

    Sleep deprivation during pregnancy is an emerging concern, as it can adversely affect the development of the offspring brain. This study was conducted to evaluate the effects of deprivation of rapid eye movement (REM) sleep during the third term of pregnancy on the sleep-wake profiles of neonates in the Wistar rat model. Sleep-wake patterns were assessed through electrophysiological measures and behavioural observations during postnatal days 1-21 on pups born to REM sleep-deprived dams and control rats. Pups of REM sleep-deprived dams had active sleep that was not only markedly higher in percentage during all the days studied, but also had reduced latency during later postnatal days 15-21. Quiet sleep and wake periods were lower. These factors, along with less frequent but longer sleep-wake cycles, indicated maturational delay in the sleep-wake neural networks. The disruption of time-bound growth of sleep-wake neural networks was substantiated further by the decreased slope of survival plots in the sleep bouts. Examination of altered sleep-wake patterns during early development may provide crucial information concerning deranged neural development in the offspring. This is the first report, to our knowledge, to show that maternal sleep deprivation during pregnancy can delay and impair the development of sleep-wake profile in the offspring. © 2017 European Sleep Research Society.

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

    PubMed

    Salin-Pascual, R J; Grandos-Fuentes, D; Galicia-Polo, L; Nieves, E; Roehrs, T A; Roth, T

    1992-06-01

    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.

  17. Cues of Fatigue: Effects of Sleep Deprivation on Facial Appearance

    PubMed Central

    Sundelin, Tina; Lekander, Mats; Kecklund, Göran; Van Someren, Eus J. W.; Olsson, Andreas; Axelsson, John

    2013-01-01

    Study Objective: To investigate the facial cues by which one recognizes that someone is sleep deprived versus not sleep deprived. Design: Experimental laboratory study. Setting: Karolinska Institutet, Stockholm, Sweden. Participants: Forty observers (20 women, mean age 25 ± 5 y) rated 20 facial photographs with respect to fatigue, 10 facial cues, and sadness. The stimulus material consisted of 10 individuals (five women) photographed at 14:30 after normal sleep and after 31 h of sleep deprivation following a night with 5 h of sleep. Measurements: Ratings of fatigue, fatigue-related cues, and sadness in facial photographs. Results: The faces of sleep deprived individuals were perceived as having more hanging eyelids, redder eyes, more swollen eyes, darker circles under the eyes, paler skin, more wrinkles/fine lines, and more droopy corners of the mouth (effects ranging from b = +3 ± 1 to b = +15 ± 1 mm on 100-mm visual analog scales, P < 0.01). The ratings of fatigue were related to glazed eyes and to all the cues affected by sleep deprivation (P < 0.01). Ratings of rash/eczema or tense lips were not significantly affected by sleep deprivation, nor associated with judgements of fatigue. In addition, sleep-deprived individuals looked sadder than after normal sleep, and sadness was related to looking fatigued (P < 0.01). Conclusions: The results show that sleep deprivation affects features relating to the eyes, mouth, and skin, and that these features function as cues of sleep loss to other people. Because these facial regions are important in the communication between humans, facial cues of sleep deprivation and fatigue may carry social consequences for the sleep deprived individual in everyday life. Citation: Sundelin T; Lekander M; Kecklund G; Van Someren EJW; Olsson A; Axelsson J. Cues of fatigue: effects of sleep deprivation on facial appearance. SLEEP 2013;36(9):1355-1360. PMID:23997369

  18. The prospective association between sleep deprivation and depression among adolescents.

    PubMed

    Roberts, Robert E; Duong, Hao T

    2014-02-01

    To examine the prospective, reciprocal association between sleep deprivation and depression among adolescents. A community-based two-wave cohort study. A metropolitan area with a population of over 4 million. 4,175 youths 11-17 at baseline, and 3,134 of these followed up a year later. Depression is measured using both symptoms of depression and DSM-IV major depression. Sleep deprivation is defined as ≤ 6 h of sleep per night. Sleep deprivation at baseline predicted both measures of depression at follow-up, controlling for depression at baseline. Examining the reciprocal association, major depression at baseline, but not symptoms predicted sleep deprivation at follow-up. These results are the first to document reciprocal effects for major depression and sleep deprivation among adolescents using prospective data. The data suggest reduced quantity of sleep increases risk for major depression, which in turn increases risk for decreased sleep.

  19. REM sleep phase preference in the crepuscular Octodon degus assessed by selective REM sleep deprivation.

    PubMed

    Ocampo-Garcés, Adrián; Hernández, Felipe; Palacios, Adrian G

    2013-08-01

    To determine rapid eye movement (REM) sleep phase preference in a crepuscular mammal (Octodon degus) by challenging the specific REM sleep homeostatic response during the diurnal and nocturnal anticrepuscular rest phases. We have investigated REM sleep rebound, recovery, and documented REM sleep propensity measures during and after diurnal and nocturnal selective REM sleep deprivations. Nine male wild-captured O. degus prepared for polysomnographic recordings. Animals were recorded during four consecutive baseline and two separate diurnal or nocturnal deprivation days, under a 12:12 light-dark schedule. Three-h selective REM sleep deprivations were performed, starting at midday (zeitgeber time 6) or midnight (zeitgeber time 18). Diurnal and nocturnal REM sleep deprivations provoked equivalent amounts of REM sleep debt, but a consistent REM sleep rebound was found only after nocturnal deprivation. The nocturnal rebound was characterized by a complete recovery of REM sleep associated with an augment in REM/total sleep time ratio and enhancement in REM sleep episode consolidation. Our results support the notion that the circadian system actively promotes REM sleep. We propose that the sleep-wake cycle of O. degus is modulated by a chorus of circadian oscillators with a bimodal crepuscular modulation of arousal and a unimodal promotion of nocturnal REM sleep

  20. Stress-free automatic sleep deprivation using air puffs

    PubMed Central

    Gross, Brooks A.; Vanderheyden, William M.; Urpa, Lea M.; Davis, Devon E.; Fitzpatrick, Christopher J.; Prabhu, Kaustubh; Poe, Gina R.

    2015-01-01

    Background Sleep deprivation via gentle handling is time-consuming and personnel-intensive. New Method We present here an automated sleep deprivation system via air puffs. Implanted EMG and EEG electrodes were used to assess sleep/waking states in six male Sprague-Dawley rats. Blood samples were collected from an implanted intravenous catheter every 4 hours during the 12-hour light cycle on baseline, 8 hours of sleep deprivation via air puffs, and 8 hours of sleep deprivation by gentle handling days. Results The automated system was capable of scoring sleep and waking states as accurately as our offline version (~90% for sleep) and with sufficient speed to trigger a feedback response within an acceptable amount of time (1.76 s). Manual state scoring confirmed normal sleep on the baseline day and sleep deprivation on the two manipulation days (68% decrease in non-REM, 63% decrease in REM, and 74% increase in waking). No significant differences in levels of ACTH and corticosterone (stress hormones indicative of HPA axis activity) were found at any time point between baseline sleep and sleep deprivation via air puffs. Comparison with Existing Method There were no significant differences in ACTH or corticosterone concentrations between sleep deprivation by air puffs and gentle handling over the 8-hour period. Conclusions Our system accurately detects sleep and delivers air puffs to acutely deprive rats of sleep with sufficient temporal resolution during the critical 4-5 h post learning sleep-dependent memory consolidation period. The system is stress-free and a viable alternative to existing sleep deprivation techniques. PMID:26014662

  1. Stress-free automatic sleep deprivation using air puffs.

    PubMed

    Gross, Brooks A; Vanderheyden, William M; Urpa, Lea M; Davis, Devon E; Fitzpatrick, Christopher J; Prabhu, Kaustubh; Poe, Gina R

    2015-08-15

    Sleep deprivation via gentle handling is time-consuming and personnel-intensive. We present here an automated sleep deprivation system via air puffs. Implanted EMG and EEG electrodes were used to assess sleep/waking states in six male Sprague-Dawley rats. Blood samples were collected from an implanted intravenous catheter every 4h during the 12-h light cycle on baseline, 8h of sleep deprivation via air puffs, and 8h of sleep deprivation by gentle handling days. The automated system was capable of scoring sleep and waking states as accurately as our offline version (∼90% for sleep) and with sufficient speed to trigger a feedback response within an acceptable amount of time (1.76s). Manual state scoring confirmed normal sleep on the baseline day and sleep deprivation on the two manipulation days (68% decrease in non-REM, 63% decrease in REM, and 74% increase in waking). No significant differences in levels of ACTH and corticosterone (stress hormones indicative of HPA axis activity) were found at any time point between baseline sleep and sleep deprivation via air puffs. There were no significant differences in ACTH or corticosterone concentrations between sleep deprivation by air puffs and gentle handling over the 8-h period. Our system accurately detects sleep and delivers air puffs to acutely deprive rats of sleep with sufficient temporal resolution during the critical 4-5h post learning sleep-dependent memory consolidation period. The system is stress-free and a viable alternative to existing sleep deprivation techniques. Copyright © 2015 Elsevier B.V. All rights reserved.

  2. Sleep Deprivation: A Cause of High Blood Pressure?

    MedlinePlus

    ... High blood pressure (hypertension) Is it true that sleep deprivation can cause high blood pressure? Answers from ... be linked to increased blood pressure. People who sleep five hours or less a night may be ...

  3. A new model to study sleep deprivation-induced seizure.

    PubMed

    Lucey, Brendan P; Leahy, Averi; Rosas, Regine; Shaw, Paul J

    2015-05-01

    A relationship between sleep and seizures is well-described in both humans and rodent animal models; however, the mechanism underlying this relationship is unknown. Using Drosophila melanogaster mutants with seizure phenotypes, we demonstrate that seizure activity can be modified by sleep deprivation. Seizure activity was evaluated in an adult bang-sensitive seizure mutant, stress sensitive B (sesB(9ed4)), and in an adult temperature sensitive seizure mutant seizure (sei(ts1)) under baseline and following 12 h of sleep deprivation. The long-term effect of sleep deprivation on young, immature sesB(9ed4) flies was also assessed. Laboratory. Drosophila melanogaster. Sleep deprivation. Sleep deprivation increased seizure susceptibility in adult sesB(9ed4)/+ and sei(ts1) mutant flies. Sleep deprivation also increased seizure susceptibility when sesB was disrupted using RNAi. The effect of sleep deprivation on seizure activity was reduced when sesB(9ed4)/+ flies were given the anti-seizure drug, valproic acid. In contrast to adult flies, sleep deprivation during early fly development resulted in chronic seizure susceptibility when sesB(9ed4)/+ became adults. These findings show that Drosophila is a model organism for investigating the relationship between sleep and seizure activity. © 2015 Associated Professional Sleep Societies, LLC.

  4. Sleep deprivation and the effect on exercise performance.

    PubMed

    VanHelder, T; Radomski, M W

    1989-04-01

    Sleep deprivation or partial sleep loss are common in work conditions as rotating shifts and prolonged work hours, in sustained military operations and in athletes competing in events after crossing several time zones or engaged in ultramarathon or triathlon events. Although it is well established that sleep loss has negative effects on mental performance, its effects on physical performance are equivocal. This review examines the latter question in light of recent studies published on this problem. Sleep deprivation of 30 to 72 hours does not affect cardiovascular and respiratory responses to exercise of varying intensity, or the aerobic and anaerobic performance capability of individuals. Muscle strength and electromechanical responses are also not affected. Time to exhaustion, however, is decreased by sleep deprivation. Although ratings of perceived exertion always increased during exercise in sleep-deprived (30 to 60 hours) subjects compared with normal sleep, this is not a reliable assessment of a subject's ability to perform physical work as the ratings of perceived exertion are dissociated from any cardiovascular changes in sleep deprivation. Examination of the various hormonal and metabolic parameters which have been measured in the studies reviewed reveals that the major metabolic perturbations accompanying sleep deprivation in humans are an increase in insulin resistance and a decrease in glucose tolerance. This may explain the reduction in observed time to exhaustion in sleep-deprived subjects. The role of growth hormone in mediating altered carbohydrate metabolism may be of particular relevance as to how sleep deprivation alters the supply of energy substrate to the muscle.

  5. Changes in the waking EEG as a consequence of sleep and sleep deprivation.

    PubMed

    Corsi-Cabrera, M; Ramos, J; Arce, C; Guevara, M A; Ponce-de León, M; Lorenzo, I

    1992-12-01

    Electroencephalographic (EEG) activity was monopolarly recorded during resting wakefulness in 10 volunteers under the following conditions: at night before going to sleep, at night before total sleep deprivation, in the morning after waking, in the morning after sleep deprivation and at night after having slept during the day. Absolute and relative power and inter- and intrahemispheric correlation were established. After diurnal and nocturnal sleep as compared to sleep deprivation, we obtained the following significant results: interhemispheric correlations were higher; intrahemispheric correlations were lower; absolute power of alpha 2, beta 1 and beta 2 was lower; and relative power of alpha 2 and beta 2 was lower. EEG changes as a consequence of sleep or lack of sleep are dependent on prior sleep and/or wakefulness and not on circadian phase. EEG activity during wakefulness is a sensitive parameter and a useful tool to assess the consequences of sleep on brain functional organization.

  6. Effect of normal sleep and sleep deprivation on interhemispheric correlation during subsequent wakefulness in man.

    PubMed

    Corsi-Cabrera, M; Ramos, J; Meneses, S

    1989-04-01

    EEG activity was recorded from the right and left central, temporal, parietal and occipital derivations in 10 volunteers under the following conditions: at night before going to sleep, at night before sleep deprivation, in the morning after waking, in the morning after sleep deprivation and in the morning 48 h after recovery. Interhemispheric correlation and relative power were calculated for EEG samples of 20.48 sec. In the morning after normal sleep interhemispheric correlations were higher in all derivations in comparison to presleep values, while in the morning after sleep deprivation, interhemispheric correlations were lower or similar to predeprivation values in all derivations except the temporal cortex. The relative power of beta was significantly lower after normal sleep and higher after sleep loss, while the relative power of low frequencies was higher in the morning after sleep and lower in the morning after deprivation.

  7. Cues of fatigue: effects of sleep deprivation on facial appearance.

    PubMed

    Sundelin, Tina; Lekander, Mats; Kecklund, Göran; Van Someren, Eus J W; Olsson, Andreas; Axelsson, John

    2013-09-01

    To investigate the facial cues by which one recognizes that someone is sleep deprived versus not sleep deprived. Experimental laboratory study. Karolinska Institutet, Stockholm, Sweden. Forty observers (20 women, mean age 25 ± 5 y) rated 20 facial photographs with respect to fatigue, 10 facial cues, and sadness. The stimulus material consisted of 10 individuals (five women) photographed at 14:30 after normal sleep and after 31 h of sleep deprivation following a night with 5 h of sleep. Ratings of fatigue, fatigue-related cues, and sadness in facial photographs. The faces of sleep deprived individuals were perceived as having more hanging eyelids, redder eyes, more swollen eyes, darker circles under the eyes, paler skin, more wrinkles/fine lines, and more droopy corners of the mouth (effects ranging from b = +3 ± 1 to b = +15 ± 1 mm on 100-mm visual analog scales, P < 0.01). The ratings of fatigue were related to glazed eyes and to all the cues affected by sleep deprivation (P < 0.01). Ratings of rash/eczema or tense lips were not significantly affected by sleep deprivation, nor associated with judgements of fatigue. In addition, sleep-deprived individuals looked sadder than after normal sleep, and sadness was related to looking fatigued (P < 0.01). The results show that sleep deprivation affects features relating to the eyes, mouth, and skin, and that these features function as cues of sleep loss to other people. Because these facial regions are important in the communication between humans, facial cues of sleep deprivation and fatigue may carry social consequences for the sleep deprived individual in everyday life.

  8. Sleep Deprivation Influences Circadian Gene Expression in the Lateral Habenula

    PubMed Central

    Gao, Yanxia

    2016-01-01

    Sleep is governed by homeostasis and the circadian clock. Clock genes play an important role in the generation and maintenance of circadian rhythms but are also involved in regulating sleep homeostasis. The lateral habenular nucleus (LHb) has been implicated in sleep-wake regulation, since LHb gene expression demonstrates circadian oscillation characteristics. This study focuses on the participation of LHb clock genes in regulating sleep homeostasis, as the nature of their involvement is unclear. In this study, we observed changes in sleep pattern following sleep deprivation in LHb-lesioned rats using EEG recording techniques. And then the changes of clock gene expression (Per1, Per2, and Bmal1) in the LHb after 6 hours of sleep deprivation were detected by using real-time quantitative PCR (qPCR). We found that sleep deprivation increased the length of Non-Rapid Eye Movement Sleep (NREMS) and decreased wakefulness. LHb-lesioning decreased the amplitude of reduced wake time and increased NREMS following sleep deprivation in rats. qPCR results demonstrated that Per2 expression was elevated after sleep deprivation, while the other two genes were unaffected. Following sleep recovery, Per2 expression was comparable to the control group. This study provides the basis for further research on the role of LHb Per2 gene in the regulation of sleep homeostasis. PMID:27413249

  9. Sleep Deprivation Influences Circadian Gene Expression in the Lateral Habenula.

    PubMed

    Zhang, Beilin; Gao, Yanxia; Li, Yang; Yang, Jing; Zhao, Hua

    2016-01-01

    Sleep is governed by homeostasis and the circadian clock. Clock genes play an important role in the generation and maintenance of circadian rhythms but are also involved in regulating sleep homeostasis. The lateral habenular nucleus (LHb) has been implicated in sleep-wake regulation, since LHb gene expression demonstrates circadian oscillation characteristics. This study focuses on the participation of LHb clock genes in regulating sleep homeostasis, as the nature of their involvement is unclear. In this study, we observed changes in sleep pattern following sleep deprivation in LHb-lesioned rats using EEG recording techniques. And then the changes of clock gene expression (Per1, Per2, and Bmal1) in the LHb after 6 hours of sleep deprivation were detected by using real-time quantitative PCR (qPCR). We found that sleep deprivation increased the length of Non-Rapid Eye Movement Sleep (NREMS) and decreased wakefulness. LHb-lesioning decreased the amplitude of reduced wake time and increased NREMS following sleep deprivation in rats. qPCR results demonstrated that Per2 expression was elevated after sleep deprivation, while the other two genes were unaffected. Following sleep recovery, Per2 expression was comparable to the control group. This study provides the basis for further research on the role of LHb Per2 gene in the regulation of sleep homeostasis.

  10. Sleep deprivation affects extinction but not acquisition memory in honeybees.

    PubMed

    Hussaini, Syed Abid; Bogusch, Lisa; Landgraf, Tim; Menzel, Randolf

    2009-11-01

    Sleep-like behavior has been studied in honeybees before, but the relationship between sleep and memory formation has not been explored. Here we describe a new approach to address the question if sleep in bees, like in other animals, improves memory consolidation. Restrained bees were observed by a web camera, and their antennal activities were used as indicators of sleep. We found that the bees sleep more during the dark phase of the day compared with the light phase. Sleep phases were characterized by two distinct patterns of antennal activities: symmetrical activity, more prominent during the dark phase; and asymmetrical activity, more common during the light phase. Sleep-deprived bees showed rebound the following day, confirming effective deprivation of sleep. After appetitive conditioning of the bees to various olfactory stimuli, we observed their sleep. Bees conditioned to odor with sugar reward showed lesser sleep compared with bees that were exposed to either reward alone or air alone. Next, we asked whether sleep deprivation affects memory consolidation. While sleep deprivation had no effect on retention scores after odor acquisition, retention for extinction learning was significantly reduced, indicating that consolidation of extinction memory but not acquisition memory was affected by sleep deprivation.

  11. Augmented Reality as a Countermeasure for Sleep Deprivation.

    PubMed

    Baumeister, James; Dorrlan, Jillian; Banks, Siobhan; Chatburn, Alex; Smith, Ross T; Carskadon, Mary A; Lushington, Kurt; Thomas, Bruce H

    2016-04-01

    Sleep deprivation is known to have serious deleterious effects on executive functioning and job performance. Augmented reality has an ability to place pertinent information at the fore, guiding visual focus and reducing instructional complexity. This paper presents a study to explore how spatial augmented reality instructions impact procedural task performance on sleep deprived users. The user study was conducted to examine performance on a procedural task at six time points over the course of a night of total sleep deprivation. Tasks were provided either by spatial augmented reality-based projections or on an adjacent monitor. The results indicate that participant errors significantly increased with the monitor condition when sleep deprived. The augmented reality condition exhibited a positive influence with participant errors and completion time having no significant increase when sleep deprived. The results of our study show that spatial augmented reality is an effective sleep deprivation countermeasure under laboratory conditions.

  12. REM Sleep Phase Preference in the Crepuscular Octodon degus Assessed by Selective REM Sleep Deprivation

    PubMed Central

    Ocampo-Garcés, Adrián; Hernández, Felipe; Palacios, Adrian G.

    2013-01-01

    Study Objectives: To determine rapid eye movement (REM) sleep phase preference in a crepuscular mammal (Octodon degus) by challenging the specific REM sleep homeostatic response during the diurnal and nocturnal anticrepuscular rest phases. Design: We have investigated REM sleep rebound, recovery, and documented REM sleep propensity measures during and after diurnal and nocturnal selective REM sleep deprivations. Subjects: Nine male wild-captured O. degus prepared for polysomnographic recordings Interventions: Animals were recorded during four consecutive baseline and two separate diurnal or nocturnal deprivation days, under a 12:12 light-dark schedule. Three-h selective REM sleep deprivations were performed, starting at midday (zeitgeber time 6) or midnight (zeitgeber time 18). Measurements and Results: Diurnal and nocturnal REM sleep deprivations provoked equivalent amounts of REM sleep debt, but a consistent REM sleep rebound was found only after nocturnal deprivation. The nocturnal rebound was characterized by a complete recovery of REM sleep associated with an augment in REM/total sleep time ratio and enhancement in REM sleep episode consolidation. Conclusions: Our results support the notion that the circadian system actively promotes REM sleep. We propose that the sleep-wake cycle of O. degus is modulated by a chorus of circadian oscillators with a bimodal crepuscular modulation of arousal and a unimodal promotion of nocturnal REM sleep. Citation: Ocampo-Garcés A; Hernández F; Palacios AG. REM sleep phase preference in the crepuscular Octodon degus assessed by selective REM sleep deprivation. SLEEP 2013;36(8):1247-1256. PMID:23904685

  13. Sleep deprived and sweating it out: the effects of total sleep deprivation on skin conductance reactivity to psychosocial stress.

    PubMed

    Liu, Jean C J; Verhulst, Silvan; Massar, Stijn A A; Chee, Michael W L

    2015-01-01

    We examined how sleep deprivation alters physiological responses to psychosocial stress by evaluating changes in skin conductance. Between-subjects design with one group allocated to 24 h of total sleep deprivation and the other to rested wakefulness. The study took place in a research laboratory. Participants were 40 healthy young adults recruited from a university. Sleep deprivation and feedback. Electrodermal activity was monitored while participants completed a difficult perceptual task with false feedback. All participants showed increased skin conductance levels following stress. However, compared to well-rested participants, sleep deprived participants showed higher skin conductance reactivity with increasing stress levels. Our results suggest that sleep deprivation augments allostatic responses to increasing psychosocial stress. Consequentially, we propose sleep loss as a risk factor that can influence the pathogenic effects of stress. © 2014 Associated Professional Sleep Societies, LLC.

  14. Sleep Deprivation Selectively Impairs Memory Consolidation for Contextual Fear Conditioning

    PubMed Central

    Graves, Laurel A.; Heller, Elizabeth A.; Pack, Allan I.; Abel, Ted

    2003-01-01

    Many behavioral and electrophysiological studies in animals and humans have suggested that sleep and circadian rhythms influence memory consolidation. In rodents, hippocampus-dependent memory may be particularly sensitive to sleep deprivation after training, as spatial memory in the Morris water maze is impaired by rapid eye movement sleep deprivation following training. Spatial learning in the Morris water maze, however, requires multiple training trials and performance, as measured by time to reach the hidden platform is influenced by not only spatial learning but also procedural learning. To determine if sleep is important for the consolidation of a single-trial, hippocampus-dependent task, we sleep deprived animals for 0–5 and 5–10 h after training for contextual and cued fear conditioning. We found that sleep deprivation from 0–5 h after training for this task impaired memory consolidation for contextual fear conditioning whereas sleep deprivation from 5–10 h after training had no effect. Sleep deprivation at either time point had no effect on cued fear conditioning, a hippocampus-independent task. Previous studies have determined that memory consolidation for fear conditioning is impaired when protein kinase A and protein synthesis inhibitors are administered at the same time as when sleep deprivation is effective, suggesting that sleep deprivation may act by modifying these molecular mechanisms of memory storage. PMID:12773581

  15. Sleep deprivation in pigeons and rats using motion detection.

    PubMed

    Newman, Sarah M; Paletz, Elliott M; Obermeyer, William H; Benca, Ruth M

    2009-10-01

    Forced sleep deprivation results in substantial behavioral and physiologic effects in mammals. The disk-over-water (DOW) method produces a syndrome characterized by increased energy expenditure and a robust preferentially rapid-eye-movement sleep rebound upon recovery or eventual death after several weeks of sleep deprivation. The DOW has been used successfully only in rats. This paper presents a method to enforce long-term controlled sleep deprivation across species and to compare its effects in rats and pigeons. A conveyor was substituted for the DOW disk. Behavior rather than electroencephalography was used to trigger arousal stimuli, as in gentle-handling deprivation. Rats and pigeons were deprived using this apparatus, and the results were compared with each other and with published reports. The physiologic consequences and recovery sleep in rats were like those published for DOW rats. Magnitude of sleep loss and recovery patterns in pigeons were similar to those seen in rats, but expected symptoms of the sleep deprivation syndrome were absent in pigeons. The use of a motion trigger allowed us to measure and, thus, to assess the quality and impact of the procedure. Prolonged and controlled sleep deprivation can be enforced using automated motion detection and a conveyor-over-water system. Pigeons and rats, deprived of sleep to the same extent, showed similar patterns of recovery sleep, but pigeons did not exhibit the hyperphagia, weight loss, and debilitation seen in rats.

  16. The Effects of Total Sleep Deprivation and Recovery Sleep on Cognitive Performance and Brain Function

    DTIC Science & Technology

    2004-08-01

    bedsharing infants and mothers. Sleep . 1996, 19(9):685-90. 4) Mosko, S., Richard, C., McKenna, J., Drummond, S. Infant sleep architecture during bedsharing...Dyche, J., Coard, B., & Drummond, S. P. A. Actigraphy in Ambulatory Sleep -Wake Measurement. Paper presented at the 1 st annual Fleet Review at Naval...AD Award Number: DAMD17-02-1-0201 TITLE: The Effects of Total Sleep Deprivation and Recovery Sleep on Cognitive Performance and Brain Function

  17. Beauty sleep: experimental study on the perceived health and attractiveness of sleep deprived people.

    PubMed

    Axelsson, John; Sundelin, Tina; Ingre, Michael; Van Someren, Eus J W; Olsson, Andreas; Lekander, Mats

    2010-12-14

    To investigate whether sleep deprived people are perceived as less healthy, less attractive, and more tired than after a normal night's sleep. Experimental study. Sleep laboratory in Stockholm, Sweden. 23 healthy, sleep deprived adults (age 18-31) who were photographed and 65 untrained observers (age 18-61) who rated the photographs. Participants were photographed after a normal night's sleep (eight hours) and after sleep deprivation (31 hours of wakefulness after a night of reduced sleep). The photographs were presented in a randomised order and rated by untrained observers. Difference in observer ratings of perceived health, attractiveness, and tiredness between sleep deprived and well rested participants using a visual analogue scale (100 mm). Sleep deprived people were rated as less healthy (visual analogue scale scores, mean 63 (SE 2) v 68 (SE 2), P<0.001), more tired (53 (SE 3) v 44 (SE 3), P<0.001), and less attractive (38 (SE 2) v 40 (SE 2), P<0.001) than after a normal night's sleep. The decrease in rated health was associated with ratings of increased tiredness and decreased attractiveness. Our findings show that sleep deprived people appear less healthy, less attractive, and more tired compared with when they are well rested. This suggests that humans are sensitive to sleep related facial cues, with potential implications for social and clinical judgments and behaviour. Studies are warranted for understanding how these effects may affect clinical decision making and can add knowledge with direct implications in a medical context.

  18. Functional connectivity during rested wakefulness predicts vulnerability to sleep deprivation.

    PubMed

    Yeo, B T Thomas; Tandi, Jesisca; Chee, Michael W L

    2015-05-01

    Significant inter-individual differences in vigilance decline following sleep deprivation exist. We characterized functional connectivity in 68 healthy young adult participants in rested wakefulness and following a night of total sleep deprivation. After whole brain signal regression, functionally connected cortical networks during the well-rested state exhibited reduced correlation following sleep deprivation, suggesting that highly integrated brain regions become less integrated during sleep deprivation. In contrast, anti-correlations in the well-rested state became less so following sleep deprivation, suggesting that highly segregated networks become less segregated during sleep deprivation. Subjects more resilient to vigilance decline following sleep deprivation showed stronger anti-correlations among several networks. The weaker anti-correlations overlapped with connectivity alterations following sleep deprivation. Resilient individuals thus evidence clearer separation of highly segregated cortical networks in the well-rested state. In contrast to corticocortical connectivity, subcortical-cortical connectivity was comparable across resilient and vulnerable groups despite prominent state-related changes in both groups. Because sleep deprivation results in a significant elevation of whole brain signal amplitude, the aforesaid signal changes and group contrasts may be masked in analyses omitting their regression, suggesting possible value in regressing whole brain signal in certain experimental contexts.

  19. Effects of Sleep Deprivation on Dissociated Components of Executive Functioning

    PubMed Central

    Tucker, Adrienne M.; Whitney, Paul; Belenky, Gregory; Hinson, John M.; Van Dongen, Hans P.A.

    2010-01-01

    Study Objectives: We studied the effects of sleep deprivation on executive functions using a task battery which included a modified Sternberg task, a probed recall task, and a phonemic verbal fluency task. These tasks were selected because they allow dissociation of some important executive processes from non-executive components of cognition. Design: Subjects were randomized to a total sleep deprivation condition or a control condition. Performance on the executive functions task battery was assessed at baseline, after 51 h of total sleep deprivation (or no sleep deprivation in the control group), and following 2 nights of recovery sleep, at fixed time of day (11:00). Performance was also measured repeatedly throughout the experiment on a control task battery, for which the effects of total sleep deprivation had been documented in previously published studies. Setting: Six consecutive days and nights in a controlled laboratory environment with continuous behavioral monitoring. Participants: Twenty-three healthy adults (age range 22–38 y; 11 women). Twelve subjects were randomized to the sleep deprivation condition; the others were controls. Results: Performance on the control task battery was considerably degraded during sleep deprivation. Overall performance on the modified Sternberg task also showed impairment during sleep deprivation, as compared to baseline and recovery and compared to controls. However, two dissociated components of executive functioning on this task—working memory scanning efficiency and resistance to proactive interference—were maintained at levels equivalent to baseline. On the probed recall task, resistance to proactive interference was also preserved. Executive aspects of performance on the phonemic verbal fluency task showed improvement during sleep deprivation, as did overall performance on this task. Conclusion: Sleep deprivation affected distinct components of cognitive processing differentially. Dissociated non

  20. Sleep Deprivation of Rats: The Hyperphagic Response Is Real

    PubMed Central

    Koban, Michael; Sita, Luciane V.; Le, Wei Wei; Hoffman, Gloria E.

    2008-01-01

    Study Objectives: Chronic sleep deprivation of rats causes hyperphagia without body weight gain. Sleep deprivation hyperphagia is prompted by changes in pathways governing food intake; hyperphagia may be adaptive to sleep deprivation hypermetabolism. A recent paper suggested that sleep deprivation might inhibit ability of rats to increase food intake and that hyperphagia may be an artifact of uncorrected chow spillage. To resolve this, a palatable liquid diet (Ensure) was used where spillage is insignificant. Design: Sleep deprivation of male Sprague Dawley rats was enforced for 10 days by the flowerpot/platform paradigm. Daily food intake and body weight were measured. On day 10, rats were transcardially perfused for analysis of hypothalamic mRNA expression of the orexigen, neuropeptide Y (NPY). Setting: Morgan State University, sleep deprivation and transcardial perfusion; University of Maryland, NPY in situ hybridization and analysis. Measurements and Results: Using a liquid diet for accurate daily measurements, there was no change in food intake in the first 5 days of sleep deprivation. Importantly, from days 6–10 it increased significantly, peaking at 29% above baseline. Control rats steadily gained weight but sleep-deprived rats did not. Hypothalamic NPY mRNA levels were positively correlated to stimulation of food intake and negatively correlated with changes in body weight. Conclusion: Sleep deprivation hyperphagia may not be apparent over the short term (i.e., ≤5 days), but when extended beyond 6 days, it is readily observed. The timing of changes in body weight and food intake suggests that the negative energy balance induced by sleep deprivation prompts the neural changes that evoke hyperphagia. Citation: Koban M; Sita LV; Le WW; Hoffman GE. Sleep deprivation of rats: the hyperphagic response is real. SLEEP 2008;31(7):927-933. PMID:18652088

  1. Selective REM Sleep Deprivation Improves Expectation-Related Placebo Analgesia

    PubMed Central

    Chouchou, Florian; Chauny, Jean-Marc; Rainville, Pierre; Lavigne, Gilles J.

    2015-01-01

    The placebo effect is a neurobiological and psychophysiological process known to influence perceived pain relief. Optimization of placebo analgesia may contribute to the clinical efficacy and effectiveness of medication for acute and chronic pain management. We know that the placebo effect operates through two main mechanisms, expectations and learning, which is also influenced by sleep. Moreover, a recent study suggested that rapid eye movement (REM) sleep is associated with modulation of expectation-mediated placebo analgesia. We examined placebo analgesia following pharmacological REM sleep deprivation and we tested the hypothesis that relief expectations and placebo analgesia would be improved by experimental REM sleep deprivation in healthy volunteers. Following an adaptive night in a sleep laboratory, 26 healthy volunteers underwent classical experimental placebo analgesic conditioning in the evening combined with pharmacological REM sleep deprivation (clonidine: 13 volunteers or inert control pill: 13 volunteers). Medication was administered in a double-blind manner at bedtime, and placebo analgesia was tested in the morning. Results revealed that 1) placebo analgesia improved with REM sleep deprivation; 2) pain relief expectations did not differ between REM sleep deprivation and control groups; and 3) REM sleep moderated the relationship between pain relief expectations and placebo analgesia. These results support the putative role of REM sleep in modulating placebo analgesia. The mechanisms involved in these improvements in placebo analgesia and pain relief following selective REM sleep deprivation should be further investigated. PMID:26678391

  2. Selective REM Sleep Deprivation Improves Expectation-Related Placebo Analgesia.

    PubMed

    Chouchou, Florian; Chauny, Jean-Marc; Rainville, Pierre; Lavigne, Gilles J

    2015-01-01

    The placebo effect is a neurobiological and psychophysiological process known to influence perceived pain relief. Optimization of placebo analgesia may contribute to the clinical efficacy and effectiveness of medication for acute and chronic pain management. We know that the placebo effect operates through two main mechanisms, expectations and learning, which is also influenced by sleep. Moreover, a recent study suggested that rapid eye movement (REM) sleep is associated with modulation of expectation-mediated placebo analgesia. We examined placebo analgesia following pharmacological REM sleep deprivation and we tested the hypothesis that relief expectations and placebo analgesia would be improved by experimental REM sleep deprivation in healthy volunteers. Following an adaptive night in a sleep laboratory, 26 healthy volunteers underwent classical experimental placebo analgesic conditioning in the evening combined with pharmacological REM sleep deprivation (clonidine: 13 volunteers or inert control pill: 13 volunteers). Medication was administered in a double-blind manner at bedtime, and placebo analgesia was tested in the morning. Results revealed that 1) placebo analgesia improved with REM sleep deprivation; 2) pain relief expectations did not differ between REM sleep deprivation and control groups; and 3) REM sleep moderated the relationship between pain relief expectations and placebo analgesia. These results support the putative role of REM sleep in modulating placebo analgesia. The mechanisms involved in these improvements in placebo analgesia and pain relief following selective REM sleep deprivation should be further investigated.

  3. Sleep Deprivation Impairs the Accurate Recognition of Human Emotions

    PubMed Central

    van der Helm, Els; Gujar, Ninad; Walker, Matthew P.

    2010-01-01

    Study Objectives: Investigate the impact of sleep deprivation on the ability to recognize the intensity of human facial emotions. Design: Randomized total sleep-deprivation or sleep-rested conditions, involving between-group and within-group repeated measures analysis. Setting: Experimental laboratory study. Participants: Thirty-seven healthy participants, (21 females) aged 18–25 y, were randomly assigned to the sleep control (SC: n = 17) or total sleep deprivation group (TSD: n = 20). Interventions: Participants performed an emotional face recognition task, in which they evaluated 3 different affective face categories: Sad, Happy, and Angry, each ranging in a gradient from neutral to increasingly emotional. In the TSD group, the task was performed once under conditions of sleep deprivation, and twice under sleep-rested conditions following different durations of sleep recovery. In the SC group, the task was performed twice under sleep-rested conditions, controlling for repeatability. Measurements and Results: In the TSD group, when sleep-deprived, there was a marked and significant blunting in the recognition of Angry and Happy affective expressions in the moderate (but not extreme) emotional intensity range; differences that were most reliable and significant in female participants. No change in the recognition of Sad expressions was observed. These recognition deficits were, however, ameliorated following one night of recovery sleep. No changes in task performance were observed in the SC group. Conclusions: Sleep deprivation selectively impairs the accurate judgment of human facial emotions, especially threat relevant (Anger) and reward relevant (Happy) categories, an effect observed most significantly in females. Such findings suggest that sleep loss impairs discrete affective neural systems, disrupting the identification of salient affective social cues. Citation: van der Helm E; Gujar N; Walker MP. Sleep deprivation impairs the accurate recognition of human

  4. Emotional expressiveness in sleep-deprived healthy adults.

    PubMed

    Minkel, Jared; Htaik, Oo; Banks, Siobhan; Dinges, David

    2011-01-01

    The purpose of this study was to evaluate the influence of sleep deprivation on emotional expression and subjective emotional experience in a highly controlled, laboratory setting. Twenty-three healthy adult participants watched positive (amusing) and negative (sad) film clips before and after they were randomly assigned to a night of sleep deprivation or a normal sleep control condition. The intensity of their facial expressiveness while viewing the films was coded by human judges and compared to their subjective emotional responses. Relative to the control group, sleep-deprived participants demonstrated less expressiveness, especially in response to positive stimuli. Subjective responses were not significantly different between the sleep-deprived and control groups. These preliminary results suggest that sleep deprivation is associated with attenuated emotional expressiveness in healthy adults.

  5. Effects of Sleep Deprivation on Brain Bioenergetics, Sleep, and Cognitive Performance in Cocaine-Dependent Individuals

    PubMed Central

    Trksak, George H.; Bracken, Bethany K.; Jensen, J. Eric; Plante, David T.; Penetar, David M.; Tartarini, Wendy L.; Maywalt, Melissa A.; Dorsey, Cynthia M.; Renshaw, Perry F.; Lukas, Scott E.

    2013-01-01

    In cocaine-dependent individuals, sleep is disturbed during cocaine use and abstinence, highlighting the importance of examining the behavioral and homeostatic response to acute sleep loss in these individuals. The current study was designed to identify a differential effect of sleep deprivation on brain bioenergetics, cognitive performance, and sleep between cocaine-dependent and healthy control participants. 14 healthy control and 8 cocaine-dependent participants experienced consecutive nights of baseline, total sleep deprivation, and recovery sleep in the research laboratory. Participants underwent [31]P magnetic resonance spectroscopy (MRS) brain imaging, polysomnography, Continuous Performance Task, and Digit Symbol Substitution Task. Following recovery sleep, [31]P MRS scans revealed that cocaine-dependent participants exhibited elevated global brain β-NTP (direct measure of adenosine triphosphate), α-NTP, and total NTP levels compared to those of healthy controls. Cocaine-dependent participants performed worse on the Continuous Performance Task and Digit Symbol Substitution Task at baseline compared to healthy control participants, but sleep deprivation did not worsen cognitive performance in either group. Enhancements of brain ATP levels in cocaine dependent participants following recovery sleep may reflect a greater impact of sleep deprivation on sleep homeostasis, which may highlight the importance of monitoring sleep during abstinence and the potential influence of sleep loss in drug relapse. PMID:24250276

  6. Effects of sleep deprivation on brain bioenergetics, sleep, and cognitive performance in cocaine-dependent individuals.

    PubMed

    Trksak, George H; Bracken, Bethany K; Jensen, J Eric; Plante, David T; Penetar, David M; Tartarini, Wendy L; Maywalt, Melissa A; Dorsey, Cynthia M; Renshaw, Perry F; Lukas, Scott E

    2013-01-01

    In cocaine-dependent individuals, sleep is disturbed during cocaine use and abstinence, highlighting the importance of examining the behavioral and homeostatic response to acute sleep loss in these individuals. The current study was designed to identify a differential effect of sleep deprivation on brain bioenergetics, cognitive performance, and sleep between cocaine-dependent and healthy control participants. 14 healthy control and 8 cocaine-dependent participants experienced consecutive nights of baseline, total sleep deprivation, and recovery sleep in the research laboratory. Participants underwent ³¹P magnetic resonance spectroscopy (MRS) brain imaging, polysomnography, Continuous Performance Task, and Digit Symbol Substitution Task. Following recovery sleep, ³¹P MRS scans revealed that cocaine-dependent participants exhibited elevated global brain β-NTP (direct measure of adenosine triphosphate), α-NTP, and total NTP levels compared to those of healthy controls. Cocaine-dependent participants performed worse on the Continuous Performance Task and Digit Symbol Substitution Task at baseline compared to healthy control participants, but sleep deprivation did not worsen cognitive performance in either group. Enhancements of brain ATP levels in cocaine dependent participants following recovery sleep may reflect a greater impact of sleep deprivation on sleep homeostasis, which may highlight the importance of monitoring sleep during abstinence and the potential influence of sleep loss in drug relapse.

  7. Effects of acute and chronic sleep deprivation on cardiovascular regulation.

    PubMed

    Tobaldini, E; Pecis, M; Montano, N

    2014-01-01

    Sleep is a fundamental physiological process, characterized by the activation of several cortical and subcortical neural networks. The relation between sleep and cardiovascular system is complex and bidirectional: sleep disorders may alter cardiovascular system, leading to an increased cardiovascular risk, while, on the contrary, cardio- vascular diseases are characterized by an alteration of physiological sleep. Autonomic nervous system (ANS) plays a key role in the regulation of cardiovascular functions during different sleep stages, with sympatho-vagal balance dynamically shifting towards sympathetic or vagal predominance across different sleep stages. Sleep deprivation (SD) has becoming one of the most relevant health problem in modern societies. SD can be related to aging, which is associated with increased sleep fragmentation, and to sleep disorders, such as sleep disordered breathing and neurological disorders. Experimental studies in animals showed that SD significantly affects cardiovascular functions, altering heart rate and blood pressure responses, and increasing sympathetic activity and neuroendocrine response to stressor stimuli. Clinical studies in humans have shown that SD, either due to experimental sleep loss and to sleep disorders, can affect different biological pathways, such as cardiovascular autonomic control, inflammation, immunity responses and metabolism. All these alterations may predispose subjects with SD to an increased cardiovascular risk. Hence, it is fundamental to identify the presence of a sleep disorder, which could be per se responsible for sleep loss, or the presence of sleep deprivation due to other factors, such as social life, habits etc., in order to identify subjects at high risk for cardiovascular events.

  8. Increased voluntary alcohol drinking concurrent with REM-sleep deprivation.

    PubMed

    Aalto, J; Kiianmaa, K

    1984-01-01

    The alcohol intake of twenty adult Long-Evans male rats was recorded before, during and after rapid eye movement sleep (REM) deprivation produced with the flowerpot technique modified by using a cuff pedestal and an electrified grid floor instead of water. The alcohol intake reached a steady level of 2.8 g/kg/day in the 3 weeks before REM deprivation. During seven REM-sleep deprivation days the alcohol intake was significantly elevated, finally increasing to 3.7 g/kg/day. A rebound decrease in alcohol drinking was then observed during the "REM-rebound" phase immediately after the termination of REM-sleep deprivation. The results suggest a possible vicious circle of REM-sleep deprivation increasing alcohol drinking and alcohol intake causing REM-sleep deprivation.

  9. Effect of sleep deprivation on the human metabolome.

    PubMed

    Davies, Sarah K; Ang, Joo Ern; Revell, Victoria L; Holmes, Ben; Mann, Anuska; Robertson, Francesca P; Cui, Nanyi; Middleton, Benita; Ackermann, Katrin; Kayser, Manfred; Thumser, Alfred E; Raynaud, Florence I; Skene, Debra J

    2014-07-22

    Sleep restriction and circadian clock disruption are associated with metabolic disorders such as obesity, insulin resistance, and diabetes. The metabolic pathways involved in human sleep, however, have yet to be investigated with the use of a metabolomics approach. Here we have used untargeted and targeted liquid chromatography (LC)/MS metabolomics to examine the effect of acute sleep deprivation on plasma metabolite rhythms. Twelve healthy young male subjects remained in controlled laboratory conditions with respect to environmental light, sleep, meals, and posture during a 24-h wake/sleep cycle, followed by 24 h of wakefulness. Two-hourly plasma samples collected over the 48 h period were analyzed by LC/MS. Principal component analysis revealed a clear time of day variation with a significant cosine fit during the wake/sleep cycle and during 24 h of wakefulness in untargeted and targeted analysis. Of 171 metabolites quantified, daily rhythms were observed in the majority (n = 109), with 78 of these maintaining their rhythmicity during 24 h of wakefulness, most with reduced amplitude (n = 66). During sleep deprivation, 27 metabolites (tryptophan, serotonin, taurine, 8 acylcarnitines, 13 glycerophospholipids, and 3 sphingolipids) exhibited significantly increased levels compared with during sleep. The increased levels of serotonin, tryptophan, and taurine may explain the antidepressive effect of acute sleep deprivation and deserve further study. This report, to our knowledge the first of metabolic profiling during sleep and sleep deprivation and characterization of 24 h rhythms under these conditions, offers a novel view of human sleep/wake regulation.

  10. The Prospective Association between Sleep Deprivation and Depression among Adolescents

    PubMed Central

    Roberts, Robert E.; Duong, Hao T.

    2014-01-01

    Study Objectives: To examine the prospective, reciprocal association between sleep deprivation and depression among adolescents. Design: A community-based two-wave cohort study. Setting: A metropolitan area with a population of over 4 million. Participants: 4,175 youths 11-17 at baseline, and 3,134 of these followed up a year later. Measurements: Depression is measured using both symptoms of depression and DSM-IV major depression. Sleep deprivation is defined as ≤ 6 h of sleep per night. Results: Sleep deprivation at baseline predicted both measures of depression at follow-up, controlling for depression at baseline. Examining the reciprocal association, major depression at baseline, but not symptoms predicted sleep deprivation at follow-up. Conclusion: These results are the first to document reciprocal effects for major depression and sleep deprivation among adolescents using prospective data. The data suggest reduced quantity of sleep increases risk for major depression, which in turn increases risk for decreased sleep. Citation: Roberts RE; Duong HT. The prospective association between sleep deprivation and depression among adolescents. SLEEP 2014;37(2):239-244. PMID:24497652

  11. Sleep Deprivation in Pigeons and Rats Using Motion Detection

    PubMed Central

    Newman, Sarah M.; Paletz, Elliott M.; Obermeyer, William H.; Benca, Ruth M.

    2009-01-01

    Study Objectives: Forced sleep deprivation results in substantial behavioral and physiologic effects in mammals. The disk-over-water (DOW) method produces a syndrome characterized by increased energy expenditure and a robust preferentially rapid-eye-movement sleep rebound upon recovery or eventual death after several weeks of sleep deprivation. The DOW has been used successfully only in rats. This paper presents a method to enforce long-term controlled sleep deprivation across species and to compare its effects in rats and pigeons. Design and Intervention: A conveyor was substituted for the DOW disk. Behavior rather than electroencephalography was used to trigger arousal stimuli, as in gentle-handling deprivation. Rats and pigeons were deprived using this apparatus, and the were compared with each other and with published reports. Measurements and Results: The physiologic consequences and recovery sleep in rats were like those published for DOW rats. Magnitude of sleep loss and recovery patterns in pigeons were similar to those seen in rats, but expected symptoms of the sleep deprivation syndrome were absent in pigeons. The use of a motion trigger allowed us to measure and, thus, to assess the quality and impact of the procedure. Conclusion: Prolonged and controlled sleep deprivation can be enforced using automated motion detection and a conveyor-over-water system. Pigeons and rats, deprived of sleep to the same extent, showed similar patterns of recovery sleep, but pigeons did not exhibit the hyperphagia, weight loss, and debilitation seen in rats. Citation: Newman SM; Paletz EM; Obermeyer WH; Benca RM. Sleep Deprivation In Pigeons And Rats Using Motion Detection. SLEEP 2009;32(10):1299-1312. PMID:19848359

  12. Spatial reversal learning is robust to total sleep deprivation.

    PubMed

    Leenaars, Cathalijn H C; Joosten, Ruud N J M A; Kramer, Michiel; Post, Ger; Eggels, Leslie; Wuite, Mark; Dematteis, Maurice; Feenstra, Matthijs G P; Van Someren, Eus J W

    2012-04-21

    Sleep deprivation affects cognitive functions that depend on the prefrontal cortex (PFC) such as cognitive flexibility, and the consolidation of newly learned information. The identification of cognitive processes that are either robustly sensitive or robustly insensitive to the same experimental sleep deprivation procedure, will allow us to better focus on the specific effects of sleep on cognition, and increase understanding of the mechanisms involved. In the present study we investigate whether sleep deprivation differentially affects the two separate cognitive processes of acquisition and consolidation of a spatial reversal task. After training on a spatial discrimination between two levers in a Skinner box, male Wistar rats were exposed to a reversal of the previously learned stimulus-response contingency. We first evaluated the effect of sleep deprivation on the acquisition of reversal learning. Performance on reversal learning after 12h of sleep deprivation (n=12) was compared to performance after control conditions (n=12). The second experiment evaluated the effect of sleep deprivation on the consolidation of reversal learning; the first session of reversal learning was followed by 3h of nap prevention (n=8) or undisturbed control conditions (n=8). The experiments had sufficient statistical power (0.90 and 0.81, respectively) to detect differences with medium effect sizes. Neither the acquisition, nor the consolidation, of reversal learning was affected by acute sleep deprivation. Together with previous findings, these results help to further delineate the role of sleep in cognitive processing.

  13. Sleep deprivation and sleep recovery modifies connexin36 and connexin43 protein levels in rat brain.

    PubMed

    Franco-Pérez, Javier; Ballesteros-Zebadúa, Paola; Fernández-Figueroa, Edith A; Ruiz-Olmedo, Isabel; Reyes-Grajeda, Pablo; Paz, Carlos

    2012-01-25

    Gap junctional communication is mainly mediated by connexin36 and connexin43 in neurons and astrocytes, respectively. It has been suggested that connexin36 allows electrical coupling between neurons whereas connexin43 participates in several process including release of ATP. It was recently reported that blockage of gap junctional communication mediated by connexin36 can disrupt the sleep architecture of the rat. However, there is no experimental approach about effects of sleep deprivation on connexins expression. Therefore, we examined in adult male Wistar rats whether protein levels of connexin36 and connexin43 change in pons, hypothalamus, and frontal cortex after 24 h of total sleep deprivation and 4 h of sleep recovery. Western blot revealed that total sleep deprivation significantly decreases the levels of connexin36 in the hypothalamus and this decrease maintains after sleep recovery. Meanwhile, connexin43 is not altered by total sleep deprivation but interestingly the sleep recovery period induces an increase of this connexin. These results suggest that electrical coupling between hypothalamic neurons could be altered by sleep deprivation and that sleep recovery drives changes in connexin43 expression probably as a mechanism related to ATP release and energy regulation during sleep.

  14. Sleep mechanisms: Sleep deprivation and detection of changing levels of consciousness

    NASA Technical Reports Server (NTRS)

    Dement, W. C.; Barchas, J. D.

    1972-01-01

    An attempt was made to obtain information relevant to assessing the need to sleep and make up for lost sleep. Physiological and behavioral parameters were used as measuring parameters. Sleep deprivation in a restricted environment, derivation of data relevant to determining sleepiness from EEG, and the development of the Sanford Sleepiness Scale were discussed.

  15. Tempol prevents chronic sleep-deprivation induced memory impairment.

    PubMed

    Alzoubi, Karem H; Khabour, Omar F; Albawaana, Amal S; Alhashimi, Farah H; Athamneh, Rabaa Y

    2016-01-01

    Sleep deprivation is associated with oxidative stress that causes learning and memory impairment. Tempol is a nitroxide compound that promotes the metabolism of many reactive oxygen species (ROS) and has antioxidant and neuroprotective effect. The current study investigated whether chronic administration of tempol can overcome oxidative stress and prevent learning and memory impairment induced by sleep deprivation. Sleep deprivation was induced in rats using multiple platform model. Tempol was administered to rats via oral gavages. Behavioral studies were conducted to test the spatial learning and memory using radial arm water maze. The hippocampus was dissected; antioxidant biomarkers (GSH, GSSG, GSH/GSSG ratio, GPx, SOD, and catalase) were assessed. The result of this project revealed that chronic sleep deprivation impaired both short and long term memory (P<0.05), while tempol treatment prevented such effect. Furthermore, tempol normalized chronic sleep deprivation induced reduction in the hippocampus activity of catalase, GPx, and SOD (P<0.05). Tempol also enhanced the ratio of GSH/GSSG in chronically sleep deprived rats treated with tempol as compared with only sleep deprived rats (P<0.05). In conclusion chronic sleep deprivation induced memory impairment, and treatment with tempol prevented this impairment probably through normalizing antioxidant mechanisms in the hippocampus.

  16. Sleep Deprivation, Allergy Symptoms, and Negatively Reinforced Problem Behavior.

    ERIC Educational Resources Information Center

    Kennedy, Craig H.; Meyer, Kim A.

    1996-01-01

    A study of the relationship between presence or absence of sleep deprivation, allergy symptoms, and the rate and function of problem behavior in three adolescents with moderate to profound mental retardation found that problem behavior was negatively reinforced by escape from instruction, and both allergy symptoms and sleep deprivation influenced…

  17. Are seizures in the setting of sleep deprivation provoked?

    PubMed

    Lawn, Nicholas; Lieblich, Sam; Lee, Judy; Dunne, John

    2014-04-01

    It is generally accepted that sleep deprivation contributes to seizures. However, it is unclear whether a seizure occurring in the setting of sleep deprivation should be considered as provoked or not and whether this is influenced by seizure type and etiology. This information may have an important impact on epilepsy diagnosis and management. We prospectively analyzed the influence of sleep deprivation on the risk of seizure recurrence in patients with first-ever unprovoked seizures and compared the findings with patients with first-ever provoked seizures. Of 1026 patients with first-ever unprovoked seizures, 204 (20%) were associated with sleep deprivation. While the overall likelihood of seizure recurrence was slightly lower in sleep-deprived patients with first-ever seizures (log-rank p=0.03), sleep deprivation was not an independent predictor of seizure recurrence on multivariate analysis. Seizure recurrence following a first-ever unprovoked seizure associated with sleep deprivation was far more likely than for 174 patients with a provoked first-ever seizure (log-rank p<0.0001). Our findings support the International League Against Epilepsy recommendation that seizures occurring in the setting of sleep deprivation should not be regarded as provoked.

  18. Sleep Deprivation, Allergy Symptoms, and Negatively Reinforced Problem Behavior.

    ERIC Educational Resources Information Center

    Kennedy, Craig H.; Meyer, Kim A.

    1996-01-01

    A study of the relationship between presence or absence of sleep deprivation, allergy symptoms, and the rate and function of problem behavior in three adolescents with moderate to profound mental retardation found that problem behavior was negatively reinforced by escape from instruction, and both allergy symptoms and sleep deprivation influenced…

  19. Sleep deprivation and obesity in shift workers in southern Brazil.

    PubMed

    Canuto, Raquel; Pattussi, Marcos Pascoal; Macagnan, Jamile Block Araldi; Henn, Ruth Liane; Olinto, Maria Teresa Anselmo

    2014-11-01

    The objective of our study was to explore the association between sleep deprivation and obesity among shift workers. A cross-sectional study was conducted. Obesity was defined as BMI ≥30 kg/m2. Time of sleep was categorized as: >5 h of continuous sleep/d; ≤5 h of continuous sleep/d with some additional rest (sleep deprivation level I); and ≤5 h of continuous sleep/d without any additional rest (sleep deprivation level II). Sociodemographic, parental and behavioural variables were evaluated by means of a standardized pre-tested questionnaire. Potential confounding factors were controlled for in the multivariable model. A poultry-processing plant in southern Brazil. Nine hundred and five shift workers (63 % female). Obesity was more prevalent in the participants who were female, aged 40 years and older, who had less schooling and reported excess weight in both parents. Sleep deprivation levels I and II were associated with increased income, number of meals consumed throughout the day and nightshift work. All of the workers who exhibited a degree of sleep deprivation worked the night shift. After controlling for potential confounding factors, the prevalence ratios of obesity were 1·4 (95 % CI 0·8, 2·2) and 4·4 (95 % CI 2·4, 8·0) in the workers with sleep deprivation levels I and II, respectively, compared with the reference group. These results show a strong association between sleep deprivation and obesity in shift workers and that sleep deprivation may be a direct consequence of working at night.

  20. Sleep Deprived and Sweating It Out: The Effects of Total Sleep Deprivation on Skin Conductance Reactivity to Psychosocial Stress

    PubMed Central

    Liu, Jean C.J.; Verhulst, Silvan; Massar, Stijn A.A.; Chee, Michael W.L.

    2015-01-01

    Study Objectives: We examined how sleep deprivation alters physiological responses to psychosocial stress by evaluating changes in skin conductance. Design: Between-subjects design with one group allocated to 24 h of total sleep deprivation and the other to rested wakefulness. Setting: The study took place in a research laboratory. Participants: Participants were 40 healthy young adults recruited from a university. Interventions: Sleep deprivation and feedback. Measurements and Results: Electrodermal activity was monitored while participants completed a difficult perceptual task with false feedback. All participants showed increased skin conductance levels following stress. However, compared to well-rested participants, sleep deprived participants showed higher skin conductance reactivity with increasing stress levels. Conclusions: Our results suggest that sleep deprivation augments allostatic responses to increasing psychosocial stress. Consequentially, we propose sleep loss as a risk factor that can influence the pathogenic effects of stress. Citation: Liu JC, Verhulst S, Massar SA, Chee MW. Sleep deprived and sweating it out: the effects of total sleep deprivation on skin conductance reactivity to psychosocial stress. SLEEP 2015;38(1):155–159. PMID:25325448

  1. Selective REM sleep deprivation during daytime. II. Muscle atonia in non-REM sleep.

    PubMed

    Werth, Esther; Achermann, Peter; Borbély, Alexander A

    2002-08-01

    One of the hallmarks of rapid eye movement (REM) sleep is muscle atonia. Here we report extended epochs of muscle atonia in non-REM sleep (MAN). Their extent and time course was studied in a protocol that included a baseline night, a daytime sleep episode with or without selective REM sleep deprivation, and a recovery night. The distribution of the latency to the first occurrence of MAN was bimodal with a first mode shortly after sleep onset and a second mode 40 min later. Within a non-REM sleep episode, MAN showed a U-shaped distribution with the highest values before and after REM sleep. Whereas MAN was at a constant level over consecutive 2-h intervals of nighttime sleep, MAN showed high initial values when sleep began in the morning. Selective daytime REM sleep deprivation caused an initial enhancement of MAN during recovery sleep. It is concluded that episodes of MAN may represent an REM sleep equivalent and that it may be a marker of homeostatic and circadian REM sleep regulating processes. MAN episodes may contribute to the compensation of an REM sleep deficit.

  2. Night shifts, sleep deprivation, and attention performance in medical students.

    PubMed

    Pérez-Olmos, Isabel; Ibáñez-Pinilla, Milcíades

    2014-03-29

    To determine attention performance of medical students after sleep deprivation due to night shift work. Prospective cohort design. All seventh, eighth and ninth semester students were invited to participate (n= 209). The effectiveness and concentration indices (d2 Test for attention, dependent variable) from 180 students at 3 evaluations during the semester were compared. Eighth and ninth semester students underwent their second evaluation after a night shift. The independent variables were nocturnal sleep measurements. No differences in nocturnal sleep hours during the previous week (p=0.966), sleep deprivation (p=0.703) or effectiveness in the d2 Test (p=0.428) were found between the groups at the beginning of the semester. At the beginning and the end of the semester, the d2 Test results were not different between groups (p=0.410, p=0.394) respectively. The second evaluation showed greater sleep deprivation in students with night shift work (p=0.001). The sleep deprived students had lower concentration indices (p=0.001).The differences were associated with the magnitude of sleep deprivation (p=0.008). Multivariate regression analysis showed that attention performance was explained by sleep deprivation due to night shift work, adjusting for age and gender. Students with sleep deprivation had worse concentration than those without. Sleep deprivation due to night shift work in medical students had a negative impact on their attention performance. Medical educators should address these potential negative learning and patient care consequences of sleep deprivation in medical students due to night shifts.

  3. Night shifts, sleep deprivation, and attention performance in medical students

    PubMed Central

    Ibanez-Pinilla, Milciades

    2014-01-01

    Objectives To determine attention performance of medical students after sleep deprivation due to night shift work. Methods Prospective cohort design. All seventh, eighth and ninth semester students were invited to participate (n= 209). The effectiveness and concentration indices (d2 Test for attention, dependent variable) from 180 students at 3 evaluations during the semester were compared. Eighth and ninth semester students underwent their second evaluation after a night shift. The independent variables were nocturnal sleep measurements. Results No differences in nocturnal sleep hours during the previous week (p=0.966), sleep deprivation (p=0.703) or effectiveness in the d2 Test (p=0.428) were found between the groups at the beginning of the semester. At the beginning and the end of the semester, the d2 Test results were not different between groups (p=0.410, p=0.394) respectively. The second evaluation showed greater sleep deprivation in students with night shift work (p<0.001). The sleep deprived students had lower concentration indices (p<0.001).The differences were associated with the magnitude of sleep deprivation (p=0.008). Multivariate regression analysis showed that attention performance was explained by sleep deprivation due to night shift work, adjusting for age and gender. Students with sleep deprivation had worse concentration than those without. Conclusions Sleep deprivation due to night shift work in medical students had a negative impact on their attention performance. Medical educators should address these potential negative learning and patient care consequences of sleep deprivation in medical students due to night shifts. PMID:25341213

  4. Acute Sleep Deprivation Enhances Post-Infection Sleep and Promotes Survival during Bacterial Infection in Drosophila

    PubMed Central

    Kuo, Tzu-Hsing; Williams, Julie A.

    2014-01-01

    Study Objectives: Sleep is known to increase as an acute response to infection. However, the function of this behavioral response in host defense is not well understood. To address this problem, we evaluated the effect of acute sleep deprivation on post-infection sleep and immune function in Drosophila. Setting: Laboratory. Participants: Drosophila melanogaster. Methods and Results: Flies were subjected to sleep deprivation before (early DEP) or after (late DEP) bacterial infection. Relative to a non-deprived control, flies subjected to early DEP had enhanced sleep after infection as well as increased bacterial clearance and survival outcome. Flies subjected to late DEP experienced enhanced sleep following the deprivation period, and showed a modest improvement in survival outcome. Continuous DEP (early and late DEP) throughout infection also enhanced sleep later during infection and improved survival. However, improved survival in flies subjected to late or continuous DEP did not occur until after flies had experienced sleep. During infection, both early and late DEP enhanced NFκB transcriptional activity as measured by a luciferase reporter (κB-luc) in living flies. Early DEP also increased NFκB activity prior to infection. Flies that were deficient in expression of either the Relish or Dif NFκB transcription factors showed normal responses to early DEP. However, the effect of early DEP on post-infection sleep and survival was abolished in double mutants, which indicates that Relish and Dif have redundant roles in this process. Conclusions: Acute sleep deprivation elevated NFκB-dependent activity, increased post-infection sleep, and improved survival during bacterial infection. Citation: Kuo TH, Williams JA. Acute sleep deprivation enhances post-infection sleep and promotes survival during bacterial infection in Drosophila. SLEEP 2014;37(5):859-869. PMID:24790264

  5. Sleep deprivation in adolescents and adults: changes in affect.

    PubMed

    Talbot, Lisa S; McGlinchey, Eleanor L; Kaplan, Katherine A; Dahl, Ronald E; Harvey, Allison G

    2010-12-01

    The present study investigated the impact of sleep deprivation on several aspects of affective functioning in healthy participants selected from three different developmental periods: early adolescence (ages 10-13), midadolescence (ages 13-16), and adulthood (ages 30-60). Participants completed an affective functioning battery under conditions of sleep deprivation (a maximum of 6.5 hours total sleep time on the first night followed by a maximum of 2 hours total sleep time on the second night) and rest (approximately 7-8 hours total sleep time each night for two consecutive nights). Less positive affect was observed in the sleep-deprived, compared to rested, condition. This effect held for 9 of the 12 positive affect items on the PANAS-C. Participants also reported a greater increase in anxiety during a catastrophizing task and rated the likelihood of potential catastrophes as higher when sleep deprived, relative to when rested. Early adolescents appraised their main worry as more threatening when sleep deprived, relative to when rested. These results support and extend previous research underscoring the adverse affective consequences of sleep deprivation.

  6. The sleep-deprived electroencephalogram: evidence and practice.

    PubMed

    Glick, Thomas H

    2002-08-01

    Sleep deprivation for the initial electroencephalogram for suspected seizures is a widespread but inconsistent practice not informed by balanced evidence. Daily practice suggests that nonneurologists are confused by the meaning and value of, and indications for, "sleep" (tracing) vs "sleep deprivation" (and other alternatives). They need specific, informed guidance from general neurologists on best practices. To document illustratively the variability of neurologists' practices, the level of relevant information among nonneurologists, and the current state of published evidence; and to stimulate formulation of consensus advisories. I surveyed knowledge and practices of (1) nonneurologists in a community teaching hospital; (2) local and national neurologists and epileptologists; (3) electroencephalogram laboratory protocols; and (4) textbook accounts and recommendations and the relevant journal literature. National professional organizations were contacted for advisories or guidelines. Most nonneurologists surveyed misunderstood "sleep" vs "sleep-deprived" electroencephalograms and their actual protocols. They are unaware of evidence on benefits vs burdens. Neurologists' practices are inconsistent. Experts generally agree that sleep deprivation produces substantial activation of interictal epileptiform discharges beyond the activation of sleep per se. However, most published recommendations and interviewed epileptologists do not suggest sleep deprivation for the initial electroencephalogram because of "inconvenience" (burdens) for the patient. Evidence-based or reasoned guidance is minimal, and professional societies have not issued advisories. Confusion over sleep deprivation, disparities between evidence and recommendations, and inconsistent practices create a need for expert consensus for guidance, as well as comparative research on alternative methods of increasing diagnostic yield.

  7. Sleep deprivation of rats: the hyperphagic response is real.

    PubMed

    Koban, Michael; Sita, Luciane V; Le, Wei Wei; Hoffman, Gloria E

    2008-07-01

    Chronic sleep deprivation of rats causes hyperphagia without body weight gain. Sleep deprivation hyperphagia is prompted by changes in pathways governing food intake; hyperphagia may be adaptive to sleep deprivation hypermetabolism. A recent paper suggested that sleep deprivation might inhibit ability of rats to increase food intake and that hyperphagia may be an artifact of uncorrected chow spillage. To resolve this, a palatable liquid diet (Ensure) was used where spillage is insignificant. Sleep deprivation of male Sprague Dawley rats was enforced for 10 days by the flowerpot/platform paradigm. Daily food intake and body weight were measured. On day 10, rats were transcardially perfused for analysis of hypothalamic mRNA expression of the orexigen, neuropeptide Y (NPY). Morgan State University, sleep deprivation and transcardial perfusion; University of Maryland, NPY in situ hybridization and analysis. Using a liquid diet for accurate daily measurements, there was no change in food intake in the first 5 days of sleep deprivation. Importantly, from days 6-10 it increased significantly, peaking at 29% above baseline. Control rats steadily gained weight but sleep-deprived rats did not. Hypothalamic NPY mRNA levels were positively correlated to stimulation of food intake and negatively correlated with changes in body weight. Sleep deprivation hyperphagia may not be apparent over the short term (i.e., < or = 5 days), but when extended beyond 6 days, it is readily observed. The timing of changes in body weight and food intake suggests that the negative energy balance induced by sleep deprivation prompts the neural changes that evoke hyperphagia.

  8. Melatonin improves experimental colitis with sleep deprivation

    PubMed Central

    PARK, YOUNG-SOOK; CHUNG, SOOK-HEE; LEE, SEONG-KYU; KIM, JA-HYUN; KIM, JUN-BONG; KIM, TAE-KYUN; KIM, DONG-SHIN; BAIK, HAING-WOON

    2015-01-01

    Sleep deprivation (SD) is an epidemic phenomenon in modern countries, and its harmful effects are well known. SD acts as an aggravating factor in inflammatory bowel disease. Melatonin is a sleep-related neurohormone, also known to have antioxidant and anti-inflammatory effects in the gastrointestinal tract; however, the effects of melatonin on colitis have been poorly characterized. Thus, in this study, we assessed the measurable effects of SD on experimental colitis and the protective effects of melatonin. For this purpose, male imprinting control region (ICR) mice (n=24) were used; the mice were divided into 4 experimental groups as follows: the control, colitis, colitis with SD and colitis with SD and melatonin groups. Colitis was induced by the administration of 5% dextran sulfate sodium (DSS) in the drinking water for 6 days. The mice were sleep-deprived for 3 days. Changes in body weight, histological analyses of colon tissues and the expression levels of pro-inflammatory cytokines and genes were evaluated. SD aggravated inflammation and these effects were reversed by melatonin in the mice with colitis. In addition, weight loss in the mice with colitis with SD was significantly reduced by the injection of melatonin. Treatment with melatonin led to high survival rates in the mice, in spite of colitis with SD. The levels of pro-inflammatory cytokines, such as interleukin (IL)-1β, IL-6, IL-17, interferon-γ and tumor necrosis factor-α, in the serum of mice were significantly increased by SD and reduced by melatonin treatment. The melatonin-treated group showed a histological improvement of inflammation. Upon gene analysis, the expression of the inflammatory genes, protein kinase Cζ (PKCζ) and calmodulin 3 (CALM3), was increased by SD, and the levels decreased following treatment with melatonin. The expression levels of the apoptosis-related inducible nitric oxide synthase (iNOS) and wingless-type MMTV integration site family, member 5A (Wnt5a) genes was

  9. Melatonin improves experimental colitis with sleep deprivation.

    PubMed

    Park, Young-Sook; Chung, Sook-Hee; Lee, Seong-Kyu; Kim, Ja-Hyun; Kim, Jun-Bong; Kim, Tae-Kyun; Kim, Dong-Shin; Baik, Haing-Woon

    2015-04-01

    Sleep deprivation (SD) is an epidemic phenomenon in modern countries, and its harmful effects are well known. SD acts as an aggravating factor in inflammatory bowel disease. Melatonin is a sleep-related neurohormone, also known to have antioxidant and anti-inflammatory effects in the gastrointestinal tract; however, the effects of melatonin on colitis have been poorly characterized. Thus, in this study, we assessed the measurable effects of SD on experimental colitis and the protective effects of melatonin. For this purpose, male imprinting control region (ICR) mice (n = 24) were used; the mice were divided into 4 experimental groups as follows: the control, colitis, colitis with SD and colitis with SD and melatonin groups. Colitis was induced by the administration of 5% dextran sulfate sodium (DSS) in the drinking water for 6 days. The mice were sleep-deprived for 3 days. Changes in body weight, histological analyses of colon tissues and the expression levels of pro-inflammatory cytokines and genes were evaluated. SD aggravated inflammation and these effects were reversed by melatonin in the mice with colitis. In addition, weight loss in the mice with colitis with SD was significantly reduced by the injection of melatonin. Treatment with melatonin led to high survival rates in the mice, in spite of colitis with SD. The levels of pro-inflammatory cytokines, such as interleukin (IL)-1β, IL-6, IL-17, interferon-γ and tumor necrosis factor-α, in the serum of mice were significantly increased by SD and reduced by melatonin treatment. The melatonin-treated group showed a histological improvement of inflammation. Upon gene analysis, the expression of the inflammatory genes, protein kinase Cζ (PKCζ) and calmodulin 3 (CALM3), was increased by SD, and the levels decreased following treatment with melatonin. The expression levels of the apoptosis-related inducible nitric oxide synthase (iNOS) and wingless-type MMTV integration site family, member 5A (Wnt5a) genes was

  10. Impact of Acute Sleep Deprivation on Sarcasm Detection

    PubMed Central

    Mary, Alison; Slama, Hichem; Cleeremans, Axel; Peigneux, Philippe; Kissine, Mikhail

    2015-01-01

    There is growing evidence that sleep plays a pivotal role on health, cognition and emotional regulation. However, the interplay between sleep and social cognition remains an uncharted research area. In particular, little is known about the impact of sleep deprivation on sarcasm detection, an ability which, once altered, may hamper everyday social interactions. The aim of this study is to determine whether sleep-deprived participants are as able as sleep-rested participants to adopt another perspective in gauging sarcastic statements. At 9am, after a whole night of sleep (n = 15) or a sleep deprivation night (n = 15), participants had to read the description of an event happening to a group of friends. An ambiguous voicemail message left by one of the friends on another's phone was then presented, and participants had to decide whether the recipient would perceive the message as sincere or as sarcastic. Messages were uttered with a neutral intonation and were either: (1) sarcastic from both the participant’s and the addressee’s perspectives (i.e. both had access to the relevant background knowledge to gauge the message as sarcastic), (2) sarcastic from the participant’s but not from the addressee’s perspective (i.e. the addressee lacked context knowledge to detect sarcasm) or (3) sincere. A fourth category consisted in messages sarcastic from both the participant’s and from the addressee’s perspective, uttered with a sarcastic tone. Although sleep-deprived participants were as accurate as sleep-rested participants in interpreting the voice message, they were also slower. Blunted reaction time was not fully explained by generalized cognitive slowing after sleep deprivation; rather, it could reflect a compensatory mechanism supporting normative accuracy level in sarcasm understanding. Introducing prosodic cues compensated for increased processing difficulties in sarcasm detection after sleep deprivation. Our findings support the hypothesis that sleep

  11. Impact of Acute Sleep Deprivation on Sarcasm Detection.

    PubMed

    Deliens, Gaétane; Stercq, Fanny; Mary, Alison; Slama, Hichem; Cleeremans, Axel; Peigneux, Philippe; Kissine, Mikhail

    2015-01-01

    There is growing evidence that sleep plays a pivotal role on health, cognition and emotional regulation. However, the interplay between sleep and social cognition remains an uncharted research area. In particular, little is known about the impact of sleep deprivation on sarcasm detection, an ability which, once altered, may hamper everyday social interactions. The aim of this study is to determine whether sleep-deprived participants are as able as sleep-rested participants to adopt another perspective in gauging sarcastic statements. At 9am, after a whole night of sleep (n = 15) or a sleep deprivation night (n = 15), participants had to read the description of an event happening to a group of friends. An ambiguous voicemail message left by one of the friends on another's phone was then presented, and participants had to decide whether the recipient would perceive the message as sincere or as sarcastic. Messages were uttered with a neutral intonation and were either: (1) sarcastic from both the participant's and the addressee's perspectives (i.e. both had access to the relevant background knowledge to gauge the message as sarcastic), (2) sarcastic from the participant's but not from the addressee's perspective (i.e. the addressee lacked context knowledge to detect sarcasm) or (3) sincere. A fourth category consisted in messages sarcastic from both the participant's and from the addressee's perspective, uttered with a sarcastic tone. Although sleep-deprived participants were as accurate as sleep-rested participants in interpreting the voice message, they were also slower. Blunted reaction time was not fully explained by generalized cognitive slowing after sleep deprivation; rather, it could reflect a compensatory mechanism supporting normative accuracy level in sarcasm understanding. Introducing prosodic cues compensated for increased processing difficulties in sarcasm detection after sleep deprivation. Our findings support the hypothesis that sleep deprivation might

  12. Impact of partial sleep deprivation on immune markers.

    PubMed

    Wilder-Smith, A; Mustafa, F B; Earnest, A; Gen, L; Macary, P A

    2013-10-01

    Sleep quality is considered to be an important predictor of immunity. Lack of sleep therefore may reduce immunity, thereby increasing the susceptibility to respiratory pathogens. A previous study showed that reduced sleep duration was associated with an increased likelihood of the common cold. It is important to understand the role of sleep in altering immune responses to understand how sleep deprivation leads to an increased susceptibility to the common cold or other respiratory infections. We sought to examine the impact of partial sleep deprivation on various immune markers. Fifty-two healthy volunteers were partially sleep deprived for one night. We took blood samples before the sleep deprivation, immediately after, and 4 and 7 days after sleep deprivation. We measured various immune markers and used a generalized estimating equation (GEE) to examine the differences in the repeated measures. CD4, CD8, CD14, and CD16 all showed significant time-dependent changes, but CD3 did not. The most striking time-dependent change was observed for the mitogen proliferation assay and for HLA-DR. There was a significant decrease in the mitogen proliferation values and HLA-DR immediately after the sleep deprivation experiment, which started to rise again on day 4 and normalized by day 7. The transiently impaired mitogen proliferation, the decreased HLA-DR, the upregulated CD14, and the variations in CD4 and CD8 that we observed in temporal relationship with partial sleep deprivation could be one possible explanation for the increased susceptibility to respiratory infections reported after reduced sleep duration. Copyright © 2013 Elsevier B.V. All rights reserved.

  13. Sleep deprivation and cellular responses to oxidative stress.

    PubMed

    Gopalakrishnan, Anupama; Ji, Li Li; Cirelli, Chiara

    2004-02-01

    It has been hypothesized that sleep deprivation represents an oxidative challenge for the brain and that sleep may have a protective role against oxidative damage. This study was designed to test this hypothesis by measuring in rats the effects of sleep loss on markers of oxidative stress (oxidant production and antioxidant enzyme activities) as well as on markers of cellular oxidative damage (lipid peroxidation and protein oxidation). The analyses were performed in the brain and in peripheral tissues (liver and skeletal muscle), after short-term sleep deprivation (8 hours), after long-term sleep deprivation (3-14 days), and during recovery sleep after 1 week of sleep loss. Short-term sleep deprivation was performed by gentle handling; long-term sleep deprivation was performed using the disk-over-water method. Sleep research laboratory at University of Wisconsin-Madison. Adult male Wistar Kyoto rats (n = 69) implanted for polygraphic (electroencephalogram, electromyogram) recording. Aliquots of brain, liver, or skeletal muscle homogenate were used to assess oxidant production, superoxide dismutase activity, lipid peroxidation, and protein oxidation. No evidence of oxidative damage was observed at the lipid and/or at the protein level in long-term sleep-deprived animals relative to their yoked controls, nor in the cerebral cortex or in peripheral tissues. Also, no consistent change in antioxidant enzymatic activities was found after prolonged sleep deprivation, nor was any evidence of increased oxidant production in the brain or in peripheral tissues. The available data do not support the assumption that prolonged wakefulness may cause oxidative damage, nor that it can represent an oxidative stress for the brain or for peripheral tissue such as liver and skeletal muscle.

  14. Effect of total sleep deprivation on the landmarks of stage 2 sleep.

    PubMed

    Curcio, Giuseppe; Ferrara, Michele; Pellicciari, Maria Concetta; Cristiani, Riccardo; De Gennaro, Luigi

    2003-12-01

    To assess the effects of total sleep deprivation on sleep spindle and K-complex (KC) density. Eight healthy male subjects (mean age=23.4 years) participated in the experiment: they slept in the laboratory for 3 nights (one adaptation, one baseline, one recovery); baseline and recovery night were separated by a period of 40 h of continuous wake. One night of total sleep deprivation caused a doubling of slow-wave sleep (SWS) amount, an increase of sleep efficiency and a reduction of the latencies of non-rapid eye movement (NREM) sleep stages during the recovery night. These effects were accompanied by a significant reduction in spindle density in the first sleep cycle of the recovery night. Mean KC density did not change as a result of total sleep deprivation, while KC density and inter-KC intervals showed linear trends across the first 4 sleep cycles, respectively decreasing and increasing. Finally, a clear evidence of an antagonist relationship between spindle and KC changes across sleep cycles was provided. The present study further supports the existence of a reciprocal relationship between SWS and sleep spindles, but fails to show an increase of KC density after total sleep deprivation. The opposite time courses of spindle and KC density across sleep cycles points to an antagonist relation between the two main phasic events of NREM sleep. The latter result, together with the increase of inter-KC distance and the decrease of KC density across subsequent sleep cycles, is consistent with the hypothesis of a role of the spontaneous KC as the "forerunner" of delta waves.

  15. Sleep Deprivation Reveals Altered Brain Perfusion Patterns in Somnambulism

    PubMed Central

    Dang-Vu, Thien Thanh; Zadra, Antonio; Labelle, Marc-Antoine; Petit, Dominique; Soucy, Jean-Paul; Montplaisir, Jacques

    2015-01-01

    Background Despite its high prevalence, relatively little is known about the pathophysiology of somnambulism. Increasing evidence indicates that somnambulism is associated with functional abnormalities during wakefulness and that sleep deprivation constitutes an important drive that facilitates sleepwalking in predisposed patients. Here, we studied the neural mechanisms associated with somnambulism using Single Photon Emission Computed Tomography (SPECT) with 99mTc-Ethylene Cysteinate Dimer (ECD), during wakefulness and after sleep deprivation. Methods Ten adult sleepwalkers and twelve controls with normal sleep were scanned using 99mTc-ECD SPECT in morning wakefulness after a full night of sleep. Eight of the sleepwalkers and nine of the controls were also scanned during wakefulness after a night of total sleep deprivation. Between-group comparisons of regional cerebral blood flow (rCBF) were performed to characterize brain activity patterns during wakefulness in sleepwalkers. Results During wakefulness following a night of total sleep deprivation, rCBF was decreased bilaterally in the inferior temporal gyrus in sleepwalkers compared to controls. Conclusions Functional neural abnormalities can be observed during wakefulness in somnambulism, particularly after sleep deprivation and in the inferior temporal cortex. Sleep deprivation thus not only facilitates the occurrence of sleepwalking episodes, but also uncovers patterns of neural dysfunction that characterize sleepwalkers during wakefulness. PMID:26241047

  16. Reduced visual processing capacity in sleep deprived persons.

    PubMed

    Kong, Danyang; Soon, Chun Siong; Chee, Michael W L

    2011-03-15

    Multiple experiments have found sleep deprivation to lower task-related parietal and extrastriate visual activation, suggesting a reduction of visual processing capacity in this state. The perceptual load theory of attention (Lavie, 1995) predicts that our capacity to process unattended distractors will be reduced by increasing perceptual difficulty of task-relevant stimuli. Here, we evaluated the effects of sleep deprivation and perceptual load on visual processing capacity by measuring neural repetition-suppression to unattended scenes while healthy volunteers attended to faces embedded in face-scene pictures. Perceptual load did not affect repetition suppression after a normal night of sleep. Sleep deprivation reduced repetition suppression in the parahippocampal place area (PPA) in the high but not low perceptual load condition. Additionally, the extent to which task-related fusiform face area (FFA) activation was reduced after sleep deprivation correlated with behavioral performance and lowered repetition suppression in the PPA. The findings concerning correct responses indicate that a portion of stimulus related activation following a normal night of sleep contributes to potentially useful visual processing capacity that is attenuated following sleep deprivation. Finally, when unattended stimuli are not highly intrusive, sleep deprivation does not appear to increase distractibility.

  17. Is sleep deprivation a contributor to obesity in children?

    PubMed

    Chaput, Jean-Philippe

    2016-03-01

    Chronic lack of sleep (called "sleep deprivation") is common in modern societies with 24/7 availability of commodities. Accumulating evidence supports the role of reduced sleep as contributing to the current obesity epidemic in children and youth. Longitudinal studies have consistently shown that short sleep duration is associated with weight gain and the development of obesity. Recent experimental studies have reported that sleep restriction leads to weight gain in humans. Increased food intake appears to be the main mechanism by which insufficient sleep results in weight gain. Voluntary sleep restriction has been shown to increase snacking, the number of meals eaten per day, and the preference for energy-dense foods. Although the causes of sleep loss in the pediatric population are numerous, more research looking at screen exposure before bedtime and its effects on sleep is needed given the pervasiveness of electronic media devices in today's environment. Health professionals should routinely ask questions about sleep and promote a good night's sleep because insufficient sleep impacts activity and eating behaviors. Future research should examine the clinical benefits of increasing sleep duration on eating behaviors and body weight control and determine the importance of adequate sleep to improve the treatment of obesity.

  18. Sleep Disturbance, Sleep Duration, and Inflammation: A Systematic Review and Meta-Analysis of Cohort Studies and Experimental Sleep Deprivation

    PubMed Central

    Irwin, Michael R.; Olmstead, Richard; Carroll, Judith E.

    2015-01-01

    Background Sleep disturbance is associated with inflammatory disease risk and all-cause mortality. Here, we assess global evidence linking sleep disturbance, sleep duration, and inflammation in adult humans. Methods A systematic search of English language publications was performed, with inclusion of primary research articles that characterized sleep disturbance and/or sleep duration or performed experimental sleep deprivation, and assessed inflammation by levels of circulating markers. Effect sizes (ES) and 95% confidence intervals (CI) were extracted and pooled using a random effect model. Results A total of 72 studies (n>50000) were analyzed with assessment of C-reactive protein (CRP), interleukin-6 (IL-6), and tumor necrosis factor α (TNF). Sleep disturbance was associated with higher levels of CRP (ES 0.12; 95% CI 0.05 – 0.19) and IL-6 (ES 0.20; 95% CI 0.08 – 0.31). Shorter sleep duration, but not the extreme of short sleep, was associated with higher levels of CRP (ES 0.09; 95% CI 0.01 – 0.17) but not IL-6 (ES 0.03; 95% CI −0.09 – 0.14). The extreme of long sleep duration was associated with higher levels of CRP (ES 0.17; 95% CI 0.01 – 0.34) and IL-6 (ES 0.11; 95% CI 0.02 – 0.20). Neither sleep disturbances nor sleep duration was associated with TNF. Neither experimental sleep deprivation nor sleep restriction was associated with CRP, IL-6, or TNF. Some heterogeneity among studies was found, but no evidence of publication bias. Conclusions Sleep disturbance and long sleep duration, but not short sleep duration, are associated with increases in markers of systemic inflammation. PMID:26140821

  19. Sleep Disturbance, Sleep Duration, and Inflammation: A Systematic Review and Meta-Analysis of Cohort Studies and Experimental Sleep Deprivation.

    PubMed

    Irwin, Michael R; Olmstead, Richard; Carroll, Judith E

    2016-07-01

    Sleep disturbance is associated with inflammatory disease risk and all-cause mortality. Here, we assess global evidence linking sleep disturbance, sleep duration, and inflammation in adult humans. A systematic search of English language publications was performed, with inclusion of primary research articles that characterized sleep disturbance and/or sleep duration or performed experimental sleep deprivation and assessed inflammation by levels of circulating markers. Effect sizes (ES) and 95% confidence intervals (CI) were extracted and pooled using a random effect model. A total of 72 studies (n > 50,000) were analyzed with assessment of C-reactive protein (CRP), interleukin-6 (IL-6), and tumor necrosis factor α (TNFα). Sleep disturbance was associated with higher levels of CRP (ES .12; 95% CI = .05-.19) and IL-6 (ES .20; 95% CI = .08-.31). Shorter sleep duration, but not the extreme of short sleep, was associated with higher levels of CRP (ES .09; 95% CI = .01-.17) but not IL-6 (ES .03; 95% CI: -.09 to .14). The extreme of long sleep duration was associated with higher levels of CRP (ES .17; 95% CI = .01-.34) and IL-6 (ES .11; 95% CI = .02-20). Neither sleep disturbances nor sleep duration was associated with TNFα. Neither experimental sleep deprivation nor sleep restriction was associated with CRP, IL-6, or TNFα. Some heterogeneity among studies was found, but there was no evidence of publication bias. Sleep disturbance and long sleep duration, but not short sleep duration, are associated with increases in markers of systemic inflammation. Copyright © 2016 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.

  20. Cardiovascular effects of partial sleep deprivation in healthy volunteers.

    PubMed

    Dettoni, Josilene L; Consolim-Colombo, Fernanda Marciano; Drager, Luciano F; Rubira, Marcelo C; Souza, Silvia Beatriz P Cavasin de; Irigoyen, Maria Claudia; Mostarda, Cristiano; Borile, Suellen; Krieger, Eduardo M; Moreno, Heitor; Lorenzi-Filho, Geraldo

    2012-07-01

    Sleep deprivation is common in Western societies and is associated with increased cardiovascular morbidity and mortality in epidemiological studies. However, the effects of partial sleep deprivation on the cardiovascular system are poorly understood. In the present study, we evaluated 13 healthy male volunteers (age: 31 ± 2 yr) monitoring sleep diary and wrist actigraphy during their daily routine for 12 nights. The subjects were randomized and crossover to 5 nights of control sleep (>7 h) or 5 nights of partial sleep deprivation (<5 h), interposed by 2 nights of unrestricted sleep. At the end of control and partial sleep deprivation periods, heart rate variability (HRV), blood pressure variability (BPV), serum norepinephrine, and venous endothelial function (dorsal hand vein technique) were measured at rest in a supine position. The subjects slept 8.0 ± 0.5 and 4.5 ± 0.3 h during control and partial sleep deprivation periods, respectively (P < 0.01). Compared with control, sleep deprivation caused significant increase in sympathetic activity as evidenced by increase in percent low-frequency (50 ± 15 vs. 59 ± 8) and a decrease in percent high-frequency (50 ± 10 vs. 41 ± 8) components of HRV, increase in low-frequency band of BPV, and increase in serum norepinephrine (119 ± 46 vs. 162 ± 58 ng/ml), as well as a reduction in maximum endothelial dependent venodilatation (100 ± 22 vs. 41 ± 20%; P < 0.05 for all comparisons). In conclusion, 5 nights of partial sleep deprivation is sufficient to cause significant increase in sympathetic activity and venous endothelial dysfunction. These results may help to explain the association between short sleep and increased cardiovascular risk in epidemiological studies.

  1. Diurnal rhythms in the human urine metabolome during sleep and total sleep deprivation

    PubMed Central

    Giskeødegård, Guro F.; Davies, Sarah K.; Revell, Victoria L.; Keun, Hector; Skene, Debra J.

    2015-01-01

    Understanding how metabolite levels change over the 24 hour day is of crucial importance for clinical and epidemiological studies. Additionally, the association between sleep deprivation and metabolic disorders such as diabetes and obesity requires investigation into the links between sleep and metabolism. Here, we characterise time-of-day variation and the effects of sleep deprivation on urinary metabolite profiles. Healthy male participants (n = 15) completed an in-laboratory study comprising one 24 h sleep/wake cycle prior to 24 h of continual wakefulness under highly controlled environmental conditions. Urine samples were collected over set 2–8 h intervals and analysed by 1H NMR spectroscopy. Significant changes were observed with respect to both time of day and sleep deprivation. Of 32 identified metabolites, 7 (22%) exhibited cosine rhythmicity over at least one 24 h period; 5 exhibiting a cosine rhythm on both days. Eight metabolites significantly increased during sleep deprivation compared with sleep (taurine, formate, citrate, 3-indoxyl sulfate, carnitine, 3-hydroxyisobutyrate, TMAO and acetate) and 8 significantly decreased (dimethylamine, 4-DTA, creatinine, ascorbate, 2-hydroxyisobutyrate, allantoin, 4-DEA, 4-hydroxyphenylacetate). These data indicate that sampling time, the presence or absence of sleep and the response to sleep deprivation are highly relevant when identifying biomarkers in urinary metabolic profiling studies. PMID:26450397

  2. Diurnal rhythms in the human urine metabolome during sleep and total sleep deprivation.

    PubMed

    Giskeødegård, Guro F; Davies, Sarah K; Revell, Victoria L; Keun, Hector; Skene, Debra J

    2015-10-09

    Understanding how metabolite levels change over the 24 hour day is of crucial importance for clinical and epidemiological studies. Additionally, the association between sleep deprivation and metabolic disorders such as diabetes and obesity requires investigation into the links between sleep and metabolism. Here, we characterise time-of-day variation and the effects of sleep deprivation on urinary metabolite profiles. Healthy male participants (n = 15) completed an in-laboratory study comprising one 24 h sleep/wake cycle prior to 24 h of continual wakefulness under highly controlled environmental conditions. Urine samples were collected over set 2-8 h intervals and analysed by (1)H NMR spectroscopy. Significant changes were observed with respect to both time of day and sleep deprivation. Of 32 identified metabolites, 7 (22%) exhibited cosine rhythmicity over at least one 24 h period; 5 exhibiting a cosine rhythm on both days. Eight metabolites significantly increased during sleep deprivation compared with sleep (taurine, formate, citrate, 3-indoxyl sulfate, carnitine, 3-hydroxyisobutyrate, TMAO and acetate) and 8 significantly decreased (dimethylamine, 4-DTA, creatinine, ascorbate, 2-hydroxyisobutyrate, allantoin, 4-DEA, 4-hydroxyphenylacetate). These data indicate that sampling time, the presence or absence of sleep and the response to sleep deprivation are highly relevant when identifying biomarkers in urinary metabolic profiling studies.

  3. Sleep Deprivation and Time-Based Prospective Memory

    PubMed Central

    Esposito, Maria José; Occhionero, Miranda; Cicogna, PierCarla

    2015-01-01

    Study Objectives: To evaluate the effect of sleep deprivation on time-based prospective memory performance, that is, realizing delayed intentions at an appropriate time in the future (e.g., to take a medicine in 30 minutes). Design: Between-subjects experimental design. The experimental group underwent 24 h of total sleep deprivation, and the control group had a regular sleep-wake cycle. Participants were tested at 08:00. Settings: Laboratory. Participants: Fifty healthy young adults (mean age 22 ± 2.1, 31 female). Interventions: 24 h of total sleep deprivation. Measurements and Results: Participants were monitored by wrist actigraphy for 3 days before the experimental session. The following cognitive tasks were administered: one time-based prospective memory task and 3 reasoning tasks as ongoing activity. Objective and subjective vigilance was assessed by the psychomotor vigilance task and a visual analog scale, respectively. To measure the time-based prospective memory task we assessed compliance and clock checking behavior (time monitoring). Sleep deprivation negatively affected time-based prospective memory compliance (P < 0.001), objective vigilance (mean RT: P < 0.001; slowest 10% RT: P < 0.001; lapses: P < 0.005), and subjective vigilance (P < 0.0001). Performance on reasoning tasks and time monitoring behavior did not differ between groups. Conclusions: The results highlight the potential dangerous effects of total sleep deprivation on human behavior, particularly the ability to perform an intended action after a few minutes. Sleep deprivation strongly compromises time-based prospective memory compliance but does not affect time check frequency. Sleep deprivation may impair the mechanism that allows the integration of information related to time monitoring with the prospective intention. Citation: Esposito MJ, Occhionero M, Cicogna P. Sleep deprivation and time-based prospective memory. SLEEP 2015;38(11):1823–1826. PMID:26085303

  4. Oculomotor responses during partial and total sleep deprivation.

    PubMed

    Rowland, Laura M; Thomas, Maria L; Thorne, David R; Sing, Helen C; Krichmar, Jeffrey L; Davis, H Quigg; Balwinski, Sharon M; Peters, Robert D; Kloeppel-Wagner, Esther; Redmond, Daniel P; Alicandri, Elizabeth; Belenky, Gregory

    2005-07-01

    Oculomotor responses related to the pupil light reflex (PLR) and saccadic velocity may be sensitive to the effects of sleepiness and therefore could be used to evaluate an individual's fitness for duty. There were 12 normal subjects who completed an 8-d study. They were allowed 8 h in bed on the first three nights, 4 h in bed on the fourth night, and then were sleep deprived for the following 64 h. Approximately every 3 h, subjects performed a battery of tests which included a 45-s automated oculomotor test and a 40-min PC-based driving simulator task. Sleepiness was evaluated with a self-assessment instrument. Subjects were allowed 10 h of recovery sleep following sleep deprivation. Oculomotor results for nine subjects showed a significant increase in latency to pupil constriction and a significant decrease in saccadic velocity with total, but not partial, sleep deprivation. The most robust changes during sleep deprivation occurred for saccadic velocity. A night of recovery sleep reversed the effects of total sleep deprivation on latency to pupil constriction and saccadic velocity. Subjective sleepiness and off-road accidents were found to significantly increase over the sleep deprivation period. A significant positive correlation between increasing latency to pupil constriction and increasing sleepiness and driving accidents, and a significant negative correlation between decreasing saccadic velocity and increasing sleepiness and driving accidents during sleep deprivation were found. These findings suggest that oculomotor functions, particularly saccadic velocity, are feasible for assessing neurophysiological changes associated with and predictive of sleep deprivation-induced operational performance degradation.

  5. Slow wave and REM sleep deprivation effects on explicit and implicit memory during sleep.

    PubMed

    Casey, Sarah J; Solomons, Luke C; Steier, Joerg; Kabra, Neeraj; Burnside, Anna; Pengo, Martino F; Moxham, John; Goldstein, Laura H; Kopelman, Michael D

    2016-11-01

    It has been debated whether different stages in the human sleep cycle preferentially mediate the consolidation of explicit and implicit memories, or whether all of the stages in succession are necessary for optimal consolidation. Here we investigated whether the selective deprivation of slow wave sleep (SWS) or rapid eye movement (REM) sleep over an entire night would have a specific effect on consolidation in explicit and implicit memory tasks. Participants completed a set of explicit and implicit memory tasks at night, prior to sleep. They had 1 control night of undisturbed sleep and 2 experimental nights, during which either SWS or REM sleep was selectively deprived across the entire night (sleep conditions counterbalanced across participants). Polysomnography recordings quantified precisely the amount of SWS and REM sleep that occurred during each of the sleep conditions, and spindle counts were recorded. In the morning, participants completed the experimental tasks in the same sequence as the night before. SWS deprivation disrupted the consolidation of explicit memories for visuospatial information (ηp2 = .23), and both SWS (ηp2 = .53) and REM sleep (ηp2 = .52) deprivation adversely affected explicit verbal recall. Neither SWS nor REM sleep deprivation affected aspects of short-term or working memory, and did not affect measures of verbal implicit memory. Spindle counts did not correlate significantly with memory performance. These findings demonstrate the importance of measuring the sleep cycles throughout the entire night, and the contribution of both SWS and REM sleep to memory consolidation. (PsycINFO Database Record (c) 2016 APA, all rights reserved).

  6. Sleep Deficiency and Deprivation Leading to Cardiovascular Disease

    PubMed Central

    Kohansieh, Michelle; Makaryus, Amgad N.

    2015-01-01

    Sleep plays a vital role in an individual's mental, emotional, and physiological well-being. Not only does sleep deficiency lead to neurological and psychological disorders, but also the literature has explored the adverse effects of sleep deficiency on the cardiovascular system. Decreased quantity and quality of sleep have been linked to cardiovascular disease (CVD) risk factors, such as hypertension, obesity, diabetes, and dyslipidemia. We explore the literature correlating primary sleep deficiency and deprivation as a cause for cardiovascular disease and cite endothelial dysfunction as a common underlying mechanism. PMID:26495139

  7. Deconstructing and reconstructing cognitive performance in sleep deprivation.

    PubMed

    Jackson, Melinda L; Gunzelmann, Glenn; Whitney, Paul; Hinson, John M; Belenky, Gregory; Rabat, Arnaud; Van Dongen, Hans P A

    2013-06-01

    Mitigation of cognitive impairment due to sleep deprivation in operational settings is critical for safety and productivity. Achievements in this area are hampered by limited knowledge about the effects of sleep loss on actual job tasks. Sleep deprivation has different effects on different cognitive performance tasks, but the mechanisms behind this task-specificity are poorly understood. In this context it is important to recognize that cognitive performance is not a unitary process, but involves a number of component processes. There is emerging evidence that these component processes are differentially affected by sleep loss. Experiments have been conducted to decompose sleep-deprived performance into underlying cognitive processes using cognitive-behavioral, neuroimaging and cognitive modeling techniques. Furthermore, computational modeling in cognitive architectures has been employed to simulate sleep-deprived cognitive performance on the basis of the constituent cognitive processes. These efforts are beginning to enable quantitative prediction of the effects of sleep deprivation across different task contexts. This paper reviews a rapidly evolving area of research, and outlines a theoretical framework in which the effects of sleep loss on cognition may be understood from the deficits in the underlying neurobiology to the applied consequences in real-world job tasks.

  8. Deconstructing and Reconstructing Cognitive Performance in Sleep Deprivation

    PubMed Central

    Jackson, Melinda L.; Gunzelmann, Glenn; Whitney, Paul; Hinson, John M.; Belenky, Gregory; Rabat, Arnaud; Van Dongen, Hans P. A.

    2012-01-01

    Summary Mitigation of cognitive impairment due to sleep deprivation in operational settings is critical for safety and productivity. Achievements in this area are hampered by limited knowledge about the effects of sleep loss on actual job tasks. Sleep deprivation has different effects on different cognitive performance tasks, but the mechanisms behind this task-specificity are poorly understood. In this context it is important to recognize that cognitive performance is not a unitary process, but involves a number of component processes. There is emerging evidence that these component processes are differentially affected by sleep loss. Experiments have been conducted to decompose sleep-deprived performance into underlying cognitive processes using cognitive-behavioral, neuroimaging and cognitive modeling techniques. Furthermore, computational modeling in cognitive architectures has been employed to simulate sleep-deprived cognitive performance on the basis of the constituent cognitive processes. These efforts are beginning to enable quantitative prediction of the effects of sleep deprivation across different task contexts. This paper reviews a rapidly evolving area of research, and outlines a theoretical framework in which the effects of sleep loss on cognition may be understood from the deficits in the underlying neurobiology to the applied consequences in real-world job tasks. PMID:22884948

  9. [Sleep deprivation and pain: a review of the newest literature].

    PubMed

    Karmann, A J; Kundermann, B; Lautenbacher, S

    2014-04-01

    It has now been established that sleep deprivation or fragmentation causes hyperalgesia which cannot be explained by a general change in somatosensory perception. However, it has not yet been clarified which of the sleep stages are most relevant for this effect. The seemingly paradoxical effects of sleep deprivation on pain-evoked brain potentials on the one hand and the subjective pain report on the other hand suggest complex changes in gating mechanisms. As the effects on pain and affect can be dissociated a common mechanism of action seems unlikely. Data from animal studies suggest that hyperalgesia due to sleep deprivation might be particularly strong under preexisting neuropathic conditions. Together with results from animal research the finding that endogenous pain modulation (CPM) is impaired by sleep deprivation suggests that the serotoninergic system mediates the effect of sleep deprivation on pain perception. However, other neurotransmitters and neuromodulators still have to be considered. The clinically relevant question arises why sleep deprivation induces hyperalgesia more easily in certain individuals than in others and why this effect then has a longer duration?

  10. Regional differences of the human sleep electroencephalogram in response to selective slow-wave sleep deprivation.

    PubMed

    Ferrara, Michele; De Gennaro, Luigi; Curcio, Giuseppe; Cristiani, Riccardo; Corvasce, Chiara; Bertini, Mario

    2002-07-01

    The purpose of this study was to assess the topographic changes in sleep recuperative processes in response to selective slow-wave sleep (SWS) deprivation. SWS was suppressed on two consecutive nights by means of acoustic stimulation. The electroencephalogram (EEG) power of baseline, deprivation and recovery nights was analysed in 1 Hz bins. During the SWS deprivation nights, large decreases of EEG power were found at frontopolar, central and parietal derivations encompassing the delta, theta and alpha range, while only slow delta (0.5-2 Hz) was affected at the frontal derivation. Recovery sleep was characterized by a generalized increase of power during non-REM sleep encompassing the delta, theta and alpha bands, with a clear antero-posterior gradient. The coherent behaviour of different EEG bands with traditionally different electrophysiological meanings during non-REM sleep suggests that, in light of the recent advances in sleep neurophysiology, a re-examination of the functional role of EEG rhythms during sleep is needed. The 'resistance' to selective SWS deprivation of the frontal area, together with its larger increase of EEG power during recovery, may be interpreted as a sign of a greater sleep need of the frontal cortical areas, confirming that some aspects of the regulatory processes of human sleep are local in nature and may show use-dependent characteristics.

  11. Sleep deprivation and the postnatal blues.

    PubMed

    Wilkie, G; Shapiro, C M

    1992-05-01

    This prospective study of 63 women was designed to investigate the relationship between sleep disruption prior to the birth, during labour and in the early postpartum period and the subsequent development of the postnatal blues. The results from this preliminary study suggest that two factors: (a) a night-time labour; and (b) a history of sleep disruption in the latter stages of pregnancy, may have aetiological importance in the development of postnatal blues. There was little evidence from this study to suggest that sleep disruption on the nights following the birth, the third sleep factor investigated, had any impact on the expression of the blues.

  12. Neighborhood Economic Deprivation and Social Fragmentation: Associations With Children's Sleep.

    PubMed

    Bagley, Erika J; Fuller-Rowell, Thomas E; Saini, Ekjyot K; Philbrook, Lauren E; El-Sheikh, Mona

    2016-12-09

    A growing body of work indicates that experiences of neighborhood disadvantage place children at risk for poor sleep. This study aimed to examine how both neighborhood economic deprivation (a measure of poverty) and social fragmentation (an index of instability) are associated with objective measures of the length and quality of children's sleep. Participants were 210 children (54.3% boys) living predominantly in small towns and semirural communities in Alabama. On average children were 11.3 years old (SD = .63); 66.7% of the children were European American and 33.3% were African American. The sample was socioeconomically diverse with 67.9% of the participants living at or below the poverty line and 32.1% from lower-middle-class or middle-class families. Indicators of neighborhood characteristics were derived from the 2012 American Community Survey and composited to create two variables representing neighborhood economic deprivation and social fragmentation. Child sleep period, actual sleep minutes, and efficiency were examined using actigraphy. Higher levels of neighborhood economic deprivation were associated with fewer sleep minutes and poorer sleep efficiency. More neighborhood social fragmentation was also linked with poorer sleep efficiency. Analyses controlled for demographic characteristics, child health, and family socioeconomic status. Findings indicate that living in economically and socially disadvantaged neighborhoods predicts risk for shorter and lower-quality sleep in children. Examination of community context in addition to family and individual characteristics may provide a more comprehensive understanding of the factors shaping child sleep.

  13. Sleep Deprivation and Time-Based Prospective Memory.

    PubMed

    Esposito, Maria José; Occhionero, Miranda; Cicogna, PierCarla

    2015-11-01

    To evaluate the effect of sleep deprivation on time-based prospective memory performance, that is, realizing delayed intentions at an appropriate time in the future (e.g., to take a medicine in 30 minutes). Between-subjects experimental design. The experimental group underwent 24 h of total sleep deprivation, and the control group had a regular sleep-wake cycle. Participants were tested at 08:00. Laboratory. Fifty healthy young adults (mean age 22 ± 2.1, 31 female). 24 h of total sleep deprivation. Participants were monitored by wrist actigraphy for 3 days before the experimental session. The following cognitive tasks were administered: one time-based prospective memory task and 3 reasoning tasks as ongoing activity. Objective and subjective vigilance was assessed by the psychomotor vigilance task and a visual analog scale, respectively. To measure the time-based prospective memory task we assessed compliance and clock checking behavior (time monitoring). Sleep deprivation negatively affected time-based prospective memory compliance (P < 0.001), objective vigilance (mean RT: P < 0.001; slowest 10% RT: P < 0.001; lapses: P < 0.005), and subjective vigilance (P < 0.0001). Performance on reasoning tasks and time monitoring behavior did not differ between groups. The results highlight the potential dangerous effects of total sleep deprivation on human behavior, particularly the ability to perform an intended action after a few minutes. Sleep deprivation strongly compromises time-based prospective memory compliance but does not affect time check frequency. Sleep deprivation may impair the mechanism that allows the integration of information related to time monitoring with the prospective intention. © 2015 Associated Professional Sleep Societies, LLC.

  14. Sleep and Nutritional Deprivation and Performance of House Officers.

    ERIC Educational Resources Information Center

    Hawkins, Michael R.; And Others

    1985-01-01

    A study to compare cognitive functioning in acutely and chronically sleep-deprived house officers is described. A multivariate analysis of variance revealed significant deficits in primary mental tasks involving basic rote memory, language, and numeric skills. (Author/MLW)

  15. Sleep and Nutritional Deprivation and Performance of House Officers.

    ERIC Educational Resources Information Center

    Hawkins, Michael R.; And Others

    1985-01-01

    A study to compare cognitive functioning in acutely and chronically sleep-deprived house officers is described. A multivariate analysis of variance revealed significant deficits in primary mental tasks involving basic rote memory, language, and numeric skills. (Author/MLW)

  16. Sleep Duration and Area-Level Deprivation in Twins

    PubMed Central

    Watson, Nathaniel F.; Horn, Erin; Duncan, Glen E.; Buchwald, Dedra; Vitiello, Michael V.; Turkheimer, Eric

    2016-01-01

    Study Objectives: We used quantitative genetic models to assess whether area-level deprivation as indicated by the Singh Index predicts shorter sleep duration and modifies its underlying genetic and environmental contributions. Methods: Participants were 4,218 adult twin pairs (2,377 monozygotic and 1,841 dizygotic) from the University of Washington Twin Registry. Participants self-reported habitual sleep duration. The Singh Index was determined by linking geocoding addresses to 17 indicators at the census-tract level using data from Census of Washington State and Census Tract Cartographic Boundary Files from 2000 and 2010. Data were analyzed using univariate and bivariate genetic decomposition and quantitative genetic interaction models that assessed A (additive genetics), C (common environment), and E (unique environment) main effects of the Singh Index on sleep duration and allowed the magnitude of residual ACE variance components in sleep duration to vary with the Index. Results: The sample had a mean age of 38.2 y (standard deviation [SD] = 18), and was predominantly female (62%) and Caucasian (91%). Mean sleep duration was 7.38 h (SD = 1.20) and the mean Singh Index score was 0.00 (SD = 0.89). The heritability of sleep duration was 39% and the Singh Index was 12%. The uncontrolled phenotypic regression of sleep duration on the Singh Index showed a significant negative relationship between area-level deprivation and sleep length (b = −0.080, P < 0.001). Every 1 SD in Singh Index was associated with a ∼4.5 min change in sleep duration. For the quasi-causal bivariate model, there was a significant main effect of E (b0E = −0.063; standard error [SE] = 0.30; P < 0.05). Residual variance components unique to sleep duration were significant for both A (b0Au = 0.734; SE = 0.020; P < 0.001) and E (b0Eu = 0.934; SE = 0.013; P < 0.001). Conclusions: Area-level deprivation has a quasi-causal association with sleep duration, with greater deprivation being related to

  17. Acute sleep deprivation enhances post-infection sleep and promotes survival during bacterial infection in Drosophila.

    PubMed

    Kuo, Tzu-Hsing; Williams, Julie A

    2014-05-01

    Sleep is known to increase as an acute response to infection. However, the function of this behavioral response in host defense is not well understood. To address this problem, we evaluated the effect of acute sleep deprivation on post-infection sleep and immune function in Drosophila. Laboratory. Drosophila melanogaster. Flies were subjected to sleep deprivation before (early DEP) or after (late DEP) bacterial infection. Relative to a non-deprived control, flies subjected to early DEP had enhanced sleep after infection as well as increased bacterial clearance and survival outcome. Flies subjected to late DEP experienced enhanced sleep following the deprivation period, and showed a modest improvement in survival outcome. Continuous DEP (early and late DEP) throughout infection also enhanced sleep later during infection and improved survival. However, improved survival in flies subjected to late or continuous DEP did not occur until after flies had experienced sleep. During infection, both early and late DEP enhanced NFκB transcriptional activity as measured by a luciferase reporter (κB-luc) in living flies. Early DEP also increased NFκB activity prior to infection. Flies that were deficient in expression of either the Relish or Dif NFκB transcription factors showed normal responses to early DEP. However, the effect of early DEP on post-infection sleep and survival was abolished in double mutants, which indicates that Relish and Dif have redundant roles in this process. Acute sleep deprivation elevated NFκB-dependent activity, increased post-infection sleep, and improved survival during bacterial infection.

  18. Auditory Evoked Potentials as a Function of Sleep Deprivation and Recovery Sleep. Addendum.

    DTIC Science & Technology

    1985-09-29

    77 494 AUDITORY EVOICED POTENTIALS AS A FUNCTION OF SLEEPvi 4T DEPIVATION AND RECOVER.. (U) DOILIES SREEN STATE UII ON DEPT OF PSYCHOLOGY P MOIA ET...J-- d , AUDITORY EVOKED POTENTIALS AS A FUNCTION OF SLEEP DEPRIVATION AND RECOVERY SLEEP 0or 00- ADDENDUM Final Report September 29, 1985...PERSONNEL AT USAHEL ............ 2 3.0 RECOMMENDATIONS REGARDING ELECTRODE PLACEMENT FOR SLEEP STAGE RECORDINGS .................. 3 3.1

  19. Auditory Evoked Potentials as a Function of Sleep Deprivation and Recovery Sleep

    DTIC Science & Technology

    1985-09-29

    performance levels. ... ’.I •.5 PROJECT SUMMARY This research studied changes in event-related brain potentials (ERPs) in sleep -deprived subjects over...sleepiness involves monitoring ongoing electroencephalographic (EEG) activity . EEG activity changes with wakefulness, drowsiness and sleep and investigators...rapid-eye- movement ( NREM ) sleep , the amplitude of certain components of the ERPs (P1 and N2) increased while the amplitude of other compone’nts (Ni

  20. Estradiol treatment modulates spontaneous sleep and recovery after sleep deprivation in castrated male rats.

    PubMed

    Wibowo, Erik; Deurveilher, Samüel; Wassersug, Richard J; Semba, Kazue

    2012-01-15

    Exogenous estradiol (E) is used occasionally to treat the side effects associated with androgen-deprivation in men, but its effects on sleep patterns have received little attention. We examined whether E modulates sleep patterns and recovery from sleep loss in castrated male rats. Adult male rats were castrated and implanted subcutaneously with Silastic tubes containing either oil (Cast+Oil) or E (Cast+E). Sham-operated male rats (Intact) were implanted with oil-filled tubes. All rats were also implanted with EEG and EMG electrodes for sleep/wake recordings. After two weeks, polysomnographic recordings were made before, during, and following 6h of sleep deprivation (SD). At baseline, the Cast+Oil group showed sleep and EEG patterns similar to those in the Intact group. Compared to these groups, the Cast+E group spent more time awake during the dark (active) phase, and showed higher EEG theta power (a measure of cortical activation) during wake and rapid eye movement (REM) sleep in both the light and dark phases. Following SD, the Cast+E group showed a larger increase from baseline in REM sleep amount, compared to the Cast+Oil group. The Cast+Oil group showed prolonged rebound in non-REM sleep and EEG delta power, and reduced REM sleep rebound, compared to the other two groups. These results indicate that E treatment in castrated male rats promotes baseline wakefulness during the active phase, and facilitates recovery of REM sleep after acute sleep loss. The possible benefit of E treatment for improving sleep quality in androgen-deprived men remains to be investigated. Copyright © 2011 Elsevier B.V. All rights reserved.

  1. Advice for the Sleep-Deprived

    ERIC Educational Resources Information Center

    Wolfe, Pat

    2005-01-01

    A research has uncovered that adolescent sleep patterns are influenced not so much by the activities of the young adults as by the changes taking place in the biological timing system of their brains. It is evident that teenagers are not getting the amount of sleep they require and suggestions are presented to help diminish if not entirely avoid…

  2. Advice for the Sleep-Deprived

    ERIC Educational Resources Information Center

    Wolfe, Pat

    2005-01-01

    A research has uncovered that adolescent sleep patterns are influenced not so much by the activities of the young adults as by the changes taking place in the biological timing system of their brains. It is evident that teenagers are not getting the amount of sleep they require and suggestions are presented to help diminish if not entirely avoid…

  3. The effects of sleep deprivation on emotional empathy.

    PubMed

    Guadagni, Veronica; Burles, Ford; Ferrara, Michele; Iaria, Giuseppe

    2014-12-01

    Previous studies have shown that sleep loss has a detrimental effect on the ability of the individuals to process emotional information. In this study, we tested the hypothesis that this negative effect extends to the ability of experiencing emotions while observing other individuals, i.e. emotional empathy. To test this hypothesis, we assessed emotional empathy in 37 healthy volunteers who were assigned randomly to one of three experimental groups: one group was tested before and after a night of total sleep deprivation (sleep deprivation group), a second group was tested before and after a usual night of sleep spent at home (sleep group) and the third group was tested twice during the same day (day group). Emotional empathy was assessed by using two parallel versions of a computerized test measuring direct (i.e. explicit evaluation of empathic concern) and indirect (i.e. the observer's reported physiological arousal) emotional empathy. The results revealed that the post measurements of both direct and indirect emotional empathy of participants in the sleep deprivation group were significantly lower than those of the sleep and day groups; post measurement scores of participants in the day and sleep groups did not differ significantly for either direct or indirect emotional empathy. These data are consistent with previous studies showing the negative effect of sleep deprivation on the processing of emotional information, and extend these effects to emotional empathy. The findings reported in our study are relevant to healthy individuals with poor sleep habits, as well as clinical populations suffering from sleep disturbances.

  4. Acute sleep deprivation reduces energy expenditure in healthy men.

    PubMed

    Benedict, Christian; Hallschmid, Manfred; Lassen, Arne; Mahnke, Christin; Schultes, Bernd; Schiöth, Helgi Birgir; Born, Jan; Lange, Tanja

    2011-06-01

    Epidemiologic evidence indicates that chronic sleep curtailment increases risk of developing obesity, but the mechanisms behind this relation are largely unknown. We examined the influence of a single night of total sleep deprivation on morning energy expenditures and food intakes in healthy humans. According to a balanced crossover design, we examined 14 normal-weight male subjects on 2 occasions during a regular 24-h sleep-wake cycle (including 8 h of nocturnal sleep) and a 24-h period of continuous wakefulness. On the morning after regular sleep and total sleep deprivation, resting and postprandial energy expenditures were assessed by indirect calorimetry, and the free-choice food intake from an opulent buffet was tested in the late afternoon at the end of the experiment. Circulating concentrations of ghrelin, leptin, norepinephrine, cortisol, thyreotropin, glucose, and insulin were repeatedly measured over the entire 24-h session. In comparison with normal sleep, resting and postprandial energy expenditures assessed on the subsequent morning were significantly reduced after sleep deprivation by ≈5% and 20%, respectively (P < 0.05 and P < 0.0001). Nocturnal wakefulness increased morning plasma ghrelin concentrations (P < 0.02) and nocturnal and daytime circulating concentrations of thyreotropin, cortisol, and norepinephrine (P < 0.05) as well as morning postprandial plasma glucose concentrations (P < 0.05). Changes in food intakes were variable, and no differences between wake and sleep conditions were detected. Our findings show that one night of sleep deprivation acutely reduces energy expenditure in healthy men, which suggests that sleep contributes to the acute regulation of daytime energy expenditure in humans.

  5. Sleep Deprivation and Recovery Sleep Prior to a Noxious Inflammatory Insult Influence Characteristics and Duration of Pain.

    PubMed

    Vanini, Giancarlo

    2016-01-01

    Insufficient sleep and chronic pain are public health epidemics. Sleep loss worsens pain and predicts the development of chronic pain. Whether previous, acute sleep loss and recovery sleep determine pain levels and duration remains poorly understood. This study tested whether acute sleep deprivation and recovery sleep prior to formalin injection alter post-injection pain levels and duration. Male Sprague-Dawley rats (n = 48) underwent sleep deprivation or ad libitum sleep for 9 hours. Thereafter, rats received a subcutaneous injection of formalin or saline into a hind paw. In the recovery sleep group, rats were allowed 24 h between sleep deprivation and the injection of formalin. Mechanical and thermal nociception were assessed using the von Frey test and Hargreaves' method. Nociceptive measures were performed at 1, 3, 7, 10, 14, 17 and 21 days post-injection. Formalin caused bilateral mechanical hypersensitivity (allodynia) that persisted for up to 21 days post-injection. Sleep deprivation significantly enhanced bilateral allodynia. There was a synergistic interaction when sleep deprivation preceded a formalin injection. Rats allowed a recovery sleep period prior to formalin injection developed allodynia only in the injected limb, with higher mechanical thresholds (less allodynia) and a shorter recovery period. There were no persistent changes in thermal nociception. The data suggest that acute sleep loss preceding an inflammatory insult enhances pain and can contribute to chronic pain. The results encourage studies in a model of surgical pain to test whether enhancing sleep reduces pain levels and duration. © 2016 Associated Professional Sleep Societies, LLC.

  6. Changes in Plasma Lipids during Exposure to Total Sleep Deprivation

    PubMed Central

    Chua, Eric Chern-Pin; Shui, Guanghou; Cazenave-Gassiot, Amaury; Wenk, Markus R.; Gooley, Joshua J.

    2015-01-01

    Study Objectives: The effects of sleep loss on plasma lipids, which play an important role in energy homeostasis and signaling, have not been systematically examined. Our aim was to identify lipid species in plasma that increase or decrease reliably during exposure to total sleep deprivation. Design: Twenty individuals underwent sleep deprivation in a laboratory setting. Blood was drawn every 4 h and mass spectrometry techniques were used to analyze concentrations of 263 lipid species in plasma, including glycerolipids, glycerophospholipids, sphingolipids, and sterols. Setting: Chronobiology and Sleep Laboratory, Duke-NUS Graduate Medical School. Participants: Healthy ethnic-Chinese males aged 21–28 y (n = 20). Interventions: Subjects were kept awake for 40 consecutive hours. Measurements and Results: Each metabolite time series was modeled as a sum of sinusoidal (circadian) and linear components, and we assessed whether the slope of the linear component differed from zero. More than a third of all individually analyzed lipid profiles exhibited a circadian rhythm and/or a linear change in concentration during sleep deprivation. Twenty-five lipid species showed a linear and predominantly unidirectional trend in concentration levels that was consistent across participants. Choline plasmalogen levels decreased, whereas several phosphatidylcholine (PC) species and triacylglycerides (TAG) carrying polyunsaturated fatty acids increased. Conclusions: The decrease in choline plasmalogen levels during sleep deprivation is consistent with prior work demonstrating that these lipids are susceptible to degradation by oxidative stress. The increase in phosphatidylcholines and triacylglycerides suggests that sleep loss might modulate lipid metabolism, which has potential implications for metabolic health in individuals who do not achieve adequate sleep. Citation: Chua EC, Shui G, Cazenave-Gassiot A, Wenk MR, Gooley JJ. Changes in plasma lipids during exposure to total sleep

  7. High-Throughput Analysis of Dynamic Gene Expression Associated with Sleep Deprivation and Recovery Sleep in the Mouse Brain

    DTIC Science & Technology

    2006-12-01

    2006 4. TITLE AND SUBTITLE 5a. CONTRACT NUMBER High -Throughput Analysis of Dynamic Gene Expression Associated with Sleep Deprivation and...waking (W), rapid eye movement sleep (REMS), and non-rapid eye movement sleep (NREMS). Waking is defined by low voltage, low theta EEG with high ...voltage EMG. REM sleep is defined by the lowest voltage EMG and low voltage EEG with high theta activity. Non-REM sleep is all sleep other than REM

  8. Binocular and monocular/unihemispheric sleep in the domestic chick (Gallus gallus) after a moderate sleep deprivation.

    PubMed

    Bobbo, Daniela; Nelini, Cristian; Mascetti, Gian G

    2008-03-01

    Binocular (Bin-sleep) and monocular/unihemispheric sleep (Mo-Un sleep) were studied in domestic chicks (Gallus gallus) after an 8 h period of sleep deprivation. Eleven-day-old chicks were divided into three groups: two non-deprived (N-DEP1 and N-DEP2) and one deprived for 8 h (DEP-8H). Deprivation was performed by placing chicks on a treadmill on which they were forced to walk continuously. Sleep behaviour was recorded for 6 h consecutively immediately after the end of sleep deprivation. During the recovery period, sleep-deprived chicks slept for a longer duration, spent significantly more time in binocular sleep and slept for significantly longer episodes that did control chicks. Regarding Mo-Un sleep, sleep deprivation seems to affect the right hemisphere by reducing the number of episodes and the time spent sleeping with the left eye closed. These results suggest that sleep-deprivation significantly influences the pattern of sleep in domestic chicks allowing for a better recovery.

  9. Increased Automaticity and Altered Temporal Preparation Following Sleep Deprivation

    PubMed Central

    Kong, Danyang; Asplund, Christopher L.; Ling, Aiqing; Chee, Michael W.L.

    2015-01-01

    Study Objectives: Temporal expectation enables us to focus limited processing resources, thereby optimizing perceptual and motor processing for critical upcoming events. We investigated the effects of total sleep deprivation (TSD) on temporal expectation by evaluating the foreperiod and sequential effects during a psychomotor vigilance task (PVT). We also examined how these two measures were modulated by vulnerability to TSD. Design: Three 10-min visual PVT sessions using uniformly distributed foreperiods were conducted in the wake-maintenance zone the evening before sleep deprivation (ESD) and three more in the morning following approximately 22 h of TSD. TSD vulnerable and nonvulnerable groups were determined by a tertile split of participants based on the change in the number of behavioral lapses recorded during ESD and TSD. A subset of participants performed six additional 10-min modified auditory PVTs with exponentially distributed foreperiods during rested wakefulness (RW) and TSD to test the effect of temporal distribution on foreperiod and sequential effects. Setting: Sleep laboratory. Participants: There were 172 young healthy participants (90 males) with regular sleep patterns. Nineteen of these participants performed the modified auditory PVT. Measurements and Results: Despite behavioral lapses and slower response times, sleep deprived participants could still perceive the conditional probability of temporal events and modify their level of preparation accordingly. Both foreperiod and sequential effects were magnified following sleep deprivation in vulnerable individuals. Only the foreperiod effect increased in nonvulnerable individuals. Conclusions: The preservation of foreperiod and sequential effects suggests that implicit time perception and temporal preparedness are intact during total sleep deprivation. Individuals appear to reallocate their depleted preparatory resources to more probable event timings in ongoing trials, whereas vulnerable

  10. Sleep deprivation alters thyroid hormone economy in rats.

    PubMed

    Rodrigues, Nayana Coutinho; da Cruz, Natália Santos; de Paula Nascimento, Cristine; da Conceição, Rodrigo Rodrigues; da Silva, Alba Cenélia Matos; Olivares, Emerson Lopes; Marassi, Michelle Porto

    2015-02-01

    What is the central question of this study? The relationship between the thyroid system and sleep deprivation has seldom been assessed in the literature, and mounting evidence exists that sleep disturbances influence human lifestyles. The aim of this study was to investigate the hypothalamic-pituitary-thyroid axis and thyroid hormone metabolism in sleep-deprived and sleep-restricted rats. What is the main finding and its importance? Central hypothyroidism and high thyroxine (T4 ) to 3,5,3'-triiodothyronine (T3 ) activation in brown adipose tissue were observed following sleep deprivation. Sleep-restricted rats exhibited normal thyroid-stimulating hormone and T4 concentrations despite increased circulating T3 . Sleep recovery for 24 h did not normalize the high T3 concentrations, suggesting that high T3 is a powerful counterregulatory mechanism activated following sleep deprivation. Modern life has shortened sleep time, and the consequences of sleep deprivation have been examined in both human subjects and animal models. As the relationship between thyroid function and sleep deprivation has not been fully investigated, the aim of this study was to assess the hypothalamic-pituitary-thyroid axis and thyroid hormone metabolism following paradoxical sleep deprivation (PSD) and sleep restriction (SR) in rats. The effects of a 24 h rebound period were also studied. Male Wistar rats (200-250 g, n = 10 per group) were subjected to sleep deprivation via the modified multiple platform method. Rats were assigned to the following seven groups: control, PSD for 24 or 96 h, 24 or 96 h of sleep deprivation with rebound (PSD24R and PSD96R), SR for 21 days (SR21) and SR21 with rebound (SR21R). Blood samples were collected to determine the 3,5,3'-triiodothyronine (T3 ), thyroxine (T4 ) and thyroid-stimulating hormone concentrations. Brown adipose tissue iodothyronine deiodinase type 2 (D2) activity was also evaluated. Body weight gain was dramatically reduced (by ∼50-100%) in all

  11. [Effects of chronic partial sleep deprivation on growth and learning/memory in young rats].

    PubMed

    Jiang, Fan; Shen, Xiao-Ming; Li, Sheng-Hui; Cui, Mao-Long; Zhang, Yin; Wang, Cheng; Yu, Xiao-Gang; Yan, Chong-Huai

    2009-02-01

    The effects of sleep deprivation on the immature brain remain unknown. Based on a computer controlled chronic sleep deprivation animal model, the effects of chronic partial sleep deprivation on growth, learning and memory in young rats were explored. Twelve weaned male Spraque-Dawley rats (3-week-old) were randomly divided into sleep deprivation, test control and blank control groups. Sleep deprivation was performed using computer-controlled "disc-over-water" technique at 8-11 am daily, for 14 days. The temperature and weights were measured every 7 days. Morris water maze was used to test spatial learning and memory abilities before and 7 and 14 days after sleep deprivation. After 14 days of sleep deprivation, the rats were sacrificed for weighting their major organs. After 14 days of sleep deprivation, the rats' temperature increased significantly. During the sleep deprivation, the rate of weight gain in the sleep deprivation group was much slower than that in the test control and blank control groups. The thymus of the rats subjected to sleep deprivation was much lighter than that of the blank control group. After 7 days of sleep deprivation, the rats showed slower acquisition of reference memory, but were capable of successfully performing the task by repeated exposure to the test. Such impairment of reference memory was not seen 14 days after sleep deprivation. Chronic sleep deprivation can affect growth of immature rats, as well as their abilities to acquire spatial reference memory.

  12. Sleep deprivation and the organization of the behavioral states.

    NASA Technical Reports Server (NTRS)

    Dement, W. C.

    1972-01-01

    Questions concerning the significance of sleep in the developing organism are investigated, together with the mechanisms that underlie the unique distribution of behavioral states at any particular age and during any particular experimental manipulation. It is attempted to define the states of sleep and wakefulness in terms of a temporal confluence of a number of more or less independent processes, taking also into account the functional consequences of these attributes. The results of a selective deprivation of rapid eye movement sleep are explored, giving attention to effects on sleep, behavioral changes, brain excitability, pharmacological changes, and biochemical changes.

  13. Occurrence of epileptiform discharges and sleep during EEG recordings in children after melatonin intake versus sleep-deprivation.

    PubMed

    Gustafsson, Greta; Broström, Anders; Ulander, Martin; Vrethem, Magnus; Svanborg, Eva

    2015-08-01

    To determine if melatonin is equally efficient as partial sleep deprivation in inducing sleep without interfering with epileptiform discharges in EEG recordings in children 1-16 years old. We retrospectively analysed 129 EEGs recorded after melatonin intake and 113 EEGs recorded after partial sleep deprivation. Comparisons were made concerning occurrence of epileptiform discharges, the number of children who fell asleep and the technical quality of EEG recordings. Comparison between different age groups was also made. No significant differences were found regarding occurrence of epileptiform discharges (33% after melatonin intake, 36% after sleep deprivation), or proportion of unsuccessful EEGs (8% and 10%, respectively). Melatonin and sleep deprivation were equally efficient in inducing sleep (70% in both groups). Significantly more children aged 1-4 years obtained sleep after melatonin intake in comparison to sleep deprivation (82% vs. 58%, p⩽0.01), and in comparison to older children with melatonin induced sleep (58-67%, p⩽0.05). Sleep deprived children 9-12 years old had higher percentage of epileptiform discharges (62%, p⩽0.05) compared to younger sleep deprived children. Melatonin is equally efficient as partial sleep deprivation to induce sleep and does not affect the occurrence of epileptiform discharges in the EEG recording. Sleep deprivation could still be preferable in older children as melatonin probably has less sleep inducing effect. Melatonin induced sleep have advantages, especially in younger children as they fall asleep easier than after sleep deprivation. The procedure is easier for the parents than keeping a young child awake for half the night. Copyright © 2014 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rights reserved.

  14. Individual Differences in Response to Sleep Deprivation: Assessment of Fatigue Following Sleep Loss

    NASA Technical Reports Server (NTRS)

    Carskadon, Mary A.

    1997-01-01

    Previous work has indicated that a small but significant number of participants in sleep deprivation studies or in simulated shift work experiments manifests an exaggerated performance decrement when they reach a critical point in the experiment, usually near the trough of the circadian cycle or the middle of the night. Those who show this exaggerated response do not appear to differ from other normal volunteers in any substantial way according to usual screening criteria or baseline values. The present study aims to examine factors that may provide the basis for this extreme response. We propose that a preexisting sleep deficit-as manifested by low values on the Multiple Sleep Latency Test (MSLT)-may account for extreme responders. Roth and colleagues (1993) have shown that among normal volunteers screened for a variety of studies, approximately 20 to 25 percent show low (< or = 6 minutes) MSLT scores on a consistent basis, whereas a like proportion shows consistently high MSLT scores (> or = 13 minutes). Additionally, studies by this group have indicated that subjects with low MSLT scores may suffer from chronic insufficient sleep (Roth et al., 1993), as further substantiated by the finding that they have consistently higher nocturnal sleep efficiency and that their MSLT scores rise to normal values when sleep is extended (Roehrs et al., 1996). We hypothesize that the short MSLT subjects have a significant long-term sleep deficit that leads to a marked intolerance for sleep deprivation or shift work. We further suggest that this sleep debt may signify an increased sleep need in these individuals that is not met either due to personal preference or to societal pressures (or both). If this speculation is accurate, then we predict that the tolerance for sleep deprivation in such individuals can be increased by "pretreatment" with sleep extension. Thus, the present study is designed to test the following two hypotheses: subjects with nominal sleep patterns who have

  15. Individual Differences in Response to Sleep Deprivation: Assessment of Fatigue Following Sleep Loss

    NASA Technical Reports Server (NTRS)

    Carskadon, Mary A.

    1997-01-01

    Previous work has indicated that a small but significant number of participants in sleep deprivation studies or in simulated shift work experiments manifests an exaggerated performance decrement when they reach a critical point in the experiment, usually near the trough of the circadian cycle or the middle of the night. Those who show this exaggerated response do not appear to differ from other non-nal volunteers in any substantial way according to usual screening criteria or baseline values. The present study aims to examine factors that may provide the basis for this extreme response. We propose that a preexisting sleep deficit-as manifested by low values on the Multiple Sleep Latency Test (MSLT)-may account for extreme responders. Roth and colleagues (1993) have shown that among normal volunteers screened for a variety of studies, approximately 20 to 25 percent show low (< 6 minutes) MSLT scores on a consistent basis, whereas a like proportion shows consistently high MSLT scores (> 13 minutes). Additionally, studies by this group have indicated that subjects with low MSLT scores may suffer from chronic insufficient sleep (Roth et al., 1993), as further substantiated by the finding that they have consistently higher nocturnal sleep efficiency and that their MSLT scores rise to normal values when sleep is extended (Roehrs et al., 1996). We hypothesize that the short MSLT subjects have a significant long-term sleep deficit that leads to a marked intolerance for sleep deprivation or shift work. We further suggest that this sleep debt may signify an increased sleep need in these individuals that is not met either due to personal preference or to societal pressures (or both). If this speculation is accurate, then we predict that the tolerance for sleep deprivation in such individuals can be increased by "pretreatment" with sleep extension. Thus, the present study is designed to test the following two hypotheses: subjects with nominal sleep patterns who have low MSLT

  16. Individual Differences in Response to Sleep Deprivation: Assessment of Fatigue Following Sleep Loss

    NASA Technical Reports Server (NTRS)

    Carskadon, Mary A.

    1997-01-01

    Previous work has indicated that a small but significant number of participants in sleep deprivation studies or in simulated shift work experiments manifests an exaggerated performance decrement when they reach a critical point in the experiment, usually near the trough of the circadian cycle or the middle of the night. Those who show this exaggerated response do not appear to differ from other non-nal volunteers in any substantial way according to usual screening criteria or baseline values. The present study aims to examine factors that may provide the basis for this extreme response. We propose that a preexisting sleep deficit-as manifested by low values on the Multiple Sleep Latency Test (MSLT)-may account for extreme responders. It has been shown that among normal volunteers screened for a variety of studies, approximately 20 to 25 percent show low (< 6 minutes) MSLT scores on a consistent basis, whereas a like proportion shows consistently high MSLT scores (> 13 minutes). Additionally, studies by this group have indicated that subjects with low MSLT scores may suffer from chronic insufficient sleep, as further substantiated by the finding that they have consistently higher nocturnal sleep efficiency and that their MSLT scores rise to normal values when sleep is extended. We hypothesize that the short MSLT subjects have a significant long-term sleep deficit that leads to a marked intolerance for sleep deprivation or shift work. We further suggest that this sleep debt may signify an increased sleep need in these individuals that is not met either due to personal preference or to societal pressures (or both). If this speculation is accurate, then we predict that the tolerance for sleep deprivation in such individuals can be increased by "pretreatment" with sleep extension. Thus, the present study is designed to test the following two hypotheses: (1) subjects with nominal sleep patterns who have low MSLT scores (e.g., Sleepy subjects) will show an exaggerated

  17. [A world record in marathon tennis: sleep deprivation and performance].

    PubMed

    Tafti, M; Vergé, M; Besset, A; Billiard, M

    1989-01-01

    We studied the effects of marked sleep deprivation on the EEG patterns and performance of a physically fit man (age 26) on the occasion of the world record continuous marathon tennis play (147 hours, 20 minutes). Before and immediately after the marathon, the sleep patterns of the player were recorded in our laboratory. After playing for 40 and 80 hours and within 24 hours, the performance changes were evaluated each hour. Amounts of the different sleep stages during the first recovery night compared with those of the baseline indicate an increase of 56% for total sleep time, 54% for stages 1 and 2, 154% for stages 3 and 4 and 20% for REM sleep. During the second recovery night, only REM sleep showed an increase. Activity index showed a marked decrease after 80 hours of sleep deprivation compared with that after 40 hours and was dramatically worsened during nighttime. The number of faults and pauses was also increased after 80 hours, suggesting a clear performance deterioration. Our results confirmed the effects of sleep deprivation on the recovery and performance deterioration.

  18. Aging worsens the effects of sleep deprivation on postural control.

    PubMed

    Robillard, Rébecca; Prince, François; Filipini, Daniel; Carrier, Julie

    2011-01-01

    Falls increase with age and cause significant injuries in the elderly. This study aimed to determine whether age modulates the interactions between sleep deprivation and postural control and to evaluate how attention influences these interactions in the elderly. Fifteen young (24±2.7 y.o.) and 15 older adults (64±3.2 y.o.) stood still on a force plate after a night of sleep and after total sleep deprivation. Center of pressure range and velocity were measured with eyes open and with eyes closed while participants performed an interference task, a control task, and no cognitive task. Sleep deprivation increased the antero-posterior range of center of pressure in both age groups and center of pressure speed in older participants only. In elderly participants, the destabilizing effects of sleep deprivation were more pronounced with eyes closed. The interference task did not alter postural control beyond the destabilization induced by sleep loss in older subjects. It was concluded that sleep loss has greater destabilizing effects on postural control in older than in younger participants, and may therefore increase the risk of falls in the elderly.

  19. Confinement and sleep deprivation effects on propensity to take risks.

    PubMed

    Chaumet, Guillaume; Taillard, Jacques; Sagaspe, Patricia; Pagani, Massimo; Dinges, David F; Pavy-Le-Traon, Anne; Bareille, Marie-Pierre; Rascol, Olivier; Philip, Pierre

    2009-02-01

    The impact of confinement and sleep deprivation on risk-taking propensity is a key issue in crew management. We investigated both confinement and gender effects on risk propensity and performance during up to 36 h of extended wakefulness. We studied 4 groups of 3 men and 3 women [N = 24, mean age (+/- SD) = 32.9 +/- 5.8 yr] for 10 consecutive days: a 7-d confined period (CONF) or a 7-d baseline (BASE) condition preceding one control night of normal sleep, one night of sleep deprivation, and one recovery night in the laboratory. Risk propensity (EVAR scale) and simple reaction time task (SRTT) performances were monitored every 2.25 h (0930-1945) during CONF and every 2.11 h (0930-0745) during the sleep deprivation condition. Overall risk propensity during extended wakefulness showed a variation in both conditions with two diurnal peaks separated by a nocturnal minima. After the confinement period, no second peak was found. Number of lapses (reaction time > 500 ms) on the SRTT varied daily in both conditions. In the normal sleep schedule, subjects increased their level of impulsiveness between the first day and the end of confinement (P < 0.05). During the night of sleep deprivation, risk-taking propensity decreases and remains stable the following day in the confinement condition while it increases after the baseline period. In a confined environment under a normal sleep-wake schedule, impulsiveness increases in men and women.

  20. Chronic sleep deprivation and seasonality: implications for the obesity epidemic.

    PubMed

    Cizza, G; Requena, M; Galli, G; de Jonge, L

    2011-11-01

    Sleep duration has progressively fallen over the last 100 years while obesity has increased in the past 30 years. Several studies have reported an association between chronic sleep deprivation and long-term weight gain. Increased energy intake due to sleep loss has been listed as the main mechanism. The consequences of chronic sleep deprivation on energy expenditure have not been fully explored. Sleep, body weight, mood and behavior are subjected to circannual changes. However, in our modern environment seasonal changes in light and ambient temperature are attenuated. Seasonality, defined as cyclic changes in mood and behavior, is a stable personality trait with a strong genetic component. We hypothesize that the attenuation in seasonal changes in the environment may produce negative consequences, especially in individuals more predisposed to seasonality, such as women. Seasonal affective disorder, a condition more common in women and characterized by depressed mood, hypersomnia, weight gain, and carbohydrate craving during the winter, represents an extreme example of seasonality. One of the postulated functions of sleep is energy preservation. Hibernation, a phenomenon characterized by decreased energy expenditure and changes in the state of arousal, may offer useful insight into the mechanisms behind energy preservation during sleep. The goals of this article are to: a) consider the contribution of changes in energy expenditure to the weight gain due to sleep loss; b) review the phenomena of seasonality, hibernation, and their neuroendocrine mechanisms as they relate to sleep, energy expenditure, and body weight regulation.

  1. Chronic sleep deprivation and seasonality: Implications for the obesity epidemic

    PubMed Central

    Cizza, G.; Requena, M.; Galli, G.; de Jonge, L.

    2012-01-01

    Sleep duration has progressively fallen over the last 100 years while obesity has increased in the past 30 years. Several studies have reported an association between chronic sleep deprivation and long-term weight gain. Increased energy intake due to sleep loss has been listed as the main mechanism. The consequences of chronic sleep deprivation on energy expenditure have not been fully explored. Sleep, body weight, mood and behavior are subjected to circannual changes. However, in our modern environment seasonal changes in light and ambient temperature are attenuated. Seasonality, defined as cyclic changes in mood and behavior, is a stable personality trait with a strong genetic component. We hypothesize that the attenuation in seasonal changes in the environment may produce negative consequences, especially in individuals more predisposed to seasonality, such as women. Seasonal affective disorder, a condition more common in women and characterized by depressed mood, hypersomnia, weight gain, and carbohydrate craving during the winter, represents an extreme example of seasonality. One of the postulated functions of sleep is energy preservation. Hibernation, a phenomenon characterized by decreased energy expenditure and changes in the state of arousal, may offer useful insight into the mechanisms behind energy preservation during sleep. The goals of this article are to: a) consider the contribution of changes in energy expenditure to the weight gain due to sleep loss; b) review the phenomena of seasonality, hibernation, and their neuroendocrine mechanisms as they relate to sleep, energy expenditure, and body weight regulation. PMID:21720205

  2. Transition to daylight saving time reduces sleep duration plus sleep efficiency of the deprived sleep.

    PubMed

    Lahti, Tuuli A; Leppämäki, Sami; Lönnqvist, Jouko; Partonen, Timo

    2006-10-09

    Daylight saving time (DST) is widely adopted. We explored the effects of transition to daylight saving time on sleep. With the use of wrist-worn accelerometers, we monitored the rest-activity cycles on a sample of 10 healthy adults for 10 days around the transition to summer time. Identical measurement protocols were carried out twice on the same individuals during the transitions in the years of 2003 and 2004, yielding data on 200 person-days for analysis. Both sleep duration and sleep efficiency were reduced after the transition both years. After the transition sleep time was shortened by 60.14min (P<0.01) and sleep efficiency was reduced by 10% (P<0.01) on average. Transition to daylight saving time appears to compromise the process of sleep by decreasing both sleep duration and sleep efficiency.

  3. Effects of sleep deprivation on spontaneous arousals in humans.

    PubMed

    Sforza, Emilia; Chapotot, Florian; Pigeau, Ross; Paul, Paul Naitoh; Buguet, Alain

    2004-09-15

    The hierarchical definition of arousals from sleep includes a range of physiologic responses including microarousals, delta and K-complex bursts, and variations in autonomic system. Whether patterns in slow-wave electroencephalographic activity and autonomic activation are primary forms of arousal response can be addressed by studying effects of total sleep deprivation. We therefore examined changes in arousal density during recovery sleep in healthy subjects. Participants spent 6 consecutive 24-hour periods in the laboratory. Nights 1 and 2 were baseline nights followed by 64-hour total sleep deprivation, then 2 consecutive recovery nights. Sleep-deprivation protocol was conducted under laboratory conditions with continuous behavioral and electrophysiologic monitoring. Twelve drug-free men aged 27.4 +/- 7.9 years were studied. None reported sleepiness or altered sleep-wake cycle, and none had neurologic, psychiatric or sleep disorders. N/A. Arousals were classified into 4 levels: microarousals, phases of transitory activation, and delta and K-complex bursts. Sleep deprivation induced changes in the density of considered arousals except phases of transitory activation, with a distinct pattern among the different types. The greatest change was found for microarousals, which showed a significant decrease in the first recovery night (P = .01), with return to baseline thereafter. A fall in K-complex and delta-burst density was noted in the first recovery night, not, however, reaching statistical significance. The phases of transitory activation rate were virtually unaffected throughout the experimental nights. We conclude that homeostatic sleep processes exert an inhibitory effect on arousal response from sleep with a significant effect only on the microarousal density. Decreased delta and K-complex burst rates, though not significant, support the hypothesis that they may be activating processes, probably modulated by factors independent from those implicated in

  4. Effects of sleep deprivation on short-term recognition memory.

    PubMed

    Polzella, D J

    1975-03-01

    A probe-recognition short-term memory paradigm was used to inquire into the precise effects of sleep deprivation on human memory. It was found that recognition performance, as measured by d', was generally impaired for each subjects after 24 hr of sleep deprivation. While d' was shown to decrease exponentially as the number of items intervening between the target and the probe increased, this decay rate was not affected by sleep loss. In addition there was confirmation of a previously observed increase in the positive skewness of reaction times after wakefulness. The data were consistent with the hypothesis that sleep deprivation increases the occurrence of lapses, periods of lowered reactive capacity, which prevent the encoding of items in short-term memory.

  5. Sleep Duration and Area-Level Deprivation in Twins.

    PubMed

    Watson, Nathaniel F; Horn, Erin; Duncan, Glen E; Buchwald, Dedra; Vitiello, Michael V; Turkheimer, Eric

    2016-01-01

    We used quantitative genetic models to assess whether area-level deprivation as indicated by the Singh Index predicts shorter sleep duration and modifies its underlying genetic and environmental contributions. Participants were 4,218 adult twin pairs (2,377 monozygotic and 1,841 dizygotic) from the University of Washington Twin Registry. Participants self-reported habitual sleep duration. The Singh Index was determined by linking geocoding addresses to 17 indicators at the census-tract level using data from Census of Washington State and Census Tract Cartographic Boundary Files from 2000 and 2010. Data were analyzed using univariate and bivariate genetic decomposition and quantitative genetic interaction models that assessed A (additive genetics), C (common environment), and E (unique environment) main effects of the Singh Index on sleep duration and allowed the magnitude of residual ACE variance components in sleep duration to vary with the Index. The sample had a mean age of 38.2 y (standard deviation [SD] = 18), and was predominantly female (62%) and Caucasian (91%). Mean sleep duration was 7.38 h (SD = 1.20) and the mean Singh Index score was 0.00 (SD = 0.89). The heritability of sleep duration was 39% and the Singh Index was 12%. The uncontrolled phenotypic regression of sleep duration on the Singh Index showed a significant negative relationship between area-level deprivation and sleep length (b = -0.080, P < 0.001). Every 1 SD in Singh Index was associated with a ∼4.5 min change in sleep duration. For the quasi-causal bivariate model, there was a significant main effect of E (b(0E) = -0.063; standard error [SE] = 0.30; P < 0.05). Residual variance components unique to sleep duration were significant for both A (b(0Au) = 0.734; SE = 0.020; P < 0.001) and E (b(0Eu) = 0.934; SE = 0.013; P < 0.001). Area-level deprivation has a quasi-causal association with sleep duration, with greater deprivation being related to shorter sleep. As area-level deprivation

  6. Voluntary oculomotor performance upon awakening after total sleep deprivation.

    PubMed

    Ferrara, M; De Gennaro MFL; Bertini, M

    2000-09-15

    The potential impact of sleep inertia on measures of voluntary oculomotor control have been surprisingly neglected. The present study examined the effects of 40 hours of sleep deprivation on saccadic (SAC) and smooth pursuit (SP) performance, attentional/visual search performance (Letter Cancellation Task, LCT) and subjective sleepiness (Sleepiness Visual Analog Scale, SVAS) recorded immediately after awakening. Standard polysomnography of nine normal subjects was recorded for 3 nights (1 adaptation, AD; 1 baseline, BSL; 1 recovery, REC); BSL and REC were separated by a period of 40 h of continuous wakefulness, during which subjects were tested every two hours. Within 30 s of each morning awakening, a test battery (SAC, SP, LCT, SVAS) was administered to subjects in bed. For data analysis, mean performance obtained during the day preceding the sleep deprivation night was considered as "Diurnal Baseline" and compared to performance upon awakening from nocturnal sleep. As a consequence of sleep deprivation, SWS percentage was doubled during REC. Saccade latency increased and velocity decreased significantly upon awakening from REC as compared to the other three conditions (Diurnal baseline, AD awakening, BSL awakening); accuracy was unaffected. As regards SP, phase did not show any impairment upon awakening, while velocity gain upon awakening from REC was significantly lower as compared to the other conditions. Finally, number of hits on LCT upon awakening from REC was significantly lower and subjective sleepiness higher as compared to Diurnal Baseline. It is concluded that 40 h of sleep deprivation significantly impaired performance to SAC and SP tasks recorded upon awakening from recovery sleep. This performance worsening is limited to the measures of speed, while both SAC accuracy and SP phase do not show a significant decrease upon awakening. Since saccadic velocity has recently been found to negatively correlate with simulator vehicle crash rates, it is

  7. Salivary Biomarkers of Physical Fatigue as Markers of Sleep Deprivation

    PubMed Central

    Michael, Darren J.; Valle, Bianca; Cox, Jennifer; Kalns, John E.; Fogt, Donovan L.

    2013-01-01

    Study Objective: Determine whether a salivary biomarker of physical fatigue, referred to as the fatigue biomarker index (FBI), can discriminate a control group from a sleep deprived group when saliva is collected under controlled conditions. The study expands on previous work examining changes in the composition of saliva during periods of prolonged exercise. Methods: Thirty (30) young adults (14 Control [CON]; 16 Sleep Deprived [SDEP]) were monitored for mood state (Profile of Mood States [POMS]), cognitive performance (Stroop Color-Conflict Tests), and salivary biomarkers of physical fatigue over a 48-h period with sampling at 3-h intervals. Trials lasted from 06:00 on day 1 (time = -3 h) to 09:00 on day 3 (time = 48 h). Levels of salivary biomarkers were calculated from liquid chromatography-mass spectrometry (LC-MS) data. Statistical comparisons were made using Wilcoxon rank sum tests with a Bonferroni correction to limit type 1 error. Receiver-operator characteristic (ROC) analysis was used to evaluate the ability of the various parameters to distinguish the SDEP population from the CON population. Results: Longitudinal analysis demonstrated significant between-group differences in all three parameters. ROC analysis demonstrated that cognitive performance tests and salivary biomarkers of physical fatigue distinguish the SDEP population from the CON population. Conclusions: A previously identified salivary biomarker of physical fatigue may provide an alternative method for discriminating sleep deprived from rested individuals. The salivary biomarker of physical fatigue holds promise as an objective measure of sleep deprivation, perhaps eventually removing the reliance on self-reported sleep diaries and/or repeated polysomnographs for longitudinal tracking of sleep quality and/or diagnosis of sleep disorders. Citation: Michael DJ; Valle B; Cox J; Kalns JE; Fogt DL. Salivary biomarkers of physical fatigue as markers of sleep deprivation. J Clin Sleep Med 2013

  8. REM sleep deprivation impairs muscle regeneration in rats.

    PubMed

    Mônico-Neto, Marcos; Dáttilo, Murilo; Ribeiro, Daniel Araki; Lee, Kil Sun; de Mello, Marco Túlio; Tufik, Sergio; Antunes, Hanna Karen Moreira

    2017-02-01

    The aim was observe the influence of sleep deprivation (SD) and sleep recovery on muscle regeneration process in rats submitted to cryolesion. Thirty-two Wistar rats were randomly allocated in four groups: control (CTL), SD for 96 h (SD96), control plus sleep recovery period (CTL + R) and SD96h plus 96 h of sleep recovery (SD96 + R). The animals were submitted to muscle injury by cryolesioning, after to SD and sleep recovery. The major outcomes of this study were the reduction of muscular IGF-1 in both legs (injured and uninjured) and a delay in muscle regeneration process of animals submitted to SD compared to animals that slept, with increase connective tissue, inflammatory infiltrate and minor muscle fibers. SD impairs muscle regeneration in rats, moreover reduces muscular IGF-1 and sleep recovery was able to restore it to basal levels, but it was not enough to normalize the muscle regeneration.

  9. Notch signaling modulates sleep homeostasis and learning after sleep deprivation in Drosophila

    PubMed Central

    Seugnet, Laurent; Suzuki, Yasuko; Merlin, Gabriel; Gottschalk, Laura; Duntley, Stephen P.

    2013-01-01

    Summary The role of the trans-membrane receptor Notch in the adult brain is poorly understood. Here, we provide evidence that bunched, a negative regulator of Notch is involved in sleep homeostasis. Genetic evidence indicates that interfering with bunched activity in the mushroom bodies (MBs) abolishes sleep homeostasis. Combining bunched and Delta loss-of-function mutations rescued normal homeostasis, suggesting that Notch signaling may be involved in regulating sensitivity to sleep loss. Preventing the down regulation of Delta by over-expressing a wild-type transgene in MBs reduces sleep homeostasis and, importantly, prevents learning impairments induced by sleep deprivation. Similar resistance to sleep loss is observed with the Notchspl-1 gain-of-function mutants. Immunohistochemistry reveals that the Notch receptor is expressed in glia, whereas Delta is localized in neurons. Importantly the expression of the intracellular domain of Notch, a dominant activated form of the receptor, in glia is sufficient to prevent learning deficits after sleep deprivation. Together these results identify a novel neuronal-glia signalling pathway dependent on Notch and regulated by bunched. These data highlight the emerging role of neuron-glia interactions in regulating both sleep and learning impairments associated with sleep loss. PMID:21549599

  10. [Circadian fluctuations in the muscular efficiency of athletes: with sleep versus sleep deprivation].

    PubMed

    Callard, D; Gauthier, A; Maffiuletti, N; Davenne, D; Van Hoecke, J

    2000-01-01

    The influence of time of day on muscular performance was studied. From part of the results of two different studies (EAS et EPS), the effects of sleep deprivation were appreciated. Seven times over the 24-h period, developed torque and myoelectric activity were estimated during maximal isometric voluntary contractions using an isokinetic dynamometer: elbow flexion for EAS in standardised sleep, and knee extension for EPS in complete sleep deprivation. The results showed nycthemeral changes in torque in both conditions (p < 0.005), with maximal values recorded at the beginning of night. Although during sleep deprivation (EPS) the rhythm followed neurophysiological factors, during EAS, this rhythm was accounted for by the variations in the contractile state of muscle.

  11. Sleep extension increases IGF-I concentrations before and during sleep deprivation in healthy young men.

    PubMed

    Chennaoui, Mounir; Arnal, Pierrick J; Drogou, Catherine; Sauvet, Fabien; Gomez-Merino, Danielle

    2016-09-01

    Sleep deprivation is known to suppress circulating trophic factors such as insulin-like growth factor (IGF)-I and brain-derived neurotrophic factor (BDNF). This experiment examined the effect of an intervention involving 6 nights of extended sleep before total sleep deprivation on this catabolic profile. In a randomized crossover design, 14 young men (age range: 26-37 years) were either in an extended (EXT; time in bed: 2100-0700 h) or habitual (HAB: 2230-0700 h) sleep condition, followed by 3 days in the laboratory with blood sampling at baseline (B), after 24 h of sleep deprivation (24h-SD), and after 1 night of recovery sleep (R). In the EXT condition compared with the HAB condition, free IGF-I levels were significantly higher at B, 24h-SD, and R (P < 0.001), and those of total IGF-I at B and 24h-SD (P < 0.05). EXT did not influence growth hormone, IGF binding protein 3, BDNF, insulin, and glucose levels. The only effect of 24 h of sleep deprivation was for insulin levels, which were significantly higher after R compared with B. In a healthy adult, additional sleep over 1 week increased blood concentrations of the anabolic factor IGF-I before and during 24 h of sleep deprivation and after the subsequent recovery night without effects on BDNF. With further research, these findings may prove to be important in guiding effective lifestyle modifications to limit physical or cognitive deficits associated with IGF-I decrease with age.

  12. A novel BHLHE41 variant is associated with short sleep and resistance to sleep deprivation in humans.

    PubMed

    Pellegrino, Renata; Kavakli, Ibrahim Halil; Goel, Namni; Cardinale, Christopher J; Dinges, David F; Kuna, Samuel T; Maislin, Greg; Van Dongen, Hans P A; Tufik, Sergio; Hogenesch, John B; Hakonarson, Hakon; Pack, Allan I

    2014-08-01

    Earlier work described a mutation in DEC2 also known as BHLHE41 (basic helix-loophelix family member e41) as causal in a family of short sleepers, who needed just 6 h sleep per night. We evaluated whether there were other variants of this gene in two well-phenotyped cohorts. Sequencing of the BHLHE41 gene, electroencephalographic data, and delta power analysis and functional studies using cell-based luciferase. We identified new variants of the BHLHE41 gene in two cohorts who had either acute sleep deprivation (n = 200) or chronic partial sleep deprivation (n = 217). One variant, Y362H, at another location in the same exon occurred in one twin in a dizygotic twin pair and was associated with reduced sleep duration, less recovery sleep following sleep deprivation, and fewer performance lapses during sleep deprivation than the homozygous twin. Both twins had almost identical amounts of non rapid eye movement (NREM) sleep. This variant reduced the ability of BHLHE41 to suppress CLOCK/BMAL1 and NPAS2/BMAL1 transactivation in vitro. Another variant in the same exome had no effect on sleep or response to sleep deprivation and no effect on CLOCK/BMAL1 transactivation. Random mutagenesis identified a number of other variants of BHLHE41 that affect its function. There are a number of mutations of BHLHE41. Mutations reduce total sleep while maintaining NREM sleep and provide resistance to the effects of sleep loss. Mutations that affect sleep also modify the normal inhibition of BHLHE41 of CLOCK/BMAL1 transactivation. Thus, clock mechanisms are likely involved in setting sleep length and the magnitude of sleep homeostasis. Pellegrino R, Kavakli IH, Goel N, Cardinale CJ, Dinges DF, Kuna ST, Maislin G, Van Dongen HP, Tufik S, Hogenesch JB, Hakonarson H, Pack AI. A novel BHLHE41 variant is associated with short sleep and resistance to sleep deprivation in humans. SLEEP 2014;37(8):1327-1336.

  13. Cognitive Performance, Sleepiness, and Mood in Partially Sleep Deprived Adolescents: The Need for Sleep Study

    PubMed Central

    Lo, June C.; Ong, Ju Lynn; Leong, Ruth L.F.; Gooley, Joshua J.; Chee, Michael W.L.

    2016-01-01

    Study Objectives: To investigate the effects of sleep restriction (7 nights of 5 h time in bed [TIB]) on cognitive performance, subjective sleepiness, and mood in adolescents. Methods: A parallel-group design was adopted in the Need for Sleep Study. Fifty-six healthy adolescents (25 males, age = 15–19 y) who studied in top high schools and were not habitual short sleepers were randomly assigned to Sleep Restriction (SR) or Control groups. Participants underwent a 2-w protocol consisting of 3 baseline nights (TIB = 9 h), 7 nights of sleep opportunity manipulation (TIB = 5 h for the SR and 9 h for the control groups), and 3 nights of recovery sleep (TIB = 9 h) at a boarding school. A cognitive test battery was administered three times each day. Results: During the manipulation period, the SR group demonstrated incremental deterioration in sustained attention, working memory and executive function, increase in subjective sleepiness, and decrease in positive mood. Subjective sleepiness and sustained attention did not return to baseline levels even after 2 recovery nights. In contrast, the control group maintained baseline levels of cognitive performance, subjective sleepiness, and mood throughout the study. Incremental improvement in speed of processing, as a result of repeated testing and learning, was observed in the control group but was attenuated in the sleep-restricted participants, who, despite two recovery sleep episodes, continued to perform worse than the control participants. Conclusions: A week of partial sleep deprivation impairs a wide range of cognitive functions, subjective alertness, and mood even in high-performing high school adolescents. Some measures do not recover fully even after 2 nights of recovery sleep. Commentary: A commentary on this article appears in this issue on page 497. Citation: Lo JC, Ong JL, Leong RL, Gooley JJ, Chee MW. Cognitive performance, sleepiness, and mood in partially sleep deprived adolescents: the need for sleep study

  14. Changes in Plasma Lipids during Exposure to Total Sleep Deprivation.

    PubMed

    Chua, Eric Chern-Pin; Shui, Guanghou; Cazenave-Gassiot, Amaury; Wenk, Markus R; Gooley, Joshua J

    2015-11-01

    The effects of sleep loss on plasma lipids, which play an important role in energy homeostasis and signaling, have not been systematically examined. Our aim was to identify lipid species in plasma that increase or decrease reliably during exposure to total sleep deprivation. Twenty individuals underwent sleep deprivation in a laboratory setting. Blood was drawn every 4 h and mass spectrometry techniques were used to analyze concentrations of 263 lipid species in plasma, including glycerolipids, glycerophospholipids, sphingolipids, and sterols. Chronobiology and Sleep Laboratory, Duke-NUS Graduate Medical School. Healthy ethnic-Chinese males aged 21-28 y (n = 20). Subjects were kept awake for 40 consecutive hours. Each metabolite time series was modeled as a sum of sinusoidal (circadian) and linear components, and we assessed whether the slope of the linear component differed from zero. More than a third of all individually analyzed lipid profiles exhibited a circadian rhythm and/or a linear change in concentration during sleep deprivation. Twenty-five lipid species showed a linear and predominantly unidirectional trend in concentration levels that was consistent across participants. Choline plasmalogen levels decreased, whereas several phosphatidylcholine (PC) species and triacylglycerides (TAG) carrying polyunsaturated fatty acids increased. The decrease in choline plasmalogen levels during sleep deprivation is consistent with prior work demonstrating that these lipids are susceptible to degradation by oxidative stress. The increase in phosphatidylcholines and triacylglycerides suggests that sleep loss might modulate lipid metabolism, which has potential implications for metabolic health in individuals who do not achieve adequate sleep. © 2015 Associated Professional Sleep Societies, LLC.

  15. Sleep deprivation and its effects on object-selective attention.

    PubMed

    Chee, Michael W L; Tan, Jiat Chow; Parimal, Sarayu; Zagorodnov, Vitali

    2010-01-15

    Sleep deprivation (SD) affects attention but it is an open question as to whether all subtypes of attention are similarly affected. We investigated the effects of 24 h of total SD on object-selective attention. 26 healthy, young adults viewed quartets of alternating faces or place scenes and performed selective judgments on faces only, scenes only or both faces and scenes. Volunteers underwent fMRI following a normal night of sleep and again following approximately 24 h of total sleep deprivation in a counterbalanced fashion. Sleep deprivation resulted in slower and less accurate picture classification as well as poorer recognition memory for scenes. Attention strongly modulated activation in the Parahippocampal Place Area (PPA). Task-related activation in the fronto-parietal cortex and PPA was reduced in SD, but the relative modulation of PPA activation by attention was preserved. Psychophysiological interaction between the left intra-parietal sulcus and the PPA that was clearly present after a normal night of sleep was reduced below threshold following SD suggesting that PPI may be a more sensitive method of detecting change in selective attention. Sleep deprivation may affect object-selective attention in addition to exerting a task-independent deficit in attention.

  16. The Effects of Sleep Deprivation on Soccer Skills.

    PubMed

    Pallesen, Ståle; Gundersen, Hilde Stokvold; Kristoffersen, Morten; Bjorvatn, Bjørn; Thun, Eirunn; Harris, Anette

    2017-08-01

    Many athletes sleep poorly due to stress, travel, and competition anxiety. In the present study, we investigated the effects of sleep deprivation on soccer skills (juggling, dribbling, ball control, continuous kicking, 20 and 40 m sprint, and 30 m sprint with changes of direction). In all, 19 male junior soccer players (14-19 years old) were recruited and participated in a cross-balanced experimental study comprising two conditions; habitual sleep and 24 hours sleep deprivation. In both conditions, testing took place between 8 a.m. and 10 a.m. Order of tests was counterbalanced. Each test was conducted once or twice in a sequence repeated three times. The results revealed a negative effect of sleep deprivation on the continuous kicking test. On one test, 30 meter sprint with directional changes, a significant condition × test repetition interaction was found, indicating a steeper learning curve in the sleep deprived condition from Test 1 to Test 2 and a steeper learning curve in the rested condition from Test 2 to Test 3. The results are discussed in terms of limitations and strengths, and recommendations for future studies are outlined.

  17. Increased Automaticity and Altered Temporal Preparation Following Sleep Deprivation.

    PubMed

    Kong, Danyang; Asplund, Christopher L; Ling, Aiqing; Chee, Michael W L

    2015-08-01

    Temporal expectation enables us to focus limited processing resources, thereby optimizing perceptual and motor processing for critical upcoming events. We investigated the effects of total sleep deprivation (TSD) on temporal expectation by evaluating the foreperiod and sequential effects during a psychomotor vigilance task (PVT). We also examined how these two measures were modulated by vulnerability to TSD. Three 10-min visual PVT sessions using uniformly distributed foreperiods were conducted in the wake-maintenance zone the evening before sleep deprivation (ESD) and three more in the morning following approximately 22 h of TSD. TSD vulnerable and nonvulnerable groups were determined by a tertile split of participants based on the change in the number of behavioral lapses recorded during ESD and TSD. A subset of participants performed six additional 10-min modified auditory PVTs with exponentially distributed foreperiods during rested wakefulness (RW) and TSD to test the effect of temporal distribution on foreperiod and sequential effects. Sleep laboratory. There were 172 young healthy participants (90 males) with regular sleep patterns. Nineteen of these participants performed the modified auditory PVT. Despite behavioral lapses and slower response times, sleep deprived participants could still perceive the conditional probability of temporal events and modify their level of preparation accordingly. Both foreperiod and sequential effects were magnified following sleep deprivation in vulnerable individuals. Only the foreperiod effect increased in nonvulnerable individuals. The preservation of foreperiod and sequential effects suggests that implicit time perception and temporal preparedness are intact during total sleep deprivation. Individuals appear to reallocate their depleted preparatory resources to more probable event timings in ongoing trials, whereas vulnerable participants also rely more on automatic processes. © 2015 Associated Professional Sleep

  18. Sustained attention performance during sleep deprivation: evidence of state instability

    NASA Technical Reports Server (NTRS)

    Doran, S. M.; Van Dongen, H. P.; Dinges, D. F.

    2001-01-01

    Nathaniel Kleitman was the first to observe that sleep deprivation in humans did not eliminate the ability to perform neurobehavioral functions, but it did make it difficult to maintain stable performance for more than a few minutes. To investigate variability in performance as a function of sleep deprivation, n = 13 subjects were tested every 2 hours on a 10-minute, sustained-attention, psychomotor vigilance task (PVT) throughout 88 hours of total sleep deprivation (TSD condition), and compared to a control group of n = 15 subjects who were permitted a 2-hour nap every 12 hours (NAP condition) throughout the 88-hour period. PVT reaction time means and standard deviations increased markedly among subjects and within each individual subject in the TSD condition relative to the NAP condition. TSD subjects also had increasingly greater performance variability as a function of time on task after 18 hours of wakefulness. During sleep deprivation, variability in PVT performance reflected a combination of normal timely responses, errors of omission (i.e., lapses), and errors of commission (i.e., responding when no stimulus was present). Errors of omission and errors of commission were highly intercorrelated across deprivation in the TSD condition (r = 0.85, p = 0.0001), suggesting that performance instability is more likely to include compensatory effort than a lack of motivation. The marked increases in PVT performance variability as sleep loss continued supports the "state instability" hypothesis, which posits that performance during sleep deprivation is increasingly variable due to the influence of sleep initiating mechanisms on the endogenous capacity to maintain attention and alertness, thereby creating an unstable state that fluctuates within seconds and that cannot be characterized as either fully awake or asleep.

  19. Prolonged Eyelid Closure Episodes during Sleep Deprivation in Professional Drivers

    PubMed Central

    Alvaro, Pasquale K.; Jackson, Melinda L.; Berlowitz, David J.; Swann, Philip; Howard, Mark E.

    2016-01-01

    Study Objectives: Real life ocular measures of drowsiness use average blink duration, amplitude and velocity of eyelid movements to reflect drowsiness in drivers. However, averaged data may conceal the variability in duration of eyelid closure episodes, and more prolonged episodes that indicate higher levels of drowsiness. The current study aimed to describe the frequency and duration of prolonged eyelid closure episodes during acute sleep deprivation. Methods: Twenty male professional drivers (mean age ± standard deviation = 41.9 ± 8.3 years) were recruited from the Transport Workers Union newsletter and newspaper advertisements in Melbourne, Australia. Each participant underwent 24 hours of sleep deprivation and completed a simulated driving task (AusEd), the Psychomotor Vigilance Task, and the Karolinska Sleepiness Scale. Eyelid closure episodes during the driving task were recorded and analyzed manually from digital video recordings. Results: Eyelid closure episodes increased in frequency and duration with a median of zero s/h of eyelid closure after 3 h increasing to 34 s/h after 23 h awake. Eyelid closure episodes were short and infrequent from 3 to 14 h of wakefulness. After 17 h of sleep deprivation, longer and more frequent eyelid closure episodes began to occur. Episodes lasting from 7 seconds up to 18 seconds developed after 20 h of wakefulness. Length of eyelid closure episodes was moderately to highly correlated with the standard deviation of lateral lane position, braking reaction time, crashes, impaired vigilance, and subjective sleepiness. Conclusions: The frequency and duration of episodes of prolonged eyelid closure increases during acute sleep deprivation, with very prolonged episodes after 17 hours awake. Automated devices that assess drowsiness using averaged measures of eyelid closure episodes need to be able to detect prolonged eyelid closure episodes that occur during more severe sleep deprivation. Citation: Alvaro PK, Jackson ML

  20. Sustained attention performance during sleep deprivation: evidence of state instability

    NASA Technical Reports Server (NTRS)

    Doran, S. M.; Van Dongen, H. P.; Dinges, D. F.

    2001-01-01

    Nathaniel Kleitman was the first to observe that sleep deprivation in humans did not eliminate the ability to perform neurobehavioral functions, but it did make it difficult to maintain stable performance for more than a few minutes. To investigate variability in performance as a function of sleep deprivation, n = 13 subjects were tested every 2 hours on a 10-minute, sustained-attention, psychomotor vigilance task (PVT) throughout 88 hours of total sleep deprivation (TSD condition), and compared to a control group of n = 15 subjects who were permitted a 2-hour nap every 12 hours (NAP condition) throughout the 88-hour period. PVT reaction time means and standard deviations increased markedly among subjects and within each individual subject in the TSD condition relative to the NAP condition. TSD subjects also had increasingly greater performance variability as a function of time on task after 18 hours of wakefulness. During sleep deprivation, variability in PVT performance reflected a combination of normal timely responses, errors of omission (i.e., lapses), and errors of commission (i.e., responding when no stimulus was present). Errors of omission and errors of commission were highly intercorrelated across deprivation in the TSD condition (r = 0.85, p = 0.0001), suggesting that performance instability is more likely to include compensatory effort than a lack of motivation. The marked increases in PVT performance variability as sleep loss continued supports the "state instability" hypothesis, which posits that performance during sleep deprivation is increasingly variable due to the influence of sleep initiating mechanisms on the endogenous capacity to maintain attention and alertness, thereby creating an unstable state that fluctuates within seconds and that cannot be characterized as either fully awake or asleep.

  1. Sleep Deprivation and Recovery Sleep Prior to a Noxious Inflammatory Insult Influence Characteristics and Duration of Pain

    PubMed Central

    Vanini, Giancarlo

    2016-01-01

    Study Objectives: Insufficient sleep and chronic pain are public health epidemics. Sleep loss worsens pain and predicts the development of chronic pain. Whether previous, acute sleep loss and recovery sleep determine pain levels and duration remains poorly understood. This study tested whether acute sleep deprivation and recovery sleep prior to formalin injection alter post-injection pain levels and duration. Methods: Male Sprague-Dawley rats (n = 48) underwent sleep deprivation or ad libitum sleep for 9 hours. Thereafter, rats received a subcutaneous injection of formalin or saline into a hind paw. In the recovery sleep group, rats were allowed 24 h between sleep deprivation and the injection of formalin. Mechanical and thermal nociception were assessed using the von Frey test and Hargreaves' method. Nociceptive measures were performed at 1, 3, 7, 10, 14, 17 and 21 days post-injection. Results: Formalin caused bilateral mechanical hypersensitivity (allodynia) that persisted for up to 21 days post-injection. Sleep deprivation significantly enhanced bilateral allodynia. There was a synergistic interaction when sleep deprivation preceded a formalin injection. Rats allowed a recovery sleep period prior to formalin injection developed allodynia only in the injected limb, with higher mechanical thresholds (less allodynia) and a shorter recovery period. There were no persistent changes in thermal nociception. Conclusion: The data suggest that acute sleep loss preceding an inflammatory insult enhances pain and can contribute to chronic pain. The results encourage studies in a model of surgical pain to test whether enhancing sleep reduces pain levels and duration. Citation: Vanini G. Sleep deprivation and recovery sleep prior to a noxious inflammatory insult influence characteristics and duration of pain. SLEEP 2016;39(1):133–142. PMID:26237772

  2. Sleep extension improves neurocognitive functions in chronically sleep-deprived obese individuals.

    PubMed

    Lucassen, Eliane A; Piaggi, Paolo; Dsurney, John; de Jonge, Lilian; Zhao, Xiong-ce; Mattingly, Megan S; Ramer, Angela; Gershengorn, Janet; Csako, Gyorgy; Cizza, Giovanni

    2014-01-01

    Sleep deprivation and obesity, are associated with neurocognitive impairments. Effects of sleep deprivation and obesity on cognition are unknown, and the cognitive long-term effects of improvement of sleep have not been prospectively assessed in short sleeping, obese individuals. To characterize neurocognitive functions and assess its reversibility. Prospective cohort study. Tertiary Referral Research Clinical Center. A cohort of 121 short-sleeping (<6.5 h/night) obese (BMI 30-55 kg/m(2)) men and pre-menopausal women. Sleep extension (468±88 days) with life-style modifications. Neurocognitive functions, sleep quality and sleep duration. At baseline, 44% of the individuals had an impaired global deficit score (t-score 0-39). Impaired global deficit score was associated with worse subjective sleep quality (p = 0.02), and lower urinary dopamine levels (p = 0.001). Memory was impaired in 33%; attention in 35%; motor skills in 42%; and executive function in 51% of individuals. At the final evaluation (N = 74), subjective sleep quality improved by 24% (p<0.001), self-reported sleep duration increased by 11% by questionnaires (p<0.001) and by 4% by diaries (p = 0.04), and daytime sleepiness tended to improve (p = 0.10). Global cognitive function and attention improved by 7% and 10%, respectively (both p = 0.001), and memory and executive functions tended to improve (p = 0.07 and p = 0.06). Serum cortisol increased by 17% (p = 0.02). In a multivariate mixed model, subjective sleep quality and sleep efficiency, urinary free cortisol and dopamine and plasma total ghrelin accounted for 1/5 of the variability in global cognitive function. Drop-out rate. Chronically sleep-deprived obese individuals exhibit substantial neurocognitive deficits that are partially reversible upon improvement of sleep in a non-pharmacological way. These findings have clinical implications for large segments of the US population. www.ClinicalTrials.gov NCT00261898

  3. Effects of cocaine, methamphetamine and modafinil challenge on sleep rebound after paradoxical sleep deprivation in rats.

    PubMed

    Martins, R C S; Andersen, M L; Shih, M C; Tufik, S

    2008-01-01

    Sleep loss is both common and critically relevant to our society and might lead to the abuse of psychostimulants such as amphetamines, cocaine and modafinil. Since psychoactive substance abuse often occurs within a scenario of sleep deficit, the purpose of this investigation was to compare the sleep patterns of rats challenged with cocaine (7 mg/kg, ip), methamphetamine (7 mg/kg, ip), or modafinil (100 mg/kg, ip) subsequent to paradoxical sleep deprivation (PSD) for 96 h. Our results show that, immediately after 96 h of PSD, rats (10 per group) that were injected with a psychostimulant presented lower percentages of paradoxical sleep compared to those injected with saline (P < 0.01). Regarding slow wave sleep (SWS), rats injected with psychostimulants after PSD presented a late rebound (on the second night subsequent to the injection) in the percentage of this phase of sleep when compared to PSD rats injected with saline (P < 0.05). In addition, the current study has produced evidence of the characteristic effect of each drug on sleep architecture. Home cage control rats injected with modafinil and methamphetamine showed a reduction in SWS compared with the saline group. Methamphetamine affected sleep patterns most, since it significantly reduced paradoxical sleep, SWS and sleep efficiency before and after PSD compared to control (P < 0.05). Cocaine was the psychostimulant causing the least changes in sleep pattern in relation to those observed after saline injection. Therefore, our results suggest that abuse of these psychostimulants in a PSD paradigm aggravates their impact on sleep patterns.

  4. Effects of daytime food intake on memory consolidation during sleep or sleep deprivation.

    PubMed

    Herzog, Nina; Friedrich, Alexia; Fujita, Naoko; Gais, Steffen; Jauch-Chara, Kamila; Oltmanns, Kerstin M; Benedict, Christian

    2012-01-01

    Sleep enhances memory consolidation. Bearing in mind that food intake produces many metabolic signals that can influence memory processing in humans (e.g., insulin), the present study addressed the question as to whether the enhancing effect of sleep on memory consolidation is affected by the amount of energy consumed during the preceding daytime. Compared to sleep, nocturnal wakefulness has been shown to impair memory consolidation in humans. Thus, a second question was to examine whether the impaired memory consolidation associated with sleep deprivation (SD) could be compensated by increased daytime energy consumption. To these aims, 14 healthy normal-weight men learned a finger tapping sequence (procedural memory) and a list of semantically associated word pairs (declarative memory). After the learning period, standardized meals were administered, equaling either ∼50% or ∼150% of the estimated daily energy expenditure. In the morning, after sleep or wakefulness, memory consolidation was tested. Plasma glucose was measured both before learning and retrieval. Polysomnographic sleep recordings were performed by electroencephalography (EEG). Independent of energy intake, subjects recalled significantly more word pairs after sleep than they did after SD. When subjects stayed awake and received an energy oversupply, the number of correctly recalled finger sequences was equal to those seen after sleep. Plasma glucose did not differ among conditions, and sleep time in the sleep conditions was not influenced by the energy intake interventions. These data indicate that the daytime energy intake level affects neither sleep's capacity to boost the consolidation of declarative and procedural memories, nor sleep's quality. However, high energy intake was followed by an improved procedural but not declarative memory consolidation under conditions of SD. This suggests that the formation of procedural memory is not only triggered by sleep but is also sensitive to the

  5. Role of Sleep Deprivation in Fear Conditioning and Extinction: Implications for Treatment of PTSD

    DTIC Science & Technology

    2013-10-01

    of the model is the impact on sleep . In animals, fear conditioning disrupts sleep , especially REM sleep . Sleep deprivation, in whole or just of REM ...was tested. We examined the effects of initial learning on REM sleep and whether REM sleep subsequent to learning facilitated memory consolidation of...threat and safety. Results showed increased safety learning was associated with increased consolidation of REM sleep the subsequent night. Increased

  6. Detrimental role of prolonged sleep deprivation on adult neurogenesis

    PubMed Central

    Fernandes, Carina; Rocha, Nuno Barbosa F.; Rocha, Susana; Herrera-Solís, Andrea; Salas-Pacheco, José; García-García, Fabio; Murillo-Rodríguez, Eric; Yuan, Ti-Fei; Machado, Sergio; Arias-Carrión, Oscar

    2015-01-01

    Adult mammalian brains continuously generate new neurons, a phenomenon called adult neurogenesis. Both environmental stimuli and endogenous factors are important regulators of adult neurogenesis. Sleep has an important role in normal brain physiology and its disturbance causes very stressful conditions, which disrupt normal brain physiology. Recently, an influence of sleep in adult neurogenesis has been established, mainly based on sleep deprivation studies. This review provides an overview on how rhythms and sleep cycles regulate hippocampal and subventricular zone neurogenesis, discussing some potential underlying mechanisms. In addition, our review highlights some interacting points between sleep and adult neurogenesis in brain function, such as learning, memory, and mood states, and provides some insights on the effects of antidepressants and hypnotic drugs on adult neurogenesis. PMID:25926773

  7. Sleep Deprivation in Humans, Immunodepression and Glutamine Supplementation

    DTIC Science & Technology

    2007-11-02

    include: shiftworkers (Miller, 1992), intensive care patients (Schwab, 1994), infants (Kahn et al., 1994), ship crews and submariners (Miller et al...administering antibiotics to rats in the first four days of sleep deprivation were inconclusive (Bergmann et al., 1996). With regard to sleep quality...non-existent levels of plasma leptin have been observed in genetically obese mice and humans. The actions of leptin are mainly thought to be

  8. Effects of partial sleep deprivation on slow waves during non-rapid eye movement sleep: a high density EEG investigation

    PubMed Central

    Plante, David T.; Goldstein, Michael R.; Cook, Jesse D.; Smith, Richard; Riedner, Brady A.; Rumble, Meredith E.; Jelenchick, Lauren; Roth, Andrea; Tononi, Giulio; Benca, Ruth M.; Peterson, Michael J.

    2015-01-01

    Objective Changes in slow waves during non-rapid eye movement (NREM) sleep in response to acute total sleep deprivation are well-established measures of sleep homeostasis. This investigation utilized high-density electroencephalography (hdEEG) to examine topographic changes in slow waves during repeated partial sleep deprivation. Methods Twenty-four participants underwent a 6-day sleep restriction protocol. Spectral and period-amplitude analyses of sleep hdEEG data were used to examine changes in slow wave energy, count, amplitude, and slope relative to baseline. Results Changes in slow wave energy were dependent on the quantity of NREM sleep utilized for analysis, with widespread increases during sleep restriction and recovery when comparing data from the first portion of the sleep period, but restricted to recovery sleep if the entire sleep episode was considered. Period-amplitude analysis was less dependent on the quantity of NREM sleep utilized, and demonstrated topographic changes in the count, amplitude, and distribution of slow waves, with frontal increases in slow wave amplitude, numbers of high-amplitude waves, and amplitude/slopes of low amplitude waves resulting from partial sleep deprivation. Conclusions Topographic changes in slow waves occur across the course of partial sleep restriction and recovery. Significance These results demonstrate a homeostatic response to partial sleep loss in humans. PMID:26596212

  9. Effects of partial sleep deprivation on slow waves during non-rapid eye movement sleep: A high density EEG investigation.

    PubMed

    Plante, David T; Goldstein, Michael R; Cook, Jesse D; Smith, Richard; Riedner, Brady A; Rumble, Meredith E; Jelenchick, Lauren; Roth, Andrea; Tononi, Giulio; Benca, Ruth M; Peterson, Michael J

    2016-02-01

    Changes in slow waves during non-rapid eye movement (NREM) sleep in response to acute total sleep deprivation are well-established measures of sleep homeostasis. This investigation utilized high-density electroencephalography (hdEEG) to examine topographic changes in slow waves during repeated partial sleep deprivation. Twenty-four participants underwent a 6-day sleep restriction protocol. Spectral and period-amplitude analyses of sleep hdEEG data were used to examine changes in slow wave energy, count, amplitude, and slope relative to baseline. Changes in slow wave energy were dependent on the quantity of NREM sleep utilized for analysis, with widespread increases during sleep restriction and recovery when comparing data from the first portion of the sleep period, but restricted to recovery sleep if the entire sleep episode was considered. Period-amplitude analysis was less dependent on the quantity of NREM sleep utilized, and demonstrated topographic changes in the count, amplitude, and distribution of slow waves, with frontal increases in slow wave amplitude, numbers of high-amplitude waves, and amplitude/slopes of low amplitude waves resulting from partial sleep deprivation. Topographic changes in slow waves occur across the course of partial sleep restriction and recovery. These results demonstrate a homeostatic response to partial sleep loss in humans. Copyright © 2015 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rights reserved.

  10. The effects of sleep restriction and sleep deprivation in producing false memories.

    PubMed

    Chatburn, Alex; Kohler, Mark J; Payne, Jessica D; Drummond, Sean P A

    2017-01-01

    False memory has been claimed to be the result of an associative process of generalisation, as well as to be representative of memory errors. These can occur at any stage of memory encoding, consolidation, or retrieval, albeit through varied mechanisms. The aim of this paper is to experimentally determine: (i) if cognitive dysfunction brought about by sleep loss at the time of stimulus encoding can influence false memory production; and (ii) whether this relationship holds across sensory modalities. Subjects undertook both the Deese-Roedigger-McDermott (DRM) false memory task and a visual task designed to produce false memories. Performance was measured while subjects were well-rested (9h Time in Bed or TIB), and then again when subjects were either sleep restricted (4h TIB for 4 nights) or sleep deprived (30h total SD). Results indicate (1) that partial and total sleep loss produced equivalent effects in terms of false and veridical verbal memory, (2) that subjects performed worse after sleep loss (regardless of whether this was partial or total sleep loss) on cued recognition-based false and veridical verbal memory tasks, and that sleep loss interfered with subjects' ability to recall veridical, but not false memories under free recall conditions, and (3) that there were no effects of sleep loss on a visual false memory task. This is argued to represent the dysfunction and slow repair of an online verbal associative process in the brain following inadequate sleep.

  11. Monitoring sleep depth: analysis of bispectral index (BIS) based on polysomnographic recordings and sleep deprivation.

    PubMed

    Giménez, Sandra; Romero, Sergio; Alonso, Joan Francesc; Mañanas, Miguel Ángel; Pujol, Anna; Baxarias, Pilar; Antonijoan, Rosa Maria

    2017-02-01

    The assessment and management of sleep are increasingly recommended in the clinical practice. Polysomnography (PSG) is considered the gold standard test to monitor sleep objectively, but some practical and technical constraints exist due to environmental and patient considerations. Bispectral index (BIS) monitoring is commonly used in clinical practice for guiding anesthetic administration and provides an index based on relationships between EEG components. Due to similarities in EEG synchronization between anesthesia and sleep, several studies have assessed BIS as a sleep monitor with contradictory results. The aim of this study was to evaluate objectively both the feasibility and reliability of BIS for sleep monitoring through a robust methodology, which included full PSG recordings at a baseline situation and after 40 h of sleep deprivation. Results confirmed that the BIS index was highly correlated with the hypnogram (0.89 ± 0.02), showing a progressive decrease as sleep deepened, and an increase during REM sleep (awake: 91.77 ± 8.42; stage N1: 83.95 ± 11.05; stage N2: 71.71 ± 11.99; stage N3: 42.41 ± 9.14; REM: 80.11 ± 8.73). Mean and median BIS values were lower in the post-deprivation night than in the baseline night, showing statistical differences for the slow wave sleep (baseline: 42.41 ± 9.14 vs. post-deprivation: 39.49 ± 10.27; p = 0.02). BIS scores were able to discriminate properly between deep (N3) and light (N1, N2) sleep. BIS values during REM overlapped those of other sleep stages, although EMG activity provided by the BIS monitor could help to identify REM sleep if needed. In conclusion, BIS monitors could provide a useful measure of sleep depth in especially particular situations such as intensive care units, and they could be used as an alternative for sleep monitoring in order to reduce PSG-derived costs and to increase capacity in ambulatory care.

  12. Changes in brain glycogen after sleep deprivation vary with genotype.

    PubMed

    Franken, Paul; Gip, Phung; Hagiwara, Grace; Ruby, Norman F; Heller, H Craig

    2003-08-01

    Sleep has been functionally implicated in brain energy homeostasis in that it could serve to replenish brain energy stores that become depleted while awake. Sleep deprivation (SD) should therefore lower brain glycogen content. We tested this hypothesis by sleep depriving mice of three inbred strains, i.e., AKR/J (AK), DBA/2J (D2), and C57BL/6J (B6), that differ greatly in their sleep regulation. After a 6-h SD, these mice and their controls were killed by microwave irradiation, and glycogen and glucose were quantified in the cerebral cortex, brain stem, and cerebellum. After SD, both measures significantly increased by approximately 40% in the cortex of B6 mice, while glycogen significantly decreased by 20-38% in brain stem and cerebellum of AK and D2 mice. In contrast, after SD, glucose content increased in all three structures in AK mice and did not change in D2 mice. The increase in glycogen after SD in B6 mice persisted under conditions of food deprivation that, by itself, lowered cortical glycogen. Furthermore, the strains that differ most in their compensatory response to sleep loss, i.e., AK and D2, did not differ in their glycogen response. Thus glycogen content per se is an unlikely end point of sleep's functional role in brain energy homeostasis.

  13. The effects of acute sleep deprivation during residency training.

    PubMed

    Bartle, E J; Sun, J H; Thompson, L; Light, A I; McCool, C; Heaton, S

    1988-08-01

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

  14. Acute sleep deprivation increases food purchasing in men.

    PubMed

    Chapman, Colin D; Nilsson, Emil K; Nilsson, Victor C; Cedernaes, Jonathan; Rångtell, Frida H; Vogel, Heike; Dickson, Suzanne L; Broman, Jan-Erik; Hogenkamp, Pleunie S; Schiöth, Helgi B; Benedict, Christian

    2013-12-01

    To investigate if acute sleep deprivation affects food purchasing choices in a mock supermarket. On the morning after one night of total sleep deprivation (TSD) or after one night of sleep, 14 normal-weight men were given a fixed budget (300 SEK-approximately 50 USD). They were instructed to purchase as much as they could out of a possible 40 items, including 20 high-caloric foods (>2 kcal/g) and 20 low-caloric foods (<2 kcal/g). The prices of the high-caloric foods were then varied (75%, 100% (reference price), and 125%) to determine if TSD affects the flexibility of food purchasing. Before the task, participants received a standardized breakfast, thereby minimizing the potential confound produced by hunger. In addition, morning plasma concentrations of the orexigenic hormone ghrelin were measured under fasting conditions. Independent of both type of food offered and price condition, sleep-deprived men purchased significantly more calories (+9%) and grams (+18%) of food than they did after one night of sleep (both P < 0.05). Morning plasma ghrelin concentrations were also higher after TSD (P < 0.05). However, this increase did not correlate with the effects of TSD on food purchasing. This experiment demonstrates that acute sleep loss alters food purchasing behavior in men. Copyright © 2013 The Obesity Society.

  15. Rapid eye movement sleep deprivation affects sleep similarly in castrated and noncastrated rats.

    PubMed

    Peder, M

    1987-03-01

    Twenty-four-hour recordings of electrophysiological correlates of the sleep-waking cycle in castrated and noncastrated Wistar rats were performed to validate the cuff pedestal technique in the deprivation of rapid eye movement sleep. An undisturbed pattern of sleep was found in both castrated and noncastrated rats when the cuffs were in the raised position. The lowering of the cuff for 4 days virtually abolished REMs in both groups of rats. During neither the dark nor the light period was there any difference between the castrated and noncastrated rats in the total amount of REMs rebound. The results accord with the data obtained by the conventional flowerpot procedure and show that castration does not influence the amount of REMs before, during, and after REMs deprivation in the rat. It is suggested that testicular testosterone, contrary to growth hormone, is not essential for the triggering of REMs sleep, although both have anabolic actions.

  16. Functional imaging correlates of impaired distractor suppression following sleep deprivation.

    PubMed

    Kong, Danyang; Soon, Chun Siong; Chee, Michael W L

    2012-05-15

    Sleep deprivation (SD) has been shown to affect selective attention but it is not known how two of its component processes: target enhancement and distractor suppression, are affected. To investigate, young volunteers either attended to houses or were obliged to ignore them (when attending to faces) while viewing superimposed face-house pictures. MR signal enhancement and suppression in the parahippocampal place area (PPA) were determined relative to a passive viewing control condition. Sleep deprivation was associated with lower PPA activation across conditions. Critically SD specifically impaired distractor suppression in selective attention, leaving target enhancement relatively preserved. These findings parallel some observations in cognitive aging. Additionally, following SD, attended houses were not significantly better recognized than ignored houses in a post-experiment test of recognition memory contrasting with the finding of superior recognition of attended houses in the well-rested state. These results provide evidence for co-encoding of distracting information with targets into memory when one is sleep deprived.

  17. Double Trouble? The Effects of Sleep Deprivation and Chronotype on Adolescent Affect

    ERIC Educational Resources Information Center

    Dagys, Natasha; McGlinchey, Eleanor L.; Talbot, Lisa S.; Kaplan, Katherine A.; Dahl, Ronald E.; Harvey, Allison G.

    2012-01-01

    Background: Two understudied risk factors that have been linked to emotional difficulties in adolescence are chronotype and sleep deprivation. This study extended past research by using an experimental design to investigate the role of sleep deprivation and chronotype on emotion in adolescents. It was hypothesized that sleep deprivation and an…

  18. Double Trouble? The Effects of Sleep Deprivation and Chronotype on Adolescent Affect

    ERIC Educational Resources Information Center

    Dagys, Natasha; McGlinchey, Eleanor L.; Talbot, Lisa S.; Kaplan, Katherine A.; Dahl, Ronald E.; Harvey, Allison G.

    2012-01-01

    Background: Two understudied risk factors that have been linked to emotional difficulties in adolescence are chronotype and sleep deprivation. This study extended past research by using an experimental design to investigate the role of sleep deprivation and chronotype on emotion in adolescents. It was hypothesized that sleep deprivation and an…

  19. Role of Sleep Deprivation in Fear Conditioning and Extinction: Implications for Treatment of PTSD

    DTIC Science & Technology

    2014-10-01

    Annual 3. DATES COVERED (From - To) 4. TITLE AND SUBTITLE Role of Sleep Deprivation in Fear Conditioning and Extinction: Implications for...the mechanism underlying the most successful treatment for PTSD, Prolonged Exposure. In animal models, sleep deprivation has been shown to impair...acquisition, consolidation, and generalization of extinction memory in humans. 15. SUBJECT TERMS PTSD, sleep deprivation , fear conditioning

  20. Effects of 72-Hour Partial Sleep Deprivation on Human Behavioral and Physiological Response Measures.

    DTIC Science & Technology

    Ten adult males were subjected to partial sleep deprivation experiments in order to study the effects of progressive sleep deprivation on the basic...progressive loss of performance capability. Power spectral data also show changes as a function of sleep deprivation , indicating that one feature of this type of stress may be an alteration of basic human biorhythms. (Author)

  1. Meta-Analysis of the Antidepressant Effects of Acute Sleep Deprivation.

    PubMed

    Boland, Elaine M; Rao, Hengyi; Dinges, David F; Smith, Rachel V; Goel, Namni; Detre, John A; Basner, Mathias; Sheline, Yvette I; Thase, Michael E; Gehrman, Philip R

    2017-09-19

    To provide a quantitative meta-analysis of the antidepressant effects of sleep deprivation to complement qualitative reviews addressing response rates. English-language studies from 1974 to 2016 using the keywords sleep deprivation and depression searched through PubMed and PsycINFO databases. A total of 66 independent studies met criteria for inclusion: conducted experimental sleep deprivation, reported the percentage of the sample that responded to sleep deprivation, provided a priori definition of antidepressant response, and did not seamlessly combine sleep deprivation with other therapies (eg, chronotherapeutics, repetitive transcranial magnetic stimulation). Data extracted included percentage of responders, type of sample (eg, bipolar, unipolar), type of sleep deprivation (eg, total, partial), demographics, medication use, type of outcome measure used, and definition of response (eg, 30% reduction in depression ratings). Data were analyzed with meta-analysis of proportions and a Poisson mixed-effects regression model. The overall response rate to sleep deprivation was 45% among studies that utilized a randomized control group and 50% among studies that did not. The response to sleep deprivation was not affected significantly by the type of sleep deprivation performed, the nature of the clinical sample, medication status, the definition of response used, or age and gender of the sample. These findings support a significant effect of sleep deprivation and suggest the need for future studies on the phenotypic nature of the antidepressant response to sleep deprivation, on the neurobiological mechanisms of action, and on moderators of the sleep deprivation treatment response in depression.

  2. Hormonal responses to exercise after partial sleep deprivation and after a hypnotic drug-induced sleep.

    PubMed

    Mougin, F; Bourdin, H; Simon-Rigaud, M L; Nguyen, N U; Kantelip, J P; Davenne, D

    2001-02-01

    The aim of this study was to determine the hormonal responses, which are dependent on the sleep wake cycle, to strenuous physical exercise. Exercise was performed after different nocturnal regimens: (i) a baseline night preceded by a habituation night; (ii) two nights of partial sleep deprivation caused by a delayed bedtime or by an early awakening; and (iii) two nights of sleep after administration of either a hypnotic compound (10 mg zolpidem) or a placebo. Eight well-trained male endurance athletes with a maximal oxygen uptake of 63.5 +/- 3.8 ml x kg(-1) x min(-1) (mean value +/- s(x)) were selected on the basis of their sleeping habits and their physical training. Polygraphic recordings of EEG showed that both nights with partial sleep loss led to a decrease (P< 0.01) in stage 2 and rapid eye movement sleep. A delayed bedtime also led to a decrease (P < 0.05) in stage 1 sleep. Zolpidem had no effect on the different stages of sleep. During the afternoon after an experimental night, exercise was performed on a cycle ergometer. After a 10-min warm-up, the participants performed 30 min steady-state cycling at 75% VO(2-max) followed by a progressively increased workload until exhaustion. The recovery period lasted 30 min. Plasma growth hormone, prolactin, cortisol, catecholamine and lactate concentrations were measured at rest, during exercise and after recovery. The concentration of plasma growth hormone and catecholamine were not affected by partial sleep deprivation, whereas that of plasma prolactin was higher (P < 0.05) during the trial after an early awakening. Plasma cortisol was lower (P < 0.05) during recovery after both sleep deprivation conditions. Blood lactate was higher (P < 0.05) during submaximal exercise performed after both a delayed bedtime and an early awakening. Zolpidem-induced sleep did not affect the hormonal and metabolic responses to subsequent exercise. Our results demonstrate only minor alterations in the hormonal responses to exercise

  3. Free recall of word lists under total sleep deprivation and after recovery sleep.

    PubMed

    de Almeida Valverde Zanini, Gislaine; Tufik, Sérgio; Andersen, Monica Levy; da Silva, Raquel Cristina Martins; Bueno, Orlando Francisco Amodeo; Rodrigues, Camila Cruz; Pompéia, Sabine

    2012-02-01

    One task that has been used to assess memory effects of prior total sleep deprivation (TSD) is the immediate free recall of word lists; however, results have been mixed. A possible explanation for this is task impurity, since recall of words from different serial positions reflects use of distinct types of memory (last words: short-term memory; first and intermediate words: episodic memory). Here we studied the effects of 2 nights of TSD on immediate free recall of semantically unrelated word lists considering the serial position curve. Random allocation to a 2-night TSD protocol followed by one night of recovery sleep or to a control group. Study conducted under continuous behavioral monitoring. 24 young, healthy male volunteers. 2 nights of total sleep deprivation (TSD) and one night of recovery sleep. Participants were shown five 15 unrelated word-lists at baseline, after one and 2 nights of TSD, and after one night of recovery sleep. We also investigated the development of recall strategies (learning) and susceptibility to interference from previous lists. No free recall impairment occurred during TSD, irrespective of serial position. Interference was unchanged. Both groups developed recall strategies, but task learning occurred earlier in controls and was evident in the TSD group only after sleep recovery. Prior TSD spared episodic memory, short-term phonological memory, and interference, allowed the development of recall strategies, but may have decreased the advantage of using these strategies, which returned to normal after recovery sleep.

  4. Effects of sleep deprivation on central auditory processing

    PubMed Central

    2012-01-01

    Background Sleep deprivation is extremely common in contemporary society, and is considered to be a frequent cause of behavioral disorders, mood, alertness, and cognitive performance. Although the impacts of sleep deprivation have been studied extensively in various experimental paradigms, very few studies have addressed the impact of sleep deprivation on central auditory processing (CAP). Therefore, we examined the impact of sleep deprivation on CAP, for which there is sparse information. In the present study, thirty healthy adult volunteers (17 females and 13 males, aged 30.75 ± 7.14 years) were subjected to a pure tone audiometry test, a speech recognition threshold test, a speech recognition task, the Staggered Spondaic Word Test (SSWT), and the Random Gap Detection Test (RGDT). Baseline (BSL) performance was compared to performance after 24 hours of being sleep deprived (24hSD) using the Student’s t test. Results Mean RGDT score was elevated in the 24hSD condition (8.0 ± 2.9 ms) relative to the BSL condition for the whole cohort (6.4 ± 2.8 ms; p = 0.0005), for males (p = 0.0066), and for females (p = 0.0208). Sleep deprivation reduced SSWT scores for the whole cohort in both ears [(right: BSL, 98.4 % ± 1.8 % vs. SD, 94.2 % ± 6.3 %. p = 0.0005)(left: BSL, 96.7 % ± 3.1 % vs. SD, 92.1 % ± 6.1 %, p < 0.0001)]. These effects were evident within both gender subgroups [(right: males, p = 0.0080; females, p = 0.0143)(left: males, p = 0.0076; females: p = 0.0010). Conclusion Sleep deprivation impairs RGDT and SSWT performance. These findings confirm that sleep deprivation has central effects that may impair performance in other areas of life. PMID:22823997

  5. Sleep active cortical neurons expressing neuronal nitric oxide synthase are active after both acute sleep deprivation and chronic sleep restriction.

    PubMed

    Zielinski, M R; Kim, Y; Karpova, S A; Winston, S; McCarley, R W; Strecker, R E; Gerashchenko, D

    2013-09-05

    Non-rapid eye movement (NREM) sleep electroencephalographic (EEG) delta power (~0.5-4 Hz), also known as slow wave activity (SWA), is typically enhanced after acute sleep deprivation (SD) but not after chronic sleep restriction (CSR). Recently, sleep-active cortical neurons expressing neuronal nitric oxide synthase (nNOS) were identified and associated with enhanced SWA after short acute bouts of SD (i.e., 6h). However, the relationship between cortical nNOS neuronal activity and SWA during CSR is unknown. We compared the activity of cortical neurons expressing nNOS (via c-Fos and nNOS immuno-reactivity, respectively) and sleep in rats in three conditions: (1) after 18-h of acute SD; (2) after five consecutive days of sleep restriction (SR) (18-h SD per day with 6h ad libitum sleep opportunity per day); (3) and time-of-day matched ad libitum sleep controls. Cortical nNOS neuronal activity was enhanced during sleep after both 18-h SD and 5 days of SR treatments compared to control treatments. SWA and NREM sleep delta energy (the product of NREM sleep duration and SWA) were positively correlated with enhanced cortical nNOS neuronal activity after 18-h SD but not 5days of SR. That neurons expressing nNOS were active after longer amounts of acute SD (18h vs. 6h reported in the literature) and were correlated with SWA further suggest that these cells might regulate SWA. However, since these neurons were active after CSR when SWA was not enhanced, these findings suggest that mechanisms downstream of their activation are altered during CSR.

  6. Sex-dependent effects of sleep deprivation on myocardial sensitivity to ischemic injury.

    PubMed

    Zoladz, Phillip R; Krivenko, Anna; Eisenmann, Eric D; Bui, Albert D; Seeley, Sarah L; Fry, Megan E; Johnson, Brandon L; Rorabaugh, Boyd R

    2016-01-01

    Sleep deprivation is associated with increased risk of myocardial infarction. However, it is unknown whether the effects of sleep deprivation are limited to increasing the likelihood of experiencing a myocardial infarction or if sleep deprivation also increases the extent of myocardial injury. In this study, rats were deprived of paradoxical sleep for 96 h using the platform-over-water method. Control rats were subjected to the same condition except the control platform was large enough for the rats to sleep. Hearts from sleep deprived and control rats were subjected to 20 min ischemia on a Langendorff isolated heart system. Infarct size and post ischemic recovery of contractile function were unaffected by sleep deprivation in male hearts. In contrast, hearts from sleep-deprived females exhibited significantly larger infarcts than hearts from control females. Post ischemic recovery of rate pressure product and + dP/dT were significantly attenuated by sleep deprivation in female hearts, and post ischemic recovery of end diastolic pressure was significantly elevated in hearts from sleep deprived females compared to control females, indicating that post ischemic recovery of both systolic and diastolic function were worsened by sleep deprivation. These data provide evidence that sleep deprivation increases the extent of ischemia-induced injury in a sex-dependent manner.

  7. Effects of Daytime Food Intake on Memory Consolidation during Sleep or Sleep Deprivation

    PubMed Central

    Herzog, Nina; Friedrich, Alexia; Fujita, Naoko; Gais, Steffen; Jauch-Chara, Kamila; Oltmanns, Kerstin M.; Benedict, Christian

    2012-01-01

    Sleep enhances memory consolidation. Bearing in mind that food intake produces many metabolic signals that can influence memory processing in humans (e.g., insulin), the present study addressed the question as to whether the enhancing effect of sleep on memory consolidation is affected by the amount of energy consumed during the preceding daytime. Compared to sleep, nocturnal wakefulness has been shown to impair memory consolidation in humans. Thus, a second question was to examine whether the impaired memory consolidation associated with sleep deprivation (SD) could be compensated by increased daytime energy consumption. To these aims, 14 healthy normal-weight men learned a finger tapping sequence (procedural memory) and a list of semantically associated word pairs (declarative memory). After the learning period, standardized meals were administered, equaling either ∼50% or ∼150% of the estimated daily energy expenditure. In the morning, after sleep or wakefulness, memory consolidation was tested. Plasma glucose was measured both before learning and retrieval. Polysomnographic sleep recordings were performed by electroencephalography (EEG). Independent of energy intake, subjects recalled significantly more word pairs after sleep than they did after SD. When subjects stayed awake and received an energy oversupply, the number of correctly recalled finger sequences was equal to those seen after sleep. Plasma glucose did not differ among conditions, and sleep time in the sleep conditions was not influenced by the energy intake interventions. These data indicate that the daytime energy intake level affects neither sleep’s capacity to boost the consolidation of declarative and procedural memories, nor sleep’s quality. However, high energy intake was followed by an improved procedural but not declarative memory consolidation under conditions of SD. This suggests that the formation of procedural memory is not only triggered by sleep but is also sensitive to the

  8. Altered salience network connectivity predicts macronutrient intake after sleep deprivation

    PubMed Central

    Fang, Zhuo; Spaeth, Andrea M.; Ma, Ning; Zhu, Senhua; Hu, Siyuan; Goel, Namni; Detre, John A.; Dinges, David F.; Rao, Hengyi

    2015-01-01

    Although insufficient sleep is a well-recognized risk factor for overeating and weight gain, the neural mechanisms underlying increased caloric (particularly fat) intake after sleep deprivation remain unclear. Here we used resting-state functional magnetic resonance imaging and examined brain connectivity changes associated with macronutrient intake after one night of total sleep deprivation (TSD). Compared to the day following baseline sleep, healthy adults consumed a greater percentage of calories from fat and a lower percentage of calories from carbohydrates during the day following TSD. Subjects also exhibited increased brain connectivity in the salience network from the dorsal anterior cingulate cortex (dACC) to bilateral putamen and bilateral anterior insula (aINS) after TSD. Moreover, dACC-putamen and dACC-aINS connectivity correlated with increased fat and decreased carbohydrate intake during the day following TSD, but not during the day following baseline sleep. These findings provide a potential neural mechanism by which sleep loss leads to increased fat intake. PMID:25645575

  9. Altered salience network connectivity predicts macronutrient intake after sleep deprivation.

    PubMed

    Fang, Zhuo; Spaeth, Andrea M; Ma, Ning; Zhu, Senhua; Hu, Siyuan; Goel, Namni; Detre, John A; Dinges, David F; Rao, Hengyi

    2015-02-03

    Although insufficient sleep is a well-recognized risk factor for overeating and weight gain, the neural mechanisms underlying increased caloric (particularly fat) intake after sleep deprivation remain unclear. Here we used resting-state functional magnetic resonance imaging and examined brain connectivity changes associated with macronutrient intake after one night of total sleep deprivation (TSD). Compared to the day following baseline sleep, healthy adults consumed a greater percentage of calories from fat and a lower percentage of calories from carbohydrates during the day following TSD. Subjects also exhibited increased brain connectivity in the salience network from the dorsal anterior cingulate cortex (dACC) to bilateral putamen and bilateral anterior insula (aINS) after TSD. Moreover, dACC-putamen and dACC-aINS connectivity correlated with increased fat and decreased carbohydrate intake during the day following TSD, but not during the day following baseline sleep. These findings provide a potential neural mechanism by which sleep loss leads to increased fat intake.

  10. Obstructive Sleep Apnea Is a Predictor of Abnormal Glucose Metabolism in Chronically Sleep Deprived Obese Adults

    PubMed Central

    Cizza, Giovanni; Piaggi, Paolo; Lucassen, Eliane A.; de Jonge, Lilian; Walter, Mary; Mattingly, Megan S.; Kalish, Heather; Csako, Gyorgy; Rother, Kristina I.

    2013-01-01

    Context Sleep abnormalities, including obstructive sleep apnea (OSA), have been associated with insulin resistance. Objective To determine the relationship between sleep, including OSA, and glucose parameters in a prospectively assembled cohort of chronically sleep-deprived obese subjects. Design Cross-sectional evaluation of a prospective cohort study. Setting Tertiary Referral Research Clinical Center. Main Outcome Measure(s) Sleep duration and quality assessed by actigraphy, sleep diaries and questionnaires, OSA determined by a portable device; glucose metabolism assessed by oral glucose tolerance test (oGTT), and HbA1c concentrations in 96 obese individuals reporting sleeping less than 6.5 h on a regular basis. Results Sixty % of subjects had an abnormal respiratory disturbance index (RDI≥5) and 44% of these subjects had abnormal oGTT results. Severity of OSA as assessed by RDI score was associated with fasting glucose (R = 0.325, p = 0.001) and fasting insulin levels (ρ = 0.217, p = 0.033). Subjects with moderate to severe OSA (RDI>15) had higher glucose concentrations at 120 min than those without OSA (RDI<5) (p = 0.017). Subjects with OSA also had significantly higher concentrations of plasma ACTH (p = 0.009). Several pro-inflammatory cytokines were higher in subjects with OSA (p<0.050). CRP levels were elevated in this sample, suggesting increased cardiovascular risk. Conclusions OSA is associated with impaired glucose metabolism in obese, sleep deprived individuals. Since sleep apnea is common and frequently undiagnosed, health care providers should be aware of its occurrence and associated risks. Trial Registration This study was conducted under the NIDDK protocol 06-DK-0036 and is listed in ClinicalTrials.gov NCT00261898 PMID:23734252

  11. Metabolic, Endocrine, and Immune Consequences of Sleep Deprivation

    PubMed Central

    AlDabal, Laila; BaHammam, Ahmed S

    2011-01-01

    Over the last three to four decades, it has been observed that the average total hours of sleep have decreased to less than seven hours per person per night. Concomitantly, global figures relating to obesity and diabetes mellitus have increased in an alarming fashion in adults and children, and it has been hypothesized that neuro-hormonal changes accompanying this behavioral sleep deprivation may lead to insulin resistance and, subsequently, to diabetes mellitus. Sleep deprivation has been associated with multiple physiological changes, including increased cortisol and ghrelin levels, decreased leptin levels and impaired glucose metabolism. Experimental studies have also shown an increase in inflammatory and pro-inflammatory markers, which are indicators of body stress, under sleep deprivation. This review elaborates further on this hypothesis, exploring the molecular basis for the link between both entities and the underlying pathophysiology that results in insulin resistance and diabetes mellitus. We review the results of experimental and epidemiological studies, specifically examining the relationship between sleep duration and the immune and endocrine systems. PMID:21754974

  12. Effects of a selective sleep deprivation on subsequent anaerobic performance.

    PubMed

    Mougin, F; Bourdin, H; Simon-Rigaud, M L; Didier, J M; Toubin, G; Kantelip, J P

    1996-02-01

    The aim of the study was to investigate the effects of a partial sleep deprivation on a subsequent supramaximal exercise evaluated from the 30 second Wingate test, and on the following recovery. To take into account the active muscle mass, the Wingate test was performed against a constant braking force related to the data of a force-velocity test conducted on a Monark cycle ergometer (Model 814 E with weights) one week before the experimental test. Eight highly trained athletes were enrolled for this study. The changes in ventilatory and metabolic responses were analyzed during and upon completion of physical 30 second exercise, taking place after two nights, in other words, after a reference night and after a night with reduced sleep. Partial sleep deprivation was obtained by delaying bedtime until 3 a.m. The 30 second Wingate test was performed between 9 a.m. and noon the following days, using a Monark ergometer (Model 814 F). The analyses of change scores disclosed that there were no main significant effects for measures of ventilation, lactates and pH(v) levels under the two experimental conditions. The peak power, the mean power output and the peak velocity recorded after partial sleep deprivation were not modified in comparison with the values obtained after the reference night. These findings suggest that acute sleep loss did not contribute to alterations in supramaximal exercise.

  13. Sleep deprivation and phasic activity of REM sleep: independence of middle-ear muscle activity from rapid eye movements.

    PubMed

    De Gennaro, L; Ferrara, M

    2000-02-01

    In the recovery nights after total and partial sleep deprivation there is a reduction of rapid eye movements during REM sleep as compared to baseline nights; recent evidence provided by a selective SWS deprivation study also shows that the highest percentage of variance of this reduction is explained by SWS rebound. The present study assesses whether the reduction of rapid eye movements (REMs) during the recovery night after total sleep deprivation is paralleled by a decrease of middle-ear muscle activity (MEMA), another phasic muscle activity of REM sleep. Standard polysomnography, MEMA and REMs of nine subjects were recorded for three nights (one adaptation, one baseline, one recovery); baseline and recovery night were separated by a period of 40 hours of continuous wake. Results show that, in the recovery night, sleep deprivation was effective in determining an increase of SWS amount and of the sleep efficiency index, and a decrease of stage 1, stage 2, intra-sleep wake, and NREM latencies, without affecting REM duration and latency. However, MEMA frequency during REM sleep did not diminish during these nights as compared to baseline ones, while there was a clear effect of REM frequency reduction. Results indicate an independence of phasic events of REM sleep, suggesting that the inverse relation between recovery sleep after sleep deprivation and REM frequency is not paralleled by a concomitant variation in MEMA frequency.

  14. Acute Sleep Deprivation Blocks Short- and Long-Term Operant Memory in Aplysia.

    PubMed

    Krishnan, Harini C; Gandour, Catherine E; Ramos, Joshua L; Wrinkle, Mariah C; Sanchez-Pacheco, Joseph J; Lyons, Lisa C

    2016-12-01

    Insufficient sleep in individuals appears increasingly common due to the demands of modern work schedules and technology use. Consequently, there is a growing need to understand the interactions between sleep deprivation and memory. The current study determined the effects of acute sleep deprivation on short and long-term associative memory using the marine mollusk Aplysia californica, a relatively simple model system well known for studies of learning and memory. Aplysia were sleep deprived for 9 hours using context changes and tactile stimulation either prior to or after training for the operant learning paradigm, learning that food is inedible (LFI). The effects of sleep deprivation on short-term (STM) and long-term memory (LTM) were assessed. Acute sleep deprivation prior to LFI training impaired the induction of STM and LTM with persistent effects lasting at least 24 h. Sleep deprivation immediately after training blocked the consolidation of LTM. However, sleep deprivation following the period of molecular consolidation did not affect memory recall. Memory impairments were independent of handling-induced stress, as daytime handled control animals demonstrated no memory deficits. Additional training immediately after sleep deprivation failed to rescue the induction of memory, but additional training alleviated the persistent impairment in memory induction when training occurred 24 h following sleep deprivation. Acute sleep deprivation inhibited the induction and consolidation, but not the recall of memory. These behavioral studies establish Aplysia as an effective model system for studying the interactions between sleep and memory formation.

  15. Circadian Modulation of Consolidated Memory Retrieval Following Sleep Deprivation in Drosophila

    PubMed Central

    Glou, Eric Le; Seugnet, Laurent; Shaw, Paul J.; Preat, Thomas; Goguel, Valérie

    2012-01-01

    Objectives: Several lines of evidence indicate that sleep plays a critical role in learning and memory. The aim of this study was to evaluate anesthesia resistant memory following sleep deprivation in Drosophila. Design: Four to 16 h after aversive olfactory training, flies were sleep deprived for 4 h. Memory was assessed 24 h after training. Training, sleep deprivation, and memory tests were performed at different times during the day to evaluate the importance of the time of day for memory formation. The role of circadian rhythms was further evaluated using circadian clock mutants. Results Memory was disrupted when flies were exposed to 4 h of sleep deprivation during the consolidation phase. Interestingly, normal memory was observed following sleep deprivation when the memory test was performed during the 2 h preceding lights-off, a period characterized by maximum wake in flies. We also show that anesthesia resistant memory was less sensitive to sleep deprivation in flies with disrupted circadian rhythms. Conclusions Our results indicate that anesthesia resistant memory, a consolidated memory less costly than long-term memory, is sensitive to sleep deprivation. In addition, we provide evidence that circadian factors influence memory vulnerability to sleep deprivation and memory retrieval. Taken together, the data show that memories weakened by sleep deprivation can be retrieved if the animals are tested at the optimal circadian time. Citation: Le Glou E; Seugnet L; Shaw PJ; Preat T; Goguel V. Circadian modulation of consolidated memory retrieval following sleep deprivation in Drosophila. SLEEP 2012;35(10):1377-1384. PMID:23024436

  16. Increased EEG spectral power density during sleep following short-term sleep deprivation in pigeons (Columba livia): evidence for avian sleep homeostasis.

    PubMed

    Martinez-Gonzalez, Dolores; Lesku, John A; Rattenborg, Niels C

    2008-06-01

    Birds provide a unique opportunity to evaluate current theories for the function of sleep. Like mammalian sleep, avian sleep is composed of two states, slow-wave sleep (SWS) and rapid eye-movement (REM) sleep that apparently evolved independently in mammals and birds. Despite this resemblance, however, it has been unclear whether avian SWS shows a compensatory response to sleep loss (i.e., homeostatic regulation), a fundamental aspect of mammalian sleep potentially linked to the function of SWS. Here, we prevented pigeons (Columba livia) from taking their normal naps during the last 8 h of the day. Although time spent in SWS did not change significantly following short-term sleep deprivation, electroencephalogram (EEG) slow-wave activity (SWA; i.e., 0.78-2.34 Hz power density) during SWS increased significantly during the first 3 h of the recovery night when compared with the undisturbed night, and progressively declined thereafter in a manner comparable to that observed in similarly sleep-deprived mammals. SWA was also elevated during REM sleep on the recovery night, a response that might reflect increased SWS pressure and the concomitant 'spill-over' of SWS-related EEG activity into short episodes of REM sleep. As in rodents, power density during SWS also increased in higher frequencies (9-25 Hz) in response to short-term sleep deprivation. Finally, time spent in REM sleep increased following sleep deprivation. The mammalian-like increase in EEG spectral power density across both low and high frequencies, and the increase in time spent in REM sleep following sleep deprivation suggest that some aspects of avian and mammalian sleep are regulated in a similar manner.

  17. Migraine, arousal and sleep deprivation: comment on: "sleep quality, arousal and pain thresholds in migraineurs: a blinded controlled polysomnographic study".

    PubMed

    Vollono, Catello; Testani, Elisa; Losurdo, Anna; Mazza, Salvatore; Della Marca, Giacomo

    2013-06-10

    We discuss the hypothesis proposed by Engstrom and coworkers that Migraineurs have a relative sleep deprivation, which lowers the pain threshold and predispose to attacks. Previous data indicate that Migraineurs have a reduction of Cyclic Alternating Pattern (CAP), an essential mechanism of NREM sleep regulation which allows to dump the effect of incoming disruptive stimuli, and to protect sleep. The modifications of CAP observed in Migraineurs are similar to those observed in patients with impaired arousal (narcolepsy) and after sleep deprivation. The impairment of this mechanism makes Migraineurs more vulnerable to stimuli triggering attacks during sleep, and represents part of a more general vulnerability to incoming stimuli.

  18. Effects of Extreme Sleep Deprivation on Human Performance

    SciTech Connect

    Tuan Tran; Kimberly R. Raddatz; Elizabeth T. Cady; Bradford Amstutz; Pete D. Elgin; Christopher Vowels; Gerald Deehan

    2007-04-01

    Sleep is a fundamental recuperative process for the nervous system. Disruption of this homeostatic drive can lead to severe impairments of the operator’s ability to perceive, recognize, and respond to emergencies and/or unanticipated events, putting the operator at risk. Therefore, establishing a comprehensive understanding of how sleep deprivation influences human performance is essential in order to counter fatigue or to develop mitigation strategies. The goal of the present study was to examine the psychological effects of prolonged sleep deprivation (approx. 75 hrs) over a four-day span on a general aviation pilot flying a fixed-based flight simulator. During the study, a series of tasks were employed every four hours in order to examine the pilot’s perceptual and higher level cognitive abilities. Overall, results suggest that the majority of cognitive and perceptual degradation occurs between 30-40 hours into the flight. Limitations and future research directions are also discussed.

  19. Deprivation and Recovery of Sleep in Succession Enhances Reflexive Motor Behavior

    PubMed Central

    Sprenger, Andreas; Weber, Frederik D.; Machner, Bjoern; Talamo, Silke; Scheffelmeier, Sabine; Bethke, Judith; Helmchen, Christoph; Gais, Steffen; Kimmig, Hubert; Born, Jan

    2015-01-01

    Sleep deprivation impairs inhibitory control over reflexive behavior, and this impairment is commonly assumed to dissipate after recovery sleep. Contrary to this belief, here we show that fast reflexive behaviors, when practiced during sleep deprivation, is consolidated across recovery sleep and, thereby, becomes preserved. As a model for the study of sleep effects on prefrontal cortex-mediated inhibitory control in humans, we examined reflexive saccadic eye movements (express saccades), as well as speeded 2-choice finger motor responses. Different groups of subjects were trained on a standard prosaccade gap paradigm before periods of nocturnal sleep and sleep deprivation. Saccade performance was retested in the next morning and again 24 h later. The rate of express saccades was not affected by sleep after training, but slightly increased after sleep deprivation. Surprisingly, this increase augmented even further after recovery sleep and was still present 4 weeks later. Additional experiments revealed that the short testing after sleep deprivation was sufficient to increase express saccades across recovery sleep. An increase in speeded responses across recovery sleep was likewise found for finger motor responses. Our findings indicate that recovery sleep can consolidate motor disinhibition for behaviors practiced during prior sleep deprivation, thereby persistently enhancing response automatization. PMID:26048955

  20. Deprivation and Recovery of Sleep in Succession Enhances Reflexive Motor Behavior.

    PubMed

    Sprenger, Andreas; Weber, Frederik D; Machner, Bjoern; Talamo, Silke; Scheffelmeier, Sabine; Bethke, Judith; Helmchen, Christoph; Gais, Steffen; Kimmig, Hubert; Born, Jan

    2015-11-01

    Sleep deprivation impairs inhibitory control over reflexive behavior, and this impairment is commonly assumed to dissipate after recovery sleep. Contrary to this belief, here we show that fast reflexive behaviors, when practiced during sleep deprivation, is consolidated across recovery sleep and, thereby, becomes preserved. As a model for the study of sleep effects on prefrontal cortex-mediated inhibitory control in humans, we examined reflexive saccadic eye movements (express saccades), as well as speeded 2-choice finger motor responses. Different groups of subjects were trained on a standard prosaccade gap paradigm before periods of nocturnal sleep and sleep deprivation. Saccade performance was retested in the next morning and again 24 h later. The rate of express saccades was not affected by sleep after training, but slightly increased after sleep deprivation. Surprisingly, this increase augmented even further after recovery sleep and was still present 4 weeks later. Additional experiments revealed that the short testing after sleep deprivation was sufficient to increase express saccades across recovery sleep. An increase in speeded responses across recovery sleep was likewise found for finger motor responses. Our findings indicate that recovery sleep can consolidate motor disinhibition for behaviors practiced during prior sleep deprivation, thereby persistently enhancing response automatization.

  1. Psychological Effect of an Analogue Traumatic Event Reduced by Sleep Deprivation.

    PubMed

    Porcheret, Kate; Holmes, Emily A; Goodwin, Guy M; Foster, Russell G; Wulff, Katharina

    2015-07-01

    To examine the effect of sleep deprivation compared to sleep, immediately after experimental trauma stimuli on the development of intrusive memories to that trauma stimuli. Participants were exposed to a film with traumatic content (trauma film). The immediate response to the trauma film was assessed, followed by either total sleep deprivation (sleep deprived group, N = 20) or sleep as usual (sleep group, N = 22). Twelve hours after the film viewing the initial psychological effect of the trauma film was measured and for the subsequent 6 days intrusive emotional memories related to the trauma film were recorded in daily life. Academic sleep laboratory and participants' home environment. Healthy paid volunteers. On the first day after the trauma film, the psychological effect as assessed by the Impact of Event Scale - Revised was lower in the sleep deprived group compared to the sleep group. In addition, the sleep deprived group reported fewer intrusive emotional memories (mean 2.28, standard deviation [SD] 2.91) compared to the sleep group (mean 3.76, SD 3.35). Because habitual sleep/circadian patterns, psychological health, and immediate effect of the trauma film were similar at baseline for participants of both groups, the results cannot be accounted for by pre-existing inequalities between groups. Our findings suggest that sleep deprivation on one night, rather than sleeping, reduces emotional effect and intrusive memories following exposure to experimental trauma. © 2015 Associated Professional Sleep Societies, LLC.

  2. Dose-Dependent Model of Caffeine Effects on Human Vigilance during Total Sleep Deprivation

    DTIC Science & Technology

    2014-05-20

    Dose-dependent model of caffeine effects on human vigilance during total sleep deprivation Sridhar Ramakrishnan a, Srinivas Laxminarayan a, Nancy J...psychomotor vigilance task (PVT) performance of sleep - deprived subjects. We used the two-process model of sleep regulation to quantify performance... sleep - deprived subjects and, therefore, can be used for determining caffeine doses that optimize the timing and duration of peak performance. Published

  3. A reassessment of the hyperphagia/weight-loss paradox during sleep deprivation.

    PubMed

    Martins, Paulo J F; D'Almeida, Vânia; Nobrega, José N; Tufik, Sergio

    2006-09-01

    Sleep deprivation is a well-known paradigm to investigate the deleterious effects of prolonged wakefulness. Previous studies have shown that, during sleep deprivation, rats are hyperphagic but, paradoxically, lose body weight. This phenomenon has been attributed to increased metabolism. However, most previous studies have failed to account for food spillage, which may be considerable during sleep deprivation. In the present study, we revisited the issue of feeding changes in sleep-deprived rats and introduced different procedures to allow accurate estimation of food spillage prior to, during, and after 120 hours of sleep deprivation by a single platform technique. Animal Sleep Research Laboratory, Psychobiology Department, Universidade Federal de São Paulo, Brazil. The main finding was that, once corrected for spillage, food intake was not significantly increased during sleep deprivation. Increases in food removed from feeders were accompanied by proportional increases in food spillage, resulting in no net changes in food intake. Further, weight loss did occur during the sleep-deprivation period, especially in the first 24 hours, and it was actually explained by a reduction in food intake. The hyperphagia/weight-loss paradox previously seen during prolonged sleep deprivation does not necessarily occur with shorter periods of deprivation. Although we found no evidence of hyperphagia for up to 5 days of sleep deprivation in chow-fed rats, our data suggest that an impairment in the ability to increase food intake in response to increased energy expenditure contributes to the energy deficit during sleep deprivation in rats.

  4. Melatonin attenuates dextran sodium sulfate induced colitis with sleep deprivation: possible mechanism by microarray analysis.

    PubMed

    Chung, Sook Hee; Park, Young Sook; Kim, Ok Soon; Kim, Ja Hyun; Baik, Haing Woon; Hong, Young Ok; Kim, Sang Su; Shin, Jae-Ho; Jun, Jin-Hyun; Jo, Yunju; Ahn, Sang Bong; Jo, Young Kwan; Son, Byoung Kwan; Kim, Seong Hwan

    2014-06-01

    Inflammatory bowel disease is a chronic inflammatory condition of the gastrointestinal tract. It can be aggravated by stress, like sleep deprivation, and improved by anti-inflammatory agents, like melatonin. We aimed to investigate the effects of sleep deprivation and melatonin on inflammation. We also investigated genes regulated by sleep deprivation and melatonin. In the 2% DSS induced colitis mice model, sleep deprivation was induced using modified multiple platform water bath. Melatonin was injected after induction of colitis and colitis with sleep deprivation. Also mRNA was isolated from the colon of mice and analyzed via microarray and real-time PCR. Sleep deprivation induced reduction of body weight, and it was difficult for half of the mice to survive. Sleep deprivation aggravated, and melatonin attenuated the severity of colitis. In microarrays and real-time PCR of mice colon tissues, mRNA of adiponectin and aquaporin 8 were downregulated by sleep deprivation and upregulated by melatonin. However, mRNA of E2F transcription factor (E2F2) and histocompatibility class II antigen A, beta 1 (H2-Ab1) were upregulated by sleep deprivation and downregulated by melatonin. Melatonin improves and sleep deprivation aggravates inflammation of colitis in mice. Adiponectin, aquaporin 8, E2F2 and H2-Ab1 may be involved in the inflammatory change aggravated by sleep deprivation and attenuated by melatonin.

  5. Residency Training: The King-Devick test and sleep deprivation

    PubMed Central

    Davies, Emma C.; Henderson, Sam; Galetta, Steven L.

    2012-01-01

    Objective: The current study investigates the effect of sleep deprivation on the speed and accuracy of eye movements as measured by the King-Devick (K-D) test, a <1-minute test that involves rapid number naming. Methods: In this cohort study, neurology residents and staff from the University of Pennsylvania Health System underwent baseline followed by postcall K-D testing (n = 25); those not taking call (n = 10) also completed baseline and follow-up K-D testing. Differences in the times and errors between baseline and follow-up K-D scores were compared between the 2 groups. Results: Residents taking call had less improvement from baseline K-D times when compared to participants not taking call (p < 0.0001, Wilcoxon rank sum test). For both groups, the change in K-D time from baseline was correlated to amount of sleep obtained (rs = −0.50, p = 0.002) and subjective evaluation of level of alertness (rs = 0.33, p = 0.05) but had no correlation to time since last caffeine consumption (rs = −0.13, p = 0.52). For those residents on their actual call night, the duration of sleep obtained did not correlate with change in K-D scores from baseline (rs = 0.13, p = 0.54). Conclusions: The K-D test is sensitive to the effects of sleep deprivation on cognitive functioning, including rapid eye movements, concentration, and language function. As with other measures of sleep deprivation, K-D performance demonstrated significant interindividual variability in vulnerability to sleep deprivation. Severe fatigue appears to reduce the degree of improvement typically observed in K-D testing. PMID:22529208

  6. Antidepressant effects of sleep deprivation require astrocyte-dependent adenosine mediated signaling

    PubMed Central

    Hines, D J; Schmitt, L I; Hines, R M; Moss, S J; Haydon, P G

    2013-01-01

    Major depressive disorder is a debilitating condition with a lifetime risk of ten percent. Most treatments take several weeks to achieve clinical efficacy, limiting the ability to bring instant relief needed in psychiatric emergencies. One intervention that rapidly alleviates depressive symptoms is sleep deprivation; however, its mechanism of action is unknown. Astrocytes regulate responses to sleep deprivation, raising the possibility that glial signaling mediates antidepressive-like actions of sleep deprivation. Here, we found that astrocytic signaling to adenosine (A1) receptors was required for the robust reduction of depressive-like behaviors following 12 hours of sleep deprivation. As sleep deprivation activates synaptic A1 receptors, we mimicked the effect of sleep deprivation on depression phenotypes by administration of the A1 agonist CCPA. These results provide the first mechanistic insight into how sleep deprivation impacts mood, and provide a novel pathway for rapid antidepressant development by modulation of glial signaling in the brain. PMID:23321809

  7. Cognitive Performance, Sleepiness, and Mood in Partially Sleep Deprived Adolescents: The Need for Sleep Study.

    PubMed

    Lo, June C; Ong, Ju Lynn; Leong, Ruth L F; Gooley, Joshua J; Chee, Michael W L

    2016-03-01

    To investigate the effects of sleep restriction (7 nights of 5 h time in bed [TIB]) on cognitive performance, subjective sleepiness, and mood in adolescents. A parallel-group design was adopted in the Need for Sleep Study. Fifty-six healthy adolescents (25 males, age = 15-19 y) who studied in top high schools and were not habitual short sleepers were randomly assigned to Sleep Restriction (SR) or Control groups. Participants underwent a 2-w protocol consisting of 3 baseline nights (TIB = 9 h), 7 nights of sleep opportunity manipulation (TIB = 5 h for the SR and 9 h for the control groups), and 3 nights of recovery sleep (TIB = 9 h) at a boarding school. A cognitive test battery was administered three times each day. During the manipulation period, the SR group demonstrated incremental deterioration in sustained attention, working memory and executive function, increase in subjective sleepiness, and decrease in positive mood. Subjective sleepiness and sustained attention did not return to baseline levels even after 2 recovery nights. In contrast, the control group maintained baseline levels of cognitive performance, subjective sleepiness, and mood throughout the study. Incremental improvement in speed of processing, as a result of repeated testing and learning, was observed in the control group but was attenuated in the sleep-restricted participants, who, despite two recovery sleep episodes, continued to perform worse than the control participants. A week of partial sleep deprivation impairs a wide range of cognitive functions, subjective alertness, and mood even in high-performing high school adolescents. Some measures do not recover fully even after 2 nights of recovery sleep. A commentary on this article appears in this issue on page 497. © 2016 Associated Professional Sleep Societies, LLC.

  8. Comparing Technical Dexterity of Sleep-Deprived Versus Intoxicated Surgeons

    PubMed Central

    Thiele, Allison; Karreman, Erwin; Thiel, John

    2014-01-01

    Background: The evidence on the effect of sleep deprivation on the cognitive and motor skills of physicians in training is sparse and conflicting, and the evidence is nonexistent on surgeons in practice. Work-hour limitations based on these data have contributed to challenges in the quality of surgical education under the apprentice model, and as a result there is an increasing focus on competency-based education. Whereas the effects of alcohol intoxication on psychometric performance are well studied in many professions, the effects on performance in surgery are not well documented. To study the effects of sleep deprivation on the surgical performance of surgeons, we compared simulated the laparoscopic skills of staff gynecologists “under 2 conditions”: sleep deprivation and ethanol intoxication. We hypothesized that the performance of unconsciously competent surgeons does not deteriorate postcall as it does under the influence of alcohol. Methods: Nine experienced staff gynecologists performed 3 laparoscopic tasks in increasing order of difficulty (cup drop, rope passing, pegboard exchange) on a box trainer while sleep deprived (<3 hours in 24 hours) and subsequently when legally intoxicated (>0.08 mg/mL blood alcohol concentration). Three expert laparoscopic surgeons scored the anonymous clips online using Global Objective Assessment of Laparoscopic Skills criteria: depth perception, bimanual dexterity, and efficiency. Data were analyzed by a mixed-design analysis of variance. Results: There were large differences in mean performance between the tasks. With increasing task difficulty, mean scores became significantly (P < .05) poorer. For the easy tasks, the scores for sleep-deprived and intoxicated participants were similar for all variables except time. Surprisingly, participants took less time to complete the easy tasks when intoxicated. However, the most difficult task took less time but was performed significantly worse compared with being sleep

  9. Aging does not affect the sleep endocrine response to total sleep deprivation in humans.

    PubMed

    Murck, H; Antonijevic, I A; Schier, T; Frieboes, R M; Barthelmes, J; Steiger, A

    1999-01-01

    Aging is associated with decreased sleep continuity, slow wave sleep (SWS), growth hormone (GH) release and an increased hypothalamo-pituitary-adrenocortical (HPA) system activity. Total sleep deprivation (TSD) is a strong stimulus for sleep. To determine if aging affects the response to TSD, for the first time the combined effects of TSD on conventional and spectral sleep electroencephalographic (EEG) parameters and GH, cortisol and prolactin secretion were compared in elderly (60-80 years; n = 7) vs. younger subjects (20-30 years; n = 7). MANOVA revealed a reduction of SWS in the elderly. TSD led to an increase in SWS, a decrease in sleep onset latency, rapid eye movement (REM) density and by trend REM-latency without a global group difference. GH was reduced, whereas prolactin was enhanced in the elderly. After TSD GH was unchanged and prolactin secretion was enhanced without group difference. Thus, the plasticity of the sleep-endocrine system in response to TSD is sustained during aging. The possible involvement of the GABAergic system, that seems not to be severely impaired with age, is proposed.

  10. Waking electroencephalogram activity as a consequence of sleep and total sleep deprivation in the rat.

    PubMed

    Ugalde, E; Corsi-Cabrera, M; Juárez, J; Ramos, J; Arce, C

    1994-04-01

    Effects of 6 hours of total sleep deprivation (TSD) by gentle handling and 6 hours of sleep on the waking electroencephalogram (EEG) activity of 14 Wistar rats were studied during the lights-on portion of the light-dark cycle under two TSD schedules: a) TSD 0800-1400 hours and sleep 1400-2000 hours, and b) sleep 0800-1400 hours and TSD 1400-2000 hours. EEG was recorded monopolarly from left and right parietals referred to ipsilateral reference electrodes. Spectral analysis was performed on samples of waking EEG during TSD (each 30 minutes) and during sleep (each 60 minutes after enforced awakening). The following significant changes were observed: TSD induced a linear increase in the absolute power of delta (1.46-3.42 Hz) and the full band (1.6-24.9 Hz) and produced a decrease in the interparietal correlation of theta. Sleep induced the opposite results. Theta relative power (power in a band expressed as a percentage of total power between 1.46 and 24.9 Hz) showed a circadian effect. It was higher at 1400 hours than at 0800 and 2000 hours after both sleep and TSD conditions. Six hours of TSD were enough to induce significant changes in the waking EEG regardless of position of TSD in the lights-on period of the light-dark cycle.

  11. Mutual relations between sleep deprivation, sleep stealers and risk behaviours in adolescents

    PubMed Central

    Paiva, Teresa; Gaspar, Tania; Matos, Margarida Gaspar

    2016-01-01

    Objectives The aim is to evaluate the mutual influences between sleep duration/sleep deprivation (SD) and the sleep stealers/adolescent risk behaviours. Methods The national survey is a component of the Health Behaviour in School-Aged Children (HBSC) study, it is based on a school-based self-completed questionnaire; 3476 students were randomly selected from 139 randomly chosen Portuguese schools using as an unit the class, 53.8% were girls; 45.9% attended the 8th grade and 54.1% the 10th grade; the mean age was 14.9 years. The measured variables were: 1) gender and age; 2) sociodemographics; 3) sleep duration during the week and during weekends and computed SD; 4) screen time (computer use during the week and during the week end (PC use); watching TV and mobile phone use; 5) earlier sexual behaviour; 6) violent behaviours: fights, use of weapons; 7) use of tobacco, alcohol and drugs. The statistical analysis included Pearson chi-square tests and logistic regression. Results Excessive use of mobile phone, of computer use during weekdays, and internet facilities; substance use; violence and earlier sexual relations had significantly higher prevalence in sleep deprived adolescents. By logistic regression only using PC during weekdays, tobacco, drugs and weapons were associated to SD, while SD was associated to PC use during weekdays, tobacco use and drugs’ use. Computer uses tend to be associated among themselves. Mobile phone is associated with computer practices and with alcohol and tobacco use. Tobacco is associated with most risk behaviours. Alcohol use is associated with other substance use, computer use and violent behaviours. Violence behaviours, earlier sex and drugs use tend to be associated among themselves. Conclusions Sleep stealers use and risk behaviours are more prevalent in sleep deprived adolescents, but, in spite of significant individual associations, models of risk behaviours are still lacking. PMID:27226817

  12. A Unified Mathematical Model to Quantify Performance Impairment for Both Chronic Sleep Restriction and Total Sleep Deprivation

    DTIC Science & Technology

    2013-04-24

    Chronic sleep restriction Total sleep deprivation a b s t r a c t Performance prediction models based on the classical two-process model of sleep...restriction (partial sleep loss) performance predictions based on such models have been found to be less accurate. Because most modern operational...AVAILABILITY STATEMENT Approved for public release; distribution unlimited 13. SUPPLEMENTARY NOTES 14. ABSTRACT Performance prediction models based on

  13. Exercise-Induced growth hormone during acute sleep deprivation.

    PubMed

    Ritsche, Kevin; Nindl, Bradly C; Wideman, Laurie

    2014-10-01

    The effect of acute (24-h) sleep deprivation on exercise-induced growth hormone (GH) and insulin-like growth factor-1 (IGF-1) was examined. Ten men (20.6 ± 1.4 years) completed two randomized 24-h sessions including a brief, high-intensity exercise bout following either a night of sleep (SLEEP) or (24-h) sleep deprivation (SLD). Anaerobic performance (mean power [MP], peak power [PP], minimum power [MinP], time to peak power [TTPP], fatigue index, [FI]) and total work per sprint [TWPS]) was determined from four maximal 30-sec Wingate sprints on a cycle ergometer. Self-reported sleep 7 days prior to each session was similar between SLEEP and SLD sessions (7.92 ± 0.33 vs. 7.98 ± 0.39 h, P = 0.656, respectively) and during the actual SLEEP session in the lab, the total amount of sleep was similar to the 7 days leading up to the lab session (7.72 ± 0.14 h vs. 7.92 ± 0.33 h, respectively) (P = 0.166). No differences existed in MP, PP, MinP, TTPP, FI, TWPS, resting GH concentrations, time to reach exercise-induced peak GH concentration (TTP), or free IGF-1 between sessions. GH area under the curve (AUC) (825.0 ± 199.8 vs. 2212.9 ± 441.9 μg/L*min, P < 0.01), exercise-induced peak GH concentration (17.8 ± 3.7 vs. 39.6 ± 7.1 μg/L, P < 0.01) and ΔGH (peak GH - resting GH) (17.2 ± 3.7 vs. 38.2 ± 7.3 μg/L, P < 0.01) were significantly lower during the SLEEP versus SLD session. Our results indicate that the exercise-induced GH response was significantly augmented in sleep-deprived individuals.

  14. Melatonin modulates adiponectin expression on murine colitis with sleep deprivation

    PubMed Central

    Kim, Tae Kyun; Park, Young Sook; Baik, Haing-Woon; Jun, Jin Hyun; Kim, Eun Kyung; Sull, Jae Woong; Sung, Ho Joong; Choi, Jin Woo; Chung, Sook Hee; Gye, Myung Chan; Lim, Ju Yeon; Kim, Jun Bong; Kim, Seong Hwan

    2016-01-01

    AIM To determine adiponectin expression in colonic tissue of murine colitis and systemic cytokine expression after melatonin treatments and sleep deprivation. METHODS The following five groups of C57BL/6 mice were used in this study: (1) group I, control; (2) group II, 2% DSS induced colitis for 7 d; (3) group III, 2% DSS induced colitis and melatonin treatment; (4) group IV, 2% DSS induced colitis with sleep deprivation (SD) using specially designed and modified multiple platform water baths; and (5) group V, 2% DSS induced colitis with SD and melatonin treatment. Melatonin (10 mg/kg) or saline was intraperitoneally injected daily to mice for 4 d. The body weight was monitored daily. The degree of colitis was evaluated histologically after sacrificing the mice. Immunohistochemical staining and Western blot analysis was performed using anti-adiponectin antibody. After sampling by intracardiac punctures, levels of serum cytokines were measured by ELISA. RESULTS Sleep deprivation in water bath exacerbated DSS induced colitis and worsened weight loss. Melatonin injection not only alleviated the severity of mucosal injury, but also helped survival during stressful condition. The expression level of adiponectin in mucosa was decreased in colitis, with the lowest level observed in colitis combined with sleep deprivation. Melatonin injection significantly (P < 0.05) recovered the expression of adiponectin. The expression levels of IL-6 and IL-17 were increased in the serum of mice with DSS colitis but decreased after melatonin injection. CONCLUSION This study suggested that melatonin modulated adiponectin expression in colonic tissue and melatonin and adiponectin synergistically potentiated anti-inflammatory effects on colitis with sleep deprivation. PMID:27672276

  15. Melatonin modulates adiponectin expression on murine colitis with sleep deprivation.

    PubMed

    Kim, Tae Kyun; Park, Young Sook; Baik, Haing-Woon; Jun, Jin Hyun; Kim, Eun Kyung; Sull, Jae Woong; Sung, Ho Joong; Choi, Jin Woo; Chung, Sook Hee; Gye, Myung Chan; Lim, Ju Yeon; Kim, Jun Bong; Kim, Seong Hwan

    2016-09-07

    To determine adiponectin expression in colonic tissue of murine colitis and systemic cytokine expression after melatonin treatments and sleep deprivation. The following five groups of C57BL/6 mice were used in this study: (1) group I, control; (2) group II, 2% DSS induced colitis for 7 d; (3) group III, 2% DSS induced colitis and melatonin treatment; (4) group IV, 2% DSS induced colitis with sleep deprivation (SD) using specially designed and modified multiple platform water baths; and (5) group V, 2% DSS induced colitis with SD and melatonin treatment. Melatonin (10 mg/kg) or saline was intraperitoneally injected daily to mice for 4 d. The body weight was monitored daily. The degree of colitis was evaluated histologically after sacrificing the mice. Immunohistochemical staining and Western blot analysis was performed using anti-adiponectin antibody. After sampling by intracardiac punctures, levels of serum cytokines were measured by ELISA. Sleep deprivation in water bath exacerbated DSS induced colitis and worsened weight loss. Melatonin injection not only alleviated the severity of mucosal injury, but also helped survival during stressful condition. The expression level of adiponectin in mucosa was decreased in colitis, with the lowest level observed in colitis combined with sleep deprivation. Melatonin injection significantly (P < 0.05) recovered the expression of adiponectin. The expression levels of IL-6 and IL-17 were increased in the serum of mice with DSS colitis but decreased after melatonin injection. This study suggested that melatonin modulated adiponectin expression in colonic tissue and melatonin and adiponectin synergistically potentiated anti-inflammatory effects on colitis with sleep deprivation.

  16. Assessing Individual Differences in Adaptation to Extreme Environments: A 36-Hour Sleep Deprivation Study

    NASA Technical Reports Server (NTRS)

    Martinez, Jacqueline; Cowings, Patricia S.; Toscano, William B.

    2012-01-01

    In space, astronauts may experience effects of cumulative sleep loss due to demanding work schedules that can result in cognitive performance impairments, mood state deteriorations, and sleep-wake cycle disruption. Individuals who experience sleep deprivation of six hours beyond normal sleep times experience detrimental changes in their mood and performance states. Hence, the potential for life threatening errors increases exponentially with sleep deprivation. We explored the effects of 36-hours of sleep deprivation on cognitive performance, mood states, and physiological responses to identify which metrics may best predict fatigue induced performance decrements of individuals.

  17. Sleepless in adolescence: prospective data on sleep deprivation, health and functioning.

    PubMed

    Roberts, Robert E; Roberts, Catherine Ramsay; Duong, Hao T

    2009-10-01

    We estimate prevalence, incidence and persistence of short sleep or sleep deprivation in a two wave cohort study of 4175 youths 11-17 years old at baseline and 3134 of these a year later. Data were collected using computer interviews and questionnaires. Sleep deprivation was defined as 6h or less per night during the past 4 weeks. Weighted logistic regression procedures were employed to calculate prevalence, incidence, persistence/chronicity, and odds ratios. Prevalence rates and rates of persistence suggest sleep deprivation is highly prevalent and chronic. Multivariate analyses indicate that short sleep increases risk across multiple domains of dysfunction, suggesting pervasive deleterious effects. The broad impact of sleep deprivation and its pervasiveness suggests interventions will need to focus on multilevel changes to increase sleep time and reduce the negative impact of sleep deprivation among adolescents.

  18. The Effects of Two Types of Sleep Deprivation on Visual Working Memory Capacity and Filtering Efficiency

    PubMed Central

    Drummond, Sean P. A.; Anderson, Dane E.; Straus, Laura D.; Vogel, Edward K.; Perez, Veronica B.

    2012-01-01

    Sleep deprivation has adverse consequences for a variety of cognitive functions. The exact effects of sleep deprivation, though, are dependent upon the cognitive process examined. Within working memory, for example, some component processes are more vulnerable to sleep deprivation than others. Additionally, the differential impacts on cognition of different types of sleep deprivation have not been well studied. The aim of this study was to examine the effects of one night of total sleep deprivation and 4 nights of partial sleep deprivation (4 hours in bed/night) on two components of visual working memory: capacity and filtering efficiency. Forty-four healthy young adults were randomly assigned to one of the two sleep deprivation conditions. All participants were studied: 1) in a well-rested condition (following 6 nights of 9 hours in bed/night); and 2) following sleep deprivation, in a counter-balanced order. Visual working memory testing consisted of two related tasks. The first measured visual working memory capacity and the second measured the ability to ignore distractor stimuli in a visual scene (filtering efficiency). Results showed neither type of sleep deprivation reduced visual working memory capacity. Partial sleep deprivation also generally did not change filtering efficiency. Total sleep deprivation, on the other hand, did impair performance in the filtering task. These results suggest components of visual working memory are differentially vulnerable to the effects of sleep deprivation, and different types of sleep deprivation impact visual working memory to different degrees. Such findings have implications for operational settings where individuals may need to perform with inadequate sleep and whose jobs involve receiving an array of visual information and discriminating the relevant from the irrelevant prior to making decisions or taking actions (e.g., baggage screeners, air traffic controllers, military personnel, health care providers). PMID

  19. Small platform sleep deprivation selectively increases the average duration of rapid eye movement sleep episodes during sleep rebound.

    PubMed

    Kitka, Tamas; Katai, Zita; Pap, Dorottya; Molnar, Eszter; Adori, Csaba; Bagdy, Gyorgy

    2009-12-28

    The single platform-on-water (flower pot) method is extensively used for depriving rapid eye movement sleep (REMS). Detailed comparison of sleep-wake architecture, recorded during the rebound period after spending three days on either a small or large platform, could separate the effects of REMS deficit from other stress factors caused by the procedure. A further aim of the study was to find the most characteristic REMS parameter of the rebound originating from REMS deficit. Rats were kept on a small or large platform for 72 h. Their fronto-parietal electroencephalogram, electromyogram and motility were recorded during the 24 h rebound at the beginning of the passive phase. A similar period of a home cage group was also recorded. The most typical differences between the two rebound groups were the increased cumulative time and longer average duration of REMS episodes without significant change in the number of these episodes of the small platform animals during the passive phase. Results obtained by cosinor analysis were in accordance with the findings above. Since we did not find any difference in the average duration of REMS episodes comparing the large platform rebound group and the home cage group, we concluded that the increased mean duration of REMS episodes is a selective marker for the rebound caused by small platform sleep deprivation, while other changes in sleep architecture may be the consequence of stress and also some sleep deficit.

  20. Replication and Pedagogy in the History of Psychology IV: Patrick and Gilbert (1896) on Sleep Deprivation

    ERIC Educational Resources Information Center

    Fuchs, Thomas; Burgdorf, Jeffrey

    2008-01-01

    We report an attempted replication of G. T. W. Patrick and J. A. Gilbert's pioneering sleep deprivation experiment "Studies from the psychological laboratory of the University of Iowa. On the effects of loss of sleep", conducted in 1895/96. Patrick and Gilbert's study was the first sleep deprivation experiment of its kind, performed by some of the…

  1. Sleepless in Adolescence: Prospective Data on Sleep Deprivation, Health and Functioning

    ERIC Educational Resources Information Center

    Roberts, Robert E.; Roberts, Catherine Ramsay; Duong, Hao T.

    2009-01-01

    We estimate prevalence, incidence and persistence of short sleep or sleep deprivation in a two wave cohort study of 4175 youths 11-17 years old at baseline and 3134 of these a year later. Data were collected using computer interviews and questionnaires. Sleep deprivation was defined as 6 h or less per night during the past 4 weeks. Weighted…

  2. Sleepless in Adolescence: Prospective Data on Sleep Deprivation, Health and Functioning

    ERIC Educational Resources Information Center

    Roberts, Robert E.; Roberts, Catherine Ramsay; Duong, Hao T.

    2009-01-01

    We estimate prevalence, incidence and persistence of short sleep or sleep deprivation in a two wave cohort study of 4175 youths 11-17 years old at baseline and 3134 of these a year later. Data were collected using computer interviews and questionnaires. Sleep deprivation was defined as 6 h or less per night during the past 4 weeks. Weighted…

  3. Replication and Pedagogy in the History of Psychology IV: Patrick and Gilbert (1896) on Sleep Deprivation

    ERIC Educational Resources Information Center

    Fuchs, Thomas; Burgdorf, Jeffrey

    2008-01-01

    We report an attempted replication of G. T. W. Patrick and J. A. Gilbert's pioneering sleep deprivation experiment "Studies from the psychological laboratory of the University of Iowa. On the effects of loss of sleep", conducted in 1895/96. Patrick and Gilbert's study was the first sleep deprivation experiment of its kind, performed by some of the…

  4. Sleep Terrors (Night Terrors)

    MedlinePlus

    ... can contribute to sleep terrors, such as: Sleep deprivation and extreme tiredness Stress Sleep schedule disruptions, travel ... Risk factors Sleep terrors are more common if family members have a history of sleep terrors or ...

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

    PubMed

    Pilcher, J J; Walters, A S

    1997-11-01

    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.

  6. Exercise‐Induced growth hormone during acute sleep deprivation

    PubMed Central

    Ritsche, Kevin; Nindl, Bradly C.; Wideman, Laurie

    2014-01-01

    Abstract The effect of acute (24‐h) sleep deprivation on exercise‐induced growth hormone (GH) and insulin‐like growth factor‐1 (IGF‐1) was examined. Ten men (20.6 ± 1.4 years) completed two randomized 24‐h sessions including a brief, high‐intensity exercise bout following either a night of sleep (SLEEP) or (24‐h) sleep deprivation (SLD). Anaerobic performance (mean power [MP], peak power [PP], minimum power [MinP], time to peak power [TTPP], fatigue index, [FI]) and total work per sprint [TWPS]) was determined from four maximal 30‐sec Wingate sprints on a cycle ergometer. Self‐reported sleep 7 days prior to each session was similar between SLEEP and SLD sessions (7.92 ± 0.33 vs. 7.98 ± 0.39 h, P =0.656, respectively) and during the actual SLEEP session in the lab, the total amount of sleep was similar to the 7 days leading up to the lab session (7.72 ± 0.14 h vs. 7.92 ± 0.33 h, respectively) (P =0.166). No differences existed in MP, PP, MinP, TTPP, FI, TWPS, resting GH concentrations, time to reach exercise‐induced peak GH concentration (TTP), or free IGF‐1 between sessions. GH area under the curve (AUC) (825.0 ± 199.8 vs. 2212.9 ± 441.9 μg/L*min, P <0.01), exercise‐induced peak GH concentration (17.8 ± 3.7 vs. 39.6 ± 7.1 μg/L, P <0.01) and ΔGH (peak GH – resting GH) (17.2 ± 3.7 vs. 38.2 ± 7.3 μg/L, P <0.01) were significantly lower during the SLEEP versus SLD session. Our results indicate that the exercise‐induced GH response was significantly augmented in sleep‐deprived individuals. PMID:25281616

  7. Sleep deprivation increases cerebral serotonin 2A receptor binding in humans.

    PubMed

    Elmenhorst, David; Kroll, Tina; Matusch, Andreas; Bauer, Andreas

    2012-12-01

    Serotonin and its cerebral receptors play an important role in sleep-wake regulation. The aim of the current study is to investigate the effect of 24-h total sleep deprivation on the apparent serotonin 2A receptor (5-HT(2A)R) binding capacity in the human brain to test the hypothesis that sleep deprivation induces global molecular alterations in the cortical serotonergic receptor system. Volunteers were tested twice with the subtype-selective radiotracer [(18)F]altanserin and positron emission tomography (PET) for imaging of 5-HT(2A)Rs at baseline and after 24 h of sleep deprivation. [(18)F]Altanserin binding potentials were analyzed in 13 neocortical regions of interest. The efficacy of sleep deprivation was assessed by questionnaires, waking electroencephalography, and cognitive performance measurements. Sleep laboratory and neuroimaging center. Eighteen healthy volunteers. Sleep deprivation. A total of 24 hours of sleep deprivation led to a 9.6% increase of [(18)F]altanserin binding on neocortical 5-HT(2A) receptors. Significant region-specific increases were found in the medial inferior frontal gyrus, insula, and anterior cingulate, parietal, sensomotoric, and ventrolateral prefrontal cortices. This study demonstrates that a single night of total sleep deprivation causes significant increases of 5-HT(2A)R binding potentials in a variety of cortical regions although the increase declines as sleep deprivation continued. It provides in vivo evidence that total sleep deprivation induces adaptive processes in the serotonergic system of the human brain.

  8. Sleep deprivation during a specific 3-hour time window post-training impairs hippocampal synaptic plasticity and memory

    PubMed Central

    Prince, Toni-Moi; Wimmer, Mathieu; Choi, Jennifer; Havekes, Robbert; Aton, Sara; Abel, Ted

    2014-01-01

    Sleep deprivation disrupts hippocampal function and plasticity. In particular, long-term memory consolidation is impaired by sleep deprivation, suggesting that a specific critical period exists following learning during which sleep is necessary. To elucidate the impact of sleep deprivation on long-term memory consolidation and synaptic plasticity, long-term memory was assessed when mice were sleep deprived following training in the hippocampus-dependent object place recognition task. We found that 3 hours of sleep deprivation significantly impaired memory when deprivation began 1 hour after training. In contrast, 3 hours of deprivation beginning immediately post-training did not impair spatial memory. Furthermore, a 3-hour sleep deprivation beginning 1 hour after training impaired hippocampal long-term potentiation (LTP), whereas sleep deprivation immediately after training did not affect LTP. Together, our findings define a specific 3-hour critical period, extending from 1 to 4 hours after training, during which sleep deprivation impairs hippocampal function. PMID:24380868

  9. A Novel BHLHE41 Variant is Associated with Short Sleep and Resistance to Sleep Deprivation in Humans

    PubMed Central

    Pellegrino, Renata; Kavakli, Ibrahim Halil; Goel, Namni; Cardinale, Christopher J.; Dinges, David F.; Kuna, Samuel T.; Maislin, Greg; Van Dongen, Hans P.A.; Tufik, Sergio; Hogenesch, John B.; Hakonarson, Hakon; Pack, Allan I.

    2014-01-01

    Study Objectives: Earlier work described a mutation in DEC2 also known as BHLHE41 (basic helix-loophelix family member e41) as causal in a family of short sleepers, who needed just 6 h sleep per night. We evaluated whether there were other variants of this gene in two well-phenotyped cohorts. Design: Sequencing of the BHLHE41 gene, electroencephalographic data, and delta power analysis and functional studies using cell-based luciferase. Results: We identified new variants of the BHLHE41 gene in two cohorts who had either acute sleep deprivation (n = 200) or chronic partial sleep deprivation (n = 217). One variant, Y362H, at another location in the same exon occurred in one twin in a dizygotic twin pair and was associated with reduced sleep duration, less recovery sleep following sleep deprivation, and fewer performance lapses during sleep deprivation than the homozygous twin. Both twins had almost identical amounts of non rapid eye movement (NREM) sleep. This variant reduced the ability of BHLHE41 to suppress CLOCK/BMAL1 and NPAS2/BMAL1 transactivation in vitro. Another variant in the same exome had no effect on sleep or response to sleep deprivation and no effect on CLOCK/BMAL1 transactivation. Random mutagenesis identified a number of other variants of BHLHE41 that affect its function. Conclusions: There are a number of mutations of BHLHE41. Mutations reduce total sleep while maintaining NREM sleep and provide resistance to the effects of sleep loss. Mutations that affect sleep also modify the normal inhibition of BHLHE41 of CLOCK/BMAL1 transactivation. Thus, clock mechanisms are likely involved in setting sleep length and the magnitude of sleep homeostasis. Citation: Pellegrino R, Kavakli IH, Goel N, Cardinale CJ, Dinges DF, Kuna ST, Maislin G, Van Dongen HP, Tufik S, Hogenesch JB, Hakonarson H, Pack AI. A novel BHLHE41 variant is associated with short sleep and resistance to sleep deprivation in humans. SLEEP 2014;37(8):1327-1336. PMID:25083013

  10. Geranylgeranylacetone, an inducer of HSP 70, attenuates REM sleep rebound after sleep deprivation.

    PubMed

    Wada, Tadashi; Sei, Hiroyoshi; Kusumoto, Kenji; Kitaoka, Kazuyoshi; Chikahisa, Sachiko; Rokutan, Kazuhito; Morita, Yusuke

    2006-04-28

    The effect of pretreatment of geranylgeranylacetone (GGA), an inducer of heat shock protein (HSP) 70, on responses in sleep and core body temperature (Tcore) against sleep deprivation (SD) was examined in rats. After 3 days of GGA or vehicle injection, a 6-h period of SD was performed. During the recovery period, both rapid-eye movement (REM) and non-REM (NREM) sleep were increased in both GGA- and vehicle-injected rats. However, in GGA-injected rats, REM-sleep rebound was significantly suppressed, while NREM-sleep rebound remained unaffected. In addition, the increase of Tcore caused by SD was also attenuated in GGA-injected rats. In the hippocampus, both SD and the GGA pretreatment induced an increase in the expression of HSP70 mRNA, indicating that the SD functions as a stress for hippocampal neurons and that the GGA induces HSP70 expression. The findings suggest that pretreatment with GGA suppresses REM sleep rebound and the response of Tcore against SD.

  11. Effects of sleep deprivation on measures of the febrile reaction and the recovery of somatovisceral functions and sleep in endotoxemia.

    PubMed

    Lapshina, K V; Ekimova, I V

    2010-05-01

    Electroencephalographic methods were used to study the effects of total sleep deprivation on thermoregulatory measures of the fever response in pigeons (Columba livia): brain temperature, peripheral vasomotor reactions, thoracic muscle contractile activity, and the recovery of somatic functions and the time characteristics of waking and sleep in lipopolysaccharide (LPS)-induced endotoxemia. Sleep deprivation during the period in which the quantity of slow-wave sleep increased on administration of LPS induced decreases in the latent period of fever onset and in the duration of fever, along with more significant increases in brain temperature and the level of muscle contractile activity as compared with the effects of LPS alone. The period after sleep deprivation was characterized by more prolonged recovery of muscle contractile activity and the time characteristics of sleep and waking states, along with more prolonged compensatory "rebound" of slow-wave sleep as compared with the effects of sleep deprivation alone. Thus, sleep deprivation in endotoxemia led to decreases in the latent period of fever onset, exacerbation of fever, and increases in the latent period of recovery of physiological functions.

  12. Effect of 24 Hours of Sleep Deprivation on Auditory and Linguistic Perception: A Comparison among Young Controls, Sleep-Deprived Participants, Dyslexic Readers, and Aging Adults

    ERIC Educational Resources Information Center

    Fostick, Leah; Babkoff, Harvey; Zukerman, Gil

    2014-01-01

    Purpose: To test the effects of 24 hr of sleep deprivation on auditory and linguistic perception and to assess the magnitude of this effect by comparing such performance with that of aging adults on speech perception and with that of dyslexic readers on phonological awareness. Method: Fifty-five sleep-deprived young adults were compared with 29…

  13. Effect of 24 Hours of Sleep Deprivation on Auditory and Linguistic Perception: A Comparison among Young Controls, Sleep-Deprived Participants, Dyslexic Readers, and Aging Adults

    ERIC Educational Resources Information Center

    Fostick, Leah; Babkoff, Harvey; Zukerman, Gil

    2014-01-01

    Purpose: To test the effects of 24 hr of sleep deprivation on auditory and linguistic perception and to assess the magnitude of this effect by comparing such performance with that of aging adults on speech perception and with that of dyslexic readers on phonological awareness. Method: Fifty-five sleep-deprived young adults were compared with 29…

  14. Effects of sleep deprivation on impulsive behaviors in men and women.

    PubMed

    Acheson, Ashley; Richards, Jerry B; de Wit, Harriet

    2007-08-15

    The purpose of this study was to examine the effects of sleep deprivation on impulsive behavior. Patients with impulse control disorders often report sleep problems, and sleep deprivation even in healthy individuals impairs cognition, decision-making, and perhaps impulse control. To characterize the effects of sleep loss on specific forms of impulsive behavior, we tested the effects of overnight, monitored sleep deprivation on measures of impulsivity and cognition in healthy volunteers. Ten men and ten women completed two 24 h sessions in random order, in which they were either allowed to sleep normally or remained awake all night. At 8:30 am and 6:15 pm on the day after sleep or no sleep, participants were tested on the Balloon Analogue Risk Task (BART), the Experiential Discounting Task, the Adjusting Amount Delay and Probability Discounting Task, and the Stop Task. Participants also completed mood questionnaires and the Automated Neuropsychological Assessment Matrix (ANAM) throughout the course of the day. Sleep deprivation did not affect most of the measures of impulsive behavior. However, on the BART, sleep deprivation decreased risk taking in women, but not men. Sleep deprivation produced expected increases in subjective fatigue, and impaired performance on measures of attention and cognitive efficiency on the ANAM. The results indicate that sleep deprivation does not specifically increase impulsive behaviors but may differentially affect risk taking in men and women.

  15. Human Hippocampal Structure: A Novel Biomarker Predicting Mnemonic Vulnerability to, and Recovery from, Sleep Deprivation.

    PubMed

    Saletin, Jared M; Goldstein-Piekarski, Andrea N; Greer, Stephanie M; Stark, Shauna; Stark, Craig E; Walker, Matthew P

    2016-02-24

    Sleep deprivation impairs the formation of new memories. However, marked interindividual variability exists in the degree to which sleep loss compromises learning, the mechanistic reasons for which are unclear. Furthermore, which physiological sleep processes restore learning ability following sleep deprivation are similarly unknown. Here, we demonstrate that the structural morphology of human hippocampal subfields represents one factor determining vulnerability (and conversely, resilience) to the impact of sleep deprivation on memory formation. Moreover, this same measure of brain morphology was further associated with the quality of nonrapid eye movement slow wave oscillations during recovery sleep, and by way of such activity, determined the success of memory restoration. Such findings provide a novel human biomarker of cognitive susceptibility to, and recovery from, sleep deprivation. Moreover, this metric may be of special predictive utility for professions in which memory function is paramount yet insufficient sleep is pervasive (e.g., aviation, military, and medicine).

  16. Age-related changes in sleep spindles characteristics during daytime recovery following a 25-hour sleep deprivation

    PubMed Central

    Rosinvil, T.; Lafortune, M.; Sekerovic, Z.; Bouchard, M.; Dubé, J.; Latulipe-Loiselle, A.; Martin, N.; Lina, J. M.; Carrier, J.

    2015-01-01

    Objectives: The mechanisms underlying sleep spindles (~11–15 Hz; >0.5 s) help to protect sleep. With age, it becomes increasingly difficult to maintain sleep at a challenging time (e.g., daytime), even after sleep loss. This study compared spindle characteristics during daytime recovery and nocturnal sleep in young and middle-aged adults. In addition, we explored whether spindles characteristics in baseline nocturnal sleep were associated with the ability to maintain sleep during daytime recovery periods in both age groups. Methods: Twenty-nine young (15 women and 14 men; 27.3 y ± 5.0) and 31 middle-aged (19 women and 13 men; 51.6 y ± 5.1) healthy subjects participated in a baseline nocturnal sleep and a daytime recovery sleep after 25 hours of sleep deprivation. Spindles were detected on artifact-free Non-rapid eye movement (NREM) sleep epochs. Spindle density (nb/min), amplitude (μV), frequency (Hz), and duration (s) were analyzed on parasagittal (linked-ears) derivations. Results: In young subjects, spindle frequency increased during daytime recovery sleep as compared to baseline nocturnal sleep in all derivations, whereas middle-aged subjects showed spindle frequency enhancement only in the prefrontal derivation. No other significant interaction between age group and sleep condition was observed. Spindle density for all derivations and centro-occipital spindle amplitude decreased whereas prefrontal spindle amplitude increased from baseline to daytime recovery sleep in both age groups. Finally, no significant correlation was found between spindle characteristics during baseline nocturnal sleep and the marked reduction in sleep efficiency during daytime recovery sleep in both young and middle-aged subjects. Conclusion: These results suggest that the interaction between homeostatic and circadian pressure modulates spindle frequency differently in aging. Spindle characteristics do not seem to be linked with the ability to maintain daytime recovery sleep. PMID

  17. Acute Sleep Deprivation Blocks Short- and Long-Term Operant Memory in Aplysia

    PubMed Central

    Krishnan, Harini C.; Gandour, Catherine E.; Ramos, Joshua L.; Wrinkle, Mariah C.; Sanchez-Pacheco, Joseph J.; Lyons, Lisa C.

    2016-01-01

    Study Objectives: Insufficient sleep in individuals appears increasingly common due to the demands of modern work schedules and technology use. Consequently, there is a growing need to understand the interactions between sleep deprivation and memory. The current study determined the effects of acute sleep deprivation on short and long-term associative memory using the marine mollusk Aplysia californica, a relatively simple model system well known for studies of learning and memory. Methods: Aplysia were sleep deprived for 9 hours using context changes and tactile stimulation either prior to or after training for the operant learning paradigm, learning that food is inedible (LFI). The effects of sleep deprivation on short-term (STM) and long-term memory (LTM) were assessed. Results: Acute sleep deprivation prior to LFI training impaired the induction of STM and LTM with persistent effects lasting at least 24 h. Sleep deprivation immediately after training blocked the consolidation of LTM. However, sleep deprivation following the period of molecular consolidation did not affect memory recall. Memory impairments were independent of handling-induced stress, as daytime handled control animals demonstrated no memory deficits. Additional training immediately after sleep deprivation failed to rescue the induction of memory, but additional training alleviated the persistent impairment in memory induction when training occurred 24 h following sleep deprivation. Conclusions: Acute sleep deprivation inhibited the induction and consolidation, but not the recall of memory. These behavioral studies establish Aplysia as an effective model system for studying the interactions between sleep and memory formation. Citation: Krishnan HC, Gandour CE, Ramos JL, Wrinkle MC, Sanchez-Pacheco JJ, Lyons LC. Acute sleep deprivation blocks short- and long-term operant memory in Aplysia. SLEEP 2016;39(12):2161–2171. PMID:27748243

  18. Circadian modulation of consolidated memory retrieval following sleep deprivation in Drosophila.

    PubMed

    Le Glou, Eric; Seugnet, Laurent; Shaw, Paul J; Preat, Thomas; Goguel, Valérie

    2012-10-01

    Several lines of evidence indicate that sleep plays a critical role in learning and memory. The aim of this study was to evaluate anesthesia resistant memory following sleep deprivation in Drosophila. Four to 16 h after aversive olfactory training, flies were sleep deprived for 4 h. Memory was assessed 24 h after training. Training, sleep deprivation, and memory tests were performed at different times during the day to evaluate the importance of the time of day for memory formation. The role of circadian rhythms was further evaluated using circadian clock mutants. Memory was disrupted when flies were exposed to 4 h of sleep deprivation during the consolidation phase. Interestingly, normal memory was observed following sleep deprivation when the memory test was performed during the 2 h preceding lights-off, a period characterized by maximum wake in flies. We also show that anesthesia resistant memory was less sensitive to sleep deprivation in flies with disrupted circadian rhythms. Our results indicate that anesthesia resistant memory, a consolidated memory less costly than long-term memory, is sensitive to sleep deprivation. In addition, we provide evidence that circadian factors influence memory vulnerability to sleep deprivation and memory retrieval. Taken together, the data show that memories weakened by sleep deprivation can be retrieved if the animals are tested at the optimal circadian time.

  19. Proteomic changes in rat hippocampus and adrenals following short-term sleep deprivation

    PubMed Central

    Poirrier, Jean-Etienne; Guillonneau, François; Renaut, Jenny; Sergeant, Kjell; Luxen, Andre; Maquet, Pierre; Leprince, Pierre

    2008-01-01

    Background To identify the biochemical changes induced by sleep deprivation at a proteomic level, we compared the hippocampal proteome of rats either after 4 hours of sleep or sleep deprivation obtained by gentle handling. Because sleep deprivation might induce some stress, we also analyzed proteomic changes in rat adrenals in the same conditions. After sleep deprivation, proteins from both tissues were extracted and subjected to 2D-DIGE analysis followed by protein identification through mass spectrometry and database search. Results In the hippocampus, 87 spots showed significant variation between sleep and sleep deprivation, with more proteins showing higher abundance in the latter case. Of these, 16 proteins were present in sufficient amount for a sequencing attempt and among the 12 identified proteins, inferred affected cellular functions include cell metabolism, energy pathways, transport and vesicle trafficking, cytoskeleton and protein processing. Although we did not observe classical, macroscopic effect of stress in sleep-deprived rats, 47 protein spots showed significant variation in adrenal tissue between sleep and sleep deprivation, with more proteins showing higher abundance following sleep. Of these, 16 proteins were also present in sufficient amount for a sequencing attempt and among the 13 identified proteins, the most relevant cellular function that was affected was cell metabolism. Conclusion At a proteomic level, short term sleep deprivation is characterized by a higher expression of some proteins in the hippocampus and a lower abundance of other proteins in the adrenals (compared to normal sleep control). Altogether, this could indicate a general activation of a number of cellular mechanisms involved in the maintenance of wakefulness and in increased energy expenditure during sleep deprivation. These findings are relevant to suggested functions of sleep like energy repletion and the restoration of molecular stocks or a more global homeostasis of

  20. Childbirth fear, anxiety, fatigue, and sleep deprivation in pregnant women.

    PubMed

    Hall, Wendy A; Hauck, Yvonne L; Carty, Elaine M; Hutton, Eileen K; Fenwick, Jennifer; Stoll, Kathrin

    2009-01-01

    To explore women's levels of childbirth fear, sleep deprivation, anxiety, and fatigue and their relationships during the third trimester of pregnancy. A cross-sectional descriptive survey of a community sample. Six hundred and fifty English-speaking nulliparous and multiparous women, 17 to 46 years of age and between 35 and 39 weeks gestation, with uncomplicated pregnancies. Wijma Delivery Expectancy/Experience Questionnaire, Spielberger State Anxiety Inventory, Mindell's Sleep Questionnaire, and the Multidimensional Assessment of Fatigue Questionnaire. Twenty-five percent of women reported high levels of childbirth fear and 20.6% reported sleeping less than 6 hours per night. Childbirth fear, fatigue, sleep deprivation, and anxiety were positively correlated. Fewer women attending midwives reported severe fear of childbirth than those attending obstetricians. Women with high childbirth fear were more likely to have more daily stressors, anxiety, and fatigue, as well as less help. Higher levels of anxiety predicted higher levels of childbirth fear among women. One fourth of women reported high childbirth fear. Women's fear of childbirth was related to fatigue, available help, stressors, and anxiety. Fear of childbirth appears to be part of a complex picture of women's emotional experiences during pregnancy.

  1. Monotonic and rhythmic influences: a challenge for sleep deprivation research.

    PubMed

    Babkoff, H; Caspy, T; Mikulincer, M; Sing, H C

    1991-05-01

    There are both monotonic and rhythmic factors in the patterns of change seen in physiological, psychological, and performance variables during sleep deprivation. These monotonic and rhythmic factors can be orthogonal, or they may interact with each other, with various task variables, or both. The importance of separating the rhythmic from the monotonic factors and of elucidating their interactions is discussed. Experimental methods and types of analysis appropriate to evaluating these factors are examined, with special emphasis on the complex demodulation time series analysis applied to group or individual subject data. The discussion is accompanied by data illustrations. It is suggested that sleep deprivation research should be designed so as to generate physiological and behavioral data that include information on both monotonic and rhythmic factors, the nature and extent of their interaction, and how they interrelate with systematically manipulated independent variables.

  2. Degradation of Cortical Representations during Encoding following Sleep Deprivation.

    PubMed

    Poh, Jia-Hou; Chee, Michael W L

    2017-02-01

    A night of total sleep deprivation (TSD) reduces task-related activation of fronto-parietal and higher visual cortical areas. As this reduction in activation corresponds to impaired attention and perceptual processing, it might also be associated with poorer memory encoding. Related animal work has established that cortical columns stochastically enter an 'off' state in sleep deprivation, leading to predictions that neural representations are less stable and distinctive following TSD. To test these predictions participants incidentally encoded scene images while undergoing fMRI, either during rested wakefulness (RW) or after TSD. In scene-selective PPA, TSD reduced stability of neural representations across repetition. This was accompanied by poorer subsequent memory. Greater representational stability benefitted subsequent memory in RW but not TSD. Even for items subsequently recognized, representational distinctiveness was lower in TSD, suggesting that quality of encoding is degraded. Reduced representational stability and distinctiveness are two novel mechanisms by which TSD can contribute to poorer memory formation.

  3. Individualising EEG frequency bands for sleep deprivation studies.

    PubMed

    Henelius, Andreas; Korpela, Jussi; Huotilainen, Minna

    2011-01-01

    A method for determining individualised frequency bands from electroencephalographic (EEG) power spectral density (PSD) plots is presented. EEG was collected during the performance of a computerised multitask test from 21 healthy male subjects, of which an experimental group of 14 subjects underwent sleep deprivation and 7 subjects formed the control group. EEG PSD plots were compared between the groups and were used to determine individual theta, alpha and beta bands for the subjects by studying the points of intersection between the individual subjects' normalised spectra and the normalised average spectrum of the control group. The results show that the frontal and occipital locations are best suited for the determination of individualised frequency bands. The proposed method can be used to enhance EEG spectral analysis of task-induced cognitive effort during sleep deprivation.

  4. A Time for Learning and a Time for Sleep: The Effect of Sleep Deprivation on Contextual Fear Conditioning at Different Times of the Day

    PubMed Central

    Hagewoud, Roelina; Whitcomb, Shamiso N.; Heeringa, Amarins N.; Havekes, Robbert; Koolhaas, Jaap M.; Meerlo, Peter

    2010-01-01

    Study Objectives: Sleep deprivation negatively affects memory consolidation, especially in the case of hippocampus-dependent memories. Studies in rodents have shown that 5 hours of sleep deprivation immediately following footshock exposure selectively impairs the formation of a contextual fear memory. In these studies, both acquisition and subsequent sleep deprivation were performed in the animals' main resting phase. However, in everyday life, subjects most often learn during their active phase. Design: Here we examined the effects of sleep deprivation on memory consolidation for contextual fear in rats when the task was performed at different times of the day, particularly, at the beginning of the resting phase or right before the onset of the active phase. Measurements and Results: Results show that sleep deprivation immediately following training affects consolidation of contextual fear, independent of time of training. However, in the resting phase memory consolidation was impaired by 6 hours of posttraining sleep deprivation, whereas, in the active phase, the impairment was only seen after 12 hours of sleep deprivation. Since rats sleep at least twice as much during the resting phase compared with the active phase, these data suggest that the effect of sleep deprivation depends on the amount of sleep that was lost. Also, control experiments show that effects of sleep deprivation were not related to the amount of stimulation the animals received and were therefore not likely an indirect effect of the sleep-deprivation method. Conclusion: These results support the notion that sleep immediately following acquisition, independent of time of day, promotes memory consolidation and that sleep deprivation may disrupt this process depending on the amount of sleep that is lost. Citation: Hagewoud R; Whitcomb SN; Heeringa AN; Havekes R; Koolhaas JM; Meerlo P. A time for learning and a time for sleep: the effect of sleep deprivation on contextual fear conditioning at

  5. Identification of Genes Associated with Resilience/Vulnerability to Sleep Deprivation and Starvation in Drosophila

    PubMed Central

    Thimgan, Matthew S.; Seugnet, Laurent; Turk, John; Shaw, Paul J.

    2015-01-01

    Background and Study Objectives: Flies mutant for the canonical clock protein cycle (cyc01) exhibit a sleep rebound that is ∼10 times larger than wild-type flies and die after only 10 h of sleep deprivation. Surprisingly, when starved, cyc01 mutants can remain awake for 28 h without demonstrating negative outcomes. Thus, we hypothesized that identifying transcripts that are differentially regulated between waking induced by sleep deprivation and waking induced by starvation would identify genes that underlie the deleterious effects of sleep deprivation and/or protect flies from the negative consequences of waking. Design: We used partial complementary DNA microarrays to identify transcripts that are differentially expressed between cyc01 mutants that had been sleep deprived or starved for 7 h. We then used genetics to determine whether disrupting genes involved in lipid metabolism would exhibit alterations in their response to sleep deprivation. Setting: Laboratory. Patients or Participants: Drosophila melanogaster. Interventions: Sleep deprivation and starvation. Measurements and Results: We identified 84 genes with transcript levels that were differentially modulated by 7 h of sleep deprivation and starvation in cyc01 mutants and were confirmed in independent samples using quantitative polymerase chain reaction. Several of these genes were predicted to be lipid metabolism genes, including bubblegum, cueball, and CG4500, which based on our data we have renamed heimdall (hll). Using lipidomics we confirmed that knockdown of hll using RNA interference significantly decreased lipid stores. Importantly, genetically modifying bubblegum, cueball, or hll resulted in sleep rebound alterations following sleep deprivation compared to genetic background controls. Conclusions: We have identified a set of genes that may confer resilience/vulnerability to sleep deprivation and demonstrate that genes involved in lipid metabolism modulate sleep homeostasis. Citation: Thimgan MS

  6. Feedback Blunting: Total Sleep Deprivation Impairs Decision Making that Requires Updating Based on Feedback.

    PubMed

    Whitney, Paul; Hinson, John M; Jackson, Melinda L; Van Dongen, Hans P A

    2015-05-01

    To better understand the sometimes catastrophic effects of sleep loss on naturalistic decision making, we investigated effects of sleep deprivation on decision making in a reversal learning paradigm requiring acquisition and updating of information based on outcome feedback. Subjects were randomized to a sleep deprivation or control condition, with performance testing at baseline, after 2 nights of total sleep deprivation (or rested control), and following 2 nights of recovery sleep. Subjects performed a decision task involving initial learning of go and no go response sets followed by unannounced reversal of contingencies, requiring use of outcome feedback for decisions. A working memory scanning task and psychomotor vigilance test were also administered. Six consecutive days and nights in a controlled laboratory environment with continuous behavioral monitoring. Twenty-six subjects (22-40 y of age; 10 women). Thirteen subjects were randomized to a 62-h total sleep deprivation condition; the others were controls. Unlike controls, sleep deprived subjects had difficulty with initial learning of go and no go stimuli sets and had profound impairment adapting to reversal. Skin conductance responses to outcome feedback were diminished, indicating blunted affective reactions to feedback accompanying sleep deprivation. Working memory scanning performance was not significantly affected by sleep deprivation. And although sleep deprived subjects showed expected attentional lapses, these could not account for impairments in reversal learning decision making. Sleep deprivation is particularly problematic for decision making involving uncertainty and unexpected change. Blunted reactions to feedback while sleep deprived underlie failures to adapt to uncertainty and changing contingencies. Thus, an error may register, but with diminished effect because of reduced affective valence of the feedback or because the feedback is not cognitively bound with the choice. This has important

  7. Evidence That Sleep Deprivation Downregulates Dopamine D2R in Ventral Striatum in the Human Brain

    SciTech Connect

    Volkow N. D.; Fowler J.; Volkow, N.D.; Tomasi, D.; Wang, G.-J.; Fowler, J.S.; Logan, J.; Benveniste, H.; Kin, R.; Thanos, P.K.; Sergi F.

    2012-03-23

    Dopamine D2 receptors are involved with wakefulness, but their role in the decreased alertness associated with sleep deprivation is unclear. We had shown that sleep deprivation reduced dopamine D2/D3 receptor availability (measured with PET and [{sup 11}C]raclopride in controls) in striatum, but could not determine whether this reflected dopamine increases ([{sup 11}C]raclopride competes with dopamine for D2/D3 receptor binding) or receptor downregulation. To clarify this, we compared the dopamine increases induced by methylphenidate (a drug that increases dopamine by blocking dopamine transporters) during sleep deprivation versus rested sleep, with the assumption that methylphenidate's effects would be greater if, indeed, dopamine release was increased during sleep deprivation. We scanned 20 controls with [{sup 11}C]raclopride after rested sleep and after 1 night of sleep deprivation; both after placebo and after methylphenidate. We corroborated a decrease in D2/D3 receptor availability in the ventral striatum with sleep deprivation (compared with rested sleep) that was associated with reduced alertness and increased sleepiness. However, the dopamine increases induced by methylphenidate (measured as decreases in D2/D3 receptor availability compared with placebo) did not differ between rested sleep and sleep deprivation, and were associated with the increased alertness and reduced sleepiness when methylphenidate was administered after sleep deprivation. Similar findings were obtained by microdialysis in rodents subjected to 1 night of paradoxical sleep deprivation. These findings are consistent with a downregulation of D2/D3 receptors in ventral striatum with sleep deprivation that may contribute to the associated decreased wakefulness and also corroborate an enhancement of D2 receptor signaling in the arousing effects of methylphenidate in humans.

  8. A comparison of tyrosine against placebo, phentermine, caffeine, and D-amphetamine during sleep deprivation.

    PubMed

    Waters, William F; Magill, Richard A; Bray, George A; Volaufova, Julia; Smith, Steven R; Lieberman, Harris R; Rood, Jennifer; Hurry, Mark; Anderson, Tai; Ryan, Donna H

    2003-08-01

    Sleep deprivation can impair alertness and cognitive and motor performance. We hypothesized that the amino acid tyrosine might reduce deleterious effects of sleep deprivation. Seventy-six healthy males, age 18-35 years, participated in a four-day protocol that included a habituation night, a baseline night, a 40.5 h period without sleep, and a recovery night. Tyrosine 150 mg/kg, caffeine 300 mg/70 kg, phentermine 37.5 mg, D-amphetamine 20 mg and placebo were administered in a double-blind, randomized fashion to compare their effects on the time it took to fall asleep, on endocrine responses during sleep deprivation, and on sleep quantity, quality and architecture as measured by polysomnography during recovery sleep. When given after 36 h without sleep, tyrosine had no significant effect on any parameter of sleep. D-amphetamine produced marked decrease in sleep drive but caused deleterious effects on many aspects of recovery sleep. Still, D-amphetamine was associated with increased alertness on the first recovery day. Phentermine and caffeine both decreased sleep drive during sleep deprivation, but phentermine impaired rapid-eye-movement (REM) recovery sleep. Tyrosine (when compared to placebo) had no effect on any sleep related measure, but it did stimulate prolactin release.

  9. Effects of adaptogens on granulocytopoiesis during paradoxical sleep deprivation.

    PubMed

    Provalova, N V; Skurikhin, E G; Suslov, N I; Dygai, A M; Gol'dberg, E D

    2002-03-01

    We studied the effects of extracts from Siberian ginseng, Rhodiola rosea, bergenia, and ginseng (G115) and pantohematogen on granulocytopoiesis after paradoxical sleep deprivation. The effects of adaptogens on the blood system were most pronounced during hyperplasia of granulocytopoiesis. Natural preparations were divided into groups depending on their activity. Extracts of Siberian ginseng and Rhodiola rosea did not modulate granulocytopoiesis. Ginseng G115 extract suppressed granulocytopoiesis. Bergenia extract and pantohematogen produced ambiguous effects on the granulocytic hemopoietic stem.

  10. Sleep deprivation, allergy symptoms, and negatively reinforced problem behavior.

    PubMed

    Kennedy, C H; Meyer, K A

    1996-01-01

    We studied the relation between the presence versus the absence of sleep deprivation or allergy symptoms and the rate and function of problem behavior. Three students whose problem behavior was negatively reinforced by escape form instruction were studied across several weeks using analogue functional analyses. Our results indicated that the extraexperimental events were associated with (a) termination of instruction functioning as a negative reinforcer, (b) increased rates of negatively reinforced problem behavior, or (c) increased rates of problem behavior across all conditions.

  11. The effect of REM sleep deprivation on motivation for food reward.

    PubMed

    Hanlon, Erin C; Andrzejewski, Matthew E; Harder, Bridgette K; Kelley, Ann E; Benca, Ruth M

    2005-08-30

    Prolonged sleep deprivation in rats produces a characteristic syndrome consisting of an increase in food intake yet a decrease in weight. Moreover, the increase in food intake generally precedes the weight loss, suggesting that sleep deprivation may affect appetitive behaviors. Using the multiple platform method to produce rapid eye movement (REM) sleep deprivation, we investigated the effect of REM sleep deprivation (REMSD) on motivation for food reward utilizing food-reinforced operant tasks. In acquisition or maintenance of an operant task, REM sleep-deprived rats, with or without simultaneous food restriction, decreased responding for sucrose pellet reward in comparison to controls, despite the fact that all REM sleep-deprived rats lost weight. Furthermore, the overall response deficit of the REM sleep-deprived rats was due to a within-session decline in responding. REM sleep-deprived rats showed evidence of understanding the contingency of the task comparable to controls throughout deprivation period, suggesting that the decrements in responding were not primarily related to deficits in learning or memory. Rather, REM sleep deprivation appears to alter systems involved in motivational processes, reward, and/or attention.

  12. Short-term sleep deprivation leads to decreased systemic redox metabolites and altered epigenetic status.

    PubMed

    Trivedi, Malav S; Holger, Dana; Bui, Anh Tuyet; Craddock, Travis J A; Tartar, Jaime L

    2017-01-01

    Sleep is critical for repair as well as the rejuvenation processes in the body and many of these functions are regulated via underlying cellular metabolic homeostasis. Changes in sleep pattern are reported to alter such metabolic function resulting in altered disease susceptibility or behavior. Here, we measured the extent to which overnight total sleep deprivation (SD) in young adult humans can influence systemic (plasma-derived) redox-metabolism including the major antioxidant, glutathione as well as DNA methylation levels. Nineteen participants (n = 19, μ age = 21, SD = 3.09) underwent morning testing before and after overnight total SD. Biochemical measures before and after SD revealed that glutathione, ATP, cysteine, and homocysteine levels were significantly reduced following one night of sleep deprivation (all p's < 0.01). Parallel to the well-recognized fact that sleep deprivation (maintaining wakefulness) uses up metabolic reserves, we observed that morning cortisol levels were blunted after sleep deprivation. There were no significant correlations between self-reported or actigraphy-measured sleep and the biochemical measurements, strongly indicating that prior sleep behavior did not have any direct influence on the biochemical measures taken at baseline or after sleep deprivation. Results from the current investigation supports the previous literature implicating the induction of oxidative stress and ATP depletion with sleep deprivation. Furthermore, such altered antioxidant status can also induce downstream epigenetic changes. Although we did not measure the specific genes that were altered under the influence of such sleep deprivation, such epigenetic changes could potentially contribute towards disease predisposition.

  13. [Effects of sleep deprivation on the intelligence structure of school-age children in Changsha, China].

    PubMed

    Wang, Xiang-Yu; Wang, Xiang; Huang, Chao-Quan; Guo, Zi-Ying; Qian, Yan-Fei; Yang, Yan; Tan, Mo; Tan, Xin; Tu, Qiu-Yun; Wang, Lian

    2013-10-01

    To investigate the effects of sleep deprivation on intelligence development in primary school students. Between June 2009 and April 2010, 316 grade 5 students aged 10-11 years were selected from four primary schools in four administrative districts of Changsha, China by stratified random sampling. The intelligence characteristics of children with varying degrees of sleep deprivation were investigated using the Chinese Wechsler Intelligence Scale for Children. A total of 286 valid questionnaires were received, with a response rate of 90.5%. The survey was comprised of a sleep deprivation group (sleep time <8 hours per night; n=180) and a control group (sleep time ≥8 hours per night; n=106). The sleep deprivation group had significantly lower subtest scores, verbal intelligence quotient (IQ) (VIQ), performance IQ (PIQ) and full scale IQ (P<0.05) and significantly lower verbal comprehension factor score and memory/attention factor score compared with the control group (P<0.05). Compared with the control group, the moderate sleep deprivation subgroup had significantly decreased VIQ and full scale IQ as well as verbal comprehension factor score and memory/attention factor score (P<0.05), and the severe sleep deprivation subgroup showed decreases in all scores (P<0.05). The sleep deprivation group and moderate and severe sleep deprivation subgroups had significantly higher proportions of children with VIQ-PIQ imbalance than the control group. Sleep deprivation adversely affects intelligence development, especially VIQ, in primary school students, and the adverse effects of sleep deprivation are mainly seen in students with moderate and severe sleep deprivation.

  14. Sleep Deprivation Attack Detection in Wireless Sensor Network

    NASA Astrophysics Data System (ADS)

    Bhattasali, Tapalina; Chaki, Rituparna; Sanyal, Sugata

    2012-02-01

    Deployment of sensor network in hostile environment makes it mainly vulnerable to battery drainage attacks because it is impossible to recharge or replace the battery power of sensor nodes. Among different types of security threats, low power sensor nodes are immensely affected by the attacks which cause random drainage of the energy level of sensors, leading to death of the nodes. The most dangerous type of attack in this category is sleep deprivation, where target of the intruder is to maximize the power consumption of sensor nodes, so that their lifetime is minimized. Most of the existing works on sleep deprivation attack detection involve a lot of overhead, leading to poor throughput. The need of the day is to design a model for detecting intrusions accurately in an energy efficient manner. This paper proposes a hierarchical framework based on distributed collaborative mechanism for detecting sleep deprivation torture in wireless sensor network efficiently. Proposed model uses anomaly detection technique in two steps to reduce the probability of false intrusion.

  15. Psychological Effect of an Analogue Traumatic Event Reduced by Sleep Deprivation

    PubMed Central

    Porcheret, Kate; Holmes, Emily A.; Goodwin, Guy M.; Foster, Russell G.; Wulff, Katharina

    2015-01-01

    Study Objective: To examine the effect of sleep deprivation compared to sleep, immediately after experimental trauma stimuli on the development of intrusive memories to that trauma stimuli. Design: Participants were exposed to a film with traumatic content (trauma film). The immediate response to the trauma film was assessed, followed by either total sleep deprivation (sleep deprived group, N = 20) or sleep as usual (sleep group, N = 22). Twelve hours after the film viewing the initial psychological effect of the trauma film was measured and for the subsequent 6 days intrusive emotional memories related to the trauma film were recorded in daily life. Setting: Academic sleep laboratory and participants' home environment. Participants: Healthy paid volunteers. Measurements and results: On the first day after the trauma film, the psychological effect as assessed by the Impact of Event Scale – Revised was lower in the sleep deprived group compared to the sleep group. In addition, the sleep deprived group reported fewer intrusive emotional memories (mean 2.28, standard deviation [SD] 2.91) compared to the sleep group (mean 3.76, SD 3.35). Because habitual sleep/circadian patterns, psychological health, and immediate effect of the trauma film were similar at baseline for participants of both groups, the results cannot be accounted for by pre-existing inequalities between groups. Conclusions: Our findings suggest that sleep deprivation on one night, rather than sleeping, reduces emotional effect and intrusive memories following exposure to experimental trauma. Citation: Porcheret K, Holmes EA, Goodwin GM, Foster RG, Wulff K. Psychological effect of an analogue traumatic event reduced by sleep deprivation. SLEEP 2015;38(7):1017–1025. PMID:26118556

  16. The spectrum of the non-rapid eye movement sleep electroencephalogram following total sleep deprivation is trait-like.

    PubMed

    Tarokh, Leila; Rusterholz, Thomas; Achermann, Peter; Van Dongen, Hans P A

    2015-08-01

    The sleep electroencephalogram (EEG) spectrum is unique to an individual and stable across multiple baseline recordings. The aim of this study was to examine whether the sleep EEG spectrum exhibits the same stable characteristics after acute total sleep deprivation. Polysomnography (PSG) was recorded in 20 healthy adults across consecutive sleep periods. Three nights of baseline sleep [12 h time in bed (TIB)] following 12 h of wakefulness were interleaved with three nights of recovery sleep (12 h TIB) following 36 h of sustained wakefulness. Spectral analysis of the non-rapid eye movement (NREM) sleep EEG (C3LM derivation) was used to calculate power in 0.25 Hz frequency bins between 0.75 and 16.0 Hz. Intraclass correlation coefficients (ICCs) were calculated to assess stable individual differences for baseline and recovery night spectra separately and combined. ICCs were high across all frequencies for baseline and recovery and for baseline and recovery combined. These results show that the spectrum of the NREM sleep EEG is substantially different among individuals, highly stable within individuals and robust to an experimental challenge (i.e. sleep deprivation) known to have considerable impact on the NREM sleep EEG. These findings indicate that the NREM sleep EEG represents a trait.

  17. Sleep deprivation effects on object discrimination task in zebrafish (Danio rerio).

    PubMed

    Pinheiro-da-Silva, Jaquelinne; Silva, Priscila Fernandes; Nogueira, Marcelo Borges; Luchiari, Ana Carolina

    2017-03-01

    The zebrafish is an ideal vertebrate model for neurobehavioral studies with translational relevance to humans. Many aspects of sleep have been studied, but we still do not understand how and why sleep deprivation alters behavioral and physiological processes. A number of hypotheses suggest its role in memory consolidation. In this respect, the aim of this study was to analyze the effects of sleep deprivation on memory in zebrafish (Danio rerio), using an object discrimination paradigm. Four treatments were tested: control, partial sleep deprivation, total sleep deprivation by light pulses, and total sleep deprivation by extended light. The control group explored the new object more than the known object, indicating clear discrimination. The partially sleep-deprived group explored the new object more than the other object in the discrimination phase, suggesting a certain degree of discriminative performance. By contrast, both total sleep deprivation groups equally explored all objects, regardless of their novelty. It seems that only one night of sleep deprivation is enough to affect discriminative response in zebrafish, indicating its negative impact on cognitive processes. We suggest that this study could be a useful screening tool for cognitive dysfunction and a better understanding of the effect of sleep-wake cycles on cognition.

  18. The effects of sleep and sleep deprivation on task-switching performance.

    PubMed

    Couyoumdjian, Alessandro; Sdoia, Stefano; Tempesta, Daniela; Curcio, Giuseppe; Rastellini, Elisabetta; DE Gennaro, Luigi; Ferrara, Michele

    2010-03-01

    Neural systems of the prefrontal cortex (PFC) involved in executive functions are particularly vulnerable to sleep deprivation (SD). In this study, we investigated whether SD selectively affects specific components of the executive control processes involved in task-switching performance. Two different tasks are performed in rapid and random succession in this procedure, so that the to-be-executed task may change from one trial to the next (switch trial), or may be repeated (repetition trial). Task-switches are usually slower than task repetitions, giving way to the 'switch cost'. One hundred and eight university students were assigned randomly to the sleep (S) or the SD group. Each of them was tested on a task-switching paradigm before and after an experimental night (S or SD), and after one recovery night. SD impaired both task-switching accuracy and speed. A higher proportion of errors and increased switch costs after SD have been observed, compared to normal sleep. Control analyses on switch and repetition trials showed that the SD group was significantly worse only on the switch trials. The effects of SD are reverted by one night of recovery sleep. It is concluded that the ability to adjust behaviour rapidly and flexibly to changing environmental demands, which relies on the functional integrity of the PFC, is impacted negatively by sleep loss.

  19. Auditory and Visual Evoked Potentials as a Function of Sleep Deprivation and Irregular Sleep

    DTIC Science & Technology

    1989-08-15

    Broughton, 1968). If the cyclicity of REM sleep is a sleep -dependent phenomenon as purported by Moses et al. (1977), rather than the sleeping ...1977). The auditory evoked brain response during adult human sleep . Waking and Sleeping , 1, 189-194. Aserinsky, E., & Kleitman, N. (1953). Regularly...wave versus REM sleep . Psychophysiology, 5, 231. Globus, G.G., Drury, R. L., Phoebus, E.C., & Boyd, R. (1971). Ultradian rhythms in human performance

  20. Sleep deprivation does not affect seizure frequency during inpatient video-EEG monitoring.

    PubMed

    Malow, B A; Passaro, E; Milling, C; Minecan, D N; Levy, K

    2002-11-12

    To determine whether acute sleep deprivation facilitates seizures during inpatient monitoring in a controlled protocol. Eighty-four patients with medically refractory partial epilepsy undergoing inpatient monitoring were assigned in consecutive blocks to either sleep deprivation every other night or to normal sleep. In both groups, subjects were requested to stay awake during the day, from 6 AM to 10 PM. In the sleep deprivation group, patients also stayed awake between 10 PM and 6 AM every other night beginning with Day 2. Patients were removed from sleep deprivation if they had two or more secondarily generalized seizures within 24 hours. Patients were removed from the normal sleep group and were sleep deprived if they did not have a complex partial or secondarily generalized seizure by Day 6 of monitoring. In these patients removed from sleep deprivation or from normal sleep, data were analyzed up to and including the day of removal from the protocol. The sleep deprivation and normal sleep subjects did not differ in age, sex, seizure localization, or percent dosage reduction in antiepileptic drugs from baseline at days 1 to 3 of monitoring. Protocol duration was 6.5 +/- 2.4 days (mean +/- SD) for the sleep deprivation group and 5.8 +/- 2.0 days for the normal sleep group. Seizures per day for complex partial, secondarily generalized, and combined complex partial and secondarily generalized, calculated from admission until end of protocol, did not differ significantly between the two groups. Acute sleep deprivation did not affect seizure frequency during inpatient monitoring in our patients with intractable complex partial seizures with secondary generalization.

  1. Sleep Deprivation Increases Cerebral Serotonin 2A Receptor Binding in Humans

    PubMed Central

    Elmenhorst, David; Kroll, Tina; Matusch, Andreas; Bauer, Andreas

    2012-01-01

    Study Objectives: Serotonin and its cerebral receptors play an important role in sleep-wake regulation. The aim of the current study is to investigate the effect of 24-h total sleep deprivation on the apparent serotonin 2A receptor (5-HT2AR) binding capacity in the human brain to test the hypothesis that sleep deprivation induces global molecular alterations in the cortical serotonergic receptor system. Design: Volunteers were tested twice with the subtype-selective radiotracer [18F]altanserin and positron emission tomography (PET) for imaging of 5-HT2ARs at baseline and after 24 h of sleep deprivation. [18F]Altanserin binding potentials were analyzed in 13 neocortical regions of interest. The efficacy of sleep deprivation was assessed by questionnaires, waking electroencephalography, and cognitive performance measurements. Setting: Sleep laboratory and neuroimaging center. Patients or Participants: Eighteen healthy volunteers. Interventions: Sleep deprivation. Measurements and Results: A total of 24 hours of sleep deprivation led to a 9.6% increase of [18F]altanserin binding on neocortical 5-HT2A receptors. Significant region-specific increases were found in the medial inferior frontal gyrus, insula, and anterior cingulate, parietal, sensomotoric, and ventrolateral prefrontal cortices. Conclusions: This study demonstrates that a single night of total sleep deprivation causes significant increases of 5-HT2AR binding potentials in a variety of cortical regions although the increase declines as sleep deprivation continued. It provides in vivo evidence that total sleep deprivation induces adaptive processes in the serotonergic system of the human brain. Citation: Elmenhorst D; Kroll T; Matusch A; Bauer A. Sleep Deprivation Increases Cerebral Serotonin 2A Receptor Binding in Humans. SLEEP 2012;35(12):1615-1623. PMID:23204604

  2. Effects of paradoxical sleep deprivation on the performance of rats in a model of visual attention.

    PubMed

    Godoi, Francisco Rafael do Lago; Oliveira, Maria Gabriela Menezes; Tufik, Sergio

    2005-11-30

    In the present work we sought to evaluate the effects of paradoxical sleep deprivation (PSD) on the performance of rats in the five-choice serial reaction time task, a test designed to assess attentional function. Adult male Wistar rats were trained to detect a brief (1 s) light stimulus randomly presented in one of five locations in a box specially designed for the task. After achieving stable performance, the animals were submitted to 96 h of sleep deprivation by the platform technique, in which the rats are placed on top of small platforms in a tank filled with water. During sleep, particularly during the paradoxical stage, the loss of muscle tone make the animals fall into the water, thus awakening them and so depriving of sleep. Performance in the task was assessed daily during the 96 h deprivation period and also during seven recovery days afterwards. Paradoxical sleep deprivation reduced accuracy on the on the third (72 h) and fourth (96 h) days of sleep deprivation compared to home-cage controls, and this impairment reverted soon after the beginning of the recovery period. Sleep-deprived animals also showed an increase in omissions in the first day of PSD and a reduction on the number of trials started on the fourth day of sleep deprivation. No significant group differences were observed in premature and perseverative responses, correct response latency and reward latency. Our results thus indicate that paradoxical sleep deprivation impairs attentional function.

  3. Sleep deprivation induces excess diuresis and natriuresis in healthy children.

    PubMed

    Mahler, B; Kamperis, K; Schroeder, M; Frøkiær, J; Djurhuus, J C; Rittig, S

    2012-01-15

    Urine production is reduced at night, allowing undisturbed sleep. This study was undertaken to show the effect of sleep deprivation (SD) on urine production in healthy children. Special focus was on gender and children at an age where enuresis is still prominent. Twenty healthy children (10 girls) underwent two 24-h studies, randomly assigned to either sleep or SD on the first study night. Diet and fluid intake were standardized. Blood samples were drawn every 4 h during daytime and every 2 h at night. Urine was fractionally collected. Blood pressure and heart rate were noninvasively monitored. Blood was analyzed for plasma antidiuretic hormone (AVP), atrial natriuretic peptide (ANP), angiotensin II, aldosterone, and renin. Urine was analyzed for aquaporin-2 and PGE(2). Successful SD was achieved in all participants with a minimum of 4 h 50 min, and full-night SD was obtained in 50% of the participants. During SD, both boys and girls produced markedly larger amounts of urine than during normal sleep (477 ± 145 vs. 291 ± 86 ml, P < 0.01). SD increased urinary excretion of sodium (0.17 ± 0.05 vs. 0.10 ± 0.03 mmol·kg(-1)·h(-1)) whereas solute-free water reabsorption remained unchanged. SD induced a significant fall in nighttime plasma AVP (P < 0.01), renin (P < 0.05), angiotensin II (P < 0.001), and aldosterone (P < 0.05) whereas plasma ANP levels remained uninfluenced (P = 0.807). Nighttime blood pressure and heart rate were significantly higher during SD (mean arterial pressure: 78.5 ± 8.0 vs. 74.7 ± 8.7 mmHg, P < 0.001). SD leads to natriuresis and excess diuresis in healthy children. The underlying mechanism could be a reduced nighttime dip in blood pressure and a decrease in renin-angiotensin-aldosterone system levels during sleep deprivation.

  4. Effects of acute sleep deprivation on motor and reversal learning in mice.

    PubMed

    Varga, Andrew W; Kang, Mihwa; Ramesh, Priyanka V; Klann, Eric

    2014-10-01

    Sleep supports the formation of a variety of declarative and non-declarative memories, and sleep deprivation often impairs these types of memories. In human subjects, natural sleep either during a nap or overnight leads to long-lasting improvements in visuomotor and fine motor tasks, but rodent models recapitulating these findings have been scarce. Here we present evidence that 5h of acute sleep deprivation impairs mouse skilled reach learning compared to a matched period of ad libitum sleep. In sleeping mice, the duration of total sleep time during the 5h of sleep opportunity or during the first bout of sleep did not correlate with ultimate gain in motor performance. In addition, we observed that reversal learning during the skilled reaching task was also affected by sleep deprivation. Consistent with this observation, 5h of sleep deprivation also impaired reversal learning in the water-based Y-maze. In conclusion, acute sleep deprivation negatively impacts subsequent motor and reversal learning and memory.

  5. Effects of Acute Sleep Deprivation on Motor and Reversal Learning in Mice

    PubMed Central

    Varga, Andrew W.; Kang, Mihwa; Ramesh, Priyanka V.; Klann, Eric

    2014-01-01

    Sleep supports the formation of a variety of declarative and non-declarative memories, and sleep deprivation often impairs these types of memories. In human subjects, natural sleep either during a nap or overnight leads to long-lasting improvements in visuomotor and fine motor tasks, but rodent models recapitulating these findings have been scarce. Here we present evidence that 5 hours of acute sleep deprivation impairs mouse skilled reach learning compared to a matched period of ad libitum sleep. In sleeping mice, the duration of total sleep time during the 5 hours of sleep opportunity or during the first bout of sleep did not correlate with ultimate gain in motor performance. In addition, we observed that reversal learning during the skilled reaching task was also affected by sleep deprivation. Consistent with this observation, 5 hours of sleep deprivation also impaired reversal learning in the water-based Y-maze. In conclusion, acute sleep deprivation negatively impacts subsequent motor and reversal learning and memory. PMID:25046627

  6. Glucocorticoids Are Not Responsible for Paradoxical Sleep Deprivation-Induced Memory Impairments

    PubMed Central

    Tiba, Paula Ayako; de Menezes Oliveira, Maria Gabriela; Rossi, Vanessa Contatto; Tufik, Sergio; Suchecki, Deborah

    2008-01-01

    Study Objectives: To evaluate whether paradoxical sleep deprivation-induced memory impairments are due to release of glucocorticoids, by means of corticosterone inhibition with metyrapone. Design: The design was a 2 (Groups [control, paradoxical sleep-deprived]) × 2 (Treatments [vehicle, metyrapone]) study, performed in 2 experiments: Acute treatment (single injection given immediately after 96 hours of sleep deprivation) and chronic treatment (8 injections, twice per day, throughout the sleep-deprivation period). Animals were either paradoxical sleep-deprived or remained in their home cages for 96 hours before training in contextual fear conditioning and received intraperitoneal injections of a corticosterone synthesis inhibitor, metyrapone. Memory performance was tested 24 hours after training. Subjects: Three-month old Wistar male rats. Measurements: Freezing behavior was considered as the conditioning index, and adrenocorticotropic hormone and corticosterone plasma levels were determined from trunk blood of animals sacrificed in different time points. Animals were weighed before and after the paradoxical sleep-deprivation period. Results: Acute metyrapone treatment impaired memory in control animals and did not prevent paradoxical sleep deprivation-induced memory impairment. Likewise, in the chronic treatment, paradoxical sleep-deprived animals did not differ from control rats in their corticosterone or adrenocorticotropic hormone response to training, but still did not learn as well, and did not show any stress responses to the testing. Chronic metyrapone was, however, effective in preventing the weight loss typically observed in paradoxical sleep-deprived animals. Conclusions: Our results suggest that glucocorticoids do not mediate memory impairments but might be responsible for the weight loss induced by paradoxical sleep deprivation. Citation: Tiba PA; de Menezes Oliveira MG; Rossi VC; Tufik S; Suchecki D. Glucocorticoids are not responsible for

  7. Partial sleep deprivation and energy balance in adults: an emerging issue for consideration by dietetics practitioners.

    PubMed

    Shlisky, Julie D; Hartman, Terryl J; Kris-Etherton, Penny M; Rogers, Connie J; Sharkey, Neil A; Nickols-Richardson, Sharon M

    2012-11-01

    During the past 30 years, rates of partial sleep deprivation and obesity have increased in the United States. Evidence linking partial sleep deprivation, defined as sleeping <6 hours per night, to energy imbalance is relevant to weight gain prevention and weight loss promotion. With a majority of Americans overweight or obese, weight loss is a recommended strategy for reducing comorbid conditions. Our purpose was to review the literature regarding the role of partial sleep deprivation on energy balance and weight regulation. An inverse relationship between obesity and sleep duration has been demonstrated in cross-sectional and prospective studies. Several intervention studies have tested mechanisms by which partial sleep deprivation affects energy balance. Reduced sleep may disrupt appetitive hormone regulation, specifically increasing ghrelin and decreasing leptin and, thereby, influence energy intake. Increased wakefulness also may promote food intake episodes and energy imbalance. Energy expenditure may not be greatly affected by partial sleep deprivation, although additional and more accurate methods of measurements may be necessary to detect subtle changes in energy expenditure. Body weight loss achieved by reduced energy intake and/or increased energy expenditure combined with partial sleep deprivation may contribute to undesirable body composition change with proportionately more fat-free soft tissue mass lost compared with fat mass. Evaluating sleep patterns and recommending regular, sufficient sleep for individuals striving to manage weight may be prudent. Copyright © 2012 Academy of Nutrition and Dietetics. Published by Elsevier Inc. All rights reserved.

  8. Effect of 24 hours of sleep deprivation on auditory and linguistic perception: a comparison among young controls, sleep-deprived participants, dyslexic readers, and aging adults.

    PubMed

    Fostick, Leah; Babkoff, Harvey; Zukerman, Gil

    2014-06-01

    To test the effects of 24 hr of sleep deprivation on auditory and linguistic perception and to assess the magnitude of this effect by comparing such performance with that of aging adults on speech perception and with that of dyslexic readers on phonological awareness. Fifty-five sleep-deprived young adults were compared with 29 aging adults (older than 60 years) and with 18 young controls on auditory temporal order judgment (TOJ) and on speech perception tasks (Experiment 1). The sleep deprived were also compared with 51 dyslexic readers and with the young controls on TOJ and phonological awareness tasks (One-Minute Test for Pseudowords, Phoneme Deletion, Pig Latin, and Spoonerism; Experiment 2). Sleep deprivation resulted in longer TOJ thresholds, poorer speech perception, and poorer nonword reading compared with controls. The TOJ thresholds of the sleep deprived were comparable to those of the aging adults, but their pattern of speech performance differed. They also performed better on TOJ and phonological awareness than dyslexic readers. A variety of linguistic skills are affected by sleep deprivation. The comparison of sleep-deprived individuals with other groups with known difficulties in these linguistic skills might suggest that different groups exhibit common difficulties.

  9. Partial sleep deprivation by environmental noise increases food intake and body weight in obesity resistant rats

    PubMed Central

    Mavanji, Vijayakumar; Teske, Jennifer A.; Billington, Charles J.; Kotz, Catherine M.

    2012-01-01

    Objective Sleep-restriction in humans increases risk for obesity, but previous rodent studies show weight loss following sleep deprivation, possibly due to stressful-methods used to prevent sleep. Obesity-resistant (OR) rats exhibit consolidated-sleep and resistance to weight-gain. We hypothesized that sleep disruption by a less-stressful method would increase body weight, and examined effect of partial sleep deprivation (PSD) on body weight in OR and Sprague-Dawley (SD) rats. Design and Methods OR and SD rats (n=12/group) were implanted with transmitters to record sleep/wake. After baseline recording, six SD and six OR rats underwent 8 h PSD during light-phase for 9 d. Sleep was reduced using recordings of random noise. Sleep/wake states were scored as wakefulness (W), slow-wave-sleep (SWS) and rapid-eye-movement-sleep (REMS). Total number of transitions between stages, SWS-delta-power, food intake and body weight were documented. Results Exposure to noise decreased SWS and REMS time, while increasing W time. Sleep-deprivation increased number of transitions between stages and SWS-delta-power. Further, PSD during the rest phase increased recovery-sleep during active phase. The PSD SD and OR rats had greater food intake and body weight compared to controls Conclusions PSD by less-stressful means increases body weight in rats. Also, PSD during rest phase increases active period sleep. PMID:23666828

  10. Sleep deprivation influences some but not all processes of supervisory attention

    NASA Technical Reports Server (NTRS)

    Jennings, J. R.; Monk, T. H.; van der Molen, M. W.

    2003-01-01

    Does one night of sleep deprivation alter processes of supervisory attention in general or only a specific subset of such processes? Twenty college-aged volunteers, half female, performed a choice reaction time task. A cue indicated that compatible (e.g., right button, right-pointing arrow) or incompatible (e.g., left button, right-pointing arrow) responses were to be given to a stimulus that followed 50 or 500 ms later. The paradigm assessed response inhibition, task-shifting skill, and task strategy-processes inherent in supervisory attention. Performance, along with heart rate, was assessed for 12 hr following normal sleep or a night of complete sleep deprivation. Sleep deprivation altered neither preparation for task shifting nor response inhibition. The ability to use preparatory bias to speed performance did decrease with sleep deprivation. Sleep deprivation appears to selectively affect this supervisory attention process, which is perceived as an active effort to cope with a challenging task.

  11. Sleep deprivation influences some but not all processes of supervisory attention

    NASA Technical Reports Server (NTRS)

    Jennings, J. R.; Monk, T. H.; van der Molen, M. W.

    2003-01-01

    Does one night of sleep deprivation alter processes of supervisory attention in general or only a specific subset of such processes? Twenty college-aged volunteers, half female, performed a choice reaction time task. A cue indicated that compatible (e.g., right button, right-pointing arrow) or incompatible (e.g., left button, right-pointing arrow) responses were to be given to a stimulus that followed 50 or 500 ms later. The paradigm assessed response inhibition, task-shifting skill, and task strategy-processes inherent in supervisory attention. Performance, along with heart rate, was assessed for 12 hr following normal sleep or a night of complete sleep deprivation. Sleep deprivation altered neither preparation for task shifting nor response inhibition. The ability to use preparatory bias to speed performance did decrease with sleep deprivation. Sleep deprivation appears to selectively affect this supervisory attention process, which is perceived as an active effort to cope with a challenging task.

  12. The effect of 60-h sleep deprivation on cardiovascular regulation and body temperature.

    PubMed

    Vaara, Jani; Kyröläinen, Heikki; Koivu, Mikko; Tulppo, Mikko; Finni, Taija

    2009-02-01

    This study examined cardiovascular regulation and body temperature (BT) during 60 h of sleep deprivation in 20 young healthy cadets. Heart rate variability was measured during an active orthostatic test (AOT). Measurements were performed each day in the morning and evening after 2, 14, 26, 38, 50 and 60 h of sleep deprivation. In AOT, in the sitting and standing positions, heart rate decreased (P < 0.001), while high frequency and low frequency power increased (P < 0.05-0.001) during sleep deprivation. Body temperature also decreased (P < 0.001), but no changes were detected in blood pressure. In conclusion, the accumulation of 60 h of sleep loss resulted in increased vagal outflow, as evidenced by decreased heart rate. In addition, BT decreased during sleep deprivation. Thus, sleep deprivation causes alterations in autonomic regulation of the heart, and in thermoregulation.

  13. Identification of genes associated with resilience/vulnerability to sleep deprivation and starvation in Drosophila.

    PubMed

    Thimgan, Matthew S; Seugnet, Laurent; Turk, John; Shaw, Paul J

    2015-05-01

    Flies mutant for the canonical clock protein cycle (cyc(01)) exhibit a sleep rebound that is ∼10 times larger than wild-type flies and die after only 10 h of sleep deprivation. Surprisingly, when starved, cyc(01) mutants can remain awake for 28 h without demonstrating negative outcomes. Thus, we hypothesized that identifying transcripts that are differentially regulated between waking induced by sleep deprivation and waking induced by starvation would identify genes that underlie the deleterious effects of sleep deprivation and/or protect flies from the negative consequences of waking. We used partial complementary DNA microarrays to identify transcripts that are differentially expressed between cyc(01) mutants that had been sleep deprived or starved for 7 h. We then used genetics to determine whether disrupting genes involved in lipid metabolism would exhibit alterations in their response to sleep deprivation. Laboratory. Drosophila melanogaster. Sleep deprivation and starvation. We identified 84 genes with transcript levels that were differentially modulated by 7 h of sleep deprivation and starvation in cyc(01) mutants and were confirmed in independent samples using quantitative polymerase chain reaction. Several of these genes were predicted to be lipid metabolism genes, including bubblegum, cueball, and CG4500, which based on our data we have renamed heimdall (hll). Using lipidomics we confirmed that knockdown of hll using RNA interference significantly decreased lipid stores. Importantly, genetically modifying bubblegum, cueball, or hll resulted in sleep rebound alterations following sleep deprivation compared to genetic background controls. We have identified a set of genes that may confer resilience/vulnerability to sleep deprivation and demonstrate that genes involved in lipid metabolism modulate sleep homeostasis. © 2015 Associated Professional Sleep Societies, LLC.

  14. Total sleep deprivation decreases immobility in the forced-swim test.

    PubMed

    Lopez-Rodriguez, Faustino; Kim, Joseph; Poland, Russell E

    2004-06-01

    Sleep deprivation can exert antidepressant effects in humans in less than 24 h, making it the fastest acting antidepressant treatment. However, it is rarely used clinically because the effect disappears once the subject goes back to sleep. An understanding of the neurobiological mechanisms underlying the antidepressant effect of sleep deprivation should help to develop new rapidly acting antidepressant strategies. In the present report, an animal model of depression (the forced-swim test) was used to determine whether the effects of total sleep deprivation parallel those obtained with antidepressant drugs. Using the disk-over-water method, rats deprived of sleep for 24 h exhibited increased swimming behavior when compared to cage control rats, mimicking the effects of serotonergic antidepressants. After 48 h, sleep-deprived rats exhibited increased swimming when compared to both cage control and stimulus control rats, demonstrating that the effect is due to sleep deprivation per se, and not to extraneous factors inherent in the sleep deprivation protocol (such as stress and movement). We believe that this paradigm can be used to study the neurobiological mechanisms of rapid antidepressant effects induced by sleep deprivation.

  15. Sleep deprivation reduces perceived emotional intelligence and constructive thinking skills.

    PubMed

    Killgore, William D S; Kahn-Greene, Ellen T; Lipizzi, Erica L; Newman, Rachel A; Kamimori, Gary H; Balkin, Thomas J

    2008-07-01

    Insufficient sleep can adversely affect a variety of cognitive abilities, ranging from simple alertness to higher-order executive functions. Although the effects of sleep loss on mood and cognition are well documented, there have been no controlled studies examining its effects on perceived emotional intelligence (EQ) and constructive thinking, abilities that require the integration of affect and cognition and are central to adaptive functioning. Twenty-six healthy volunteers completed the Bar-On Emotional Quotient Inventory (EQi) and the Constructive Thinking Inventory (CTI) at rested baseline and again after 55.5 and 58 h of continuous wakefulness, respectively. Relative to baseline, sleep deprivation was associated with lower scores on Total EQ (decreased global emotional intelligence), Intrapersonal functioning (reduced self-regard, assertiveness, sense of independence, and self-actualization), Interpersonal functioning (reduced empathy toward others and quality of interpersonal relationships), Stress Management skills (reduced impulse control and difficulty with delay of gratification), and Behavioral Coping (reduced positive thinking and action orientation). Esoteric Thinking (greater reliance on formal superstitions and magical thinking processes) was increased. These findings are consistent with the neurobehavioral model suggesting that sleep loss produces temporary changes in cerebral metabolism, cognition, emotion, and behavior consistent with mild prefrontal lobe dysfunction.

  16. The cumulative cost of additional wakefulness: dose-response effects on neurobehavioral functions and sleep physiology from chronic sleep restriction and total sleep deprivation

    NASA Technical Reports Server (NTRS)

    Van Dongen, Hans P A.; Maislin, Greg; Mullington, Janet M.; Dinges, David F.

    2003-01-01

    OBJECTIVES: To inform the debate over whether human sleep can be chronically reduced without consequences, we conducted a dose-response chronic sleep restriction experiment in which waking neurobehavioral and sleep physiological functions were monitored and compared to those for total sleep deprivation. DESIGN: The chronic sleep restriction experiment involved randomization to one of three sleep doses (4 h, 6 h, or 8 h time in bed per night), which were maintained for 14 consecutive days. The total sleep deprivation experiment involved 3 nights without sleep (0 h time in bed). Each study also involved 3 baseline (pre-deprivation) days and 3 recovery days. SETTING: Both experiments were conducted under standardized laboratory conditions with continuous behavioral, physiological and medical monitoring. PARTICIPANTS: A total of n = 48 healthy adults (ages 21-38) participated in the experiments. INTERVENTIONS: Noctumal sleep periods were restricted to 8 h, 6 h or 4 h per day for 14 days, or to 0 h for 3 days. All other sleep was prohibited. RESULTS: Chronic restriction of sleep periods to 4 h or 6 h per night over 14 consecutive days resulted in significant cumulative, dose-dependent deficits in cognitive performance on all tasks. Subjective sleepiness ratings showed an acute response to sleep restriction but only small further increases on subsequent days, and did not significantly differentiate the 6 h and 4 h conditions. Polysomnographic variables and delta power in the non-REM sleep EEG-a putative marker of sleep homeostasis--displayed an acute response to sleep restriction with negligible further changes across the 14 restricted nights. Comparison of chronic sleep restriction to total sleep deprivation showed that the latter resulted in disproportionately large waking neurobehavioral and sleep delta power responses relative to how much sleep was lost. A statistical model revealed that, regardless of the mode of sleep deprivation, lapses in behavioral alertness

  17. The cumulative cost of additional wakefulness: dose-response effects on neurobehavioral functions and sleep physiology from chronic sleep restriction and total sleep deprivation

    NASA Technical Reports Server (NTRS)

    Van Dongen, Hans P A.; Maislin, Greg; Mullington, Janet M.; Dinges, David F.

    2003-01-01

    OBJECTIVES: To inform the debate over whether human sleep can be chronically reduced without consequences, we conducted a dose-response chronic sleep restriction experiment in which waking neurobehavioral and sleep physiological functions were monitored and compared to those for total sleep deprivation. DESIGN: The chronic sleep restriction experiment involved randomization to one of three sleep doses (4 h, 6 h, or 8 h time in bed per night), which were maintained for 14 consecutive days. The total sleep deprivation experiment involved 3 nights without sleep (0 h time in bed). Each study also involved 3 baseline (pre-deprivation) days and 3 recovery days. SETTING: Both experiments were conducted under standardized laboratory conditions with continuous behavioral, physiological and medical monitoring. PARTICIPANTS: A total of n = 48 healthy adults (ages 21-38) participated in the experiments. INTERVENTIONS: Noctumal sleep periods were restricted to 8 h, 6 h or 4 h per day for 14 days, or to 0 h for 3 days. All other sleep was prohibited. RESULTS: Chronic restriction of sleep periods to 4 h or 6 h per night over 14 consecutive days resulted in significant cumulative, dose-dependent deficits in cognitive performance on all tasks. Subjective sleepiness ratings showed an acute response to sleep restriction but only small further increases on subsequent days, and did not significantly differentiate the 6 h and 4 h conditions. Polysomnographic variables and delta power in the non-REM sleep EEG-a putative marker of sleep homeostasis--displayed an acute response to sleep restriction with negligible further changes across the 14 restricted nights. Comparison of chronic sleep restriction to total sleep deprivation showed that the latter resulted in disproportionately large waking neurobehavioral and sleep delta power responses relative to how much sleep was lost. A statistical model revealed that, regardless of the mode of sleep deprivation, lapses in behavioral alertness

  18. Effects of sleep deprivation on serum cortisol level and mental health in servicemen.

    PubMed

    Song, Hong-Tao; Sun, Xin-Yang; Yang, Ting-Shu; Zhang, Li-Yi; Yang, Jia-Lin; Bai, Jing

    2015-06-01

    This study aimed to investigate the effects of sleep deprivation on serum cortisol level and mental health and explore the correlations between them in servicemen. A total of 149 out of the 207 Chinese servicemen were randomly selected to go through 24hour sleep deprivation, leaving the rest (58) as the control group, before and after which their blood samples were drawn for cortisol measurement. Following the procedure, all the participants were administered the Military Personnel Mental Disorder Prediction Scale, taking the military norm as baseline. The results revealed that the post-deprivation serum cortisol level was positively correlated with the factor score of mania in the sleep deprivation group (rSp=0.415, p<0.001). Sleep deprivation could significantly increase serum cortisol level and may affect mental health in servicemen. The increase of serum cortisol level is significantly related to mania disorder during sleep deprivation. Copyright © 2015 Elsevier B.V. All rights reserved.

  19. Global Prevalence of Sleep Deprivation in Students and Heavy Media Use

    ERIC Educational Resources Information Center

    Zhang, Meilan; Tillman, Daniel A.; An, Song A.

    2017-01-01

    The latest two international educational assessments found global prevalence of sleep deprivation in students, consistent with what has been reported in sleep research. However, despite the fundamental role of adequate sleep in cognitive and social functioning, this important issue has been largely overlooked by educational researchers. Drawing…

  20. Global Prevalence of Sleep Deprivation in Students and Heavy Media Use

    ERIC Educational Resources Information Center

    Zhang, Meilan; Tillman, Daniel A.; An, Song A.

    2017-01-01

    The latest two international educational assessments found global prevalence of sleep deprivation in students, consistent with what has been reported in sleep research. However, despite the fundamental role of adequate sleep in cognitive and social functioning, this important issue has been largely overlooked by educational researchers. Drawing…

  1. Effects of selective REM sleep deprivation on prefrontal gamma activity and executive functions.

    PubMed

    Corsi-Cabrera, M; Rosales-Lagarde, A; del Río-Portilla, Y; Sifuentes-Ortega, R; Alcántara-Quintero, B

    2015-05-01

    Given that the dorsolateral prefrontal cortex is involved in executive functions and is deactivated and decoupled from posterior associative regions during REM sleep, that Gamma temporal coupling involved in information processing is enhanced during REM sleep, and that adult humans spend about 90 min of every 24h in REM sleep, it might be expected that REM sleep deprivation would modify Gamma temporal coupling and have a deteriorating effect on executive functions. We analyzed EEG Gamma activity and temporal coupling during implementation of a rule-guided task before and after REM sleep deprivation and its effect on verbal fluency, flexible thinking and selective attention. After two nights in the laboratory for adaptation, on the third night subjects (n=18) were randomly assigned to either selective REM sleep deprivation effectuated by awakening them at each REM sleep onset or, the same number of NREM sleep awakenings as a control for unspecific effects of sleep interruptions. Implementation of abstract rules to guide behavior required greater activation and synchronization of Gamma activity in the frontopolar regions after REM sleep reduction from 20.6% at baseline to just 3.93% of total sleep time. However, contrary to our hypothesis, both groups showed an overall improvement in executive task performance and no effect on their capacity to sustain selective attention. These results suggest that after one night of selective REM sleep deprivation executive functions can be compensated by increasing frontal activation and they still require the participation of supervisory control by frontopolar regions.

  2. Changes in attention to an emotional task after sleep deprivation: neurophysiological and behavioral findings.

    PubMed

    Alfarra, Ramey; Fins, Ana I; Chayo, Isaac; Tartar, Jaime L

    2015-01-01

    While sleep loss is shown to have widespread effects on cognitive processes, little is known about the impact of sleep loss on emotion processes. In order to expand on previous behavioral and physiological findings on how sleep loss influences emotion processing, we administered positive, negative, and neutral affective visual stimuli to individuals after one night of sleep deprivation while simultaneously acquiring EEG event related potential (ERP) data and recording affective behavioral responses. We compared these responses to a baseline testing session. We specifically looked at the late positive potential (LPP) component of the visual ERP as an established sensitive measure of attention to emotionally-charged visual stimuli. Our results show that after sleep deprivation, the LPP no longer discriminates between emotional and non-emotional pictures; after sleep deprivation the LPP amplitude was of similar amplitude for neutral, positive, and negative pictures. This effect was driven by an increase in the LPP to neutral pictures. Our behavioral measures show that, relative to baseline testing, emotional pictures are rated as less emotional following sleep deprivation with a concomitant reduction in emotional picture-induced anxiety. We did not observe any change in cortisol concentrations after sleep deprivation before or after emotional picture exposure, suggesting that the observed changes in emotion processing are independent of potential stress effects of sleep deprivation. Combined, our findings suggest that sleep loss interferes with proper allocation of attention resources during an emotional task.

  3. Mood, alertness, and performance in response to sleep deprivation and recovery sleep in experienced shiftworkers versus non-shiftworkers.

    PubMed

    Wehrens, Sophie M T; Hampton, Shelagh M; Kerkhofs, Myriam; Skene, Debra J

    2012-06-01

    Previous studies have shown increased sleepiness and mood changes in shiftworkers, which may be due to sleep deprivation or circadian disruption. Few studies, however, have compared responses of experienced shiftworkers and non-shiftworkers to sleep deprivation in an identical laboratory setting. The aim of this laboratory study, therefore, was to compare long-term shiftworkers and non-shiftworkers and to investigate the effects of one night of total sleep deprivation (30.5 h of continuous wakefulness) and recovery sleep on psychomotor vigilance, self-rated alertness, and mood. Eleven experienced male shiftworkers (shiftwork ≥5 yrs) were matched with 14 non-shiftworkers for age (mean ± SD: 35.7 ± 7.2 and 32.5 ± 6.2 yrs, respectively) and body mass index (BMI) (28.7 ± 3.8 and 26.6 ± 3.4 kg/m(2), respectively). After keeping a 7-d self-selected sleep/wake cycle (7.5/8 h nocturnal sleep), both groups entered a laboratory session consisting of a night of adaptation sleep and a baseline sleep (each 7.5/8 h), a sleep deprivation night, and recovery sleep (4-h nap plus 7.5/8 h nighttime sleep). Subjective alertness and mood were assessed with the Karolinska Sleepiness Scale (KSS) and 9-digit rating scales, and vigilance was measured by the visual psychomotor vigilance test (PVT). A mixed-model regression analysis was carried out on data collected every hour during the sleep deprivation night and on all days (except for the adaptation day), at .25, 4.25, 5.25, 11.5, 12.5, and 13.5 h after habitual wake-up time. Despite similar circadian phase (melatonin onset), demographics, food intake, body posture, and environmental light, shiftworkers felt significantly more alert, more cheerful, more elated, and calmer than non-shiftworkers throughout the laboratory study. In addition, shiftworkers showed a faster median reaction time (RT) compared to non-shiftworkers, although four other PVT parameters did not differ between the groups. As expected, both groups showed a

  4. The effects of biperiden on nap sleep after sleep deprivation in depressed patients.

    PubMed

    Dressing, H; Riemann, D; Gann, H; Berger, M

    1992-08-01

    Sixteen patients with a major depressive disorder were allowed to take a nap at 5 A.M. after a period of total sleep deprivation. The patients were randomly assigned to biperiden or placebo treatment prior to the nap to test the hypothesis that anticholinergic medication is capable of preventing a nap-related worsening of mood. Total sleep deprivation positively influenced mood for the whole group. Contrary to expectations, the rate of nap-related relapses of mood did not differ between placebo- and biperiden-treated individuals, and biperiden did not significantly suppress rapid eye movement (REM) sleep. There was only a tendency for lower REM time after administration of biperiden compared to placebo. This unexpected result may be due to a high cholinergic tone in the patient group investigated and a high REM propensity in the early morning hours. Studies with more selective M1/M2 receptor antagonists are necessary to clarify whether nap-related changes of mood can be prevented by anticholinergic blockade.

  5. The Effect of Total Sleep Deprivation and Recovery Sleep on Cognitive on Performance and Brain Function

    DTIC Science & Technology

    2005-08-01

    Performance on other Cognitive Tasks. Sleep 2005 28(Suppl 1):A353. 7. Chen, T, Salamat, JS, Yanagi, MA, Stiller, CS, Drummond, SPA. Actigraphy Measures vs...suggest that these variations within a normal range of sleep , as measured with actigraphy , were not extreme enough to influence cognitive performance...appear to alter normal sleep architecture during recovery sleep . Here, we compared sleep parameters on baseline and for two consecutive nights of

  6. Too tired to inspire or be inspired: Sleep deprivation and charismatic leadership.

    PubMed

    Barnes, Christopher M; Guarana, Cristiano L; Nauman, Shazia; Kong, Dejun Tony

    2016-08-01

    We draw from theory on sleep and affect regulation to extend the emotional labor model of leadership. We examine both leader and follower sleep as important antecedents of attributions of charismatic leadership. In Study 1, we manipulate the sleep of leaders, and find that leader emotional labor in the form of deep acting (but not surface acting or authentically experienced positive affect) mediates the harmful effect of leader sleep deprivation on follower ratings of charismatic leadership. In Study 2, we manipulate the sleep of followers, and find that follower experienced positive affect mediates the harmful effect of follower sleep deprivation on follower ratings of charismatic leadership of the leader. Thus, both leader and follower sleep deprivation harm attributions of charismatic leadership, with the regulation and experience of affect as causal mechanisms. (PsycINFO Database Record

  7. Sleep Terrors (Night Terrors)

    MedlinePlus

    ... factors can contribute to sleep terrors, such as: Sleep deprivation and extreme tiredness Stress Fever (in children) Sleeping in unfamiliar surroundings Lights or noise An overfull bladder Sleep terrors sometimes are associated with underlying conditions that ...

  8. Intensive sleep deprivation and cognitive behavioral therapy for pharmacotherapy refractory insomnia in a hospitalized patient.

    PubMed

    Breitstein, Joshua; Penix, Brandon; Roth, Bernard J; Baxter, Tristin; Mysliwiec, Vincent

    2014-06-15

    The case of a 59-year-old woman psychiatrically hospitalized with comorbid insomnia, suicidal ideation, and generalized anxiety disorder is presented. Pharmacologic therapies were unsuccessful for treating insomnia prior to and during hospitalization. Intensive sleep deprivation was initiated for 40 consecutive hours followed by a recovery sleep period of 8 hours. Traditional components of cognitive behavioral therapy for insomnia (CBTi), sleep restriction, and stimulus control therapies, were initiated on the ward. After two consecutive nights with improved sleep, anxiety, and absence of suicidal ideation, the patient was discharged. She was followed in the sleep clinic for two months engaging in CBTi. Treatment resulted in substantial improvement in her insomnia, daytime sleepiness, and anxiety about sleep. Sleep deprivation regimens followed by a restricted sleep recovery period have shown antidepressant effects in depressed patients. Similar treatment protocols have not been investigated in patients with pharmacotherapy refractory insomnia and generalized anxiety disorder.

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

    PubMed

    Beaumont, Maurice; Batéjat, Denise; Coste, Olivier; Doireau, Philippe; Chauffard, Françoise; Enslen, Marc; Lagarde, Didier; Pierard, Christophe

    2005-01-01

    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.

  10. Effects of biperiden on sleep at baseline and after 72 h of REM sleep deprivation in the cat.

    PubMed

    Salin-Pascual, R J; Jimenez-Anguiano, A; Granados-Fuentes, D; Drucker-Colin, R

    1992-01-01

    We examined the effects of the muscarinic M1 antagonist biperiden in cats. In the first experiment a dose-response analysis was performed with intraventricular injection (IV ventricle) of biperiden. In the second experiment after REM sleep deprivation cats were injected with either biperiden (0.1 mg/kg) or saline. Biperiden produced a reduction in REM sleep percentage and an increase in REM sleep latency with these high doses. The 0.1 mg/kg biperiden dose, which did not suppress REM sleep at baseline, did reduce the REM sleep rebound. The present study suggests a modulatory role of biperiden on REM sleep regulatory processes. The fact that an effect of biperiden is noted only at the high doses suggests that at these doses the drug is influencing non-M1 receptors. Changes in the sensitivity of these receptors as a result of REM sleep deprivation might explain why a dose of biperiden will reduce REM sleep rebound, while being ineffective in suppressing REM sleep at baseline.

  11. Human Hippocampal Structure: A Novel Biomarker Predicting Mnemonic Vulnerability to, and Recovery from, Sleep Deprivation

    PubMed Central

    Goldstein-Piekarski, Andrea N.; Greer, Stephanie M.; Stark, Shauna; Stark, Craig E.

    2016-01-01

    Sleep deprivation impairs the formation of new memories. However, marked interindividual variability exists in the degree to which sleep loss compromises learning, the mechanistic reasons for which are unclear. Furthermore, which physiological sleep processes restore learning ability following sleep deprivation are similarly unknown. Here, we demonstrate that the structural morphology of human hippocampal subfields represents one factor determining vulnerability (and conversely, resilience) to the impact of sleep deprivation on memory formation. Moreover, this same measure of brain morphology was further associated with the quality of nonrapid eye movement slow wave oscillations during recovery sleep, and by way of such activity, determined the success of memory restoration. Such findings provide a novel human biomarker of cognitive susceptibility to, and recovery from, sleep deprivation. Moreover, this metric may be of special predictive utility for professions in which memory function is paramount yet insufficient sleep is pervasive (e.g., aviation, military, and medicine). SIGNIFICANCE STATEMENT Sleep deprivation does not impact all people equally. Some individuals show cognitive resilience to the effects of sleep loss, whereas others express striking vulnerability, the reasons for which remain largely unknown. Here, we demonstrate that structural features of the human brain, specifically those within the hippocampus, accurately predict which individuals are susceptible (or conversely, resilient) to memory impairments caused by sleep deprivation. Moreover, this same structural feature determines the success of memory restoration following subsequent recovery sleep. Therefore, structural properties of the human brain represent a novel biomarker predicting individual vulnerability to (and recovery from) the effects of sleep loss, one with occupational relevance in professions where insufficient sleep is pervasive yet memory function is paramount. PMID:26911684

  12. A time for learning and a time for sleep: the effect of sleep deprivation on contextual fear conditioning at different times of the day.

    PubMed

    Hagewoud, Roelina; Whitcomb, Shamiso N; Heeringa, Amarins N; Havekes, Robbert; Koolhaas, Jaap M; Meerlo, Peter

    2010-10-01

    Sleep deprivation negatively affects memory consolidation, especially in the case of hippocampus-dependent memories. Studies in rodents have shown that 5 hours of sleep deprivation immediately following footshock exposure selectively impairs the formation of a contextual fear memory. In these studies, both acquisition and subsequent sleep deprivation were performed in the animals' main resting phase. However, in everyday life, subjects most often learn during their active phase. Here we examined the effects of sleep deprivation on memory consolidation for contextual fear in rats when the task was performed at different times of the day, particularly, at the beginning of the resting phase or right before the onset of the active phase. Results show that sleep deprivation immediately following training affects consolidation of contextual fear, independent of time of training. However, in the resting phase memory consolidation was impaired by 6 hours of posttraining sleep deprivation, whereas, in the active phase, the impairment was only seen after 12 hours of sleep deprivation. Since rats sleep at least twice as much during the resting phase compared with the active phase, these data suggest that the effect of sleep deprivation depends on the amount of sleep that was lost. Also, control experiments show that effects of sleep deprivation were not related to the amount of stimulation the animals received and were therefore not likely an indirect effect of the sleep-deprivation method. These results support the notion that sleep immediately following acquisition, independent of time of day, promotes memory consolidation and that sleep deprivation may disrupt this process depending on the amount of sleep that is lost.

  13. Sleep deprivation affects inflammatory marker expression in adipose tissue

    PubMed Central

    2010-01-01

    Sleep deprivation has been shown to increase inflammatory markers in rat sera and peripheral blood mononuclear cells. Inflammation is a condition associated with pathologies such as obesity, cancer, and cardiovascular diseases. We investigated changes in the pro and anti-inflammatory cytokines and adipokines in different depots of white adipose tissue in rats. We also assessed lipid profiles and serum levels of corticosterone, leptin, and adiponectin after 96 hours of sleep deprivation. Methods The study consisted of two groups: a control (C) group and a paradoxical sleep deprivation by 96 h (PSD) group. Ten rats were randomly assigned to either the control group (C) or the PSD. Mesenteric (MEAT) and retroperitoneal (RPAT) adipose tissue, liver and serum were collected following completion of the PSD protocol. Levels of interleukin (IL)-6, interleukin (IL)-10 and tumour necrosis factor (TNF)-α were analysed in MEAT and RPAT, and leptin, adiponectin, glucose, corticosterone and lipid profile levels were analysed in serum. Results IL-6 levels were elevated in RPAT but remained unchanged in MEAT after PSD. IL-10 protein concentration was not altered in either depot, and TNF-α levels decreased in MEAT. Glucose, triglycerides (TG), VLDL and leptin decreased in serum after 96 hours of PSD; adiponectin was not altered and corticosterone was increased. Conclusion PSD decreased fat mass and may modulate the cytokine content in different depots of adipose tissue. The inflammatory response was diminished in both depots of adipose tissue, with increased IL-6 levels in RPAT and decreased TNF-α protein concentrations in MEAT and increased levels of corticosterone in serum. PMID:21034496

  14. Creatine supplementation, sleep deprivation, cortisol, melatonin and behavior.

    PubMed

    McMorris, T; Harris, R C; Howard, A N; Langridge, G; Hall, B; Corbett, J; Dicks, M; Hodgson, C

    2007-01-30

    The effect of creatine supplementation and sleep deprivation, with intermittent moderate-intensity exercise, on cognitive and psychomotor performance, mood state, effort and salivary concentrations of cortisol and melatonin were examined. Subjects were divided into a creatine supplementation group and a placebo group. They took 5 g of creatine monohydrate or a placebo, dependent on their group, four times a day for 7 days immediately prior to the experiment. They undertook tests examining central executive functioning, short-term memory, choice reaction time, balance, mood state and effort at baseline and following 18-, 24- and 36-h sleep deprivation, with moderate intermittent exercise. Saliva samples were taken prior to each set of tests. A group x time analysis of covariance, with baseline performance the covariate, showed that the creatine group performed significantly (p < 0.05) better than the placebo group on the central executive task but only at 36 h. The creatine group demonstrated a significant (p < 0.01) linear improvement in performance of the central executive task throughout the experiment, while the placebo group showed no significant effects. There were no significant differences between the groups for any of the other variables. A significant (p < 0.001) main effect of time was found for the balance test with a linear improvement being registered. Cortisol concentrations on Day 1 were significantly (p < 0.01) higher than on Day 2. Mood significantly (p < 0.001) deteriorated up to 24 h with no change from 24 to 36 h. Effort at baseline was significantly (p < 0.01) lower than in the other conditions. It was concluded that, during sleep deprivation with moderate-intensity exercise, creatine supplementation only affects performance of complex central executive tasks.

  15. Electrophysiological correlates of cognition improve with nap during sleep deprivation.

    PubMed

    Panjwani, Usha; Ray, Koushik; Chatterjee, Abhirup; Bhaumik, Sangeet; Kumar, Sanjeev

    2010-02-01

    The efficacy of a 30-min nap as a countermeasure in the reduction of cognitive decline following 24 h of sleep deprivation (SD) on subjective sleepiness scales, event-related potential (ERP) P300, and contingent negative variation (CNV) was evaluated. The experiment was performed in three sessions on different days between 7 and 8 a.m. on nine normal, healthy males, of age 25-30 years: Session 1. Baseline recordings; Session 2, after one night's total sleep deprivation, and; Session 3, after 1 week of Session 1, following one night's sleep deprivation along with a 30-min nap opportunity between 1.00 and 3.00 a.m. Subjective sleepiness scores increased after SD as compared to baseline, but reduced significantly after nap (P < 0.05). There was an increase in P3 peak latency of ERP following SD (16%, P < 0.01), which was reduced with nap (10.7%, P < 0.05).There was an increase in CNV M1 peak latency after SD (18%) which decreased with the use of nap (12.5%) (P < 0.01). The CNV reaction time increased following SD (39.3%) and decreased with the use of nap (24%) (P < 0.01). No significant effects on ERP N1, P1, N2 latencies, P2 and P3 amplitudes and CNV N1, P3, M2 peak latencies and M1, and M2 amplitudes were observed. It was concluded that a 30-min nap, between 1.00 and 3.00 a.m. during night SD, reduces the cognitive decline following 24 h of SD in terms of its electro-physiological correlates. The study is of applied value in optimization of cognitive performance in professions demanding night work schedules.

  16. [Effect of paradoxical sleep deprivation on elaboration and differentiation of alimentary conditioned reflexes].

    PubMed

    Koridze, M G; Nemsadze, N D

    1980-01-01

    Paradoxical sleep deprivation of cats by means of awakening them without any significant emotional stress does not affect the acquisition of sound discrimination. Paradoxical sleep deprivation by Jouvet's method producing emotional stress impairs the acquisition of sound discrimination. However, it fails to affect the reproduction of preliminary elaborated sound discrimination.

  17. An Overview of Sleep Deprivation and The Ameliorative Effects of Modafinil

    DTIC Science & Technology

    2002-11-01

    H., and Jouvet, M., Successful treatment of idiopathic hypersomnia and narcolepsy with modafinil. Progress in Neuro-Psychopharmacology and Biological...Laffont, F., Cathala, H.P., and Kohler, F. Effect of modafinil on narcolepsy and idiopathic hypersomnia . in the 5th European Congress of Sleep Research...amphetamine and modafinil on the sleep/wake cycle during experimental hypersomnia induced by sleep deprivation in the cat. Journal of Sleep Research, 2000. 9

  18. Does experimental paradoxical sleep deprivation (EPSD) is an appropriate model for evaluation of cardiovascular complications of obstructive sleep apnea?

    PubMed

    Joukar, Siyavash; Ghorbani-Shahrbabaki, Soodabe

    2016-05-01

    Some of the previous studies have used animal model of paradoxical sleep deprivation for investigation of sleep loss complications. The present study is designed to examine the effectiveness and reliability of this model for investigation and assessment of some cardiovascular complications of obstructive sleep apnea syndrome. The Wistar rat groups were divided into the control group, the Test48 and Test72 groups, who experienced paradoxical sleep deprivation for 48 and 72 h, and the Sham48 and Sham72 groups, who were exposed to environmental conditions same to test groups but without sleep deprivation, respectively. At the end of the experiment, blood pressure and heart rate variability were assessed. The results showed that 72 h rapid eye movements sleep deprivation significantly increased the systolic blood pressure compared to the control (p < 0.01), Sham48 and Test48 groups (p < 0.05). The comparison of the heart rate and heart rate variability parameters such as time domain indices (RR interval, SDNN, RMSSD, SD1, SD2, and SD1/SD2) as well as frequency-domain variables (total power, LF and HF power, and LF/HF) had no significant difference among animal groups. These findings suggest that rat paradoxical sleep deprivation may be a suitable model for induction and investigation of hemodynamic alterations which occurs in obstructive sleep apnea syndrome; however, it cannot be an alternative model to induce heart rate variability alterations similar to those reported in patient with obstructive sleep apnea.

  19. Ovarian hormones promote recovery from sleep deprivation by increasing sleep intensity in middle-aged ovariectomized rats.

    PubMed

    Deurveilher, Samuel; Seary, M Elizabeth; Semba, Kazue

    2013-04-01

    Sleep disturbances are commonly associated with menopause. Hormone replacement therapy is often used to treat various menopausal symptoms, but its efficacy for improving sleep is a matter of debate. We addressed this question by using a rodent model of ovarian hormone loss and replacement in midlife. Middle-aged female rats were ovariectomized and implanted with capsules containing estradiol with or without progesterone, or oil. After two weeks, sleep/wake states were recorded polygraphically during a 24-h baseline period, followed by 6h of sleep deprivation in the second half of the light phase, and a 24-h recovery period. During the baseline dark phase, hormone treatments increased wakefulness, and decreased non-rapid eye movement sleep (NREMS) by shortening NREMS episodes; however, NREMS EEG delta power or energy (cumulative power) was unaffected by combined hormones. Following sleep deprivation, all the groups showed NREMS and rapid eye movement sleep (REMS) rebounds, with similar relative increases from respective baseline levels. The increases in NREMS EEG delta power/energy during recovery were enhanced by combined hormones. These results from middle-aged ovariectomized rats indicate that replacement with estrogen with or without progesterone reduces baseline NREMS without affecting sleep intensity, particularly during the dark (active) phase, whereas following sleep deprivation the same hormone treatments do not affect the ability to increase NREMS or REMS, but treatment with both hormones, in particular, enhances the intensity of recovery sleep. These results support the usefulness of ovariectomized middle-aged rats as a model system to study the biological effects of hormone replacement on sleep regulation. Copyright © 2013 Elsevier Inc. All rights reserved.

  20. The effect of one night's sleep deprivation on adolescent neurobehavioral performance.

    PubMed

    Louca, Mia; Short, Michelle A

    2014-11-01

    To investigate the effects of one night's sleep deprivation on neurobehavioral functioning in adolescents. Participants completed a neurobehavioral test battery measuring sustained attention, reaction speed, cognitive processing speed, sleepiness, and fatigue every 2 h during wakefulness. Baseline performance (defined as those test bouts between 09:00 and 19:00 on days 2 and 3, following two 10-h sleep opportunities) were compared to performance at the same clock time the day following total sleep deprivation. The sleep laboratory at the Centre for Sleep Research. Twelve healthy adolescents (6 male), aged 14-18 years (mean = 16.17, standard deviation = 0.83). Sustained attention, reaction speed, cognitive processing speed, and subjective sleepiness were all significantly worse following one night without sleep than following 10-h sleep opportunities (all main effects of day, P < 0.05). Sleep deprivation led to increased variability on objective performance measures. There were between-subjects differences in response to sleep loss that were task-specific, suggesting that adolescents may not only vary in terms of the degree to which they are affected by sleep loss but also the domains in which they are affected. These findings suggest that one night of total sleep deprivation has significant deleterious effects upon neurobehavioral performance and subjective sleepiness. These factors impair daytime functioning in adolescents, leaving them at greater risk of poor academic and social functioning and accidents and injuries.

  1. Sleep deprivation impairs recall of social transmission of food preference in rats

    PubMed Central

    Wooden, Jessica I; Pido, Jennifer; Mathews, Hunter; Kieltyka, Ryan; Montemayor, Bertha A; Ward, Christopher P

    2014-01-01

    Evidence indicates that sleep plays an important role in learning and memory, and disruption of sleep especially seems to interfere with hippocampal memory processes. Social transmission of food preference (STFP), a natural test of paired associative learning, has been shown to be dependent on the hippocampus. While social transmission of food preference is not a novel task, it has not been used to examine the role of sleep in memory consolidation. Male Sprague-Dawley rats were randomly divided into three groups: cage control; sleep-deprived; and device control. Demonstrator rats were given powdered food mixed with a target spice. Test rats then interacted with demonstrator rats before being given a two choice test of powered food with the target spice or a novel spice. Sleep-deprived rats were then placed in an automated device that prevented sleep for 24 hours. After sleep deprivation, animals were given a preference test again to determine memory for the target spice at both 24 hours and 72 hours. Polysomnography was used to validate the method of sleep deprivation. During immediate preference testing, rats demonstrated a clear preference for the food containing the target spice. Rats that experienced 24 hours of sleep deprivation following the initial testing indicated a significant reduction in the recall of the target spice at 24 and 72 hours. The cage control and device animals maintained their preference for food containing the target spice. Therefore, the loss of sleep interfered with memory consolidation for food preference learned via social transmission. PMID:25395874

  2. Sleep deprivation impairs recall of social transmission of food preference in rats.

    PubMed

    Wooden, Jessica I; Pido, Jennifer; Mathews, Hunter; Kieltyka, Ryan; Montemayor, Bertha A; Ward, Christopher P

    2014-01-01

    Evidence indicates that sleep plays an important role in learning and memory, and disruption of sleep especially seems to interfere with hippocampal memory processes. Social transmission of food preference (STFP), a natural test of paired associative learning, has been shown to be dependent on the hippocampus. While social transmission of food preference is not a novel task, it has not been used to examine the role of sleep in memory consolidation. Male Sprague-Dawley rats were randomly divided into three groups: cage control; sleep-deprived; and device control. Demonstrator rats were given powdered food mixed with a target spice. Test rats then interacted with demonstrator rats before being given a two choice test of powered food with the target spice or a novel spice. Sleep-deprived rats were then placed in an automated device that prevented sleep for 24 hours. After sleep deprivation, animals were given a preference test again to determine memory for the target spice at both 24 hours and 72 hours. Polysomnography was used to validate the method of sleep deprivation. During immediate preference testing, rats demonstrated a clear preference for the food containing the target spice. Rats that experienced 24 hours of sleep deprivation following the initial testing indicated a significant reduction in the recall of the target spice at 24 and 72 hours. The cage control and device animals maintained their preference for food containing the target spice. Therefore, the loss of sleep interfered with memory consolidation for food preference learned via social transmission.

  3. A unified mathematical model to quantify performance impairment for both chronic sleep restriction and total sleep deprivation.

    PubMed

    Rajdev, Pooja; Thorsley, David; Rajaraman, Srinivasan; Rupp, Tracy L; Wesensten, Nancy J; Balkin, Thomas J; Reifman, Jaques

    2013-08-21

    Performance prediction models based on the classical two-process model of sleep regulation are reasonably effective at predicting alertness and neurocognitive performance during total sleep deprivation (TSD). However, during sleep restriction (partial sleep loss) performance predictions based on such models have been found to be less accurate. Because most modern operational environments are predominantly characterized by chronic sleep restriction (CSR) rather than by episodic TSD, the practical utility of this class of models has been limited. To better quantify performance during both CSR and TSD, we developed a unified mathematical model that incorporates extant sleep debt as a function of a known sleep/wake history, with recent history exerting greater influence. This incorporation of sleep/wake history into the classical two-process model captures an individual's capacity to recover during sleep as a function of sleep debt and naturally bridges the continuum from CSR to TSD by reducing to the classical two-process model in the case of TSD. We validated the proposed unified model using psychomotor vigilance task data from three prior studies involving TSD, CSR, and sleep extension. We compared and contrasted the fits, within-study predictions, and across-study predictions from the unified model against predictions generated by two previously published models, and found that the unified model more accurately represented multiple experimental studies and consistently predicted sleep restriction scenarios better than the existing models. In addition, we found that the model parameters obtained by fitting TSD data could be used to predict performance in other sleep restriction scenarios for the same study populations, and vice versa. Furthermore, this model better accounted for the relatively slow recovery process that is known to characterize CSR, as well as the enhanced performance that has been shown to result from sleep banking. Published by Elsevier Ltd.

  4. Are adolescents chronically sleep-deprived? An investigation of sleep habits of adolescents in the Southwest of Germany.

    PubMed

    Loessl, B; Valerius, G; Kopasz, M; Hornyak, M; Riemann, D; Voderholzer, U

    2008-09-01

    Adolescent sleep receives increasing attention. Several studies have shown that adolescents generally do not sleep enough. This survey assessed adolescents' sleep patterns, and results were compared with sleep logs. A total of 818 students aged 12-18 attending three different school types were asked to complete a questionnaire, adapted from the 'School Sleep Habits Survey', and filled in a sleep protocol over 2 weeks. Information on sleep patterns and demographic data were obtained additionally. A total of 601 students completed the questionnaire (i.e. 73.5% return rate), 55.1% female and 44.9% male. Average sleep duration during the week amounted to 8.04+/-0.89 h and 9.51+/-1.65 h on weekends. Sleep duration times on school days decreased from an average 8.64+/-0.83 h for the age category 12-13 years to 7.83+/-0.72 h for students above 16 years. 91.6% of all students slept less than 9.2 h per night during the week. Data from the 153 returned sleep logs showed even lower sleep times (7.75+/-0.82 h for school nights). The main hypothesis that students sleep on average considerably less than the recommended 9 h during weekdays was confirmed. Bedtimes changed throughout the week with the latest on Friday and Saturday nights and the least sleep around midweek. There were no significant group differences regarding school type and environment (rural vs. urban). Interestingly, the majority reported only little daytime sleepiness and no impaired performance. Results regarding the consequences of chronic sleep deprivation in the literature are inconclusive. The impact on physiological parameters, especially metabolic functions, requires further investigations.

  5. Effect of 72 h of Sleep Deprivation on the Iowa Gambling Task

    PubMed Central

    LIU, Lei; ZHOU, Renlai

    2016-01-01

    Introduction Sleep deprivation has detrimental effects on cognitive processes, including decision making. The present study investigated how 72 h of sleep deprivation influenced individual neural performance in the Iowa gambling task using event-related potential technology. Methods Eleven healthy male adults who participated in our study were randomized to be either in group with 72 h of social isolation condition or 72 h of sleep deprivation condition. Results Results showed that, in the feedback stage, the N250–400 amplitude was smaller in post-test than in pre-test for the sleep deprivation condition, especially in the frontal cortex. No significant difference between the pre-test and post-test condition was found in the social isolation condition. Conclusion These results suggested that 72 h of sleep deprivation affected an individual’s response to feedback stimuli, causing the individual to evaluate the stimuli slowly. PMID:28360813

  6. The tired hippocampus: the molecular impact of sleep deprivation on hippocampal function.

    PubMed

    Havekes, Robbert; Abel, Ted

    2017-02-27

    Memory consolidation, the process by which information is stored following training, consists of synaptic consolidation and systems consolidation. It is widely acknowledged that sleep deprivation has a profound effect on synaptic consolidation, particularly for memories that require the hippocampus. It is unclear, however, which of the many molecular changes associated with sleep deprivation directly contribute to memory deficits. In this review, we highlight recent studies showing that sleep deprivation impairs hippocampal cAMP and mTOR signaling, and ultimately causes spine loss in CA1 neurons in a cofilin-dependent fashion. Reversing these molecular alterations made memory consolidation resistant to the negative impact of sleep deprivation. Together, these studies have started to identify the molecular underpinnings by which sleep deprivation impairs synaptic consolidation.

  7. Genomic analysis of sleep deprivation reveals translational regulation in the hippocampus

    PubMed Central

    Vecsey, Christopher G.; Peixoto, Lucia; Choi, Jennifer H. K.; Wimmer, Mathieu; Jaganath, Devan; Hernandez, Pepe J.; Blackwell, Jennifer; Meda, Karuna; Park, Alan J.; Hannenhalli, Sridhar

    2012-01-01

    Sleep deprivation is a common problem of considerable health and economic impact in today's society. Sleep loss is associated with deleterious effects on cognitive functions such as memory and has a high comorbidity with many neurodegenerative and neuropsychiatric disorders. Therefore, it is crucial to understand the molecular basis of the effect of sleep deprivation in the brain. In this study, we combined genome-wide and traditional molecular biological approaches to determine the cellular and molecular impacts of sleep deprivation in the mouse hippocampus, a brain area crucial for many forms of memory. Microarray analysis examining the effects of 5 h of sleep deprivation on gene expression in the mouse hippocampus found 533 genes with altered expression. Bioinformatic analysis revealed that a prominent effect of sleep deprivation was to downregulate translation, potentially mediated through components of the insulin signaling pathway such as the mammalian target of rapamycin (mTOR), a key regulator of protein synthesis. Consistent with this analysis, sleep deprivation reduced levels of total and phosphorylated mTOR, and levels returned to baseline after 2.5 h of recovery sleep. Our findings represent the first genome-wide analysis of the effects of sleep deprivation on the mouse hippocampus, and they suggest that the detrimental effects of sleep deprivation may be mediated by reductions in protein synthesis via downregulation of mTOR. Because protein synthesis and mTOR activation are required for long-term memory formation, our study improves our understanding of the molecular mechanisms underlying the memory impairments induced by sleep deprivation. PMID:22930738

  8. The Effect of Acute Sleep Deprivation on Visual Evoked Potentials in Professional Drivers

    PubMed Central

    Jackson, Melinda L.; Croft, Rodney J.; Owens, Katherine; Pierce, Robert J.; Kennedy, Gerard A.; Crewther, David; Howard, Mark E.

    2008-01-01

    Study Objectives: Previous studies have demonstrated that as little as 18 hours of sleep deprivation can cause deleterious effects on performance. It has also been suggested that sleep deprivation can cause a “tunnel-vision” effect, in which attention is restricted to the center of the visual field. The current study aimed to replicate these behavioral effects and to examine the electrophysiological underpinnings of these changes. Design: Repeated-measures experimental study. Setting: University laboratory. Patients or Participants: Nineteen professional drivers (1 woman; mean age = 45.3 ± 9.1 years). Interventions: Two experimental sessions were performed; one following 27 hours of sleep deprivation and the other following a normal night of sleep, with control for circadian effects. Measurements & Results: A tunnel-vision task (central versus peripheral visual discrimination) and a standard checkerboard-viewing task were performed while 32-channel EEG was recorded. For the tunnel-vision task, sleep deprivation resulted in an overall slowing of reaction times and increased errors of omission for both peripheral and foveal stimuli (P < 0.05). These changes were related to reduced P300 amplitude (indexing cognitive processing) but not measures of early visual processing. No evidence was found for an interaction effect between sleep deprivation and visual-field position, either in terms of behavior or electrophysiological responses. Slower processing of the sustained parvocellular visual pathway was demonstrated. Conclusions: These findings suggest that performance deficits on visual tasks during sleep deprivation are due to higher cognitive processes rather than early visual processing. Sleep deprivation may differentially impair processing of more-detailed visual information. Features of the study design (eg, visual angle, duration of sleep deprivation) may influence whether peripheral visual-field neglect occurs. Citation: Jackson ML; Croft RJ; Owens K; Pierce

  9. Sleep deprivation impairs memory by attenuating mTORC1-dependent protein synthesis†

    PubMed Central

    Tudor, Jennifer C.; Davis, Emily J.; Peixoto, Lucia; Wimmer, Mathieu E.; van Tilborg, Erik; Park, Alan J.; Poplawski, Shane G.; Chung, Caroline W.; Havekes, Robbert; Huang, Jiayan; Gatti, Evelina; Pierre, Philippe; Abel, Ted

    2016-01-01

    Sleep deprivation is a public health epidemic that causes wide-ranging deleterious consequences, including impaired memory and cognition. Protein synthesis in hippocampal neurons promotes memory and cognition. The kinase complex mammalian target of rapamycin complex 1 (mTORC1) stimulates protein synthesis by phosphorylating and inhibiting the eukaryotic translation initiation factor 4E binding protein 2 (4EBP2). We investigated the involvement of the mTORC1-4EBP2 axis in the molecular mechanisms mediating the cognitive deficits caused by sleep deprivation in mice. Using an in vivo protein translation assay, we found that loss of sleep impaired protein synthesis in the hippocampus. Five hours of sleep loss attenuated both mTORC1-mediated phosphorylation of 4EBP2 and the interaction between eukaryotic initiation factor 4E (eIF4E) and eukaryotic initiation factor 4G (eIF4G) in the hippocampi of sleep-deprived mice. Increasing the abundance of 4EBP2 in hippocampal excitatory neurons prior to sleep deprivation increased the abundance of phosphorylated 4EBP2, restored the amount of eIF4E-eIF4G interaction and hippocampal protein synthesis to that seen in mice that were not sleep-deprived, and prevented the hippocampus-dependent memory deficits associated with sleep loss. These findings collectively demonstrate that 4EBP2-regulated protein synthesis is a critical mediator of the memory deficits caused by sleep deprivation. PMID:27117251

  10. Effect of rapid eye movement sleep deprivation on rat brain monoamine oxidases.

    PubMed

    Thakkar, M; Mallick, B N

    1993-08-01

    Monoamine oxidase, monoamine oxidase-A, and monoamine oxidase-B activities were compared in free moving, rapid eye movement sleep-deprived, recovered, and control rat brains. The activities were estimated in the whole brain, cerebrum, cerebellum, whole brainstem, medulla, pons, and midbrain. The flowerpot method was used for continuing deprivation for one, two, or four days. Monoamine oxidase activity decreased significantly in the cerebrum and the cerebellum of the sleep-deprived rats, whereas monoamine oxidase-A and monoamine oxidase-B were differentially affected. Medullary MAO-A was the first to be affected, showing an increase after just one day of rapid eye movement sleep deprivation, while longer deprivation decreased its activity. The activity of monoamine oxidase-B was not significantly affected in any brain areas of the deprived rats until after two days of rapid eye movement sleep deprivation. All the altered enzyme activities returned to control levels after recovery. Control experiments suggest that the decrease was primarily caused by the rapid eye movement sleep deprivation and was not due to nonspecific effects. These findings are consistent with past studies and may help to explain earlier observations. The results support the involvement of aminergic mechanisms in rapid eye movement sleep. The plausible reasons for the changes in the activities of monoamine oxidases, after rapid eye movement sleep deprivation, are discussed.

  11. The impact of sleep deprivation on visual perspective taking.

    PubMed

    Deliens, Gaétane; Bukowski, Henryk; Slama, Hichem; Surtees, Andrew; Cleeremans, Axel; Samson, Dana; Peigneux, Philippe

    2017-10-11

    Total sleep deprivation (TSD) is known to alter cognitive processes. Surprisingly little attention has been paid to its impact on social cognition. Here, we investigated whether TSD alters levels-1 and -2 visual perspective-taking abilities, i.e. the capacity to infer (a) what can be seen and (b) how it is seen from another person's visual perspective, respectively. Participants completed levels-1 and -2 visual perspective-taking tasks after a night of sleep and after a night of TSD. In these tasks, participants had to take their own (self trials) or someone else's (other trials) visual perspective in trials where both perspectives were either the same (consistent trials) or different (inconsistent trials). An instruction preceding each trial indicated the perspective to take (i.e. the relevant perspective). Results show that TSD globally deteriorates social performance. In the level-1 task, TSD affects the selection of relevant over irrelevant perspectives. In the level-2 task, the effect of TSD cannot be unequivocally explained. This implies that visual perspective taking should be viewed as partially state-dependent, rather than a wholly static trait-like characteristic. © 2017 European Sleep Research Society.

  12. Effects of chronic sleep deprivation on glucose homeostasis in rats.

    PubMed

    Xu, Xiaowen; Wang, Liang; Zhang, Yan; Su, Tianjiao; Chen, Liying; Zhang, Yan; Ma, Weifeng; Xie, Yuanyuan; Wang, Tiantian; Yang, Fan; He, Li; Wang, Wenjiao; Fu, Xuemei; Hao, Hongxia; Ma, Yuanzheng

    2016-01-01

    Epidemiological studies have shown that chronic sleep disturbances resulted in metabolic disorders. The purpose of this study was to assess the relationship between chronic sleep deprivation (CSD) and the glucose homeostasis in rats. Twenty-four rats were randomly divided into CSD group and control (CON) group. The CSD rats were intervened by a modified multiple platform method (MMPM) to establish an animal model of chronic sleep disturbances. After 3-month intervention, all rats were subjected to an intraperitoneal glucose tolerance test (IPGTT) and an insulin tolerance test (ITT), and the body weight, aspartate aminotransferase (AST), alanine aminotransferase (ALT), creatinine, lipid profile group, and homeostasis model assessment-IR (HOMA-IR) were measured. Both the CSD and CON groups had an attenuation of weight gain after 3-month intervention. The plasma glucose level of CSD group was higher than that of the CON group during the IPGTT (P < 0.01). The CSD rats showed a marked increase in HOMA-IR and ITT compared with the CON group (P < 0.01). There were no significant differences of AST, ALT, creatinine, and most lipid parameters between the CSD and CON groups (P > 0.05). The CSD has a marked effect on glucose homeostasis, comprising glucose intolerance and insulin resistance.

  13. Sleep deprivation selectively disrupts top-down adaptation to cognitive conflict in the Stroop test.

    PubMed

    Gevers, Wim; Deliens, Gaetane; Hoffmann, Sophie; Notebaert, Wim; Peigneux, Philippe

    2015-12-01

    Sleep deprivation is known to exert detrimental effects on various cognitive domains, including attention, vigilance and working memory. Seemingly at odds with these findings, prior studies repeatedly failed to evidence an impact of prior sleep deprivation on cognitive interference in the Stroop test, a hallmark paradigm in the study of cognitive control abilities. The present study investigated further the effect of sleep deprivation on cognitive control using an adapted version of the Stroop test that allows to segregate top-down (attentional reconfiguration on incongruent items) and bottom-up (facilitated processing after repetitions in responses and/or features of stimuli) components of performance. Participants underwent a regular night of sleep or a night of total sleep deprivation before cognitive testing. Results disclosed that sleep deprivation selectively impairs top-down adaptation mechanisms: cognitive control no longer increased upon detection of response conflict at the preceding trial. In parallel, bottom-up abilities were found unaffected by sleep deprivation: beneficial effects of stimulus and response repetitions persisted. Changes in vigilance states due to sleep deprivation selectively impact on cognitive control in the Stroop test by affecting top-down, but not bottom-up, mechanisms that guide adaptive behaviours.

  14. Feedback Blunting: Total Sleep Deprivation Impairs Decision Making that Requires Updating Based on Feedback

    PubMed Central

    Whitney, Paul; Hinson, John M.; Jackson, Melinda L.; Van Dongen, Hans P.A.

    2015-01-01

    Study Objectives: To better understand the sometimes catastrophic effects of sleep loss on naturalistic decision making, we investigated effects of sleep deprivation on decision making in a reversal learning paradigm requiring acquisition and updating of information based on outcome feedback. Design: Subjects were randomized to a sleep deprivation or control condition, with performance testing at baseline, after 2 nights of total sleep deprivation (or rested control), and following 2 nights of recovery sleep. Subjects performed a decision task involving initial learning of go and no go response sets followed by unannounced reversal of contingencies, requiring use of outcome feedback for decisions. A working memory scanning task and psychomotor vigilance test were also administered. Setting: Six consecutive days and nights in a controlled laboratory environment with continuous behavioral monitoring. Subjects: Twenty-six subjects (22–40 y of age; 10 women). Interventions: Thirteen subjects were randomized to a 62-h total sleep deprivation condition; the others were controls. Results: Unlike controls, sleep deprived subjects had difficulty with initial learning of go and no go stimuli sets and had profound impairment adapting to reversal. Skin conductance responses to outcome feedback were diminished, indicating blunted affective reactions to feedback accompanying sleep deprivation. Working memory scanning performance was not significantly affected by sleep deprivation. And although sleep deprived subjects showed expected attentional lapses, these could not account for impairments in reversal learning decision making. Conclusions: Sleep deprivation is particularly problematic for decision making involving uncertainty and unexpected change. Blunted reactions to feedback while sleep deprived underlie failures to adapt to uncertainty and changing contingencies. Thus, an error may register, but with diminished effect because of reduced affective valence of the feedback

  15. The behavioral and health consequences of sleep deprivation among U.S. high school students: relative deprivation matters.

    PubMed

    Meldrum, Ryan Charles; Restivo, Emily

    2014-06-01

    To evaluate whether the strength of the association between sleep deprivation and negative behavioral and health outcomes varies according to the relative amount of sleep deprivation experienced by adolescents. 2011 Youth Risk Behavior Survey data of high school students (N=15,364) were analyzed. Associations were examined on weighted data using logistic regression. Twelve outcomes were examined, ranging from weapon carrying to obesity. The primary independent variable was a self-reported measure of average number of hours slept on school nights. Participants who reported deprivations in sleep were at an increased risk of a number of negative outcomes. However, this varied considerably across different degrees of sleep deprivation. For each of the outcomes considered, those who slept less than 5h were more likely to report negative outcomes (adjusted odds ratios ranging from 1.38 to 2.72; p<.05 across all models) relative to sleeping 8 or more hours. However, less extreme forms of sleep deprivation were, in many instances, unrelated to the outcomes considered. Among U.S. high school students, deficits in sleep are significantly and substantively associated with a variety of negative outcomes, and this association is particularly pronounced for students achieving fewer than 5h of sleep at night. Copyright © 2014 Elsevier Inc. All rights reserved.

  16. Cold hands, warm feet: sleep deprivation disrupts thermoregulation and its association with vigilance.

    PubMed

    Romeijn, Nico; Verweij, Ilse M; Koeleman, Anne; Mooij, Anne; Steimke, Rosa; Virkkala, Jussi; van der Werf, Ysbrand; Van Someren, Eus J W

    2012-12-01

    Vigilance is affected by induced and spontaneous skin temperature fluctuations. Whereas sleep deprivation strongly affects vigilance, no previous study examined in detail its effect on human skin temperature fluctuations and their association with vigilance. In a repeated-measures constant routine design, skin temperatures were assessed continuously from 14 locations while performance was assessed using a reaction time task, including eyes-open video monitoring, performed five times a day for 2 days, after a normal sleep or sleep deprivation night. Participants were seated in a dimly lit, temperature-controlled laboratory. Eight healthy young adults (five males, age 22.0 ± 1.8 yr (mean ± standard deviation)). One night of sleep deprivation. Mixed-effect regression models were used to evaluate the effect of sleep deprivation on skin temperature gradients of the upper (ear-mastoid), middle (hand-arm), and lower (foot-leg) body, and on the association between fluctuations in performance and in temperature gradients. Sleep deprivation induced a marked dissociation of thermoregulatory skin temperature gradients, indicative of attenuated heat loss from the hands co-occurring with enhanced heat loss from the feet. Sleep deprivation moreover attenuated the association between fluctuations in performance and temperature gradients; the association was best preserved for the upper body gradient. Sleep deprivation disrupts coordination of fluctuations in thermoregulatory skin temperature gradients. The dissociation of middle and lower body temperature gradients may therefore be evaluated as a marker for sleep debt, and the upper body gradient as a possible aid in vigilance assessment when sleep debt is unknown. Importantly, our findings suggest that sleep deprivation affects the coordination between skin blood flow fluctuations and the baroreceptor-mediated cardiovascular regulation that prevents venous pooling of blood in the lower limbs when there is the orthostatic

  17. The impact of sleep deprivation in military surgical teams: a systematic review.

    PubMed

    Parker, Rachael Sv; Parker, P

    2017-06-01

    Fatigue in military operations leads to safety and operational problems due to a decrease in alertness and performance. The primary method of counteracting the effects of sleep deprivation is to increase nightly sleep time, which in operational situations is not always feasible. History has taught us that surgeons and surgical teams are finite resources that cannot operate on patients indefinitely. A systematic review was conducted using the search terms 'sleep' and 'deprivation' examining the impact of sleep deprivation on cognitive performance in military surgical teams. Studies examining outcomes on intensive care patients and subjects with comorbidities were not addressed in this review. Sleep deprivation in any 'out-of-hours' surgery has a significant impact on overall morbidity and mortality. Sleep deprivation in surgeons and surgical trainees negatively impacts cognitive performance and puts their own and patients' health at risk. All published research lacks consensus when defining 'sleep deprivation' and 'rested' states. It is recognised that it would be unethical to conduct a well-designed randomised controlled trial, to determine the effects of fatigue on performance in surgery; however, there is a paucity between surrogate markers and applying simulated results to actual clinical performance. This requires further research. Recommended methods of combating fatigue include: prophylactically 'sleep-banking' prior to known periods of sleep deprivation, napping, use of stimulant or alerting substances such as modafinil, coordinated work schedules to reduce circadian desynchronisation and regular breaks with enforced rest periods. A forward surgical team will become combat-ineffective after 48 hours of continuous operations. This systematic review recommends implementing on-call periods of no more than 12 hours in duration, with adequate rest periods every 24 hours. Drug therapies and sleep banking may, in the short term, prevent negative effects of

  18. Sleep Deprivation affects Extinction but Not Acquisition Memory in Honeybees

    ERIC Educational Resources Information Center

    Hussaini, Syed Abid; Bogusch, Lisa; Landgraf, Tim; Menzel, Randolf

    2009-01-01

    Sleep-like behavior has been studied in honeybees before, but the relationship between sleep and memory formation has not been explored. Here we describe a new approach to address the question if sleep in bees, like in other animals, improves memory consolidation. Restrained bees were observed by a web camera, and their antennal activities were…

  19. Sleep Deprivation affects Extinction but Not Acquisition Memory in Honeybees

    ERIC Educational Resources Information Center

    Hussaini, Syed Abid; Bogusch, Lisa; Landgraf, Tim; Menzel, Randolf

    2009-01-01

    Sleep-like behavior has been studied in honeybees before, but the relationship between sleep and memory formation has not been explored. Here we describe a new approach to address the question if sleep in bees, like in other animals, improves memory consolidation. Restrained bees were observed by a web camera, and their antennal activities were…

  20. [The effects of overnight sleep deprivation on cardiovascular autonomic modulation].

    PubMed

    Zhong, Xu; Xiao, Yi; Huang, Rong; Huang, Xi-zhen

    2005-08-01

    This study aimed to delineate cardiovascular autonomic modulation associated with overnight total sleep deprivation (TSD) in humans. Cardiovascular autonomic modulation during overnight total sleep deprivation was assessed in 18 normal male subjects [age: (26.2 +/- 4.2) years, BMI (23.9 +/- 1.7) kg/m(2)]. ECG and continuous blood pressure from radial artery tonometry were obtained in seated position before TSD (baseline) and after overnight TSD. Spectral analysis of heart rate variability (HRV) and BP variability (BPV) were computed for cardiac parasympathetic modulation (high frequency power, HF); sympathetic modulation (low frequency power, LF), sympatho-vagal balance (LF/HF power of R-R variability, LF/HF) and BPV sympathetic modulation (low frequency power, BPV LF) in normalized (N) units [(total power of the components)/(total power-very low frequency power) x 100]. No significant changes were found in BP and heart rate. HRV LF was increased significantly from baseline (59.4 +/- 15.7)% to overnight SD (67.0 +/- 13.9)%. HRV LF/HF was increased significantly from baseline (2.7 +/- 1.7) to overnight SD (3.8 +/- 2.3), HRV HFN was decreased from baseline (29.0 +/- 11.6)% to overnight SD (22.8 +/- 10.4)%, BPV LF was significantly increased from baseline (63.2 +/- 16.5)% to overnight SD (72.4 +/- 13.2)%. Acute SD was associated with increased sympathetic and decreased parasympathetic cardiovascular modulation.

  1. Sleep deprivation induces abnormal bone metabolism in temporomandibular joint

    PubMed Central

    Geng, Wei; Wu, Gaoyi; Huang, Fei; Zhu, Yong; Nie, Jia; He, Yuhong; Chen, Lei

    2015-01-01

    Background: The purpose of this study was to explore the effect of experimental sleep deprivation (SD) on the temporomandibular joint (TMJ) of rats and the possible mechanism related to abnormal bone metabolism. Material and methods: SD was induced by a modified multiple platform method and assessed by serum adrenocorticotropic hormone (ACTH) level. TMJs were detached and stained with hematoxylin and eosin (H&E). Expression of interleukin-1β (IL-1β), tumor necrosis factor alpha (TNF-α), osteoprotegerin (OPG) and receptor activator of nuclear factor kappa B ligand (RANKL) was evaluated by quantitative reverse transcription polymerase chain reaction, H&E staining, immunohistochemical staining and enzyme linked immunosorbent assay. Results: Compared with controls, SD significantly increased serum ACTH, indicating that the SD model was successful. In the SD group, H&E staining revealed greater vessel hyperplasia in the synovial membrane and thicker hypertrophic layers in condylar cartilages. Compared with controls, RNA and protein expression of the inflammatory factors IL-1β and TNF-α and the bone metabolism-related factor RANKL increased in condylar cartilage in the SD group, whereas OPG and the OPG/RANKL ratio decreased. Immunohistochemical staining revealed that OPG/RANKL immunopositive cells were mainly located in hypertrophic layers. Conclusions: These results suggest that sleep deprivation might play an important role in the occurrence and development of temporomandibular disorders, which may occur through abnormal secretion of inflammatory and bone metabolism-related factors. PMID:25785010

  2. Synaptic plasticity model of therapeutic sleep deprivation in major depression.

    PubMed

    Wolf, Elias; Kuhn, Marion; Normann, Claus; Mainberger, Florian; Maier, Jonathan G; Maywald, Sarah; Bredl, Aliza; Klöppel, Stefan; Biber, Knut; van Calker, Dietrich; Riemann, Dieter; Sterr, Annette; Nissen, Christoph

    2016-12-01

    Therapeutic sleep deprivation (SD) is a rapid acting treatment for major depressive disorder (MDD). Within hours, SD leads to a dramatic decrease in depressive symptoms in 50-60% of patients with MDD. Scientifically, therapeutic SD presents a unique paradigm to study the neurobiology of MDD. Yet, up to now, the neurobiological basis of the antidepressant effect, which is most likely different from today's first-line treatments, is not sufficiently understood. This article puts the idea forward that sleep/wake-dependent shifts in synaptic plasticity, i.e., the neural basis of adaptive network function and behavior, represent a critical mechanism of therapeutic SD in MDD. Particularly, this article centers on two major hypotheses of MDD and sleep, the synaptic plasticity hypothesis of MDD and the synaptic homeostasis hypothesis of sleep-wake regulation, and on how they can be integrated into a novel synaptic plasticity model of therapeutic SD in MDD. As a major component, the model proposes that therapeutic SD, by homeostatically enhancing cortical synaptic strength, shifts the initially deficient inducibility of associative synaptic long-term potentiation (LTP) in patients with MDD in a more favorable window of associative plasticity. Research on the molecular effects of SD in animals and humans, including observations in the neurotrophic, adenosinergic, monoaminergic, and glutamatergic system, provides some support for the hypothesis of associative synaptic plasticity facilitation after therapeutic SD in MDD. The model proposes a novel framework for a mechanism of action of therapeutic SD that can be further tested in humans based on non-invasive indices and in animals based on direct studies of synaptic plasticity. Further determining the mechanisms of action of SD might contribute to the development of novel fast acting treatments for MDD, one of the major health problems worldwide. Copyright © 2015 Elsevier Ltd. All rights reserved.

  3. Impairment of male reproductive function after sleep deprivation.

    PubMed

    Alvarenga, Tathiana A; Hirotsu, Camila; Mazaro-Costa, Renata; Tufik, Sergio; Andersen, Monica L

    2015-05-01

    To evaluate the influence of sleep loss on sexual behavior, hormone levels, sperm parameters, and testis-specific gene expression in male rats. Experimental research. Animal laboratory. Male adult Wistar-Hannover rats. Sexually experienced rats were subjected to paradoxic sleep deprivation (PSD) for 96 hours or sleep restriction (SR) for 21 days or kept in their home cage as control (CTRL). Sexual behavior, hormone levels, sperm parameters and expression of stress and nitric oxide-related genes were evaluated. PSD significantly decreased sexual behavior compared with the CTRL group, whereas SR had no effect. The PSD group had significantly lower testosterone levels than the CTRL group. Both PSD and SR groups had lower sperm viabilities than the CTRL group. The decrease in the number of live sperm compared with the CTRL group was larger in the PSD group than in the SR group. Regarding testicular gene expression, both PSD and SR led to an increase of iNOS and hydroxysteroid 11β-dehydrogenase 1 expressions compared with the CTRL group. These changes were more pronounced in the PSD group. A significant increase in endothelial nitric oxide synthase expression was observed in the PSD groups compared with the CTRL group. No changes were observed in dimethylarginine dimethylaminohydrolase 1 and casein kinase 2β-polypeptide expressions. Sleep loss can promote marked changes in the male reproductive system of rats, particularly affecting spermatic function in part by interfering in the testicular nitric oxide pathway. Copyright © 2015 American Society for Reproductive Medicine. Published by Elsevier Inc. All rights reserved.

  4. Effects of sleep deprivation on sleep homeostasis and restoration during methadone-maintenance: a [31] P MRS brain imaging study

    PubMed Central

    Trksak, George H.; Jensen, J. Eric; Plante, David T.; Penetar, David M.; Tartarini, Wendy L.; Maywalt, Melissa A.; Brendel, Michael; Dorsey, Cynthia M.; Renshaw, Perry F.; Lukas, Scott E.

    2009-01-01

    SUMMARY Insomnia afflicts many individuals, but particularly those in chronic methadone treatment. Studies examining sleep deprivation (SD) have begun to identify sleep restoration processes involving brain bioenergetics. The technique [31]P magnetic resonance spectroscopy (MRS) can measure brain changes in the high-energy phosphates: alpha-, beta-, and gamma-nucleoside triphosphate (NTP). In the present study, 21 methadone-maintained (MM) and 16 control participants underwent baseline (BL), SD (40 wakeful hrs), recovery1 (RE1), and recovery2 (RE2) study nights. Polysomnographic sleep was recorded each night and [31]P MRS brain scanning conducted each morning using a 4T MR scanner (dual-tuned proton/phosphorus headcoil). Interestingly, increases in total sleep time (TST) and sleep efficiency index (SEI) commonly associated with RE sleep were not apparent in MM participants. Analysis of methadone treatment duration revealed that the lack of RE sleep increases in TST and SEI were primarily exhibited by short-term MM participants (methadone<12 months), while RE sleep in long-term MM (methadone>12 months) participants was more comparable to control participants. Slow wave sleep increased during RE1, but there was no difference between MM and control participants. Spectral power analysis revealed that compared to control participants; MM participants had greater delta, theta, and alpha spectral power during BL and RE sleep. [31]P MRS revealed that elevations in brain beta-NTP (a direct measure of ATP) following RE sleep were greater in MM compared to control participants. Results suggest that differences in sleep and brain chemistry during RE in MM participants may be reflective of a disruption in homeostatic sleep function. PMID:19775835

  5. Differential impact of REM sleep deprivation on cytoskeletal proteins of brain regions involved in sleep regulation.

    PubMed

    Rodríguez-Vázquez, Jennifer; Camacho-Arroyo, Ignacio; Velázquez-Moctezuma, Javier

    2012-01-01

    Rapid eye movement (REM) sleep is involved in memory consolidation, which implies synaptic plasticity. This process requires protein synthesis and the reorganization of the neural cytoskeleton. REM sleep deprivation (REMSD) has an impact on some neuronal proteins involved in synaptic plasticity, such as glutamate receptors and postsynaptic density protein 95, but its effects on cytoskeletal proteins is unknown. In this study, the effects of REMSD on the content of the cytoskeletal proteins MAP2 and TAU were analyzed. Adult female rats were submitted to selective REMSD by using the multiple platform technique. After 24, 48 or 72 h of REMSD, rats were decapitated and the following brain areas were dissected: pons, preoptic area, hippocampus and frontal cortex. Protein extraction and Western blot were performed. Results showed an increase in TAU content in the pons, preoptic area and hippocampus after 24 h of REMSD, while in the frontal cortex a significant increase in TAU content was observed after 72 h of REMSD. A TAU content decrease was observed in the hippocampus after 48 h of REMSD. Interestingly, a marked increase in TAU content was observed after 72 h of REMSD. MAP2 content only increased in the preoptic area at 24 h, and in the frontal cortex after 24 and 72 h of REMSD, without significant changes in the pons and hippocampus. These results support the idea that REM sleep plays an important role in the organization of neural cytoskeleton, and that this effect is tissue-specific.

  6. REM-sleep deprivation-induced increase in ethanol intake: role of brain monoaminergic neurons.

    PubMed

    Aalto, J; Kiianmaa, K

    1986-01-01

    The ethanol intake of Long-Evans male rats was recorded before, during and after deprivation of rapid eye movement (REM) sleep produced with the flowerpot technique modified by using a cuff pedestal and electrified grid floor instead of water. Ethanol intake increased significantly during REM-sleep deprivation. A rebound decrease in ethanol drinking was then observed during the REM-rebound phase immediately after the termination of REM-sleep deprivation. Because REM-sleep deprivation has been reported to impair the function of central monoamine neuronal systems and because some studies have implicated these systems in the control of voluntary ethanol intake, we studied whether different monoamine uptake blocking agents could antagonize the increase in ethanol intake caused by REM-sleep deprivation. After three days of REM-sleep deprivation, the rats were given uptake blocking agents for serotonin (citalopram, 5, 10 and 20 mg/kg/day, IP), dopamine (GBR 12909, 5 mg/kg/day, IP) and noradrenaline (talsupram, 1, 5 and 10 mg/kg/day, IP). Citalopram and GBR 12909 did not modify the increased level of ethanol intake, but talsupram decreased ethanol intake to the levels seen prior to deprivation, and during the REM-rebound phase amplified the decrease found. These effects of talsupram could be antagonized by blocking mg/kg/day, IP). Prazosin alone tended to increase ethanol consumption. These findings suggest that functional alterations in central noradrenergic neurons during REM-sleep deprivation may contribute to the concurrent increase in ethanol intake.

  7. The impact of sleep deprivation on food desire in the human brain.

    PubMed

    Greer, Stephanie M; Goldstein, Andrea N; Walker, Matthew P

    2013-01-01

    Epidemiological evidence supports a link between sleep loss and obesity. However, the detrimental impact of sleep deprivation on central brain mechanisms governing appetitive food desire remains unknown. Here we report that sleep deprivation significantly decreases activity in appetitive evaluation regions within the human frontal cortex and insular cortex during food desirability choices, combined with a converse amplification of activity within the amygdala. Moreover, this bi-directional change in the profile of brain activity is further associated with a significant increase in the desire for weight-gain promoting high-calorie foods following sleep deprivation, the extent of which is predicted by the subjective severity of sleep loss across participants. These findings provide an explanatory brain mechanism by which insufficient sleep may lead to the development/maintenance of obesity through diminished activity in higher-order cortical evaluation regions, combined with excess subcortical limbic responsivity, resulting in the selection of foods most capable of triggering weight-gain.

  8. Sleep deprivation-induced multi-organ injury: role of oxidative stress and inflammation

    PubMed Central

    Periasamy, Srinivasan; Hsu, Dur-Zong; Fu, Yu-Hsuan; Liu, Ming-Yie

    2015-01-01

    Sleep deprivation affects all aspects of health. Adverse health effects by sleep deviation are still underestimated and undervalued in clinical practice and, to a much greater extent in monitoring human health. We hypothesized that sleep deprivation-induced mild organ injuries; oxidative stress and inflammation might play a crucial role in inducing multi-organ injury. Male C57BL/6J mice (n = 6-7) were sleep-deprived for 0-72 h using a modified multiple platform boxes method. Blood and tissue were collected. Liver, heart, kidney, lung, and pancreatic injuries were evaluated using biochemical and histological analyses. Glutamic oxaloacetic transaminase (GOT), glutamic pyruvic transaminase (GPT), total billirubin (TBIL), creatine phosphokinase (CPK), creatine phosphokinase-myocardial band (CKMB), lactic dehydrogenase (LDH), creatinine (CRE), and blood urea nitrogen (BUN) were assayed in blood. Malondialdehyde (MDA), nitric oxide (NO), tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6 levels were measured. Histology revealed mild-to-moderate liver and lung injury in sleep-deprived mice. Sleep-deprived mice had significantly higher GOT, GPT, TBIL, CPK, CKMB, LDH, BUN, and α-amylase (AMYL) levels, which indicated liver, heart, kidney, and pancreatic injuries. Serum IL-1β at 24 h and IL-6 at 72 h were significantly higher in sleep-deprived than in control mice. Hepatic TNF-α and IL-1β were significantly higher, but IL-6 significantly lower in mice that had been sleep-deprived for 72 h. Sleep deprivation-mediated inflammation may be associated with mild to moderate multi-organ damage in mice. The implication of this study indicates sleep deprivation in humans may induce multi-organ injury that negatively affects cardiovascular and gastrointestinal health. PMID:26648820

  9. Acute versus chronic partial sleep deprivation in middle-aged people: differential effect on performance and sleepiness.

    PubMed

    Philip, Pierre; Sagaspe, Patricia; Prague, Mélanie; Tassi, Patricia; Capelli, Aurore; Bioulac, Bernard; Commenges, Daniel; Taillard, Jacques

    2012-07-01

    To evaluate the effects of acute sleep deprivation and chronic sleep restriction on vigilance, performance, and self-perception of sleepiness. Habitual night followed by 1 night of total sleep loss (acute sleep deprivation) or 5 consecutive nights of 4 hr of sleep (chronic sleep restriction) and recovery night. Eighteen healthy middle-aged male participants (age [(± standard deviation] = 49.7 ± 2.6 yr, range 46-55 yr). Multiple sleep latency test trials, Karolinska Sleepiness Scale scores, simple reaction time test (lapses and 10% fastest reaction times), and nocturnal polysomnography data were recorded. Objective and subjective sleepiness increased immediately in response to sleep restriction. Sleep latencies after the second and third nights of sleep restriction reached levels equivalent to those observed after acute sleep deprivation, whereas Karolinska Sleepiness Scale scores did not reach these levels. Lapse occurrence increased after the second day of sleep restriction and reached levels equivalent to those observed after acute sleep deprivation. A statistical model revealed that sleepiness and lapses did not progressively worsen across days of sleep restriction. Ten percent fastest reaction times (i.e., optimal alertness) were not affected by acute or chronic sleep deprivation. Recovery to baseline levels of alertness and performance occurred after 8-hr recovery night. In middle-aged study participants, sleep restriction induced a high increase in sleep propensity but adaptation to chronic sleep restriction occurred beyond day 3 of restriction. This sleepiness attenuation was underestimated by the participants. One recovery night restores daytime sleepiness and cognitive performance deficits induced by acute or chronic sleep deprivation. Philip P; Sagaspe P; Prague M; Tassi P; Capelli A; Bioulac B; Commenges D; Taillard J. Acute versus chronic partial sleep deprivation in middle-aged people: differential effect on performance and sleepiness. SLEEP 2012;35(7):997-1002.

  10. Acute Versus Chronic Partial Sleep Deprivation in Middle-Aged People: Differential Effect on Performance and Sleepiness

    PubMed Central

    Philip, Pierre; Sagaspe, Patricia; Prague, Mélanie; Tassi, Patricia; Capelli, Aurore; Bioulac, Bernard; Commenges, Daniel; Taillard, Jacques

    2012-01-01

    Study Objective: To evaluate the effects of acute sleep deprivation and chronic sleep restriction on vigilance, performance, and self-perception of sleepiness. Design: Habitual night followed by 1 night of total sleep loss (acute sleep deprivation) or 5 consecutive nights of 4 hr of sleep (chronic sleep restriction) and recovery night. Participants: Eighteen healthy middle-aged male participants (age [(± standard deviation] = 49.7 ± 2.6 yr, range 46-55 yr). Measurements: Multiple sleep latency test trials, Karolinska Sleepiness Scale scores, simple reaction time test (lapses and 10% fastest reaction times), and nocturnal polysomnography data were recorded. Results: Objective and subjective sleepiness increased immediately in response to sleep restriction. Sleep latencies after the second and third nights of sleep restriction reached levels equivalent to those observed after acute sleep deprivation, whereas Karolinska Sleepiness Scale scores did not reach these levels. Lapse occurrence increased after the second day of sleep restriction and reached levels equivalent to those observed after acute sleep deprivation. A statistical model revealed that sleepiness and lapses did not progressively worsen across days of sleep restriction. Ten percent fastest reaction times (i.e., optimal alertness) were not affected by acute or chronic sleep deprivation. Recovery to baseline levels of alertness and performance occurred after 8-hr recovery night. Conclusions: In middle-aged study participants, sleep restriction induced a high increase in sleep propensity but adaptation to chronic sleep restriction occurred beyond day 3 of restriction. This sleepiness attenuation was underestimated by the participants. One recovery night restores daytime sleepiness and cognitive performance deficits induced by acute or chronic sleep deprivation. Citation: Philip P; Sagaspe P; Prague M; Tassi P; Capelli A; Bioulac B; Commenges D; Taillard J. Acute versus chronic partial sleep deprivation in

  11. The Effect of One Night's Sleep Deprivation on Adolescent Neurobehavioral Performance

    PubMed Central

    Louca, Mia; Short, Michelle A.

    2014-01-01

    Study Objectives: To investigate the effects of one night's sleep deprivation on neurobehavioral functioning in adolescents. Design: Participants completed a neurobehavioral test battery measuring sustained attention, reaction speed, cognitive processing speed, sleepiness, and fatigue every 2 h during wakefulness. Baseline performance (defined as those test bouts between 09:00 and 19:00 on days 2 and 3, following two 10-h sleep opportunities) were compared to performance at the same clock time the day following total sleep deprivation. Setting: The sleep laboratory at the Centre for Sleep Research. Participants: Twelve healthy adolescents (6 male), aged 14-18 years (mean = 16.17, standard deviation = 0.83). Measurements and Results: Sustained attention, reaction speed, cognitive processing speed, and subjective sleepiness were all significantly worse following one night without sleep than following 10-h sleep opportunities (all main effects of day, P < 0.05). Sleep deprivation led to increased variability on objective performance measures. There were between-subjects differences in response to sleep loss that were task-specific, suggesting that adolescents may not only vary in terms of the degree to which they are affected by sleep loss but also the domains in which they are affected. Conclusions: These findings suggest that one night of total sleep deprivation has significant deleterious effects upon neurobehavioral performance and subjective sleepiness. These factors impair daytime functioning in adolescents, leaving them at greater risk of poor academic and social functioning and accidents and injuries. Citation: Louca M, Short MA. The effect of one night's sleep deprivation on adolescent neurobehavioral performance. SLEEP 2014;37(11):1799-1807. PMID:25364075

  12. Blood-Gene Expression Reveals Reduced Circadian Rhythmicity in Individuals Resistant to Sleep Deprivation

    PubMed Central

    Arnardottir, Erna S.; Nikonova, Elena V.; Shockley, Keith R.; Podtelezhnikov, Alexei A.; Anafi, Ron C.; Tanis, Keith Q.; Maislin, Greg; Stone, David J.; Renger, John J.; Winrow, Christopher J.; Pack, Allan I.

    2014-01-01

    Study Objectives: To address whether changes in gene expression in blood cells with sleep loss are different in individuals resistant and sensitive to sleep deprivation. Design: Blood draws every 4 h during a 3-day study: 24-h normal baseline, 38 h of continuous wakefulness and subsequent recovery sleep, for a total of 19 time-points per subject, with every 2-h psychomotor vigilance task (PVT) assessment when awake. Setting: Sleep laboratory. Participants: Fourteen subjects who were previously identified as behaviorally resistant (n = 7) or sensitive (n = 7) to sleep deprivation by PVT. Intervention: Thirty-eight hours of continuous wakefulness. Measurements and Results: We found 4,481 unique genes with a significant 24-h diurnal rhythm during a normal sleep-wake cycle in blood (false discovery rate [FDR] < 5%). Biological pathways were enriched for biosynthetic processes during sleep. After accounting for circadian effects, two genes (SREBF1 and CPT1A, both involved in lipid metabolism) exhibited small, but significant, linear changes in expression with the duration of sleep deprivation (FDR < 5%). The main change with sleep deprivation was a reduction in the amplitude of the diurnal rhythm of expression of normally cycling probe sets. This reduction was noticeably higher in behaviorally resistant subjects than sensitive subjects, at any given P value. Furthermore, blood cell type enrichment analysis showed that the expression pattern difference between sensitive and resistant subjects is mainly found in cells of myeloid origin, such as monocytes. Conclusion: Individual differences in behavioral effects of sleep deprivation are associated with differences in diurnal amplitude of gene expression for genes that show circadian rhythmicity. Citation: Arnardottir ES, Nikonova EV, Shockley KR, Podtelezhnikov AA, Anafi RC, Tanis KQ, Maislin G, Stone DJ, Renger JJ, Winrow CJ, Pack AI. Blood-gene expression reveals reduced circadian rhythmicity in individuals resistant to

  13. Sleep deprivation and divergent toll-like receptor-4 activation of cellular inflammation in aging.

    PubMed

    Carroll, Judith E; Carrillo, Carmen; Olmstead, Richard; Witarama, Tuff; Breen, Elizabeth C; Yokomizo, Megumi; Seeman, Teresa; Irwin, Michael R

    2015-02-01

    Sleep disturbance and aging are associated with increases in inflammation, as well as increased risk of infectious disease. However, there is limited understanding of the role of sleep loss on age-related differences in immune responses. This study examines the effects of sleep deprivation on toll-like receptor activation of monocytic inflammation in younger compared to older adults. Community-dwelling adults (n = 70) who were categorized as younger (25-39 y old, n = 21) and older (60-84 y old, n = 49) participants, underwent a sleep laboratory-based experimental partial sleep deprivation (PSD) protocol including adaptation, an uninterrupted night of sleep, sleep deprivation (sleep restricted to 03:00-07:00), and recovery. Blood samples were obtained each morning to measure toll-like receptor-4 activation of monocyte intracellular production of the inflammatory cytokines interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α). Partial sleep deprivation induced a significant increase in the production of IL-6 and/or TNF-α that persisted after a night of recovery sleep (F(2,121.2) = 3.8, P < 0.05). Age moderated the effects of sleep loss, such that younger adults had an increase in inflammatory cytokine production that was not present in older adults (F(2,121.2) = 4.0, P < 0.05). Older adults exhibit reduced toll-like receptor 4 stimulated cellular inflammation that, unlike in younger adults, is not activated after a night of partial sleep loss. Whereas sleep loss increases cellular inflammation in younger adults and may contribute to inflammatory disorders, blunted toll-like receptor activation in older adults may increase the risk of infectious disease seen with aging. © 2015 Associated Professional Sleep Societies, LLC.

  14. Acute total sleep deprivation potentiates cocaine-induced hyperlocomotion in mice.

    PubMed

    Berro, L F; Santos, R; Hollais, A W; Wuo-Silva, R; Fukushiro, D F; Mári-Kawamoto, E; Costa, J M; Trombin, T F; Patti, C L; Grapiglia, S B; Tufik, S; Andersen, M L; Frussa-Filho, R

    2014-09-05

    Sleep deprivation is common place in modern society. Nowadays, people tend to self-impose less sleep in order to achieve professional or social goals. In the social context, late-night parties are frequently associated with higher availability of recreational drugs with abuse potential. Physiologically, all of these drugs induce an increase in dopamine release in the mesolimbic dopaminergic system, which leads to hyperlocomotion in rodents. Sleep deprivation also seems to play an important role in the events related to the neurotransmission of the dopaminergic system by potentiating its behavioral effects. In this scenario, the aim of the present study was to investigate the effects of total sleep deprivation (6h) on the acute cocaine-induced locomotor stimulation in male mice. Animals were sleep deprived or maintained in their home cages and subsequently treated with an acute i.p. injection of 15mg/kg cocaine or saline and observed in the open field. Total sleep deprivation for 6h potentiated the hyperlocomotion induced by acute cocaine administration. In addition, the cocaine sleep deprived group showed a decreased ratio central/total locomotion compared to the cocaine control group, which might be related to an increase in the impulsiveness of mice. Our data indicate that acute periods of sleep loss should be considered risk factors for cocaine abuse.

  15. Psychomotor performance of medical students: effect of 24 hours of sleep deprivation.

    PubMed

    Dixit, Abhinav; Thawani, Rajat; Goyal, Abhishek; Vaney, Neelam

    2012-04-01

    Sleep deprivation is known to have detrimental effects on attentional resources and cognitive functions. The aim of this study is to assess the changes in performance, due to 24 h of sleep deprivation, in medical students The performance was assessed using simple paper-pencil tasks, such as digit symbol substitution test, digit vigilance test, and letter cancellation tasks. The results revealed an increase in the number of errors in letter cancellation tasks and digit vigilance test, with a significant decrease in the number of correct responses on the letter cancellation task. The time taken to complete the tests increased with lack of sleep, with the digit symbol substitution test being affected the most. This study infers that sleep deprivation for 24 h affected the judgment ability more than the response speed. Sleep deprivation might lead to compromised performance of medical students in examinations.

  16. Coping with Sleep Deprivation: Shifts in Regional Brain Activity and Learning Strategy

    PubMed Central

    Hagewoud, Roelina; Havekes, Robbert; Tiba, Paula A.; Novati, Arianna; Hogenelst, Koen; Weinreder, Pim; Van der Zee, Eddy A.; Meerlo, Peter

    2010-01-01

    Study Objectives: Dissociable cognitive strategies are used for place navigation. Spatial strategies rely on the hippocampus, an area important for flexible integration of novel information. Response strategies are more rigid and involve the dorsal striatum. These memory systems can compensate for each other in case of temporal or permanent damage. Sleep deprivation has adverse effects on hippocampal function. However, whether the striatal memory system can compensate for sleep-deprivation–induced hippocampal impairments is unknown. Design: With a symmetrical maze paradigm for mice, we examined the effect of sleep deprivation on learning the location of a food reward (training) and on learning that a previously nonrewarded arm was now rewarded (reversal training). Measurements and Results: Five hours of sleep deprivation after each daily training session did not affect performance during training. However, in contrast with controls, sleep-deprived mice avoided a hippocampus-dependent spatial strategy and preferentially used a striatum-dependent response strategy. In line with this, the training-induced increase in phosphorylation of the transcription factor cAMP response-element binding protein (CREB) shifted from hippocampus to dorsal striatum. Importantly, although sleep-deprived mice performed well during training, performance during reversal training was attenuated, most likely due to rigidity of the striatal system they used. Conclusions: Together, these findings suggest that the brain compensates for negative effects of sleep deprivation on the hippocampal memory system by promoting the use of a striatal memory system. However, effects of sleep deprivation can still appear later on because the alternative learning mechanisms and brain regions involved may result in reduced flexibility under conditions requiring adaptation of previously formed memories. Citation: Hagewoud R; Havekes R; Tiba PA; Novati A; Hogenelst K; Weinreder P; Van der Zee EA; Meerlo P

  17. Classifying Vulnerability to Sleep Deprivation Using Baseline Measures of Psychomotor Vigilance

    PubMed Central

    Patanaik, Amiya; Kwoh, Chee Keong; Chua, Eric C.P.; Gooley, Joshua J.; Chee, Michael W.L.

    2015-01-01

    Objective: To identify measures derived from baseline psychomotor vigilance task (PVT) performance that can reliably predict vulnerability to sleep deprivation. Design: Subjects underwent total sleep deprivation and completed a 10-min PVT every 1–2 h in a controlled laboratory setting. Participants were categorized as vulnerable or resistant to sleep deprivation, based on a median split of lapses that occurred following sleep deprivation. Standard reaction time, drift diffusion model (DDM), and wavelet metrics were derived from PVT response times collected at baseline. A support vector machine model that incorporated maximum relevance and minimum redundancy feature selection and wrapper-based heuristics was used to classify subjects as vulnerable or resistant using rested data. Setting: Two academic sleep laboratories. Participants: Independent samples of 135 (69 women, age 18 to 25 y), and 45 (3 women, age 22 to 32 y) healthy adults. Measurements and Results: In both datasets, DDM measures, number of consecutive reaction times that differ by more than 250 ms, and two wavelet features were selected by the model as features predictive of vulnerability to sleep deprivation. Using the best set of features selected in each dataset, classification accuracy was 77% and 82% using fivefold stratified cross-validation, respectively. Conclusions: Despite differences in experimental conditions across studies, drift diffusion model parameters associated reliably with individual differences in performance during total sleep deprivation. These results demonstrate the utility of drift diffusion modeling of baseline performance in estimating vulnerability to psychomotor vigilance decline following sleep deprivation. Citation: Patanaik A, Kwoh CK, Chua EC, Gooley JJ, Chee MW. Classifying vulnerability to sleep deprivation using baseline measures of psychomotor vigilance. SLEEP 2015;38(5):723–734. PMID:25325482

  18. Classifying vulnerability to sleep deprivation using baseline measures of psychomotor vigilance.

    PubMed

    Patanaik, Amiya; Kwoh, Chee Keong; Chua, Eric C P; Gooley, Joshua J; Chee, Michael W L

    2015-05-01

    To identify measures derived from baseline psychomotor vigilance task (PVT) performance that can reliably predict vulnerability to sleep deprivation. Subjects underwent total sleep deprivation and completed a 10-min PVT every 1-2 h in a controlled laboratory setting. Participants were categorized as vulnerable or resistant to sleep deprivation, based on a median split of lapses that occurred following sleep deprivation. Standard reaction time, drift diffusion model (DDM), and wavelet metrics were derived from PVT response times collected at baseline. A support vector machine model that incorporated maximum relevance and minimum redundancy feature selection and wrapper-based heuristics was used to classify subjects as vulnerable or resistant using rested data. Two academic sleep laboratories. Independent samples of 135 (69 women, age 18 to 25 y), and 45 (3 women, age 22 to 32 y) healthy adults. In both datasets, DDM measures, number of consecutive reaction times that differ by more than 250 ms, and two wavelet features were selected by the model as features predictive of vulnerability to sleep deprivation. Using the best set of features selected in each dataset, classification accuracy was 77% and 82% using fivefold stratified cross-validation, respectively. In both datasets, DDM measures, number of consecutive reaction times that differ by more than 250 ms, and two wavelet features were selected by the model as features predictive of vulnerability to sleep deprivation. Using the best set of features selected in each dataset, classification accuracy was 77% and 82% using fivefold stratified cross-validation, respectively. Despite differences in experimental conditions across studies, drift diffusion model parameters associated reliably with individual differences in performance during total sleep deprivation. These results demonstrate the utility of drift diffusion modeling of baseline performance in estimating vulnerability to psychomotor vigilance decline

  19. Novel application of brain-targeting polyphenol compounds in sleep deprivation-induced cognitive dysfunction

    PubMed Central

    Zhao, Wei; Wang, Jun; Bi, Weina; Ferruzzi, Mario; Yemul, Shrishailam; Freire, Daniel; Mazzola, Paolo; Ho, Lap; Dubner, Lauren; Pasinetti, Giulio Maria

    2016-01-01

    Sleep deprivation produces deficits in hippocampal synaptic plasticity and hippocampal-dependent memory storage. Recent evidence suggests that sleep deprivation disrupts memory consolidation through multiple mechanisms, including the down-regulation of the cAMP-response element-binding protein (CREB) and of mammalian target of rapamycin (mTOR) signaling. In this study, we tested the effects of a Bioactive Dietary Polyphenol Preparation (BDPP), comprised of grape seed polyphenol extract, Concord grape juice, and resveratrol, on the attenuation of sleep deprivation-induced cognitive impairment. We found that BDPP significantly improves sleep deprivation-induced contextual memory deficits, possibly through the activation of CREB and mTOR signaling pathways. We also identified brain-available polyphenol metabolites from BDPP, among which quercetin-3-O-glucuronide activates CREB signaling and malvidin-3-O-glucoside activates mTOR signaling. In combination, quercetin and malvidin-glucoside significantly attenuated sleep deprivation-induced cognitive impairment in -a mouse model of acute sleep deprivation. Our data suggests the feasibility of using select brain-targeting polyphenol compounds derived from BDPP as potential therapeutic agents in promoting resilience against sleep deprivation-induced cognitive dysfunction. PMID:26235983

  20. Effects of sleep deprivation and exercise on cognitive, motor performance and mood.

    PubMed

    Scott, Jonathon P R; McNaughton, Lars R; Polman, Remco C J

    2006-02-28

    This study examined the effect of 30 h of sleep deprivation and intermittent physical exercise, on both cognitive and psychomotor function as well subjective ratings of mood. Six subjects with the following physical characteristics participated in the study (Mean +/- S.D.): age 22 +/- 0.3 years, height 180 +/- 5 cm, body mass: 77 +/- 5 kg, VO2peak 44 +/- 5 ml kg(-1) min(-1). Three subjects engaged in normal sedentary activities while three others cycled on a cycle ergometer at 50% VO2peak for 20 min out of every 2 h during 30 h of sleep deprivation. One week later sleep deprivation was repeated with a cross over of subjects. Every 4 h, subjects completed simple and two-choice reaction time tasks at both rest and during exercise, a computerized tracking task, a number cancellation task, and an assessment of subjective mood state as measured by the POMS questionnaire. A 3 x 4 repeated measures ANOVA revealed that resting but not exercising reaction times were significantly slower with sleep deprivation. Sleep deprivation was also associated with significantly greater negative disturbances to subjective vigour, fatigue and depression assessed by the Profile of Mood States questionnaire. Compared to those who have been deprived of sleep alone, individuals that performed 5 h of intermittent moderate exercise during 30 h of sleep deprivation appeared to be more vulnerable to negative mood disturbances and impairment in reaction times. This could result in greater risk of accident due to a reduced capacity to respond quickly.

  1. Novel application of brain-targeting polyphenol compounds in sleep deprivation-induced cognitive dysfunction.

    PubMed

    Zhao, Wei; Wang, Jun; Bi, Weina; Ferruzzi, Mario; Yemul, Shrishailam; Freire, Daniel; Mazzola, Paolo; Ho, Lap; Dubner, Lauren; Pasinetti, Giulio Maria

    2015-10-01

    Sleep deprivation produces deficits in hippocampal synaptic plasticity and hippocampal-dependent memory storage. Recent evidence suggests that sleep deprivation disrupts memory consolidation through multiple mechanisms, including the down-regulation of the cAMP-response element-binding protein (CREB) and of mammalian target of rapamycin (mTOR) signaling. In this study, we tested the effects of a Bioactive Dietary Polyphenol Preparation (BDPP), comprised of grape seed polyphenol extract, Concord grape juice, and resveratrol, on the attenuation of sleep deprivation-induced cognitive impairment. We found that BDPP significantly improves sleep deprivation-induced contextual memory deficits, possibly through the activation of CREB and mTOR signaling pathways. We also identified brain-available polyphenol metabolites from BDPP, among which quercetin-3-O-glucuronide activates CREB signaling and malvidin-3-O-glucoside activates mTOR signaling. In combination, quercetin and malvidin-glucoside significantly attenuated sleep deprivation-induced cognitive impairment in -a mouse model of acute sleep deprivation. Our data suggests the feasibility of using select brain-targeting polyphenol compounds derived from BDPP as potential therapeutic agents in promoting resilience against sleep deprivation-induced cognitive dysfunction.

  2. Sleep deprivation and anxiety in humans and rodents--translational considerations and hypotheses.

    PubMed

    Pires, Gabriel Natan; Tufik, Sergio; Andersen, Monica Levy

    2015-10-01

    The effects of acute sleep deprivation on anxiety are the focus of controversy in the literature. While clinical research studies on the effects of sleep deprivation seem to show a consistent increase in acute anxiety, rodent studies have produced inconsistent results, with some experiments pointing to anxiogenesis and others to anxiolysis. Such observations impair the translational applicability of rodent models on the paradigm between sleep deprivation and anxiety. Current studies fail in the very basic principle of biomedical translational research: to provide relevant and reliable knowledge from basic experimental science that can be applied in clinical environments. Possible explanations for the disparity between human and animal studies include the accuracy of both human and rodent research, the ability of current behavioral protocols to truly reflect the anxiety response of rodents to sleep deprivation, and the nature of sleep deprivation-induced anxiety in rodents. Based on these hypotheses, we performed a brief overview of the literature on the relationship between sleep deprivation and anxiety and propose a research agenda that could lead to a better understanding of the reasons for the discrepancies found in the literature and provide more reliable data on the translational relationship between sleep deprivation and anxiety.

  3. Effects of mental resilience on neuroendocrine hormones level changes induced by sleep deprivation in servicemen.

    PubMed

    Sun, Xinyang; Dai, Xuyan; Yang, Tingshu; Song, Hongtao; Yang, Jialin; Bai, Jing; Zhang, Liyi

    2014-12-01

    The aim of this study was to investigate the effects of mental resilience on the changes of serum rennin, angiotensin, and cortisol level induced by sleep deprivation in servicemen. By random cluster sampling, a total of 160 servicemen, aged from 18 to 30, were selected to undergo 24-hour total sleep deprivation and administered the military personnel mental resilience scale after the deprivation procedure. The sleep deprivation procedure started at 8 a.m. on Day 8 and ended at 8 a.m. on Day 9 after 7 days of normal sleep for baseline preparation. Blood samples were drawn from the 160 participants at 8 a.m. respectively on Day 8 and Day 9 for hormonal measurements. All blood samples were analyzed using radioimmunoassay. As hypothesized, serum rennin, angiotensin II, and cortisol level of the participants after sleep deprivation were significantly higher than those before (P < 0.05). The changes of serum rennin and cortisol in the lower mental resilience subgroup were significantly greater (P < 0.05); problem-solving skill and willpower were the leading influence factors for the increases of serum rennin and cortisol respectively induced by sleep deprivation. We conclude that mental resilience plays a significant role in alleviating the changes of neurohormones level induced by sleep deprivation in servicemen.

  4. Does sleep deprivation alter functional EEG networks in children with focal epilepsy?

    PubMed

    van Diessen, Eric; Otte, Willem M; Braun, Kees P J; Stam, Cornelis J; Jansen, Floor E

    2014-01-01

    Electroencephalography (EEG) recordings after sleep deprivation increase the diagnostic yield in patients suspected of epilepsy if the routine EEG remains inconclusive. Sleep deprivation is associated with increased interictal EEG abnormalities in patients with epilepsy, but the exact mechanism is unknown. In this feasibility study, we used a network analytical approach to provide novel insights into this clinical observation. The aim was to characterize the effect of sleep deprivation on the interictal functional network organization using a unique dataset of paired routine and sleep deprivation recordings in patients and controls. We included 21 children referred to the first seizure clinic of our center with suspected new onset focal epilepsy in whom a routine interictal and a sleep deprivation EEG (SD-EEG) were performed. Seventeen children, in whom the diagnosis of epilepsy was excluded, served as controls. For both time points weighted functional networks were constructed based on interictal artifact free time-series. Routine and sleep deprivation networks were characterized at different frequency bands using minimum spanning tree (MST) measures (leaf number and diameter) and classical measures of integration (path length) and segregation (clustering coefficient). A significant interaction was found for leaf number and diameter between patients and controls after sleep deprivation: patients showed a shift toward a more path-like MST network whereas controls showed a shift toward a more star-like MST network. This shift in network organization after sleep deprivation in patients is in accordance with previous studies showing a more regular network organization in the ictal state and might relate to the increased epileptiform abnormalities found in patients after sleep deprivation. Larger studies are needed to verify these results. Finally, MST measures were more sensitive in detecting network changes as compared to the classical measures of integration and

  5. Rapid antidepressant effects of sleep deprivation therapy correlates with serum BDNF changes in major depression.

    PubMed

    Gorgulu, Yasemin; Caliyurt, Okan

    2009-09-28

    Recent reports have suggested that brain-derived neurotrophic factor (BDNF) levels are reduced in individuals suffering major depressive disorder and these levels normalize following antidepressant treatment. Various antidepressants and electroconvulsive therapy are shown to have a positive effect on brain-derived neurotrophic factor levels in depressive patients. The aim of this study was to assess the effect of total sleep deprivation therapy on BDNF levels in major depressive patients. Patients were assigned to two treatment groups which consisted of 22 patients in the sertraline group and 19 patients in the total sleep deprivation plus sertraline group. Patients in the sleep deprivation group were treated with three total sleep deprivations in the first week of their treatment and received sertraline. Patients in sertraline group received only sertraline. BDNF levels were measured in the two treatment groups at baseline, 7th, 14th, and 42nd days. Patients were also evaluated using the Hamilton Rating Scale for Depression (HAM-D). A control group, consisting of 33 healthy volunteers had total sleep deprivation, BDNF levels and depression measured at baseline and after the total sleep deprivation. Results showed that serum BDNF levels were significantly lower at baseline in both treatment groups compared to controls. Decreased levels of BDNF were also negatively correlated with HAM-D scores. First single sleep deprivation and a series of three sleep deprivations accelerated the treatment response that significantly decreased HAM-D scores and increased BDNF levels. Total sleep deprivation and sertraline therapy is introduced to correlate with the rapid treatment response and BDNF changes in this study.

  6. The effects of 53 hours of sleep deprivation on moral judgment.

    PubMed

    Killgore, William D S; Killgore, Desiree B; Day, Lisa M; Li, Christopher; Kamimori, Gary H; Balkin, Thomas J

    2007-03-01

    Functional neuroimaging studies suggest a prominent role for the medial prefrontal cortex in the formation of moral judgments. Activity in this region has also been shown to decline significantly during sleep loss. We therefore examined the effects of 2 nights of sleep deprivation on several aspects of moral judgment. Participants made judgments about the "appropriateness" of various courses of action in response to 3 types of moral dilemmas at rested baseline and again following 53 hours of continuous wakefulness. In-residence sleep laboratory at the Walter Reed Army Institute of Research. Twenty-six healthy adults (21 men, 5 women). N/A. Compared to baseline, sleep deprivation resulted in significantly longer response latencies (suggesting greater difficulty deciding upon a course of action) only for Moral Personal (i.e., emotionally evocative) dilemmas, whereas response times to Moral Impersonal (less emotionally evocative) and Non Moral dilemmas did not change significantly with sleep loss. The effect of sleep deprivation on the willingness to agree with solutions that violate personally held moral beliefs was moderated by the level of emotional intelligence, as measured by the Bar-On EQ-i. Persons high in emotional intelligence were less susceptible to changes in moral judgments as a function of sleep loss. These findings suggest that sleep deprivation impairs the ability to integrate emotion and cognition to guide moral judgments, although susceptibility to the effects of sleep loss on this ability is moderated by the level of emotional intelligence.

  7. GABAA receptor-mediated input change on orexin neurons following sleep deprivation in mice.

    PubMed

    Matsuki, T; Takasu, M; Hirose, Y; Murakoshi, N; Sinton, C M; Motoike, T; Yanagisawa, M

    2015-01-22

    Orexins are bioactive peptides, which have been shown to play a pivotal role in vigilance state transitions: the loss of orexin-producing neurons (orexin neurons) leads to narcolepsy with cataplexy in the human. However, the effect of the need for sleep (i.e., sleep pressure) on orexin neurons remains largely unknown. Here, we found that immunostaining intensities of the α1 subunit of the GABAA receptor and neuroligin 2, which is involved in inhibitory synapse specialization, on orexin neurons of mouse brain were significantly increased by 6-h sleep deprivation. In contrast, we noted that immunostaining intensities of the α2, γ2, and β2/3 subunits of the GABAA receptor and Huntingtin-associated protein 1, which is involved in GABAAR trafficking, were not changed by 6-h sleep deprivation. Using a slice patch recording, orexin neurons demonstrated increased sensitivity to a GABAA receptor agonist together with synaptic plasticity changes after sleep deprivation when compared with an ad lib sleep condition. In summary, the GABAergic input property of orexin neurons responds rapidly to sleep deprivation. This molecular response of orexin neurons may thus play a role in the changes that accompany the need for sleep following prolonged wakefulness, in particular the decreased probability of a transition to wakefulness once recovery sleep has begun.

  8. Sustained attention performance during sleep deprivation associates with instability in behavior and physiologic measures at baseline.

    PubMed

    Chua, Eric Chern-Pin; Yeo, Sing-Chen; Lee, Ivan Tian-Guang; Tan, Luuan-Chin; Lau, Pauline; Cai, Shiwei; Zhang, Xiaodong; Puvanendran, Kathiravelu; Gooley, Joshua J

    2014-01-01

    To identify baseline behavioral and physiologic markers that associate with individual differences in sustained attention during sleep deprivation. In a retrospective study, ocular, electrocardiogram, and electroencephalogram (EEG) measures were compared in subjects who were characterized as resilient (n = 15) or vulnerable (n = 15) to the effects of total sleep deprivation on sustained attention. Chronobiology and Sleep Laboratory, Duke-NUS Graduate Medical School Singapore. Healthy volunteers aged 22-32 years from the general population. Subjects were kept awake for at least 26 hours under constant environmental conditions. Every 2 hours, sustained attention was assessed using a 10-minute psychomotor vigilance task (PVT). During baseline sleep and recovery sleep, EEG slow wave activity was similar in resilient versus vulnerable subjects, suggesting that individual differences in vulnerability to sleep loss were not related to differences in homeostatic sleep regulation. Rather, irrespective of time elapsed since wake, subjects who were vulnerable to sleep deprivation exhibited slower and more variable PVT response times, lower and more variable heart rate, and higher and more variable EEG spectral power in the theta frequency band (6.0-7.5 Hz). Performance decrements in sustained attention during sleep deprivation associate with instability in behavioral and physiologic measures at baseline. Small individual differences in sustained attention that are present at baseline are amplified during prolonged wakefulness, thus contributing to large between-subjects differences in performance and sleepiness.

  9. Sleep deprivation impairs precision of waggle dance signaling in honey bees

    PubMed Central

    Klein, Barrett A.; Klein, Arno; Wray, Margaret K.; Mueller, Ulrich G.; Seeley, Thomas D.

    2010-01-01

    Sleep is essential for basic survival, and insufficient sleep leads to a variety of dysfunctions. In humans, one of the most profound consequences of sleep deprivation is imprecise or irrational communication, demonstrated by degradation in signaling as well as in receiving information. Communication in nonhuman animals may suffer analogous degradation of precision, perhaps with especially damaging consequences for social animals. However, society-specific consequences of sleep loss have rarely been explored, and no function of sleep has been ascribed to a truly social (eusocial) organism in the context of its society. Here we show that sleep-deprived honey bees (Apis mellifera) exhibit reduced precision when signaling direction information to food sources in their waggle dances. The deterioration of the honey bee's ability to communicate is expected to reduce the foraging efficiency of nestmates. This study demonstrates the impact of sleep deprivation on signaling in a eusocial animal. If the deterioration of signals made by sleep-deprived honey bees and humans is generalizable, then imprecise communication may be one detrimental effect of sleep loss shared by social organisms. PMID:21156830

  10. Effect of sleep deprivation on tolerance of prolonged exercise.

    PubMed

    Martin, B J

    1981-01-01

    Acute loss of sleep produces few apparent physiological effects at rest. Nevertheless, many anecdotes suggest that adequate sleep is essential for optimum endurance athletic performance. To investigate this question, heavy exercise performance after 36 h without sleep was compared with that after normal sleep in eight subjects. During prolonged treadmill walking at about 80% of the VO2 max, sleep loss reduced work time to exhaustion by an average of 11% (p = 0.05). This decrease occurred despite doubling monetary incentives for subjects during work after sleeplessness. Subjects appeared to fall into "resistant" and "susceptible" categories: four showed less than a 5% change in performance after sleep loss, while four others showed decrements in exercise tolerance ranging from 15 to 40%. During the walk, sleep loss resulted in significantly greater perceived exertion (p less than 0.05), even though exercise heart rate and metabolic rate (VO2 and VCO2) were unchanged. Minute ventilation was significantly elevated during exercise after sleep loss ( p less than 0.05). Sleep loss failed to alter the continuous slow rises in VE and heart rate that occurred as work was prolonged. These findings suggest that the psychological effects of acute sleep loss may contribute to decreased tolerance of prolonged heavy exercise.

  11. Intensive Sleep Deprivation and Cognitive Behavioral Therapy for Pharmacotherapy Refractory Insomnia in a Hospitalized Patient

    PubMed Central

    Breitstein, Joshua; Penix, Brandon; Roth, Bernard J.; Baxter, Tristin; Mysliwiec, Vincent

    2014-01-01

    The case of a 59-year-old woman psychiatrically hospitalized with comorbid insomnia, suicidal ideation, and generalized anxiety disorder is presented. Pharmacologic therapies were unsuccessful for treating insomnia prior to and during hospitalization. Intensive sleep deprivation was initiated for 40 consecutive hours followed by a recovery sleep period of 8 hours. Traditional components of cognitive behavioral therapy for insomnia (CBTi), sleep restriction, and stimulus control therapies, were initiated on the ward. After two consecutive nights with improved sleep, anxiety, and absence of suicidal ideation, the patient was discharged. She was followed in the sleep clinic for two months engaging in CBTi. Treatment resulted in substantial improvement in her insomnia, daytime sleepiness, and anxiety about sleep. Sleep deprivation regimens followed by a restricted sleep recovery period have shown antidepressant effects in depressed patients. Similar treatment protocols have not been investigated in patients with pharmacotherapy refractory insomnia and generalized anxiety disorder. Citation: Breitstein J, Penix B, Roth BJ, Baxter T, Mysliwiec V. Intensive sleep deprivation and cognitive behavioral therapy for pharmacotherapy refractory insomnia in a hospitalized patient. J Clin Sleep Med 2014;10(6):689-690. PMID:24932151

  12. The effect of sleep deprivation on BOLD activity elicited by a divided attention task.

    PubMed

    Jackson, Melinda L; Hughes, Matthew E; Croft, Rodney J; Howard, Mark E; Crewther, David; Kennedy, Gerard A; Owens, Katherine; Pierce, Rob J; O'Donoghue, Fergal J; Johnston, Patrick

    2011-06-01

    Sleep loss, widespread in today's society and associated with a number of clinical conditions, has a detrimental effect on a variety of cognitive domains including attention. This study examined the sequelae of sleep deprivation upon BOLD fMRI activation during divided attention. Twelve healthy males completed two randomized sessions; one after 27 h of sleep deprivation and one after a normal night of sleep. During each session, BOLD fMRI was measured while subjects completed a cross-modal divided attention task (visual and auditory). After normal sleep, increased BOLD activation was observed bilaterally in the superior frontal gyrus and the inferior parietal lobe during divided attention performance. Subjects reported feeling significantly more sleepy in the sleep deprivation session, and there was a trend towards poorer divided attention task performance. Sleep deprivation led to a down regulation of activation in the left superior frontal gyrus, possibly reflecting an attenuation of top-down control mechanisms on the attentional system. These findings have implications for understanding the neural correlates of divided attention and the neurofunctional changes that occur in individuals who are sleep deprived.

  13. The impact of one night of sleep deprivation on moral judgments.

    PubMed

    Tempesta, D; Couyoumdjian, A; Moroni, F; Marzano, C; De Gennaro, L; Ferrara, M

    2012-01-01

    Recent studies have shown the existence of a relationship between sleep and moral judgment. In this study, we investigated whether one night of sleep deprivation affects the ability to judge the appropriateness of moral dilemmas. Forty-eight students had to judge 30 moral dilemmas at test, after a night of home sleep, and another 30 dilemmas at retest, following one night of continuous wakefulness. The 60 dilemmas (20 moral impersonal, 20 moral personal, and 20 non-moral) were selected from Greene's dilemmas. Both groups judged the appropriateness of personal and impersonal dilemmas in the same way. A close to significant effect of sleep deprivation was observed on the reaction times for impersonal moral dilemmas, to which the deprived subjects responded faster (p = .05) than the control subjects. However, this was not the case for personal ones, for which no difference was significant. This result shows a greater ease/speed in responding to the (impersonal) dilemmas, which induce low emotional engagement after sleep deprivation, although the willingness to accept moral violations is not affected. This suggests that one night of sleep loss selectively influences the response speed only for moral impersonal dilemmas, probably due to disinhibition processes. The quality of moral judgment dilemmas does not seem to be easily influenced by a single night of sleep deprivation, but only by a longer lack of sleep.

  14. The unrested resting brain: sleep deprivation alters activity within the default-mode network.

    PubMed

    Gujar, Ninad; Yoo, Seung-Schik; Hu, Peter; Walker, Matthew P

    2010-08-01

    The sleep-deprived brain has principally been characterized by examining dysfunction during cognitive task performance. However, far less attention has been afforded the possibility that sleep deprivation may be as, if not more, accurately characterized on the basis of abnormal resting-state brain activity. Here we report that one night of sleep deprivation significantly disrupts the canonical signature of task-related deactivation, resulting in a double dissociation within anterior as well as posterior midline regions of the default network. Indeed, deactivation within these regions alone discriminated sleep-deprived from sleep-control subjects with a 93% degree of sensitivity and 92% specificity. In addition, the relative balance of deactivation within these default nodes significantly correlated with the amount of prior sleep in the control group (and not extended time awake in the deprivation group). Therefore, the stability and the balance of task-related deactivation in key default-mode regions may be dependent on prior sleep, such that a lack thereof disrupts this signature pattern of brain activity, findings that may offer explanatory insights into conditions associated with sleep loss at both a clinical as well as societal level.

  15. [The effects of sleep deprivation on sleepiness, performance, stress and immune system].

    PubMed

    2009-01-01

    Sleep loss has been a common practice in modern society. However, it has been only recently that the effects of sleep loss on human health have received more attention. This review summarizes the experimental findings of the effects of total and partial sleep deprivation on stress hormones and pro-inflammatory cytokines. Specifically, studies have consistently demonstrated that total or partial sleep loss is associated with increased sleepiness and decreased performance and elevation of pro-inflammatory cytokines, i. e., IL-6 and TNF-alpha, which have been proposed as mediators of excessive daytime sleepiness and cardiometabolic morbidity in humans. In addition, non-stressful sleep loss is not associated with elevation of cortisol, the end-product of the hypothalamic-pituitary-adrenal (HPA) axis. Also, alertness and performance measured with objective tests (Multiple Sleep Latency Test and Performance Vigilance Test) are significantly impaired following total or partial sleep loss. Furthermore, napping or extended sleep have been shown to decrease sleepiness, improve performance and cause beneficial changes in cortisol and IL-6 secretion. Collectively, these studies show that sleep loss has adverse effects on alertness, performance and inflammation markers suggesting that insufficient sleep may influence health and longevity in a negative manner. On the other hand it appears that more sleep either in the form of napping or extended sleep may protect from these adverse effects of sleep loss.

  16. Effects of food or sleep deprivation during civilian survival training on clinical chemistry variables.

    PubMed

    Ståhle, Lars; Granström, Elisabeth; Ljungdahl Ståhle, Ewa; Isaksson, Sven; Samuelsson, Anders; Rudling, Mats; Sepp, Harry

    2013-06-01

    To describe clinical chemistry and weight changes after short-term food or sleep deprivation or multiple deprivations during civilian survival training. Data from one baseline-controlled two-period crossover study designed to compare sleep deprivation for up to 50 hours with food deprivation for up to 66 hours (n = 12) and data from regular multiple-deprivations survival training comparing participants (n = 33) with nondeprived instructors (n = 10). Food deprivation was associated with decreased body weight, blood glucose, serum triglycerides, sodium, chloride, and urine pH, and there were increases in blood and urine ketones and serum free fatty acids. Sleep deprivation was associated with a minor decrease in hemoglobin and erythrocyte particle count and volume fraction and an increase in leukocytes. The clinical chemistry and body weight changes associated with food deprivation were qualitatively similar to those observed in fasting obese patients but developed quicker in the survival training setting. Sleep deprivation had few effects on the clinical chemistry profile except for hematological variables. Physicians evaluating clinical chemistry data from patients subjected to short-term food or sleep deprivation should take the physiological state into account in their assessment. Copyright © 2013 Wilderness Medical Society. Published by Elsevier Inc. All rights reserved.

  17. Gender Differences in Sleep Deprivation Effects on Risk and Inequality Aversion: Evidence from an Economic Experiment

    PubMed Central

    Ferrara, Michele; Bottasso, Anna; Tempesta, Daniela; Carrieri, Marika; De Gennaro, Luigi; Ponti, Giovanni

    2015-01-01

    Excessive working hours—even at night—are becoming increasingly common in our modern 24/7 society. The prefrontal cortex (PFC) is particularly vulnerable to the effects of sleep loss and, consequently, the specific behaviors subserved by the functional integrity of the PFC, such as risk-taking and pro-social behavior, may be affected significantly. This paper seeks to assess the effects of one night of sleep deprivation on subjects’ risk and social preferences, which are probably the most explored behavioral domains in the tradition of Experimental Economics. This novel cross-over study employs thirty-two university students (gender-balanced) participating to 2 counterbalanced laboratory sessions in which they perform standard risk and social preference elicitation protocols. One session was after one night of undisturbed sleep at home, and the other was after one night of sleep deprivation in the laboratory. Sleep deprivation causes increased sleepiness and decreased alertness in all subjects. After sleep loss males make riskier decisions compared to the rested condition, while females do the opposite. Females likewise show decreased inequity aversion after sleep deprivation. As for the relationship between cognitive ability and economic decisions, sleep deprived individuals with higher cognitive reflection show lower risk aversion and more altruistic behavior. These results show that one night of sleep deprivation alters economic behavior in a gender-sensitive way. Females’ reaction to sleep deprivation, characterized by reduced risky choices and increased egoism compared to males, may be related to intrinsic psychological gender differences, such as in the way men and women weigh up probabilities in their decision-making, and/or to the different neurofunctional substrate of their decision-making. PMID:25793869

  18. Gender differences in sleep deprivation effects on risk and inequality aversion: evidence from an economic experiment.

    PubMed

    Ferrara, Michele; Bottasso, Anna; Tempesta, Daniela; Carrieri, Marika; De Gennaro, Luigi; Ponti, Giovanni

    2015-01-01

    Excessive working hours--even at night--are becoming increasingly common in our modern 24/7 society. The prefrontal cortex (PFC) is particularly vulnerable to the effects of sleep loss and, consequently, the specific behaviors subserved by the functional integrity of the PFC, such as risk-taking and pro-social behavior, may be affected significantly. This paper seeks to assess the effects of one night of sleep deprivation on subjects' risk and social preferences, which are probably the most explored behavioral domains in the tradition of Experimental Economics. This novel cross-over study employs thirty-two university students (gender-balanced) participating to 2 counterbalanced laboratory sessions in which they perform standard risk and social preference elicitation protocols. One session was after one night of undisturbed sleep at home, and the other was after one night of sleep deprivation in the laboratory. Sleep deprivation causes increased sleepiness and decreased alertness in all subjects. After sleep loss males make riskier decisions compared to the rested condition, while females do the opposite. Females likewise show decreased inequity aversion after sleep deprivation. As for the relationship between cognitive ability and economic decisions, sleep deprived individuals with higher cognitive reflection show lower risk aversion and more altruistic behavior. These results show that one night of sleep deprivation alters economic behavior in a gender-sensitive way. Females' reaction to sleep deprivation, characterized by reduced risky choices and increased egoism compared to males, may be related to intrinsic psychological gender differences, such as in the way men and women weigh up probabilities in their decision-making, and/or to the different neurofunctional substrate of their decision-making.

  19. Sleep deprivation worsens inflammation and delays recovery in a mouse model of colitis.

    PubMed

    Tang, Yueming; Preuss, Fabian; Turek, Fred W; Jakate, Shriram; Keshavarzian, Ali

    2009-06-01

    We recently showed that patients with inflammatory bowel disease (IBD) report significantly more sleep disturbances. To determine whether disrupted sleep can affect the severity of inflammation and the course of IBD, we used an animal model of colonic inflammation to determine the effects of acute and chronic intermittent sleep deprivation on the severity of colonic inflammation and tissue damage in colitis and recovery from this damage. Acute sleep deprivation (ASD) consisted of 24h of forced locomotor activity in a mechanical wheel rotating at a constant speed. Chronic intermittent sleep deprivation (CISD) consisted of an acute sleep deprivation episode, followed by additional sleep deprivation periods in the wheel for 6h every other day throughout the 10day study period. To induce colitis, mice were given 2% dextran sodium sulfate (DSS) in their daily drinking water for 7days. The development and severity of colitis were monitored by measuring weight loss and tissue myeloperoxidase (MPO) activity daily and colon histology scores 10days after initiation of colitis. ASD or CISD did not cause colonic inflammation in vehicle-treated mice. Changes in daily body weight, tissue MPO levels and colon histopathology score were similar between mice that were sleep deprived and controls. Daily DSS ingestion caused colitis in mice. ASD worsened colonic inflammation: tissue MPO levels in ASD/DSS-treated mice were significantly higher than in DSS-treated mice that were not sleep deprived. However, the worsening of colonic inflammation by ASD was not enough to exacerbate clinical manifestations of colitis such as weight loss. In contrast, the deleterious effects of CISD were severe enough to cause worsening of histological and clinical manifestations of colitis. The deleterious effects of sleep deprivation on severity of colitis appeared to be due to both increased colonic inflammation and a decrease in the ability of mice to recover from DSS-induced colonic injury. Both acute

  20. Neurobehavioral and Cognitive Changes Induced by Sleep Deprivation in Healthy Volunteers.

    PubMed

    Cassé-Perrot, Catherine; Lanteaume, Laura; Deguil, Julie; Bordet, Régis; Auffret, Alexandra; Otten, Lisa; Blin, Olivier; Bartrés-Faz, David; Micallef, Joëlle

    2016-01-01

    To this day, the pharmacological treatment of Alzheimer's disease remains limited to the temporary stabilisation of cognitive decline and the reduction of neuropsychiatric symptoms. It is moreover with great difficulty to predict and select promising drug candidates in the early stages of the discovery and developmental process. In this context, scientists have developed new experimental paradigms to artificially induce transient cognitive impairments in healthy volunteers akin to those observed in Alzheimer's disease, i.e. the Cognitive Challenge Models. In the last decade, a great amount of literature on Sleep Deprivation was published which mainly focused on the consequences of sleep loss for public health. However, sleep deprivation paradigm may also be regarded as a cognitive challenge model. It is commonly accepted that sleep deprivation induces cognitive impairments related to a global decrease in vigilance, while in fact, there is a controversial approach related to the selective effects on cognitive functions. The identification and validation of cognitive challenge models in healthy volunteers are suitable in early clinical development of drugs to determine the 'hint of efficacy' of drug candidates. The present review aims at exploring in detail the methods, designs and cognitive paradigms used in non pharmacological sleep deprivation studies. Sleep deprivation can be induced by different methods. Probing the four main cognitive functions will allow identifying the extent to which different sleep deprivation designs selectively compromise executive function, working memory, episodic memory and attention. Findings will be discussed in line with cognitive processing levels that are required according to the tasks.

  1. Effects of 24-h and 36-h sleep deprivation on human postural control and adaptation.

    PubMed

    Patel, M; Gomez, S; Berg, S; Almbladh, P; Lindblad, J; Petersen, H; Magnusson, M; Johansson, R; Fransson, P A

    2008-02-01

    This study investigated whether human postural stability and adaptation were affected by sleep deprivation and the relationship between motor performance and subjective scores of sleepiness (visuo-anlogue sleepiness scores, VAS). Postural stability and subjective sleepiness were examined in 18 healthy subjects (mean age 23.8 years) following 24 and 36 h of continued wakefulness, ensured by portable EEG recordings, and compared to a control test where the assessments were made after a normal night of sleep. The responses were assessed using posturography with eyes open and closed, and vibratory proprioceptive stimulations were used to challenge postural control. Postural control was significantly affected after 24 h of sleep deprivation both in anteroposterior and in lateral directions, but less so after 36 h. Subjective VAS scores showed poor correlation with indicators of postural control performance. The clearest evidence that sleep deprivation decreased postural control was the reduction of adaptation. Also several near falls after 2-3 min during the posturographic tests showed that sleep deprivation might affect stability through momentary lapses of attention. Access to vision, somewhat, but not entirely reduced the effect of sleep deprivation. In conclusion, sleep deprivation can be a contributing factor to decreased postural control and falls.

  2. L-carnitine prevents memory impairment induced by chronic REM-sleep deprivation.

    PubMed

    Alzoubi, Karem H; Rababa'h, Abeer M; Owaisi, Amani; Khabour, Omar F

    2017-05-01

    Sleep deprivation (SD) negatively impacts memory, which was related to oxidative stress induced damage. L-carnitine is a naturally occurring compound, synthesized endogenously in mammalian species and known to possess antioxidant properties. In this study, the effect of L-carnitine on learning and memory impairment induced by rapid eye movement sleep (REM-sleep) deprivation was investigated. REM-sleep deprivation was induced using modified multiple platform model (8h/day, for 6 weeks). Simultaneously, L-carnitine was administered (300mg/kg/day) intraperitoneally for 6 weeks. Thereafter, the radial arm water maze (RAWM) was used to assess spatial learning and memory. Additionally, the hippocampus levels of antioxidant biomarkers/enzymes: reduced glutathione (GSH), oxidized glutathione (GSSG), GSH/GSSG ratio, glutathione peroxidase (GPx), catalase, and superoxide dismutase (SOD) and thiobarbituric acid reactive substance (TBARS) were assessed. The results showed that chronic REM-sleep deprivation impaired both short- and long-term memory (P<0.05), whereas L-carnitine treatment protected against this effect. Furthermore, L-carnitine normalized chronic REM-sleep deprivation induced reduction in the hippocampus ratio of GSH/GSSG, activity of catalase, GPx, and SOD. No change was observed in TBARS among tested groups (P>0.05). In conclusion, chronic REM-sleep deprivation induced memory impairment, and treatment with L-carnitine prevented this impairment through normalizing antioxidant mechanisms in the hippocampus. Copyright © 2017 Elsevier Inc. All rights reserved.

  3. Chronic caffeine treatment prevents sleep deprivation-induced impairment of cognitive function and synaptic plasticity.

    PubMed

    Alhaider, Ibrahim A; Aleisa, Abdulaziz M; Tran, Trinh T; Alzoubi, Karem H; Alkadhi, Karim A

    2010-04-01

    This study was undertaken to provide a detailed account of the effect of chronic treatment with a small dose of caffeine on the deleterious effects of sleep loss on brain function in rats. We investigated the effects of chronic (4 weeks) caffeine treatment (0.3 g/L in drinking water) on memory impairment in acutely (24 h) sleep-deprived adult male Wistar rats. Sleep deprivation was induced using the modified multiple platform model. The effects of caffeine on sleep deprivation-induced hippocampus-dependent learning and memory deficits were studied by 3 approaches: learning and memory performance in the radial arm water maze task, electrophysiological recording of early long-term potentiation (E-LTP) in area CA1 of the hippocampus, and levels of memory- and synaptic plasticity-related signaling molecules after E-LTP induction. The results showed that chronic caffeine treatment prevented impairment of hippocampus-dependent learning, shortterm memory and E-LTP of area CA1 in the sleep-deprived rats. In correlation, chronic caffeine treatment prevented sleep deprivation-associated decrease in the levels of phosphorylated calcium/calmodulin-dependent protein kinase II (P-CaMKII) during expression of E-LTP. The results suggest that long-term use of a low dose of caffeine prevents impairment of short-term memory and E-LTP in acutely sleep-deprived rats.

  4. Sleep Deprivation Aggravates Median Nerve Injury-Induced Neuropathic Pain and Enhances Microglial Activation by Suppressing Melatonin Secretion

    PubMed Central

    Huang, Chun-Ta; Chiang, Rayleigh Ping-Ying; Chen, Chih-Li; Tsai, Yi-Ju

    2014-01-01

    Study Objectives: Sleep deprivation is common in patients with neuropathic pain, but the effect of sleep deprivation on pathological pain remains uncertain. This study investigated whether sleep deprivation aggravates neuropathic symptoms and enhances microglial activation in the cuneate nucleus (CN) in a median nerve chronic constriction injury (CCI) model. Also, we assessed if melatonin supplements during the sleep deprived period attenuates these effects. Design: Rats were subjected to sleep deprivation for 3 days by the disc-on-water method either before or after CCI. In the melatonin treatment group, CCI rats received melatonin supplements at doses of 37.5, 75, 150, or 300 mg/kg during sleep deprivation. Melatonin was administered at 23:00 once a day. Participants: Male Sprague-Dawley rats, weighing 180-250 g (n = 190), were used. Measurements: Seven days after CCI, behavioral testing was conducted, and immunohistochemistry, immunoblotting, and enzyme-linked immunosorbent assay were used for qualitative and quantitative analyses of microglial activation and measurements of proinflammatory cytokines. Results: In rats who underwent post-CCI sleep deprivation, microglia were more profoundly activated and neuropathic pain was worse than those receiving pre-CCI sleep deprivation. During the sleep deprived period, serum melatonin levels were low over the 24-h period. Administration of melatonin to CCI rats with sleep deprivation significantly attenuated activation of microglia and development of neuropathic pain, and markedly decreased concentrations of proinflammatory cytokines. Conclusions: Sleep deprivation makes rats more vulnerable to nerve injury-induced neuropathic pain, probably because of associated lower melatonin levels. Melatonin supplements to restore a circadian variation in melatonin concentrations during the sleep deprived period could alleviate nerve injury-induced behavioral hypersensitivity. Citation: Huang CT, Chiang RP, Chen CL, Tsai YJ. Sleep

  5. Sleep Deprivation Alters Valuation Signals in the Ventromedial Prefrontal Cortex

    PubMed Central

    Libedinsky, Camilo; Smith, David V.; Teng, Chieh Schen; Namburi, Praneeth; Chen, Vanessa W.; Huettel, Scott A.; Chee, Michael W. L.

    2011-01-01

    Even a single night of total sleep deprivation (SD) can have dramatic effects on economic decision making. Here we tested the novel hypothesis that SD influences economic decisions by altering the valuation process. Using functional magnetic resonance imaging we identified value signals related to the anticipation and the experience of monetary and social rewards (attractive female faces). We then derived decision value signals that were predictive of each participant’s willingness to exchange money for brief views of attractive faces in an independent market task. Strikingly, SD altered decision value signals in ventromedial prefrontal cortex (VMPFC) in proportion to the corresponding change in economic preferences. These changes in preference were independent of the effects of SD on attention and vigilance. Our results provide novel evidence that signals in VMPFC track the current state of the individual, and thus reflect not static but constructed preferences. PMID:22028686

  6. Some measures to reduce effects of prolonged sleep deprivation.

    PubMed

    Lagarde, D; Batejat, D

    1995-01-01

    Prolonged sleep deprivation is an exceptional situation, encountered in special environments such as sports, civilian and military, and which induces deficits in vigilance and performance. Among the array of measures which may be used to counteract these effects, the authors described a protocol using the combination of small naps, and administration of a pharmacological aid. A detailed description of advantages and drawbacks of each one of these measures is given, illustrated by several examples extracted from different studies. Four aspects of pharmacological aid are reviewed: the effects of amphetamines and amphetamine-like substances, caffeine, eugregoric substances, and the effect of the association small nap + eugregoric substances. The use of these various aids is discussed, and findings show that each one of them finds an application in a specific context.

  7. The Impact of Partial Sleep Deprivation on Moral Reasoning in Military Officers

    PubMed Central

    Olsen, Olav Kjellevold; Pallesen, Ståle; Eid, Jarle

    2010-01-01

    Study Objectives: The present study explores the impact of long-term partial sleep deprivation on the activation of moral justice schemas, which are suggested to play a prominent role in moral reasoning and the formation of moral judgments and behavior. Design: Participants judged 5 dilemmas in rested and partially sleep deprived condition, in a counterbalanced design. Setting: In classroom and field exercises at the Norwegian Naval Academy and the Norwegian Army Academy. Participants: Seventy-one Norwegian naval and army officer cadets. Measurements and Results: The results showed that the officers' ability to conduct mature and principally oriented moral reasoning was severely impaired during partial sleep deprivation compared to the rested state. At the same time, the officers became substantially more rules-oriented in the sleep deprived condition, while self-oriented moral reasoning did not change. Interaction effects showed that those officers who displayed high levels of mature moral reasoning (n = 24) in the rested condition, lost much of this capacity during sleep deprivation in favor of a strong increase in rules-oriented moral reasoning as well as self-orientation. Conversely, officers at low levels of mature moral reasoning in rested condition (n = 23) were unaffected by sleep deprivation. Conclusions: The present data show that long-term partial sleep deprivation has an impact on the activation of moral justice schemas, and consequently on the ability to make moral justice judgments. Citation: Olsen OK; Pallesen S; Eid J. The impact of partial sleep deprivation on moral reasoning in military officers. SLEEP 2010;33(8):1086-1090. PMID:20815191

  8. Hormone treatment gives no benefit against cognitive changes caused by acute sleep deprivation in postmenopausal women.

    PubMed

    Karakorpi, Maija; Alhola, Paula; Urrila, Anna Sofia; Kylmälä, Mervi; Portin, Raija; Kalleinen, Nea; Polo-Kantola, Päivi

    2006-09-01

    The objective was to evaluate whether hormone therapy (HT) gives any benefit against the possible impairment of cognitive performance when challenged by acute sleep deprivation. Twenty postmenopausal women volunteered (age range 59-72 years, mean=64.4 years, SD=4.4): 10 HT users and 10 nonusers. Eleven young women served as a control group for the cognitive age effect (age range 20-26 years, mean age 23.1 years, SD=1.6). The subjects spent four consecutive nights at the sleep laboratory and were exposed to acute sleep deprivation of 40 h. Measures of attention (reaction speed and vigilance), alertness, and mood were administered every 2 h during the daytime and every hour during the sleep deprivation night. Postmenopausal women performed slower than young controls, whereas young controls made more errors. In HT users, the recovery night did not fully restore the performance in the simple and two-choice reaction time tasks, but in nonusers it did so. Sleep deprivation had a detrimental, yet reversible effect on vigilance in all groups. In all groups, sleepiness started to increase after 15 h of sleep deprivation and remained elevated in the morning after the recovery night. Prolonged wakefulness or HT had no effect on mood. In conclusion, sleep deprivation impaired cognitive performance in postmenopausal as well as young women. Postmenopausal women kept up their performance at the expense of reaction speed and young women at the expense of accuracy. One night was not enough for HT users to recover from sleep deprivation. Thus, HT gave no benefit in maintaining the attention and alertness during sleep deprivation.

  9. Lack of estradiol modulation of sleep deprivation-induced c-Fos in the rat brain.

    PubMed

    Mashoodh, Rahia; Stamp, Jennifer A; Wilkinson, Michael; Rusak, Benjamin; Semba, Kazue

    2008-11-28

    Women recover from sleep deprivation more efficiently than men, but the mechanism for this difference is unknown. Effects of estrogen on sleep suggest that it could play a role, but the brain targets on which estrogen may act to have this effect have not been identified. Sleep deprivation increases levels of the immediate-early gene protein c-Fos in selected brain regions, but it is unknown whether estrogen modulates this response. We investigated the influence of different levels of exogenous estradiol on the c-Fos response to sleep deprivation in ovariectomized female rats. Female rats were treated with low or high levels of estradiol (mimicking diestrous and proestrous levels, respectively) delivered via subcutaneous silastic tubes. Control ovariectomized females and sham-operated males were implanted with tubes filled with cholesterol. One week after surgery, half of the rats underwent a 3 h period of sleep deprivation during the light phase in a motorized Wahmann activity wheel that rotated constantly at a slow speed, while half were confined to fixed wheels. Immediately after sleep deprivation, animals were killed and their brains processed to detect c-Fos using immunohistochemistry. Sleep deprivation increased the number of c-Fos positive cells in a number of brain areas, including the caudate putamen, medial preoptic area, perifornical hypothalamus, and anterior paraventricular thalamic nucleus. Other areas, including the suprachiasmatic nucleus, posterior paraventricular hypothalamic nucleus, posterior paraventricular thalamic nucleus, arcuate nucleus, and central amygdala, did not respond to 3 h sleep deprivation with a significant increase in c-Fos levels. Levels of c-Fos induced in the selected brain regions by sleep deprivation were not modulated by estrogen levels, nor by sex.

  10. The effect of a REM sleep deprivation procedure on different aspects of memory function in humans.

    PubMed

    Saxvig, Ingvild West; Lundervold, Astri Johansen; Grønli, Janne; Ursin, Reidun; Bjorvatn, Bjørn; Portas, Chiara Maria

    2008-03-01

    Previous studies have suggested that memory is dependent on the occurrence of REM sleep. Research has mainly focused on two distinct types of memory function, declarative and procedural, and it seems that the latter may more directly depend on REM sleep. Memory consolidation has been more investigated than acquisition, maintenance, and recall, despite the fact that sleep may affect flow of information into/from storage. Moreover, tests have often been limited to stimuli within only one modality (usually visual or verbal). This study aimed to clarify the role of REM sleep in memory by investigating aspects of memory function, processing, and modality in the same experimental setting. Tests of acquisition and consolidation of multiple aspects of memory function within the visual and verbal modalities were administrated to subjects before and after REM sleep deprivation. Results show that test performance was not affected by REM sleep deprivation.

  11. Essential Roles of GABA Transporter-1 in Controlling Rapid Eye Movement Sleep and in Increased Slow Wave Activity after Sleep Deprivation

    PubMed Central

    Xu, Xin-Hong; Qu, Wei-Min; Bian, Min-Juan; Huang, Fang; Fei, Jian; Urade, Yoshihiro; Huang, Zhi-Li

    2013-01-01

    GABA is the major inhibitory neurotransmitter in the mammalian central nervous system that has been strongly implicated in the regulation of sleep. GABA transporter subtype 1 (GAT1) constructs high affinity reuptake sites for GABA and regulates GABAergic transmission in the brain. However, the role of GAT1 in sleep-wake regulation remains elusive. In the current study, we characterized the spontaneous sleep-wake cycle and responses to sleep deprivation in GAT1 knock-out (KO) mice. GAT1 KO mice exhibited dominant theta-activity and a remarkable reduction of EEG power in low frequencies across all vigilance stages. Under baseline conditions, spontaneous rapid eye movement (REM) sleep of KO mice was elevated both during the light and dark periods, and non-REM (NREM) sleep was reduced during the light period only. KO mice also showed more state transitions from NREM to REM sleep and from REM sleep to wakefulness, as well as more number of REM and NREM sleep bouts than WT mice. During the dark period, KO mice exhibited more REM sleep bouts only. Six hours of sleep deprivation induced rebound increases in NREM and REM sleep in both genotypes. However, slow wave activity, the intensity component of NREM sleep was briefly elevated in WT mice but remained completely unchanged in KO mice, compared with their respective baselines. These results indicate that GAT1 plays a critical role in the regulation of REM sleep and homeostasis of NREM sleep. PMID:24155871

  12. Essential roles of GABA transporter-1 in controlling rapid eye movement sleep and in increased slow wave activity after sleep deprivation.

    PubMed

    Xu, Xin-Hong; Qu, Wei-Min; Bian, Min-Juan; Huang, Fang; Fei, Jian; Urade, Yoshihiro; Huang, Zhi-Li

    2013-01-01

    GABA is the major inhibitory neurotransmitter in the mammalian central nervous system that has been strongly implicated in the regulation of sleep. GABA transporter subtype 1 (GAT1) constructs high affinity reuptake sites for GABA and regulates GABAergic transmission in the brain. However, the role of GAT1 in sleep-wake regulation remains elusive. In the current study, we characterized the spontaneous sleep-wake cycle and responses to sleep deprivation in GAT1 knock-out (KO) mice. GAT1 KO mice exhibited dominant theta-activity and a remarkable reduction of EEG power in low frequencies across all vigilance stages. Under baseline conditions, spontaneous rapid eye movement (REM) sleep of KO mice was elevated both during the light and dark periods, and non-REM (NREM) sleep was reduced during the light period only. KO mice also showed more state transitions from NREM to REM sleep and from REM sleep to wakefulness, as well as more number of REM and NREM sleep bouts than WT mice. During the dark period, KO mice exhibited more REM sleep bouts only. Six hours of sleep deprivation induced rebound increases in NREM and REM sleep in both genotypes. However, slow wave activity, the intensity component of NREM sleep was briefly elevated in WT mice but remained completely unchanged in KO mice, compared with their respective baselines. These results indicate that GAT1 plays a critical role in the regulation of REM sleep and homeostasis of NREM sleep.

  13. Effect of sleep deprivation on rhythms of clock gene expression and melatonin in humans.

    PubMed

    Ackermann, Katrin; Plomp, Rosina; Lao, Oscar; Middleton, Benita; Revell, Victoria L; Skene, Debra J; Kayser, Manfred

    2013-08-01

    This study investigated the impact of sleep deprivation on the human circadian system. Plasma melatonin and cortisol levels and leukocyte expression levels of 12 genes were examined over 48 h (sleep vs. no-sleep nights) in 12 young males (mean±SD: 23±5 yrs). During one night of total sleep deprivation, BMAL1 expression was suppressed, the heat shock gene HSPA1B expression was induced, and the amplitude of the melatonin rhythm increased, whereas other high-amplitude clock gene rhythms (e.g., PER1-3, REV-ERBα) remained unaffected. These data suggest that the core clock mechanism in peripheral oscillators is compromised during acute sleep deprivation.

  14. Sleep homeostatic pressure and PER3 VNTR gene polymorphism influence antidepressant response to sleep deprivation in bipolar depression.

    PubMed

    Dallaspezia, Sara; Locatelli, Clara; Lorenzi, Cristina; Pirovano, Adele; Colombo, Cristina; Benedetti, Francesco

    2016-03-01

    Combined Total sleep deprivation (TSD) and light therapy (LT) cause a rapid improvement in bipolar depression which has been hypothesized to be paralleled by changes in sleep homeostasis. Recent studies showed that bipolar patients had lower changes of EEG theta power after sleep and responders to antidepressant TSD+LT slept less and showed a lower increase of EEG theta power then non-responders. A polymorphism in PER3 gene has been associated with diurnal preference, sleep structure and homeostatic response to sleep deprivation in healthy subjects. We hypothesized that the individual variability in the homeostatic response to TSD could be a correlate of antidepressant response and be influenced by genetic factors. We administered three TSD+LT cycles to bipolar depressed patients. Severity of depression was rated on Hamilton Depression Rating Scale. Actigraphic recordings were performed in a group of patients. PER3 polymorphism influenced changes in total sleep time (F=2.24; p=0.024): while PER3(4/4) and PER3(4/5) patients showed a reduction in it after treatment, PER3(5/5) subjects showed an increase of about 40min, suggesting a higher homeostatic pressure. The same polymorphism influenced the change of depressive symptomatology during treatment (F=3.72; p=0.028). Sleep information was recorded till the day after the end of treatment: a longer period of observation could give more information about the possible maintenance of allostatic adaptation. A higher sleep homeostatic pressure reduced the antidepressant response to TSD+LT, while an allostatic adaptation to sleep loss was associated with better response. This process seems to be under genetic control. Copyright © 2015 Elsevier B.V. All rights reserved.

  15. Sustained Attention Performance during Sleep Deprivation Associates with Instability in Behavior and Physiologic Measures at Baseline

    PubMed Central

    Chua, Eric Chern-Pin; Yeo, Sing-Chen; Lee, Ivan Tian-Guang; Tan, Luuan-Chin; Lau, Pauline; Cai, Shiwei; Zhang, Xiaodong; Puvanendran, Kathiravelu; Gooley, Joshua J.

    2014-01-01

    Study Objectives: To identify baseline behavioral and physiologic markers that associate with individual differences in sustained attention during sleep deprivation. Design: In a retrospective study, ocular, electrocardiogram, and electroencephalogram (EEG) measures were compared in subjects who were characterized as resilient (n = 15) or vulnerable (n = 15) to the effects of total sleep deprivation on sustained attention. Setting: Chronobiology and Sleep Laboratory, Duke-NUS Graduate Medical School Singapore. Participants: Healthy volunteers aged 22-32 years from the general population. Interventions: Subjects were kept awake for at least 26 hours under constant environmental conditions. Every 2 hours, sustained attention was assessed using a 10-minute psychomotor vigilance task (PVT). Measurements and Results: During baseline sleep and recovery sleep, EEG slow wave activity was similar in resilient versus vulnerable subjects, suggesting that individual differences in vulnerability to sleep loss were not related to differences in homeostatic sleep regulation. Rather, irrespective of time elapsed since wake, subjects who were vulnerable to sleep deprivation exhibited slower and more variable PVT response times, lower and more variable heart rate, and higher and more variable EEG spectral power in the theta frequency band (6.0-7.5 Hz). Conclusions: Performance decrements in sustained attention during sleep deprivation associate with instability in behavioral and physiologic measures at baseline. Small individual differences in sustained attention that are present at baseline are amplified during prolonged wakefulness, thus contributing to large between-subjects differences in performance and sleepiness. Citation: Chua EC; Yeo SC; Lee IT; Tan LC; Lau P; Cai S; Zhang X; Puvanendran K; Gooley JJ. Sustained attention performance during sleep deprivation associates with instability in behavior and physiologic measures at baseline. SLEEP 2014;37(1):27-39. PMID:24470693

  16. Blood-gene expression reveals reduced circadian rhythmicity in individuals resistant to sleep deprivation.

    PubMed

    Arnardottir, Erna S; Nikonova, Elena V; Shockley, Keith R; Podtelezhnikov, Alexei A; Anafi, Ron C; Tanis, Keith Q; Maislin, Greg; Stone, David J; Renger, John J; Winrow, Christopher J; Pack, Allan I

    2014-10-01

    To address whether changes in gene expression in blood cells with sleep loss are different in individuals resistant and sensitive to sleep deprivation. Blood draws every 4 h during a 3-day study: 24-h normal baseline, 38 h of continuous wakefulness and subsequent recovery sleep, for a total of 19 time-points per subject, with every 2-h psychomotor vigilance task (PVT) assessment when awake. Sleep laboratory. Fourteen subjects who were previously identified as behaviorally resistant (n = 7) or sensitive (n = 7) to sleep deprivation by PVT. Thirty-eight hours of continuous wakefulness. We found 4,481 unique genes with a significant 24-h diurnal rhythm during a normal sleep-wake cycle in blood (false discovery rate [FDR] < 5%). Biological pathways were enriched for biosynthetic processes during sleep. After accounting for circadian effects, two genes (SREBF1 and CPT1A, both involved in lipid metabolism) exhibited small, but significant, linear changes in expression with the duration of sleep deprivation (FDR < 5%). The main change with sleep deprivation was a reduction in the amplitude of the diurnal rhythm of expression of normally cycling probe sets. This reduction was noticeably higher in behaviorally resistant subjects than sensitive subjects, at any given P value. Furthermore, blood cell type enrichment analysis showed that the expression pattern difference between sensitive and resistant subjects is mainly found in cells of myeloid origin, such as monocytes. Individual differences in behavioral effects of sleep deprivation are associated with differences in diurnal amplitude of gene expression for genes that show circadian rhythmicity. © 2014 Associated Professional Sleep Societies, LLC.

  17. Energy Stores Are Not Altered by Long-Term Partial Sleep Deprivation in Drosophila melanogaster

    PubMed Central

    Harbison, Susan T.; Sehgal, Amita

    2009-01-01

    Recent human studies reveal a widespread association between short sleep and obesity. Two hypotheses, which are not mutually exclusive, might explain this association. First, genetic factors that reduce endogenous sleep times might also impact energy stores, an assertion that we confirmed in a previous study. Second, metabolism may be altered by chronic partial sleep deprivation. Here we address the second assertion by measuring the impact of long-term partial sleep deprivation on energy stores using Drosophila as a model. We subjected flies to long-term partial sleep deprivation via two different methods: a mechanical stimulus and a light stimulus. We then measured whole-body triglycerides and glycogen, two important sources of energy for the fly, and compared them to un-stimulated controls. We also measured changes in energy stores in response to a random circadian clock shift. Sex and line-dependent alterations in glycogen and/or triglyceride levels occurred in response to the circadian clock shift and in flies subjected to a single night of sleep deprivation using light. Thus, consistent with previous studies, our findings suggest that acute sleep loss and changes to the circadian clock can alter metabolism. Significant changes in energy stores were also observed when flies were subjected to chronic sleep loss via the mechanical stimulus, although not the light stimulus. Interestingly, mechanical stimulation resulted in the same change in energy stores even when it was not associated with sleep deprivation, suggesting that the changes are caused by stress rather than sleep loss. These findings emphasize the importance of taking stress into account when evaluating the relationship between sleep loss and metabolism. PMID:19593430

  18. Pemoline and Methylphenidate: Interaction With Mood, Sleepiness, and Cognitive Performance During 64 Hours of Sleep Deprivation

    DTIC Science & Technology

    1992-07-07

    AD-A256 601 PEMOLINE AND METHYLPHENIDATE : INTERACTION WITH MOOD, SLEEP:7NESS, AND COGNITIVE PERFORMANCE DURING 64 HOURS OF SLEEP DEPRIVATION H...COMMAND BETHESDA, MARYLAND Pemoline and Methylphenidate : Interaction with Mood, Sleepiness, and Cognitive Performance During 64 Hours of Sleep...Report No. 90-41. ABSTRACT Moderate doses of the stimulant drugs methylphenidate (10 mg every 6 hr x 8 doses) or pemoline (37.5 mg every 12 hr x 4 doses

  19. Mapping Slow Waves by EEG Topography and Source Localization: Effects of Sleep Deprivation.

    PubMed

    Bersagliere, Alessia; Pascual-Marqui, Roberto D; Tarokh, Leila; Achermann, Peter

    2017-10-05

    Slow waves are a salient feature of the electroencephalogram (EEG) during non-rapid eye movement (non-REM) sleep. The aim of this study was to assess the topography of EEG power and the activation of brain structures during slow wave sleep under normal conditions and after sleep deprivation. Sleep EEG recordings during baseline and recovery sleep after 40 h of sustained wakefulness were analyzed (eight healthy young men, 27 channel EEG). Power maps were computed for the first non-REM sleep episode (where sleep pressure is highest) in baseline and recovery sleep, at frequencies between 0.5 and 2 Hz. Power maps had a frontal predominance at all frequencies between 0.5 and 2 Hz. An additional occipital focus of activity was observed below 1 Hz. Power maps ≤ 1 Hz were not affected by sleep deprivation, whereas an increase in power was observed in the maps ≥ 1.25 Hz. Based on the response to sleep deprivation, low-delta (0.5-1 Hz) and mid-delta activity (1.25-2 Hz) were dissociated. Electrical sources within the cortex of low- and mid-delta activity were estimated using eLORETA. Source localization revealed a predominantly frontal distribution of activity for low-delta and mid-delta activity. Sleep deprivation resulted in an increase in source strength only for mid-delta activity, mainly in parietal and frontal regions. Low-delta activity dominated in occipital and temporal regions and mid-delta activity in limbic and frontal regions independent of the level of sleep pressure. Both, power maps and electrical sources exhibited trait-like aspects.

  20. Urinary Metabolite Profiles May be Predictive of Cognitive Performance Under Conditions of Acute Sleep Deprivation

    DTIC Science & Technology

    2016-01-01

    A.I. Cumulative sleepiness, mood disturbance , and psychomotor vigilance performance decrements during a week of sleep restricted to 4-5 hours per...Cognitive Performance Under Conditions of Acute Sleep Deprivation 5a. CONTRACT NUMBER 5b. GRANT NUMBER 5c. PROGRAM ELEMENT NUMBER Nicholas J...and sustained actions in military and civilian operational environments typically lead to reduced sleep normally required to perform optimally

  1. Sleep in Othello

    PubMed Central

    Dimsdale, Joel E.

    2009-01-01

    Some of our best descriptions of sleep disorders come from literature. While Shakespeare is well known for his references to insomnia and sleep walking, his works also demonstrate a keen awareness of many other sleep disorders. This paper examines sleep themes in Shakespeare's play Othello. The play indicates Shakespeare's astute eye for sleep deprivation, sexual parasomnias, and effects of stress and drugs on sleep. Citation: Dimsdale JE. Sleep in Othello. J Clin Sleep Med 2009;5(3):280-281. PMID:19960651

  2. Cold Hands, Warm Feet: Sleep Deprivation Disrupts Thermoregulation and Its Association with Vigilance

    PubMed Central

    Romeijn, Nico; Verweij, Ilse M.; Koeleman, Anne; Mooij, Anne; Steimke, Rosa; Virkkala, Jussi; van der Werf, Ysbrand; Van Someren, Eus J.W.

    2012-01-01

    Study Objectives: Vigilance is affected by induced and spontaneous skin temperature fluctuations. Whereas sleep deprivation strongly affects vigilance, no previous study examined in detail its effect on human skin temperature fluctuations and their association with vigilance. Design: In a repeated-measures constant routine design, skin temperatures were assessed continuously from 14 locations while performance was assessed using a reaction time task, including eyes-open video monitoring, performed five times a day for 2 days, after a normal sleep or sleep deprivation night. Setting: Participants were seated in a dimly lit, temperature-controlled laboratory. Patients or Participants: Eight healthy young adults (five males, age 22.0 ± 1.8 yr (mean ± standard deviation)). Intervention: One night of sleep deprivation. Measurements and Results: Mixed-effect regression models were used to evaluate the effect of sleep deprivation on skin temperature gradients of the upper (ear-mastoid), middle (hand-arm), and lower (foot-leg) body, and on the association between fluctuations in performance and in temperature gradients. Sleep deprivation induced a marked dissociation of thermoregulatory skin temperature gradients, indicative of attenuated heat loss from the hands co-occurring with enhanced heat loss from the feet. Sleep deprivation moreover attenuated the association between fluctuations in performance and temperature gradients; the association was best preserved for the upper body gradient. Conclusions: Sleep deprivation disrupts coordination of fluctuations in thermoregulatory skin temperature gradients. The dissociation of middle and lower body temperature gradients may therefore be evaluated as a marker for sleep debt, and the upper body gradient as a possible aid in vigilance assessment when sleep debt is unknown. Importantly, our findings suggest that sleep deprivation affects the coordination between skin blood flow fluctuations and the baroreceptor

  3. Orexin activation precedes increased NPY expression, hyperphagia, and metabolic changes in response to sleep deprivation.

    PubMed

    Martins, Paulo José Forcina; Marques, Marina Soares; Tufik, Sergio; D'Almeida, Vânia

    2010-03-01

    Several pieces of evidence support that sleep duration plays a role in body weight control. Nevertheless, it has been assumed that, after the identification of orexins (hypocretins), the molecular basis of the interaction between sleep and energy homeostasis has been provided. However, no study has verified the relationship between neuropeptide Y (NPY) and orexin changes during hyperphagia induced by sleep deprivation. In the current study we aimed to establish the time course of changes in metabolite, endocrine, and hypothalamic neuropeptide expression of Wistar rats sleep deprived by the platform method for a distinct period (from 24 to 96 h) or sleep restricted for 21 days (SR-21d). Despite changes in the stress hormones, we found no changes in food intake and body weight in the SR-21d group. However, sleep-deprived rats had a 25-35% increase in their food intake from 72 h accompanied by slight weight loss. Such changes were associated with increased hypothalamus mRNA levels of prepro-orexin (PPO) at 24 h followed by NPY at 48 h of sleep deprivation. Conversely, sleep recovery reduced the expression of both PPO and NPY, which rapidly brought the animals to a hypophagic condition. Our data also support that sleep deprivation rapidly increases energy expenditure and therefore leads to a negative energy balance and a reduction in liver glycogen and serum triacylglycerol levels despite the hyperphagia. Interestingly, such changes were associated with increased serum levels of glucagon, corticosterone, and norepinephrine, but no effects on leptin, insulin, or ghrelin were observed. In conclusion, orexin activation accounts for the myriad changes induced by sleep deprivation, especially the hyperphagia induced under stress and a negative energy balance.

  4. Reduced Neurobehavioral Impairment from Sleep Deprivation in Older Adults: Contribution of Adenosinergic Mechanisms

    PubMed Central

    Landolt, Hans-Peter; Rétey, Julia V.; Adam, Martin

    2012-01-01

    A night without sleep is followed by enhanced sleepiness, increased low-frequency activity in the waking EEG, and reduced vigilant attention. The magnitude of these changes is highly variable among healthy individuals. Findings in young men of low and high subjective caffeine sensitivity suggest that adenosinergic mechanisms contribute to inter-individual differences in sleep deprivation-induced changes in EEG theta activity, as well as optimal performance on the psychomotor vigilance task (PVT). In comparison to young subjects, healthy adults of older age typically feel less sleepy after sleep deprivation, and show fewer response lapses, and faster reaction times on the PVT, especially in the morning after the night without sleep. We hypothesized that age-related changes in adenosine signal transmission underlie reduced vulnerability to sleep deprivation in older individuals. To test this hypothesis, the combined effects of prolonged wakefulness and the adenosine receptor antagonist, caffeine, on an antero-posterior power gradient in EEG theta activity and PVT performance were analyzed in healthy older and caffeine-insensitive and -sensitive young men. The results show that age-related differences in sleep loss-induced changes in brain rhythmic activity and neurobehavioral functions are mirrored in young individuals of low and high sensitivity to the stimulant effects of caffeine. Moreover, the effects of sleep deprivation and caffeine on regional theta power and vigilant attention are inversely correlated across older and young age groups. Genetic variants of the adenosine A2A receptor gene contribute to individual differences in neurobehavioral performance in rested and sleep deprived state, and modulate the actions of caffeine in wakefulness and sleep. Based upon this evidence, we propose that age-related differences in A2A receptor-mediated signal transduction could be involved in age-related changes in the vulnerability to acute sleep deprivation. PMID

  5. Migraine, arousal and sleep deprivation: comment on: “sleep quality, arousal and pain thresholds in migraineurs: a blinded controlled polysomnographic study”

    PubMed Central

    2013-01-01

    We discuss the hypothesis proposed by Engstrom and coworkers that Migraineurs have a relative sleep deprivation, which lowers the pain threshold and predispose to attacks. Previous data indicate that Migraineurs have a reduction of Cyclic Alternating Pattern (CAP), an essential mechanism of NREM sleep regulation which allows to dump the effect of incoming disruptive stimuli, and to protect sleep. The modifications of CAP observed in Migraineurs are similar to those observed in patients with impaired arousal (narcolepsy) and after sleep deprivation. The impairment of this mechanism makes Migraineurs more vulnerable to stimuli triggering attacks during sleep, and represents part of a more general vulnerability to incoming stimuli. PMID:23758606

  6. Sleep Deprivation Impairs the Human Central and Peripheral Nervous System Discrimination of Social Threat

    PubMed Central

    Goldstein-Piekarski, Andrea N.; Greer, Stephanie M.; Saletin, Jared M.

    2015-01-01

    Facial expressions represent one of the most salient cues in our environment. They communicate the affective state and intent of an individual and, if interpreted correctly, adaptively influence the behavior of others in return. Processing of such affective stimuli is known to require reciprocal signaling between central viscerosensory brain regions and peripheral-autonomic body systems, culminating in accurate emotion discrimination. Despite emerging links between sleep and affective regulation, the impact of sleep loss on the discrimination of complex social emotions within and between the CNS and PNS remains unknown. Here, we demonstrate in humans that sleep deprivation impairs both viscerosensory brain (anterior insula, anterior cingulate cortex, amygdala) and autonomic-cardiac discrimination of threatening from affiliative facial cues. Moreover, sleep deprivation significantly degrades the normally reciprocal associations between these central and peripheral emotion-signaling systems, most prominent at the level of cardiac-amygdala coupling. In addition, REM sleep physiology across the sleep-rested night significantly predicts the next-day success of emotional discrimination within this viscerosensory network across individuals, suggesting a role for REM sleep in affective brain recalibration. Together, these findings establish that sleep deprivation compromises the faithful signaling of, and the “embodied” reciprocity between, viscerosensory brain and peripheral autonomic body processing of complex social signals. Such impairments hold ecological relevance in professional contexts in which the need for accurate interpretation of social cues is paramount yet insufficient sleep is pervasive. PMID:26180190

  7. Sleep Deprivation Impairs the Human Central and Peripheral Nervous System Discrimination of Social Threat.

    PubMed

    Goldstein-Piekarski, Andrea N; Greer, Stephanie M; Saletin, Jared M; Walker, Matthew P

    2015-07-15

    Facial expressions represent one of the most salient cues in our environment. They communicate the affective state and intent of an individual and, if interpreted correctly, adaptively influence the behavior of others in return. Processing of such affective stimuli is known to require reciprocal signaling between central viscerosensory brain regions and peripheral-autonomic body systems, culminating in accurate emotion discrimination. Despite emerging links between sleep and affective regulation, the impact of sleep loss on the discrimination of complex social emotions within and between the CNS and PNS remains unknown. Here, we demonstrate in humans that sleep deprivation impairs both viscerosensory brain (anterior insula, anterior cingulate cortex, amygdala) and autonomic-cardiac discrimination of threatening from affiliative facial cues. Moreover, sleep deprivation significantly degrades the normally reciprocal associations between these central and peripheral emotion-signaling systems, most prominent at the level of cardiac-amygdala coupling. In addition, REM sleep physiology across the sleep-rested night significantly predicts the next-day success of emotional discrimination within this viscerosensory network across individuals, suggesting a role for REM sleep in affective brain recalibration. Together, these findings establish that sleep deprivation compromises the faithful signaling of, and the "embodied" reciprocity between, viscerosensory brain and peripheral autonomic body processing of complex social signals. Such impairments hold ecological relevance in professional contexts in which the need for accurate interpretation of social cues is paramount yet insufficient sleep is pervasive.

  8. Mood and metabolic consequences of sleep deprivation as a potential endophenotype' in bipolar disorder.

    PubMed

    Aydin, Adem; Selvi, Yavuz; Besiroglu, Lutfullah; Boysan, Murat; Atli, Abdullah; Ozdemir, Osman; Kilic, Sultan; Balaharoglu, Ragıp

    2013-09-05

    It has been commonly recognized that circadian rhythm and sleep/wake cycle are causally involved in bipolar disorder. There has been a paucity of systematic research considering the relations between sleep and mood states in bipolar disorder. The current study examines the possible influences of sleep deprivation on mood states and endocrine functions among first-degree relatives of patients with bipolar disorder and healthy controls. Blood samples were taken at two time points in the consecutive mornings at predeprivation and postdeprivation periods. Participants simultaneously completed the Profiles of Mood States at two time points after giving blood samples. Plasma T3 and TSH levels increased after total sleep deprivation in both groups. Sleep deprivation induced TSH levels were reversely associated with depression-dejection among healthy controls. A paradoxical effect was detected for only the first-degree relatives of the patients that changes in plasma cortisol levels negatively linked to depression-dejection and anger-hostility scores after total sleep deprivation. Plasma DHEA levels became correlated with vigor-activity scores after sleep deprivation among first-degree relatives of bipolar patients. On the contrary, significant associations of depression-dejection, anger-hostility, and confusion-bewilderment with the baseline plasma DHEA levels became statistically trivial in the postdeprivation period. Findings suggested that first-degree relatives of patients with bipolar disorder had completely distinct characteristics with respect to sleep deprivation induced responses in terms of associations between endocrine functions and mood states as compared to individuals whose relatives had no psychiatric problems. Considering the relationships between endocrine functions and mood states among relatives of the patients, it appears like sleep deprivation changes the receptor sensitivity which probably plays a pivotal role on mood outcomes among the first

  9. Chronic Caffeine Treatment Prevents Sleep Deprivation-Induced Impairment of Cognitive Function and Synaptic Plasticity

    PubMed Central

    Alhaider, Ibrahim A.; Aleisa, Abdulaziz M.; Tran, Trinh T.; Alzoubi, Karem H.; Alkadhi, Karim A.

    2010-01-01

    Study Objectives: This study was undertaken to provide a detailed account of the effect of chronic treatment with a small dose of caffeine on the deleterious effects of sleep loss on brain function in rats. Experimental Design: We investigated the effects of chronic (4 weeks) caffeine treatment (0.3 g/L in drinking water) on memory impairment in acutely (24 h) sleep-deprived adult male Wistar rats. Sleep deprivation was induced using the modified multiple platform model. The effects of caffeine on sleep deprivation-induced hippocampus-dependent learning and memory deficits were studied by 3 approaches: learning and memory performance in the radial arm water maze task, electrophysiological recording of early long-term potentiation (E-LTP) in area CA1 of the hippocampus, and levels of memory- and synaptic plasticity-related signaling molecules after E-LTP induction. Measurement and Results: The results showed that chronic caffeine treatment prevented impairment of hippocampus-dependent learning, short-term memory and E-LTP of area CA1 in the sleep-deprived rats. In correlation, chronic caffeine treatment prevented sleep deprivation-associated decrease in the levels of phosphorylated calcium/calmodulin-dependent protein kinase II (P-CaMKII) during expression of E-LTP. Conclusions: The results suggest that long-term use of a low dose of caffeine prevents impairment of short-term memory and E-LTP in acutely sleep-deprived rats. Citation: Alhaider IA; Aleisa AM; Tran TT; Alzoubi KH; Alkadhi KA. Chronic caffeine treatment prevents sleep deprivation-induced impairment of cognitive function and synaptic plasticity. SLEEP 2010;33(4):437-444. PMID:20394312

  10. Influence of sleep deprivation on learning among surgical house staff and medical students.

    PubMed

    Browne, B J; Van Susteren, T; Onsager, D R; Simpson, D; Salaymeh, B; Condon, R E

    1994-05-01

    Sleep deprivation as a result of in-house night call may alter capacity to learn. Surgical residents and medical students, in both sleep-deprived and rested states, read surgical journal articles and later answered questions regarding their content as a measure of ability to learn while participating in scheduled night call. Medical students (n = 35) and residents (n = 21) rotating on surgical services kept logs of hours slept during a 4-week study period. Subjects read six selected articles at separate early morning sittings during weeks 1 and 3. A multiple choice test was given 1 week after each session to assess short-term recall, and all tests were given again 3 months later to assess retention of information over the longer term. Scores were compared with the sleep data. Subjective measures of fatigue and motivation elicited from subjects also were evaluated. Sleep deprivation (4 hours or less uninterrupted sleep per night) resulted in increased fatigue and decreased motivation among medical students and residents (p < 0.05, t test). Objective scores on tests administered 1 week and 3 months after reading did not show an effect attributable to sleep deprivation (p > 0.05, t test). Sleep deprivation leads to subjective feelings of increased fatigue and decreased motivation. Residents and medical students, however, whether sleep deprived or not, obtain comparable scores on objective tests measuring both short-term and long-term retention of newly learned material. The ability to learn medically relevant information does not appear to be significantly altered by the degree of sleep deprivation associated with clinical rotations on surgical services.

  11. Caffeine and REM sleep deprivation: Effect on basal levels of signaling molecules in area CA1.

    PubMed

    Alkadhi, Karim A; Alhaider, Ibrahim A

    2016-03-01

    We have investigated the neuroprotective effect of chronic caffeine treatment on basal levels of memory-related signaling molecules in area CA1 of sleep-deprived rats. Animals in the caffeine groups were treated with caffeine in drinking water (0.3g/l) for four weeks before they were REM sleep-deprived for 24h in the Modified Multiple Platforms paradigm. Western blot analysis of basal protein levels of plasticity- and memory-related signaling molecules in hippocampal area CA1 showed significant down regulation of the basal levels of phosphorylated- and total-CaMKII, phosphorylated- and total-CREB as well as those of BDNF and CaMKIV in sleep deprived rats. All these changes were completely prevented in rats that chronically consumed caffeine. The present findings suggest an important neuroprotective property of caffeine in sleep deprivation.

  12. How does one night of sleep deprivation affect the internal clock?

    PubMed

    Casini, Laurence; Ramdani-Beauvir, Céline; Burle, Boris; Vidal, Franck

    2013-01-01

    Twelve subjects performed two temporal tasks, one explicit (Experiment 1) and one implicit (Experiment 2) after one night of sleep deprivation and after one night of normal rest. Experiment 1 involved a 1100-ms duration production task, and in Experiment 2 subjects performed a word identification task requiring implicit estimation of vowel duration (around 150 ms). One night of sleep deprivation had the same pattern of effect on explicit timing in the suprasecond range and implicit timing in the millisecond range. Specifically, sleep deprivation induced productions of shorter intervals in the duration production task and estimation of segmental durations as being longer in the word identification task. Both results are consistent with an acceleration of pacemaker rate.Moreover, in both experiments, we found a correlation between the alertness level of participants and the size of the effect. Therefore, sleep deprivation, which physiologically manipulates cortical arousal level, produced similar performance modulation in suprasecond explicit and subsecond implicit tasks suggesting a common mechanism.

  13. Increased ultrasonic vocalizations and risk-taking in rat pups of sleep-deprived dams.

    PubMed

    Gulia, Kamalesh K; Patel, Niraj; Kumar, Velayudhan Mohan

    2015-02-01

    Ultrasonic vocalizations (USVs) in rodent pups are analogous to cries in human babies. There is reduction in USVs in pups after experimental deprivation of rapid eye movement sleep of dams during pregnancy. However, the effects of total sleep deprivation on the USVs of newborns and their emotional development are not documented. Male pups born to the rats that underwent total sleep deprivation for 5h during the third trimester made higher vocalizations, when tested on early postnatal days (pnds) in an isolation-paradigm. Their anxiety-related behaviors during pnds 25-28, were tested using elevated plus maze (EPM). In comparison to the control pups, weanlings of sleep-deprived dams made increased entries into the open arms and higher mobility in the EPM. Enhanced distress calls during early pnds and reduction in risk assessment in weanlings indicate a link between the two behaviors. The USVs during ontogeny may provide early signals about altered emotional development.

  14. Transiently increasing cAMP levels selectively in hippocampal excitatory neurons during sleep deprivation prevents memory deficits caused by sleep loss.