Effects of acute caffeine withdrawal on Short Category Test performance in sleep-deprived individuals.

PubMed

Killgore, William D S; Kahn-Greene, Ellen T; Killgore, Desiree B; Kamimori, Gary H; Balkin, Thomas J

2007-12-01

Caffeine is a popular stimulant often used to counter the effects of sleep loss and fatigue. Withdrawal from caffeine may produce mild declines in simple cognitive capacities such as attention and concentration, but it is unclear whether more complex cognitive functions, such as abstract reasoning or concept formation, may be similarly affected. To assess the effect of acute caffeine withdrawal on executive functioning during sleep deprivation, 26 healthy volunteers were administered in double-blind form either repeated doses of caffeine or placebo over two nights of continuous wakefulness. The 108-item Short Category Test was administered after 56 hr. of total sleep deprivation (9 hr. post-caffeine administration). The caffeine group scored significantly more poorly, making approximately 57% more errors on the test than the placebo group. These findings suggest that acute caffeine withdrawal during prolonged sleep deprivation has an adverse effect on abstract reasoning and concept formation.

Sleep and protein synthesis-dependent synaptic plasticity: impacts of sleep loss and stress

PubMed Central

Grønli, Janne; Soulé, Jonathan; Bramham, Clive R.

2014-01-01

Sleep has been ascribed a critical role in cognitive functioning. Several lines of evidence implicate sleep in the consolidation of synaptic plasticity and long-term memory. Stress disrupts sleep while impairing synaptic plasticity and cognitive performance. Here, we discuss evidence linking sleep to mechanisms of protein synthesis-dependent synaptic plasticity and synaptic scaling. We then consider how disruption of sleep by acute and chronic stress may impair these mechanisms and degrade sleep function. PMID:24478645

The metabolic burden of sleep loss.

PubMed

Schmid, Sebastian M; Hallschmid, Manfred; Schultes, Bernd

2015-01-01

In parallel with the increasing prevalence of obesity and type 2 diabetes, sleep loss has become common in modern societies. An increasing number of epidemiological studies show an association between short sleep duration, sleep disturbances, and circadian desynchronisation of sleep with adverse metabolic traits, in particular obesity and type 2 diabetes. Furthermore, experimental studies point to distinct mechanisms by which insufficient sleep adversely affects metabolic health. Changes in the activity of neuroendocrine systems seem to be major mediators of the detrimental metabolic effects of insufficient sleep, through favouring neurobehavioural outcomes such as increased appetite, enhanced sensitivity to food stimuli, and, ultimately, a surplus in energy intake. The effect of curtailed sleep on physical activity and energy expenditure is less clear, but changes are unlikely to outweigh increases in food intake. Although long-term interventional studies proving a cause and effect association are still scarce, sleep loss seems to be an appealing target for the prevention, and probably treatment, of metabolic disease. Copyright © 2015 Elsevier Ltd. All rights reserved.

Medical and Genetic Differences in the Adverse Impact of Sleep Loss on Performance: Ethical Considerations for the Medical Profession

PubMed Central

Czeisler, Charles A.

2009-01-01

The Institute of Medicine recently concluded that-on average-medical residents make more serious medical errors and have more motor vehicle crashes when they are deprived of sleep. In the interest of public safety, society has required limitations on work hours in many other safety sensitive occupations, including transportation and nuclear power generation. Those who argue in favor of traditional extended duration resident work hours often suggest that there are inter- individual differences in response to acute sleep loss or chronic sleep deprivation, implying that physicians may be more resistant than the average person to the detrimental effects of sleep deprivation on performance, although there is no evidence that physicians are particularly resistant to such effects. Indeed, recent investigations have identified genetic polymorphisms that may convey a relative resistance to the effects of prolonged wakefulness on a subset of the healthy population, although there is no evidence that physicians are over-represented in this cohort. Conversely, there are also genetic polymorphisms, sleep disorders and other inter-individual differences that appear to convey an increased vulnerability to the performance-impairing effects of 24 hours of wakefulness. Given the magnitude of inter-individual differences in the effect of sleep loss on cognitive performance, and the sizeable proportion of the population affected by sleep disorders, hospitals face a number of ethical dilemmas. How should the work hours of physicians be limited to protect patient safety optimally? For example, some have argued that, in contrast to other professions, work schedules that repeatedly induce acute and chronic sleep loss are uniquely essential to the training of physicians. If evidence were to prove this premise to be correct, how should such training be ethically accomplished in the quartile of physicians and surgeons who are most vulnerable to the effects of sleep loss on performance

Medical and genetic differences in the adverse impact of sleep loss on performance: ethical considerations for the medical profession.

PubMed

Czeisler, Charles A

2009-01-01

The Institute of Medicine recently concluded that-on average-medical residents make more serious medical errors and have more motor vehicle crashes when they are deprived of sleep. In the interest of public safety, society has required limitations on work hours in many other safety sensitive occupations, including transportation and nuclear power generation. Those who argue in favor of traditional extended duration resident work hours often suggest that there are inter- individual differences in response to acute sleep loss or chronic sleep deprivation, implying that physicians may be more resistant than the average person to the detrimental effects of sleep deprivation on performance, although there is no evidence that physicians are particularly resistant to such effects. Indeed, recent investigations have identified genetic polymorphisms that may convey a relative resistance to the effects of prolonged wakefulness on a subset of the healthy population, although there is no evidence that physicians are over-represented in this cohort. Conversely, there are also genetic polymorphisms, sleep disorders and other inter-individual differences that appear to convey an increased vulnerability to the performance-impairing effects of 24 hours of wakefulness. Given the magnitude of inter-individual differences in the effect of sleep loss on cognitive performance, and the sizeable proportion of the population affected by sleep disorders, hospitals face a number of ethical dilemmas. How should the work hours of physicians be limited to protect patient safety optimally? For example, some have argued that, in contrast to other professions, work schedules that repeatedly induce acute and chronic sleep loss are uniquely essential to the training of physicians. If evidence were to prove this premise to be correct, how should such training be ethically accomplished in the quartile of physicians and surgeons who are most vulnerable to the effects of sleep loss on performance

Cardiovascular reactivity to acute psychological stress following sleep deprivation.

PubMed

Franzen, Peter L; Gianaros, Peter J; Marsland, Anna L; Hall, Martica H; Siegle, Greg J; Dahl, Ronald E; Buysse, Daniel J

2011-10-01

Psychological stress and sleep disturbances are highly prevalent and are both implicated in the etiology of cardiovascular diseases. Given the common co-occurrence of psychological distress and sleep disturbances including short sleep duration, this study examined the combined effects of these two factors on blood pressure reactivity to immediate mental challenge tasks after well-rested and sleep-deprived experimental conditions. Participants (n = 20) were healthy young adults free from current or past sleep, psychiatric, or major medical disorders. Using a within-subjects crossover design, we examined acute stress reactivity under two experimental conditions: after a night of normal sleep in the laboratory and after a night of total sleep deprivation. Two standardized psychological stress tasks were administered, a Stroop color-word naming interference task and a speech task, which were preceded by a prestress baseline period and followed by a poststress recovery period. Each period was 10 minutes in duration, and blood pressure recordings were collected every 2.5 minutes throughout each period. Mean blood pressure responses during stress and recovery periods were examined with a mixed-effects analysis of covariance, controlling for baseline blood pressure. There was a significant interaction between sleep deprivation and stress on systolic blood pressure (F(2,82.7) = 4.05, p = .02). Systolic blood pressure was higher in the sleep deprivation condition compared with the normal sleep condition during the speech task and during the two baseline periods. Sleep deprivation amplified systolic blood pressure increases to psychological stress. Sleep loss may increase cardiovascular risk by dysregulating stress physiology.

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

Insufficient sleep: Enhanced risk-seeking relates to low local sleep intensity.

PubMed

Maric, Angelina; Montvai, Eszter; Werth, Esther; Storz, Matthias; Leemann, Janina; Weissengruber, Sebastian; Ruff, Christian C; Huber, Reto; Poryazova, Rositsa; Baumann, Christian R

2017-09-01

Chronic sleep restriction is highly prevalent in modern society and is, in its clinical form, insufficient sleep syndrome, one of the most prevalent diagnoses in clinical sleep laboratories, with substantial negative impact on health and community burden. It reflects every-day sleep loss better than acute sleep deprivation, but its effects and particularly the underlying mechanisms remain largely unknown for a variety of critical cognitive domains, as, for example, risky decision making. We assessed financial risk-taking behavior after 7 consecutive nights of sleep restriction and after 1 night of acute sleep deprivation compared to a regular sleep condition in a within-subject design. We further investigated potential underlying mechanisms of sleep-loss-induced changes in behavior by high-density electroencephalography recordings during restricted sleep. We show that chronic sleep restriction increases risk-seeking, whereas this was not observed after acute sleep deprivation. This increase was subjectively not noticed and was related to locally lower values of slow-wave energy during preceding sleep, an electrophysiological marker of sleep intensity and restoration, in electrodes over the right prefrontal cortex. This study provides, for the first time, evidence that insufficient sleep restoration over circumscribed cortical areas leads to aberrant behavior. In chronically sleep restricted subjects, low slow-wave sleep intensity over the right prefrontal cortex-which has been shown to be linked to risk behavior-may lead to increased and subjectively unnoticed risk-seeking. Ann Neurol 2017;82:409-418. © 2017 American Neurological Association.

Countermeasures for sleep loss and deprivation.

PubMed

Kushida, Clete A

2006-09-01

Sleep deprivation is ubiquitous and carries profound consequences in terms of personal and public health and safety. There is no substitute for a good night's sleep. Sleep that is optimal in quality and quantity for individuals, factoring in their age and personal sleep requirements, will minimize sleep debt and maximize daytime performance. Therefore, setting aside an adequate amount of time for sleep should be a priority; sleep should not be sacrificed at the expense of other activities of daily living. Nevertheless, there are certain therapeutic countermeasures available for individuals who are unable to obtain adequate sleep because of medical or sleep-related conditions (eg, narcolepsy, obstructive sleep apnea) when excessive daytime sleepiness is the main feature of the condition, or residual sleepiness despite treatment for the main conditions is present. These therapeutic countermeasures may also be considered in situations in which occupational constraints (eg, rotating shift work, military duty) dictate that constant or heightened vigilance is important or critical to work performance, crucial decision making, and/or survival. Exploration of the causes of sleep loss or deprivation, whether it is voluntary, or work or family induced, and/or the effects of a medical or sleep disorder, is a necessary first step in the evaluation of a patient who has significant daytime fatigue or sleepiness. Wake-promoting substances and medications such as caffeine, modafinil, methylphenidate, and dextroamphetamine may be considered in situations in which sleep loss is unavoidable or persists despite treatment of an underlying disorder that is characterized by or associated with daytime fatigue or sleepiness.

Public health implications of sleep loss: the community burden.

PubMed

Hillman, David R; Lack, Leon C

2013-10-21

Poor sleep imparts a significant personal and societal burden. Therefore, it is important to have accurate estimates of its causes, prevalence and costs to inform health policy. A recent evaluation of the sleep habits of Australians demonstrates that frequent (daily or near daily) sleep difficulties (initiating and maintaining sleep, and experiencing inadequate sleep), daytime fatigue, sleepiness and irritability are highly prevalent (20%-35%). These difficulties are generally more prevalent among females, with the exception of snoring and related difficulties. While about half of these problems are likely to be attributable to specific sleep disorders, the balance appears attributable to poor sleep habits or choices to limit sleep opportunity. Study of the economic impact of sleep disorders demonstrates financial costs to Australia of $5.1 billion per year. This comprises $270 million for health care costs for the conditions themselves, $540 million for care of associated medical conditions attributable to sleep disorders, and about $4.3 billion largely attributable to associated productivity losses and non-medical costs resulting from sleep loss-related accidents. Loss of life quality added a substantial further non-financial cost. While large, these costs were for sleep disorders alone. Additional costs relating to inadequate sleep from poor sleep habits in people without sleep disorders were not considered. Based on the high prevalence of such problems and the known impacts of sleep loss in all its forms on health, productivity and safety, it is likely that these poor sleep habits would add substantially to the costs from sleep disorders alone.

Loss of Sleep Affects the Ultrastructure of Pyramidal Neurons in the Adolescent Mouse Frontal Cortex

PubMed Central

de Vivo, Luisa; Nelson, Aaron B.; Bellesi, Michele; Noguti, Juliana; Tononi, Giulio; Cirelli, Chiara

2016-01-01

Study Objective: The adolescent brain may be uniquely affected by acute sleep deprivation (ASD) and chronic sleep restriction (CSR), but direct evidence is lacking. We used electron microscopy to examine how ASD and CSR affect pyramidal neurons in the frontal cortex of adolescent mice, focusing on mitochondria, endosomes, and lysosomes that together perform most basic cellular functions, from nutrient intake to prevention of cellular stress. Methods: Adolescent (1-mo-old) mice slept (S) or were sleep deprived (ASD, with novel objects and running wheels) during the first 6–8 h of the light period, chronically sleep restricted (CSR) for > 4 days (using novel objects, running wheels, social interaction, forced locomotion, caffeinated water), or allowed to recover sleep (RS) for ∼32 h after CSR. Ultrastructural analysis of 350 pyramidal neurons was performed (S = 82; ASD = 86; CSR = 103; RS = 79; 4 to 5 mice/group). Results: Several ultrastructural parameters differed in S versus ASD, S versus CSR, CSR versus RS, and S versus RS, although the different methods used to enforce wake may have contributed to some of the differences between short and long sleep loss. Differences included larger cytoplasmic area occupied by mitochondria in CSR versus S, and higher number of secondary lysosomes in CSR versus S and RS. We also found that sleep loss may unmask interindividual differences not obvious during baseline sleep. Moreover, using a combination of 11 ultrastructural parameters, we could predict in up to 80% of cases whether sleep or wake occurred at the single cell level. Conclusions: Ultrastructural analysis may be a powerful tool to identify which cellular organelles, and thus which cellular functions, are most affected by sleep and sleep loss. Citation: de Vivo L, Nelson AB, Bellesi M, Noguti J, Tononi G, Cirelli C. Loss of sleep affects the ultrastructure of pyramidal neurons in the adolescent mouse frontal cortex. SLEEP 2016;39(4):861–874. PMID:26715225

Acute Sleep Loss Induces Tissue-Specific Epigenetic and Transcriptional Alterations to Circadian Clock Genes in Men.

PubMed

Cedernaes, Jonathan; Osler, Megan E; Voisin, Sarah; Broman, Jan-Erik; Vogel, Heike; Dickson, Suzanne L; Zierath, Juleen R; Schiöth, Helgi B; Benedict, Christian

2015-09-01

Shift workers are at increased risk of metabolic morbidities. Clock genes are known to regulate metabolic processes in peripheral tissues, eg, glucose oxidation. This study aimed to investigate how clock genes are affected at the epigenetic and transcriptional level in peripheral human tissues following acute total sleep deprivation (TSD), mimicking shift work with extended wakefulness. In a randomized, two-period, two-condition, crossover clinical study, 15 healthy men underwent two experimental sessions: x sleep (2230-0700 h) and overnight wakefulness. On the subsequent morning, serum cortisol was measured, followed by skeletal muscle and subcutaneous adipose tissue biopsies for DNA methylation and gene expression analyses of core clock genes (BMAL1, CLOCK, CRY1, PER1). Finally, baseline and 2-h post-oral glucose load plasma glucose concentrations were determined. In adipose tissue, acute sleep deprivation vs sleep increased methylation in the promoter of CRY1 (+4%; P = .026) and in two promoter-interacting enhancer regions of PER1 (+15%; P = .036; +9%; P = .026). In skeletal muscle, TSD vs sleep decreased gene expression of BMAL1 (-18%; P = .033) and CRY1 (-22%; P = .047). Concentrations of serum cortisol, which can reset peripheral tissue clocks, were decreased (2449 ± 932 vs 3178 ± 723 nmol/L; P = .039), whereas postprandial plasma glucose concentrations were elevated after TSD (7.77 ± 1.63 vs 6.59 ± 1.32 mmol/L; P = .011). Our findings demonstrate that a single night of wakefulness can alter the epigenetic and transcriptional profile of core circadian clock genes in key metabolic tissues. Tissue-specific clock alterations could explain why shift work may disrupt metabolic integrity as observed herein.

Sleep Quantity and Quality during Acute Concussion: A Pilot Study

PubMed Central

Raikes, Adam C.; Schaefer, Sydney Y.

2016-01-01

Study Objectives: A number of subjective and objective studies provide compelling evidence of chronic post-concussion changes in sleep, yet very little is known about the acute effects of concussion on sleep quality and quantity. Therefore, the purpose of this prospective pilot study was to use actigraphy to examine the changes in sleep quality and quantity acutely following concussion at home rather than in a hospital or sleep laboratory. Methods: Seventeen young adults (7 with acute concussion, 10 controls) were recruited for this study. All participants completed two 5-day testing sessions separated by 30 days from intake (controls) or day of injury (concussion). Participants wore actigraphs and kept a sleep journal. Sleep parameter outcomes included nighttime total sleep time (nTST), 24-h total sleep time (TST), wake after sleep onset (WASO), and sleep efficiency (SE). The coefficient of variation (CV) for each sleep parameter was computed for each session. Results: nTST and TST CV was significantly greater in the concussion group. There is the additional indication that individuals with a concussion may require and obtain more sleep shortly after injury and subsequently have a shorter duration of sleep at 1 mo post-injury. This pattern was not seen in the measures of sleep quality (WASO, SE). Conclusions: Individuals with a concussion demonstrated increased nighttime sleep duration variability. This increase persisted at 1 mo post-injury and may be associated with previously documented self-reports of poor sleep quality lasting months and years after a concussion. Additionally, this increase may predispose individuals to numerous negative health outcomes if left untreated. Citation: Raikes AC, Schaefer SY. Sleep quantity and quality during acute concussion: a pilot study. SLEEP 2016;39(12):2141–2147. PMID:27748242

Involvement of the α1-adrenoceptor in sleep-waking and sleep loss-induced anxiety behavior in zebrafish.

PubMed

Singh, A; Subhashini, N; Sharma, S; Mallick, B N

2013-08-15

Sleep is a universal phenomenon in vertebrates, and its loss affects various behaviors. Independent studies have reported that sleep loss increases anxiety; however, the detailed mechanism is unknown. Because sleep deprivation increases noradrenalin (NA), which modulates many behaviors and induces patho-physiological changes, this study utilized zebrafish as a model to investigate whether sleep loss-induced increased anxiety is modulated by NA. Continuous behavioral quiescence for at least 6s was considered to represent sleep in zebrafish; although some authors termed it as a sleep-like state, in this study we have termed it as sleep. The activity of fish that signified sleep-waking was recorded in light-dark, during continuous dark and light; the latter induced sleep loss in fish. The latency, number of entries, time spent and distance travelled in the light chamber were assessed in a light-dark box test to estimate the anxiety behavior of normal, sleep-deprived and prazosin (PRZ)-treated fish. Zebrafish showed increased waking during light and complete loss of sleep upon continuous exposure to light for 24h. PRZ significantly increased sleep in normal fish. Sleep-deprived fish showed an increased preference for dark (expression of increased anxiety), and this effect was prevented by PRZ, which increased sleep as well. Our findings suggest that sleep loss-induced anxiety-like behavior in zebrafish is likely to be mediated by NA's action on the α1-adrenoceptor. Copyright © 2013 IBRO. Published by Elsevier Ltd. All rights reserved.

Loss of Sleep Affects the Ultrastructure of Pyramidal Neurons in the Adolescent Mouse Frontal Cortex.

PubMed

de Vivo, Luisa; Nelson, Aaron B; Bellesi, Michele; Noguti, Juliana; Tononi, Giulio; Cirelli, Chiara

2016-04-01

The adolescent brain may be uniquely affected by acute sleep deprivation (ASD) and chronic sleep restriction (CSR), but direct evidence is lacking. We used electron microscopy to examine how ASD and CSR affect pyramidal neurons in the frontal cortex of adolescent mice, focusing on mitochondria, endosomes, and lysosomes that together perform most basic cellular functions, from nutrient intake to prevention of cellular stress. Adolescent (1-mo-old) mice slept (S) or were sleep deprived (ASD, with novel objects and running wheels) during the first 6-8 h of the light period, chronically sleep restricted (CSR) for > 4 days (using novel objects, running wheels, social interaction, forced locomotion, caffeinated water), or allowed to recover sleep (RS) for ∼32 h after CSR. Ultrastructural analysis of 350 pyramidal neurons was performed (S = 82; ASD = 86; CSR = 103; RS = 79; 4 to 5 mice/group). Several ultrastructural parameters differed in S versus ASD, S versus CSR, CSR versus RS, and S versus RS, although the different methods used to enforce wake may have contributed to some of the differences between short and long sleep loss. Differences included larger cytoplasmic area occupied by mitochondria in CSR versus S, and higher number of secondary lysosomes in CSR versus S and RS. We also found that sleep loss may unmask interindividual differences not obvious during baseline sleep. Moreover, using a combination of 11 ultrastructural parameters, we could predict in up to 80% of cases whether sleep or wake occurred at the single cell level. Ultrastructural analysis may be a powerful tool to identify which cellular organelles, and thus which cellular functions, are most affected by sleep and sleep loss. © 2016 Associated Professional Sleep Societies, LLC.

Sleep modifications in acute transient global amnesia.

PubMed

Della Marca, Giacomo; Mazza, Marianna; Losurdo, Anna; Testani, Elisa; Broccolini, Aldobrando; Frisullo, Giovanni; Marano, Giuseppe; Morosetti, Roberta; Pilato, Fabio; Profice, Paolo; Vollono, Catello; Di Lazzaro, Vincenzo

2013-09-15

Transient global amnesia (TGA) is a temporary memory loss characterized by an abrupt onset of antero-grade and retrograde amnesia, totally reversible. Since sleep plays a major role in memory consolidation, and in the storage of memory-related traces into the brain cortex, the aims of the present study were: (1) to evaluate changes in sleep macro-structure in TGA; (2) to assess modifications in sleep micro-structure in TGA, with particular reference to the arousal EEG and to cyclic alternating pattern (CAP); (3) to compare sleep parameters in TGA patients with a control group of patients with acute ischemic events ("minor stroke" or transient ischemic attack [TIA]) clinically and neuroradiologically "similar" to the TGA. TGA GROUP: 17 patients, (8 men and 9 women, 60.2 ± 12.5 years). Stroke or TIA (SoT) group: 17 patients hospitalized in the Stroke Unit for recent onset of minor stroke or TIA with hemispheric localization; healthy controls (HC) group: 17 healthy volunteers, matched for age and sex. Patients and controls underwent full-night polysomnography. In the multivariate analysis (conditions TGA, SoT, and HC) a significant effect of the condition was observed for sleep efficiency index, number of awakenings longer 1 min, REM latency, CAP time, and CAP rate. TGA and SoT differed only for CAP time and CAP rate, which were lower in the TGA group. Microstructural modification associated with tga could be consequent to: (1) hippocampal dysfunction and memory impairment; (2) impairment of arousal-related structures (in particular, cholinergic pathways); (3) emotional distress.

Effects of Partial and Acute Total Sleep Deprivation on Performance across Cognitive Domains, Individuals and Circadian Phase

PubMed Central

Lo, June C.; Groeger, John A.; Santhi, Nayantara; Arbon, Emma L.; Lazar, Alpar S.; Hasan, Sibah; von Schantz, Malcolm; Archer, Simon N.; Dijk, Derk-Jan

2012-01-01

Background Cognitive performance deteriorates during extended wakefulness and circadian phase misalignment, and some individuals are more affected than others. Whether performance is affected similarly across cognitive domains, or whether cognitive processes involving Executive Functions are more sensitive to sleep and circadian misalignment than Alertness and Sustained Attention, is a matter of debate. Methodology/Principal Findings We conducted a 2 × 12-day laboratory protocol to characterize the interaction of repeated partial and acute total sleep deprivation and circadian phase on performance across seven cognitive domains in 36 individuals (18 males; mean ± SD of age = 27.6±4.0 years). The sample was stratified for the rs57875989 polymorphism in PER3, which confers cognitive susceptibility to total sleep deprivation. We observed a deterioration of performance during both repeated partial and acute total sleep deprivation. Furthermore, prior partial sleep deprivation led to poorer cognitive performance in a subsequent total sleep deprivation period, but its effect was modulated by circadian phase such that it was virtually absent in the evening wake maintenance zone, and most prominent during early morning hours. A significant effect of PER3 genotype was observed for Subjective Alertness during partial sleep deprivation and on n-back tasks with a high executive load when assessed in the morning hours during total sleep deprivation after partial sleep loss. Overall, however, Subjective Alertness and Sustained Attention were more affected by both partial and total sleep deprivation than other cognitive domains and tasks including n-back tasks of Working Memory, even when implemented with a high executive load. Conclusions/Significance Sleep loss has a primary effect on Sleepiness and Sustained Attention with much smaller effects on challenging Working Memory tasks. These findings have implications for understanding how sleep debt and circadian rhythmicity

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.

Maximizing Sensitivity of the Psychomotor Vigilance Test (PVT) to Sleep Loss

PubMed Central

Basner, Mathias; Dinges, David F.

2011-01-01

Study Objectives: The psychomotor vigilance test (PVT) is among the most widely used measures of behavioral alertness, but there is large variation among published studies in PVT performance outcomes and test durations. To promote standardization of the PVT and increase its sensitivity and specificity to sleep loss, we determined PVT metrics and task durations that optimally discriminated sleep deprived subjects from alert subjects. Design: Repeated-measures experiments involving 10-min PVT assessments every 2 h across both acute total sleep deprivation (TSD) and 5 days of chronic partial sleep deprivation (PSD). Setting: Controlled laboratory environment. Participants: 74 healthy subjects (34 female), aged 22–45 years. Interventions: TSD experiment involving 33 h awake (N = 31 subjects) and a PSD experiment involving 5 nights of 4 h time in bed (N = 43 subjects). Measurements and Results: In a paired t-test paradigm and for both TSD and PSD, effect sizes of 10 different PVT performance outcomes were calculated. Effect sizes were high for both TSD (1.59–1.94) and PSD (0.88–1.21) for PVT metrics related to lapses and to measures of psychomotor speed, i.e., mean 1/RT (response time) and mean slowest 10% 1/RT. In contrast, PVT mean and median RT outcomes scored low to moderate effect sizes influenced by extreme values. Analyses facilitating only portions of the full 10-min PVT indicated that for some outcomes, high effect sizes could be achieved with PVT durations considerably shorter than 10 min, although metrics involving lapses seemed to profit from longer test durations in TSD. Conclusions: Due to their superior conceptual and statistical properties and high sensitivity to sleep deprivation, metrics involving response speed and lapses should be considered primary outcomes for the 10-min PVT. In contrast, PVT mean and median metrics, which are among the most widely used outcomes, should be avoided as primary measures of alertness. Our analyses also suggest

Research of Sleep Disorders in Patients with Acute Cerebral Infarction.

PubMed

Chen, Xiaofang; Bi, Hongye; Zhang, Meiyun; Liu, Haiyan; Wang, Xueying; Zu, Ruonan

2015-11-01

The purpose of this study is to investigate the incidence of sleep disorders (SD), characteristic of cerebral infarction patients with different parts affected. The research selected 101 patients with a first occurrence of acute cerebral infarction as the experimental group, and 86 patients without cerebral infarction as controls. Polysomnography, Pittsburgh Sleep Quality Index, Epworth Sleepiness Scale, and US National Stroke Scale were assessed. Compared with control group, the incidence of SD was higher in experimental group (P < .05), and the incidence of SD in women was more frequent in experimental group (P < .05). There was no significant difference in the types of SD patients with acute cerebral infarction. In addition, the sleep quality of cerebral infarction patients with different parts affected was different: the sleep quality of left hemisphere infarction patients was poor compared with the right one, and the sleep quality of anterior circulation patients was poor compared with posterior circulation patients. Patients with thalamus infarction had a longer sleep time and a shorter sleep latency and stage 2 of non-rapid eye movement sleep compared with non-thalamus infarction group. The prevalence of SD was relatively high in acute cerebral infarction patients, and the detailed classification of acute cerebral infarction may provide a more effective therapeutic method and therefore relieve patients' pain and supply a better quality of sleep. Copyright © 2015 National Stroke Association. Published by Elsevier Inc. All rights reserved.

Repeated Exposure to Conditioned Fear Stress Increases Anxiety and Delays Sleep Recovery Following Exposure to an Acute Traumatic Stressor

PubMed Central

Greenwood, Benjamin N.; Thompson, Robert S.; Opp, Mark R.; Fleshner, Monika

2014-01-01

Repeated stressor exposure can sensitize physiological responses to novel stressors and facilitate the development of stress-related psychiatric disorders including anxiety. Disruptions in diurnal rhythms of sleep–wake behavior accompany stress-related psychiatric disorders and could contribute to their development. Complex stressors that include fear-eliciting stimuli can be a component of repeated stress experienced by human beings, but whether exposure to repeated fear can prime the development of anxiety and sleep disturbances is unknown. In the current study, adult male F344 rats were exposed to either control conditions or repeated contextual fear conditioning for 22 days followed by exposure to no, mild (10), or severe (100) acute uncontrollable tail shock stress. Exposure to acute stress produced anxiety-like behavior as measured by a reduction in juvenile social exploration and exaggerated shock-elicited freezing in a novel context. Prior exposure to repeated fear enhanced anxiety-like behavior as measured by shock-elicited freezing, but did not alter social exploratory behavior. The potentiation of anxiety produced by prior repeated fear was temporary; exaggerated fear was present 1 day but not 4 days following acute stress. Interestingly, exposure to acute stress reduced rapid eye movement (REM) and non-REM (NREM) sleep during the hours immediately following acute stress. This initial reduction in sleep was followed by robust REM rebound and diurnal rhythm flattening of sleep/wake behavior. Prior repeated fear extended the acute stress-induced REM and NREM sleep loss, impaired REM rebound, and prolonged the flattening of the diurnal rhythm of NREM sleep following acute stressor exposure. These data suggest that impaired recovery of sleep/wake behavior following acute stress could contribute to the mechanisms by which a history of prior repeated stress increases vulnerability to subsequent novel stressors and stress-related disorders. PMID

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.

Sleep and athletic performance: the effects of sleep loss on exercise performance, and physiological and cognitive responses to exercise.

PubMed

Fullagar, Hugh H K; Skorski, Sabrina; Duffield, Rob; Hammes, Daniel; Coutts, Aaron J; Meyer, Tim

2015-02-01

Although its true function remains unclear, sleep is considered critical to human physiological and cognitive function. Equally, since sleep loss is a common occurrence prior to competition in athletes, this could significantly impact upon their athletic performance. Much of the previous research has reported that exercise performance is negatively affected following sleep loss; however, conflicting findings mean that the extent, influence, and mechanisms of sleep loss affecting exercise performance remain uncertain. For instance, research indicates some maximal physical efforts and gross motor performances can be maintained. In comparison, the few published studies investigating the effect of sleep loss on performance in athletes report a reduction in sport-specific performance. The effects of sleep loss on physiological responses to exercise also remain equivocal; however, it appears a reduction in sleep quality and quantity could result in an autonomic nervous system imbalance, simulating symptoms of the overtraining syndrome. Additionally, increases in pro-inflammatory cytokines following sleep loss could promote immune system dysfunction. Of further concern, numerous studies investigating the effects of sleep loss on cognitive function report slower and less accurate cognitive performance. Based on this context, this review aims to evaluate the importance and prevalence of sleep in athletes and summarises the effects of sleep loss (restriction and deprivation) on exercise performance, and physiological and cognitive responses to exercise. Given the equivocal understanding of sleep and athletic performance outcomes, further research and consideration is required to obtain a greater knowledge of the interaction between sleep and performance.

Effects of Sleep Loss on Subjective Complaints and Objective Neurocognitive Performance as Measured by the Immediate Post-Concussion Assessment and Cognitive Testing.

PubMed

Stocker, Ryan P J; Khan, Hassen; Henry, Luke; Germain, Anne

2017-05-01

This study examined the effects of total and partial sleep deprivation on subjective symptoms and objective neurocognitive performance, as measured by the Immediate Post-Concussion Assessment and Cognitive Testing (ImPACT) in a sample of healthy adults. One-hundred and two, right-handed, healthy participants (between ages 18 and 30 years old) completed three consecutive nights in the sleep laboratory with concurrent continuous polysomnography monitoring. Night 1 served as a baseline night. Prior to Night 2, they were randomly assigned to one of three sleep conditions: undisrupted normal sleep (N = 34), sleep restriction (50% of habitual sleep, N = 37), or total sleep deprivation (N = 31). Participants slept undisturbed on Night 3. ImPACT was administered on three separate occasions. Sleep loss was associated with increased severity of subjectively reported affective, cognitive, physical, and sleep symptoms. Although objective neurocognitive task scores derived from the ImPACT battery did not corroborate subjective complaints, sleep loss was associated with significant differences on tasks of visual memory, reaction time, and visual motor speed over time. While self-report measures suggested marked impairments following sleep loss, deficits in neurocognitive performance were observed only on three domains measured with ImPACT. ImPACT may capture subtle changes in neurocognitive performance following sleep loss; however, independent and larger validation studies are needed to determine its sensitivity to acute sleep loss and recovery sleep. Neurocognitive screening batteries may be useful for detecting the effects of more severe or chronic sleep loss under high-stress conditions that mimic high-risk occupations. © The Author 2017. Published by Oxford University Press. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.

Cell Injury and Repair Resulting from Sleep Loss and Sleep Recovery in Laboratory Rats

PubMed Central

Everson, Carol A.; Henchen, Christopher J.; Szabo, Aniko; Hogg, Neil

2014-01-01

Study Objectives: Increased cell injury would provide the type of change in constitution that would underlie sleep disruption as a risk factor for multiple diseases. The current study was undertaken to investigate cell injury and altered cell fate as consequences of sleep deprivation, which were predicted from systemic clues. Design: Partial (35% sleep reduction) and total sleep deprivation were produced in rats for 10 days, which was tolerated and without overtly deteriorated health. Recovery rats were similarly sleep deprived for 10 days, then allowed undisturbed sleep for 2 days. The plasma, liver, lung, intestine, heart, and spleen were analyzed and compared to control values for damage to DNA, proteins, and lipids; apoptotic cell signaling and death; cell proliferation; and concentrations of glutathione peroxidase and catalase. Measurements and Results: Oxidative DNA damage in totally sleep deprived rats was 139% of control values, with organ-specific effects in the liver (247%), lung (166%), and small intestine (145%). Overall and organ-specific DNA damage was also increased in partially sleep deprived rats. In the intestinal epithelium, total sleep deprivation resulted in 5.3-fold increases in dying cells and 1.5-fold increases in proliferating cells, compared with control. Two days of recovery sleep restored the balance between DNA damage and repair, and resulted in normal or below-normal metabolic burdens and oxidative damage. Conclusions: These findings provide physical evidence that sleep loss causes cell damage, and in a manner expected to predispose to replication errors and metabolic abnormalities; thereby providing linkage between sleep loss and disease risk observed in epidemiological findings. Properties of recovery sleep include biochemical and molecular events that restore balance and decrease cell injury. Citation: Everson CA, Henchen CJ, Szabo A, Hogg N. Cell injury and repair resulting from sleep loss and sleep recovery in laboratory rats

Sleep Quantity and Quality during Acute Concussion: A Pilot Study.

PubMed

Raikes, Adam C; Schaefer, Sydney Y

2016-12-01

A number of subjective and objective studies provide compelling evidence of chronic post-concussion changes in sleep, yet very little is known about the acute effects of concussion on sleep quality and quantity. Therefore, the purpose of this prospective pilot study was to use actigraphy to examine the changes in sleep quality and quantity acutely following concussion at home rather than in a hospital or sleep laboratory. Seventeen young adults (7 with acute concussion, 10 controls) were recruited for this study. All participants completed two 5-day testing sessions separated by 30 days from intake (controls) or day of injury (concussion). Participants wore actigraphs and kept a sleep journal. Sleep parameter outcomes included nighttime total sleep time (nTST), 24-h total sleep time (TST), wake after sleep onset (WASO), and sleep efficiency (SE). The coefficient of variation (CV) for each sleep parameter was computed for each session. nTST and TST CV was significantly greater in the concussion group. There is the additional indication that individuals with a concussion may require and obtain more sleep shortly after injury and subsequently have a shorter duration of sleep at 1 mo post-injury. This pattern was not seen in the measures of sleep quality (WASO, SE). Individuals with a concussion demonstrated increased nighttime sleep duration variability. This increase persisted at 1 mo post-injury and may be associated with previously documented self-reports of poor sleep quality lasting months and years after a concussion. Additionally, this increase may predispose individuals to numerous negative health outcomes if left untreated. © 2016 Associated Professional Sleep Societies, LLC.

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

Modeling the adenosine system as a modulator of cognitive performance and sleep patterns during sleep restriction and recovery.

PubMed

Phillips, Andrew J K; Klerman, Elizabeth B; Butler, James P

2017-10-01

Sleep loss causes profound cognitive impairments and increases the concentrations of adenosine and adenosine A1 receptors in specific regions of the brain. Time courses for performance impairment and recovery differ between acute and chronic sleep loss, but the physiological basis for these time courses is unknown. Adenosine has been implicated in pathways that generate sleepiness and cognitive impairments, but existing mathematical models of sleep and cognitive performance do not explicitly include adenosine. Here, we developed a novel receptor-ligand model of the adenosine system to test the hypothesis that changes in both adenosine and A1 receptor concentrations can capture changes in cognitive performance during acute sleep deprivation (one prolonged wake episode), chronic sleep restriction (multiple nights with insufficient sleep), and subsequent recovery. Parameter values were estimated using biochemical data and reaction time performance on the psychomotor vigilance test (PVT). The model closely fit group-average PVT data during acute sleep deprivation, chronic sleep restriction, and recovery. We tested the model's ability to reproduce timing and duration of sleep in a separate experiment where individuals were permitted to sleep for up to 14 hours per day for 28 days. The model accurately reproduced these data, and also correctly predicted the possible emergence of a split sleep pattern (two distinct sleep episodes) under these experimental conditions. Our findings provide a physiologically plausible explanation for observed changes in cognitive performance and sleep during sleep loss and recovery, as well as a new approach for predicting sleep and cognitive performance under planned schedules.

Modeling the adenosine system as a modulator of cognitive performance and sleep patterns during sleep restriction and recovery

PubMed Central

Phillips, Andrew J. K.

2017-01-01

Sleep loss causes profound cognitive impairments and increases the concentrations of adenosine and adenosine A1 receptors in specific regions of the brain. Time courses for performance impairment and recovery differ between acute and chronic sleep loss, but the physiological basis for these time courses is unknown. Adenosine has been implicated in pathways that generate sleepiness and cognitive impairments, but existing mathematical models of sleep and cognitive performance do not explicitly include adenosine. Here, we developed a novel receptor-ligand model of the adenosine system to test the hypothesis that changes in both adenosine and A1 receptor concentrations can capture changes in cognitive performance during acute sleep deprivation (one prolonged wake episode), chronic sleep restriction (multiple nights with insufficient sleep), and subsequent recovery. Parameter values were estimated using biochemical data and reaction time performance on the psychomotor vigilance test (PVT). The model closely fit group-average PVT data during acute sleep deprivation, chronic sleep restriction, and recovery. We tested the model’s ability to reproduce timing and duration of sleep in a separate experiment where individuals were permitted to sleep for up to 14 hours per day for 28 days. The model accurately reproduced these data, and also correctly predicted the possible emergence of a split sleep pattern (two distinct sleep episodes) under these experimental conditions. Our findings provide a physiologically plausible explanation for observed changes in cognitive performance and sleep during sleep loss and recovery, as well as a new approach for predicting sleep and cognitive performance under planned schedules. PMID:29073206

Impact of sleep loss before learning on cortical dynamics during memory retrieval.

PubMed

Alberca-Reina, E; Cantero, J L; Atienza, M

2015-12-01

Evidence shows that sleep loss before learning decreases activation of the hippocampus during encoding and promotes forgetting. But it remains to be determined which neural systems are functionally affected during memory retrieval after one night of recovery sleep. To investigate this issue, we evaluated memory for pairs of famous people's faces with the same or different profession (i.e., semantically congruent or incongruent faces) after one night of undisturbed sleep in subjects who either underwent 4hours of acute sleep restriction (ASR, N=20) or who slept 8hours the pre-training night (controls, N=20). EEG recordings were collected during the recognition memory task in both groups, and the cortical sources generating this activity localized by applying a spatial beamforming filter in the frequency domain. Even though sleep restriction did not affect accuracy of memory performance, controls showed a much larger decrease of alpha power relative to a baseline period when compared to sleep-deprived subjects. These group differences affected a widespread frontotemporoparietal network involved in retrieval of episodic/semantic memories. Regression analyses further revealed that associative memory in the ASR group was negatively correlated with alpha power in the occipital regions, whereas the benefit of congruency in the same group was positively correlated with delta power in the left lateral prefrontal cortex. Retrieval-related decreases of alpha power have been associated with the reactivation of material-specific memory representations, whereas increases of delta power have been related to inhibition of interferences that may affect the performance of the task. We can therefore draw the conclusion that a few hours of sleep loss in the pre-training night, though insufficient to change the memory performance, is sufficient to alter the processes involved in retrieving and manipulating episodic and semantic information. Copyright © 2015 Elsevier Inc. All rights

Astrocytic modulation of sleep homeostasis and cognitive consequences of sleep loss.

PubMed

Halassa, Michael M; Florian, Cedrick; Fellin, Tommaso; Munoz, James R; Lee, So-Young; Abel, Ted; Haydon, Philip G; Frank, Marcos G

2009-01-29

Astrocytes modulate neuronal activity by releasing chemical transmitters via a process termed gliotransmission. The role of this process in the control of behavior is unknown. Since one outcome of SNARE-dependent gliotransmission is the regulation of extracellular adenosine and because adenosine promotes sleep, we genetically inhibited the release of gliotransmitters and asked if astrocytes play an unsuspected role in sleep regulation. Inhibiting gliotransmission attenuated the accumulation of sleep pressure, assessed by measuring the slow wave activity of the EEG during NREM sleep, and prevented cognitive deficits associated with sleep loss. Since the sleep-suppressing effects of the A1 receptor antagonist CPT were prevented following inhibition of gliotransmission and because intracerebroventricular delivery of CPT to wild-type mice mimicked the transgenic phenotype, we conclude that astrocytes modulate the accumulation of sleep pressure and its cognitive consequences through a pathway involving A1 receptors.

Sleep loss and acute drug abuse can induce DNA damage in multiple organs of mice.

PubMed

Alvarenga, T A; Ribeiro, D A; Araujo, P; Hirotsu, C; Mazaro-Costa, R; Costa, J L; Battisti, M C; Tufik, S; Andersen, M L

2011-09-01

The purpose of the present study was to characterize the genetic damage induced by paradoxical sleep deprivation (PSD) in combination with cocaine or ecstasy (3,4-methylenedioxymethamphetamine; MDMA) in multiple organs of male mice using the single cell gel (comet) assay. C57BL/6J mice were submitted to PSD by the platform technique for 72 hours, followed by drug administration and evaluation of DNA damage in peripheral blood, liver and brain tissues. Cocaine was able to induce genetic damage in the blood, brain and liver cells of sleep-deprived mice at the majority of the doses evaluated. Ecstasy also induced increased DNA migration in peripheral blood cells for all concentrations tested. Analysis of damaged cells by the tail moment data suggests that ecstasy is a genotoxic chemical at the highest concentrations tested, inducing damage in liver or brain cells after sleep deprivation in mice. Taken together, our results suggest that cocaine and ecstasy/MDMA act as potent genotoxins in multiple organs of mice when associated with sleep loss.

Acute physical exercise under hypoxia improves sleep, mood and reaction time.

PubMed

de Aquino-Lemos, Valdir; Santos, Ronaldo Vagner T; Antunes, Hanna Karen Moreira; Lira, Fabio S; Luz Bittar, Irene G; Caris, Aline V; Tufik, Sergio; de Mello, Marco Tulio

2016-02-01

This study aimed to assess the effect of two sessions of acute physical exercise at 50% VO2peak performed under hypoxia (equivalent to an altitude of 4500 m for 28 h) on sleep, mood and reaction time. Forty healthy men were randomized into 4 groups: Normoxia (NG) (n = 10); Hypoxia (HG) (n = 10); Exercise under Normoxia (ENG) (n = 10); and Exercise under Hypoxia (EHG) (n = 10). All mood and reaction time assessments were performed 40 min after awakening. Sleep was reassessed on the first day at 14 h after the initiation of hypoxia; mood and reaction time were measured 28 h later. Two sessions of acute physical exercise at 50% VO2peak were performed for 60 min on the first and second days after 3 and 27 h, respectively, after starting to hypoxia. Improved sleep efficiency, stage N3 and REM sleep and reduced wake after sleep onset were observed under hypoxia after acute physical exercise. Tension, anger, depressed mood, vigor and reaction time scores improved after exercise under hypoxia. We conclude that hypoxia impairs sleep, reaction time and mood. Acute physical exercise at 50% VO2peak under hypoxia improves sleep efficiency, reversing the aspects that had been adversely affected under hypoxia, possibly contributing to improved mood and reaction time.

Sleep quality but not sleep quantity effects on cortisol responses to acute psychosocial stress.

PubMed

Bassett, Sarah M; Lupis, Sarah B; Gianferante, Danielle; Rohleder, Nicolas; Wolf, Jutta M

2015-01-01

Given the well-documented deleterious health effects, poor sleep has become a serious public health concern and increasing efforts are directed toward understanding underlying pathways. One potential mechanism may be stress and its biological correlates; however, studies investigating the effects of poor sleep on a body's capacity to deal with challenges are lacking. The current study thus aimed at testing the effects of sleep quality and quantity on cortisol responses to acute psychosocial stress. A total of 73 college-aged adults (44 females) were investigated. Self-reported sleep behavior was assessed via the Pittsburgh Sleep Quality Index and salivary cortisol responses to the Trier Social Stress Test were measured. In terms of sleep quality, we found a significant three-way interaction, such that relative to bad sleep quality, men who reported fairly good or very good sleep quality showed blunted or exaggerated cortisol responses, respectively, while women's stress responses were less dependent on their self-reported sleep quality. Contrarily, average sleep duration did not appear to impact cortisol stress responses. Lastly, participants who reported daytime dysfunctions (i.e. having trouble staying awake or keeping up enthusiasm) also showed a trend to blunted cortisol stress responses compared to participants who did not experience these types of daytime dysfunctions. Overall, the current study suggests gender-specific stress reactivity dysfunctions as one mechanism linking poor sleep with detrimental physical health outcomes. Furthermore, the observed differential sleep effects may indicate that while the body may be unable to maintain normal hypothalamic-pituitary-adrenal functioning in an acute psychosocial stress situation after falling prey to low sleep quality, it may retain capacities to deal with challenges during extended times of sleep deprivation.

Improving sleep for patients in acute hospitals.

PubMed

Norton, Christine; Flood, David; Brittin, Andy; Miles, Jane

2015-03-11

Sleep is important to health and recovery from illness, but is known to be difficult in hospital. This article describes a quality improvement project conducted on 18 wards in acute hospitals. Patients reported sleeping an average of five hours per night, and 47% (352/749) rated their sleep quality as good or excellent in hospital. Individualised ward action plans were implemented. At follow up, disturbance by noise and light had fallen significantly and 69% (540/783) of patients rated their sleep as good or excellent, 22% more than before the intervention (P<0.001). Local interventions such as improving staff awareness of noise, installing window blinds and turning down equipment alarms improved the patient experience of sleep.

Voluntary Sleep Loss in Rats

PubMed Central

Oonk, Marcella; Krueger, James M.; Davis, Christopher J.

2016-01-01

Study Objectives: Animal sleep deprivation (SDEP), in contrast to human SDEP, is involuntary and involves repeated exposure to aversive stimuli including the inability of the animal to control the waking stimulus. Therefore, we explored intracranial self-stimulation (ICSS), an operant behavior, as a method for voluntary SDEP in rodents. Methods: Male Sprague-Dawley rats were implanted with electroencephalography/electromyography (EEG/EMG) recording electrodes and a unilateral bipolar electrode into the lateral hypothalamus. Rats were allowed to self-stimulate, or underwent gentle handling-induced SDEP (GH-SDEP), during the first 6 h of the light phase, after which they were allowed to sleep. Other rats performed the 6 h ICSS and 1 w later were subjected to 6 h of noncontingent stimulation (NCS). During NCS the individual stimulation patterns recorded during ICSS were replayed. Results: After GH-SDEP, ICSS, or NCS, time in nonrapid eye movement (NREM) sleep and rapid eye movement (REM) sleep increased. Further, in the 24 h after SDEP, rats recovered all of the REM sleep lost during SDEP, but only 75% to 80% of the NREM sleep lost, regardless of the SDEP method. The magnitude of EEG slow wave responses occurring during NREM sleep also increased after SDEP treatments. However, NREM sleep EEG slow wave activity (SWA) responses were attenuated following ICSS, compared to GH-SDEP and NCS. Conclusions: We conclude that ICSS and NCS can be used to sleep deprive rats. Changes in rebound NREM sleep EEG SWA occurring after ICSS, NCS, and GH-SDEP suggest that nonspecific effects of the SDEP procedure differentially affect recovery sleep phenotypes. Citation: Oonk M, Krueger JM, Davis CJ. Voluntary sleep loss in rats. SLEEP 2016;39(7):1467–1479. PMID:27166236

Sleep quality but not sleep quantity effects on cortisol responses to acute psychosocial stress

PubMed Central

Bassett, Sarah M.; Lupis, Sarah B.; Gianferante, Danielle; Rohleder, Nicolas; Wolf, Jutta M.

2016-01-01

Given the well-documented deleterious health effects, poor sleep has become a serious public health concern and increasing efforts are directed towards understanding underlying pathways. One potential mechanism may be stress and its biological correlates; however, studies investigating the effects of poor sleep on a body’s capacity to deal with challenges are lacking. The current study thus aimed at testing the effects of sleep quality and sleep quantity on cortisol responses to acute psychosocial stress. A total of 73 college-aged adults (44 females) were investigated. Self-reported sleep behavior was assessed via the Pittsburgh Sleep Quality Index and salivary cortisol responses to the Trier Social Stress Test (TSST) were measured. In terms of sleep quality, we found a significant three-way interaction, such that relative to bad sleep quality, men who reported fairly good or very good sleep quality showed blunted or exaggerated cortisol responses, respectively, while women’s stress responses were less dependent on their self-reported sleep quality. Contrarily, average sleep duration did not appear to impact cortisol stress responses. Lastly, participants who reported daytime dysfunctions (i.e., having trouble staying awake or keeping up enthusiasm) also showed a trend to blunted cortisol stress responses compared to participants who did not experience these types of daytime dysfunctions. Overall, the current study suggests gender-specific stress reactivity dysfunctions as one mechanism linking poor sleep with detrimental physical health outcomes. Furthermore, the observed differential sleep effects may indicate that while the body may be unable to maintain normal HPA functioning in an acute psychosocial stress situation after falling prey to low sleep quality, it may retain capacities to deal with challenges during extended times of sleep deprivation. PMID:26414625

Decreased alertness due to sleep loss increases pain sensitivity in mice

PubMed Central

Alexandre, Chloe; Latremoliere, Alban; Ferreira, Ashley; Miracca, Giulia; Yamamoto, Mihoko; Scammell, Thomas E; Woolf, Clifford J

2018-01-01

Extended daytime and nighttime activities are major contributors to the growing sleep deficiency epidemic1,2, as is the high prevalence of sleep disorders like insomnia. The consequences of chronic insufficient sleep for health remain uncertain3. Sleep quality and duration predict presence of pain the next day in healthy subjects4–7, suggesting that sleep disturbances alone may worsen pain, and experimental sleep deprivation in humans supports this claim8,9. We demonstrate that sleep loss, but not sleep fragmentation, in healthy mice increases sensitivity to noxious stimuli (referred to as ‘pain’) without general sensory hyper-responsiveness. Moderate daily repeated sleep loss leads to a progressive accumulation of sleep debt and also to exaggerated pain responses, both of which are rescued after restoration of normal sleep. Caffeine and modafinil, two wake-promoting agents that have no analgesic activity in rested mice, immediately normalize pain sensitivity in sleep-deprived animals, without affecting sleep debt. The reversibility of mild sleep-loss-induced pain by wake-promoting agents reveals an unsuspected role for alertness in setting pain sensitivity. Clinically, insufficient or poor-quality sleep may worsen pain and this enhanced pain may be reduced not by analgesics, whose effectiveness is reduced, but by increasing alertness or providing better sleep. PMID:28481358

Maximizing sensitivity of the psychomotor vigilance test (PVT) to sleep loss.

PubMed

Basner, Mathias; Dinges, David F

2011-05-01

The psychomotor vigilance test (PVT) is among the most widely used measures of behavioral alertness, but there is large variation among published studies in PVT performance outcomes and test durations. To promote standardization of the PVT and increase its sensitivity and specificity to sleep loss, we determined PVT metrics and task durations that optimally discriminated sleep deprived subjects from alert subjects. Repeated-measures experiments involving 10-min PVT assessments every 2 h across both acute total sleep deprivation (TSD) and 5 days of chronic partial sleep deprivation (PSD). Controlled laboratory environment. 74 healthy subjects (34 female), aged 22-45 years. TSD experiment involving 33 h awake (N = 31 subjects) and a PSD experiment involving 5 nights of 4 h time in bed (N = 43 subjects). In a paired t-test paradigm and for both TSD and PSD, effect sizes of 10 different PVT performance outcomes were calculated. Effect sizes were high for both TSD (1.59-1.94) and PSD (0.88-1.21) for PVT metrics related to lapses and to measures of psychomotor speed, i.e., mean 1/RT (response time) and mean slowest 10% 1/RT. In contrast, PVT mean and median RT outcomes scored low to moderate effect sizes influenced by extreme values. Analyses facilitating only portions of the full 10-min PVT indicated that for some outcomes, high effect sizes could be achieved with PVT durations considerably shorter than 10 min, although metrics involving lapses seemed to profit from longer test durations in TSD. Due to their superior conceptual and statistical properties and high sensitivity to sleep deprivation, metrics involving response speed and lapses should be considered primary outcomes for the 10-min PVT. In contrast, PVT mean and median metrics, which are among the most widely used outcomes, should be avoided as primary measures of alertness. Our analyses also suggest that some shorter-duration PVT versions may be sensitive to sleep loss, depending on the outcome variable

Sleep loss impairs short and novel language tasks having a prefrontal focus.

PubMed

Harrison, Y; Horne, J A

1998-06-01

Most cognitive tests administered during sleep loss are well rehearsed to remove practice effects. This can introduce tedium and a loss of novelty, which may be the key to the test's subsequent sensitivity to sleep loss, and why it may need only a few minutes administration before sleep loss effects are apparent. There is little evidence to show that any of these tests are actually affected by sleep loss is given de novo, without practice, but using a non-sleep deprived control group. Although the sleep deprivation literature advocates that short, novel and stimulating tests would not be expected to be sensitive to sleep loss, recent sleep loss findings using neuropsychological tests focussing on the prefrontal cortex, indicate that such tests may challenge this maxim. Twenty healthy young adults were randomly assigned to two groups: nil sleep deprivation (control). and 36h continuous sleep deprivation (SD). Two, novel, interesting and short (6 min) language tests, known (by brain imaging) to have predominantly a PFC focus, were given, once, towards the end of SD: (i) the Haylings test--which measures the capacity to inhibit strong associations in favour of novel responses, and (ii) a variant of the word fluency test--innovation in a verb-to-noun association. Subjects were exhorted to do their best. Compared with control subjects both tasks were significantly impaired by SD. As a check on the effects on the Haylings test, a repeat study was undertaken with 30 more subjects randomly divided as before. The outcome was similar. Linguistically, sleep loss appears to interfere with novel responses and the ability to suppress routine answers.

Enhancing Slow Wave Sleep with Sodium Oxybate Reduces the Behavioral and Physiological Impact of Sleep Loss

PubMed Central

Walsh, James K.; Hall-Porter, Janine M.; Griffin, Kara S.; Dodson, Ehren R.; Forst, Elizabeth H.; Curry, Denise T.; Eisenstein, Rhody D.; Schweitzer, Paula K.

2010-01-01

Study Objectives: To investigate whether enhancement of slow wave sleep (SWS) with sodium oxybate reduces the impact of sleep deprivation. Design: Double-blind, parallel group, placebo-controlled design Setting: Sleep research laboratory Participants: Fifty-eight healthy adults (28 placebo, 30 sodium oxybate), ages 18-50 years. Interventions: A 5-day protocol included 2 screening/baseline nights and days, 2 sleep deprivation nights, each followed by a 3-h daytime (08:00-11:00) sleep opportunity and a recovery night. Sodium oxybate or placebo was administered prior to each daytime sleep period. Multiple sleep latency test (MSLT), psychomotor vigilance test (PVT), Karolinska Sleepiness Scale (KSS), and Profile of Mood States were administered during waking hours. Measurements and Results: During daytime sleep, the sodium oxybate group had more SWS, more EEG spectral power in the 1-9 Hz range, and less REM. Mean MSLT latency was longer for the sodium oxybate group on the night following the first daytime sleep period and on the day following the second day sleep period. Median PVT reaction time was faster in the sodium oxybate group following the second day sleep period. The change from baseline in SWS was positively correlated with the change in MSLT and KSS. During recovery sleep the sodium oxybate group had less TST, SWS, REM, and slow wave activity (SWA) than the placebo group. Conclusions: Pharmacological enhancement of SWS with sodium oxybate resulted in a reduced response to sleep loss on measures of alertness and attention. In addition, SWS enhancement during sleep restriction appears to result in a reduced homeostatic response to sleep loss. Citation: Walsh JK; Hall-Porter JM; Griffin KS; Dodson ER; Forst EH; Curry DT; Eisenstein RD; Schweitzer PK. Enhancing slow wave sleep with sodium oxybate reduces the behavioral and physiological impact of sleep loss. SLEEP 2010;33(9):1217-1225. PMID:20857869

Trait-Like Vulnerability to Total and Partial Sleep Loss

PubMed Central

Rupp, Tracy L.; Wesensten, Nancy J.; Balkin, Thomas J.

2012-01-01

Objective: To determine the extent to which individual differences in vulnerability to total sleep deprivation also reflect individual differences in vulnerability to multiple nights of sleep restriction. Design: Two sleep loss conditions (order counterbalanced) separated by 2 to 4 weeks: (a) total sleep deprivation (TSD) of 2 nights (63 h continuous wakefulness); (b) sleep restriction (SR) of 7 nights of 3 h nightly time in bed (TIB). Both conditions were preceded by 7 in-laboratory nights with 10 h nightly TIB; and followed by 3 recovery nights with 8 h nightly TIB. Measures of cognitive performance (psychomotor vigilance, working memory [1-Back], and mathematical processing), objective alertness, subjective sleepiness, and mood were obtained at regular intervals under both conditions. Intra-class correlation coefficients (ICC) were computed using outcome metrics averaged over the last day (08:00-20:00) of TSD and SR. Setting: Residential sleep/performance testing facility. Participants: Nineteen healthy adults (ages 18-39; 11 males, 8 females). Interventions: 2 nights of TSD and 7 nights SR (3 h nightly TIB). Results: Volunteers who displayed greater vulnerability to TSD displayed greater vulnerability to SR on cognitive performance tasks (ICC: PVT lapses = 0.89; PVT speed = 0.86; 1-Back = 0.88; mathematical processing = 0.68, Ps < 0.05). In addition, trait-like responsivity to TSD/SR was found for mood variables vigor (ICC = 0.91), fatigue (ICC = 0.73), and happiness (ICC = 0.85) (all Ps < 0.05). Conclusion: Resilience to sleep loss is a trait-like characteristic that reflects an individual's ability to maintain performance during both types of sleep loss (SR and TSD). Whether the findings extend to sleep schedules other than those investigated here (63 h of TSD and 7 nights of 3 h nightly TIB) will be the focus of future studies. Citation: Rupp TL; Wesensten NJ; Balkin TJ. Trait-like vulnerability to total and partial sleep loss. SLEEP 2012

Nutrition Influences Caffeine-Mediated Sleep Loss in Drosophila.

PubMed

Keebaugh, Erin S; Park, Jin Hong; Su, Chenchen; Yamada, Ryuichi; Ja, William W

2017-11-01

Plant-derived caffeine is regarded as a defensive compound produced to prevent herbivory. Caffeine is generally repellent to insects and often used to study the neurological basis for aversive responses in the model insect, Drosophila melanogaster. Caffeine is also studied for its stimulatory properties where sleep or drowsiness is suppressed across a range of species. Since limiting access to food also inhibits fly sleep-an effect known as starvation-induced sleep suppression-we tested whether aversion to caffeinated food results in reduced nutrient intake and assessed how this might influence fly studies on the stimulatory effects of caffeine. We measured sleep and total consumption during the first 24 hours of exposure to caffeinated diets containing a range of sucrose concentrations to determine the relative influence of caffeine and nutrient ingestion on sleep. Experiments were replicated using three fly strains. Caffeine reduced total consumption and nighttime sleep, but only at intermediate sucrose concentrations. Although sleep can be modeled by an exponential dose response to nutrient intake, caffeine-mediated sleep loss cannot be explained by absolute caffeine or sucrose ingestion alone. Instead, reduced sleep strongly correlates with changes in total consumption due to caffeine. Other bitter compounds phenocopy the effect of caffeine on sleep and food intake. Our results suggest that a major effect of dietary caffeine is on fly feeding behavior. Changes in feeding behavior may drive caffeine-mediated sleep loss. Future studies using psychoactive compounds should consider the potential impact of nutrition when investigating effects on sleep. © Sleep Research Society 2017. Published by Oxford University Press on behalf of the Sleep Research Society. All rights reserved. For permissions, please e-mail journals.permissions@oup.com.

Sleep loss and accidents--work hours, life style, and sleep pathology.

PubMed

Akerstedt, Torbjörn; Philip, Pierre; Capelli, Aurore; Kecklund, Göran

2011-01-01

A very important outcome of reduced sleep is accidents. The present chapter will attempt to bring together some of the present knowledge in this area. We will focus on the driving situation, for which the evidence of the link between sleep loss and accidents is quite well established, but we will also bring up working life in general where evidence is more sparse. It should be emphasized that reduced sleep as a cause of accidents implies that the mediating factor is sleepiness (or fatigue). This link is discussed elsewhere in this volume, but here we will bring in sleepiness (subjective or physiological) as an explanatory factor of accidents. Another central observation is that many real life accident studies do not link accidents to reduced sleep, but infer reduced sleep and/or sleepiness from the context, like, for example, from work schedules, life styles, or sleep pathology. Reduced sleep is mainly due to suboptimal work schedules (or to a suboptimal life style) or to sleep pathology. We have divided the present chapter into two areas. Copyright © 2011 Elsevier B.V. All rights reserved.

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

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.

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

Hypocretin underlies the evolution of sleep loss in the Mexican cavefish

PubMed Central

Jaggard, James B; Stahl, Bethany A; Lloyd, Evan; Prober, David A; Duboue, Erik R

2018-01-01

The duration of sleep varies dramatically between species, yet little is known about the genetic basis or evolutionary factors driving this variation in behavior. The Mexican cavefish, Astyanax mexicanus, exists as surface populations that inhabit rivers, and multiple cave populations with convergent evolution on sleep loss. The number of Hypocretin/Orexin (HCRT)-positive hypothalamic neurons is increased significantly in cavefish, and HCRT is upregulated at both the transcript and protein levels. Pharmacological or genetic inhibition of HCRT signaling increases sleep in cavefish, suggesting enhanced HCRT signaling underlies the evolution of sleep loss. Ablation of the lateral line or starvation, manipulations that selectively promote sleep in cavefish, inhibit hcrt expression in cavefish while having little effect on surface fish. These findings provide the first evidence of genetic and neuronal changes that contribute to the evolution of sleep loss, and support a conserved role for HCRT in sleep regulation. PMID:29405117

Age, circadian rhythms, and sleep loss in flight crews

NASA Technical Reports Server (NTRS)

Gander, Philippa H.; Nguyen, DE; Rosekind, Mark R.; Connell, Linda J.

1993-01-01

Age-related changes in trip-induced sleep loss, personality, and the preduty temperature rhythm were analyzed in crews from various flight operations. Eveningness decreased with age. The minimum of the baseline temperature rhythm occurred earlier with age. The amplitude of the baseline temperature rhythm declined with age. Average daily percentage sleep loss during trips increased with age. Among crewmembers flying longhaul flight operations, subjects aged 50-60 averaged 3.5 times more sleep loss per day than subjects aged 20-30. These studies support previous findings that evening types and subjects with later peaking temperature rhythms adapt better to shift work and time zone changes. Age and circadian type may be important considerations for duty schedules and fatigue countermeasures.

Cell injury and repair resulting from sleep loss and sleep recovery in laboratory rats.

PubMed

Everson, Carol A; Henchen, Christopher J; Szabo, Aniko; Hogg, Neil

2014-12-01

Increased cell injury would provide the type of change in constitution that would underlie sleep disruption as a risk factor for multiple diseases. The current study was undertaken to investigate cell injury and altered cell fate as consequences of sleep deprivation, which were predicted from systemic clues. Partial (35% sleep reduction) and total sleep deprivation were produced in rats for 10 days, which was tolerated and without overtly deteriorated health. Recovery rats were similarly sleep deprived for 10 days, then allowed undisturbed sleep for 2 days. The plasma, liver, lung, intestine, heart, and spleen were analyzed and compared to control values for damage to DNA, proteins, and lipids; apoptotic cell signaling and death; cell proliferation; and concentrations of glutathione peroxidase and catalase. Oxidative DNA damage in totally sleep deprived rats was 139% of control values, with organ-specific effects in the liver (247%), lung (166%), and small intestine (145%). Overall and organ-specific DNA damage was also increased in partially sleep deprived rats. In the intestinal epithelium, total sleep deprivation resulted in 5.3-fold increases in dying cells and 1.5-fold increases in proliferating cells, compared with control. Recovery sleep restored the balance between DNA damage and repair, and resulted in normal or below-normal metabolic burdens and oxidative damage. These findings provide physical evidence that sleep loss causes cell damage, and in a manner expected to predispose to replication errors and metabolic abnormalities; thereby providing linkage between sleep loss and disease risk observed in epidemiological findings. Properties of recovery sleep include biochemical and molecular events that restore balance and decrease cell injury. © 2014 Associated Professional Sleep Societies, LLC.

Non-invasive Positive Pressure Ventilation during Sleep at 3800m: relationship to Acute Mountain Sickness and sleeping oxyhemoglobin saturation

PubMed Central

Johnson, PL; Popa, DA; Prisk, GK; Sullivan, CE; Edwards, N

2014-01-01

Background and objectives Ascent to high altitude results in hypobaric hypoxia and some individuals will develop Acute Mountain Sickness, which has been shown to be associated with low oxyhemoglobin saturation during sleep. Previous research has shown that positive end-expiratory pressure by use of expiratory valves in a face mask while awake, results in a reduction in AMS symptoms and higher oxyhemoglobin saturation. We aimed to test whether pressure ventilation during sleep would prevent AMS by keeping oxyhaemoglobin higher during sleep. Methods We compared sleeping oxyhemoglobin saturation and the incidence and severity of Acute Mountain Sickness in seven subjects sleeping for two consecutive nights at 3800m above sea level using either non-invasive positive pressure ventilation that delivered positive inspiratory and expiratory airway pressure via a face mask, or sleeping without assisted ventilation. The presence and severity of Acute Mountain Sickness was assessed by administration of the Lake Louise questionnaire. Results We found significant increases in the mean and minimum sleeping oxyhemoglobin saturation and decreases in AMS symptoms in subjects who used positive pressure ventilation during sleep. Mean and minimum sleeping SaO2 was lower in subjects who developed AMS after the night spent without positive pressure ventilation. Conclusion The use of positive pressure ventilation during sleep at 3800m significantly increased the sleeping oxygen saturation; we suggest that the marked reduction in symptoms of AMS is due to this higher sleeping SaO2. We agree with the findings from previous studies that the development of AMS is associated with a lower sleeping oxygen saturation. PMID:20051046

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

NASA Technical Reports Server (NTRS)

Carskadon, Mary A.

1997-01-01

response (performance decrement) to sleep loss compared to subjects who have high MSLT scores (Alert subjects) on a nominal sleep schedule; (2) when permitted to extend sleep--thus discharging their sleep debt-the Sleepy subjects will show a sleep-loss response resembling that of the Alert subjects.

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

NASA Technical Reports Server (NTRS)

Carskadon, Mary A.

1997-01-01

scores (e.g., Sleepy subjects) will show an exaggerated response (performance decrement) to sleep loss compared to subjects who have high MSLT scores (Alert subjects) on a nominal sleep schedule. when permitted to extend sleep-thus discharging their sleep debt-the Sleepy subjects will show a sleep-loss response resembling that of the Alert subjects.

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

NASA Technical Reports Server (NTRS)

Carskadon, Mary A.

1997-01-01

low MSLT scores (e.g., Sleepy subjects) will show an exaggerated response (performance decrement) to sleep loss compared to subjects who have high MSLT scores (Alert subjects) on a nominal sleep schedule. When permitted to extend sleep-thus discharging their sleep debt-the Sleepy subjects will show a sleep-loss response resembling that of the Alert subjects.

Sleep loss increases dissociation and affects memory for emotional stimuli.

PubMed

van Heugten-van der Kloet, Dalena; Giesbrecht, Timo; Merckelbach, Harald

2015-06-01

Because of their dreamlike character, authors have speculated about the role that the sleep-wake cycle plays in dissociative symptoms. We investigated whether sleep loss fuels dissociative symptoms and undermines cognitive efficiency, particularly memory functioning. Fifty-six healthy undergraduate students were randomly assigned to an experimental group (n = 28) and a control group (n = 28). The experimental group was deprived of sleep for 36 h in a sleep laboratory; the control group had a regular night of sleep. Sleepiness, mood, and dissociative symptoms were assessed 6 times in the experimental group (control group: 4 times). Several cognitive tasks were administered. Sleep deprivation led to an increase in dissociative symptoms, which was mediated by levels of general distress. Feelings of sleepiness preceded an increase of dissociative symptoms and deterioration of mood. Finally, sleep loss also undermined memory of emotional material, especially in highly dissociative individuals. Limitations included moderate reliability of the mood scale, limited generalizability due to student sample, and a relatively short period of intensive sleep deprivation rather than lengthy but intermittent sleep loss, representative of a clinical population. We found that sleep deprivation had significant effects on dissociation, sleepiness, and mood. Specifically, sleepiness and dissociation increased during the night, while mood deteriorated. Our findings stress the importance of sleep deficiencies in the development of dissociative symptoms. They support the view that sleep disruptions fuel distress, but also degrade memory and attentional control. It is against this background that dissociative symptoms may arise. Copyright © 2014 Elsevier Ltd. All rights reserved.

Dynamic circadian modulation in a biomathematical model for the effects of sleep and sleep loss on waking neurobehavioral performance.

PubMed

McCauley, Peter; Kalachev, Leonid V; Mollicone, Daniel J; Banks, Siobhan; Dinges, David F; Van Dongen, Hans P A

2013-12-01

Recent experimental observations and theoretical advances have indicated that the homeostatic equilibrium for sleep/wake regulation--and thereby sensitivity to neurobehavioral impairment from sleep loss--is modulated by prior sleep/wake history. This phenomenon was predicted by a biomathematical model developed to explain changes in neurobehavioral performance across days in laboratory studies of total sleep deprivation and sustained sleep restriction. The present paper focuses on the dynamics of neurobehavioral performance within days in this biomathematical model of fatigue. Without increasing the number of model parameters, the model was updated by incorporating time-dependence in the amplitude of the circadian modulation of performance. The updated model was calibrated using a large dataset from three laboratory experiments on psychomotor vigilance test (PVT) performance, under conditions of sleep loss and circadian misalignment; and validated using another large dataset from three different laboratory experiments. The time-dependence of circadian amplitude resulted in improved goodness-of-fit in night shift schedules, nap sleep scenarios, and recovery from prior sleep loss. The updated model predicts that the homeostatic equilibrium for sleep/wake regulation--and thus sensitivity to sleep loss--depends not only on the duration but also on the circadian timing of prior sleep. This novel theoretical insight has important implications for predicting operator alertness during work schedules involving circadian misalignment such as night shift work.

Catechol-O-Methyltransferase Val158Met Polymorphism Associates with Individual Differences in Sleep Physiologic Responses to Chronic Sleep Loss

PubMed Central

Goel, Namni; Banks, Siobhan; Lin, Ling; Mignot, Emmanuel; Dinges, David F.

2011-01-01

Background The COMT Val158Met polymorphism modulates cortical dopaminergic catabolism, and predicts individual differences in prefrontal executive functioning in healthy adults and schizophrenic patients, and associates with EEG differences during sleep loss. We assessed whether the COMT Val158Met polymorphism was a novel marker in healthy adults of differential vulnerability to chronic partial sleep deprivation (PSD), a condition distinct from total sleep loss and one experienced by millions on a daily and persistent basis. Methodology/Principal Findings 20 Met/Met, 64 Val/Met, and 45 Val/Val subjects participated in a protocol of two baseline 10h time in bed (TIB) nights followed by five consecutive 4 h TIB nights. Met/Met subjects showed differentially steeper declines in non-REM EEG slow-wave energy (SWE)—the putative homeostatic marker of sleep drive—during PSD, despite comparable baseline SWE declines. Val/Val subjects showed differentially smaller increases in slow-wave sleep and smaller reductions in stage 2 sleep during PSD, and had more stage 1 sleep across nights and a shorter baseline REM sleep latency. The genotypes, however, did not differ in performance across various executive function and cognitive tasks and showed comparable increases in subjective and physiological sleepiness in response to chronic sleep loss. Met/Met genotypic and Met allelic frequencies were higher in whites than African Americans. Conclusions/Significance The COMT Val158Met polymorphism may be a genetic biomarker for predicting individual differences in sleep physiology—but not in cognitive and executive functioning—resulting from sleep loss in a healthy, racially-diverse adult population of men and women. Beyond healthy sleepers, our results may also provide insight for predicting sleep loss responses in patients with schizophrenia and other psychiatric disorders, since these groups repeatedly experience chronically-curtailed sleep and demonstrate COMT

Identification of Genes that Maintain Behavioral and Structural Plasticity during Sleep Loss

PubMed Central

Seugnet, Laurent; Dissel, Stephane; Thimgan, Matthew; Cao, Lijuan; Shaw, Paul J.

2017-01-01

Although patients with primary insomnia experience sleep disruption, they are able to maintain normal performance on a variety of cognitive tasks. This observation suggests that insomnia may be a condition where predisposing factors simultaneously increase the risk for insomnia and also mitigate against the deleterious consequences of waking. To gain insight into processes that might regulate sleep and buffer neuronal circuits during sleep loss, we manipulated three genes, fat facet (faf), highwire (hiw) and the GABA receptor Resistance to dieldrin (Rdl), that were differentially modulated in a Drosophila model of insomnia. Our results indicate that increasing faf and decreasing hiw or Rdl within wake-promoting large ventral lateral clock neurons (lLNvs) induces sleep loss. As expected, sleep loss induced by decreasing hiw in the lLNvs results in deficits in short-term memory and increases of synaptic growth. However, sleep loss induced by knocking down Rdl in the lLNvs protects flies from sleep-loss induced deficits in short-term memory and increases in synaptic markers. Surprisingly, decreasing hiw and Rdl within the Mushroom Bodies (MBs) protects against the negative effects of sleep deprivation (SD) as indicated by the absence of a subsequent homeostatic response, or deficits in short-term memory. Together these results indicate that specific genes are able to disrupt sleep and protect against the negative consequences of waking in a circuit dependent manner. PMID:29109678

Parallel recovery of consciousness and sleep in acute traumatic brain injury.

PubMed

Duclos, Catherine; Dumont, Marie; Arbour, Caroline; Paquet, Jean; Blais, Hélène; Menon, David K; De Beaumont, Louis; Bernard, Francis; Gosselin, Nadia

2017-01-17

To investigate whether the progressive recuperation of consciousness was associated with the reconsolidation of sleep and wake states in hospitalized patients with acute traumatic brain injury (TBI). This study comprised 30 hospitalized patients (age 29.1 ± 13.5 years) in the acute phase of moderate or severe TBI. Testing started 21.0 ± 13.7 days postinjury. Consciousness level and cognitive functioning were assessed daily with the Rancho Los Amigos scale of cognitive functioning (RLA). Sleep and wake cycle characteristics were estimated with continuous wrist actigraphy. Mixed model analyses were performed on 233 days with the RLA (fixed effect) and sleep-wake variables (random effects). Linear contrast analyses were performed in order to verify if consolidation of the sleep and wake states improved linearly with increasing RLA score. Associations were found between scores on the consciousness/cognitive functioning scale and measures of sleep-wake cycle consolidation (p < 0.001), nighttime sleep duration (p = 0.018), and nighttime fragmentation index (p < 0.001). These associations showed strong linear relationships (p < 0.01 for all), revealing that consciousness and cognition improved in parallel with sleep-wake quality. Consolidated 24-hour sleep-wake cycle occurred when patients were able to give context-appropriate, goal-directed responses. Our results showed that when the brain has not sufficiently recovered a certain level of consciousness, it is also unable to generate a 24-hour sleep-wake cycle and consolidated nighttime sleep. This study contributes to elucidating the pathophysiology of severe sleep-wake cycle alterations in the acute phase of moderate to severe TBI. © 2016 American Academy of Neurology.

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. Copyright © 2014 Elsevier Inc. All rights reserved.

The perilipin homologue, lipid storage droplet 2, regulates sleep homeostasis and prevents learning impairments following sleep loss.

PubMed

Thimgan, Matthew S; Suzuki, Yasuko; Seugnet, Laurent; Gottschalk, Laura; Shaw, Paul J

2010-08-31

Extended periods of waking result in physiological impairments in humans, rats, and flies. Sleep homeostasis, the increase in sleep observed following sleep loss, is believed to counter the negative effects of prolonged waking by restoring vital biological processes that are degraded during sleep deprivation. Sleep homeostasis, as with other behaviors, is influenced by both genes and environment. We report here that during periods of starvation, flies remain spontaneously awake but, in contrast to sleep deprivation, do not accrue any of the negative consequences of prolonged waking. Specifically, the homeostatic response and learning impairments that are a characteristic of sleep loss are not observed following prolonged waking induced by starvation. Recently, two genes, brummer (bmm) and Lipid storage droplet 2 (Lsd2), have been shown to modulate the response to starvation. bmm mutants have excess fat and are resistant to starvation, whereas Lsd2 mutants are lean and sensitive to starvation. Thus, we hypothesized that bmm and Lsd2 may play a role in sleep regulation. Indeed, bmm mutant flies display a large homeostatic response following sleep deprivation. In contrast, Lsd2 mutant flies, which phenocopy aspects of starvation as measured by low triglyceride stores, do not exhibit a homeostatic response following sleep loss. Importantly, Lsd2 mutant flies are not learning impaired after sleep deprivation. These results provide the first genetic evidence, to our knowledge, that lipid metabolism plays an important role in regulating the homeostatic response and can protect against neuronal impairments induced by prolonged waking.

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. © 2016 Associated Professional Sleep Societies, LLC.

Caffeine dosing strategies to optimize alertness during sleep loss.

PubMed

Vital-Lopez, Francisco G; Ramakrishnan, Sridhar; Doty, Tracy J; Balkin, Thomas J; Reifman, Jaques

2018-05-28

Sleep loss, which affects about one-third of the US population, can severely impair physical and neurobehavioural performance. Although caffeine, the most widely used stimulant in the world, can mitigate these effects, currently there are no tools to guide the timing and amount of caffeine consumption to optimize its benefits. In this work, we provide an optimization algorithm, suited for mobile computing platforms, to determine when and how much caffeine to consume, so as to safely maximize neurobehavioural performance at the desired time of the day, under any sleep-loss condition. The algorithm is based on our previously validated Unified Model of Performance, which predicts the effect of caffeine consumption on a psychomotor vigilance task. We assessed the algorithm by comparing the caffeine-dosing strategies (timing and amount) it identified with the dosing strategies used in four experimental studies, involving total and partial sleep loss. Through computer simulations, we showed that the algorithm yielded caffeine-dosing strategies that enhanced performance of the predicted psychomotor vigilance task by up to 64% while using the same total amount of caffeine as in the original studies. In addition, the algorithm identified strategies that resulted in equivalent performance to that in the experimental studies while reducing caffeine consumption by up to 65%. Our work provides the first quantitative caffeine optimization tool for designing effective strategies to maximize neurobehavioural performance and to avoid excessive caffeine consumption during any arbitrary sleep-loss condition. © 2018 The Authors. Journal of Sleep Research published by John Wiley & Sons Ltd on behalf of European Sleep Research Society.

Sleep Loss Effects on Continuous Sustained Performance.

DTIC Science & Technology

1982-11-30

Sleep loss, continuous performance, sustained performance, sleep deprivation, sleepiness, fatigue, circadian rhythm, hallucination . 20, ABSTRACT...complete the 42 hours and 9 experienced "psychological events such as hallucinations , visual illusions, and disorientation. Of the 20 subjects who... hallucinations , derealizations, and distortions (Mullaney, Kripke, and Fleck, 1981). All 20 subjects who were given either one 6-hour or six 1-hour

Improvement in Obstructive Sleep Apnea With Weight Loss is Dependent on Body Position During Sleep.

PubMed

Joosten, Simon A; Khoo, Jun K; Edwards, Bradley A; Landry, Shane A; Naughton, Matthew T; Dixon, John B; Hamilton, Garun S

2017-05-01

Weight loss fails to resolve obstructive sleep apnea (OSA) in most patients; however, it is unknown as to whether weight loss differentially affects OSA in the supine compared with nonsupine sleeping positions. We aimed to determine if weight loss in obese patients with OSA results in a greater reduction in the nonsupine apnea/hypopnea index (AHI) compared with the supine AHI, thus converting participants into supine-predominant OSA. Post hoc analysis of data from a randomized controlled trial assessing the effect of weight loss (bariatric surgery vs. medical weight loss) on OSA in 60 participants with obesity (body mass index: >35 and <55) with recently diagnosed (<6 months) OSA and AHI of ≥ 20 events/hour. Patients were randomized to very low calorie diet with regular review (n = 30) or to laproscopic adjustable gastric banding (n = 30) with follow-up sleep study at 2 years. Eight of 37 (22%) patients demonstrated a normal nonsupine AHI (<5 events/hour) on follow-up compared to 0/37 (0%) patients at baseline (p = .003). These patients were younger (40.0 ± 9.6 years vs. 48.4 ± 6.5 years, p = .007) and lost significantly more weight (percentage weight change -23.0 [-21.0 to -31.6]% vs. -6.9 [1.9 to -17.4], p = .001). The percentage change in nonsupine AHI was greater than the percentage change in supine AHI (-54.0 [-15.4 to -87.9]% vs -33.1 [-1.8 to -69.1]%, p = .05). However, the change in absolute nonsupine AHI was not related to change in absolute supine AHI (p = .23). Following weight loss, a significant proportion (22%) of patients with obesity have normalization of the nonsupine AHI. For these patients, supine sleep avoidance may cure their OSA. © Sleep Research Society 2017. Published by Oxford University Press on behalf of the Sleep Research Society. All rights reserved. For permissions, please e-mail journals.permissions@oup.com.

Cross-Translational Studies in Human and Drosophila Identify Markers of Sleep Loss

PubMed Central

Thimgan, Matthew S.; Gottschalk, Laura; Toedebusch, Cristina; McLeland, Jennifer; Rechtschaffen, Allan; Gilliland-Roberts, Marcia; Duntley, Stephen P.; Shaw, Paul J.

2013-01-01

Inadequate sleep has become endemic, which imposes a substantial burden for public health and safety. At present, there are no objective tests to determine if an individual has gone without sleep for an extended period of time. Here we describe a novel approach that takes advantage of the evolutionary conservation of sleep to identify markers of sleep loss. To begin, we demonstrate that IL-6 is increased in rats following chronic total sleep deprivation and in humans following 30 h of waking. Discovery experiments were then conducted on saliva taken from sleep-deprived human subjects to identify candidate markers. Given the relationship between sleep and immunity, we used Human Inflammation Low Density Arrays to screen saliva for novel markers of sleep deprivation. Integrin αM (ITGAM) and Anaxin A3 (AnxA3) were significantly elevated following 30 h of sleep loss. To confirm these results, we used QPCR to evaluate ITGAM and AnxA3 in independent samples collected after 24 h of waking; both transcripts were increased. The behavior of these markers was then evaluated further using the power of Drosophila genetics as a cost-effective means to determine whether the marker is associated with vulnerability to sleep loss or other confounding factors (e.g., stress). Transcript profiling in flies indicated that the Drosophila homologues of ITGAM were not predictive of sleep loss. Thus, we examined transcript levels of additional members of the integrin family in flies. Only transcript levels of scab, the Drosophila homologue of Integrin α5 (ITGA5), were associated with vulnerability to extended waking. Since ITGA5 was not included on the Low Density Array, we returned to human samples and found that ITGA5 transcript levels were increased following sleep deprivation. These cross-translational data indicate that fly and human discovery experiments are mutually reinforcing and can be used interchangeably to identify candidate biomarkers of sleep loss. PMID:23637783

A neuron-glia interaction involving GABA Transaminase contributes to sleep loss in sleepless mutants

PubMed Central

Chen, Wen-Feng; Maguire, Sarah; Sowcik, Mallory; Luo, Wenyu; Koh, Kyunghee; Sehgal, Amita

2014-01-01

Sleep is an essential process and yet mechanisms underlying it are not well understood. Loss of the Drosophila quiver/sleepless (qvr/sss) gene increases neuronal excitability and diminishes daily sleep, providing an excellent model for exploring the underpinnings of sleep regulation. Here, we used a proteomic approach to identify proteins altered in sss brains. We report that loss of sleepless post-transcriptionally elevates the CG7433 protein, a mitochondrial γ-aminobutyric acid transaminase (GABAT), and reduces GABA in fly brains. Loss of GABAT increases daily sleep and improves sleep consolidation, indicating that GABAT promotes wakefulness. Importantly, disruption of the GABAT gene completely suppresses the sleep phenotype of sss mutants, demonstrating that GABAT is required for loss of sleep in sss mutants. While SSS acts in distinct populations of neurons, GABAT acts in glia to reduce sleep in sss flies. Our results identify a novel mechanism of interaction between neurons and glia that is important for the regulation of sleep. PMID:24637426

Neuropsychological Function in Patients With Acute Tetraplegia and Sleep Disordered Breathing.

PubMed

Schembri, Rachel; Spong, Jo; Graco, Marnie; Berlowitz, David J

2017-02-01

To investigate the relationship between apnea severity and neuropsychological function in patients with acute-onset tetraplegia and sleep disordered breathing. Polysomnography and neuropsychological testing were performed on 104 participants (age M = 45.60, SD = 16.38; 10 female) across 11 international sites, 2 months postinjury (M = 60.70 days, SD = 39.48). Neuropsychological tests assessed attention, information processing, executive function, memory, learning, mood, and quality of life. More severe sleep apnea was associated with poorer attention, information processing, and immediate recall. Deficits did not extend to memory. Higher preinjury intelligence and being younger reduced the associations with sleep disordered breathing; however, these protective factors were insufficient to counter the damage to attention, immediate recall, and information processing associated with sleep disordered breathing. These data suggest that new spinal cord injury may function as a model of "acute sleep apnea" and that more widespread sleep apnea-related deficits, including memory, may only be seen with longer exposure to apnea. These findings have important implications for functioning and skill acquisition during rehabilitation and, as such, highlight the importance of sleep health following tetraplegia. © Sleep Research Society 2016. Published by Oxford University Press on behalf of the Sleep Research Society. All rights reserved. For permissions, please e-mail journals.permissions@oup.com.

Dynamic Circadian Modulation in a Biomathematical Model for the Effects of Sleep and Sleep Loss on Waking Neurobehavioral Performance

PubMed Central

McCauley, Peter; Kalachev, Leonid V.; Mollicone, Daniel J.; Banks, Siobhan; Dinges, David F.; Van Dongen, Hans P. A.

2013-01-01

Recent experimental observations and theoretical advances have indicated that the homeostatic equilibrium for sleep/wake regulation—and thereby sensitivity to neurobehavioral impairment from sleep loss—is modulated by prior sleep/wake history. This phenomenon was predicted by a biomathematical model developed to explain changes in neurobehavioral performance across days in laboratory studies of total sleep deprivation and sustained sleep restriction. The present paper focuses on the dynamics of neurobehavioral performance within days in this biomathematical model of fatigue. Without increasing the number of model parameters, the model was updated by incorporating time-dependence in the amplitude of the circadian modulation of performance. The updated model was calibrated using a large dataset from three laboratory experiments on psychomotor vigilance test (PVT) performance, under conditions of sleep loss and circadian misalignment; and validated using another large dataset from three different laboratory experiments. The time-dependence of circadian amplitude resulted in improved goodness-of-fit in night shift schedules, nap sleep scenarios, and recovery from prior sleep loss. The updated model predicts that the homeostatic equilibrium for sleep/wake regulation—and thus sensitivity to sleep loss—depends not only on the duration but also on the circadian timing of prior sleep. This novel theoretical insight has important implications for predicting operator alertness during work schedules involving circadian misalignment such as night shift work. Citation: McCauley P; Kalachev LV; Mollicone DJ; Banks S; Dinges DF; Van Dongen HPA. Dynamic circadian modulation in a biomathematical model for the effects of sleep and sleep loss on waking neurobehavioral performance. SLEEP 2013;36(12):1987-1997. PMID:24293775

Sleep Loss Exacerbates Fatigue, Depression, and Pain in Rheumatoid Arthritis

PubMed Central

Irwin, Michael R.; Olmstead, Richard; Carrillo, Carmen; Sadeghi, Nina; FitzGerald, John D.; Ranganath, Veena K.; Nicassio, Perry M.

2012-01-01

Study Objectives: Disturbances of sleep are hypothesized to contribute to pain. However, experimental data are limited to healthy pain-free individuals. This study evaluated the effect of sleep loss during part of the night on daytime mood symptoms and pain perceptions in patients with rheumatoid arthritis in comparison with control subjects. Design: A between-groups laboratory study with assessment of mood symptoms and pain perception before and after partial night sleep deprivation (PSD; awake 23:00 hr to 03:00 hr). Setting: General clinical research center. Participants: Patients with rheumatoid arthritis (n = 27) and volunteer comparison control subjects (n = 27). Measurements: Subjective reports of sleep, mood symptoms and pain, polysomnographic assessment of sleep continuity, and subjective and objective assessment of rheumatoid arthritis-specific joint pain. Results: PSD induced differential increases in self-reported fatigue (P < 0.09), depression (P < 0.04), anxiety (P < 0.04), and pain (P < 0.01) in patients with rheumatoid arthritis compared with responses in control subjects, in whom differential increases of self-reported pain were independent of changes in mood symptoms, subjective sleep quality, and objective measures of sleep fragmentation. In the patients with rheumatoid arthritis, PSD also induced increases in disease-specific activity as indexed by self-reported pain severity (P < 0.01) and number of painful joints (P < 0.02) as well as clinician-rated joint counts (P < 0.03). Conclusion: This study provides the first evidence of an exaggerated increase in symptoms of mood and pain in patients with rheumatoid arthritis after sleep loss, along with an activation of rheumatoid arthritis-related joint pain. Given the reciprocal relationship between sleep disturbances and pain, clinical management of pain in patients with rheumatoid arthritis should include an increased focus on the prevention and treatment of sleep disturbance in this clinical

Polysomnographic measures of sleep in cocaine dependence and alcohol dependence: Implications for age‐related loss of slow wave, stage 3 sleep

PubMed Central

Bjurstrom, Martin F.; Olmstead, Richard

2016-01-01

Abstract Background and aims Sleep disturbance is a prominent complaint in cocaine and alcohol dependence. This controlled study evaluated differences of polysomnographic (PSG) sleep in cocaine‐ and alcohol‐dependent subjects, and examined whether substance dependence interacts with age to alter slow wave sleep and rapid eye movement (REM) sleep. Design Cross‐sectional comparison. Setting Los Angeles and San Diego, CA, USA. Participants Abstinent cocaine‐dependent subjects (n = 32), abstinent alcohol‐dependent subjects (n = 73) and controls (n = 108); mean age 40.3 years recruited 2005–12. Measurements PSG measures of sleep continuity and sleep architecture primary outcomes of Stage 3 sleep and REM sleep. Covariates included age, ethnicity, education, smoking, body mass index and depressive symptoms. Findings Compared with controls, both groups of substance dependent subjects showed loss of Stage 3 sleep (P < 0.001). A substance dependence × age interaction was found in which both cocaine‐ and alcohol‐dependent groups showed loss of Stage 3 sleep at an earlier age than controls (P < 0.05 for all), and cocaine‐dependent subjects showed loss of Stage 3 sleep at an earlier age than alcoholics (P < 0.05). Compared with controls, REM sleep was increased in both substance‐dependent groups (P < 0.001), and cocaine and alcohol dependence were associated with earlier age‐related increase in REM sleep (P < 0.05 for all). Conclusions Cocaine and alcohol dependence appear to be associated with marked disturbances of sleep architecture, including increased rapid eye movement sleep and accelerated age‐related loss of slow wave, Stage 3 sleep. PMID:26749502

Homer1a is a core brain molecular correlate of sleep loss.

PubMed

Maret, Stéphanie; Dorsaz, Stéphane; Gurcel, Laure; Pradervand, Sylvain; Petit, Brice; Pfister, Corinne; Hagenbuchle, Otto; O'Hara, Bruce F; Franken, Paul; Tafti, Mehdi

2007-12-11

Sleep is regulated by a homeostatic process that determines its need and by a circadian process that determines its timing. By using sleep deprivation and transcriptome profiling in inbred mouse strains, we show that genetic background affects susceptibility to sleep loss at the transcriptional level in a tissue-dependent manner. In the brain, Homer1a expression best reflects the response to sleep loss. Time-course gene expression analysis suggests that 2,032 brain transcripts are under circadian control. However, only 391 remain rhythmic when mice are sleep-deprived at four time points around the clock, suggesting that most diurnal changes in gene transcription are, in fact, sleep-wake-dependent. By generating a transgenic mouse line, we show that in Homer1-expressing cells specifically, apart from Homer1a, three other activity-induced genes (Ptgs2, Jph3, and Nptx2) are overexpressed after sleep loss. All four genes play a role in recovery from glutamate-induced neuronal hyperactivity. The consistent activation of Homer1a suggests a role for sleep in intracellular calcium homeostasis for protecting and recovering from the neuronal activation imposed by wakefulness.

What drives sleep-dependent memory consolidation: greater gain or less loss?

PubMed

Fenn, Kimberly M; Hambrick, David Z

2013-06-01

When memory is tested after a delay, performance is typically better if the retention interval includes sleep. However, it is unclear what accounts for this well-established effect. It is possible that sleep enhances the retrieval of information, but it is also possible that sleep protects against memory loss that normally occurs during waking activity. We developed a new research approach to investigate these possibilities. Participants learned a list of paired-associate items and were tested on the items after a 12-h interval that included waking or sleep. We analyzed the number of items gained versus the number of items lost across time. The sleep condition showed more items gained and fewer items lost than did the wake condition. Furthermore, the difference between the conditions (favoring sleep) in lost items was greater than the difference in gain, suggesting that loss prevention may primarily account for the effect of sleep on declarative memory consolidation. This finding may serve as an empirical constraint on theories of memory consolidation.

More daytime sleeping predicts less functional recovery among older people undergoing inpatient post-acute rehabilitation.

PubMed

Alessi, Cathy A; Martin, Jennifer L; Webber, Adam P; Alam, Tarannum; Littner, Michael R; Harker, Judith O; Josephson, Karen R

2008-09-01

To study the association between sleep/wake patterns among older adults during inpatient post-acute rehabilitation and their immediate and long-term functional recovery Prospective, observational cohort study. Two inpatient post-acute rehabilitation sites (one community and one Veterans Administration). Older patients (aged > or = 65 years, N = 245) admitted for inpatient post-acute rehabilitation. None. Based on 7-day wrist actigraphy during the rehabilitation stay, mean nighttime percent sleep was only 52.2% and mean daytime percent sleep was 15.8% (16.3% based on structured behavioral observations). Using the Pittsburgh Sleep Quality Index (PSQI), participants reported their sleep was worse during rehabilitation compared to their premorbid sleep. Functional recovery between admission and discharge from rehabilitation (measured by the motor component of the Functional Independence Measure) was not significantly associated with reported sleep quality (PSQI scores) or actigraphically measured nighttime sleep. However, more daytime percent sleep (estimated by actigraphy and observations) during the rehabilitation stay was associated with less functional recovery from admission to discharge, even after adjusting for other significant predictors of functional recovery (mental status, hours of rehabilitation therapy received, rehospitalization, and reason for admission; adjusted R2= 0.267, P < 0.0001). More daytime sleeping during rehabilitation remained a significant predictor of less functional recovery in adjusted analyses at 3-month follow-up. Sleep disturbance is common among older people undergoing inpatient post-acute rehabilitation. These data suggest that more daytime sleeping during the rehabilitation stay is associated with less functional recovery for up to three months after admission for rehabilitation.

Poor Self-Reported Sleep Quality Predicts Mortality within One Year of Inpatient Post-Acute Rehabilitation among Older Adults

PubMed Central

Martin, Jennifer L.; Fiorentino, Lavinia; Jouldjian, Stella; Mitchell, Michael; Josephson, Karen R.; Alessi, Cathy A.

2011-01-01

Study Objective: To evaluate the association between self-reported sleep quality among older adults during inpatient post-acute rehabilitation and one-year survival. Design: Prospective, observational cohort study. Setting: Two inpatient post-acute rehabilitation sites (one community and one Veterans Administration). Participants: Older patients (aged ≥ 65 years, n = 245) admitted for inpatient post-acute rehabilitation. Interventions: None. Measurements and Results: Within one year of post-acute rehabilitation, 57 participants (23%) were deceased. Cox proportional hazards models showed that worse Pittsburgh Sleep Quality Index (PSQI) total scores during the post-acute care stay were associated with increased mortality risk when controlling for amount of rehabilitation therapy received, comorbidities, and cognitive functioning (Hazard ratio [95% CI] = 1.11 [1.02-1.20]). Actigraphically estimated sleep was unrelated to mortality risk. Conclusions: Poorer self-reported sleep quality, but not objectively estimated sleep parameters, during post-acute rehabilitation was associated with shorter survival among older adults. This suggests self-reported poor sleep may be an important and potentially modifiable risk factor for negative outcomes in these vulnerable older adults. Studies of interventions to improve sleep quality during inpatient rehabilitation should therefore be undertaken, and the long-term health benefits of improved sleep should be explored. Citation: Martin JL; Fiorentino L; Jouldjian S; Mitchell M; Josephson KR; Alessi CA. Poor self-reported sleep quality predicts mortality within one year of inpatient post-acute rehabilitation among older adults. SLEEP 2011;34(12):1715-1721. PMID:22131610

Increased impulsivity in response to food cues after sleep loss in healthy young men

PubMed Central

Cedernaes, Jonathan; Brandell, Jon; Ros, Olof; Broman, Jan-Erik; Hogenkamp, Pleunie S; Schiöth, Helgi B; Benedict, Christian

2014-01-01

Objective To investigate whether acute total sleep deprivation (TSD) leads to decreased cognitive control when food cues are presented during a task requiring active attention, by assessing the ability to cognitively inhibit prepotent responses. Methods Fourteen males participated in the study on two separate occasions in a randomized, crossover within-subject design: one night of TSD versus normal sleep (8.5 hours). Following each nighttime intervention, hunger ratings and morning fasting plasma glucose concentrations were assessed before performing a go/no-go task. Results Following TSD, participants made significantly more commission errors when they were presented “no-go” food words in the go/no-go task, as compared with their performance following sleep (+56%; P<0.05). In contrast, response time and omission errors to “go” non-food words did not differ between the conditions. Self-reported hunger after TSD was increased without changes in fasting plasma glucose. The increase in hunger did not correlate with the TSD-induced commission errors. Conclusions Our results suggest that TSD impairs cognitive control also in response to food stimuli in healthy young men. Whether such loss of inhibition or impulsiveness is food cue-specific as seen in obesity—thus providing a mechanism through which sleep disturbances may promote obesity development—warrants further investigation. PMID:24839251

Effects of sleep loss on vestibular response during simple and complex vestibular stimulation.

DOT National Transportation Integrated Search

1986-07-01

Few data are available concerning the effects of sleep loss on vestibular responses although those responses are significant products of motion in aviation environments. This study assessed periodically throughout approx. 55 hrs. of sleep loss the oc...

Mania triggered by sleep loss and risk of postpartum psychosis in women with bipolar disorder.

PubMed

Lewis, Katie J S; Di Florio, Arianna; Forty, Liz; Gordon-Smith, Katherine; Perry, Amy; Craddock, Nick; Jones, Lisa; Jones, Ian

2018-01-01

Women with bipolar disorder are at high risk of affective psychoses following childbirth (i.e. "postpartum psychosis", PP) and there is a need to identify which factors underlie this increased risk. Vulnerability to mood dysregulation following sleep loss may influence risk of PP, as childbirth is typified by sleep disruption. We investigated whether a history of mood episodes triggered by sleep loss was associated with PP in women with bipolar disorder (BD). Participants were 870 parous women with BD recruited to the Bipolar Disorder Research Network. Lifetime diagnoses of BD and perinatal episodes were identified via interview and case notes. Information on whether mood episodes had been triggered by sleep loss was derived at interview. Rates of PP were compared between women who did and did not report mood episodes following sleep loss. Women who reported sleep loss triggering episodes of mania were twice as likely to have experienced an episode of PP (OR = 2.09, 95% CI = 1.47-2.97, p < 0.001) compared to women who did not report this. There was no significant association between depression triggered by sleep loss and PP (p = 0.526). Data were cross-sectional therefore may be subject to recall bias. We also did not have objective data on sleep disruption that had occurred during the postpartum period or prior to mood episodes. In clinical practice, a history of mania following sleep loss could be a marker of increased vulnerability to PP, and should be discussed with BD women who are pregnant or planning to conceive. Copyright © 2017. Published by Elsevier B.V.

Sleep Disturbance and Short Sleep as Risk Factors for Depression and Perceived Medical Errors in First-Year Residents.

PubMed

Kalmbach, David A; Arnedt, J Todd; Song, Peter X; Guille, Constance; Sen, Srijan

2017-03-01

While short and poor quality sleep among training physicians has long been recognized as problematic, the longitudinal relationships among sleep, work hours, mood, and work performance are not well understood. Here, we prospectively characterize the risk of depression and medical errors based on preinternship sleep disturbance, internship-related sleep duration, and duty hours. Survey data from 1215 nondepressed interns were collected at preinternship baseline, then 3 and 6 months into internship. We examined how preinternship sleep quality and internship sleep and work hours affected risk of depression at 3 months, per the Patient Health Questionnaire 9. We then examined the impact of sleep loss and work hours on depression persistence from 3 to 6 months. Finally, we compared self-reported errors among interns based on nightly sleep duration (≤6 hr vs. >6 hr), weekly work hours (<70 hr vs. ≥70 hr), and depression (non- vs. acutely vs. chronically depressed). Poorly sleeping trainees obtained less sleep and were at elevated risk of depression in the first months of internship. Short sleep (≤6 hr nightly) during internship mediated the relationship between sleep disturbance and depression risk, and sleep loss led to a chronic course for depression. Depression rates were highest among interns with both sleep disturbance and short sleep. Elevated medical error rates were reported by physicians sleeping ≤6 hr per night, working ≥ 70 weekly hours, and who were acutely or chronically depressed. Sleep disturbance and internship-enforced short sleep increase risk of depression development and chronicity and medical errors. Interventions targeting sleep problems prior to and during residency hold promise for curbing depression rates and improving patient care. © Sleep Research Society 2017. Published by Oxford University Press on behalf of the Sleep Research Society. All rights reserved. For permissions, please e-mail journals.permissions@oup.com.

Acute and subchronic administration of anandamide or oleamide increases REM sleep in rats.

PubMed

Herrera-Solís, Andrea; Vásquez, Khalil Guzmán; Prospéro-García, Oscar

2010-03-01

Anandamide and oleamide, induce sleep when administered acutely, via the CB1 receptor. Their subchronic administration must be tested to demonstrate the absence of tolerance to this effect, and that the sudden withdrawal of these endocannabinoids (eCBs) does not affect sleep negatively. The sleep-waking cycle of rats was evaluated for 24h, under the effect of an acute or subchronic administration of eCBs, and during sudden eCBs withdrawal. AM251, a CB1 receptor antagonist (CB1Ra) was utilized to block eCBs effects. Our results indicated that both acute and subchronic administration of eCBs increase REMS. During eCBs withdrawal, rats lack the expression of an abstinence-like syndrome. AM251 was efficacious to prevent REMS increase caused by both acute and subchronic administration of these eCBs, suggesting that this effect is mediated by the CB1 receptor. Our data further support a role of the eCBs in REMS regulation. (c) 2009 Elsevier Inc. All rights reserved.

Short Sleep Duration, Obstructive Sleep Apnea, Shiftwork, and the Risk of Adverse Cardiovascular Events in Patients After an Acute Coronary Syndrome.

PubMed

Barger, Laura K; Rajaratnam, Shantha M W; Cannon, Christopher P; Lukas, Mary Ann; Im, KyungAh; Goodrich, Erica L; Czeisler, Charles A; O'Donoghue, Michelle L

2017-10-10

It is unknown whether short sleep duration, obstructive sleep apnea, and overnight shift work are associated with the risk of recurrent cardiovascular events in patients after an acute coronary syndrome. SOLID-TIMI 52 (The Stabilization of PLaques UsIng Darapladib-Thrombolysis in Myocardial Infarction 52 Trial) was a multinational, double-blind, placebo-controlled trial that enrolled 13 026 patients ≤30 days of acute coronary syndrome. At baseline, all patients were to complete the Berlin questionnaire to assess risk of obstructive sleep apnea and a sleep and shift work survey. Median follow-up was 2.5 years. The primary outcome was major coronary events (MCE; coronary heart disease death, myocardial infarction, or urgent revascularization). Cox models were adjusted for clinical predictors. Patients who reported <6 hours sleep per night had a 29% higher risk of MCE (adjusted hazard ratio, 1.29; 95% confidence interval, 1.12-1.49; P <0.001) compared with those with longer sleep. Patients who screened positive for obstructive sleep apnea had a 12% higher risk of MCE (1.12; 1.00-1.24; P =0.04) than those who did not screen positive. Overnight shift work (≥3 night shifts/week for ≥1 year) was associated with a 15% higher risk of MCE (1.15; 1.03-1.29; P =0.01). A step-wise increase in cardiovascular risk was observed for individuals with more than 1 sleep-related risk factor. Individuals with all 3 sleep-related risk factors had a 2-fold higher risk of MCE (2.01; 1.49-2.71; P <0.0001). Short sleep duration, obstructive sleep apnea, and overnight shift work are under-recognized as predictors of adverse outcomes after acute coronary syndrome. Increased efforts should be made to identify, treat, and educate patients about the importance of sleep for the potential prevention of cardiovascular events. URL: http://www.clinicaltrials.gov. Unique identifier: NCT01000727. © 2017 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley.

Rapid Eye Movement Sleep Abnormalities in Children with Pediatric Acute-Onset Neuropsychiatric Syndrome (PANS)

PubMed Central

Gaughan, Thomas; Buckley, Ashura; Hommer, Rebecca; Grant, Paul; Williams, Kyle; Leckman, James F.; Swedo, Susan E.

2016-01-01

Study Objectives: Polysomnographic investigation of sleep architecture in children presenting with pediatric acute-onset neuropsychiatric syndrome (PANS). Methods: Fifteen consecutive subjects meeting criteria for PANS (mean age = 7.2 y; range 3–10 y) underwent single-night full polysomnography (PSG) read by a pediatric neurologist. Results: Thirteen of 15 subjects (87%) had abnormalities detected with PSG. Twelve of 15 had evidence of rapid eye movement (REM) sleep motor disinhibition, as characterized by excessive movement, laughing, hand stereotypies, moaning, or the continuation of periodic limb movements during sleep (PLMS) into REM sleep. Conclusions: This study shows various forms of REM sleep motor disinhibition present in a population of children with PANS. Citation: Gaughan T, Buckley A, Hommer R, Grant P; Williams K, Leckman JF, Swedo SE. Rapid eye movement sleep abnormalities in children with pediatric acute-onset neuropsychiatric syndrome (PANS). J Clin Sleep Med 2016;12(7):1027–1032. PMID:27166296

Sleep Loss and the Inflammatory Response in Mice Under Chronic Environmental Circadian Disruption

PubMed Central

Castanon-Cervantes, Oscar; Natarajan, Divya; Delisser, Patrick; Davidson, Alec J.; Paul, Ketema N.

2013-01-01

Shift work and trans-time zone travel lead to insufficient sleep and numerous pathologies. Here, we examined sleep/wake dynamics during chronic exposure to environmental circadian disruption (ECD), and if chronic partial sleep loss associated with ECD influences the induction of shift-related inflammatory disorder. Sleep and wakefulness were telemetrically recorded across three months of ECD, in which the dark-phase of a light-dark cycle was advanced weekly by 6 h. A three month regimen of ECD caused a temporary reorganization of sleep (NREM and REM) and wake processes across each week, resulting in an approximately 10% net loss of sleep each week relative to baseline levels. A separate group of mice were subjected to ECD or a regimen of imposed wakefulness (IW) aimed to mimic sleep amounts under ECD for one month. Fos-immunoreactivity (IR) was quantified in sleep-wake regulatory areas: the nucleus accumbens (NAc), basal forebrain (BF), and medial preoptic area (MnPO). To assess the inflammatory response, trunk blood was treated with lipopolysaccharide (LPS) and subsequent release of IL-6 was measured. Fos-IR was greatest in the NAc, BF, and MnPO of mice subjected to IW. The inflammatory response to LPS was elevated in mice subjected to ECD, but not mice subjected to IW. Thus, the net sleep loss that occurs under ECD is not associated with a pathological immune response. PMID:23696854

Increased impulsivity in response to food cues after sleep loss in healthy young men.

PubMed

Cedernaes, Jonathan; Brandell, Jon; Ros, Olof; Broman, Jan-Erik; Hogenkamp, Pleunie S; Schiöth, Helgi B; Benedict, Christian

2014-08-01

To investigate whether acute total sleep deprivation (TSD) leads to decreased cognitive control when food cues are presented during a task requiring active attention, by assessing the ability to cognitively inhibit prepotent responses. Fourteen males participated in the study on two separate occasions in a randomized, crossover within-subject design: one night of TSD versus normal sleep (8.5 hours). Following each nighttime intervention, hunger ratings and morning fasting plasma glucose concentrations were assessed before performing a go/no-go task. Following TSD, participants made significantly more commission errors when they were presented "no-go" food words in the go/no-go task, as compared with their performance following sleep (+56%; P<0.05). In contrast, response time and omission errors to "go" non-food words did not differ between the conditions. Self-reported hunger after TSD was increased without changes in fasting plasma glucose. The increase in hunger did not correlate with the TSD-induced commission errors. Our results suggest that TSD impairs cognitive control also in response to food stimuli in healthy young men. Whether such loss of inhibition or impulsiveness is food cue-specific as seen in obesity-thus providing a mechanism through which sleep disturbances may promote obesity development-warrants further investigation. Copyright © 2014 The Authors Obesity published by Wiley Periodicals, Inc. on behalf of The Obesity Society (TOS).

Acute Exacerbation of Sleep Apnea by Hyperoxia Impairs Cognitive Flexibility in Brown-Norway Rats

PubMed Central

Topchiy, Irina; Amodeo, Dionisio A.; Ragozzino, Michael E.; Waxman, Jonathan; Radulovacki, Miodrag; Carley, David W.

2014-01-01

Study Objectives: To determine whether learning deficits occur during acute exacerbation of spontaneous sleep related breathing disorder (SRBD) in rats with high (Brown Norway; BN) and low (Zucker Lean; ZL) apnea propensity. Design: Spatial acquisition (3 days) and reversal learning (3 days) in the Morris water maze (MWM) with polysomnography (12:00–08:00): (1) with acute SRBD exacerbation (by 20-h hyperoxia immediately preceding reversal learning) or (2) without SRBD exacerbation (room air throughout). Setting: Randomized, placebo-controlled, repeated-measures design. Participants: 14 BN rats; 16 ZL rats. Interventions: 20-h hyperoxia. Measurements and Results: Apneas were detected as cessation of respiration ≥ 2 sec. Swim latency in MWM, apnea indices (AI; apneas/hour of sleep) and percentages of recording time for nonrapid eye movement (NREM), rapid eye movement (REM), and total sleep were assessed. Baseline AI in BN rats was more than double that of ZL rats (22.46 ± 2.27 versus 10.7 ± 0.9, P = 0.005). Hyperoxia increased AI in both BN (34.3 ± 7.4 versus 22.46 ± 2.27) and ZL rats (15.4 ± 2.7 versus 10.7 ± 0.9) without changes in sleep stage percentages. Control (room air) BN and ZL rats exhibited equivalent acquisition and reversal learning. Acute exacerbation of AI by hyperoxia produced a reversal learning performance deficit in BN but not ZL rats. In addition, the percentage of REM sleep and REM apnea index in BN rats during hyperoxia negatively correlated with reversal learning performance. Conclusions: Acute exacerbation of sleep related breathing disorder by hyperoxia impairs reversal learning in a rat strain with high apnea propensity, but not a strain with a low apnea propensity. This suggests a non-linear threshold effect may contribute to the relationships between sleep apnea and cognitive dysfunctions, but strain-specific differences also may be important. Citation: Topchiy I, Amodeo DA, Ragozzino ME, Waxman J, Radulovacki M, Carley DW. Acute

Effects of Acute Sleep Deprivation Resulting from Night Shift Work on Young Doctors.

PubMed

Sanches, Inês; Teixeira, Fátima; dos Santos, José Moutinho; Ferreira, António Jorge

2015-01-01

To evaluate sleep deprivation and its effects on young physicians in relation to concentration capacity and psychomotor performance. Eighteen physicians aged 26 - 33 years were divided into 2 groups: non-sleep deprived group (with no night work) and sleep deprived group (minimum 12 hour of night work/week). We applied Pittsburgh Sleep Quality Index to screen the presence of sleep pathology and Epworth Sleepiness Scale to evaluate subjective daytime sleepiness; we used actigraphy and sleep diary to assess sleep hygiene and standard sleep-wake cycles. To demonstrate the effects of sleep deprivation, we applied Toulouse-Piéron's test (concentration test) and a battery of three reaction time tasks after the night duty. Sleep deprived group had higher daytime sleepiness on Epworth Sleepiness Scale (p < 0.05) and during week sleep deprivation was higher (p < 0.010). The mean duration of sleep during the period of night duty was 184.2 minutes to sleep deprived group and 397.7 minutes to non-sleep deprived group (p < 0.001). In the Toulouse-Piéron's test, the sleep deprived group had more omissions (p < 0.05) with a poorer result in concentration (p < 0.05). Psychomotor tests that evaluated response to simple stimuli revealed longer response latency (p < 0.05) and more errors (p < 0.05) in Sleep deprived group; in reaction to instruction test the sleep deprived group showed worse perfection index (p < 0.05); in the fine movements test there was no statistically significant difference between the groups. Acute sleep deprivation resulting from nocturnal work in medical professions is associated with a reduction in attention and concentration and delayed response to stimuli. This may compromise patient care as well as the physician's health and quality of life. It is essential to study the effects of acute sleep deprivation on the cognitive abilities and performance of health professionals.

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

Toll-Like Receptor 4 Is a Regulator of Monocyte and Electroencephalographic Responses to Sleep Loss

PubMed Central

Wisor, Jonathan P.; Clegern, William C.; Schmidt, Michelle A.

2011-01-01

Study Objectives: Sleep loss triggers changes in inflammatory signaling pathways in the brain and periphery. The mechanisms that underlie these changes are ill-defined. The Toll-like receptor 4 (TLR4) activates inflammatory signaling cascades in response to endogenous and pathogen-associated ligands known to be elevated in association with sleep loss. TLR4 is therefore a possible mediator of some of the inflammation-related effects of sleep loss. Here we describe the baseline electroencephalographic sleep phenotype and the biochemical and electroencephalographic responses to sleep loss in TLR4-deficient mice. Design, Measurements and Results: TLR4-deficient mice and wild type controls were subjected to electroencephalographic and electromyographic recordings during spontaneous sleep/wake cycles and during and after sleep restriction sessions of 3, 6, and 24-h duration, during which sleep was disrupted by an automated sleep restriction system. Relative to wild type control mice, TLR4-deficient mice exhibited an increase in the duration of the primary daily waking bout occurring at dark onset in a light/dark cycle. The amount of time spent in non-rapid eye movement sleep by TLR4-deficient mice was reduced in proportion to increased wakefulness in the hours immediately after dark onset. Subsequent to sleep restriction, EEG measures of increased sleep drive were attenuated in TLR4-deficient mice relative to wild-type mice. TLR4 was enriched 10-fold in brain cells positive for the cell surface marker CD11b (cells of the monocyte lineage) relative to CD11b-negative cells in wild type mouse brains. To assess whether this population was affected selectively by TLR4 knockout, flow cytometry was used to count F4/80- and CD45-positive cells in the brains of sleep deprived and time of day control mice. While wild-type mice exhibited a significant reduction in the number of CD11b-positive cells in the brain after 24-h sleep restriction, TLR4-deficient mice did not. Conclusion

One night of sleep loss impairs innovative thinking and flexible decision making.

PubMed

Harrison, Y; Horne, J A

1999-05-01

Recent findings with clinically oriented neuropsychological tests suggest that one night without sleep causes particular impairment to tasks requiring flexible thinking and the updating of plans in the light of new information. This relatively little investigated field of sleep deprivation research has real-world implications for decision makers having lost a night's sleep. To explore this latter perspective further, we adapted a dynamic and realistic marketing decision making "game" embodying the need for these skills, and whereby such performance could be measured. As the task relied on the comprehension of a large amount of written information, a critical reasoning test was also administered to ascertain whether any failure at the marketing game might lie with information acquisition rather than with failures in decision making. Ten healthy highly motivated and trained participants underwent two counterbalanced 36 h trials, sleep vs no sleep. The critical reasoning task was unaffected by sleep loss, whereas performance at the game significantly deteri orated after 32-36 h of sleep loss, when sleep deprivation led to more rigid thinking, increased perseverative errors, and marked difficulty in appreciating an updated situation. At this point, and despite the sleep-deprived participants' best efforts to do well, their play collapsed, unlike that of the nonsleep-deprived participants. Copyright 1999 Academic Press.

Sleep Impairment and Prognosis of Acute Myocardial Infarction: A Prospective Cohort Study

PubMed Central

Clark, Alice; Lange, Theis; Hallqvist, Johan; Jennum, Poul; Rod, Naja Hulvej

2014-01-01

Study Objectives: Impaired sleep is an established risk factor for the development of cardiovascular disease, whereas less is known about how impaired sleep affects cardiovascular prognosis. The aim of this study is to determine how different aspects of impaired sleep affect the risk of case fatality and subsequent cardiovascular events following first-time acute myocardial infarction (AMI). Design: Prospective cohort study. Setting: The Stockholm Heart Epidemiology Program, Sweden. Participants: There were 2,246 first-time AMI cases. Measurements and Results: Sleep impairment was assessed by the Karolina Sleep Questionnaire, which covers various indices of impaired sleep: disturbed sleep, impaired awakening, daytime sleepiness, and nightmares. Case fatality, defined as death within 28 days of initial AMI, and new cardiovascular events within up to 10 y of follow-up were identified through national registries. In women, disturbed sleep showed a consistently higher risk of long-term cardiovascular events: AMI (hazard ratio [HR] = 1.69; 95% confidence interval [CI] 0.95–3.00), stroke (HR = 2.61; 95% CI: 1.19–5.76), and heart failure (HR = 2.43; 95% CI: 1.18–4.97), whereas no clear effect of impaired sleep on case fatality was found in women. In men, a strong effect on case fatality (odds ratio = 3.27; 95% CI: 1.76–6.06) was observed in regard to impaired awakening; however, no consistent effect of impaired sleep was seen on long-term cardiovascular prognosis. Conclusion: Results suggest sex-specific effects of impaired sleep that differ by short- and long-term prognosis. Sleep complaints are frequent, easily recognizable, and potentially manageable. Evaluation of sleep complaints may, even if they represent prognostic markers rather than risk factors, provide additional information in clinical risk assessment that could benefit secondary cardiovascular prevention. Citation: Clark A, Lange T, Hallqvist J, Jennum P, Rod NH. Sleep impairment and prognosis of

The Effects of Insomnia and Sleep Loss on Cardiovascular Disease.

PubMed

Khan, Meena S; Aouad, Rita

2017-06-01

Sleep loss has negative impacts on quality of life, mood, cognitive function, and heath. Insomnia is linked to poor mood, increased use of health care resources, decreased quality of life, and possibly cardiovascular risk factors and disease. Studies have shown increase in cortisol levels, decreased immunity, and increased markers of sympathetic activity in sleep-deprived healthy subjects and those with chronic insomnia. The literature shows subjective complaints consistent with chronic insomnia and shortened sleep can be associated with development of diabetes, hypertension, and cardiovascular disease. This article explores the relationship between insufficient sleep and insomnia with these health conditions. Copyright © 2017 Elsevier Inc. All rights reserved.

Dysphagia and Obstructive Sleep Apnea in Acute, First-Ever, Ischemic Stroke.

PubMed

Losurdo, Anna; Brunetti, Valerio; Broccolini, Aldobrando; Caliandro, Pietro; Frisullo, Giovanni; Morosetti, Roberta; Pilato, Fabio; Profice, Paolo; Giannantoni, Nadia Mariagrazia; Sacchetti, Maria Luisa; Testani, Elisa; Vollono, Catello; Della Marca, Giacomo

2018-03-01

Obstructive sleep apnea (OSA) and dysphagia are common in acute stroke and are both associated with increased risk of complications and worse prognosis. The aims of the present study were (1) to evaluate the prevalence of OSA and dysphagia in patients with acute, first-ever, ischemic stroke; (2) to investigate their clinical correlates; and (3) to verify if these conditions are associated in acute ischemic stroke. We enrolled a cohort of 140 consecutive patients with acute-onset (<48 hours), first-ever ischemic stroke. Computed tomography (CT) and magnetic resonance imaging scans confirmed the diagnosis. Neurological deficit was measured using the National Institutes of Health Stroke Scale (NIHSS) by examiners trained and certified in the use of this scale. Patients underwent a clinical evaluation of dysphagia (Gugging Swallowing Screen) and a cardiorespiratory sleep study to evaluate the presence of OSA. There are 72 patients (51.4%) with obstructive sleep apnea (OSA+), and there are 81 patients (57.8%) with dysphagia (Dys+). OSA+ patients were significantly older (P = .046) and had greater body mass index (BMI) (P = .002), neck circumference (P = .001), presence of diabetes (P = .013), and hypertension (P < .001). Dys+ patients had greater NIHSS (P < .001), lower Alberta Stroke Programme Early CT Score (P < .001), with greater BMI (P = .030). The association of OSA and dysphagia was greater than that expected based on the prevalence of each condition in acute stroke (P < .001). OSA and dysphagia are associated in first-ever, acute ischemic stroke. Copyright © 2018 National Stroke Association. Published by Elsevier Inc. All rights reserved.

Influence of sleep restriction on weight loss outcomes associated with caloric restriction.

PubMed

Wang, Xuewen; Sparks, Joshua R; Bowyer, Kimberly P; Youngstedt, Shawn D

2018-05-01

To examine the effects of moderate sleep restriction (SR) on body weight, body composition, and metabolic variables in individuals undergoing caloric restriction (CR). Overweight or obese adults were randomized to an 8 week caloric restriction (CR) regimen alone (n = 15) or combined with sleep restriction (CR + SR) (n = 21). All participants were instructed to restrict daily calorie intake to 95 per cent of their measured resting metabolic rate. Participants in the CR + SR group were also instructed to reduce time in bed on five nights and to sleep ad libitum on the other two nights each week. The CR + SR group reduced sleep by 57 ± 36 min per day during SR days and increased sleep by 59 ± 38 min per day during ad libitum sleep days, resulting in a sleep reduction of 169 ± 75 min per week. The CR and CR + SR groups lost similar amounts of weight, lean mass, and fat mass. However, the proportion of total mass lost as fat was significantly greater (p = 0.016) in the CR group. This proportion was greater than body fat percentage at baseline for the CR (p = 0.0035), but not the CR + SR group. Resting respiratory quotient was reduced (p = 0.033) only in CR, and fasting leptin concentration was reduced only in CR + SR (p = 0.029). Approximately 1 hr of SR on five nights a week led to less proportion of fat mass loss in individuals undergoing hypocaloric weight loss, despite similar weight loss. SR may adversely affect changes in body composition and "catch-up" sleep may not completely reverse it. ClinicalTrials.gov (NCT02413866).

Loss of polyubiquitin gene Ubb leads to metabolic and sleep abnormalities in mice

PubMed Central

Ryu, K.-Y.; Fujiki, N.; Kazantzis, M.; Garza, J. C.; Bouley, D. M.; Stahl, A.; Lu, X.-Y.; Nishino, S.; Kopito, R. R.

2010-01-01

Aims Ubiquitin performs essential roles in a myriad of signalling pathways required for cellular function and survival. Recently, we reported that disruption of the stress-inducible ubiquitin-encoding gene Ubb reduces ubiquitin content in the hypothalamus and leads to adult-onset obesity coupled with a loss of arcuate nucleus neurones and disrupted energy homeostasis in mice. Neuropeptides expressed in the hypothalamus control both metabolic and sleep behaviours. In order to demonstrate that the loss of Ubb results in broad hypothalamic abnormalities, we attempted to determine whether metabolic and sleep behaviours were altered in Ubb knockout mice. Methods Metabolic rate and energy expenditure were measured in a metabolic chamber, and sleep stage was monitored via electroencephalographic/electromyographic recording. The presence of neurodegeneration and increased reactive gliosis in the hypothalamus were also evaluated. Results We found that Ubb disruption leads to early-onset reduced activity and metabolic rate. Additionally, we have demonstrated that sleep behaviour is altered and sleep homeostasis is disrupted in Ubb knockout mice. These early metabolic and sleep abnormalities are accompanied by persistent reactive gliosis and the loss of arcuate nucleus neurones, but are independent of neurodegeneration in the lateral hypothalamus. Conclusions Ubb knockout mice exhibit phenotypes consistent with hypothalamic dysfunction. Our data also indicate that Ubb is essential for the maintenance of the ubiquitin levels required for proper regulation of metabolic and sleep behaviours in mice. PMID:20002312

Sleep Loss, Circadian Mismatch, and Abnormalities in Reorienting of Attention in Night Workers with Shift Work Disorder

PubMed Central

Gumenyuk, Valentina; Howard, Ryan; Roth, Thomas; Korzyukov, Oleg; Drake, Christopher L.

2014-01-01

Study Objectives: Permanent night-shift workers may develop shift-work disorder (SWD). In the current study, we evaluated neurophysiological and behavioral indices of distractibility across times prior to the night shift (T1), during night hours (T2), and after acute sleep deprivation (T3) in permanent hospital night workers with and without SWD. Methods: Ten asymptomatic night workers (NW) and 18 NW with SWD participated in a 25-h sleep deprivation study. Circadian phase was evaluated by dim-light salivary melatonin onset (DLMO). Objective sleepiness was evaluated using the Multiple Sleep Latency Test (MSLT). Electrophysiological distractibility was evaluated by brain event-related potentials (ERP), whereas behavioral distractibility was evaluated by performance on a visual task in an auditory-visual distraction paradigm. Statistical analyses: Comparisons of ERP results were performed by repeated-measures analysis of variance, and t-tests were used where appropriate. A Mann-Whitney U test was used for comparison of variables (MLST, Stanford Sleepiness Scale, and DLMO) that deviated from normal. Results: First, in the SWD group, the reorienting negativity ERP amplitude was significantly attenuated compared to that in the NW group. Second, the SWD group had shorter MSLT during night shift hours (4.8 ± 4.9 min) compared to that in NW (7.8 ± 3.7 min; U = 47; z = -2.1; P < 0.03). Third, NW with SWD had a DLMO at 20:27 ± 5.0 h, whereas healthy NW had a DLMO at 05:00 ± 3.4 h (U = 43.5; z = -2.22, P < 0.03). Finally, acute sleep deprivation impaired behavioral performance and the P3a ERP in both groups. Conclusions: Our results demonstrate specific deficits in neurophysiological activity in the attentional domain among the shift-work disorder group relative to night workers. Citation: Gumenyuk V; Howard R; Roth T; Korzyukov O; Drake CL. Sleep loss, circadian mismatch, and abnormalities in reorienting of attention in night workers with shift work disorder. SLEEP 2014

The Impact of Sleep Deprivation on the Brain

PubMed

Trošt Bobić, Tatjana; Šečić, Ana; Zavoreo, Iris; Matijević, Valentina; Filipović, Branimir; Kolak, Željka; Bašić Kes, Vanja; Ciliga, Dubravka; Sajković, Dubravka

2016-09-01

Each sleep phase is characterized by specific chemical, cellular and anatomic events of vital importance for normal neural functioning. Different forms of sleep deprivation may lead to a decline of cognitive functions in individuals. Studies in this field make a distinction between total sleep deprivation, chronic sleep restriction, and the situation of sleep disruption. Investigations covering the acute effects of sleep deprivation on the brain show that the discovered behavioral deficits in most cases regenerate after two nights of complete sleep. However, some studies done on mice emphasize the possible chronic effects of long-term sleep deprivation or chronic restriction on the occurrence of neurodegenerative diseases such as Alzheimer’s disease and dementia. In order to better understand the acute and chronic effects of sleep loss, the mechanisms of neural adaptation in the situations of insufficient sleep need to be further investigated. Future integrative research on the impact of sleep deprivation on neural functioning measured through the macro level of cognitive functions and the micro molecular and cell level could contribute to more accurate conclusions about the basic cellular mechanisms responsible for the detected behavioral deficits occurring due to sleep deprivation.

Chemogenetic inhibition of the medial prefrontal cortex reverses the effects of REM sleep loss on sucrose consumption

PubMed Central

McEown, Kristopher; Takata, Yohko; Cherasse, Yoan; Nagata, Nanae; Aritake, Kosuke; Lazarus, Michael

2016-01-01

Rapid eye movement (REM) sleep loss is associated with increased consumption of weight-promoting foods. The prefrontal cortex (PFC) is thought to mediate reward anticipation. However, the precise role of the PFC in mediating reward responses to highly palatable foods (HPF) after REM sleep deprivation is unclear. We selectively reduced REM sleep in mice over a 25–48 hr period and chemogenetically inhibited the medial PFC (mPFC) by using an altered glutamate-gated and ivermectin-gated chloride channel that facilitated neuronal inhibition through hyperpolarizing infected neurons. HPF consumption was measured while the mPFC was inactivated and REM sleep loss was induced. We found that REM sleep loss increased HPF consumption compared to control animals. However, mPFC inactivation reversed the effect of REM sleep loss on sucrose consumption without affecting fat consumption. Our findings provide, for the first time, a causal link between REM sleep, mPFC function and HPF consumption. DOI: http://dx.doi.org/10.7554/eLife.20269.001 PMID:27919319

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

Transiently Increasing cAMP Levels Selectively in Hippocampal Excitatory Neurons during Sleep Deprivation Prevents Memory Deficits Caused by Sleep Loss

PubMed Central

Bruinenberg, Vibeke M.; Tudor, Jennifer C.; Ferri, Sarah L.; Baumann, Arnd; Meerlo, Peter

2014-01-01

The hippocampus is particularly sensitive to sleep loss. Although previous work has indicated that sleep deprivation impairs hippocampal cAMP signaling, it remains to be determined whether the cognitive deficits associated with sleep deprivation are caused by attenuated cAMP signaling in the hippocampus. Further, it is unclear which cell types are responsible for the memory impairments associated with sleep deprivation. Transgenic approaches lack the spatial resolution to manipulate specific signaling pathways selectively in the hippocampus, while pharmacological strategies are limited in terms of cell-type specificity. Therefore, we used a pharmacogenetic approach based on a virus-mediated expression of a Gαs-coupled Drosophila octopamine receptor selectively in mouse hippocampal excitatory neurons in vivo. With this approach, a systemic injection with the receptor ligand octopamine leads to increased cAMP levels in this specific set of hippocampal neurons. We assessed whether transiently increasing cAMP levels during sleep deprivation prevents memory consolidation deficits associated with sleep loss in an object–location task. Five hours of total sleep deprivation directly following training impaired the formation of object–location memories. Transiently increasing cAMP levels in hippocampal neurons during the course of sleep deprivation prevented these memory consolidation deficits. These findings demonstrate that attenuated cAMP signaling in hippocampal excitatory neurons is a critical component underlying the memory deficits in hippocampus-dependent learning tasks associated with sleep deprivation. PMID:25411499

Phenotypic vulnerability of energy balance responses to sleep loss in healthy adults

PubMed Central

Spaeth, Andrea M.; Dinges, David F.; Goel, Namni

2015-01-01

Short sleep duration is a risk factor for increased hunger and caloric intake, late-night eating, attenuated fat loss when dieting, and for weight gain and obesity. It is unknown whether altered energy-balance responses to sleep loss are stable (phenotypic) over time, and the extent to which individuals differ in vulnerability to such responses. Healthy adults experienced two laboratory exposures to sleep restriction separated by 60–2132 days. Caloric intake, meal timing and weight were objectively measured. Although there were substantial phenotypic differences among participants in weight gain, increased caloric intake, and late-night eating and fat intake, responses within participants showed stability across sleep restriction exposures. Weight change was consistent in both normal-weight and overweight adults. Weight change and increased caloric intake were more stable in men whereas late-night eating was consistent in both genders. This is the first evidence of phenotypic differential vulnerability and trait-like stability of energy balance responses to repeated sleep restriction, underscoring the need for biomarkers and countermeasures to predict and mitigate this vulnerability. PMID:26446681

Phenotypic vulnerability of energy balance responses to sleep loss in healthy adults.

PubMed

Spaeth, Andrea M; Dinges, David F; Goel, Namni

2015-10-08

Short sleep duration is a risk factor for increased hunger and caloric intake, late-night eating, attenuated fat loss when dieting, and for weight gain and obesity. It is unknown whether altered energy-balance responses to sleep loss are stable (phenotypic) over time, and the extent to which individuals differ in vulnerability to such responses. Healthy adults experienced two laboratory exposures to sleep restriction separated by 60-2132 days. Caloric intake, meal timing and weight were objectively measured. Although there were substantial phenotypic differences among participants in weight gain, increased caloric intake, and late-night eating and fat intake, responses within participants showed stability across sleep restriction exposures. Weight change was consistent in both normal-weight and overweight adults. Weight change and increased caloric intake were more stable in men whereas late-night eating was consistent in both genders. This is the first evidence of phenotypic differential vulnerability and trait-like stability of energy balance responses to repeated sleep restriction, underscoring the need for biomarkers and countermeasures to predict and mitigate this vulnerability.

Diurnal Rhythms in Blood Cell Populations and the Effect of Acute Sleep Deprivation in Healthy Young Men

PubMed Central

Ackermann, Katrin; Revell, Victoria L.; Lao, Oscar; Rombouts, Elwin J.; Skene, Debra J.; Kayser, Manfred

2012-01-01

Study Objectives: The sleep/wake cycle is accompanied by changes in circulating numbers of immune cells. The goal of this study was to provide an in-depth characterization of diurnal rhythms in different blood cell populations and to investigate the effect of acute sleep deprivation on the immune system, as an indicator of the body's acute stress response. Design: Observational within-subject design. Setting: Home environment and Clinical Research Centre. Participants: 15 healthy male participants aged 23.7 ± 5.4 (standard deviation) yr. Interventions: Total sleep deprivation. Measurements and Results: Diurnal rhythms of several blood cell populations were assessed under a normal sleep/wake cycle followed by 29 hr of extended wakefulness. The effect of condition (sleep versus sleep deprivation) on peak time and amplitude was investigated. Interindividual variation of, and the level of correlation between, the different cell populations was assessed. Comprehensive nonlinear curve fitting showed significant diurnal rhythms for all blood cell types investigated, with CD4 (naïve) cells exhibiting the most robust rhythms independent of condition. For those participants exhibiting significant diurnal rhythms in blood cell populations, only the amplitude of the granulocyte rhythm was significantly reduced by sleep deprivation. Granulocytes were the most diverse population, being most strongly affected by condition, and showed the lowest correlations with any other given cell type while exhibiting the largest interindividual variation in abundance. Conclusions: Granulocyte levels and diurnal rhythmicity are directly affected by acute sleep deprivation; these changes mirror the body's immediate immune response upon exposure to stress. Citation: Ackermann K; Revell VL; Lao O; Rombouts EJ; Skene DJ; Kayser M. Diurnal rhythms in blood cell populations and the effect of acute sleep deprivation in healthy young men. SLEEP 2012;35(7):933-940. PMID:22754039

Sleep-dependent memory consolidation in patients with sleep disorders.

PubMed

Cipolli, Carlo; Mazzetti, Michela; Plazzi, Giuseppe

2013-04-01

Sleep can improve the off-line memory consolidation of new items of declarative and non-declarative information in healthy subjects, whereas acute sleep loss, as well as sleep restriction and fragmentation, impair consolidation. This suggests that, by modifying the amount and/or architecture of sleep, chronic sleep disorders may also lead to a lower gain in off-line consolidation, which in turn may be responsible for the varying levels of impaired performance at memory tasks usually observed in sleep-disordered patients. The experimental studies conducted to date have shown specific impairments of sleep-dependent consolidation overall for verbal and visual declarative information in patients with primary insomnia, for verbal declarative information in patients with obstructive sleep apnoeas, and for visual procedural skills in patients with narcolepsy-cataplexy. These findings corroborate the hypothesis that impaired consolidation is a consequence of the chronically altered organization of sleep. Moreover, they raise several novel questions as to: a) the reversibility of consolidation impairment in the case of effective treatment, b) the possible negative influence of altered prior sleep also on the encoding of new information, and c) the relationships between altered sleep and memory impairment in patients with other (medical, psychiatric or neurological) diseases associated with quantitative and/or qualitative changes of sleep architecture. Copyright © 2012 Elsevier Ltd. All rights reserved.

The prognostic value of sleep patterns in disorders of consciousness in the sub-acute phase.

PubMed

Arnaldi, Dario; Terzaghi, Michele; Cremascoli, Riccardo; De Carli, Fabrizio; Maggioni, Giorgio; Pistarini, Caterina; Nobili, Flavio; Moglia, Arrigo; Manni, Raffaele

2016-02-01

This study aimed to evaluate, through polysomnographic analysis, the prognostic value of sleep patterns, compared to other prognostic factors, in patients with disorders of consciousness (DOCs) in the sub-acute phase. Twenty-seven patients underwent 24-h polysomnography and clinical evaluation 3.5 ± 2 months after brain injury. Their clinical outcome was assessed 18.5 ± 9.9 months later. Polysomnographic recordings were evaluated using visual and quantitative indexes. A general linear model was applied to identify features able to predict clinical outcome. Clinical status at follow-up was analysed as a function of the baseline clinical status, the interval between brain injury and follow-up evaluation, patient age and gender, the aetiology of the injury, the lesion site, and visual and quantitative sleep indexes. A better clinical outcome was predicted by a visual index indicating the presence of sleep integrity (p=0.0006), a better baseline clinical status (p=0.014), and younger age (p=0.031). Addition of the quantitative sleep index strengthened the prediction. More structured sleep emerged as a valuable predictor of a positive clinical outcome in sub-acute DOC patients, even stronger than established predictors (e.g. age and baseline clinical condition). Both visual and quantitative sleep evaluation could be helpful in predicting clinical outcome in sub-acute DOCs. Copyright © 2015 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rights reserved.

The Effects of Acute Sleep Restriction on Adolescents' Pedestrian Safety in a Virtual Environment

PubMed Central

Davis, Aaron L.; Avis, Kristin T.; Schwebel, David C.

2013-01-01

Purpose Over 8,000 American adolescents ages 14-15 require medical attention due to pedestrian injury annually. Cognitive factors contributing to pedestrian safety include reaction time, impulsivity, risk-taking, attention, and decision-making. These characteristics are also influenced by sleep restriction. Experts recommend adolescents obtain 8.5 hours of uninterrupted sleep each night, but most American adolescents do not. Inadequate sleep may place adolescents at risk for pedestrian injury. Method Using a within-subjects design, fifty-five 14- and 15-year-olds engaged in a virtual reality pedestrian environment in two conditions, scheduled a week apart: sleep-restricted (4 hours sleep previous night) and adequate sleep (8.5 hours). Sleep was assessed using actigraphy and pedestrian behavior via four outcome measures: time to initiate crossing, time before contact with vehicle while crossing, virtual hits/close calls and attention to traffic (looks left and right). Results While acutely sleep restricted, adolescents took more time to initiate pedestrian crossings, crossed with less time before contact with vehicles, experienced more virtual hits/close calls and looked left and right more often compared to when adequately rested. Results were maintained after controlling for age, gender, ethnicity and average total sleep duration prior to each condition. Discussion Adolescent pedestrian behavior in the simulated virtual environment was markedly different, and generally more risky, when acutely sleep restricted compared to adequately rested. Inadequate sleep may influence cognitive functioning to the extent that pedestrian safety is jeopardized among adolescents capable of crossing streets safely when rested. Policy decisions might be educated by these results. PMID:24012066

Circadian Misalignment Augments Markers of Insulin Resistance and Inflammation, Independently of Sleep Loss

PubMed Central

Leproult, Rachel; Holmbäck, Ulf; Van Cauter, Eve

2014-01-01

Shift workers, who are exposed to irregular sleep schedules resulting in sleep deprivation and misalignment of circadian rhythms, have an increased risk of diabetes relative to day workers. In healthy adults, sleep restriction without circadian misalignment promotes insulin resistance. To determine whether the misalignment of circadian rhythms that typically occurs in shift work involves intrinsic adverse metabolic effects independently of sleep loss, a parallel group design was used to study 26 healthy adults. Both interventions involved 3 inpatient days with 10-h bedtimes, followed by 8 inpatient days of sleep restriction to 5 h with fixed nocturnal bedtimes (circadian alignment) or with bedtimes delayed by 8.5 h on 4 of the 8 days (circadian misalignment). Daily total sleep time (SD) during the intervention was nearly identical in the aligned and misaligned conditions (4 h 48 min [5 min] vs. 4 h 45 min [6 min]). In both groups, insulin sensitivity (SI) significantly decreased after sleep restriction, without a compensatory increase in insulin secretion, and inflammation increased. In male participants exposed to circadian misalignment, the reduction in SI and the increase in inflammation both doubled compared with those who maintained regular nocturnal bedtimes. Circadian misalignment that occurs in shift work may increase diabetes risk and inflammation, independently of sleep loss. PMID:24458353

Transiently increasing cAMP levels selectively in hippocampal excitatory neurons during sleep deprivation prevents memory deficits caused by sleep loss.

PubMed

Havekes, Robbert; Bruinenberg, Vibeke M; Tudor, Jennifer C; Ferri, Sarah L; Baumann, Arnd; Meerlo, Peter; Abel, Ted

2014-11-19

The hippocampus is particularly sensitive to sleep loss. Although previous work has indicated that sleep deprivation impairs hippocampal cAMP signaling, it remains to be determined whether the cognitive deficits associated with sleep deprivation are caused by attenuated cAMP signaling in the hippocampus. Further, it is unclear which cell types are responsible for the memory impairments associated with sleep deprivation. Transgenic approaches lack the spatial resolution to manipulate specific signaling pathways selectively in the hippocampus, while pharmacological strategies are limited in terms of cell-type specificity. Therefore, we used a pharmacogenetic approach based on a virus-mediated expression of a Gαs-coupled Drosophila octopamine receptor selectively in mouse hippocampal excitatory neurons in vivo. With this approach, a systemic injection with the receptor ligand octopamine leads to increased cAMP levels in this specific set of hippocampal neurons. We assessed whether transiently increasing cAMP levels during sleep deprivation prevents memory consolidation deficits associated with sleep loss in an object-location task. Five hours of total sleep deprivation directly following training impaired the formation of object-location memories. Transiently increasing cAMP levels in hippocampal neurons during the course of sleep deprivation prevented these memory consolidation deficits. These findings demonstrate that attenuated cAMP signaling in hippocampal excitatory neurons is a critical component underlying the memory deficits in hippocampus-dependent learning tasks associated with sleep deprivation. Copyright © 2014 the authors 0270-6474/14/3415715-07$15.00/0.

Homeostatic and Circadian Abnormalities in Sleep and Arousal in Gulf War Syndrome

DTIC Science & Technology

2015-10-01

for the daytime fatigue and cognitive impairments commonly reported in GWI may be that these veterans undergo frontally specific sleep deprivation ...long-term sleep loss or as a result of an unknown process related to Gulf-War participation. The notion that sleep pathology results in acute...1 Award Number: W81XWH-10-2-0129 TITLE: Homeostatic and Circadian Abnormalities in Sleep and Arousal in Gulf War Syndrome PRINCIPAL INVESTIGATOR

Sleep loss does not aggravate the deteriorating effect of hypoglycemia on neurocognitive function in healthy men.

PubMed

Jauch-Chara, Kamila; Hallschmid, Manfred; Schmid, Sebastian M; Bandorf, Nadine; Born, Jan; Schultes, Bernd

2010-05-01

Sleep deprivation (SD) impairs neurocognitive functions. Assuming that this effect is mediated by reduced cerebral glucose supply due to prolonged wakefulness inducing a progressive depletion of cerebral glycogen stores, we hypothesized that short-term sleep loss amplifies the deteriorating effects of acute hypoglycemia on neurocognitive functions. Seven healthy men were tested in a randomized and balanced order on 3 different conditions spaced 2 weeks apart. After a night of total SD (total SD), 4.5h of sleep (partial SD) and a night with 7h of regular sleep (regular sleep), subjects were exposed to a stepwise hypoglycemic clamp experiment. Reaction time (RT) and auditory evoked brain potentials (AEP) were assessed during a euglycemic baseline period and at the end of the clamp (blood glucose at 2.5mmol/l). During the euglycemic baseline, amplitude of the P3 component of the AEP was lower after total SD than after partial SD (9.2+/-3.2microV vs. 16.6+/-2.9microV; t(6)=3.2, P=0.02) and regular sleep (20.2+/-2.1microV; t(6)=18.8, P<0.01). Reaction time was longer after total SD in comparison to partial SD (367+/-45ms vs. 304+/-36ms; t(6)=2.7, P=0.04) and to regular sleep (322+/-36ms; t(6)=2.41, P=0.06) while there was no difference between partial SD and regular sleep condition (t(6)=0.60, P=0.57). Hypoglycemia decreased P3 amplitude by 11.2+/-4.1microV in the partial SD condition (t(6)=2.72, P=0.04) and by 9.3+/-0.7microV in the regular sleep condition (t(6)=12.51, P<0.01), but did not further reduce P3 amplitude after total SD (1.8+/-3.9microV; t(6)=0.46, P=0.66). Thus, at the end of hypoglycemia P3 amplitudes were similar across the 3 conditions (F(2,10)=0.89, P=0.42). RT generally showed a similar pattern with a significant prolongation due to hypoglycemia after partial SD (+42+/-12ms; t(6)=3.39, P=0.02) and regular sleep (+37+/-10ms; t(6)=3.53, P=0.01), but not after total SD (+15+/-16; t(6)=0.97, P=0.37), resulting in similar values at the end of hypoglycemia

The effects of acute sleep restriction on adolescents' pedestrian safety in a virtual environment.

PubMed

Davis, Aaron L; Avis, Kristin T; Schwebel, David C

2013-12-01

Over 8,000 American adolescents ages 14-15 years require medical attention owing to pedestrian injury annually. Cognitive factors contributing to pedestrian safety include reaction time, impulsivity, risk taking, attention, and decision making. These characteristics are also influenced by sleep restriction. Experts recommend that adolescents obtain 8.5 hours of uninterrupted sleep each night, but most American adolescents do not. Inadequate sleep may place adolescents at risk for pedestrian injury. Using a within-subjects design, 55 14- and 15-year-olds engaged in a virtual reality pedestrian environment under two conditions, scheduled a week apart: sleep-restricted (4 hours' sleep the previous night) and adequate sleep (8.5 hours). Sleep was assessed using actigraphy and pedestrian behavior via four outcome measures: time to initiate crossing, time before contact with vehicle while crossing, virtual hits or close calls and attention to traffic (looks left and right). While acutely sleep restricted, adolescents took more time to initiate pedestrian crossings, crossed with less time before contact with vehicles, experienced more virtual hits or close calls, and looked left and right more often compared with when adequately rested. Results were maintained after controlling for age, gender, ethnicity, and average total sleep duration before each condition. Adolescent pedestrian behavior in the simulated virtual environment was markedly different, and generally more risky, when acutely sleep restricted compared with adequately rested. Inadequate sleep may influence cognitive functioning to the extent that pedestrian safety is jeopardized among adolescents capable of crossing streets safely when rested. Policy decisions might be educated by these results. Copyright © 2013 Society for Adolescent Health and Medicine. Published by Elsevier Inc. All rights reserved.

Pain Sensitivity and Recovery From Mild Chronic Sleep Loss

PubMed Central

Roehrs, Timothy A.; Harris, Erica; Randall, Surilla; Roth, Thomas

2012-01-01

Study Objectives: To determine whether an extended bedtime in sleepy and otherwise healthy volunteers would increase alertness and thereby also reduce pain sensitivity. Setting: Outpatient with sleep laboratory assessments. Participants and Interventions: Healthy volunteers (n = 18), defined as having an average daily sleep latency on the Multiple Sleep Latency Test (MSLT) < 8 min, were randomized to 4 nights of extended bedtime (10 hr) (EXT) or 4 nights of their diary-reported habitual bedtimes (HAB). On day 1 and day 4 they received a standard MSLT (10:00, 12:00, 14:00, and 16:00 hr) and finger withdrawal latency pain testing to a radiant heat stimulus (10:30 and 14:30 hr). Results: During the four experimental nights the EXT group slept 1.8 hr per night more than the HAB group and average daily sleep latency on the MSLT increased in the EXT group, but not the HAB group. Similarly, finger withdrawal latency was increased (pain sensitivity was reduced) in the EXT group but not the HAB group. The nightly increase in sleep time during the four experimental nights was correlated with the improvement in MSLT, which in turn was correlated with reduced pain sensitivity. Conclusions: These are the first data to show that an extended bedtime in mildly sleepy healthy adults, which resulted in increased sleep time and reduced sleepiness, reduces pain sensitivity. Citation: Roehrs TA; Harris E; Randall S; Roth T. Pain sensitivity and recovery from mild chronic sleep loss. SLEEP 2012;35(12):1667-1672. PMID:23204609

The effects of 72 hours of sleep loss on psychological variables.

PubMed

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

1989-05-01

A study was conducted on the effects of 72 hours of sleep loss and modified continuous operations on performance and psychological variables. This paper presents the results of self-report data of 12 subjects for the following psychological variables: sleepiness, affect, motivation, cognitive difficulties, and waking dreams. The relationship between the self-report measures and performance in a visual search and memory task is also examined. Most of the psychological variables are significantly affected by the number of days of sleep deprivation, all are significantly affected by hour of day; but only sleepiness, affect and motivation are also significantly affected by the interaction between these variables. The peak hours for self-reported psychological complaints are generally between 0400 and 0800, while the lowest number of complaints are usually reported in the afternoon/early evening, between 1600 and 2000. In addition, the results showed that (a) the amplitude of the circadian component of the psychological data increased over the period of sleep loss, and (b) psychological data were more highly correlated with a measure of general performance than with accuracy. The mechanisms of sleep deprivation underlying its effects on psychological and performance measures are discussed.

Sleep deprivation elevates expectation of gains and attenuates response to losses following risky decisions.

PubMed

Venkatraman, Vinod; Chuah, Y M Lisa; Huettel, Scott A; Chee, Michael W L

2007-05-01

Using a gambling task, we investigated how 24 hours of sleep deprivation modulates the neural response to the making of risky decisions with potentially loss-bearing outcomes. Two experiments involving sleep-deprived subjects were performed. In the first, neural responses to decision making and reward outcome were evaluated. A second control experiment evaluated responses to reward outcome only. Healthy right-handed adults participated in these experiments (26 [mean age 21.3 years] in Experiment 1 and 13 [mean age 21.7 years] in Experiment 2.) Following sleep deprivation, choices involving higher relative risk elicited greater activation in the right nucleus accumbens, signifying an elevated expectation of the higher reward once the riskier choice was made. Concurrently, activation for losses in the insular and orbitofrontal cortices was reduced, denoting a diminished response to losses. This latter finding of reduced insular activation to losses was also true when volunteers were merely shown the results of the computer's decision, that is, without having to make their own choice. These results suggest that sleep deprivation poses a dual threat to competent decision making by modulating activation in nucleus accumbens and insula, brain regions associated with risky decision making and emotional processing.

Sleep loss as a trigger of mood episodes in bipolar disorder: individual differences based on diagnostic subtype and gender

PubMed Central

Lewis, Katie Swaden; Gordon-Smith, Katherine; Forty, Liz; Di Florio, Arianna; Craddock, Nick; Jones, Lisa; Jones, Ian

2017-01-01

Background Sleep loss may trigger mood episodes in people with bipolar disorder but individual differences could influence vulnerability to this trigger. Aims To determine whether bipolar subtype (bipolar disorder type I (BP-I) or II (BD-II)) and gender were associated with vulnerability to the sleep loss trigger. Method During a semi-structured interview, 3140 individuals (68% women) with bipolar disorder (66% BD-I) reported whether sleep loss had triggered episodes of high or low mood. DSM-IV diagnosis of bipolar subtype was derived from case notes and interview data. Results Sleep loss triggering episodes of high mood was associated with female gender (odds ratio (OR) = 1.43, 95% CI 1.17–1.75, P < 0.001) and BD-I subtype (OR = 2.81, 95% CI 2.26–3.50, P < 0.001). Analyses on sleep loss triggering low mood were not significant following adjustment for confounders. Conclusions Gender and bipolar subtype may increase vulnerability to high mood following sleep deprivation. This should be considered in situations where patients encounter sleep disruption, such as shift work and international travel. PMID:28684405

Behavioral and Physiological Consequences of Sleep Restriction

PubMed Central

Banks, Siobhan; Dinges, David F.

2007-01-01

Adequate sleep is essential for general healthy functioning. This paper reviews recent research on the effects of chronic sleep restriction on neurobehavioral and physiological functioning and discusses implications for health and lifestyle. Restricting sleep below an individual's optimal time in bed (TIB) can cause a range of neurobehavioral deficits, including lapses of attention, slowed working memory, reduced cognitive throughput, depressed mood, and perseveration of thought. Neurobehavioral deficits accumulate across days of partial sleep loss to levels equivalent to those found after 1 to 3 nights of total sleep loss. Recent experiments reveal that following days of chronic restriction of sleep duration below 7 hours per night, significant daytime cognitive dysfunction accumulates to levels comparable to that found after severe acute total sleep deprivation. Additionally, individual variability in neurobehavioral responses to sleep restriction appears to be stable, suggesting a traitlike (possibly genetic) differential vulnerability or compensatory changes in the neurobiological systems involved in cognition. A causal role for reduced sleep duration in adverse health outcomes remains unclear, but laboratory studies of healthy adults subjected to sleep restriction have found adverse effects on endocrine functions, metabolic and inflammatory responses, suggesting that sleep restriction produces physiological consequences that may be unhealthy. Citation: Banks S; Dinges DF. Behavioral and physiological consequences of sleep restriction. J Clin Sleep Med 2007;3(5):519-528. PMID:17803017

P-CPA pretreatment reverses the changes in sleep and behavior following acute immobilization stress rats.

PubMed

Sinha, Rakesh Kumar

2006-02-01

The effects of p-CPA (para-chlorophenylalanine) pretreatment was studied on the sleep-wake parameters and patterns of behavioral activities in an animal model of acute immobilization stress. For the experiments, young male Charles Foster rats were divided into three groups, subjected to (i) acute immobilization stress for four hours on specially designed wooden boards, (ii) a similar model of acute immobilization stress after pretreatment of p-CPA (injected through i.p. route), and (iii) control rats (p-CPA untreated and unstressed). Three channels of electrographic signals, i.e., EEG (electroencephalogram), EOG (electrooculogram), and EMG (electromyogram) were recorded continuously for four hours for all three groups of rats to analyze the changes in sleep-wake stages. The assessment of behavior was performed just after the stress on separate groups of rats in Open-Field (OF) and Elevated Plus-Maze (EPM) apparatuses. The significant changes in total sleep time (P < 0.05), total time for rapid eye movement sleep (P < 0.01), and total time in wakefulness (P < 0.01) following acute immobilization stress were found reversed in the p-CPA (a serotonin inhibitor) pretreated group of rats. Simultaneously, the results of the present work also revealed that the changes in grooming behavior (P < 0.05) in OF and the total time spent on the center of EPM (P < 0.05) were observed altered in p-CPA pretreated group of rats.

Relationship between sleep loss and economic worry among farmers: a survery of 94 active saskatchewan noncorporate farms.

PubMed

LaBrash, Leanne F; Pahwa, Punam; Pickett, William; Hagel, Louise M; Snodgrass, Phyllis R; Dosman, James A

2008-01-01

Farm work involves seasonal peak busy periods with long hours of work and potential sleep loss. Social, technological, and economic changes, and depressed commodity prices, have resulted in financial stress. There may be a relationship between sleep loss and worry about economic conditions. The objective of this study was to examine the association between hours of sleep and worry associated with cash flow shortages and worry associated with debt among a population of farmers and their family members. One hundred and ninety-five persons from 94 active farms in two rural municipalities in west central Saskatchewan were interviewed by questionnaire. Logistic regression analyses were used to quantify associations between sleep patterns and economic concerns during peak seasons and nonpeak seasons. During peak agricultural seasons, 31.6% of owners/operators reported less than 6 hours of sleep per night compared to 6.3% during the nonpeak seasons (p< .01). A significant relationship (odds ration [OR] 3.59, confidence interval [Cl] 1.58-8.13) was observed between daily cash flow worry and impaired sleep during peak busy seasons. A large proportion of farmers surveyed suffered sleep deprivation during peak seasons, and this sleep loss appeared related to worries about cash flow that were not observed during nonpeak seasons. It is possible that sleep loss during peak busy seasons may be related to impared judgment, as shown by differential worry habits, and might also be related to the high injury rates in farmers during peak busy seasons.

Rumination predicts longer sleep onset latency after an acute psychosocial stressor.

PubMed

Zoccola, Peggy M; Dickerson, Sally S; Lam, Suman

2009-09-01

Rumination has been linked to self-reported sleep quality. However, whether rumination is related to an objective sleep parameter has not been tested. This study examined whether rumination predicts sleep onset latency (SOL) on the night after an acute psychosocial stressor. We hypothesized that those who ruminate (assessed with both trait and stressor-specific measures) would have longer SOL (assessed with objective and subjective methods). Seventy participants delivered a 5-minute speech in front of an evaluative panel during an afternoon laboratory session. Trait rumination was assessed before the stressor. Stressor-specific rumination was captured with the frequency of task-related thoughts participants experienced during a 10-minute rest period after the stressor. Participants wore actigraphs on their wrists on the night after the laboratory session to measure objective sleep onset latency (SOL-O). Subjective sleep onset latency was estimated by participants on the subsequent morning. Consistent with hypotheses, trait and stressor-specific rumination predicted longer SOL-O and subjective sleep onset latency, respectively. In addition, trait and stressor-specific rumination interacted to predict longer SOL-O. SOL-O was longest among those who engaged in more stressor-specific rumination and had greater trait rumination scores. Neither rumination measure was related to sleep duration or wakefulness after sleep onset. The findings from this study are consistent with previous research linking rumination to subjective sleep quality. The results also suggest that post-stressor ruminative thought may predict delayed sleep onset for those with a propensity for rumination.

Upregulation of gene expression in reward-modulatory striatal opioid systems by sleep loss.

PubMed

Baldo, Brian A; Hanlon, Erin C; Obermeyer, William; Bremer, Quentin; Paletz, Elliott; Benca, Ruth M

2013-12-01

Epidemiological studies have shown a link between sleep loss and the obesity 'epidemic,' and several observations indicate that sleep curtailment engenders positive energy balance via increased palatable-food 'snacking.' These effects suggest alterations in reward-modulatory brain systems. We explored the effects of 10 days of sleep deprivation in rats on the expression of striatal opioid peptide (OP) genes that subserve food motivation and hedonic reward, and compared effects with those seen in hypothalamic energy balance-regulatory systems. Sleep-deprived (Sleep-Dep) rats were compared with yoked forced-locomotion apparatus controls (App-Controls), food-restricted rats (Food-Restrict), and unmanipulated controls (Home-Cage). Detection of mRNA levels with in situ hybridization revealed a subregion-specific upregulation of striatal preproenkephalin and prodynorhin gene expression in the Sleep-Dep group relative to all other groups. Neuropeptide Y (NPY) gene expression in the hippocampal dentate gyrus and throughout neocortex was also robustly upregulated selectively in the Sleep-Dep group. In contrast, parallel gene expression changes were observed in the Sleep-Dep and Food-Restrict groups in hypothalamic energy-sensing systems (arcuate nucleus NPY was upregulated, and cocaine- and amphetamine-regulated transcript was downregulated), in alignment with leptin suppression in both groups. Together, these results reveal a novel set of sleep deprivation-induced transcriptional changes in reward-modulatory peptide systems, which are dissociable from the energy-balance perturbations of sleep loss or the potentially stressful effects of the forced-locomotion procedure. The recruitment of telencephalic food-reward systems may provide a feeding drive highly resistant to feedback control, which could engender obesity through the enhancement of palatable feeding.

Sleep loss as a trigger of mood episodes in bipolar disorder: individual differences based on diagnostic subtype and gender.

PubMed

Lewis, Katie Swaden; Gordon-Smith, Katherine; Forty, Liz; Di Florio, Arianna; Craddock, Nick; Jones, Lisa; Jones, Ian

2017-09-01

Background Sleep loss may trigger mood episodes in people with bipolar disorder but individual differences could influence vulnerability to this trigger. Aims To determine whether bipolar subtype (bipolar disorder type I (BP-I) or II (BD-II)) and gender were associated with vulnerability to the sleep loss trigger. Method During a semi-structured interview, 3140 individuals (68% women) with bipolar disorder (66% BD-I) reported whether sleep loss had triggered episodes of high or low mood. DSM-IV diagnosis of bipolar subtype was derived from case notes and interview data. Results Sleep loss triggering episodes of high mood was associated with female gender (odds ratio (OR) = 1.43, 95% CI 1.17-1.75, P < 0.001) and BD-I subtype (OR = 2.81, 95% CI 2.26-3.50, P < 0.001). Analyses on sleep loss triggering low mood were not significant following adjustment for confounders. Conclusions Gender and bipolar subtype may increase vulnerability to high mood following sleep deprivation. This should be considered in situations where patients encounter sleep disruption, such as shift work and international travel. © The Royal College of Psychiatrists 2017.

Voluntary Sleep Loss in Rats.

PubMed

Oonk, Marcella; Krueger, James M; Davis, Christopher J

2016-07-01

Animal sleep deprivation (SDEP), in contrast to human SDEP, is involuntary and involves repeated exposure to aversive stimuli including the inability of the animal to control the waking stimulus. Therefore, we explored intracranial self-stimulation (ICSS), an operant behavior, as a method for voluntary SDEP in rodents. Male Sprague-Dawley rats were implanted with electroencephalography/electromyography (EEG/EMG) recording electrodes and a unilateral bipolar electrode into the lateral hypothalamus. Rats were allowed to self-stimulate, or underwent gentle handling-induced SDEP (GH-SDEP), during the first 6 h of the light phase, after which they were allowed to sleep. Other rats performed the 6 h ICSS and 1 w later were subjected to 6 h of noncontingent stimulation (NCS). During NCS the individual stimulation patterns recorded during ICSS were replayed. After GH-SDEP, ICSS, or NCS, time in nonrapid eye movement (NREM) sleep and rapid eye movement (REM) sleep increased. Further, in the 24 h after SDEP, rats recovered all of the REM sleep lost during SDEP, but only 75% to 80% of the NREM sleep lost, regardless of the SDEP method. The magnitude of EEG slow wave responses occurring during NREM sleep also increased after SDEP treatments. However, NREM sleep EEG slow wave activity (SWA) responses were attenuated following ICSS, compared to GH-SDEP and NCS. We conclude that ICSS and NCS can be used to sleep deprive rats. Changes in rebound NREM sleep EEG SWA occurring after ICSS, NCS, and GH-SDEP suggest that nonspecific effects of the SDEP procedure differentially affect recovery sleep phenotypes. © 2016 Associated Professional Sleep Societies, LLC.

Very early screening for sleep-disordered breathing in acute coronary syndrome in patients without acute heart failure.

PubMed

Van den Broecke, Sandra; Jobard, Olivier; Montalescot, Gilles; Bruyneel, Marie; Ninane, Vincent; Arnulf, Isabelle; Similowski, Thomas; Attali, Valérie

2014-12-01

Obstructive sleep apnea (OSA) is frequently associated with acute coronary syndrome (ACS). Screening of sleep-disordered breathing (SDB) has not been previously evaluated in ACS within 72 h in intensive care settings and its management could potentially enhance patients' prognosis. This pilot study assessed the feasibility of SDB screening at the early phase of ACS. All consecutive patients admitted to the coronary care unit (CCU) for ACS without acute heart failure underwent one overnight-attended polysomnography (PSG) within 72 h after admission. A telemonitoring (TM) system was set up to remotely monitor the signals and repair faulty sensors. The 27 recordings were analyzed as respiratory polygraphy (RP) and as PSG, and the results were compared. The TM system allowed successful intervention in 48% of recordings, resulting in excellent quality PSG for 89% of cases. The prevalence of SDB [apnea-hypopnea index (AHI) ≥ 15/h] was 82% and mainly consisted of central SDB and periodic breathing, except three patients with OSA. Compared with PSG, RP underestimated AHI, probably due to the poor sleep efficiency, reduction of slow-wave sleep, and alteration of rapid eye movement sleep. An early SDB screening by remote-attended PSG is feasible in ACS patients shortly after admission to CCU. The TM enhanced the quality of PSG. A high prevalence of central SDB was noticed, for which the etiology remains unknown. Further large-scale studies are needed to determine whether central SDB is an incidental finding in early ACS and whether the presence and severity of SDB have a prognostic impact. Copyright © 2014 Elsevier B.V. All rights reserved.

Concomitant changes in sleep duration and body weight and body composition during weight loss and 3-mo weight maintenance.

PubMed

Verhoef, Sanne P M; Camps, Stefan G J A; Gonnissen, Hanne K J; Westerterp, Klaas R; Westerterp-Plantenga, Margriet S

2013-07-01

An inverse relation between sleep duration and body mass index (BMI) has been shown. We assessed the relation between changes in sleep duration and changes in body weight and body composition during weight loss. A total of 98 healthy subjects (25 men), aged 20-50 y and with BMI (in kg/m(2)) from 28 to 35, followed a 2-mo very-low-energy diet that was followed by a 10-mo period of weight maintenance. Body weight, body composition (measured by using deuterium dilution and air-displacement plethysmography), eating behavior (measured by using a 3-factor eating questionnaire), physical activity (measured by using the validated Baecke's questionnaire), and sleep (estimated by using a questionnaire with the Epworth Sleepiness Scale) were assessed before and immediately after weight loss and 3- and 10-mo follow-ups. The average weight loss was 10% after 2 mo of dieting and 9% and 6% after 3- and 10-mo follow-ups, respectively. Daytime sleepiness and time to fall asleep decreased during weight loss. Short (≤7 h) and average (>7 to <9 h) sleepers increased their sleep duration, whereas sleep duration in long sleepers (≥9 h) did not change significantly during weight loss. This change in sleep duration was concomitantly negatively correlated with the change in BMI during weight loss and after the 3-mo follow-up and with the change in fat mass after the 3-mo follow-up. Sleep duration benefits from weight loss or vice versa. Successful weight loss, loss of body fat, and 3-mo weight maintenance in short and average sleepers are underscored by an increase in sleep duration or vice versa. This trial was registered at clinicaltrials.gov as NCT01015508.

Computational cognitive modeling of the temporal dynamics of fatigue from sleep loss.

PubMed

Walsh, Matthew M; Gunzelmann, Glenn; Van Dongen, Hans P A

2017-12-01

Computational models have become common tools in psychology. They provide quantitative instantiations of theories that seek to explain the functioning of the human mind. In this paper, we focus on identifying deep theoretical similarities between two very different models. Both models are concerned with how fatigue from sleep loss impacts cognitive processing. The first is based on the diffusion model and posits that fatigue decreases the drift rate of the diffusion process. The second is based on the Adaptive Control of Thought - Rational (ACT-R) cognitive architecture and posits that fatigue decreases the utility of candidate actions leading to microlapses in cognitive processing. A biomathematical model of fatigue is used to control drift rate in the first account and utility in the second. We investigated the predicted response time distributions of these two integrated computational cognitive models for performance on a psychomotor vigilance test under conditions of total sleep deprivation, simulated shift work, and sustained sleep restriction. The models generated equivalent predictions of response time distributions with excellent goodness-of-fit to the human data. More importantly, although the accounts involve different modeling approaches and levels of abstraction, they represent the effects of fatigue in a functionally equivalent way: in both, fatigue decreases the signal-to-noise ratio in decision processes and decreases response inhibition. This convergence suggests that sleep loss impairs psychomotor vigilance performance through degradation of the quality of cognitive processing, which provides a foundation for systematic investigation of the effects of sleep loss on other aspects of cognition. Our findings illustrate the value of treating different modeling formalisms as vehicles for discovery.

Mice Lacking Alternatively Activated (M2) Macrophages Show Impairments in Restorative Sleep after Sleep Loss and in Cold Environment.

PubMed

Massie, Ashley; Boland, Erin; Kapás, Levente; Szentirmai, Éva

2018-06-05

The relationship between sleep, metabolism and immune functions has been described, but the cellular components of the interaction are incompletely identified. We previously reported that systemic macrophage depletion results in sleep impairment after sleep loss and in cold environment. These findings point to the role of macrophage-derived signals in maintaining normal sleep. Macrophages exist either in resting form, classically activated, pro-inflammatory (M1) or alternatively activated, anti-inflammatory (M2) phenotypes. In the present study we determined the contribution of M2 macrophages to sleep signaling by using IL-4 receptor α-chain-deficient [IL-4Rα knockout (KO)] mice, which are unable to produce M2 macrophages. Sleep deprivation induced robust increases in non-rapid-eye-movement sleep (NREMS) and slow-wave activity in wild-type (WT) animals. NREMS rebound after sleep deprivation was ~50% less in IL-4Rα KO mice. Cold exposure induced reductions in rapid-eye-movement sleep (REMS) and NREMS in both WT and KO mice. These differences were augmented in IL-4Rα KO mice, which lost ~100% more NREMS and ~25% more REMS compared to WTs. Our finding that M2 macrophage-deficient mice have the same sleep phenotype as mice with global macrophage depletion reconfirms the significance of macrophages in sleep regulation and suggests that the main contributors are the alternatively activated M2 cells.

Lack of degradation in visuospatial perception of line orientation after one night of sleep loss.

PubMed

Killgore, William D S; Kendall, Athena P; Richards, Jessica M; McBride, Sharon A

2007-08-01

Sleep deprivation impairs a variety of cognitive abilities including vigilance, attention, and executive function. Although sleep loss has been shown to impair tasks requiring visual attention and spatial perception, it is not clear whether these deficits are exclusively a function of reduced attention and vigilance or if there are also alterations in visuospatial perception. Visuospatial perception and sustained vigilance performance were therefore examined in 54 healthy volunteers at rested baseline and again after one night of sleep deprivation using the Judgment of Line Orientation Test and a computerized test of psychomotor vigilance. Whereas psychomotor vigilance declined significantly from baseline to sleep-deprived testing, scores on the Judgment of Line Orientation did not change significantly. Results suggest that documented performance deficits associated with sleep loss are unlikely to be the result of dysfunction within systems of the brain responsible for simple visuospatial perception and processing of line angles.

Natural History of Excessive Daytime Sleepiness: Role of Obesity, Weight Loss, Depression, and Sleep Propensity

PubMed Central

Fernandez-Mendoza, Julio; Vgontzas, Alexandros N.; Kritikou, Ilia; Calhoun, Susan L.; Liao, Duanping; Bixler, Edward O.

2015-01-01

Study Objectives: Excessive daytime sleepiness (EDS) is highly prevalent in the general population and is associated with occupational and public safety hazards. However, no study has examined the clinical and polysomnographic (PSG) predictors of the natural history of EDS. Design: Representative longitudinal study. Setting: Sleep laboratory. Participants: From a random, general population sample of 1,741 individuals of the Penn State Adult Cohort, 1,395 were followed up after 7.5 years. Measurements and Results: Full medical evaluation and 1-night PSG at baseline and standardized telephone interview at follow-up. The incidence of EDS was 8.2%, while its persistence and remission were 38% and 62%, respectively. Obesity and weight gain were associated with the incidence and persistence of EDS, while weight loss was associated with its remission. Significant interactions between depression and PSG parameters on incident EDS showed that, in depressed individuals, incident EDS was associated with sleep disturbances, while in non-depressed individuals, incident EDS was associated with increased physiologic sleep propensity. Diabetes, allergy/asthma, anemia, and sleep complaints also predicted the natural history of EDS. Conclusions: Obesity, a disorder of epidemic proportions, is a major risk factor for the incidence and chronicity of excessive daytime sleepiness (EDS), while weight loss is associated with its remission. Interestingly, objective sleep disturbances predict incident EDS in depressed individuals, whereas physiologic sleep propensity predicts incident EDS in those without depression. Weight management and treatment of depression and sleep disorders should be part of public health policies. Citation: Fernandez-Mendoza J, Vgontzas AN, Kritikou I, Calhoun SL, Liao D, Bixler EO. Natural history of excessive daytime sleepiness: role of obesity, weight loss, depression, and sleep propensity. SLEEP 2015;38(3):351–360. PMID:25581913

Can a Mathematical Model Predict an Individual’s Trait-like Response to Both Total and Partial Sleep Loss?

DTIC Science & Technology

2015-01-01

Can a mathematical model predict an individual’s trait-like response to both total and partial sleep loss? SR IDHAR RAMAKR I SHNAN 1 , WE I LU 1 , SR...biomathematical model, psychomotor vigilance task, sleep -loss phenotype, trait preservation, two-process model Correspondence Jaques Reifman, PhD...trait-like response to sleep loss. However, it is not known whether this trait-like response can be captured by a mathemat- ical model from only one

Risk of Performance Decrements and Adverse Health Outcomes Resulting from Sleep Loss, Circadian Desynchronization, and Work Overload

NASA Technical Reports Server (NTRS)

Flynn-Evans, Erin; Gregory, Kevin; Arsintescu, Lucia; Whitmire, Alexandra

2016-01-01

Sleep loss, circadian desynchronization, and work overload occur to some extent for ground and flight crews, prior to and during spaceflight missions. Ground evidence indicates that such risk factors may lead to performance decrements and adverse health outcomes, which could potentially compromise mission objectives. Efforts are needed to identify the environmental and mission conditions that interfere with sleep and circadian alignment, as well as individual differences in vulnerability and resiliency to sleep loss and circadian desynchronization. Specifically, this report highlights a collection of new evidence to better characterize the risk and reveals new gaps in this risk as follows: Sleep loss is apparent during spaceflight. Astronauts consistently average less sleep during spaceflight relative to on the ground. The causes of this sleep loss remain unknown, however ground-based evidence suggests that the sleep duration of astronauts is likely to lead to performance impairment and short and long-term health consequences. Further research is needed in this area in order to develop screening tools to assess individual astronaut sleep need in order to quantify the magnitude of sleep loss during spaceflight; current and planned efforts in BHP's research portfolio address this need. In addition, it is still unclear whether the conditions of spaceflight environment lead to sleep loss or whether other factors, such as work overload lead to the reduced sleep duration. Future data mining efforts and continued data collection on the ISS will help to further characterize factors contributing to sleep loss. Sleep inertia has not been evaluated during spaceflight. Ground-based studies confirm that it takes two to four hours to achieve optimal performance after waking from a sleep episode. Sleep inertia has been associated with increased accidents and reduced performance in operational environments. Sleep inertia poses considerable risk during spaceflight when emergency

Acute Zonal Cone Photoreceptor Outer Segment Loss.

PubMed

Aleman, Tomas S; Sandhu, Harpal S; Serrano, Leona W; Traband, Anastasia; Lau, Marisa K; Adamus, Grazyna; Avery, Robert A

2017-05-01

The diagnostic path presented narrows down the cause of acute vision loss to the cone photoreceptor outer segment and will refocus the search for the cause of similar currently idiopathic conditions. To describe the structural and functional associations found in a patient with acute zonal occult photoreceptor loss. A case report of an adolescent boy with acute visual field loss despite a normal fundus examination performed at a university teaching hospital. Results of a complete ophthalmic examination, full-field flash electroretinography (ERG) and multifocal ERG, light-adapted achromatic and 2-color dark-adapted perimetry, and microperimetry. Imaging was performed with spectral-domain optical coherence tomography (SD-OCT), near-infrared (NIR) and short-wavelength (SW) fundus autofluorescence (FAF), and NIR reflectance (REF). The patient was evaluated within a week of the onset of a scotoma in the nasal field of his left eye. Visual acuity was 20/20 OU, and color vision was normal in both eyes. Results of the fundus examination and of SW-FAF and NIR-FAF imaging were normal in both eyes, whereas NIR-REF imaging showed a region of hyporeflectance temporal to the fovea that corresponded with a dense relative scotoma noted on light-adapted static perimetry in the left eye. Loss in the photoreceptor outer segment detected by SD-OCT co-localized with an area of dense cone dysfunction detected on light-adapted perimetry and multifocal ERG but with near-normal rod-mediated vision according to results of 2-color dark-adapted perimetry. Full-field flash ERG findings were normal in both eyes. The outer nuclear layer and inner retinal thicknesses were normal. Localized, isolated cone dysfunction may represent the earliest photoreceptor abnormality or a distinct entity within the acute zonal occult outer retinopathy complex. Acute zonal occult outer retinopathy should be considered in patients with acute vision loss and abnormalities on NIR-REF imaging, especially if

The effects of Dexamethasone on sleep in young children with Acute Lymphoblastic Leukemia

PubMed Central

Rosen, Gerald; Harris, Anne K.; Liu, Meixia; Dreyfus, Jill; Krueger, James; Messinger, Yoav H.

2016-01-01

Purpose Corticosteroids, which are a mainstay in the treatment of acute lymphoblastic leukemia (ALL), have a well-documented adverse effect on sleep. We sought to characterize the effects of dexamethasone on sleep over an entire 28-day treatment cycle using actigraphy, an objective measure of sleep. Methods The sleep of 25 children aged 2–9 years (mean 4.5 years) with ALL treated with dexamethasone were evaluated during maintenance chemotherapy using a within-subject experimental design, actigraphy, and standardized questionnaires to assess sleep, sleep problems, and fatigue. Results During the five days of dexamethasone treatment, sleep time increased during the night (535 vs. 498 min; p = 0.004) and daytime napping increased the following day (14 vs. 0 min; p = 0.002), and the number of wake episodes during the night was lower (14 vs. 20; p = ≤ 0.001). However, when assessed individually, sleep-onset time, efficiency, and wake after sleep onset during the night were unchanged during dexamethasone treatment; when the cumulative effect of all of these factors was assessed, there was a statistically and clinically significant increase in nighttime sleep duration during dexamethasone treatment. Conclusions During the five days of treatment with dexamethasone, an increase in nighttime sleep as well as daytime napping was observed in young children with ALL. The increases in sleep duration return to baseline one day after the discontinuation of dexamethasone. PMID:25799940

Impaired Recognition of Facially Expressed Emotions in Different Groups of Patients with Sleep Disorders.

PubMed

Crönlein, Tatjana; Langguth, Berthold; Eichhammer, Peter; Busch, Volker

2016-01-01

Recently it has been shown that acute sleep loss has a direct impact on emotional processing in healthy individuals. Here we studied the effect of chronically disturbed sleep on emotional processing by investigating two samples of patients with sleep disorders. 25 patients with psychophysiologic insomnia (23 women and 2 men, mean age: 51.6 SD; 10.9 years), 19 patients with sleep apnea syndrome (4 women and 15 men, mean age: 51.9; SD 11.1) and a control sample of 24 subjects with normal sleep (15 women and 9 men, mean age 45.3; SD 8.8) completed a Facial Expressed Emotion Labelling (FEEL) task, requiring participants to categorize and rate the intensity of six emotional expression categories: anger, anxiety, fear, happiness, disgust and sadness. Differences in FEEL score and its subscales among the three samples were analysed using ANOVA with gender as a covariate. Both patients with psychophysiologic insomnia and patients with sleep apnea showed significantly lower performance in the FEEL test as compared to the control group. Differences were seen in the scales happiness and sadness. Patient groups did not differ from each other. By demonstrating that previously known effects of acute sleep deprivation on emotional processing can be extended to persons experiencing chronically disturbed sleep, our data contribute to a deeper understanding of the relationship between sleep loss and emotions.

Acute liver injury induced by weight-loss herbal supplements.

PubMed

Chen, Gary C; Ramanathan, Vivek S; Law, David; Funchain, Pauline; Chen, George C; French, Samuel; Shlopov, Boris; Eysselein, Viktor; Chung, David; Reicher, Sonya; Pham, Binh V

2010-11-27

We report three cases of patients with acute liver injury induced by weight-loss herbal supplements. One patient took Hydroxycut while the other two took Herbalife supplements. Liver biopsies for all patients demonstrated findings consistent with drug-induced acute liver injury. To our knowledge, we are the first institute to report acute liver injury from both of these two types of weight-loss herbal supplements together as a case series. The series emphasizes the importance of taking a cautious approach when consuming herbal supplements for the purpose of weight loss.

Acute liver injury induced by weight-loss herbal supplements

PubMed Central

Chen, Gary C; Ramanathan, Vivek S; Law, David; Funchain, Pauline; Chen, George C; French, Samuel; Shlopov, Boris; Eysselein, Viktor; Chung, David; Reicher, Sonya; Pham, Binh V

2010-01-01

We report three cases of patients with acute liver injury induced by weight-loss herbal supplements. One patient took Hydroxycut while the other two took Herbalife supplements. Liver biopsies for all patients demonstrated findings consistent with drug-induced acute liver injury. To our knowledge, we are the first institute to report acute liver injury from both of these two types of weight-loss herbal supplements together as a case series. The series emphasizes the importance of taking a cautious approach when consuming herbal supplements for the purpose of weight loss. PMID:21173910

Impact of Sleeping Altitude on Symptoms of Acute Mountain Sickness on Mt. Fuji.

PubMed

Horiuchi, Masahiro; Uno, Tadashi; Endo, Junko; Handa, Yoko; Hasegawa, Tatsuya

2018-05-09

Horiuchi, Masahiro, Tadashi Uno, Junko Endo, Yoko Handa, and Tatsuya Hasegawa. Impact of sleeping altitude on symptoms of acute mountain sickness on Mt. Fuji. High Alt Med Biol. 00:000-000, 2018. We sought to investigate the factors influencing acute mountain sickness (AMS) on Mt. Fuji in Japan, in particular, to assess the effects of sleeping altitude, by means of a questionnaire survey. This study involved 1932 participants who climbed Mt. Fuji, and obtained information regarding sex, age, and whether participants stayed at the mountain lodges. The AMS survey excluded the perceived sleep difficulties assessed with the Lake Louise Scoring (LLS) system for all climbers. The overall prevalence of AMS was 31.6% for all participants (LLS score ≥3 with headache, excluding sleep difficulties). A univariate analysis revealed that overnight stay at Mt. Fuji was associated with an increased prevalence of AMS, but that sex and age were not. For overnight lodgers, the mean sleeping altitude in participants with AMS was slightly higher than that in participants without AMS (p < 0.05). Moreover, participants who stayed above 2870 m were more likely to experience AMS than those who stayed below 2815 m (p < 0.001), but sex and age were not significantly associated with the probability of experiencing AMS. Staying overnight at a mountain lodge, especially one above 2870 m, may be associated with an increased prevalence of AMS on Mt. Fuji.

Acute administration of fluoxetine normalizes rapid eye movement sleep abnormality, but not depressive behaviors in olfactory bulbectomized rats.

PubMed

Wang, Yi-Qun; Tu, Zhi-Cai; Xu, Xing-Yuan; Li, Rui; Qu, Wei-Min; Urade, Yoshihiro; Huang, Zhi-Li

2012-01-01

In humans, depression is associated with altered rapid eye movement (REM) sleep. However, the exact nature of the relationship between depressive behaviors and sleep abnormalities is debated. In this study, bilateral olfactory bulbectomy (OBX) was carried out to create a model of depression in rats. The sleep-wake profiles were assayed using a cutting-edge sleep bioassay system, and depressive behaviors were evaluated by open field and forced swimming tests. The monoamine content and monoamine metabolite levels in the brain were determined by a HPLC-electrochemical detection system. OBX rats exhibited a significant increase in REM sleep, especially between 15:00 and 18:00 hours during the light period. Acute treatment with fluoxetine (10 mg/kg, i.p.) immediately abolished the OBX-induced increase in REM sleep, but hyperactivity in the open field test and the time spent immobile in the forced swimming test remained unchanged. Neurochemistry studies revealed that acute administration of fluoxetine increased serotonin (5-HT) levels in the hippocampus, thalamus, and midbrain and decreased levels of the 5-HT metabolite 5-hydroxyindoleacetic acid (5-HIAA). The ratio of 5-HIAA to 5-HT decreased in almost all regions of the brain. These results indicate that acute administration of fluoxetine can reduce the increase in REM sleep but does not change the depressive behaviors in OBX rats, suggesting that there was no causality between REM sleep abnormalities and depressive behaviors in OBX rats. © 2011 The Authors. Journal of Neurochemistry © 2011 International Society for Neurochemistry.

Can Ayahuasca and sleep loss change sexual performance in male rats?

PubMed

Alvarenga, T A; Polesel, D N; Matos, G; Garcia, V A; Costa, J L; Tufik, S; Andersen, M L

2014-10-01

The ingestion of the beverage Ayahuasca usually occurs in religious ceremonies that are performed during the night leading to sleep deprivation. The purpose of the present study was to characterize the acute effects of Ayahuasca upon the sexual response of sleep deprived male rats. One group of sexually experienced male Wistar rats were submitted to a paradoxical sleep deprivation (PSD) protocol for 96h, while another group spent the same amount of time in the home cage (CTRL). After this period, either saline or Ayahuasca drink (250, 500 and 1000μgmL(-1)) was administered by gavage and sexual behavior and hormonal concentrations were measured. Ayahuasca alone significantly decreased sexual performance at all doses. However, in sleep deprived rats, the lower dose increased sexual performance while the intermediate dose produced a detrimental effect on sexual response compared to the CTRL rats at the same dose. Regarding the hormonal analyses, a lower testosterone concentration was observed in sleep-deprived saline rats in relation to the CTRL group. Progesterone was significantly lower only in PSD rats at the dose 500μgmL(-1) compared with CTRL-500μgmL(-1) group. Corticosterone was unchanged among the groups evaluated. Our results suggest that Ayahuasca intake markedly impaired sexual performance alone, but, when combined with sleep deprivation, had significant, but heterogeneous, effects on male sexual response. Copyright © 2014. Published by Elsevier B.V.

Non-invasive positive pressure ventilation during sleep at 3800 m: Relationship to acute mountain sickness and sleeping oxyhaemoglobin saturation.

PubMed

Johnson, Pamela L; Popa, Daniel A; Prisk, G Kim; Edwards, Natalie; Sullivan, Colin E

2010-02-01

Overnight oxyhaemoglobin desaturation is related to AMS. AMS can be debilitating and may require descent. Positive pressure ventilation during sleep at high altitude may prevent AMS and therefore be useful in people travelling to high altitude, who are known to suffer from AMS. Ascent to high altitude results in hypobaric hypoxia and some individuals will develop acute mountain sickness (AMS), which has been shown to be associated with low oxyhaemoglobin saturation during sleep. Previous research has shown that positive end-expiratory pressure by use of expiratory valves in a face mask while awake results in a reduction in AMS symptoms and higher oxyhaemoglobin saturation. We aimed to determine whether positive pressure ventilation would prevent AMS by increasing oxygenation during sleep. We compared sleeping oxyhaemoglobin saturation and the incidence and severity of AMS in seven subjects sleeping for two consecutive nights at 3800 m above sea level using either non-invasive positive pressure ventilation that delivered positive inspiratory and expiratory airway pressure via a face mask, or sleeping without assisted ventilation. The presence and severity of AMS were assessed by administration of the Lake Louise questionnaire. We found significant increases in the mean and minimum sleeping oxyhaemoglobin saturation and decreases in AMS symptoms in subjects who used positive pressure ventilation during sleep. Mean and minimum sleeping SaO2 was lower in subjects who developed AMS after the night spent without positive pressure ventilation. The use of positive pressure ventilation during sleep at 3800 m significantly increased the sleeping oxygen saturation; we suggest that the marked reduction in symptoms of AMS is due to this higher sleeping SaO2. We agree with the findings from previous studies that the development of AMS is associated with a lower sleeping oxygen saturation.

Association Between Sleep and Productivity Loss Among 598 676 Employees From Multiple Industries.

PubMed

Gingerich, Stefan B; Seaverson, Erin L D; Anderson, David R

2018-05-01

To examine the relationship between sleep habits and employee productivity. Cross-sectional health risk assessment analysis. Employer-sponsored health and well-being programs. A total of 598 676 employed adults from multiple industries. Self-reported average hours of sleep, fatigue, absence days, and presenteeism. Bivariate analyses to assess the relationships between self-reported hours of sleep and self-reported fatigue and mean and median absence and presenteeism. The relationship between sleep hours and both measures of productivity was U-shaped, with the least productivity loss among employees who reported 8 hours of sleep. More daytime fatigue correlated with more absence and presenteeism. Median absence and presenteeism was consistently lower than mean absence and presenteeism, respectively, for the various hours of sleep and levels of fatigue. Organizations looking to expand the value of their investment in employee health and well-being should consider addressing the employee sleep habits that may be negatively impacting productivity.

Effects of Positive Airway Pressure on Patients with Obstructive Sleep Apnea during Acute Ascent to Altitude

PubMed Central

Nishida, Katsufumi; Cloward, Tom V.; Weaver, Lindell K.; Brown, Samuel M.; Bell, James E.; Grissom, Colin K.

2015-01-01

Rationale: In acute ascent to altitude, untreated obstructive sleep apnea (OSA) is often replaced with central sleep apnea (CSA). In patients with obstructive sleep apnea who travel to altitude, it is unknown whether their home positive airway pressure (PAP) settings are sufficient to treat their obstructive sleep apnea, or altitude-associated central sleep apnea. Methods: Ten participants with positive airway pressure–treated obstructive sleep apnea, who reside at 1,320 m altitude, underwent polysomnography on their home positive airway pressure settings at 1,320 m and at a simulated altitude of 2,750 m in a hypobaric chamber. Six of the participants were subsequently studied without positive airway pressure at 2,750 m. Measurements and Main Results: At 1,320 m, all participants’ sleep apnea was controlled with positive airway pressure on home settings; at 2,750, no participants’ sleep apnea was controlled. At higher altitude, the apnea–hypopnea index was higher (11 vs. 2 events/h; P < 0.01), mostly due to hypopneas (10.5 vs. 2 events/h; P < 0.01). Mean oxygen saturations were lower (88 vs. 93%; P < 0.01) and total sleep time was diminished (349 vs. 393 min; P = 0.03). Four of six participants without positive airway pressure at 2,750 m required supplemental oxygen to prevent sustained oxygen saturation (as determined by pulse oximetry) less than 80%. Positive airway pressure also was associated with reduced central sleep apnea (0 vs. 1; P = 0.03), improved sleep time (358 vs. 292 min; P = 0.06), and improved sleep efficiency (78 vs. 63%; P = 0.04). Conclusions: Acute altitude exposure in patients with obstructive sleep apnea treated with positive airway pressure is associated with hypoxemia, decreased sleep time, and increased frequency of hypopneas compared with baseline altitude. Application of positive airway pressure at altitude is associated with decreased central sleep apnea and increased sleep efficiency. PMID:25884271

Loss of consciousness is related to hyper-correlated gamma-band activity in anesthetized macaques and sleeping humans.

PubMed

Bola, Michał; Barrett, Adam B; Pigorini, Andrea; Nobili, Lino; Seth, Anil K; Marchewka, Artur

2018-02-15

Loss of consciousness can result from a wide range of causes, including natural sleep and pharmacologically induced anesthesia. Important insights might thus come from identifying neuronal mechanisms of loss and re-emergence of consciousness independent of a specific manipulation. Therefore, to seek neuronal signatures of loss of consciousness common to sleep and anesthesia we analyzed spontaneous electrophysiological activity recorded in two experiments. First, electrocorticography (ECoG) acquired from 4 macaque monkeys anesthetized with different anesthetic agents (ketamine, medetomidine, propofol) and, second, stereo-electroencephalography (sEEG) from 10 epilepsy patients in different wake-sleep stages (wakefulness, NREM, REM). Specifically, we investigated co-activation patterns among brain areas, defined as correlations between local amplitudes of gamma-band activity. We found that resting wakefulness was associated with intermediate levels of gamma-band coupling, indicating neither complete dependence, nor full independence among brain regions. In contrast, loss of consciousness during NREM sleep and propofol anesthesia was associated with excessively correlated brain activity, as indicated by a robust increase of number and strength of positive correlations. However, such excessively correlated brain signals were not observed during REM sleep, and were present only to a limited extent during ketamine anesthesia. This might be related to the fact that, despite suppression of behavioral responsiveness, REM sleep and ketamine anesthesia often involve presence of dream-like conscious experiences. We conclude that hyper-correlated gamma-band activity might be a signature of loss of consciousness common across various manipulations and independent of behavioral responsiveness. Copyright © 2017 Elsevier Inc. All rights reserved.

Diet/Energy Balance Affect Sleep and Wakefulness Independent of Body Weight.

PubMed

Perron, Isaac J; Pack, Allan I; Veasey, Sigrid

2015-12-01

Excessive daytime sleepiness commonly affects obese people, even in those without sleep apnea, yet its causes remain uncertain. We sought to determine whether acute dietary changes could induce or rescue wake impairments independent of body weight. We implemented a novel feeding paradigm that generates two groups of mice with equal body weight but opposing energetic balance. Two subsets of mice consuming either regular chow (RC) or high-fat diet (HFD) for 8 w were switched to the opposite diet for 1 w. Sleep recordings were conducted at Week 0 (baseline), Week 8 (pre-diet switch), and Week 9 (post-diet switch) for all groups. Sleep homeostasis was measured at Week 8 and Week 9. Young adult, male C57BL/6J mice. Differences in total wake, nonrapid eye movement (NREM), and rapid eye movement (REM) time were quantified, in addition to changes in bout fragmentation/consolidation. At Week 9, the two diet switch groups had similar body weight. However, animals switched to HFD (and thus gaining weight) had decreased wake time, increased NREM sleep time, and worsened sleep/wake fragmentation compared to mice switched to RC (which were in weight loss). These effects were driven by significant sleep/wake changes induced by acute dietary manipulations (Week 8 → Week 9). Sleep homeostasis, as measured by delta power increase following sleep deprivation, was unaffected by our feeding paradigm. Acute dietary manipulations are sufficient to alter sleep and wakefulness independent of body weight and without effects on sleep homeostasis. © 2015 Associated Professional Sleep Societies, LLC.

Effect of Acute Intermittent CPAP Depressurization during Sleep in Obese Patients.

PubMed

Jun, Jonathan C; Unnikrishnan, Dileep; Schneider, Hartmut; Kirkness, Jason; Schwartz, Alan R; Smith, Philip L; Polotsky, Vsevolod Y

2016-01-01

Obstructive Sleep Apnea (OSA) describes intermittent collapse of the airway during sleep, for which continuous positive airway pressure (CPAP) is often prescribed for treatment. Prior studies suggest that discontinuation of CPAP leads to a gradual, rather than immediate return of baseline severity of OSA. The objective of this study was to determine the extent of OSA recurrence during short intervals of CPAP depressurization during sleep. Nine obese (BMI = 40.4 ± 3.5) subjects with severe OSA (AHI = 88.9 ± 6.8) adherent to CPAP were studied during one night in the sleep laboratory. Nasal CPAP was delivered at therapeutic (11.1 ± 0.6 cm H20) or atmospheric pressure, in alternating fashion for 1-hour periods during the night. We compared sleep architecture and metrics of OSA during CPAP-on and CPAP-off periods. 8/9 subjects tolerated CPAP withdrawal. The average AHI during CPAP-on and CPAP-off periods was 3.6 ± 0.6 and 15.8 ± 3.6 respectively (p<0.05). The average 3% ODI during CPAP-on and CPAP-off was 4.7 ± 2 and 20.4 ± 4.7 respectively (p<0.05). CPAP depressurization also induced more awake (p<0.05) and stage N1 (p<0.01) sleep, and less stage REM (p<0.05) with a trend towards decreased stage N3 (p = 0.064). Acute intermittent depressurization of CPAP during sleep led to deterioration of sleep architecture but only partial re-emergence of OSA. These observations suggest carryover effects of CPAP.

Effect of Acute Intermittent CPAP Depressurization during Sleep in Obese Patients

PubMed Central

Jun, Jonathan C.; Unnikrishnan, Dileep; Schneider, Hartmut; Kirkness, Jason; Schwartz, Alan R.; Smith, Philip L.; Polotsky, Vsevolod Y.

2016-01-01

Background Obstructive Sleep Apnea (OSA) describes intermittent collapse of the airway during sleep, for which continuous positive airway pressure (CPAP) is often prescribed for treatment. Prior studies suggest that discontinuation of CPAP leads to a gradual, rather than immediate return of baseline severity of OSA. The objective of this study was to determine the extent of OSA recurrence during short intervals of CPAP depressurization during sleep. Methods Nine obese (BMI = 40.4 ± 3.5) subjects with severe OSA (AHI = 88.9 ± 6.8) adherent to CPAP were studied during one night in the sleep laboratory. Nasal CPAP was delivered at therapeutic (11.1 ± 0.6 cm H20) or atmospheric pressure, in alternating fashion for 1-hour periods during the night. We compared sleep architecture and metrics of OSA during CPAP-on and CPAP-off periods. Results 8/9 subjects tolerated CPAP withdrawal. The average AHI during CPAP-on and CPAP-off periods was 3.6 ± 0.6 and 15.8 ± 3.6 respectively (p<0.05). The average 3% ODI during CPAP-on and CPAP-off was 4.7 ± 2 and 20.4 ± 4.7 respectively (p<0.05). CPAP depressurization also induced more awake (p<0.05) and stage N1 (p<0.01) sleep, and less stage REM (p<0.05) with a trend towards decreased stage N3 (p = 0.064). Conclusion Acute intermittent depressurization of CPAP during sleep led to deterioration of sleep architecture but only partial re-emergence of OSA. These observations suggest carryover effects of CPAP. PMID:26731735

Acute vision loss: a fuzzy presentation of sarcoidosis.

PubMed

Austin, Andrea L; Day, Luke T; Bishop, Frank M

2013-04-01

Acute vision loss is a devastating problem for patients and a challenging diagnostic dilemma for Emergency Physicians. This chief complaint is one in which we must be adept at quickly evaluating and initiating either care or referral. This case reviews the approach to acute vision loss and shows the importance of expanding the differential in atypical and complex presentations. A 31-year-old, previously healthy, white woman presented to the Emergency Department (ED) with 1 day of painless right eye vision loss. Ocular ultrasound and slit-lamp examination were unremarkable. Fundoscopic examination revealed retinal hemorrhages and papillitis. Her chest X-ray study was significant for bilateral hilar adenopathy, and subsequent lymph node biopsy confirmed the diagnosis of sarcoidosis. Although sarcoidosis is more common in African Americans, it must be considered in all patients in the appropriate clinical context. Sarcoidosis is an important diagnosis to include on the differential of many chief complaints that present to the ED, including acute vision loss and dyspnea. Published by Elsevier Inc.

Progressive Loss of the Orexin Neurons Reveals Dual Effects on Wakefulness

PubMed Central

Branch, Abigail F.; Navidi, William; Tabuchi, Sawako; Terao, Akira; Yamanaka, Akihiro; Scammell, Thomas E.; Diniz Behn, Cecilia

2016-01-01

Study Objectives: Narcolepsy is caused by loss of the orexin (also known as hypocretin) neurons. In addition to the orexin peptides, these neurons release additional neurotransmitters, which may produce complex effects on sleep/wake behavior. Currently, it remains unknown whether the orexin neurons promote the initiation as well as the maintenance of wakefulness, and whether the orexin neurons influence initiation or maintenance of sleep. To determine the effects of the orexin neurons on the dynamics of sleep/wake behavior, we analyzed sleep/wake architecture in a novel mouse model of acute orexin neuron loss. Methods: We used survival analysis and other statistical methods to analyze sleep/wake architecture in orexin-tTA ; TetO diphtheria toxin A mice at different stages of orexin neuron degeneration. Results: Progressive loss of the orexin neurons dramatically reduced survival of long wake bouts, but it also improved survival of brief wake bouts. In addition, with loss of the orexin neurons, mice were more likely to wake during the first 30 sec of nonrapid eye movement sleep and then less likely to return to sleep during the first 60 sec of wakefulness. Conclusions: These findings help explain the sleepiness and fragmented sleep that are characteristic of narcolepsy. Orexin neuron loss impairs survival of long wake bouts resulting in poor maintenance of wakefulness, but this neuronal loss also fragments sleep by increasing the risk of awakening at the beginning of sleep and then reducing the likelihood of quickly returning to sleep. Citation: Branch AF, Navidi W, Tabuchi S, Terao A, Yamanaka A, Scammell TE, Diniz Behn C. Progressive loss of the orexin neurons reveals dual effects on wakefulness. SLEEP 2016;39(2):369–377. PMID:26446125

Acute Zonal Cone Photoreceptor Outer Segment Loss

PubMed Central

Sandhu, Harpal S.; Serrano, Leona W.; Traband, Anastasia; Lau, Marisa K.; Adamus, Grazyna; Avery, Robert A.

2017-01-01

Importance The diagnostic path presented narrows down the cause of acute vision loss to the cone photoreceptor outer segment and will refocus the search for the cause of similar currently idiopathic conditions. Objective To describe the structural and functional associations found in a patient with acute zonal occult photoreceptor loss. Design, Setting, and Participants A case report of an adolescent boy with acute visual field loss despite a normal fundus examination performed at a university teaching hospital. Main Outcomes and Measures Results of a complete ophthalmic examination, full-field flash electroretinography (ERG) and multifocal ERG, light-adapted achromatic and 2-color dark-adapted perimetry, and microperimetry. Imaging was performed with spectral-domain optical coherence tomography (SD-OCT), near-infrared (NIR) and short-wavelength (SW) fundus autofluorescence (FAF), and NIR reflectance (REF). Results The patient was evaluated within a week of the onset of a scotoma in the nasal field of his left eye. Visual acuity was 20/20 OU, and color vision was normal in both eyes. Results of the fundus examination and of SW-FAF and NIR-FAF imaging were normal in both eyes, whereas NIR-REF imaging showed a region of hyporeflectance temporal to the fovea that corresponded with a dense relative scotoma noted on light-adapted static perimetry in the left eye. Loss in the photoreceptor outer segment detected by SD-OCT co-localized with an area of dense cone dysfunction detected on light-adapted perimetry and multifocal ERG but with near-normal rod-mediated vision according to results of 2-color dark-adapted perimetry. Full-field flash ERG findings were normal in both eyes. The outer nuclear layer and inner retinal thicknesses were normal. Conclusions and Relevance Localized, isolated cone dysfunction may represent the earliest photoreceptor abnormality or a distinct entity within the acute zonal occult outer retinopathy complex. Acute zonal occult outer retinopathy

Sleep restriction alters plasma endocannabinoids concentrations before but not after exercise in humans.

PubMed

Cedernaes, Jonathan; Fanelli, Flaminia; Fazzini, Alessia; Pagotto, Uberto; Broman, Jan-Erik; Vogel, Heike; Dickson, Suzanne L; Schiöth, Helgi B; Benedict, Christian

2016-12-01

Following binding to cannabinoid receptors, endocannabinoids regulate a variety of central nervous system processes including appetite and mood. Recent evidence suggests that the systemic release of these lipid metabolites can be altered by acute exercise and that their levels also vary across the 24-h sleep-wake cycle. The present study utilized a within-subject design (involving 16 normal-weight men) to determine whether daytime circulating endocannabinoid concentrations differ following three nights of partial sleep deprivation (4.25-h sleep opportunity, 2:45-7a.m. each night) vs. normal sleep (8.5-h sleep opportunity, 10:30p.m.-7a.m. each night), before and after an acute bout of ergometer cycling in the morning. In addition, subjective hunger and stress were measured. Pre-exercise plasma concentrations of 2-arachidonoylglycerol (2AG) were 80% higher 1.5h after awakening (vs. normal sleep, p<0.05) when participants were sleep-deprived. This coincided with increased hunger ratings (+25% vs. normal sleep, p<0.05). Moreover, plasma 2AG was elevated 15min post-exercise (+44%, p<0.05). Sleep duration did not however modulate this exercise-induced rise. Finally, subjective stress was generally lower on the day after three nights of short sleep vs. normal sleep, especially after exercise (p<0.05). Given that activation of the endocannabinoid system has been previously shown to acutely increase appetite and mood, our results could suggest that behavioral effects of acute sleep loss, such as increased hunger and transiently improved psychological state, may partially result from activation of this signaling pathway. In contrast, more pronounced exercise-induced elevations of endocannabinoids appear to be less affected by short sleep duration. Copyright © 2016 The Author(s). Published by Elsevier Ltd.. All rights reserved.

Clinical Predictors of Residual Sleep Apnea after Weight Loss Therapy in Obese Adolescents.

PubMed

Van Eyck, Annelies; De Guchtenaere, Ann; Van Gaal, Luc; De Backer, Wilfried; Verhulst, Stijn L; Van Hoorenbeeck, Kim

2018-05-01

To investigate clinical factors that could predict residual sleep-disordered breathing (SDB) after weight loss. Obese subjects between 10 and 19 years of age were recruited while entering an in-patient weight loss treatment program. All subjects underwent anthropometry and sleep screening using a portable device at baseline and after 4-6 months of therapy. Sleep and International Study of Asthma and Allergies in Childhood questionnaires were completed at baseline. A total of 339 patients were included. Median age was 15.4 years (10.1-19.1). Body mass index z score at baseline was 2.75 ± 0.42, and 35% of subjects were boys. SDB was present in 32%. After a mean decrease in body mass index z score of 32%, residual SDB was found in 20% of subjects with SDB at baseline. Subjects with more severe SDB (OR 1.18; CI 1.01-1.34; P = .02) and respiratory allergies (OR 7.85; CI 1.20-51.39; P = .03) were at higher risk of developing residual SDB, unlike age, sex, and anthropometric variables. Weight loss was successful for treating SDB in 80% of patients. More severe SDB and the presence of respiratory allergies at baseline were associated with a higher risk of residual SDB after weight loss. Copyright © 2017 Elsevier Inc. All rights reserved.

Natural history of excessive daytime sleepiness: role of obesity, weight loss, depression, and sleep propensity.

PubMed

Fernandez-Mendoza, Julio; Vgontzas, Alexandros N; Kritikou, Ilia; Calhoun, Susan L; Liao, Duanping; Bixler, Edward O

2015-03-01

Excessive daytime sleepiness (EDS) is highly prevalent in the general population and is associated with occupational and public safety hazards. However, no study has examined the clinical and polysomnographic (PSG) predictors of the natural history of EDS. Representative longitudinal study. Sleep laboratory. From a random, general population sample of 1,741 individuals of the Penn State Adult Cohort, 1,395 were followed up after 7.5 years. Full medical evaluation and 1-night PSG at baseline and standardized telephone interview at follow-up. The incidence of EDS was 8.2%, while its persistence and remission were 38% and 62%, respectively. Obesity and weight gain were associated with the incidence and persistence of EDS, while weight loss was associated with its remission. Significant interactions between depression and PSG parameters on incident EDS showed that, in depressed individuals, incident EDS was associated with sleep disturbances, while in non-depressed individuals, incident EDS was associated with increased physiologic sleep propensity. Diabetes, allergy/ asthma, anemia, and sleep complaints also predicted the natural history of EDS. Obesity, a disorder of epidemic proportions, is a major risk factor for the incidence and chronicity of EDS, while weight loss is associated with its remission. Interestingly, objective sleep disturbances predict incident EDS in depressed individuals, whereas physiologic sleep propensity predicts incident EDS in those without depression. Weight management and treatment of depression and sleep disorders should be part of our public health policies. © 2015 Associated Professional Sleep Societies, LLC.

Metabolic disregulation in obese adolescents with sleep-disordered breathing before and after weight loss.

PubMed

Van Hoorenbeeck, K; Franckx, H; Debode, P; Aerts, P; Ramet, J; Van Gaal, L F; Desager, K N; De Backer, W A; Verhulst, S L

2013-07-01

Sleep-disordered breathing (SDB) is prevalent in obesity. Weight loss is one of the most effective treatment options. The aim was to assess the association of SDB and metabolic disruption before and after weight loss. Obese adolescents were included when entering an in-patient weight loss program. Fasting blood analysis was performed at baseline and after 4-6 months. Sleep screening was done at baseline and at follow-up in case of baseline SDB. 224 obese adolescents were included. Median age was 15.5 years (10.1-18.0) and mean BMI z-score was 2.74 ± 0.42. About 30% had SDB at baseline (N = 68). High-density lipoprotein (HDL)-cholesterol was associated with mean nocturnal oxygen saturation () (partial r = 0.21; P = 0.002). Aspartate aminotransferase (ASAT) and alanine aminotransferase were related with oxygen desaturation index (partial r = -0.15; P = 0.03 and partial r = -0.15; P = 0.02), but this became insignificant after correction for sex. After weight loss, 24% had residual SDB. Linear regression showed an association between ASAT and (partial r = -0.34; P = 0.002). There were no significant correlations between improvements in laboratory measurements and sleep parameters. HDL-cholesterol improved in relation with the decrease in BMI z-score. SDB at baseline was associated with higher levels of liver enzymes and lower HDL-cholesterol concentration. Improvements in sleep parameters were not associated with improvements in laboratory measurements. Copyright © 2013 The Obesity Society.

Acute Total and Chronic Partial Sleep Deprivation: Effects on Neurobehavioral Functions, Waking EEG and Renin-Angiotensin System

NASA Technical Reports Server (NTRS)

Dijk, Derk-Jan

1999-01-01

Total sleep deprivation leads to decrements in neurobehavioral performance and changes in electroencephalographic (EEG) oscillations as well as the incidence of slow eye movements ad detected in the electro-oculogram (EOG) during wakefulness. Although total sleep deprivation is a powerful tool to investigate the association of EEG/EOG and neurobehavioral decrements, sleep loss during space flight is usual only partial. Furthermore exposure to the microgravity environment leads to changes in sodium and volume homeostasis and associated renal and cardio-endocrine responses. Some of these changes can be induced in head down tilt bedrest studies. We integrate research tools and research projects to enhance the fidelity of the simulated conditions of space flight which are characterized by complexity and mutual interactions. The effectiveness of countermeasures and physiologic mechanisms underlying neurobehavioral changes and renal-cardio endocrine changes are investigated in Project 3 of the Human Performance Team and Project 3 of the Cardiovascular Alterations Team respectively. Although the. specific aims of these two projects are very different, they employ very similar research protocols. Thus, both projects investigate the effects of posture/bedrest and sleep deprivation (total or partial) on outcome measures relevant to their specific aims. The main aim of this enhancement grant is to exploit the similarities in research protocols by including the assessment of outcome variables relevant to the Renal-Cardio project in the research protocol of Project 3 of the Human Performance Team and by including the assessment of outcome variables relevant to the Quantitative EEG and Sleep Deprivation Project in the research protocols of Project 3 of the Cardiovascular Alterations team. In particular we will assess Neurobehavioral Function and Waking EEG in the research protocols of the renal-cardio endocrine project and renin-angiotensin and cardiac function in the research

The Acute Effects of Intermittent Light Exposure in the Evening on Alertness and Subsequent Sleep Architecture.

PubMed

Yang, Minqi; Ma, Ning; Zhu, Yingying; Su, Ying-Chu; Chen, Qingwei; Hsiao, Fan-Chi; Ji, Yanran; Yang, Chien-Ming; Zhou, Guofu

2018-03-15

Exposure to bright light is typically intermittent in our daily life. However, the acute effects of intermittent light on alertness and sleep have seldom been explored. To investigate this issue, we employed within-subject design and compared the effects of three light conditions: intermittent bright light (30-min pulse of blue-enriched bright light (~1000 lux, ~6000 K) alternating with 30-min dim normal light (~5 lux, ~3600 K) three times); continuous bright light; and continuous dim light on subjective and objective alertness and subsequent sleep structure. Each light exposure was conducted during the three hours before bedtime. Fifteen healthy volunteers (20 ± 3.4 years; seven males) were scheduled to stay in the sleep laboratory for four separated nights (one for adaptation and the others for the light exposures) with a period of at least one week between nights. The results showed that when compared with dim light, both intermittent light and continuous bright light significantly increased subjective alertness and decreased sleep efficiency (SE) and total sleep time (TST). Intermittent light significantly increased objective alertness than dim light did during the second half of the light-exposure period. Our results suggested that intermittent light was as effective as continuous bright light in their acute effects in enhancing subjective and objective alertness and in negatively impacting subsequent sleep.

Epigenomics of Total Acute Sleep Deprivation in Relation to Genome-Wide DNA Methylation Profiles and RNA Expression.

PubMed

Nilsson, Emil K; Boström, Adrian E; Mwinyi, Jessica; Schiöth, Helgi B

2016-06-01

Despite an established link between sleep deprivation and epigenetic processes in humans, it remains unclear to what extent sleep deprivation modulates DNA methylation. We performed a within-subject randomized blinded study with 16 healthy subjects to examine the effect of one night of total sleep deprivation (TSD) on the genome-wide methylation profile in blood compared with that in normal sleep. Genome-wide differences in methylation between both conditions were assessed by applying a paired regression model that corrected for monocyte subpopulations. In addition, the correlations between the methylation of genes detected to be modulated by TSD and gene expression were examined in a separate, publicly available cohort of 10 healthy male donors (E-GEOD-49065). Sleep deprivation significantly affected the DNA methylation profile both independently and in dependency of shifts in monocyte composition. Our study detected differential methylation of 269 probes. Notably, one CpG site was located 69 bp upstream of ING5, which has been shown to be differentially expressed after sleep deprivation. Gene set enrichment analysis detected the Notch and Wnt signaling pathways to be enriched among the differentially methylated genes. These results provide evidence that total acute sleep deprivation alters the methylation profile in healthy human subjects. This is, to our knowledge, the first study that systematically investigated the impact of total acute sleep deprivation on genome-wide DNA methylation profiles in blood and related the epigenomic findings to the expression data.

Fragmentation of Rapid Eye Movement and Nonrapid Eye Movement Sleep without Total Sleep Loss Impairs Hippocampus-Dependent Fear Memory Consolidation

PubMed Central

Lee, Michael L.; Katsuyama, Ângela M.; Duge, Leanne S.; Sriram, Chaitra; Krushelnytskyy, Mykhaylo; Kim, Jeansok J.; de la Iglesia, Horacio O.

2016-01-01

and nonrapid eye movement sleep without total sleep loss impairs hippocampus-dependent fear memory consolidation. SLEEP 2016;39(11):2021–2031. PMID:27568801

Correlates and Escitalopram Treatment Effects on Sleep Disturbance in Patients with Acute Coronary Syndrome: K-DEPACS and EsDEPACS.

PubMed

Kim, Jae-Min; Stewart, Robert; Bae, Kyung-Yeol; Kang, Hee-Ju; Kim, Sung-Wan; Shin, Il-Seon; Hong, Young Joon; Ahn, Youngkeun; Jeong, Myung Ho; Yoon, Jin-Sang

2015-07-01

To investigate the correlates of sleep disturbance and to assess escitalopram treatment effects of depression on sleep disturbance in patients with acute coronary syndrome (ACS). A cross-sectional study in patients with ACS within 2 w post-ACS, and a 24-w double-blind controlled trial of escitalopram against placebo for patients with ACS who have comorbid depressive disorders. A university hospital in South Korea. There were 1,152 patients with ACS who were consecutively recruited. Of 446 patients with comorbid depressive disorders, 300 were randomized to the trial. Sleep disturbance was evaluated by the Leeds Sleep Evaluation Questionnaire. Demographic and clinical characteristics were assessed, including cardiovascular risk factors, current cardiac status, and depressive symptoms. Depressive symptoms were most strongly and consistently associated with sleep disturbance. In addition, older age, female sex, hypertension, and more severe ACS status were associated with certain aspects of sleep disturbance. Escitalopram was significantly superior to placebo for improving sleep disturbance over the 24-w treatment period. These effects were substantially explained by improvement in depressive symptoms. Depression screening is indicated in patients with acute coronary syndrome with sleep disturbance. Successful treatment of depression has beneficial effects on sleep outcomes in these patients. ClinicalTrial.gov identifier for the 24-w drug trial, NCT00419471. © 2015 Associated Professional Sleep Societies, LLC.

Influence of acute sleep loss on the neural correlates of alerting, orientating and executive attention components.

PubMed

Muto, Vincenzo; Shaffii-le Bourdiec, Anahita; Matarazzo, Luca; Foret, Ariane; Mascetti, Laura; Jaspar, Mathieu; Vandewalle, Gilles; Phillips, Christophe; Degueldre, Christian; Balteau, Evelyne; Luxen, André; Collette, Fabienne; Maquet, Pierre

2012-12-01

The Attention Network Test (ANT) is deemed to assess the alerting, orientating and executive components of human attention. Capitalizing on the opportunity to investigate three facets of attention in a single task, we used functional magnetic resonance imaging (fMRI) to assess the effect of sleep deprivation (SD) on brain responses associated with the three attentional components elicited by the ANT. Twelve healthy volunteers were scanned in two conditions 1 week apart, after a normal night of sleep (rested wakefulness, RW) or after one night of total sleep deprivation. Sleep deprivation was associated with a global increase in reaction times, which did not affect specifically any of the three attention effects. Brain responses associated with the alerting effect did not differ between RW and SD. Higher-order attention components (orientating and conflict effects) were associated with significantly larger thalamic responses during SD than during RW. These results suggest that SD influences different components of human attention non-selectively, through mechanisms that might either affect centrencephalic structures maintaining vigilance or ubiquitously perturb neuronal function. Compensatory responses can counter these effects transiently by recruiting thalamic responses, thereby supporting thalamocortical function. © 2012 European Sleep Research Society.

Risk of Performance Decrements and Adverse Health Outcomes Resulting from Sleep Loss, Circadian Desynchronization, and Work Overload

NASA Technical Reports Server (NTRS)

Evans-Flynn, Erin; Gregory, Kevin; Arsintescu, Lucia; Whitmire, Alexandra; Leveton, Lauren B.; Vessey, William

2015-01-01

Sleep loss, circadian desynchronization, and work overload occur to some extent for ground and flight crews, prior to and during spaceflight missions. Ground evidence indicates that such risk factors may lead to performance decrements and adverse health outcomes, which could potentially compromise mission objectives. Efforts are needed to identify the environmental and mission conditions that interfere with sleep and circadian alignment, as well as individual differences in vulnerability and resiliency to sleep loss and circadian desynchronization. Specifically, this report highlights a collection of new evidence to better characterize the risk and reveals new gaps in this risk.

Skill execution and sleep deprivation: effects of acute caffeine or creatine supplementation - a randomized placebo-controlled trial

PubMed Central

2011-01-01

Background We investigated the effects of sleep deprivation with or without acute supplementation of caffeine or creatine on the execution of a repeated rugby passing skill. Method Ten elite rugby players completed 10 trials on a simple rugby passing skill test (20 repeats per trial), following a period of familiarisation. The players had between 7-9 h sleep on 5 of these trials and between 3-5 h sleep (deprivation) on the other 5. At a time of 1.5 h before each trial, they undertook administration of either: placebo tablets, 50 or 100 mg/kg creatine, 1 or 5 mg/kg caffeine. Saliva was collected before each trial and assayed for salivary free cortisol and testosterone. Results Sleep deprivation with placebo application resulted in a significant fall in skill performance accuracy on both the dominant and non-dominant passing sides (p < 0.001). No fall in skill performance was seen with caffeine doses of 1 or 5 mg/kg, and the two doses were not significantly different in effect. Similarly, no deficit was seen with creatine administration at 50 or 100 mg/kg and the performance effects were not significantly different. Salivary testosterone was not affected by sleep deprivation, but trended higher with the 100 mg/kg creatine dose, compared to the placebo treatment (p = 0.067). Salivary cortisol was elevated (p = 0.001) with the 5 mg/kg dose of caffeine (vs. placebo). Conclusion Acute sleep deprivation affects performance of a simple repeat skill in elite athletes and this was ameliorated by a single dose of either caffeine or creatine. Acute creatine use may help to alleviate decrements in skill performance in situations of sleep deprivation, such as transmeridian travel, and caffeine at low doses appears as efficacious as higher doses, at alleviating sleep deprivation deficits in athletes with a history of low caffeine use. Both options are without the side effects of higher dose caffeine use. PMID:21324203

Skill execution and sleep deprivation: effects of acute caffeine or creatine supplementation - a randomized placebo-controlled trial.

PubMed

Cook, Christian J; Crewther, Blair T; Kilduff, Liam P; Drawer, Scott; Gaviglio, Chris M

2011-02-16

We investigated the effects of sleep deprivation with or without acute supplementation of caffeine or creatine on the execution of a repeated rugby passing skill. Ten elite rugby players completed 10 trials on a simple rugby passing skill test (20 repeats per trial), following a period of familiarisation. The players had between 7-9 h sleep on 5 of these trials and between 3-5 h sleep (deprivation) on the other 5. At a time of 1.5 h before each trial, they undertook administration of either: placebo tablets, 50 or 100 mg/kg creatine, 1 or 5 mg/kg caffeine. Saliva was collected before each trial and assayed for salivary free cortisol and testosterone. Sleep deprivation with placebo application resulted in a significant fall in skill performance accuracy on both the dominant and non-dominant passing sides (p < 0.001). No fall in skill performance was seen with caffeine doses of 1 or 5 mg/kg, and the two doses were not significantly different in effect. Similarly, no deficit was seen with creatine administration at 50 or 100 mg/kg and the performance effects were not significantly different. Salivary testosterone was not affected by sleep deprivation, but trended higher with the 100 mg/kg creatine dose, compared to the placebo treatment (p = 0.067). Salivary cortisol was elevated (p = 0.001) with the 5 mg/kg dose of caffeine (vs. placebo). Acute sleep deprivation affects performance of a simple repeat skill in elite athletes and this was ameliorated by a single dose of either caffeine or creatine. Acute creatine use may help to alleviate decrements in skill performance in situations of sleep deprivation, such as transmeridian travel, and caffeine at low doses appears as efficacious as higher doses, at alleviating sleep deprivation deficits in athletes with a history of low caffeine use. Both options are without the side effects of higher dose caffeine use.

The Influence of Sleep Disordered Breathing on Weight Loss in a National Weight Management Program

PubMed Central

Janney, Carol A.; Kilbourne, Amy M.; Germain, Anne; Lai, Zongshan; Hoerster, Katherine D.; Goodrich, David E.; Klingaman, Elizabeth A.; Verchinina, Lilia; Richardson, Caroline R.

2016-01-01

Study Objective: To investigate the influence of sleep disordered breathing (SDB) on weight loss in overweight/obese veterans enrolled in MOVE!, a nationally implemented behavioral weight management program delivered by the National Veterans Health Administration health system. Methods: This observational study evaluated weight loss by SDB status in overweight/obese veterans enrolled in MOVE! from May 2008–February 2012 who had at least two MOVE! visits, baseline weight, and at least one follow-up weight (n = 84,770). SDB was defined by International Classification of Diseases, Ninth Revision, Clinical Modification codes. Primary outcome was weight change (lb) from MOVE! enrollment to 6- and 12-mo assessments. Weight change over time was modeled with repeated-measures analyses. Results: SDB was diagnosed in one-third of the cohort (n = 28,269). At baseline, veterans with SDB weighed 29 [48] lb more than those without SDB (P < 0.001). On average, veterans attended eight MOVE! visits. Weight loss patterns over time were statistically different between veterans with and without SDB (P < 0.001); veterans with SDB lost less weight (−2.5 [0.1] lb) compared to those without SDB (−3.3 [0.1] lb; P = 0.001) at 6 months. At 12 mo, veterans with SDB continued to lose weight whereas veterans without SDB started to re-gain weight. Conclusions: Veterans with sleep disordered breathing (SDB) had significantly less weight loss over time than veterans without SDB. SDB should be considered in the development and implementation of weight loss programs due to its high prevalence and negative effect on health. Citation: Janney CA, Kilbourne AM, Germain A, Lai Z, Hoerster KD, Goodrich DE, Klingaman EA, Verchinina L, Richardson CR. The influence of sleep disordered breathing on weight loss in a national weight management program. SLEEP 2016;39(1):59–65. PMID:26350475

Acute stress alters autonomic modulation during sleep in women approaching menopause.

PubMed

de Zambotti, Massimiliano; Sugarbaker, David; Trinder, John; Colrain, Ian M; Baker, Fiona C

2016-04-01

Hot flashes, hormones, and psychosocial factors contribute to insomnia risk in the context of the menopausal transition. Stress is a well-recognized factor implicated in the pathophysiology of insomnia; however the impact of stress on sleep and sleep-related processes in perimenopausal women remains largely unknown. We investigated the effect of an acute experimental stress (impending Trier Social Stress Task in the morning) on pre-sleep measures of cortisol and autonomic arousal in perimenopausal women with and without insomnia that developed in the context of the menopausal transition. In addition, we assessed the macro- and micro-structure of sleep and autonomic functioning during sleep. Following adaptation to the laboratory, twenty two women with (age: 50.4 ± 3.2 years) and eighteen women without (age: 48.5 ± 2.3 years) insomnia had two randomized in-lab overnight recordings: baseline and stress nights. Anticipation of the task resulted in higher pre-sleep salivary cortisol levels and perceived tension, faster heart rate and lower vagal activity, based on heart rate variability measures, in both groups of women. The effect of the stress manipulation on the autonomic nervous system extended into the first 4 h of the night in both groups. However, vagal tone recovered 4-6 h into the stress night in controls but not in the insomnia group. Sleep macrostructure was largely unaltered by the stress, apart from a delayed latency to REM sleep in both groups. Quantitative analysis of non-rapid eye movement sleep microstructure revealed greater electroencephalographic (EEG) power in the beta1 range (15-≤23 Hz), reflecting greater EEG arousal during sleep, on the stress night compared to baseline, in the insomnia group. Hot flash frequency remained similar on both nights for both groups. These results show that pre-sleep stress impacts autonomic nervous system functioning before and during sleep in perimenopausal women with and without insomnia. Findings also indicate

Loss of Gnas imprinting differentially affects REM/NREM sleep and cognition in mice.

PubMed

Lassi, Glenda; Ball, Simon T; Maggi, Silvia; Colonna, Giovanni; Nieus, Thierry; Cero, Cheryl; Bartolomucci, Alessandro; Peters, Jo; Tucci, Valter

2012-01-01

It has been suggested that imprinted genes are important in the regulation of sleep. However, the fundamental question of whether genomic imprinting has a role in sleep has remained elusive up to now. In this work we show that REM and NREM sleep states are differentially modulated by the maternally expressed imprinted gene Gnas. In particular, in mice with loss of imprinting of Gnas, NREM and complex cognitive processes are enhanced while REM and REM-linked behaviors are inhibited. This is the first demonstration that a specific overexpression of an imprinted gene affects sleep states and related complex behavioral traits. Furthermore, in parallel to the Gnas overexpression, we have observed an overexpression of Ucp1 in interscapular brown adipose tissue (BAT) and a significant increase in thermoregulation that may account for the REM/NREM sleep phenotypes. We conclude that there must be significant evolutionary advantages in the monoallelic expression of Gnas for REM sleep and for the consolidation of REM-dependent memories. Conversely, biallelic expression of Gnas reinforces slow wave activity in NREM sleep, and this results in a reduction of uncertainty in temporal decision-making processes.

Diet/Energy Balance Affect Sleep and Wakefulness Independent of Body Weight

PubMed Central

Perron, Isaac J.; Pack, Allan I.; Veasey, Sigrid

2015-01-01

Study Objectives: Excessive daytime sleepiness commonly affects obese people, even in those without sleep apnea, yet its causes remain uncertain. We sought to determine whether acute dietary changes could induce or rescue wake impairments independent of body weight. Design: We implemented a novel feeding paradigm that generates two groups of mice with equal body weight but opposing energetic balance. Two subsets of mice consuming either regular chow (RC) or high-fat diet (HFD) for 8 w were switched to the opposite diet for 1 w. Sleep recordings were conducted at Week 0 (baseline), Week 8 (pre-diet switch), and Week 9 (post-diet switch) for all groups. Sleep homeostasis was measured at Week 8 and Week 9. Participants: Young adult, male C57BL/6J mice. Measurements and Results: Differences in total wake, nonrapid eye movement (NREM), and rapid eye movement (REM) time were quantified, in addition to changes in bout fragmentation/consolidation. At Week 9, the two diet switch groups had similar body weight. However, animals switched to HFD (and thus gaining weight) had decreased wake time, increased NREM sleep time, and worsened sleep/wake fragmentation compared to mice switched to RC (which were in weight loss). These effects were driven by significant sleep/wake changes induced by acute dietary manipulations (Week 8 → Week 9). Sleep homeostasis, as measured by delta power increase following sleep deprivation, was unaffected by our feeding paradigm. Conclusions: Acute dietary manipulations are sufficient to alter sleep and wakefulness independent of body weight and without effects on sleep homeostasis. Citation: Perron IJ, Pack AI, Veasey S. Diet/energy balance affect sleep and wakefulness independent of body weight. SLEEP 2015;38(12):1893–1903. PMID:26158893

Acute Optogenetic Silencing of Orexin/Hypocretin Neurons Induces Slow-Wave Sleep in Mice

PubMed Central

Tsunematsu, Tomomi; Kilduff, Thomas S.; Boyden, Edward S.; Takahashi, Satoru; Tominaga, Makoto; Yamanaka, Akihiro

2013-01-01

Orexin/hypocretin neurons have a crucial role in the regulation of sleep and wakefulness. To help determine how these neurons promote wakefulness, we generated transgenic mice in which orexin neurons expressed halorhodopsin (orexin/Halo mice), an orange light-activated neuronal silencer. Slice patch-clamp recordings of orexin neurons that expressed halorhodopsin demonstrated that orange light photic illumination immediately hyperpolarized membrane potential and inhibited orexin neuron discharge in proportion to illumination intensity. Acute silencing of orexin neurons in vivo during the day (the inactive period) induced synchronization of the electroencephalogram and a reduction in amplitude of the electromyogram that is characteristic of slow-wave sleep (SWS). In contrast, orexin neuron photoinhibition was ineffective during the night (active period). Acute photoinhibition of orexin neurons during the day in orexin/Halo mice also reduced discharge of neurons in an orexin terminal field, the dorsal raphe (DR) nucleus. However, serotonergic DR neurons exhibited normal discharge rates in mice lacking orexin neurons. Thus, although usually highly dependent on orexin neuronal activity, serotonergic DR neuronal activity can be regulated appropriately in the chronic absence of orexin input. Together, these results demonstrate that acute inhibition of orexin neurons results in time-of-day-dependent induction of SWS and in reduced firing rate of neurons in an efferent projection site thought to be involved in arousal state regulation. The results presented here advance our understanding of the role of orexin neurons in the regulation of sleep/wakefulness and may be relevant to the mechanisms that underlie symptom progression in narcolepsy. PMID:21775598

Effect of obstructive sleep apnoea on severity and short-term prognosis of acute coronary syndrome.

PubMed

Barbé, Ferran; Sánchez-de-la-Torre, Alicia; Abad, Jorge; Durán-Cantolla, Joaquin; Mediano, Olga; Amilibia, Jose; Masdeu, Maria José; Florés, Marina; Barceló, Antonia; de la Peña, Mónica; Aldomá, Albina; Worner, Fernando; Valls, Joan; Castellà, Gerard; Sánchez-de-la-Torre, Manuel

2015-02-01

The goal of this study was to evaluate the influence of obstructive sleep apnoea on the severity and short-term prognosis of patients admitted for acute coronary syndrome. Obstructive sleep apnoea was defined as an apnoea-hypopnoea index (AHI) >15 h(-1). We evaluated the acute coronary syndrome severity (ejection fraction, Killip class, number of diseased vessels, and plasma peak troponin) and short-term prognosis (length of hospitalisation, complications and mortality). We included 213 patients with obstructive sleep apnoea (mean±sd AHI 30±14 h(-1), 61±10 years, 80% males) and 218 controls (AHI 6±4 h(-1), 57±12 years, 82% males). Patients with obstructive sleep apnoea exhibited a higher prevalence of systemic hypertension (55% versus 37%, p<0.001), higher body mass index (29±4 kg·m(-2) versus 26±4 kg·m(-2), p<0.001), and lower percentage of smokers (61% versus 71%, p=0.04). After adjusting for smoking, age, body mass index and hypertension, the plasma peak troponin levels were significantly elevated in the obstructive sleep apnoea group (831±908 ng·L(-1) versus 987±884 ng·L(-1), p=0.03) and higher AHI severity was associated with an increased number of diseased vessels (p=0.04). The mean length of stay in the coronary care unit was higher in the obstructive sleep apnoea group (p=0.03). This study indicates that obstructive sleep apnoea is related to an increase in the peak plasma troponin levels, number of diseased vessels, and length of stay in the coronary care unit. Copyright ©ERS 2015.

Linalool Ameliorates Memory Loss and Behavioral Impairment Induced by REM-Sleep Deprivation through the Serotonergic Pathway.

PubMed

Lee, Bo Kyung; Jung, An Na; Jung, Yi-Sook

2018-07-01

Rapid eye movement (REM) sleep has an essential role in the process of learning and memory in the hippocampus. It has been reported that linalool, a major component of Lavandula angustifolia , has antioxidant, anti-inflammatory, and neuroprotective effects, along with other effects. However, the effect of linalool on the cognitive impairment and behavioral alterations that are induced by REM-sleep deprivation has not yet been elucidated. Several studies have reported that REM-sleep deprivation-induced memory deficits provide a well-known model of behavioral alterations. In the present study, we examined whether linalool elicited an anti-stress effect, reversing the behavioral alterations observed following REM-sleep deprivation in mice. Furthermore, we investigated the underlying mechanism of the effect of linalool. Spatial memory and learning memory were assessed through Y maze and passive avoidance tests, respectively, and the forced swimming test was used to evaluate anti-stress activity. The mechanisms through which linalool improves memory loss and behavioral alterations in sleep-deprived mice appeared to be through an increase in the serotonin levels. Linalool significantly ameliorated the spatial and learning memory deficits, and stress activity observed in sleep-deprived animals. Moreover, linalool led to serotonin release, and cortisol level reduction. Our findings suggest that linalool has beneficial effects on the memory loss and behavioral alterations induced by REM-sleep deprivation through the regulation of serotonin levels.

The impact of sleep loss on the facilitation of seizures: A prospective case-crossover study.

PubMed

Samsonsen, Christian; Sand, Trond; Bråthen, Geir; Helde, Grethe; Brodtkorb, Eylert

2016-11-01

The relationship between sleep and seizures is intricate. The aim of this study was to assess whether sleep loss is an independent seizure precipitant in a clinical setting. In this prospective, observational cross-over study, 179 consecutive hospital admissions for epileptic seizures were included. A semi-structured interview regarding several seizure precipitants was performed. The sleep pattern prior to the seizure, as well as alcohol, caffeine and drug use, were recorded. The interview was repeated by telephone covering the same weekday at a time when there had been no recent seizure. The Hospital Anxiety and Depression Scale (HADS) and a visual analogue scale for perceived stress were applied at admission. Student's t-test, Fisher exact test and ANOVA were used for statistical analyses. Complete data for analysis were retrieved in 144 patients. The sleep-time during the 24h prior to the seizure was lower (7.3h) compared to follow-up (8.3h; p<0.0005). Caffeine consumption and use of relevant non antiepileptic drugs (AED) were not different. HADS and stress scores at admission did not correlate with sleep-time difference. In ANOVA, controlled for alcohol consumption and AED use, the sleep-time difference remained significant (p=0.008). The interaction with alcohol intake was high, but the sleep-time difference remained highly significant also for the non- and low-consumption (≤2 units per day) subgroup (n=121, 7.50h vs 8.42h, p=0.001). Epileptic seizures are often precipitated by a combination of various clinical factors, but sleep loss stands out as an independent seizure trigger. Copyright © 2016 Elsevier B.V. All rights reserved.

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.

Evidence for Neuroinflammatory and Microglial Changes in the Cerebral Response to Sleep Loss

PubMed Central

Wisor, Jonathan P.; Schmidt, Michelle A.; Clegern, William C.

2011-01-01

Study Objectives: Sleep loss has pro-inflammatory effects, but the roles of specific cell populations in mediating these effects have not been delineated. We assessed the modulation of the electroencephalographic and molecular responses to sleep deprivation (S-DEP) by minocycline, a compound that attenuates microglial activation occurring in association with neuroinflammatory events. Design: Laboratory rodents were subjected to assessment of sleep and wake in baseline and sleep deprived conditions. Participants: Adult male CD-1 mice (30-35 g) subjected to telemetric electroencephalography. Interventions: Minocycline was administered daily. Mice were subjected to baseline data collection on the first day of minocycline administration and, on subsequent days, 2 S-DEP sessions, 1 and 3 h in duration, followed by recovery sleep. Following EEG studies, mice were euthanized either at the end of a 3 h S-DEP or as time-of day controls for sampling of brain messenger RNAs. Gene expression was measured by real-time polymerase chain reaction. Measurements and Results: Minocycline-treated mice exhibited a reduction in time spent asleep, relative to saline-treated mice, in the 3-h interval immediately after administration. S-DEP resulted in an increase in EEG slow wave activity relative to baseline in saline-treated mice. This response to S-DEP was abolished in animals subjected to chronic minocycline administration. S-DEP suppressed the expression of the microglial-specific transcript cd11b and the neuroinflammation marker peripheral benzodiazepine receptor, in the brain at the mRNA level. Minocycline attenuated the elevation of c-fos expression by S-DEP. Brain levels of pro-inflammatory cytokine mRNAs interleukin-1β (il-1β), interleukin-6 (il-6), and tumor necrosis factor-α (tnfα) were unaffected by S-DEP, but were elevated in minocycline-treated mice relative to saline-treated mice. Conclusions: The anti-neuroinflammatory agent minocycline prevents either the buildup or

Effects of Night Work, Sleep Loss and Time on Task on Simulated Threat Detection Performance

PubMed Central

Basner, Mathias; Rubinstein, Joshua; Fomberstein, Kenneth M.; Coble, Matthew C.; Ecker, Adrian; Avinash, Deepa; Dinges, David F.

2008-01-01

Study Objectives: To investigate the effects of night work and sleep loss on a simulated luggage screening task (SLST) that mimicked the x-ray system used by airport luggage screeners. Design: We developed more than 5,800 unique simulated x-ray images of luggage organized into 31 stimulus sets of 200 bags each. 25% of each set contained either a gun or a knife with low or high target difficulty. The 200-bag stimuli sets were then run on software that simulates an x-ray screening system (SLST). Signal detection analysis was used to obtain measures of hit rate (HR), false alarm rate (FAR), threat detection accuracy (A′), and response bias (B″D). Setting: Experimental laboratory study Participants: 24 healthy nonprofessional volunteers (13 women, mean age ± SD = 29.9 ± 6.5 years). Interventions: Subjects performed the SLST every 2 h during a 5-day period that included a 35 h period of wakefulness that extended to night work and then another day work period after the night without sleep. Results: Threat detection accuracy A′ decreased significantly (P < 0.001) while FAR increased significantly (P < 0.001) during night work, while both A′ (P = 0.001) and HR decreased (P = 0.008) during day work following sleep loss. There were prominent time-on-task effects on response bias B″D (P = 0.002) and response latency (P = 0.004), but accuracy A′ was unaffected. Both HR and FAR increased significantly with increasing study duration (both P < 0.001), while response latency decreased significantly (P < 0.001). Conclusions: This study provides the first systematic evidence that night work and sleep loss adversely affect the accuracy of detecting complex real world objects among high levels of background clutter. If the results can be replicated in professional screeners and real work environments, fatigue in luggage screening personnel may pose a threat for air traffic safety unless countermeasures for fatigue are deployed. Citation: Basner M; Rubinstein J

Serum Amyloid A Production Is Triggered by Sleep Deprivation in Mice and Humans: Is That the Link between Sleep Loss and Associated Comorbidities?

PubMed Central

de Oliveira, Edson M.; Visniauskas, Bruna; Tufik, Sergio; Andersen, Monica L.; Chagas, Jair R.; Campa, Ana

2017-01-01

Serum amyloid A (SAA) was recently associated with metabolic endotoxemia, obesity and insulin resistance. Concurrently, insufficient sleep adversely affects metabolic health and is an independent predisposing factor for obesity and insulin resistance. In this study we investigated whether sleep loss modulates SAA production. The serum SAA concentration increased in C57BL/6 mice subjected to sleep restriction (SR) for 15 days or to paradoxical sleep deprivation (PSD) for 72 h. Sleep restriction also induced the upregulation of Saa1.1/Saa2.1 mRNA levels in the liver and Saa3 mRNA levels in adipose tissue. SAA levels returned to the basal range after 24 h in paradoxical sleep rebound (PSR). Metabolic endotoxemia was also a finding in SR. Increased plasma levels of SAA were also observed in healthy human volunteers subjected to two nights of total sleep deprivation (Total SD), returning to basal levels after one night of recovery. The observed increase in SAA levels may be part of the initial biochemical alterations caused by sleep deprivation, with potential to drive deleterious conditions such as metabolic endotoxemia and weight gain. PMID:28335560

Intermediate stage of sleep and acute cerveau isolé preparation in the rat.

PubMed

User, P; Gioanni, H; Gottesmann, C

1980-01-01

The acute cerveau isole rat shows spindle bursts of large amplitude alternating with low voltage activity in the frontal cortex and continuous theta rhythm in the dorsal hippocampus. These patterns closely resemble an "intermediate" stage of sleep-waking cycle, when the forebrain structures seem to be functionally disconnected from the brainstem.

Health consequences of shift work and insufficient sleep.

PubMed

Kecklund, Göran; Axelsson, John

2016-11-01

This review summarises the literature on shift work and its relation to insufficient sleep, chronic diseases, and accidents. It is based on 38 meta-analyses and 24 systematic reviews, with additional narrative reviews and articles used for outlining possible mechanisms by which shift work may cause accidents and adverse health. Evidence shows that the effect of shift work on sleep mainly concerns acute sleep loss in connection with night shifts and early morning shifts. A link also exists between shift work and accidents, type 2 diabetes (relative risk range 1.09-1.40), weight gain, coronary heart disease (relative risk 1.23), stroke (relative risk 1.05), and cancer (relative risk range 1.01-1.32), although the original studies showed mixed results. The relations of shift work to cardiometabolic diseases and accidents mimic those with insufficient sleep. Laboratory studies indicate that cardiometabolic stress and cognitive impairments are increased by shift work, as well as by sleep loss. Given that the health and safety consequences of shift work and insufficient sleep are very similar, they are likely to share common mechanisms. However, additional research is needed to determine whether insufficient sleep is a causal pathway for the adverse health effects associated with shift work. Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.

Semantic congruence reverses effects of sleep restriction on associative encoding.

PubMed

Alberca-Reina, Esther; Cantero, Jose L; Atienza, Mercedes

2014-04-01

Encoding and memory consolidation are influenced by factors such as sleep and congruency of newly learned information with prior knowledge (i.e., schema). However, only a few studies have examined the contribution of sleep to enhancement of schema-dependent memory. Based on previous studies showing that total sleep deprivation specifically impairs hippocampal encoding, and that coherent schemas reduce the hippocampal consolidation period after learning, we predict that sleep loss in the pre-training night will mainly affect schema-unrelated information whereas sleep restriction in the post-training night will have similar effects on schema-related and unrelated information. Here, we tested this hypothesis by presenting participants with face-face associations that could be semantically related or unrelated under different sleep conditions: normal sleep before and after training, and acute sleep restriction either before or after training. Memory was tested one day after training, just after introducing an interference task, and two days later, without any interference. Significant results were evident on the second retesting session. In particular, sleep restriction before training enhanced memory for semantically congruent events in detriment of memory for unrelated events, supporting the specific role of sleep in hippocampal memory encoding. Unexpectedly, sleep restriction after training enhanced memory for both related and unrelated events. Although this finding may suggest a poorer encoding during the interference task, this hypothesis should be specifically tested in future experiments. All together, the present results support a framework in which encoding processes seem to be more vulnerable to sleep loss than consolidation processes. Copyright © 2014 Elsevier Inc. All rights reserved.

Sleep disruption and the sequelae associated with traumatic brain injury

PubMed Central

Lucke-Wold, Brandon P.; Smith, Kelly E.; Nguyen, Linda; Turner, Ryan C.; Logsdon, Aric F.; Jackson, Garrett J.; Huber, Jason D.; Rosen, Charles L.; Miller, Diane B.

2016-01-01

Sleep disruption, which includes a loss of sleep as well as poor quality fragmented sleep, frequently follows traumatic brain injury (TBI) impacting a large number of patients each year in the United States. Fragmented and/or disrupted sleep can worsen neuropsychiatric, behavioral, and physical symptoms of TBI. Additionally, sleep disruption impairs recovery and can lead to cognitive decline. The most common sleep disruption following TBI is insomnia, which is difficulty staying asleep. The consequences of disrupted sleep following injury range from deranged metabolomics and blood brain barrier compromise to altered neuroplasticity and degeneration. There are several theories for why sleep is necessary (e.g., glymphatic clearance and metabolic regulation) and these may help explain how sleep disruption contributes to degeneration within the brain. Experimental data indicate disrupted sleep allows hyperphosphorylated tau and amyloid β plaques to accumulate. As sleep disruption may act as a cellular stressor, target areas warranting further scientific investigation include the increase in endoplasmic reticulum and oxidative stress following acute periods of sleep deprivation. Potential treatment options for restoring the normal sleep cycle include melatonin derivatives and cognitive behavioral therapy. PMID:25956251

Sleep disruption and the sequelae associated with traumatic brain injury.

PubMed

Lucke-Wold, Brandon P; Smith, Kelly E; Nguyen, Linda; Turner, Ryan C; Logsdon, Aric F; Jackson, Garrett J; Huber, Jason D; Rosen, Charles L; Miller, Diane B

2015-08-01

Sleep disruption, which includes a loss of sleep as well as poor quality fragmented sleep, frequently follows traumatic brain injury (TBI) impacting a large number of patients each year in the United States. Fragmented and/or disrupted sleep can worsen neuropsychiatric, behavioral, and physical symptoms of TBI. Additionally, sleep disruption impairs recovery and can lead to cognitive decline. The most common sleep disruption following TBI is insomnia, which is difficulty staying asleep. The consequences of disrupted sleep following injury range from deranged metabolomics and blood brain barrier compromise to altered neuroplasticity and degeneration. There are several theories for why sleep is necessary (e.g., glymphatic clearance and metabolic regulation) and these may help explain how sleep disruption contributes to degeneration within the brain. Experimental data indicate disrupted sleep allows hyperphosphorylated tau and amyloid β plaques to accumulate. As sleep disruption may act as a cellular stressor, target areas warranting further scientific investigation include the increase in endoplasmic reticulum and oxidative stress following acute periods of sleep deprivation. Potential treatment options for restoring the normal sleep cycle include melatonin derivatives and cognitive behavioral therapy. Published by Elsevier Ltd.

Cell Death Biomarkers and Obstructive Sleep Apnea: Implications in the Acute Coronary Syndrome.

PubMed

Bauça, Josep Miquel; Yañez, Aina; Fueyo, Laura; de la Peña, Mónica; Pierola, Javier; Sánchez-de-la-Torre, Alicia; Mediano, Olga; Cabriada-Nuño, Valentín; Masdeu, María José; Teran-Santos, Joaquin; Duran-Cantolla, Joaquin; Masa, Juan Fernando; Abad, Jorge; Sanchez-de-la-Torre, Manuel; Barbé, Ferran; Barceló, Antònia

2017-05-01

Nucleosomes and cell-free double-stranded DNA (dsDNA) have been suggested as promising biomarkers in cell death-related diseases, such as acute coronary syndrome (ACS). Currently, the impact of obstructive sleep apnea (OSA) in patients with ACS is unclear. Our aim was to evaluate the relationship between OSA, dsDNA, and nucleosomes and to assess their potential implication in the development of ACS. Up to 549 patients were included in the study and divided into four groups (145 ACS; 290 ACS + OSA; 62 OSA; 52 controls). All patients underwent a sleep study, and serum concentrations of dsDNA and nucleosomes were measured. Nucleosome and dsDNA levels were higher in patients with OSA than in controls (nucleosomes: 1.47 ± 0.88 arbitary units [AU] vs. 1.00 ± 0.33 AU; p < .001, dsDNA: 315.6 ± 78.0 ng/mL vs. 282.6 ± 55.4 ng/mL; p = .007). In addition, both biomarker levels were higher in patients with ACS than in non-ACS, independently of the presence of OSA. Both nucleosomes and dsDNA are increased in patients with OSA and might be related with the high cardiovascular risk seen in these patients. The extensive cell lysis during a myocardial infarction seems to be the major contributor to the high biomarker levels, and OSA does not seem to be implicated in such elevation when this acute event occurs. NCT01335087 (clinicaltrials.gov). © Sleep Research Society 2017. Published by Oxford University Press on behalf of the Sleep Research Society. All rights reserved. For permissions, please e-mail journals.permissions@oup.com.

Implications of Sleep Restriction and Recovery on Metabolic Outcomes

PubMed Central

Killick, Roo; Banks, Siobhan

2012-01-01

Context: Alongside the growing epidemics of obesity and diabetes mellitus, chronic partial sleep restriction is also increasingly common in modern society, and the metabolic implications of this have not been fully illustrated as yet. Whether recovery sleep is sufficient to offset these detriments is an area of ongoing research. Objective: This review seeks to summarize the relevant epidemiological and experimental data in the areas of altered metabolic consequences of both shortened sleep and subsequent recovery sleep. Data Acquisition: The medical literature from 1970 to March 2012 was reviewed for key articles. Data Synthesis: Epidemiological studies suggest associations between shortened sleep and future obesity and diabetes. Experimental data thus far show a probable link between shortened sleep and altered glucose metabolism as well as appetite dysregulation. Conclusion: Sleep often seems undervalued in modern society, but this may have widespread metabolic consequences as described in this review. Acute sleep loss is often unavoidable, but chronic sleep restriction ideally should not be. Understanding the implications of both sleep restriction and recovery on metabolic outcomes will guide public health policy and allow clinical recommendations to be prescribed. PMID:22996147

Sleep-hygiene Education improves Sleep Indices in Elite Female Athletes.

PubMed

O'Donnell, Shannon; Driller, Matthew W

2017-01-01

The importance of sleep in providing psychophysiological recovery in elite athletes is often overlooked. In other populations (eg shift workers and adolescent students), sleep hygiene education may serve to acutely improve sleep indices. However, this is yet to be examined in an elite athlete setting. Therefore, the aim of the current study was to evaluate the effect of a sleep hygiene education session on sleep indices in elite athletes. The study involved 26 elite female netball athletes performing one week of baseline sleep monitoring (PRE), followed by a sleep hygiene education session and a further week of sleep monitoring (POST) in a single group, pre- post design. The sleep hygiene education session focused on providing information on the importance of sleep for athletes and practical tips to improve sleep quality and quantity. Sleep monitoring was performed using wrist actigraphy to assess total sleep time (TST), sleep efficiency (SE%), total time in bed (TTB), sleep latency (SL), wake episodes per night (WE), sleep onset variance (SOV), wake variance (WV) wake episode duration (WED), sleep onset time (SOT), and wake time (WT). There was a significant improvement in TST (mean ± SD; 22.3 ± 39.9 minutes, p=0.01) PRE to POST sleep hygiene education session, the difference associated with a small effect (ES: 0.39). A significant improvement PRE to POST was found for WV (p=0.03), and for WED (p=0.03). There were no significant differences for SE%, SL, TTB, WE, SOV, SOT, WT. The current study reports that a sleep hygiene education session is effective in improving sleep quantity in elite female athletes in an acute setting.

Heritability of Performance Deficit Accumulation During Acute Sleep Deprivation in Twins

PubMed Central

Kuna, Samuel T.; Maislin, Greg; Pack, Frances M.; Staley, Bethany; Hachadoorian, Robert; Coccaro, Emil F.; Pack, Allan I.

2012-01-01

during acute sleep deprivation in twins. SLEEP 2012;35(9):1223-1233. PMID:22942500

translin Is Required for Metabolic Regulation of Sleep.

PubMed

Murakami, Kazuma; Yurgel, Maria E; Stahl, Bethany A; Masek, Pavel; Mehta, Aradhana; Heidker, Rebecca; Bollinger, Wesley; Gingras, Robert M; Kim, Young-Joon; Ja, William W; Suter, Beat; DiAngelo, Justin R; Keene, Alex C

2016-04-04

Dysregulation of sleep or feeding has enormous health consequences. In humans, acute sleep loss is associated with increased appetite and insulin insensitivity, while chronically sleep-deprived individuals are more likely to develop obesity, metabolic syndrome, type II diabetes, and cardiovascular disease. Conversely, metabolic state potently modulates sleep and circadian behavior; yet, the molecular basis for sleep-metabolism interactions remains poorly understood. Here, we describe the identification of translin (trsn), a highly conserved RNA/DNA binding protein, as essential for starvation-induced sleep suppression. Strikingly, trsn does not appear to regulate energy stores, free glucose levels, or feeding behavior suggesting the sleep phenotype of trsn mutant flies is not a consequence of general metabolic dysfunction or blunted response to starvation. While broadly expressed in all neurons, trsn is transcriptionally upregulated in the heads of flies in response to starvation. Spatially restricted rescue or targeted knockdown localizes trsn function to neurons that produce the tachykinin family neuropeptide Leucokinin. Manipulation of neural activity in Leucokinin neurons revealed these neurons to be required for starvation-induced sleep suppression. Taken together, these findings establish trsn as an essential integrator of sleep and metabolic state, with implications for understanding the neural mechanism underlying sleep disruption in response to environmental perturbation. Copyright © 2016 Elsevier Ltd. All rights reserved.

The Influence of Sleep Disordered Breathing on Weight Loss in a National Weight Management Program.

PubMed

Janney, Carol A; Kilbourne, Amy M; Germain, Anne; Lai, Zongshan; Hoerster, Katherine D; Goodrich, David E; Klingaman, Elizabeth A; Verchinina, Lilia; Richardson, Caroline R

2016-01-01

To investigate the influence of sleep disordered breathing (SDB) on weight loss in overweight/obese veterans enrolled in MOVE!, a nationally implemented behavioral weight management program delivered by the National Veterans Health Administration health system. This observational study evaluated weight loss by SDB status in overweight/obese veterans enrolled in MOVE! from May 2008-February 2012 who had at least two MOVE! visits, baseline weight, and at least one follow-up weight (n = 84,770). SDB was defined by International Classification of Diseases, Ninth Revision, Clinical Modification codes. Primary outcome was weight change (lb) from MOVE! enrollment to 6- and 12-mo assessments. Weight change over time was modeled with repeated-measures analyses. SDB was diagnosed in one-third of the cohort (n = 28,269). At baseline, veterans with SDB weighed 29 [48] lb more than those without SDB (P < 0.001). On average, veterans attended eight MOVE! visits. Weight loss patterns over time were statistically different between veterans with and without SDB (P < 0.001); veterans with SDB lost less weight (-2.5 [0.1] lb) compared to those without SDB (-3.3 [0.1] lb; P = 0.001) at 6 months. At 12 mo, veterans with SDB continued to lose weight whereas veterans without SDB started to re-gain weight. Veterans with sleep disordered breathing (SDB) had significantly less weight loss over time than veterans without SDB. SDB should be considered in the development and implementation of weight loss programs due to its high prevalence and negative effect on health. © 2016 Associated Professional Sleep Societies, LLC.

Obstructive Sleep Apnea, Obesity, and the Development of Acute Respiratory Distress Syndrome

PubMed Central

Karnatovskaia, Lioudmila V.; Lee, Augustine S.; Bender, S. Patrick; Talmor, Daniel; Festic, Emir

2014-01-01

Background: Obstructive sleep apnea (OSA) may increase the risk of respiratory complications and acute respiratory distress syndrome (ARDS) among surgical patients. OSA is more prevalent among obese individuals; obesity can predispose to ARDS. Hypothesis: It is unclear whether OSA independently contributes towards the risk of ARDS among hospitalized patients. Methods: This is a pre-planned retrospective subgroup analysis of the prospectively identified cohort of 5,584 patients across 22 hospitals with at least one risk factor for ARDS at the time of hospitalization from a trial by the US Critical Illness and Injury Trials Group designed to validate the Lung Injury Prediction Score. A total of 252 patients (4.5%) had a diagnosis of OSA at the time of hospitalization; of those, 66% were obese. Following multivariate adjustment in the logistic regression model, there was no significant relationship between OSA and development of ARDS (OR = 0.65, 95%CI = 0.32-1.22). However, body mass index (BMI) was associated with subsequent ARDS development (OR = 1.02, 95%CI = 1.00-1.04, p = 0.03). Neither OSA nor BMI affected mechanical ventilation requirement or mortality. Conclusions: Prior diagnosis of OSA did not independently affect development of ARDS among patients with at least one predisposing condition, nor the need for mechanical ventilation or hospital mortality. Obesity appeared to independently increase the risk of ARDS. Citation: Karnatovskaia LV, Lee AS, Bender SP, Talmor D, Festic E. Obstructive sleep apnea, obesity, and the development of acute respiratory distress syndrome. J Clin Sleep Med 2014;10(6):657-662. PMID:24932146

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

RJ; Kennedy GA; Crewther D; Howard ME. The effect of acute sleep deprivation on visual evoked potentials in professional drivers. SLEEP 2008;31(9):1261-1269. PMID:18788651

Short-term memory deficits correlate with hippocampal-thalamic functional connectivity alterations following acute sleep restriction.

PubMed

Chengyang, Li; Daqing, Huang; Jianlin, Qi; Haisheng, Chang; Qingqing, Meng; Jin, Wang; Jiajia, Liu; Enmao, Ye; Yongcong, Shao; Xi, Zhang

2017-08-01

Acute sleep restriction heavily influences cognitive function, affecting executive processes such as attention, response inhibition, and memory. Previous neuroimaging studies have suggested a link between hippocampal activity and short-term memory function. However, the specific contribution of the hippocampus to the decline of short-term memory following sleep restriction has yet to be established. In the current study, we utilized resting-state functional magnetic resonance imaging (fMRI) to examine the association between hippocampal functional connectivity (FC) and the decline of short-term memory following total sleep deprivation (TSD). Twenty healthy adult males aged 20.9 ± 2.3 years (age range, 18-24 years) were enrolled in a within-subject crossover study. Short-term memory and FC were assessed using a Delay-matching short-term memory test and a resting-state fMRI scan before and after TSD. Seed-based correlation analysis was performed using fMRI data for the left and right hippocampus to identify differences in hippocampal FC following TSD. Subjects demonstrated reduced alertness and a decline in short-term memory performance following TSD. Moreover, fMRI analysis identified reduced hippocampal FC with the superior frontal gyrus (SFG), temporal regions, and supplementary motor area. In addition, an increase in FC between the hippocampus and bilateral thalamus was observed, the extent of which correlated with short-term memory performance following TSD. Our findings indicate that the disruption of hippocampal-cortical connectivity is linked to the decline in short-term memory observed after acute sleep restriction. Such results provide further evidence that support the cognitive impairment model of sleep deprivation.

Predicting risk in space: Genetic markers for differential vulnerability to sleep restriction

NASA Astrophysics Data System (ADS)

Goel, Namni; Dinges, David F.

2012-08-01

Several laboratories have found large, highly reliable individual differences in the magnitude of cognitive performance, fatigue and sleepiness, and sleep homeostatic vulnerability to acute total sleep deprivation and to chronic sleep restriction in healthy adults. Such individual differences in neurobehavioral performance are also observed in space flight as a result of sleep loss. The reasons for these stable phenotypic differential vulnerabilities are unknown: such differences are not yet accounted for by demographic factors, IQ or sleep need, and moreover, psychometric scales do not predict those individuals cognitively vulnerable to sleep loss. The stable, trait-like (phenotypic) inter-individual differences observed in response to sleep loss—with intraclass correlation coefficients accounting for 58-92% of the variance in neurobehavioral measures—point to an underlying genetic component. To this end, we utilized multi-day highly controlled laboratory studies to investigate the role of various common candidate gene variants—each independently—in relation to cumulative neurobehavioral and sleep homeostatic responses to sleep restriction. These data suggest that common genetic variations (polymorphisms) involved in sleep-wake, circadian, and cognitive regulation may serve as markers for prediction of inter-individual differences in sleep homeostatic and neurobehavioral vulnerability to sleep restriction in healthy adults. Identification of genetic predictors of differential vulnerability to sleep restriction—as determined from candidate gene studies—will help identify astronauts most in need of fatigue countermeasures in space flight and inform medical standards for obtaining adequate sleep in space. This review summarizes individual differences in neurobehavioral vulnerability to sleep deprivation and ongoing genetic efforts to identify markers of such differences.

[Relationship between sleep disordered breathing and body weight loss in patients with chronic obstructive pulmonary disease].

PubMed

Ito, Eiki; Murata, Akira; Yamamoto, Kazuo; Kudo, Shoji

2003-04-01

We evaluated body weight loss and growth hormone secretion in patients with sleep-disordered breathing associated with chronic obstructive pulmonary disease. Of 11 patients hospitalized for pulmonary rehabilitation, five (WL group) had a history of body weight loss within two years before their interviews, while the other 6 patients (NWL group) had no changes in body weight. All patients underwent body index measurements, pulmonary function tests, blood gas analyses, assessments of nutritional status, and full night polysomnography for two consecutive days. Growth hormone levels were measured in the first 3-hour period following falling asleep. There were no significant inter-group differences between the results of pulmonary function tests, blood gas analyses, or nutritional status assessment. The WL group had a significantly higher percentage loss of body weight than the NWL group (mean +/- S.D. 11.5 +/- 4.7% in the WL group versus 2.7 +/- 1.8% in the NWL group, p < 0.01). The WL group had a significantly higher sleep apnea/hypopnea index than the NWL group (42.4 +/- 9.5/hr in the WL group versus 7.8 +/- 2.9/hr in the NWL group, p < 0.01). The WL group showed a higher rate of stage I + II sleep than the NWL group (84.9 +/- 7.0% versus 64.5 +/- 8.7%), with lower rates of slow wave sleep (2.2 +/- 2.1% versus 15.0 +/- 8.7%) and rapid eye movement sleep (12.9 +/- 6.3% versus 20.6 +/- 1.0%). The WL group showed a low level of growth hormone secretion with no peak in the sequential curve, but had a higher level of insulin growth factor-1 than the NWL group (148 +/- 36 ng/ml versus 90 +/- 22 ng/ml, p < 0.01). These results suggest that chronic obstructive pulmonary disease patients undergoing weight loss are likely to have an increase of growth hormone secretions in the daytime, possibly induced by underlying psychiatric disorders such as depression. Patients with chronic obstructive pulmonary disease may lose weight regardless of nutritional status because of a

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

PubMed

Seugnet, Laurent; Suzuki, Yasuko; Merlin, Gabriel; Gottschalk, Laura; Duntley, Stephen P; Shaw, Paul J

2011-05-24

The role of the transmembrane 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 rescues normal homeostasis, suggesting that Notch signaling may be involved in regulating sensitivity to sleep loss. Preventing the downregulation of Delta by overexpressing 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 Notch(spl-1) gain-of-function mutants. Immunohistochemistry reveals that the Notch receptor is expressed in glia, whereas Delta is localized in neurons. Importantly, the expression in glia of the intracellular domain of Notch, a dominant activated form of the receptor, is sufficient to prevent learning deficits after sleep deprivation. Together, these results identify a novel neuron-glia signaling 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. Copyright © 2011 Elsevier Ltd. All rights reserved.

A gender perspective on sleeplessness behavior, effects of sleep loss, and coping resources in patients with stable coronary artery disease.

PubMed

Edéll-Gustafsson, Ulla; Svanborg, Eva; Swahn, Eva

2006-01-01

The primary aim of this study was to systematically compare perceived sleep quality, sleeplessness behavior, sense of mastery, self-esteem, depression, subjective health, and effects of sleep loss in men and women with stable coronary artery disease (CAD). Further aims were to determine possible predictors of poor sleep quality and sense of mastery, as well as the consequences of too little sleep. Comparative-correlation and predictive design were used. Patients with a history of stable angina pectoris scheduled to undergo coronary angiography at Linköping University Hospital in Sweden were included. There were 47 women and 88 men (mean age 62.4 years) with CAD. Structured interviews using validated questionnaires covered sleep quality and sleep habits, effects of sleep loss, psychologic resources, and depression. Multiple stepwise regression analysis showed that sleeplessness behavior, depressed mood, female gender, and pharmacologic treatments with inflammation inhibitors significantly (P<.0001) accounted for the variance of poorer sleep quality. The analysis also showed that the following factors in descending order significantly accounted (P<.0001) for the outcome of sleep quality: inability to feel refreshed by sleep, difficulty in maintaining sleep, gastrointestinal problems, too little sleep, final morning awakening time, sleep onset latency, lying down because of daytime tiredness, and daytime physical tiredness. Compared with men, women with stable CAD may be especially at risk of experiencing poor sleep quality, even when sleeplessness behavior and pharmacologic treatments with inflammation inhibitors are controlled. It is also possible that they may be more at risk of depressed mood.

Gray Matter-Specific Changes in Brain Bioenergetics after Acute Sleep Deprivation: A 31P Magnetic Resonance Spectroscopy Study at 4 Tesla

PubMed Central

Plante, David T.; Trksak, George H.; Jensen, J. Eric; Penetar, David M.; Ravichandran, Caitlin; Riedner, Brady A.; Tartarini, Wendy L.; Dorsey, Cynthia M.; Renshaw, Perry F.; Lukas, Scott E.; Harper, David G.

2014-01-01

Study Objectives: A principal function of sleep may be restoration of brain energy metabolism caused by the energetic demands of wakefulness. Because energetic demands in the brain are greater in gray than white matter, this study used linear mixed-effects models to examine tissue-type specific changes in high-energy phosphates derived using 31P magnetic resonance spectroscopy (MRS) after sleep deprivation and recovery sleep. Design: Experimental laboratory study. Setting: Outpatient neuroimaging center at a private psychiatric hospital. Participants: A total of 32 MRS scans performed in eight healthy individuals (mean age 35 y; range 23-51 y). Interventions: Phosphocreatine (PCr) and β-nucleoside triphosphate (NTP) were measured using 31P MRS three dimensional-chemical shift imaging at high field (4 Tesla) after a baseline night of sleep, acute sleep deprivation, and 2 nights of recovery sleep. Novel linear mixed-effects models were constructed using spectral and tissue segmentation data to examine changes in bioenergetics in gray and white matter. Measurements and Results: PCr increased in gray matter after 2 nights of recovery sleep relative to sleep deprivation with no significant changes in white matter. Exploratory analyses also demonstrated that increases in PCr were associated with increases in electroencephalographic slow wave activity during recovery sleep. No significant changes in β-NTP were observed. Conclusions: These results demonstrate that sleep deprivation and subsequent recovery-induced changes in high-energy phosphates primarily occur in gray matter, and increases in phosphocreatine after recovery sleep may be related to sleep homeostasis. Citation: Plante DT, Trksak GH, Jensen JE, Penetar DM, Ravichandran C, Riedner BA, Tartarini WL, Dorsey CM, Renshaw PF, Lukas SE, Harper DG. Gray matter-specific changes in brain bioenergetics after acute sleep deprivation: a 31P magnetic resonance spectroscopy study at 4 Tesla. SLEEP 2014

The impact of sleep loss on hippocampal function

PubMed Central

Prince, Toni-Moi; Abel, Ted

2013-01-01

Hippocampal cellular and molecular processes critical for memory consolidation are affected by the amount and quality of sleep attained. Questions remain with regard to how sleep enhances memory, what parameters of sleep after learning are optimal for memory consolidation, and what underlying hippocampal molecular players are targeted by sleep deprivation to impair memory consolidation and plasticity. In this review, we address these topics with a focus on the detrimental effects of post-learning sleep deprivation on memory consolidation. Obtaining adequate sleep is challenging in a society that values “work around the clock.” Therefore, the development of interventions to combat the negative cognitive effects of sleep deprivation is key. However, there are a limited number of therapeutics that are able to enhance cognition in the face of insufficient sleep. The identification of molecular pathways implicated in the deleterious effects of sleep deprivation on memory could potentially yield new targets for the development of more effective drugs. PMID:24045505

[Acute confusional syndrome associated with obstructive sleep apnea aggravated by acidosis secondary to oral acetazolamide treatment].

PubMed

Miguel, E; Güell, R; Antón, A; Montiel, J A; Mayos, M

2004-06-01

Acute confusional syndrome, or delirium, is a transitory mental state characterized by the fluctuating alteration of awareness and attention levels. We present the case of a patient with acute confusional syndrome associated with obstructive sleep apnea syndrome (OSAS) aggravated by metabolic acidosis induced by oral acetazolamide treatment.A 70-year-old man with no history of neurological disease was referred with a clinical picture consistent with acute confusional syndrome presenting between midnight and dawn. During the admission examination infectious, toxic, and neurologic causes, or those related to metabolic or heart disease were ruled out. Arterial blood gases measured during one of the nighttime episodes of acute confusional syndrome showed mild hypoxia and hypercapnia with mixed acidosis. Signs and symptoms suggestive of OSAS had been developing over the months prior to admission, with snoring, sleep apnea, and moderate daytime drowsiness. Polysomnography demonstrated severe OSAS with an apnea-hypopnea index of 38. Mean arterial oxygen saturation was 83%; time oxygen saturation remained below 90% was 44%. The attending physician ordered the withdrawal of oral acetazolamide, which was considered the cause of the metabolic component of acidosis. Treatment with continuous positive airway pressure was initiated at 9 cm H2O, after a titration polysomnographic study. The patient continued to improve.OSAS, for which very effective treatment is available, should be included among diseases that may trigger acute confusional syndrome.

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. Copyright © 2016 Elsevier Inc. All rights reserved.

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

Impact of Acute Changes in CPAP Flow Route in Sleep Apnea Treatment.

PubMed

Andrade, Rafaela G S; Madeiro, Fernanda; Piccin, Vivien S; Moriya, Henrique T; Schorr, Fabiola; Sardinha, Priscila S; Gregório, Marcelo G; Genta, Pedro R; Lorenzi-Filho, Geraldo

2016-12-01

CPAP is the gold standard treatment for OSA and was conceived to be applied through a nasal interface. This study was designed to determine the acute effects of changing the nasal CPAP route to oronasal and oral in upper airway patency during sleep in patients with OSA. We hypothesized that the oronasal route may compromise CPAP's effectiveness in treating OSA. Eighteen patients (mean ± SD age, 44 ± 9 years; BMI, 33.8 ± 4.7 kg/m 2 ; apnea-hypopnea index, 49.0 ± 39.1 events/hour) slept with a customized oronasal mask with nasal and oral sealed compartments connected to a multidirectional valve. Sleep was monitored by using full polysomnography and induced by low doses of midazolam. Nasal CPAP was titrated up to holding pressure. Flow route was acutely changed to the oronasal (n = 18) and oral route (n = 16) during sleep. Retroglossal area was continuously observed by using nasoendoscopy. Nasal CPAP (14.8 ± 4.1 cm H 2 O) was able to stabilize breathing in all patients. In contrast, CPAP delivered by the oronasal and oral routes promoted obstructive events in 12 (66.7%) and 14 (87.5%) patients, respectively. Compared with stable breathing during the nasal route, there was a significant and progressive reduction in the distance between the epiglottis and tongue base and the retroglossal area when CPAP was delivered by the oronasal and oral routes. CPAP delivered through the oronasal route may compromise CPAP's effectiveness in treating OSA. Copyright © 2016 American College of Chest Physicians. Published by Elsevier Inc. All rights reserved.

The genome-wide landscape of DNA methylation and hydroxymethylation in response to sleep deprivation impacts on synaptic plasticity genes.

PubMed

Massart, R; Freyburger, M; Suderman, M; Paquet, J; El Helou, J; Belanger-Nelson, E; Rachalski, A; Koumar, O C; Carrier, J; Szyf, M; Mongrain, V

2014-01-21

Sleep is critical for normal brain function and mental health. However, the molecular mechanisms mediating the impact of sleep loss on both cognition and the sleep electroencephalogram remain mostly unknown. Acute sleep loss impacts brain gene expression broadly. These data contributed to current hypotheses regarding the role for sleep in metabolism, synaptic plasticity and neuroprotection. These changes in gene expression likely underlie increased sleep intensity following sleep deprivation (SD). Here we tested the hypothesis that epigenetic mechanisms coordinate the gene expression response driven by SD. We found that SD altered the cortical genome-wide distribution of two major epigenetic marks: DNA methylation and hydroxymethylation. DNA methylation differences were enriched in gene pathways involved in neuritogenesis and synaptic plasticity, whereas large changes (>4000 sites) in hydroxymethylation where observed in genes linked to cytoskeleton, signaling and neurotransmission, which closely matches SD-dependent changes in the transcriptome. Moreover, this epigenetic remodeling applied to elements previously linked to sleep need (for example, Arc and Egr1) and synaptic partners of Neuroligin-1 (Nlgn1; for example, Dlg4, Nrxn1 and Nlgn3), which we recently identified as a regulator of sleep intensity following SD. We show here that Nlgn1 mutant mice display an enhanced slow-wave slope during non-rapid eye movement sleep following SD but this mutation does not affect SD-dependent changes in gene expression, suggesting that the Nlgn pathway acts downstream to mechanisms triggering gene expression changes in SD. These data reveal that acute SD reprograms the epigenetic landscape, providing a unique molecular route by which sleep can impact brain function and health.

Short Daytime Naps Briefly Attenuate Objectively Measured Sleepiness Under Chronic Sleep Restriction.

PubMed

Saletin, Jared M; Hilditch, Cassie J; Dement, William C; Carskadon, Mary A

2017-09-01

Napping is a useful countermeasure to the negative effects of acute sleep loss on alertness. The efficacy of naps to recover from chronic sleep loss is less well understood. Following 2 baseline nights (10 hours' time-in-bed), participants were restricted to 7 nights of 5-hour sleep opportunity. Ten adults participated in the No-Nap condition, and a further 9 were assigned to a Nap condition with a daily 45-minute nap opportunity at 1300 h. Sleepiness was assessed using the multiple sleep latency test and a visual analogue scale at 2-hour intervals. Both objective and subjective indexes of sleepiness were normalized within subject as a difference from those at baseline prior to sleep restriction. Mixed-effects models examined how the daytime nap opportunity altered sleepiness across the day and across the protocol. Short daytime naps attenuated sleepiness due to chronic sleep restriction for up to 6-8 hours after the nap. Benefits of the nap did not extend late into evening. Subjective sleepiness demonstrated a similar short-lived benefit that emerged later in the day when objective sleepiness already returned to pre-nap levels. Neither measure showed a benefit of the nap the following morning after the subsequent restriction night. These data indicate a short daytime nap may attenuate sleepiness in chronic sleep restriction, yet subjective and objective benefits emerge at different time scales. Because neither measure showed a benefit the next day, the current study underscores the need for careful consideration before naps are used as routine countermeasures to chronic sleep loss. © Sleep Research Society 2017. Published by Oxford University Press on behalf of the Sleep Research Society. All rights reserved. For permissions, please e-mail journals.permissions@oup.com.

Sleep Loss and Partner Violence Victimization

ERIC Educational Resources Information Center

Walker, Robert; Shannon, Lisa; Logan, T. K.

2011-01-01

Intimate partner violence victimization has been associated with serious health problems among women, including many disorders that involve sleep disturbances. However, there has been only limited examination of sleep duration among women with victimization experiences. A total of 756 women with a domestic violence order (DVO) against a male…

Sleep-Dependent Modulation of Metabolic Rate in Drosophila.

PubMed

Stahl, Bethany A; Slocumb, Melissa E; Chaitin, Hersh; DiAngelo, Justin R; Keene, Alex C

2017-08-01

Dysregulation of sleep is associated with metabolic diseases, and metabolic rate (MR) is acutely regulated by sleep-wake behavior. In humans and rodent models, sleep loss is associated with obesity, reduced metabolic rate, and negative energy balance, yet little is known about the neural mechanisms governing interactions between sleep and metabolism. We have developed a system to simultaneously measure sleep and MR in individual Drosophila, allowing for interrogation of neural systems governing interactions between sleep and metabolic rate. Like mammals, MR in flies is reduced during sleep and increased during sleep deprivation suggesting sleep-dependent regulation of MR is conserved across phyla. The reduction of MR during sleep is not simply a consequence of inactivity because MR is reduced ~30 minutes following the onset of sleep, raising the possibility that CO2 production provides a metric to distinguish different sleep states in the fruit fly. To examine the relationship between sleep and metabolism, we determined basal and sleep-dependent changes in MR is reduced in starved flies, suggesting that starvation inhibits normal sleep-associated effects on metabolic rate. Further, translin mutant flies that fail to suppress sleep during starvation demonstrate a lower basal metabolic rate, but this rate was further reduced in response to starvation, revealing that regulation of starvation-induced changes in MR and sleep duration are genetically distinct. Therefore, this system provides the unique ability to simultaneously measure sleep and oxidative metabolism, providing novel insight into the physiological changes associated with sleep and wakefulness in the fruit fly. © Sleep Research Society 2017. Published by Oxford University Press on behalf of the Sleep Research Society. All rights reserved. For permissions, please e-mail journals.permissions@oup.com.

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

Impact of sleep, screen time, depression and stress on weight change in the intensive weight loss phase of the LIFE study.

PubMed

Elder, C R; Gullion, C M; Funk, K L; Debar, L L; Lindberg, N M; Stevens, V J

2012-01-01

The LIFE study is a two-phase randomized clinical trial comparing two approaches to maintaining weight loss following guided weight loss. Phase I provided a nonrandomized intensive 6-month behavioral weight loss intervention to 472 obese (body mass index 30-50) adult participants. Phase II is the randomized weight loss maintenance portion of the study. This paper focuses on Phase I measures of sleep, screen time, depression and stress. The Phase I intervention consisted of 22 group sessions led over 26 weeks by behavioral counselors. Recommendations included reducing dietary intake by 500 calories per day, adopting the Dietary Approaches to Stop Hypertension (DASH) dietary pattern and increasing physical exercise to at least 180 min per week. Measures reported here are sleep time, insomnia, screen time, depression and stress at entry and post-weight loss intervention follow-up. The mean weight loss for all participants over the intensive Phase I weight loss intervention was 6.3 kg (s.d. 7.1). Sixty percent (N=285) of participants lost at least 4.5 kg (10 lbs) and were randomized into Phase II. Participants (N=472) attended a mean of 73.1% (s.d. 26.7) of sessions, completed 5.1 (s.d. 1.9) daily food records/week, and reported 195.1 min (s.d. 123.1) of exercise per week. Using logistic regression, sleep time (quadratic trend, P=0.030) and lower stress (P=0.024) at entry predicted success in the weight loss program, and lower stress predicted greater weight loss during Phase I (P=0.021). In addition, weight loss was significantly correlated with declines in stress (P=0.048) and depression (P=0.035). Results suggest that clinicians and investigators might consider targeting sleep, depression and stress as part of a behavioral weight loss intervention.

Changes in Regional Adiposity and Cardio-Metabolic Function Following a Weight Loss Program with Sibutramine in Obese Men with Obstructive Sleep Apnea

PubMed Central

Phillips, Craig L.; Yee, Brendon J.; Trenell, Mike I.; Magnussen, John S.; Wang, David; Banerjee, Dev; Berend, Norbert; Grunstein, Ronald R.

2009-01-01

Background: Although obstructive sleep apnea (OSA) is strongly linked with obesity, both conditions have been associated with increased cardiovascular risk including glucose intolerance, dyslipidemia, and hypertension independent of one another. Weight loss is known to improve both cardiovascular risk and OSA severity. The aim of this study was to evaluate cardiovascular and metabolic changes, including compartment-specific fat loss in obese OSA subjects undergoing a weight loss program. Design: Observational study. Participants: 93 men with moderate-severe OSA. Interventions: 6-month open-label weight loss trial combining sibutramine (a serotonin and noradrenaline reuptake inhibitor) with a 600-kcal deficit diet and exercise. Measurements and Results: At baseline and following 6 months of weight loss, OSA was assessed together with CT-quantified intra-abdominal and liver fat and markers of metabolic and cardiovascular function. At 6 months, weight loss and improvements in OSA were accompanied by improved insulin resistance (HOMA), increased HDL cholesterol, and reduced total cholesterol/HDL ratio. There were also reductions in measures of visceral and subcutaneous abdominal fat and liver fat. Reductions in liver fat and sleep time spent below 90% oxyhemoglobin saturation partly explained the improvement in HOMA (R2 = 0.18). In contrast, arterial stiffness (aortic augmentation index), heart rate, blood pressure, and total cholesterol did not change. Conclusions: Weight loss with sibutramine was associated with improvements in metabolic and body composition risk factors but not blood pressure or arterial stiffness. Improved insulin resistance was partly associated with reductions in liver fat and hypoxemia associated with sleep apnea. Citation: Phillips CL; Yee BJ; Trenell MI; Magnussen JS; Wang D; Banerjee D; Berend N; Grunstein RR. Changes in regional adiposity and cardio-metabolic function following a weight loss program with sibutramine in obese men with

Role of REM Sleep, Melanin Concentrating Hormone and Orexin/Hypocretin Systems in the Sleep Deprivation Pre-Ischemia

PubMed Central

Pace, Marta; Adamantidis, Antoine; Facchin, Laura; Bassetti, Claudio

2017-01-01

Study Objectives Sleep reduction after stroke is linked to poor recovery in patients. Conversely, a neuroprotective effect is observed in animals subjected to acute sleep deprivation (SD) before ischemia. This neuroprotection is associated with an increase of the sleep, melanin concentrating hormone (MCH) and orexin/hypocretin (OX) systems. This study aims to 1) assess the relationship between sleep and recovery; 2) test the association between MCH and OX systems with the pathological mechanisms of stroke. Methods Sprague-Dawley rats were assigned to four experimental groups: (i) SD_IS: SD performed before ischemia; (ii) IS: ischemia; (iii) SD_Sham: SD performed before sham surgery; (iv) Sham: sham surgery. EEG and EMG were recorded. The time-course of the MCH and OX gene expression was measured at 4, 12, 24 hours and 3, 4, 7 days following ischemic surgery by qRT-PCR. Results A reduction of infarct volume was observed in the SD_IS group, which correlated with an increase of REM sleep observed during the acute phase of stroke. Conversely, the IS group showed a reduction of REM sleep. Furthermore, ischemia induces an increase of MCH and OX systems during the acute phase of stroke, although, both systems were still increased for a long period of time only in the SD_IS group. Conclusions Our data indicates that REM sleep may be involved in the neuroprotective effect of SD pre-ischemia, and that both MCH and OX systems were increased during the acute phase of stroke. Future studies should assess the role of REM sleep as a prognostic marker, and test MCH and OXA agonists as new treatment options in the acute phase of stroke. PMID:28061506

Obstructive sleep apnea (OSA): a complication of acute infectious mononucleosis infection in a child.

PubMed

Cheng, Jeffrey

2014-03-01

Independently, obstructive sleep apnea (OSA) and infectious mononucleosis are not uncommon in the pediatric population, but acute onset of OSA, as a respiratory complication in the setting of acute EBV infection is extremely uncommon. Previous reports of this clinical entity are sparse and from nearly two decades ago. Urgent adenotonsillectomy was commonly advocated. This complication may be managed medically with systemic corticosteroids and non-invasive continuous positive airway pressure (CPAP), and a case is presented to highlight an updated management approach to this rarely encountered clinical problem in children. Copyright © 2013 Elsevier Ireland Ltd. All rights reserved.

Sleep stages, memory and learning.

PubMed Central

Dotto, L

1996-01-01

Learning and memory can be impaired by sleep loss during specific vulnerable "windows" for several days after new tasks have been learned. Different types of tasks are differentially vulnerable to the loss of different stages of sleep. Memory required to perform cognitive procedural tasks is affected by the loss of rapid-eye-movement (REM) sleep on the first night after learning occurs and again on the third night after learning. REM-sleep deprivation on the second night after learning does not produce memory deficits. Declarative memory, which is used for the recall of specific facts, is not similarly affected by REM-sleep loss. The learning of procedural motor tasks, including those required in many sports, is impaired by the loss of stage 2 sleep, which occurs primarily in the early hours of the morning. These findings have implications for the academic and athletic performance of students and for anyone whose work involves ongoing learning and demands high standards of performance. Images p1194-a PMID:8612256

Effects of night work, sleep loss and time on task on simulated threat detection performance.

PubMed

Basner, Mathias; Rubinstein, Joshua; Fomberstein, Kenneth M; Coble, Matthew C; Ecker, Adrian; Avinash, Deepa; Dinges, David F

2008-09-01

To investigate the effects of night work and sleep loss on a simulated luggage screening task (SLST) that mimicked the x-ray system used by airport luggage screeners. We developed more than 5,800 unique simulated x-ray images of luggage organized into 31 stimulus sets of 200 bags each. 25% of each set contained either a gun or a knife with low or high target difficulty. The 200-bag stimuli sets were then run on software that simulates an x-ray screening system (SLST). Signal detection analysis was used to obtain measures of hit rate (HR), false alarm rate (FAR), threat detection accuracy (A'), and response bias (B"(D)). Experimental laboratory study 24 healthy nonprofessional volunteers (13 women, mean age +/- SD = 29.9 +/- 6.5 years). Subjects performed the SLST every 2 h during a 5-day period that included a 35 h period of wakefulness that extended to night work and then another day work period after the night without sleep. Threat detection accuracy A' decreased significantly (P < 0.001) while FAR increased significantly (P < 0.001) during night work, while both A' (P = 0.001) and HR decreased (P = 0.008) during day work following sleep loss. There were prominent time-on-task effects on response bias B"(D) (P= 0.002) and response latency (P = 0.004), but accuracy A' was unaffected. Both HR and FAR increased significantly with increasing study duration (both P < 0.001), while response latency decreased significantly (P <0.001). This study provides the first systematic evidence that night work and sleep loss adversely affect the accuracy of detecting complex real world objects among high levels of background clutter. If the results can be replicated in professional screeners and real work environments, fatigue in luggage screening personnel may pose a threat for air traffic safety unless countermeasures for fatigue are deployed.

The effect of an acute sleep hygiene strategy following a late-night soccer match on recovery of players.

PubMed

Fullagar, Hugh; Skorski, Sabrina; Duffield, Rob; Meyer, Tim

2016-01-01

Elite soccer players are at risk of reduced recovery following periods of sleep disruption, particularly following late-night matches. It remains unknown whether improving sleep quality or quantity in such scenarios can improve post-match recovery. Therefore, the aim of this study was to investigate the effect of an acute sleep hygiene strategy (SHS) on physical and perceptual recovery of players following a late-night soccer match. In a randomised cross-over design, two highly-trained amateur teams (20 players) played two late-night (20:45) friendly matches against each other seven days apart. Players completed an SHS after the match or proceeded with their normal post-game routine (NSHS). Over the ensuing 48 h, objective sleep parameters (sleep duration, onset latency, efficiency, wake episodes), countermovement jump (CMJ; height, force production), YoYo Intermittent Recovery test (YYIR2; distance, maximum heart rate, lactate), venous blood (creatine kinase, urea and c-reactive protein) and perceived recovery and stress markers were collected. Sleep duration was significantly greater in SHS compared to NSHS on match night (P = 0.002, d = 1.50), with NSHS significantly less than baseline (P < 0.001, d = 1.95). Significant greater wake episodes occurred on match night for SHS (P = 0.04, d = 1.01), without significant differences between- or within-conditions for sleep onset latency (P = 0.12), efficiency (P = 0.39) or wake episode duration (P = 0.07). No significant differences were observed between conditions for any physical performance or venous blood marker (all P > 0.05); although maximum heart rate during the YYIR2 was significantly higher in NSHS than SHS at 36 h post-match (P = 0.01; d = 0.81). There were no significant differences between conditions for perceptual "overall recovery" (P = 0.47) or "overall stress" (P = 0.17). Overall, an acute SHS improved sleep quantity following a late-night soccer match; albeit without any improvement in physical

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

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.

Impact of sleep-disordered breathing in patients with acute myocardial infarction: a retrospective analysis.

PubMed

Gessner, Verena; Bitter, Thomas; Horstkotte, Dieter; Oldenburg, Olaf; Fox, Henrik

2017-10-01

Sleep-disordered breathing (SDB) is associated with an increased risk of cardiovascular events. Previous studies showed that severe SDB has a negative impact on myocardial salvage and progression of left ventricular dysfunction after acute myocardial infarction (AMI). This study investigated the frequency of SDB and the effects of SDB on left ventricular function after AMI. This retrospective study enrolled all patients with AMI who had undergone cardiorespiratory polygraphy for SDB diagnosis. The apnea-hypopnea index was used as a standard metric of SDB severity. SDB was classified as mild (apnea-hypopnea index >5 to <15 per h), moderate (≥15 to <30 per h) or severe (apnea-hypopnea index ≥30 per h). According to the majority of events, SDB was classified as predominant obstructive sleep apnea, central sleep apnea or mixed sleep apnea (mixed SDB). A total of 223 patients with AMI (112 with ST elevation and 111 without ST elevation; 63.2 ± 11.2 years, 82% male, left ventricular ejection fraction 49 ± 12%) were enrolled. SDB was present in 85.6%, and was moderate-to-severe in 63.2%; 40.8% had obstructive sleep apnea, 41.7% had central sleep apnea and 3.1% had mixed SDB. Left ventricular ejection fraction was lower in patients with AMI with severe SDB (45 ± 14%) versus those without SDB (57 ± 7%; P < 0.005). In addition, lower left ventricular ejection fraction (≤45%) was associated with increased frequency (apnea-hypopnea index ≥5 per h in 96%) and severity (apnea-hypopnea index ≥30 per h in 48%) of SDB in general and a higher percentage of central sleep apnea (57%) in particular. SDB is highly frequent in patients with AMI. SDB severity appeared to be linked to impaired left ventricular function, especially in patients with central sleep apnea. © 2017 European Sleep Research Society.

Individual differences in compliance and agreement for sleep logs and wrist actigraphy: A longitudinal study of naturalistic sleep in healthy adults

PubMed Central

Wasylyshyn, Nick; Roy, Heather; Lieberman, Gregory; Garcia, Javier O.; Asturias, Alex; Okafor, Gold N.; Elliott, James C.; Giesbrecht, Barry; Grafton, Scott T.; Mednick, Sara C.; Vettel, Jean M.

2018-01-01

There is extensive laboratory research studying the effects of acute sleep deprivation on biological and cognitive functions, yet much less is known about naturalistic patterns of sleep loss and the potential impact on daily or weekly functioning of an individual. Longitudinal studies are needed to advance our understanding of relationships between naturalistic sleep and fluctuations in human health and performance, but it is first necessary to understand the efficacy of current tools for long-term sleep monitoring. The present study used wrist actigraphy and sleep log diaries to obtain daily measurements of sleep from 30 healthy adults for up to 16 consecutive weeks. We used non-parametric Bland-Altman analysis and correlation coefficients to calculate agreement between subjectively and objectively measured variables including sleep onset time, sleep offset time, sleep onset latency, number of awakenings, the amount of wake time after sleep onset, and total sleep time. We also examined compliance data on the submission of daily sleep logs according to the experimental protocol. Overall, we found strong agreement for sleep onset and sleep offset times, but relatively poor agreement for variables related to wakefulness including sleep onset latency, awakenings, and wake after sleep onset. Compliance tended to decrease significantly over time according to a linear function, but there were substantial individual differences in overall compliance rates. There were also individual differences in agreement that could be explained, in part, by differences in compliance. Individuals who were consistently more compliant over time also tended to show the best agreement and lower scores on behavioral avoidance scale (BIS). Our results provide evidence for convergent validity in measuring sleep onset and sleep offset with wrist actigraphy and sleep logs, and we conclude by proposing an analysis method to mitigate the impact of non-compliance and measurement errors when the two

The Impact of Sleep Loss on Hippocampal Function

ERIC Educational Resources Information Center

Prince, Toni-Moi; Abel, Ted

2013-01-01

Hippocampal cellular and molecular processes critical for memory consolidation are affected by the amount and quality of sleep attained. Questions remain with regard to how sleep enhances memory, what parameters of sleep after learning are optimal for memory consolidation, and what underlying hippocampal molecular players are targeted by sleep…

Sleep deprivation alters choice strategy without altering uncertainty or loss aversion preferences

PubMed Central

Mullette-Gillman, O'Dhaniel A.; Kurnianingsih, Yoanna A.; Liu, Jean C. J.

2015-01-01

Sleep deprivation alters decision making; however, it is unclear what specific cognitive processes are modified to drive altered choices. In this manuscript, we examined how one night of total sleep deprivation (TSD) alters economic decision making. We specifically examined changes in uncertainty preferences dissociably from changes in the strategy with which participants engage with presented choice information. With high test-retest reliability, we show that TSD does not alter uncertainty preferences or loss aversion. Rather, TSD alters the information the participants rely upon to make their choices. Utilizing a choice strategy metric which contrasts the influence of maximizing and satisficing information on choice behavior, we find that TSD alters the relative reliance on maximizing information and satisficing information, in the gains domain. This alteration is the result of participants both decreasing their reliance on cognitively-complex maximizing information and a concomitant increase in the use of readily-available satisficing information. TSD did not result in a decrease in overall information use in either domain. These results show that sleep deprivation alters decision making by altering the informational strategies that participants employ, without altering their preferences. PMID:26500479

Acute otitis media associated bilateral sudden hearing loss: case report and literature review.

PubMed

Smith, A; Gutteridge, I; Elliott, D; Cronin, M

2017-07-01

Sudden sensorineural hearing loss is a rare otological condition with potential for dire outcomes including permanent hearing loss. Although the majority of cases are deemed idiopathic, bilateral sudden sensorineural hearing loss represents a rare subset typically related to systemic conditions, with higher morbidity and mortality. A controversial association with acute otitis media has been reported, with few bilateral cases published in the literature. A very rare case of bilateral sudden sensorineural hearing loss associated with acute otitis media is described, with a review of the literature. The limited evidence available suggests that acute otitis media with tinnitus and/or bacterial pathology may have an increased risk of sudden sensorineural hearing loss, which is consistent with the case described. Although there is no sufficiently powered published evidence to provide definitive treatment guidelines, the literature reviewed suggests that early myringotomy and antibiotics may greatly improve treatment outcomes.

Exploring the Lived Experience of Difficult Sleep and Good Sleep Among Psychiatric Inpatients.

PubMed

Zust, Barbara Lois; Gruenberg, Marjorie E; Sendelbach, Susan Ellen

2016-01-01

The purpose of this qualitative study was to explore psychiatric inpatients' reflections on their experiences with sleep throughout their lives. Fourteen patients in an acute care behavioral health unit agreed to participate in this study. Participants met individually with a researcher to reflect on times in their lives when they experienced good sleep; times when they had difficulty sleeping; and times when difficult sleep was resolved. The major findings of the study indicated that feeling alone with life problems triggered difficult sleep; while feelings of belonging and purpose were associated with good sleep.

Alcohol and the sleeping brain.

PubMed

Colrain, Ian M; Nicholas, Christian L; Baker, Fiona C

2014-01-01

Alcohol acts as a sedative that interacts with several neurotransmitter systems important in the regulation of sleep. Acute administration of large amounts of alcohol prior to sleep leads to decreased sleep-onset latency and changes in sleep architecture early in the night, when blood alcohol levels are high, with subsequent disrupted, poor-quality sleep later in the night. Alcohol abuse and dependence are associated with chronic sleep disturbance, lower slow-wave sleep, and more rapid-eye-movement sleep than normal, that last long into periods of abstinence and may play a role in relapse. This chapter outlines the evidence for acute and chronic alcohol effects on sleep architecture and sleep electroencephalogram, evidence for tolerance with repeated administration, and possible underlying neurochemical mechanisms for alcohol's effects on sleep. Also discussed are sex differences as well as effects of alcohol on sleep homeostasis and circadian regulation. Evidence for the role of sleep disruption as a risk factor for developing alcohol dependence is discussed in the context of research conducted in adolescents. The utility of sleep-evoked potentials in the assessment of the effects of alcoholism on sleep and the brain and in abstinence-mediated recovery is also outlined. The chapter concludes with a series of questions that need to be answered to determine the role of sleep and sleep disturbance in the development and maintenance of problem drinking and the potential beneficial effects of the treatment of sleep disorders for maintenance of abstinence in alcoholism. © 2014 Elsevier B.V. All rights reserved.

Aging induced ER stress alters sleep and sleep homeostasis

PubMed Central

Brown, Marishka K.; Chan, May T.; Zimmerman, John E.; Pack, Allan I.; Jackson, Nicholas E.; Naidoo, Nirinjini

2014-01-01

Alterations in the quality, quantity and architecture of baseline and recovery sleep have been shown to occur during aging. Sleep deprivation induces endoplasmic reticular (ER) stress and upregulates a protective signaling pathway termed the unfolded protein response (UPR). The effectiveness of the adaptive UPR is diminished by age. Previously, we showed that endogenous chaperone levels altered recovery sleep in Drosophila melanogaster. We now report that acute administration of the chemical chaperone sodium 4-phenylbutyrate (PBA) reduces ER stress and ameliorates age-associated sleep changes in Drosophila. PBA consolidates both baseline and recovery sleep in aging flies. The behavioral modifications of PBA are linked to its suppression of ER stress. PBA decreased splicing of x-box binding protein 1 (XBP1) and upregulation of phosphorylated elongation initiation factor 2 α (p-eIF2α), in flies that were subjected to sleep deprivation. We also demonstrate that directly activating ER stress in young flies fragments baseline sleep and alters recovery sleep. Alleviating prolonged/sustained ER stress during aging contributes to sleep consolidation and improves recovery sleep/ sleep debt discharge. PMID:24444805

Prevalence of impaired memory in hospitalized adults and associations with in-hospital sleep loss.

PubMed

Calev, Hila; Spampinato, Lisa M; Press, Valerie G; Meltzer, David O; Arora, Vineet M

2015-07-01

Effective inpatient teaching requires intact patient memory, but studies suggest hospitalized adults may have memory deficits. Sleep loss among inpatients could contribute to memory impairment. To assess memory in older hospitalized adults, and to test the association between sleep quantity, sleep quality, and memory, in order to identify a possible contributor to memory deficits in these patients. Prospective cohort study. General medicine and hematology/oncology inpatient wards. Fifty-nine hospitalized adults at least 50 years of age with no diagnosed sleep disorder. Immediate memory and memory after a 24-hour delay were assessed using a word recall and word recognition task from the University of Southern California Repeatable Episodic Memory Test. A vignette-based memory task was piloted as an alternative test more closely resembling discharge instructions. Sleep duration and efficiency overnight in the hospital were measured using actigraphy. Mean immediate recall was 3.8 words out of 15 (standard deviation = 2.1). Forty-nine percent of subjects had poor memory, defined as immediate recall score of 3 or lower. Median immediate recognition was 11 words out of 15 (interquartile range [IQR] = 9-13). Median delayed recall score was 1 word, and median delayed recognition was 10 words (IQR = 8-12). In-hospital sleep duration and efficiency were not significantly associated with memory. The medical vignette score was correlated with immediate recall (r = 0.49, P < 0.01). About half of the inpatients studied had poor memory while in the hospital, signaling that hospitalization might not be an ideal teachable moment. In-hospital sleep was not associated with memory scores. © 2015 Society of Hospital Medicine.

Prevalence of Impaired Memory in Hospitalized Adults and Associations with In-Hospital Sleep Loss

PubMed Central

Calev, Hila; Spampinato, Lisa M; Press, Valerie G; Meltzer, David O; Arora, Vineet M

2015-01-01

Background Effective inpatient teaching requires intact patient memory, but studies suggest hospitalized adults may have memory deficits. Sleep loss among inpatients could contribute to memory impairment. Objective To assess memory in older hospitalized adults, and to test the association between sleep quantity, sleep quality and memory, in order to identify a possible contributor to memory deficits in these patients. Design Prospective cohort study Setting General medicine and hematology/oncology inpatient wards Patients 59 hospitalized adults at least 50 years of age with no diagnosed sleep disorder. Measurements Immediate memory and memory after a 24-hour delay were assessed using a word recall and word recognition task from the University of Southern California Repeatable Episodic Memory Test (USC-REMT). A vignette-based memory task was piloted as an alternative test more closely resembling discharge instructions. Sleep duration and efficiency overnight in the hospital were measured using actigraphy. Results Mean immediate recall was 3.8 words out of 15 (SD=2.1). Forty-nine percent of subjects had poor memory, defined as immediate recall score of 3 or lower. Median immediate recognition was 11 words out of 15 (IQR=9, 13). Median delayed recall score was 1 word and median delayed recognition was 10 words (IQR= 8–12). In-hospital sleep duration and efficiency were not significantly associated with memory. The medical vignette score was correlated with immediate recall (r=0.49, p<0.01) Conclusions About half of inpatients studied had poor memory while in the hospital, signaling that hospitalization might not be an ideal teachable moment. In-hospital sleep was not associated with memory scores. PMID:25872763

Frontal Underactivation During Working Memory Processing in Adults With Acute Partial Sleep Deprivation: A Near-Infrared Spectroscopy Study.

PubMed

Yeung, Michael K; Lee, Tsz L; Cheung, Winnie K; Chan, Agnes S

2018-01-01

Individuals with partial sleep deprivation may have working memory (WM) impairment, but the underlying neural mechanism of this phenomenon is relatively unknown. The present study examined neural processing during WM performance in individuals with and without partial sleep deprivation using near-infrared spectroscopy (NIRS). Forty college students (10 males) were equally split into Sufficient Sleep (SS) and Insufficient Sleep (IS) groups based on self-reports of previous night's sleep duration. Participants in the SS group obtained the recommended amounts of sleep according to various sleep organizations (i.e., >7.0 h), whereas those in the IS group obtained amounts of sleep no greater than the lower limit of the recommendation (i.e., ≤7.0 h). All participants underwent an n -back paradigm with a WM load (i.e., 3-back) and a control condition (i.e., 0-back) while their prefrontal hemodynamics were recorded by NIRS. The IS and SS groups performed the tasks comparably well. However, unlike the SS group, which exhibited bilateral frontal activation indicated by increased oxyhemoglobin concentration and decreased deoxyhemoglobin concentration during WM processing (i.e., 3-back > 0-back), the IS group did not exhibit such activation. In addition, levels of WM-related frontal activation, especially those on the left side, correlated with sleep duration the night before, even when habitual sleep duration was controlled for. The findings suggest the presence of frontal lobe dysfunction in the absence of evident WM difficulties in individuals with acute partial sleep deprivation. They also highlight the importance of a good night's sleep to brain health.

Classifying performance impairment in response to sleep loss using pattern recognition algorithms on single session testing

PubMed Central

St. Hilaire, Melissa A.; Sullivan, Jason P.; Anderson, Clare; Cohen, Daniel A.; Barger, Laura K.; Lockley, Steven W.; Klerman, Elizabeth B.

2012-01-01

There is currently no “gold standard” marker of cognitive performance impairment resulting from sleep loss. We utilized pattern recognition algorithms to determine which features of data collected under controlled laboratory conditions could most reliably identify cognitive performance impairment in response to sleep loss using data from only one testing session, such as would occur in the “real world” or field conditions. A training set for testing the pattern recognition algorithms was developed using objective Psychomotor Vigilance Task (PVT) and subjective Karolinska Sleepiness Scale (KSS) data collected from laboratory studies during which subjects were sleep deprived for 26 – 52 hours. The algorithm was then tested in data from both laboratory and field experiments. The pattern recognition algorithm was able to identify performance impairment with a single testing session in individuals studied under laboratory conditions using PVT, KSS, length of time awake and time of day information with sensitivity and specificity as high as 82%. When this algorithm was tested on data collected under real-world conditions from individuals whose data were not in the training set, accuracy of predictions for individuals categorized with low performance impairment were as high as 98%. Predictions for medium and severe performance impairment were less accurate. We conclude that pattern recognition algorithms may be a promising method for identifying performance impairment in individuals using only current information about the individual’s behavior. Single testing features (e.g., number of PVT lapses) with high correlation with performance impairment in the laboratory setting may not be the best indicators of performance impairment under real-world conditions. Pattern recognition algorithms should be further tested for their ability to be used in conjunction with other assessments of sleepiness in real-world conditions to quantify performance impairment in

Negative effects of restricted sleep on facial appearance and social appeal

PubMed Central

Lekander, Mats; Sorjonen, Kimmo

2017-01-01

The importance of assessing evolutionarily relevant social cues suggests that humans should be sensitive to others' sleep history, as this may indicate something about their health as well as their capacity for social interaction. Recent findings show that acute sleep deprivation and looking tired are related to decreased attractiveness and health, as perceived by others. This suggests that one might also avoid contact with sleep-deprived, or sleepy-looking, individuals, as a strategy to reduce health risk and poor interactions. In this study, 25 participants (14 females, age range 18–47 years) were photographed after 2 days of sleep restriction and after normal sleep, in a balanced design. The photographs were rated by 122 raters (65 females, age range 18–65 years) on how much they would like to socialize with the participants. They also rated participants' attractiveness, health, sleepiness and trustworthiness. The results show that raters were less inclined to socialize with individuals who had gotten insufficient sleep. Furthermore, when sleep-restricted, participants were perceived as less attractive, less healthy and more sleepy. There was no difference in perceived trustworthiness. These findings suggest that naturalistic sleep loss can be detected in a face and that people are less inclined to interact with a sleep-deprived individual. PMID:28572989

Alcohol disrupts sleep homeostasis.

PubMed

Thakkar, Mahesh M; Sharma, Rishi; Sahota, Pradeep

2015-06-01

Alcohol is a potent somnogen and one of the most commonly used "over the counter" sleep aids. In healthy non-alcoholics, acute alcohol decreases sleep latency, consolidates and increases the quality (delta power) and quantity of NREM sleep during the first half of the night. However, sleep is disrupted during the second half. Alcoholics, both during drinking periods and during abstinences, suffer from a multitude of sleep disruptions manifested by profound insomnia, excessive daytime sleepiness, and altered sleep architecture. Furthermore, subjective and objective indicators of sleep disturbances are predictors of relapse. Finally, within the USA, it is estimated that societal costs of alcohol-related sleep disorders exceeds $18 billion. Thus, although alcohol-associated sleep problems have significant economic and clinical consequences, very little is known about how and where alcohol acts to affect sleep. In this review, we have described our attempts to unravel the mechanism of alcohol-induced sleep disruptions. We have conducted a series of experiments using two different species, rats and mice, as animal models. We performed microdialysis, immunohistochemical, pharmacological, sleep deprivation and lesion studies which suggest that the sleep-promoting effects of alcohol may be mediated via alcohol's action on the mediators of sleep homeostasis: adenosine (AD) and the wake-promoting cholinergic neurons of the basal forebrain (BF). Alcohol, via its action on AD uptake, increases extracellular AD resulting in the inhibition of BF wake-promoting neurons. Since binge alcohol consumption is a highly prevalent pattern of alcohol consumption and disrupts sleep, we examined the effects of binge drinking on sleep-wakefulness. Our results suggest that disrupted sleep homeostasis may be the primary cause of sleep disruption observed following binge drinking. Finally, we have also shown that sleep disruptions observed during acute withdrawal, are caused due to impaired

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

Cerebral mGluR5 availability contributes to elevated sleep need and behavioral adjustment after sleep deprivation

PubMed Central

Hefti, Katharina; Saberi-Moghadam, Sohrab; Buck, Alfred; Ametamey, Simon M; Scheidegger, Milan; Franken, Paul; Henning, Anke; Seifritz, Erich

2017-01-01

Increased sleep time and intensity quantified as low-frequency brain electrical activity after sleep loss demonstrate that sleep need is homeostatically regulated, yet the underlying molecular mechanisms remain elusive. We here demonstrate that metabotropic glutamate receptors of subtype 5 (mGluR5) contribute to the molecular machinery governing sleep-wake homeostasis. Using positron emission tomography, magnetic resonance spectroscopy, and electroencephalography in humans, we find that increased mGluR5 availability after sleep loss tightly correlates with behavioral and electroencephalographic biomarkers of elevated sleep need. These changes are associated with altered cortical myo-inositol and glycine levels, suggesting sleep loss-induced modifications downstream of mGluR5 signaling. Knock-out mice without functional mGluR5 exhibit severe dysregulation of sleep-wake homeostasis, including lack of recovery sleep and impaired behavioral adjustment to a novel task after sleep deprivation. The data suggest that mGluR5 contribute to the brain's coping mechanisms with sleep deprivation and point to a novel target to improve disturbed wakefulness and sleep. PMID:28980941

Cerebral mGluR5 availability contributes to elevated sleep need and behavioral adjustment after sleep deprivation.

PubMed

Holst, Sebastian C; Sousek, Alexandra; Hefti, Katharina; Saberi-Moghadam, Sohrab; Buck, Alfred; Ametamey, Simon M; Scheidegger, Milan; Franken, Paul; Henning, Anke; Seifritz, Erich; Tafti, Mehdi; Landolt, Hans-Peter

2017-10-05

Increased sleep time and intensity quantified as low-frequency brain electrical activity after sleep loss demonstrate that sleep need is homeostatically regulated, yet the underlying molecular mechanisms remain elusive. We here demonstrate that metabotropic glutamate receptors of subtype 5 (mGluR5) contribute to the molecular machinery governing sleep-wake homeostasis. Using positron emission tomography, magnetic resonance spectroscopy, and electroencephalography in humans, we find that increased mGluR5 availability after sleep loss tightly correlates with behavioral and electroencephalographic biomarkers of elevated sleep need. These changes are associated with altered cortical myo-inositol and glycine levels, suggesting sleep loss-induced modifications downstream of mGluR5 signaling. Knock-out mice without functional mGluR5 exhibit severe dysregulation of sleep-wake homeostasis, including lack of recovery sleep and impaired behavioral adjustment to a novel task after sleep deprivation. The data suggest that mGluR5 contribute to the brain's coping mechanisms with sleep deprivation and point to a novel target to improve disturbed wakefulness and sleep.

Electroencephalographic studies of sleep

NASA Technical Reports Server (NTRS)

Webb, W. B.; Agnew, H. W., Jr.

1975-01-01

Various experimental studies on sleep are described. The following areas are discussed: (1) effect of altered day length on sleep, (2) effect of a partial loss of sleep on subsequent nocturnal sleep; (3) effect of rigid control over sleep-wake-up times; (4) sleep and wakefulness in a time-free environment; (5) distribution of spindles during a full night of sleep; and (6) effect on sleep and performance of swiftly changing shifts of work.

Can We Predict Cognitive Performance Decrements Due to Sleep Loss and the Recuperative Effects of Caffeine

DTIC Science & Technology

2015-10-14

such as timely short naps and caffeine, are often used to mitigate the effects of sleep loss on performance. However, the timing, duration, and dosage...loss and the restorative effects of different dosages of caffeine on a specific individual’s performance. When used as a decision-aid tool, this model...provides the means to maximize Warfighter cognitive performance, resulting in peak alertness and prolonged alertness at the desired times

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

Chronic Stress is Prospectively Associated with Sleep in Midlife Women: The SWAN Sleep Study.

PubMed

Hall, Martica H; Casement, Melynda D; Troxel, Wendy M; Matthews, Karen A; Bromberger, Joyce T; Kravitz, Howard M; Krafty, Robert T; Buysse, Daniel J

2015-10-01

Evaluate whether levels of upsetting life events measured over a 9-y period prospectively predict subjective and objective sleep outcomes in midlife women. Prospective cohort study. Four sites across the United States. 330 women (46-57 y of age) enrolled in the Study of Women's Health Across the Nation (SWAN) Sleep Study. N/A. Upsetting life events were assessed annually for up to 9 y. Trajectory analysis applied to life events data quantitatively identified three distinct chronic stress groups: low stress, moderate stress, and high stress. Sleep was assessed by self-report and in-home polysomnography (PSG) during the ninth year of the study. Multivariate analyses tested the prospective association between chronic stress group and sleep, adjusting for race, baseline sleep complaints, marital status, body mass index, symptoms of depression, and acute life events at the time of the Sleep Study. Women characterized by high chronic stress had lower subjective sleep quality, were more likely to report insomnia, and exhibited increased PSG-assessed wake after sleep onset (WASO) relative to women with low to moderate chronic stress profiles. The effect of chronic stress group on WASO persisted in the subsample of participants without baseline sleep complaints. Chronic stress is prospectively associated with sleep disturbance in midlife women, even after adjusting for acute stressors at the time of the sleep study and other factors known to disrupt sleep. These results are consistent with current models of stress that emphasize the cumulative effect of stressors on health over time. © 2015 Associated Professional Sleep Societies, LLC.

Aging induced endoplasmic reticulum stress alters sleep and sleep homeostasis.

PubMed

Brown, Marishka K; Chan, May T; Zimmerman, John E; Pack, Allan I; Jackson, Nicholas E; Naidoo, Nirinjini

2014-06-01

Alterations in the quality, quantity, and architecture of baseline and recovery sleep have been shown to occur during aging. Sleep deprivation induces endoplasmic reticular (ER) stress and upregulates a protective signaling pathway termed the unfolded protein response. The effectiveness of the adaptive unfolded protein response is diminished by age. Previously, we showed that endogenous chaperone levels altered recovery sleep in Drosophila melanogaster. We now report that acute administration of the chemical chaperone sodium 4-phenylbutyrate (PBA) reduces ER stress and ameliorates age-associated sleep changes in Drosophila. PBA consolidates both baseline and recovery sleep in aging flies. The behavioral modifications of PBA are linked to its suppression of ER stress. PBA decreased splicing of X-box binding protein 1 and upregulation of phosphorylated elongation initiation factor 2 α, in flies that were subjected to sleep deprivation. We also demonstrate that directly activating ER stress in young flies fragments baseline sleep and alters recovery sleep. Alleviating prolonged or sustained ER stress during aging contributes to sleep consolidation and improves recovery sleep or sleep debt discharge. Copyright © 2014 Elsevier Inc. All rights reserved.

Flight Schedule and the Circadian Clock Influence on Sleep Loss During Overnight Cargo Operations

NASA Technical Reports Server (NTRS)

Gander, Philippa H.; Gregory, Kevin B.; Rosekind, Mark R.; Shafto, Michael G. (Technical Monitor)

1995-01-01

-0300) and were longer (average 19.2 h versus 14.8 h) than those in which they slept only once in the morning. Overnight cargo crew members are working around the time of the circadian nadir with an accumulating sleep debt. Two scheduling factors affect sleep loss during these operations: how long before the circadian wakeup signal crew members come off duty, and whether the layover lasts long enough to permit a second sleep episode in the early evening.

Maxillomandibular Volume Influences the Relationship between Weight Loss and Improvement in Obstructive Sleep Apnea

PubMed Central

Sutherland, Kate; Phillips, Craig L.; Yee, Brendon J.; Grunstein, Ronald R.; Cistulli, Peter A.

2016-01-01

Study Objectives: Obesity is the major risk factor for OSA; however, weight loss reduces OSA to a variable extent. We aimed to assess whether size of the maxillomandibular skeletal enclosure influences the relationship between weight loss and OSA reduction. Methods: Obese males (≥ 30 kg/m2) with moderate-severe OSA (AHI > 15/h) participating in a 6-mo open-label weight loss program had craniofacial computed tomography (CT) scans before and after weight loss. CT scans were analysed using three-dimensional cephalometry. Maxillomandibular volume was calculated from skeletal landmarks on the mandible (condyle, gonion, menton) and maxilla (anterior nasal spine). Multiple regression analysis was used to test for moderating effects of maxillomandibular volume on relationship between changes in weight and apnea-hypopnea index (AHI). Results: Fifty-two men (age 44.3 ± 8.8 y, AHI 42.9 ± 21.3 events/h, body mass index [BMI] 34.0 ± 2.7 kg/m2) had 7.4 ± 4.1% weight loss and 34.1 ± 32.4% AHI reduction at 6 months. BMI reduction modestly predicted AHI change (r2 = 0.17, P = 0.002). The interaction term of maxillomandibular volume and BMI change was a predictor of OSA improvement (P = 0.03), indicating maxillomandibular volume moderates this relationship. Subgroup analyses of patients by small, medium, and large maxillomandibular volume showed a strong correlation between weight loss and OSA improvement only in the small volume group (r = 0.654, P = 0.004). There was no relationship evident in those with large maxillomandibular volume (r = 0.05, P = 0.9). Conclusion: Maxillomandibular volume influences the relationship between weight loss and OSA improvement with an effect on AHI more evident in those with a smaller craniofacial skeleton. Citation: Sutherland K, Phillips CL, Yee BJ, Grunstein RR, Cistulli PA. Maxillomandibular volume influences the relationship between weight loss and improvement in obstructive sleep apnea. SLEEP 2016;39(1):43–49. PMID:26350470

Sleep and Rest Requirements: Physiological Considerations

NASA Technical Reports Server (NTRS)

Neri, David F.; Rosekind, Mark R. (Technical Monitor)

1997-01-01

Sleep is a vital physiological need which must be met to insure optimal functioning. A single night of significantly shortened sleep negatively impacts performance, alertness, and mood. Restricted sleep studies have shown that even a relatively small amount of sleep loss over several consecutive days can be additive and result in a cumulative sleep debt with similar detrimental effects. Compounding the problem of sleep loss in the operational environment is the poor correlation between subjective reports of sleepiness and objective measures of physiological sleep need. Some of the factors determining how sleepy an individual is at a given point in time are: (1) individual characteristics (e.g., amount of prior sleep and wakefulness, circadian phase, age), (2) environmental conditions (e.g., noise, temperature, amount of social interaction), and (3) task variables (e.g., signal rate, workload). Although sleep need can be masked with medications, the only way to reduce it is with sleep itself. The timing of the sleep period can affect sleep duration and quality and thus its restorative strength. The data are clear that increasing sleep time results in improved alertness. This paper will briefly review the scientific findings on sleep need, the effects of sleep loss, napping strategies, and the implications of incorporating physiologically sound sleep and rest strategies into the operational aviation environment.

Stabilising sleep for patients admitted at acute crisis to a psychiatric hospital (OWLS): an assessor-blind pilot randomised controlled trial.

PubMed

Sheaves, Bryony; Freeman, Daniel; Isham, Louise; McInerney, Josephine; Nickless, Alecia; Yu, Ly-Mee; Rek, Stephanie; Bradley, Jonathan; Reeve, Sarah; Attard, Caroline; Espie, Colin A; Foster, Russell; Wirz-Justice, Anna; Chadwick, Eleanor; Barrera, Alvaro

2018-07-01

When patients are admitted onto psychiatric wards, sleep problems are highly prevalent. We carried out the first trial testing a psychological sleep treatment at acute admission (Oxford Ward sLeep Solution, OWLS). This assessor-blind parallel-group pilot trial randomised patients to receive sleep treatment at acute crisis [STAC, plus standard care (SC)], or SC alone (1 : 1). STAC included cognitive-behavioural therapy (CBT) for insomnia, sleep monitoring and light/dark exposure for circadian entrainment, delivered over 2 weeks. Assessments took place at 0, 2, 4 and 12 weeks. Feasibility outcomes assessed recruitment, retention of participants and uptake of the therapy. Primary efficacy outcomes were the Insomnia Severity Index and Warwick-Edinburgh Mental Wellbeing Scale at week 2. Analyses were intention-to-treat, estimating treatment effect with 95% confidence intervals. Between October 2015 and July 2016, 40 participants were recruited (from 43 assessed eligible). All participants offered STAC completed treatment (mean sessions received = 8.6, s.d. = 1.5). All participants completed the primary end point. Compared with SC, STAC led to large effect size (ES) reductions in insomnia at week 2 (adjusted mean difference -4.6, 95% CI -7.7 to -1.4, ES -0.9), a small improvement in psychological wellbeing (adjusted mean difference 3.7, 95% CI -2.8 to 10.1, ES 0.3) and patients were discharged 8.5 days earlier. One patient in the STAC group had an adverse event, unrelated to participation. In this challenging environment for research, the trial was feasible. Therapy uptake was high. STAC may be a highly effective treatment for sleep disturbance on wards with potential wider benefits on wellbeing and admission length.

Sleep Extension before Sleep Loss: Effects on Performance and Neuromuscular Function.

PubMed

Arnal, Pierrick J; Lapole, Thomas; Erblang, Mégane; Guillard, Mathias; Bourrilhon, Cyprien; Léger, Damien; Chennaoui, Mounir; Millet, Guillaume Y

2016-08-01

This study aimed to investigate the effects of six nights of sleep extension on motor performance and associated neuromuscular function before and after one night of total sleep deprivation (TSD). Twelve healthy men participated in two experimental conditions (randomized crossover design): extended sleep (EXT, 9.8 ± 0.1 h time in bed) and habitual sleep (HAB, 8.2 ± 0.1 h time in bed). In each condition, subjects performed six nights of either EXT or HAB at home followed by an assessment of motor performance and neuromuscular function at baseline (D0) and after one night of TSD, i.e., 34-37 h of continuous wakefulness (D1). Maximal voluntary contractions with superimposed femoral nerve electrical and transcranial magnetic stimulations and stimulations on relaxed muscles were investigated before and after submaximal isometric knee extensor exercises performed until task failure. Time to exhaustion was longer in EXT compared with HAB (+3.9% ± 7.7% and +8.1% ± 12.3% at D0 and D1, respectively). Performance at D1 decreased from D0 similarly between conditions (-7.2% ± 5.6% and -3.7% ± 7.3% in HAB and EXT, respectively). At D1, the RPE during exercise was lower in EXT compared with HAB (-7.2% ± 7.5%) with no difference at D0. No difference was observed in voluntary activation between the two conditions. Six nights of sleep extension improved sustained contraction time to exhaustion, and this result cannot be explained by smaller reductions in voluntary activation, measured by both nerve and transcranial magnetic stimulation. The beneficial effect on motor performance in the EXT condition was likely due to reduced RPE after TSD.

Stroke patients' functions in personal activities of daily living in relation to sleep and socio-demographic and clinical variables in the acute phase after first-time stroke and at six months of follow-up.

PubMed

Bakken, Linda N; Kim, Hesook S; Finset, Arnstein; Lerdal, Anners

2012-07-01

To explore first-time stroke patients' degree of independence in activities of daily life in relation to sleep and other essential variables that might influence activities of daily life. Sleep has received little attention in rehabilitation of activities of daily life in stroke patients. This is a longitudinal survey and observational study design from the acute phase to six months poststroke. First-time stroke patients (n = 90) were recruited from two hospitals in eastern Norway in 2007 and 2008. Data were collected by survey interview, medical records and wrist actigraphy in the first two weeks at the hospital and at six months of follow-up. Actigraph measures patient activity and estimates sleep during the day and night. Linear regression showed that high dependence in personal activities of daily living was directly related to low estimated sleep time at night and higher estimated sleep during the day in the acute phase, controlling for socio-demographic and clinical variables. Furthermore, high estimated numbers of awakenings in the acute phase were related to lower activities of daily life functioning at six months of follow-up after controlling for socio-demographic and clinical variables. Stronger pain and a lower physical functioning showed direct relationships with lower independency level of in activities of daily life both in the acute phase and after six months. Sleep patterns in the acute phase may influence the patients' activities of daily life functioning up to six months poststroke. Furthermore, pain in the acute phase may influence the level of activities of daily life functioning in stroke patients. Nurses should pay attention to stroke patients' sleep quality and pain in the rehabilitation period after a stroke. Facilitating good sleep conditions and screening for pain should be an integral part of the rehabilitation programme. © 2012 Blackwell Publishing Ltd.

Ghrelin, Sleep Reduction and Evening Preference: Relationships to CLOCK 3111 T/C SNP and Weight Loss

PubMed Central

Garaulet, Marta; Sánchez-Moreno, Carmen; Smith, Caren E.; Lee, Yu-Chi; Nicolás, Francisco; Ordovás, Jose M.

2011-01-01

Background Circadian Locomotor Output Cycles Kaput (CLOCK), an essential element of the positive regulatory arm in the human biological clock, is involved in metabolic regulation. The aim was to investigate the behavioral (sleep duration, eating patterns and chronobiological characteristics) and hormonal (plasma ghrelin and leptin concentrations) factors which could explain the previously reported association between the CLOCK 3111T/C SNP and weight loss. Methodology/Principal Findings We recruited 1495 overweight/obese subjects (BMI: 25–40 kg/m2) of 20–65 y. who attended outpatient obesity clinics in Murcia, in southeastern Spain. We detected an association between the CLOCK 3111T/C SNP and weight loss, which was particularly evident after 12–14 weeks of treatment (P = 0.038). Specifically, carriers of the minor C allele were more resistant to weight loss than TT individuals (Mean±SEM) (8.71±0.59 kg vs 10.4±0.57 kg) C and TT respectively. In addition, our data show that minor C allele carriers had: 1. shorter sleep duration Mean ± SEM (7.0±0.05 vs 7.3±0.05) C and TT respectively (P = 0.039), 2. higher plasma ghrelin concentrations Mean ± SEM (pg/ml) (1108±49 vs 976±47)(P = 0.034); 3. delayed breakfast time; 4. evening preference and 5. less compliance with a Mediterranean Diet pattern, as compared with TT homozygotes. Conclusions/Significance Sleep reduction, changes in ghrelin values, alterations of eating behaviors and evening preference that characterized CLOCK 3111C carriers could be affecting weight loss. Our results support the hypothesis that the influence of the CLOCK gene may extend to a broad range of variables linked with human behaviors. PMID:21386998

Ghrelin, sleep reduction and evening preference: relationships to CLOCK 3111 T/C SNP and weight loss.

PubMed

Garaulet, Marta; Sánchez-Moreno, Carmen; Smith, Caren E; Lee, Yu-Chi; Nicolás, Francisco; Ordovás, Jose M

2011-02-28

Circadian Locomotor Output Cycles Kaput (CLOCK), an essential element of the positive regulatory arm in the human biological clock, is involved in metabolic regulation. The aim was to investigate the behavioral (sleep duration, eating patterns and chronobiological characteristics) and hormonal (plasma ghrelin and leptin concentrations) factors which could explain the previously reported association between the CLOCK 3111T/C SNP and weight loss. We recruited 1495 overweight/obese subjects (BMI: 25-40 kg/m(2)) of 20-65 y. who attended outpatient obesity clinics in Murcia, in southeastern Spain. We detected an association between the CLOCK 3111T/C SNP and weight loss, which was particularly evident after 12-14 weeks of treatment (P = 0.038). Specifically, carriers of the minor C allele were more resistant to weight loss than TT individuals (Mean±SEM) (8.71±0.59 kg vs 10.4±0.57 kg) C and TT respectively. In addition, our data show that minor C allele carriers had: 1. shorter sleep duration Mean ± SEM (7.0±0.05 vs 7.3±0.05) C and TT respectively (P = 0.039), 2. higher plasma ghrelin concentrations Mean ± SEM (pg/ml) (1108±49 vs 976±47)(P = 0.034); 3. delayed breakfast time; 4. evening preference and 5. less compliance with a Mediterranean Diet pattern, as compared with TT homozygotes. Sleep reduction, changes in ghrelin values, alterations of eating behaviors and evening preference that characterized CLOCK 3111C carriers could be affecting weight loss. Our results support the hypothesis that the influence of the CLOCK gene may extend to a broad range of variables linked with human behaviors.

Effect of repeated normobaric hypoxia exposures during sleep on acute mountain sickness, exercise performance, and sleep during exposure to terrestrial altitude.

PubMed

Fulco, Charles S; Muza, Stephen R; Beidleman, Beth A; Demes, Robby; Staab, Janet E; Jones, Juli E; Cymerman, Allen

2011-02-01

There is an expectation that repeated daily exposures to normobaric hypoxia (NH) will induce ventilatory acclimatization and lessen acute mountain sickness (AMS) and the exercise performance decrement during subsequent hypobaric hypoxia (HH) exposure. However, this notion has not been tested objectively. Healthy, unacclimatized sea-level (SL) residents slept for 7.5 h each night for 7 consecutive nights in hypoxia rooms under NH [n = 14, 24 ± 5 (SD) yr] or "sham" (n = 9, 25 ± 6 yr) conditions. The ambient percent O(2) for the NH group was progressively reduced by 0.3% [150 m equivalent (equiv)] each night from 16.2% (2,200 m equiv) on night 1 to 14.4% (3,100 m equiv) on night 7, while that for the ventilatory- and exercise-matched sham group remained at 20.9%. Beginning at 25 h after sham or NH treatment, all subjects ascended and lived for 5 days at HH (4,300 m). End-tidal Pco(2), O(2) saturation (Sa(O(2))), AMS, and heart rate were measured repeatedly during daytime rest, sleep, or exercise (11.3-km treadmill time trial). From pre- to posttreatment at SL, resting end-tidal Pco(2) decreased (P < 0.01) for the NH (from 39 ± 3 to 35 ± 3 mmHg), but not for the sham (from 39 ± 2 to 38 ± 3 mmHg), group. Throughout HH, only sleep Sa(O(2)) was higher (80 ± 1 vs. 76 ± 1%, P < 0.05) and only AMS upon awakening was lower (0.34 ± 0.12 vs. 0.83 ± 0.14, P < 0.02) in the NH than the sham group; no other between-group rest, sleep, or exercise differences were observed at HH. These results indicate that the ventilatory acclimatization induced by NH sleep was primarily expressed during HH sleep. Under HH conditions, the higher sleep Sa(O(2)) may have contributed to a lessening of AMS upon awakening but had no impact on AMS or exercise performance for the remainder of each day.

Sleep As A Strategy For Optimizing Performance.

PubMed

Yarnell, Angela M; Deuster, Patricia

2016-01-01

Recovery is an essential component of maintaining, sustaining, and optimizing cognitive and physical performance during and after demanding training and strenuous missions. Getting sufficient amounts of rest and sleep is key to recovery. This article focuses on sleep and discusses (1) why getting sufficient sleep is important, (2) how to optimize sleep, and (3) tools available to help maximize sleep-related performance. Insufficient sleep negatively impacts safety and readiness through reduced cognitive function, more accidents, and increased military friendly-fire incidents. Sufficient sleep is linked to better cognitive performance outcomes, increased vigor, and better physical and athletic performance as well as improved emotional and social functioning. Because Special Operations missions do not always allow for optimal rest or sleep, the impact of reduced rest and sleep on readiness and mission success should be minimized through appropriate preparation and planning. Preparation includes periods of "banking" or extending sleep opportunities before periods of loss, monitoring sleep by using tools like actigraphy to measure sleep and activity, assessing mental effectiveness, exploiting strategic sleep opportunities, and consuming caffeine at recommended doses to reduce fatigue during periods of loss. Together, these efforts may decrease the impact of sleep loss on mission and performance. 2016.

Chronic Stress is Prospectively Associated with Sleep in Midlife Women: The SWAN Sleep Study

PubMed Central

Hall, Martica H.; Casement, Melynda D.; Troxel, Wendy M.; Matthews, Karen A.; Bromberger, Joyce T.; Kravitz, Howard M.; Krafty, Robert T.; Buysse, Daniel J.

2015-01-01

Study Objectives: Evaluate whether levels of upsetting life events measured over a 9-y period prospectively predict subjective and objective sleep outcomes in midlife women. Design: Prospective cohort study. Setting: Four sites across the United States. Participants: 330 women (46–57 y of age) enrolled in the Study of Women's Health Across the Nation (SWAN) Sleep Study. Interventions: N/A. Measurements and Results: Upsetting life events were assessed annually for up to 9 y. Trajectory analysis applied to life events data quantitatively identified three distinct chronic stress groups: low stress, moderate stress, and high stress. Sleep was assessed by self-report and in-home polysomnography (PSG) during the ninth year of the study. Multivariate analyses tested the prospective association between chronic stress group and sleep, adjusting for race, baseline sleep complaints, marital status, body mass index, symptoms of depression, and acute life events at the time of the Sleep Study. Women characterized by high chronic stress had lower subjective sleep quality, were more likely to report insomnia, and exhibited increased PSG-assessed wake after sleep onset (WASO) relative to women with low to moderate chronic stress profiles. The effect of chronic stress group on WASO persisted in the subsample of participants without baseline sleep complaints. Conclusions: Chronic stress is prospectively associated with sleep disturbance in midlife women, even after adjusting for acute stressors at the time of the sleep study and other factors known to disrupt sleep. These results are consistent with current models of stress that emphasize the cumulative effect of stressors on health over time. Citation: Hall MH, Casement MD, Troxel WM, Matthews KA, Bromberger JT, Kravitz HM, Krafty RT, Buysse DJ. Chronic stress is prospectively associated with sleep in midlife women: the SWAN Sleep Study. SLEEP 2015;38(10):1645–1654. PMID:26039965

Acute drug induced hepatitis secondary to a weight loss product purchased over the internet

PubMed Central

Joshi, Deepak; Cross, Tim JS; Wong, Voi Shim

2007-01-01

Background Many people now seek alternative methods of weight loss. The internet provides a readily available source of weight reduction products, the ingredients of which are often unclear. The authors describe a case of acute hepatitis in a 20 year old woman caused by such a product purchased over the internet. Case Presentation A 20-year old woman presented with a two day history of abdominal pain, vomiting and jaundice. There were no identifiable risk factors for chronic liver disease. Liver function tests demonstrated an acute hepatitis (aminoaspartate transaminase 1230 IU/L). A chronic liver disease screen was negative. The patient had started a weight loss product (Pro-Lean), purchased over the internet two weeks prior to presentation. The patient was treated conservatively, and improved. The sequence of events suggests an acute hepatitis caused by an herbal weight loss product. Conclusion This case report highlights the dangers of weight loss products available to the public over the internet, and the importance of asking specifically about alternative medicines in patients who present with an acute hepatitis. PMID:17597525

Information processing during sleep and stress-related sleep vulnerability.

PubMed

Lin, Yen-Hsuan; Jen, Chun-Hui; Yang, Chien-Ming

2015-02-01

Previous studies showed enhanced attention and decreased inhibitory processes during early non-rapid eye movement sleep in primary insomnia patients, as measured by event-related potentials. The current study aims to examine information processing during sleep in non-insomniac individuals with high vulnerability (HV) to stress-related sleep disturbances. Twenty-seven non-insomniac individuals were recruited, 14 with low vulnerability and 13 with HV. After passing a screening interview and polysomnographic recording, subjects came to the sleep laboratory for 2 nights (a baseline night and a stress-inducing night) for event-related potentials recordings. The HV group demonstrated shorter P2 latency during the first 5 min of stage 2 sleep and higher P900 amplitudes under the stress condition during slow-wave sleep, which indicates an increased level of inhibitory processes. In addition, they had shorter N1 latencies during slow-wave sleep that could indicate an elevated level of attention processing during deep sleep. Unlike patients with chronic insomnia, individuals with high sleep vulnerability to stress show a compensatory process that may prevent external stimulation from interfering with their sleep. This may be one of the factors preventing their acute sleep disturbances from becoming chronic problems. © 2014 The Authors. Psychiatry and Clinical Neurosciences © 2014 Japanese Society of Psychiatry and Neurology.

Comparative efficacy of CPAP, MADs, exercise-training, and dietary weight loss for sleep apnea: a network meta-analysis.

PubMed

Iftikhar, Imran H; Bittencourt, Lia; Youngstedt, Shawn D; Ayas, Najib; Cistulli, Peter; Schwab, Richard; Durkin, Martin W; Magalang, Ulysses J

2017-02-01

To synthesize evidence from available studies on the relative efficacies of continuous positive airway pressure (CPAP), mandibular advancement device (MAD), supervised aerobic exercise training, and dietary weight loss in patients with obstructive sleep apnea (OSA). Network meta-analysis of 80 randomized controlled trials (RCTs) short-listed from PubMed, SCOPUS, Web of science, and Cochrane register (inception - September 8, 2015). Individuals with OSA. CPAP, MADs, exercise training, and dietary weight loss. CPAP decreased apnea-hypopnea index (AHI) the most [by 25.27 events/hour (22.03-28.52)] followed by exercise training, MADs, and dietary weight loss. While the difference between exercise training and CPAP was non-significant [-8.04 (-17.00 to 0.92), a significant difference was found between CPAP and MADs on AHI and oxygen desaturation index (ODI) [-10.06 (-14.21 to -5.91) and -7.82 (-13.04 to -2.59), respectively]. Exercise training significantly improved Epworth sleepiness scores (ESS) [by 3.08 (0.68-5.48)], albeit with a non-significant difference compared to MADs and CPAP. CPAP is the most efficacious in complete resolution of sleep apnea and in improving the indices of saturation during sleep. While MADs offer a reasonable alternative to CPAP, exercise training which significantly improved daytime sleepiness (ESS) could be used as adjunctive to the former two. Copyright © 2016 Elsevier B.V. All rights reserved.

Effects of sleep loss, time of day, and extended mental work on implicit and explicit learning of sequences

NASA Technical Reports Server (NTRS)

Heuer, H.; Spijkers, W.; Kiesswetter, E.; Schmidtke, V.

1998-01-01

Tacit knowledge is part of many professional skills and can be studied experimentally with implicit-learning paradigms. The authors explored the effects of 2 different stressors, loss of sleep and mental fatigue, on implicit learning in a serial-response time (RT) task. In the 1st experiment, 1 night of sleep deprivation was shown to impair implicit but not explicit sequence learning. In the 2nd experiment, no impairment of both types of sequence learning was found after 1.5 hr of mental work. Serial-RT performance, in contrast, suffered from both stressors. These findings suggest that sleep deprivation induces specific risks for automatic, skill-based behavior that are not present in consciously controlled performance.

EEG and ocular correlates of circadian melatonin phase and human performance decrements during sleep loss

NASA Technical Reports Server (NTRS)

Cajochen, C.; Khalsa, S. B.; Wyatt, J. K.; Czeisler, C. A.; Dijk, D. J.

1999-01-01

The aim of this study was to quantify the associations between slow eye movements (SEMs), eye blink rate, waking electroencephalogram (EEG) power density, neurobehavioral performance, and the circadian rhythm of plasma melatonin in a cohort of 10 healthy men during up to 32 h of sustained wakefulness. The time course of neurobehavioral performance was characterized by fairly stable levels throughout the first 16 h of wakefulness followed by deterioration during the phase of melatonin secretion. This deterioration was closely associated with an increase in SEMs. Frontal low-frequency EEG activity (1-7 Hz) exhibited a prominent increase with time awake and little circadian modulation. EEG alpha activity exhibited circadian modulation. The dynamics of SEMs and EEG activity were phase locked to changes in neurobehavioral performance and lagged the plasma melatonin rhythm. The data indicate that frontal areas of the brain are more susceptible to sleep loss than occipital areas. Frontal EEG activity and ocular parameters may be used to monitor and predict changes in neurobehavioral performance associated with sleep loss and circadian misalignment.

Sleep Problems in Children and Adolescents with Common Medical Conditions

PubMed Central

Lewandowski, Amy S.; Ward, Teresa M.; Palermo, Tonya M.

2011-01-01

Synopsis Sleep is critically important to children’s health and well-being. Untreated sleep disturbances and sleep disorders pose significant adverse daytime consequences and place children at considerable risk for poor health outcomes. Sleep disturbances occur at a greater frequency in children with acute and chronic medical conditions compared to otherwise healthy peers. Sleep disturbances in medically ill children can be associated with sleep disorders (e.g., sleep disordered breathing, restless leg syndrome), co-morbid with acute and chronic conditions (e.g., asthma, arthritis, cancer), or secondary to underlying disease-related mechanisms (e.g. airway restriction, inflammation) treatment regimens, or hospitalization. Clinical management should include a multidisciplinary approach with particular emphasis on routine, regular sleep assessments and prevention of daytime consequences and promotion of healthy sleep habits and health outcomes. PMID:21600350

Preemptive Caffeine Administration Blocks the Increase in Postoperative Pain Caused by Previous Sleep Loss in the Rat: A Potential Role for Preoptic Adenosine A2A Receptors in Sleep-Pain Interactions.

PubMed

Hambrecht-Wiedbusch, Viviane S; Gabel, Maya; Liu, Linda J; Imperial, John P; Colmenero, Angelo V; Vanini, Giancarlo

2017-09-01

Sleep and pain are reciprocally related, but the precise mechanisms underlying this relationship are poorly understood. This study used a rat model of surgical pain to examine the effect of previous sleep loss on postoperative pain and tested the hypothesis that preoptic adenosinergic mechanisms regulate sleep-pain interactions. Relative to ad libitum sleep, 6 hours of total sleep deprivation prior to a surgical incision significantly enhanced postoperative mechanical hypersensitivity in the affected paw and prolonged the time to recovery from surgery. There were no sex-specific differences in these measures. There were also no changes in adrenocorticotropic hormone and corticosterone levels after sleep deprivation, suggesting that this effect was not mediated by the stress associated with the sleep perturbation. Systemic administration of the nonselective adenosine receptor antagonist caffeine at the onset of sleep deprivation prevented the sleep deprivation-induced increase in postoperative hypersensitivity. Microinjection of the adenosine A2A receptor antagonist ZM 241385 into the median preoptic nucleus (MnPO) blocked the increase in surgical pain levels and duration caused by prior sleep deprivation and eliminated the thermal hyperalgesia induced by sleep deprivation in a group of nonoperated (i.e., without surgical incision) rats. These data show that even a brief sleep disturbance prior to surgery worsens postoperative pain and are consistent with our hypothesis that adenosine A2A receptors in the MnPO contribute to regulate these sleep-pain interactions. © Sleep Research Society 2017. Published by Oxford University Press on behalf of the Sleep Research Society. All rights reserved. For permissions, please e-mail journals.permissions@oup.com.

Estradiol and Progesterone Modulate Spontaneous Sleep Patterns and Recovery from Sleep Deprivation in Ovariectomized Rats

PubMed Central

Deurveilher, Samüel; Rusak, Benjamin; Semba, Kazue

2009-01-01

Study Objectives: Women undergo hormonal changes both naturally during their lives and as a result of sex hormone treatments. The objective of this study was to gain more knowledge about how these hormones affect sleep and responses to sleep loss. Design: Rats were ovariectomized and implanted subcutaneously with Silastic capsules containing oil vehicle, 17β-estradiol and/or progesterone. After 2 weeks, sleep/wake states were recorded during a 24-h baseline period, 6 h of total sleep deprivation induced by gentle handling during the light phase, and an 18-h recovery period. Measurements and Results: At baseline and particularly in the dark phase, ovariectomized rats treated with estradiol or estradiol plus progesterone spent more time awake at the expense of non-rapid eye movement sleep (NREMS) and/or REMS, whereas those given progesterone alone spent less time in REMS than ovariectomized rats receiving no hormones. Following sleep deprivation, all rats showed rebound increases in NREMS and REMS, but the relative increase in REMS was larger in females receiving hormones, especially high estradiol. In contrast, the normal increase in NREMS EEG delta power (an index of NREMS intensity) during recovery was attenuated by all hormone treatments. Conclusions: Estradiol promotes arousal in the active phase in sleep-satiated rats, but after sleep loss, both estradiol and progesterone selectively facilitate REMS rebound while reducing NREMS intensity. These results indicate that effects of ovarian hormones on recovery sleep differ from those on spontaneous sleep. The hormonal modulation of recovery sleep architecture may affect recovery of sleep related functions after sleep loss. Citation: Deurveilher S; Rusak B; Semba K. Estradiol and progesterone modulate spontaneous sleep patterns and recovery from sleep deprivation in ovariectomized rats. SLEEP 2009;32(7):865-877. PMID:19639749

Predictive Factors for Insufficient Weight Loss After Bariatric Surgery: Does Obstructive Sleep Apnea Influence Weight Loss?

PubMed

de Raaff, Christel A L; Coblijn, Usha K; de Vries, Nico; Heymans, Martijn W; van den Berg, Bob T J; van Tets, Willem F; van Wagensveld, Bart A

2016-05-01

Important endpoints of bariatric surgery are weight loss and improvement of comorbidities, of which obstructive sleep apnea (OSA) is the highest accompanying comorbidity (70%). This study aimed to evaluate the influence of OSA on weight loss after bariatric surgery and to provide predictive factors for insufficient weight loss (defined as ≤50% excess weight loss (EWL)) at 1 year follow-up. All consecutive patients, who underwent primary laparoscopic Roux-en-Y gastric bypass or laparoscopic sleeve gastrectomy between 2006 and 2014 were retrospectively reviewed. Patients with data on preoperative apnea-hypopnea index (AHI) and pre- and postoperative body mass index (BMI) were included. After surgery, the percentage excess weight loss (%EWL) and BMI changes were compared between preoperatively diagnosed OSA-, subdivided in mild, moderate, and severe OSA, and non-OSA patients. Multivariable logistic regression analysis evaluated predictive factors for ≤50% EWL. A total of 816 patients, 522 (64%) with and 294 (36%) without OSA, were included. After 1 year, OSA patients achieved less %EWL than non-OSA patients (65.5 SD 20.7 versus 70.3 SD 21.0; p < 0.01). The lowest %EWL was seen in severe OSA patients (61.7 SD 20.2). However, when adjusted for waist circumference, BMI, and age, no effect of OSA was seen on %EWL or changes in BMI. Although AHI, gender, age, BMI, type of surgery, and type II diabetes were predictive factors for ≤50% EWL (area under the curve 0.778), the AHI as variable was of little importance. The presence of OSA does not individually impair weight loss after bariatric surgery.

Acute Short-Term Sleep Deprivation Does Not Affect Metacognitive Monitoring Captured by Confidence Ratings: A Systematic Literature Review

ERIC Educational Resources Information Center

Jackson, Simon A.; Martin, Gregory D.; Aidman, Eugene; Kleitman, Sabina

2018-01-01

This article presents the results of a systematic review of the literature surrounding the effects that acute sleep deprivation has on metacognitive monitoring. Metacognitive monitoring refers to the ability to accurately assess one's own performance and state of knowledge. The mechanism behind this assessment is captured by subjective feelings of…

Gray matter-specific changes in brain bioenergetics after acute sleep deprivation: a 31P magnetic resonance spectroscopy study at 4 Tesla.

PubMed

Plante, David T; Trksak, George H; Jensen, J Eric; Penetar, David M; Ravichandran, Caitlin; Riedner, Brady A; Tartarini, Wendy L; Dorsey, Cynthia M; Renshaw, Perry F; Lukas, Scott E; Harper, David G

2014-12-01

A principal function of sleep may be restoration of brain energy metabolism caused by the energetic demands of wakefulness. Because energetic demands in the brain are greater in gray than white matter, this study used linear mixed-effects models to examine tissue-type specific changes in high-energy phosphates derived using 31P magnetic resonance spectroscopy (MRS) after sleep deprivation and recovery sleep. Experimental laboratory study. Outpatient neuroimaging center at a private psychiatric hospital. A total of 32 MRS scans performed in eight healthy individuals (mean age 35 y; range 23-51 y). Phosphocreatine (PCr) and β-nucleoside triphosphate (NTP) were measured using 31P MRS three dimensional-chemical shift imaging at high field (4 Tesla) after a baseline night of sleep, acute sleep deprivation (SD), and 2 nights of recovery sleep. Novel linear mixed-effects models were constructed using spectral and tissue segmentation data to examine changes in bioenergetics in gray and white matter. PCr increased in gray matter after 2 nights of recovery sleep relative to SD with no significant changes in white matter. Exploratory analyses also demonstrated that increases in PCr were associated with increases in electroencephalographic slow wave activity during recovery sleep. No significant changes in β-NTP were observed. These results demonstrate that sleep deprivation and subsequent recovery-induced changes in high-energy phosphates primarily occur in gray matter, and increases in PCr after recovery sleep may be related to sleep homeostasis. © 2014 Associated Professional Sleep Societies, LLC.

Investigating the effect of acute sleep deprivation on hypothalamic-pituitary-adrenal-axis response to a psychosocial stressor.

PubMed

Vargas, Ivan; Lopez-Duran, Nestor

2017-05-01

The hypothalamic-pituitary-adrenal (HPA) axis has been previously identified as one potential mechanism that may explain the link between sleep deprivation and negative health outcomes. However, few studies have examined the direct association between sleep deprivation and HPA-axis functioning, particularly in the context of stress. Therefore, the aim of the current study was to investigate the relationship between acute sleep deprivation and HPA-axis reactivity to a psychosocial stressor. Participants included 40 healthy, young adults between the ages of 18-29. The current protocol included spending two nights in the laboratory. After an adaptation night (night 1), participants were randomized into either a sleep deprivation condition (29 consecutive hours awake) or a control condition (night 2). Following the second night, all participants completed the Trier Social Stress Test (TSST). Salivary cortisol was collected before, during, and after the TSST. Results indicated that there were significant group differences in cortisol stress reactivity. Specifically, compared to participants in the control condition, participants in the sleep deprivation condition had greater baseline (i.e., pre-stress) cortisol, yet a blunted cortisol response to the TSST. Taken together, a combination of elevated baseline cortisol (and its subsequent effect on HPA-axis regulatory processes) and a relative 'ceiling' on the amount of cortisol a laboratory stressor can produce may explain why participants in the sleep deprivation condition demonstrated blunted cortisol responses. Copyright © 2017 Elsevier Ltd. All rights reserved.

Sleep-related laryngospasm.

PubMed

Thurnheer, R; Henz, S; Knoblauch, A

1997-09-01

The term "sleep-related laryngospasm" refers to episodic, abrupt interruption of sleep accompanied by feelings of acute suffocation followed by stridor. The condition is included in the diagnostic and coding manual of the American Sleep Disorders Association (ASDA), but there are few references in the peer-reviewed literature. Our description of the distinct clinical picture associated with this condition is based on an analysis of the histories of a series of 10 patients. The patients and their families gave precise, uniform accounts of the dramatic attacks. Diagnostic work-up included pulmonary and gastroenterological assessment. All patients reported sudden awakening from sleep due to feelings of acute suffocation, accompanied by intense fear. Apnoea lasting 5-45 s was followed by stridor. Breathing returned to normal within minutes. Patients were left exhausted by the attacks. Nine of our 10 patients had evidence of gastro-oesophageal reflux and six responded to antireflux therapy. We conclude that the nocturnal choking attacks (and the occasional daytime attacks experienced by some of the patients) are caused by laryngospasm. The pathogenesis of the apparent underlying laryngeal irritability is unknown. The condition may be related to a gastro-oesophageal reflux.

Disruption of adolescents' circadian clock: The vicious circle of media use, exposure to light at night, sleep loss and risk behaviors.

PubMed

Touitou, Yvan; Touitou, David; Reinberg, Alain

2016-11-01

Although sleep is a key element in adolescent development, teens are spending increasing amounts of time online with health risks related to excessive use of electronic media (computers, smartphones, tablets, consoles…) negatively associated with daytime functioning and sleep outcomes. Adolescent sleep becomes irregular, shortened and delayed in relation with later sleep onset and early waking time due to early school starting times on weekdays which results in rhythm desynchronization and sleep loss. In addition, exposure of adolescents to the numerous electronic devices prior to bedtime has become a great concern because LEDs emit much more blue light than white incandescent bulbs and compact fluorescent bulbs and have therefore a greater impact on the biological clock. A large number of adolescents move to evening chronotype and experience a misalignment between biological and social rhythms which, added to sleep loss, results in e.g. fatigue, daytime sleepiness, behavioral problems and poor academic achievement. This paper on adolescent circadian disruption will review the sensitivity of adolescents to light including LEDs with the effects on the circadian system, the crosstalk between the clock and the pineal gland, the role of melatonin, and the behavior of some adolescents(media use, alcohol consumption, binge drinking, smoking habits, stimulant use…). Lastly, some practical recommendations and perspectives are put forward. The permanent social jet lag resulting in clock misalignment experienced by a number of adolescents should be considered as a matter of public health. Copyright © 2017 Elsevier Ltd. All rights reserved.

Management of sleep disorders in stroke.

PubMed

Im, Kyoung Bin; Strader, Scott; Dyken, Mark Eric

2010-09-01

Scientific studies have proven a very strong association between stroke and obstructive sleep apnea (OSA). The prevalence of OSA is very high in patients with acute stroke, and untreated OSA is a stroke risk factor. In the stroke patient population, symptoms of OSA may atypically appear as isolated insomnia, hypersomnia, a dysfunction of circadian rhythm, a parasomnia, or a sleep-related movement disorder. Thus, we believe that in patients with acute stroke, OSA should be addressed first, using full in-laboratory, attended polysomnography (PSG), before other specific sleep disorders are aggressively addressed with specific therapeutic interventions. When OSA is diagnosed, supportive techniques including the application of continuous positive airway pressure (CPAP) therapy, positional therapies, or both should be considered first-line treatments. If OSA is ruled out by PSG, the therapeutic emphasis for sleep-related complaints is routinely based on instituting good sleep hygiene practices and using cognitive behavioral techniques (cognitive therapies, sleep restriction, stimulus control, and progressive relaxation therapies) because patients with stroke may be prone to the adverse effects of many of the medications that are otherwise routinely prescribed for a variety of specific sleep disorders.

Association Between Inpatient Sleep Loss and Hyperglycemia of Hospitalization

PubMed Central

DePietro, Regina H.; Knutson, Kristen L.; Spampinato, Lisa; Anderson, Samantha L.; Meltzer, David O.; Van Cauter, Eve

2017-01-01

OBJECTIVE To determine whether inpatient sleep duration and efficiency are associated with a greater risk of hyperglycemia in hospitalized patients with and without diabetes. RESEARCH DESIGN AND METHODS In this retrospective analysis of a prospective cohort study, medical inpatients ≥50 years of age were interviewed, and their charts were reviewed to obtain demographic data and diagnosis. Using World Health Organization criteria, patients were categorized as having normal blood glucose, impaired fasting blood glucose, or hyperglycemia based on morning glucose from the electronic health record. Wrist actigraphy measured sleep. Multivariable ordinal logistic regression models, controlling for subject random effects, tested the association between inpatient sleep duration and proportional odds of hyperglycemia versus impaired fasting blood glucose or impaired fasting blood glucose versus normal blood glucose in hospitalized adults. RESULTS A total of 212 patients (60% female and 74% African American) were enrolled. Roughly one-third (73, 34%) had diabetes. Objective inpatient sleep measures did not differ between patients with or without diabetes. In ordinal logistic regression models, each additional hour of in-hospital sleep was associated with an 11% (odds ratio 0.89 [95% CI 0.80, 0.99]; P = 0.043) lower proportional odds of a higher glucose category the next morning (hyperglycemia vs. elevated and elevated vs. normal). Every 10% increase in sleep efficiency was associated with an 18% lower proportional odds of a higher glucose category (odds ratio 0.82 [95% CI 0.74, 0.89]; P < 0.001). CONCLUSIONS Among medical inpatients, both shorter sleep duration and worse sleep efficiency were independently associated with greater proportional odds of hyperglycemia and impaired fasting glucose. PMID:27903614

Acute-Weight-Loss Strategies for Combat Sports and Applications to Olympic Success.

PubMed

Reale, Reid; Slater, Gary; Burke, Louise M

2017-02-01

It is common for athletes in weight-category sports to try to gain a theoretical advantage by competing in weight divisions that are lower than their day-to-day body mass (BM). Weight loss is achieved not only through chronic strategies (body-fat losses) but also through acute manipulations before weigh-in ("making weight"). Both have performance implications. This review focuses on Olympic combat sports, noting that the varied nature of regulations surrounding the weigh-in procedures, weight requirements, and recovery opportunities in these sports provide opportunity for a wider discussion of factors that can be applied to other weight-category sports. The authors summarize previous literature that has examined the performance effects of weightmaking practices before investigating the physiological nature of these BM losses. Practical recommendations in the form of a decision tree are provided to guide the achievement of acute BM loss while minimizing performance decrements.

General intelligence predicts memory change across sleep.

PubMed

Fenn, Kimberly M; Hambrick, David Z

2015-06-01

Psychometric intelligence (g) is often conceptualized as the capability for online information processing but it is also possible that intelligence may be related to offline processing of information. Here, we investigated the relationship between psychometric g and sleep-dependent memory consolidation. Participants studied paired-associates and were tested after a 12-hour retention interval that consisted entirely of wake or included a regular sleep phase. We calculated the number of word-pairs that were gained and lost across the retention interval. In a separate session, participants completed a battery of cognitive ability tests to assess g. In the wake group, g was not correlated with either memory gain or memory loss. In the sleep group, we found that g correlated positively with memory gain and negatively with memory loss. Participants with a higher level of general intelligence showed more memory gain and less memory loss across sleep. Importantly, the correlation between g and memory loss was significantly stronger in the sleep condition than in the wake condition, suggesting that the relationship between g and memory loss across time is specific to time intervals that include sleep. The present research suggests that g not only reflects the capability for online cognitive processing, but also reflects capability for offline processes that operate during sleep.

Fatigue on the flight deck: the consequences of sleep loss and the benefits of napping.

PubMed

Hartzler, Beth M

2014-01-01

The detrimental effects of fatigue in aviation are well established, as evidenced by both the number of fatigue-related mishaps and numerous studies which have found that most pilots experience a deterioration in cognitive performance as well as increased stress during the course of a flight. Further, due to the nature of the average pilot's work schedule, with frequent changes in duty schedule, early morning starts, and extended duty periods, fatigue may be impossible to avoid. Thus, it is critical that fatigue countermeasures be available which can help to combat the often overwhelming effects of sleep loss or sleep disruption. While stimulants such as caffeine are typically effective at maintaining alertness and performance, such countermeasures do nothing to address the actual source of fatigue - insufficient sleep. Consequently, strategic naps are considered an efficacious means of maintaining performance while also reducing the individual's sleep debt. These types of naps have been advocated for pilots in particular, as opportunities to sleep either in the designated rest facilities or on the flight deck may be beneficial in reducing both the performance and alertness impairments associated with fatigue, as well as the subjective feelings of sleepiness. Evidence suggests that strategic naps can reduce subjective feelings of fatigue and improve performance and alertness. Despite some contraindications to implementing strategic naps while on duty, such as sleep inertia experienced upon awakening, both researchers and pilots agree that the benefits associated with these naps far outweigh the potential risks. This article is a literature review detailing both the health and safety concerns of fatigue among commercial pilots as well as benefits and risks associated with strategic napping to alleviate this fatigue. Published by Elsevier Ltd.

Sleep Interacts with Aβ to Modulate Intrinsic Neuronal Excitability

PubMed Central

Tabuchi, Masashi; Lone, Shahnaz R.; Liu, Sha; Liu, Qili; Zhang, Julia; Spira, Adam P.; Wu, Mark N.

2015-01-01

SUMMARY Background Emerging data suggest an important relationship between sleep and Alzheimer’s Disease (AD), but how poor sleep promotes the development of AD remains unclear. Results Here, using a Drosophila model of AD, we provide evidence suggesting that changes in neuronal excitability underlie the effects of sleep loss on AD pathogenesis. β-amyloid (Aβ) accumulation leads to reduced and fragmented sleep, while chronic sleep deprivation increases Aβ burden. Moreover, enhancing sleep reduces Aβ deposition. Increasing neuronal excitability phenocopies the effects of reducing sleep on Aβ, and decreasing neuronal activity blocks the elevated Aβ accumulation induced by sleep deprivation. At the single neuron level, we find that chronic sleep deprivation, as well as Aβ expression, enhances intrinsic neuronal excitability. Importantly, these data reveal that sleep loss exacerbates Aβ–induced hyperexcitability and suggest that defects in specific K+ currents underlie the hyperexcitability caused by sleep loss and Aβ expression. Finally, we show that feeding levetiracetam, an anti-epileptic medication, to Aβ-expressing flies suppresses neuronal excitability and significantly prolongs their lifespan. Conclusions Our findings directly link sleep loss to changes in neuronal excitability and Aβ accumulation and further suggest that neuronal hyperexcitability is an important mediator of Aβ toxicity. Taken together, these data provide a mechanistic framework for a positive feedback loop, whereby sleep loss and neuronal excitation accelerate the accumulation of Aβ, a key pathogenic step in the development of AD. PMID:25754641

Youth Screen Media Habits and Sleep: Sleep-Friendly Screen Behavior Recommendations for Clinicians, Educators, and Parents.

PubMed

Hale, Lauren; Kirschen, Gregory W; LeBourgeois, Monique K; Gradisar, Michael; Garrison, Michelle M; Montgomery-Downs, Hawley; Kirschen, Howard; McHale, Susan M; Chang, Anne-Marie; Buxton, Orfeu M

2018-04-01

With the widespread use of portable electronic devices and the normalization of screen media devices in the bedroom, insufficient sleep has become commonplace. In a recent literature review, 90% of included studies found an association between screen media use and delayed bedtime and/or decreased total sleep time. This pervasive phenomenon of pediatric sleep loss has widespread implications. There is a need for basic, translational, and clinical research examining the effects of screen media on sleep loss and health consequences in children and adolescents to educate and motivate clinicians, teachers, parents and youth themselves to foster healthy sleep habits. Copyright © 2017 Elsevier Inc. All rights reserved.

Acute enhancement of non-rapid eye movement sleep in rats after drinking water contaminated with cadmium chloride.

PubMed

Unno, Katsuya; Yamoto, Kurumi; Takeuchi, Kouhei; Kataoka, Aya; Ozaki, Tomoya; Mochizuki, Takatoshi; Honda, Kazuki; Miura, Nobuhiko; Ikeda, Masayuki

2014-02-01

Cadmium (Cd) is a heavy metal widely used or effused by industries. Serious environmental Cd pollution has been reported over the past two centuries, whereas the mechanisms underlying Cd-mediated diseases are not fully understood. Interestingly, an increase in reactive oxygen species (ROS) after Cd exposure has been shown. Our group has demonstrated that sleep is triggered via accumulation of ROS during neuronal activities, and we thus hypothesize the involvement of Cd poisoning in sleep-wake irregularities. In the present study, we analyzed the effects of Cd intake (1-100 ppm CdCl₂ in drinking water) on rats by monitoring sleep encephalograms and locomotor activities. The results demonstrated that 100 ppm CdCl₂ administration for 28 h was sufficient to increase non-rapid-eye-movement (non-REM) sleep and reduce locomotor activities during the night (the rat active phase). In contrast, free-running locomotor rhythms under constant dim red light and their re-entrainment to 12:12-h light/dark cycles were intact under chronic (1 month) 100 ppm CdCl₂ administrations, suggesting a limited influence on circadian clock movements at this dosage. The relative amount of oxidized glutathione increased in the brain after the 28-h 100 ppm CdCl₂ administrations similar to the levels in cultured astrocytes receiving H₂O₂ or CdCl₂ in culture medium. Therefore, we propose Cd-induced sleep as a consequence of oxidative stress. As oxidized glutathione is an endogenous sleep substance, we suggest that Cd rapidly induces sleepiness and influences activity performance by occupying intrinsic sleep-inducing mechanisms. In conclusion, we propose increased non-REM sleep during the active phase as an index of acute Cd exposure. Copyright © 2013 John Wiley & Sons, Ltd.

Central Sleep Apnea - a Rare Cause for Acute Respiratory Insufficiency in Children. Case Report.

PubMed

Popescu, Nicoleta Aurelia; Ionescu, Marcela Daniela; Balan, Georgiana; Visan, Simina; Cinteza, Eliza; Stanescu, Diana; Gobej, Ionut; Balgradean, Mihaela

2018-03-01

Central sleep apnea is characterized by frequent cessation of breathing during sleep, resulting in repetitive episodes of insufficient ventilation and abnormalities of acid-base balance. It may be primary or secondary, and it is uncommon in children, with limited data for this population. We present here the case of a five-year-old girl, known to have thoracolumbar myelomeningocele (for which she underwent a surgical procedure in infancy), secondary hydrocephalus (with a ventriculoperitoneal shunt) and flaccid paralysis, who was admitted in our hospital with prolonged fever syndrome, productive cough, severe dyspnea and perioral cyanosis. Following physical examination, laboratory investigations and thoracic radiography, we established the diagnosis of aspiration pneumonia with acute respiratory failure. Medical treatment with multiple systemic antibiotics, antifungal agents, systemic and inhaled bronchodilator, oxygen therapy and respiratory nursing were initiated, with favorable evolution. During the entire hospitalization, the patient showed nocturnal respiratory rhythm disorders, with sleep apnea crisis of approximately 20 seconds and desaturation, followed by severe hypercapnic respiratory acidosis, manifestations that persisted even after the remission of pulmonary infection, raising the suspicion of an apnea syndrome. After excluding the causes of obstructive apnea, a cerebral CT scan was performed, revealing isolated fourth ventricle compressing the brainstem. The patient underwent neurosurgical intervention and postoperatively, the evolution was favorable, with remission of apnea crisis.

The Impact of Sleep Restriction and Simulated Physical Firefighting Work on Acute Inflammatory Stress Responses.

PubMed

Wolkow, Alexander; Ferguson, Sally A; Vincent, Grace E; Larsen, Brianna; Aisbett, Brad; Main, Luana C

2015-01-01

This study investigated the effect restricted sleep has on wildland firefighters' acute cytokine levels during 3 days and 2 nights of simulated physical wildfire suppression work. Firefighters completed multiple days of physical firefighting work separated by either an 8-h (Control condition; n = 18) or 4-h (Sleep restriction condition; n = 17) sleep opportunity each night. Blood samples were collected 4 times a day (i.e., 06:15, 11:30, 18:15, 21:30) from which plasma cytokine levels (IL-6, IL-8, IL-1β, TNF-α, IL-4, IL-10) were measured. The primary findings for cytokine levels revealed a fixed effect for condition that showed higher IL-8 levels among firefighters who received an 8-h sleep each night. An interaction effect demonstrated differing increases in IL-6 over successive days of work for the SR and CON conditions. Fixed effects for time indicated that IL-6 and IL-4 levels increased, while IL-1β, TNF-α and IL-8 levels decreased. There were no significant effects for IL-10 observed. Findings demonstrate increased IL-8 levels among firefighters who received an 8-h sleep when compared to those who had a restricted 4-h sleep. Firefighters' IL-6 levels increased in both conditions which may indicate that a 4-h sleep restriction duration and/or period (i.e., 2 nights) was not a significant enough stressor to affect this cytokine. Considering the immunomodulatory properties of IL-6 and IL-4 that inhibit pro-inflammatory cytokines, the rise in IL-6 and IL-4, independent of increases in IL-1β and TNF-α, could indicate a non-damaging response to the stress of simulated physical firefighting work. However, given the link between chronically elevated cytokine levels and several diseases, further research is needed to determine if firefighters' IL-8 and IL-6 levels are elevated following repeated firefighting deployments across a fire season and over multiple fire seasons.

Chronotype, sleep loss, and diurnal pattern of salivary cortisol in a simulated daylong driving.

PubMed

Oginska, Halszka; Fafrowicz, Magdalena; Golonka, Krystyna; Marek, Tadeusz; Mojsa-Kaja, Justyna; Tucholska, Kinga

2010-07-01

distinct diurnal variation (F = 2.950, p < .019), whereas E types showed a flattened diurnal curve. Cortisol values did not correlate with subjective assessments of workload, arousal, or sleepiness at any time-of-day. Diurnal cortisol pattern parameters (i.e., morning level, mean level, and range of diurnal changes) showed significant positive correlations with sleep length before the experiment (r = .48, .54, and .53, respectively) and with sleep index (r = .63, .64, and .56, respectively). The conclusions of this study are: (i) E-oriented types showed lower salivary cortisol levels and a flattened diurnal curve in comparison with M types; (ii) sleep loss was associated with lower morning cortisol and mean diurnal level, whereas higher cortisol levels were observed in rested individuals. In the context of stress theory, it may be hypothesized that rested subjects perceived the driving task as a challenge, whereas those with reduced sleep were not challenged, but bored/exhausted with the experimental situation.

Sleep and rhythm consequences of a genetically induced loss of serotonin.

PubMed

Leu-Semenescu, Smaranda; Arnulf, Isabelle; Decaix, Caroline; Moussa, Fathi; Clot, Fabienne; Boniol, Camille; Touitou, Yvan; Levy, Richard; Vidailhet, Marie; Roze, Emmanuel

2010-03-01

A genetic deficiency in sepiapterin reductase leads to a combined deficit of serotonin and dopamine. The motor phenotype is characterized by a dopa-responsive fluctuating generalized dystonia-parkinsonism. The non-motor symptoms are poorly recognized. In particular, the effects of brain serotonin deficiency on sleep have not been thoroughly studied. We examine the sleep, sleep-wake rhythms, CSF neurotransmitters, and melatonin profile in a patient with sepiapterin reductase deficiency. The patient was a 28-year-old man with fluctuating generalized dystonia-parkinsonism caused by sepiapterin reductase deficiency. A sleep interview, wrist actigraphy, sleep log over 14 days, 48-h continuous sleep and core temperature monitoring, and measurement of CSF neurotransmitters and circadian serum melatonin and cortisol levels before and after treatment with 5-hydroxytryptophan (the precursor of serotonin) and levodopa were performed. Before treatment, the patient had mild hypersomnia with long sleep time (704 min), ultradian sleep-wake rhythm (sleep occurred every 11.8 +/- 5.3 h), organic hyperphagia, attentionlexecutive dysfunction, and no depression. The serotonin metabolism in the CSF was reduced, and the serum melatonin profile was flat, while cortisol and core temperature profiles were normal. Supplementation with 5-hydroxytryptophan, but not with levodopa, normalized serotonin metabolism in the CSF, reduced sleep time to 540 min, normalized the eating disorder and the melatonin profile, restored a circadian sleep-wake rhythm (sleep occurred every 24 +/- 1.7 h, P < 0.0001), and improved cognition. In this unique genetic paradigm, the melatonin deficiency (caused by a lack of its substrate, serotonin) may cause the ultradian sleep-wake rhythm.

Prediction of Vigilant Attention and Cognitive Performance Using Self-Reported Alertness, Circadian Phase, Hours since Awakening, and Accumulated Sleep Loss

PubMed Central

Bermudez, Eduardo B.; Klerman, Elizabeth B.; Czeisler, Charles A.; Cohen, Daniel A.; Wyatt, James K.; Phillips, Andrew J. K.

2016-01-01

Sleep restriction causes impaired cognitive performance that can result in adverse consequences in many occupational settings. Individuals may rely on self-perceived alertness to decide if they are able to adequately perform a task. It is therefore important to determine the relationship between an individual’s self-assessed alertness and their objective performance, and how this relationship depends on circadian phase, hours since awakening, and cumulative lost hours of sleep. Healthy young adults (aged 18–34) completed an inpatient schedule that included forced desynchrony of sleep/wake and circadian rhythms with twelve 42.85-hour “days” and either a 1:2 (n = 8) or 1:3.3 (n = 9) ratio of sleep-opportunity:enforced-wakefulness. We investigated whether subjective alertness (visual analog scale), circadian phase (melatonin), hours since awakening, and cumulative sleep loss could predict objective performance on the Psychomotor Vigilance Task (PVT), an Addition/Calculation Test (ADD) and the Digit Symbol Substitution Test (DSST). Mathematical models that allowed nonlinear interactions between explanatory variables were evaluated using the Akaike Information Criterion (AIC). Subjective alertness was the single best predictor of PVT, ADD, and DSST performance. Subjective alertness alone, however, was not an accurate predictor of PVT performance. The best AIC scores for PVT and DSST were achieved when all explanatory variables were included in the model. The best AIC score for ADD was achieved with circadian phase and subjective alertness variables. We conclude that subjective alertness alone is a weak predictor of objective vigilant or cognitive performance. Predictions can, however, be improved by knowing an individual’s circadian phase, current wake duration, and cumulative sleep loss. PMID:27019198

Illness Severity and Work Productivity Loss Among Working Adults With Medically Attended Acute Respiratory Illnesses: US Influenza Vaccine Effectiveness Network 2012–2013

PubMed Central

Petrie, Joshua G.; Cheng, Caroline; Malosh, Ryan E.; VanWormer, Jeffrey J.; Flannery, Brendan; Zimmerman, Richard K.; Gaglani, Manjusha; Jackson, Michael L.; King, Jennifer P.; Nowalk, Mary Patricia; Benoit, Joyce; Robertson, Anne; Thaker, Swathi N.; Monto, Arnold S.; Ohmit, Suzanne E.

2016-01-01

Background. Influenza causes significant morbidity and mortality, with considerable economic costs, including lost work productivity. Influenza vaccines may reduce the economic burden through primary prevention of influenza and reduction in illness severity. Methods. We examined illness severity and work productivity loss among working adults with medically attended acute respiratory illnesses and compared outcomes for subjects with and without laboratory-confirmed influenza and by influenza vaccination status among subjects with influenza during the 2012–2013 influenza season. Results. Illnesses laboratory-confirmed as influenza (ie, cases) were subjectively assessed as more severe than illnesses not caused by influenza (ie, noncases) based on multiple measures, including current health status at study enrollment (≤7 days from illness onset) and current activity and sleep quality status relative to usual. Influenza cases reported missing 45% more work hours (20.5 vs 15.0; P < .001) than noncases and subjectively assessed their work productivity as impeded to a greater degree (6.0 vs 5.4; P < .001). Current health status and current activity relative to usual were subjectively assessed as modestly but significantly better for vaccinated cases compared with unvaccinated cases; however, no significant modifications of sleep quality, missed work hours, or work productivity loss were noted for vaccinated subjects. Conclusions. Influenza illnesses were more severe and resulted in more missed work hours and productivity loss than illnesses not confirmed as influenza. Modest reductions in illness severity for vaccinated cases were observed. These findings highlight the burden of influenza illnesses and illustrate the importance of laboratory confirmation of influenza outcomes in evaluations of vaccine effectiveness. PMID:26565004

Comparison of fluid types for resuscitation after acute blood loss in mallard ducks (Anas platyrhynchos).

PubMed

Lichtenberger, Marla; Orcutt, Connie; Cray, Carolyn; Thamm, Douglas H; DeBehnke, Daniel; Page, Cheryl; Mull, Lori; Kirby, Rebecca

2009-10-01

The purpose of this study was to determine the LD(50) for acute blood loss in mallard ducks (Anas platyrhynchos), compare the mortality rate among 3 fluid resuscitation groups, and determine the time required for a regenerative RBC response. Prospective study. Medical College of Wisconsin Research facility. Eighteen mallard ducks were included for the LD(50) study and 28 for the fluid resuscitation study. Phlebotomy was performed during both the LD(50) and fluid resuscitation studies. Ducks in the fluid resuscitation study received a 5 mL/kg intravenous bolus of crystalloids, hetastarch (HES), or a hemoglobin-based oxygen-carrying solution (HBOCS). The LD(50) for acute blood loss was 60% of total blood volume. This blood volume was removed in the fluid resuscitation study to create a model of acute blood loss. Following fluid administration, 6 birds in the crystalloid group (66%), 4 birds in the HES group (40%), and 2 birds in the HBOCS group (20%) died. No statistical difference in mortality rate was seen among the 3 fluid resuscitation groups. Relative polychromasia evaluated post-phlebotomy demonstrated regeneration starting at 24 hours and continuing through 48 hours. The LD(50) for acute blood loss in mallard ducks was 60% of their total blood volume. Although no statistical difference in mortality rate was appreciated among the 3 fluid resuscitation groups, a trend of decreased mortality rate was observed in the HBOCS group. An early regenerative response was apparent following acute blood loss.

The cognitive cost of sleep lost

PubMed Central

McCoy, John G.; Strecker, Robert E.

2013-01-01

A substantial body of literature supports the intuitive notion that a good night’s sleep can facilitate human cognitive performance the next day. Deficits in attention, learning & memory, emotional reactivity, and higher-order cognitive processes, such as executive function and decision making, have all been documented following sleep disruption in humans. Thus, whilst numerous clinical and experimental studies link human sleep disturbance to cognitive deficits, attempts to develop valid and reliable rodent models of these phenomena are fewer, and relatively more recent. This review focuses primarily on the cognitive impairments produced by sleep disruption in rodent models of several human patterns of sleep loss/sleep disturbance. Though not an exclusive list, this review will focus on four specific types of sleep disturbance: total sleep deprivation, experimental sleep fragmentation, selective REM sleep deprivation, and chronic sleep restriction. The use of rodent models can provide greater opportunities to understand the neurobiological changes underlying sleep loss induced cognitive impairments. Thus, this review concludes with a description of recent neurobiological findings concerning the neuroplastic changes and putative brain mechanisms that may underlie the cognitive deficits produced by sleep disturbances. PMID:21875679

Sleep in athletes and the effects of Ramadan.

PubMed

Roky, Rachida; Herrera, Christopher Paul; Ahmed, Qanta

2012-01-01

Sleep is now considered as a new frontier in performance enhancement. This article presents background content on sleep function, sleep needs and methods of sleep investigation along with data on the potential effects of Ramadan fasting on sleep in normal individuals and athletes. Accumulated sleep loss has negative impacts on cognitive function, mood, daytime sleepiness and performance. Sleep studies in athletes fasting during Ramadan are very rare. Most of them have demonstrated that during this month, sleep duration decreased and sleep timing shifted. But the direct relation between sleep changes and performance during Ramadan is not yet elucidated. Objective sleep patterns can be investigated using polysomnography, actigraphy, and standardised questionnaires and recorded in daily journals or sleep logs. The available data on sleep indicate that team doctors and coaches should consider planning sleep schedule and napping; implementing educational programmes focusing on the need for healthy sleep; and consider routine screening for sleep loss in athletes of all age groups and genders.

Sleep apnoea and stroke

PubMed Central

Sharma, Sameer; Culebras, Antonio

2016-01-01

Sleep disorders have been known to physicians for a long time. In his famous aphorisms, Hippocrates said “Sleep or watchfulness exceeding that which is customary, augurs unfavorably”. Modern medicine has been able to disentangle some of the phenomena that disturb sleep. Among the most notable offenders is sleep apnoea that has gained prominence in the past few decades. It is being proposed as one of the potentially modifiable risk factors for vascular diseases including stroke. The pathological mechanisms linking sleep apnoea to vascular risk factors include hypoxia, cardiac arrhythmias, dysautonomia, impaired glucose tolerance, hypertension, dyslipidaemia and inflammation. In this article, we review literature linking sleep apnoea and stroke, including sleep apnoea as a risk factor for primary prevention with the potential to improve outcome after acute stroke and as a secondary risk factor, amenable to modification and hence vascular risk reduction. PMID:28959482

Acute Kynurenine Challenge Disrupts Sleep-Wake Architecture and Impairs Contextual Memory in Adult Rats.

PubMed

Pocivavsek, Ana; Baratta, Annalisa M; Mong, Jessica A; Viechweg, Shaun S

2017-11-01

Tryptophan metabolism via the kynurenine pathway may represent a key molecular link between sleep loss and cognitive dysfunction. Modest increases in the kynurenine pathway metabolite kynurenic acid (KYNA), which acts as an antagonist at N-methyl-d-aspartate and α7 nicotinic acetylcholine receptors in the brain, result in cognitive impairments. As glutamatergic and cholinergic neurotransmissions are critically involved in modulation of sleep, our current experiments tested the hypothesis that elevated KYNA adversely impacts sleep quality. Adult male Wistar rats were treated with vehicle (saline) and kynurenine (25, 50, 100, and 250 mg/kg), the direct bioprecursor of KYNA, intraperitoneally at zeitgeber time (ZT) 0 to rapidly increase brain KYNA. Levels of KYNA in the brainstem, cortex, and hippocampus were determined at ZT 0, ZT 2, and ZT 4, respectively. Analyses of vigilance state-related parameters categorized as wake, rapid eye movement (REM), and non-REM (NREM) as well as spectra power analysis during NREM and REM were assessed during the light phase. Separate animals were tested in the passive avoidance paradigm, testing contextual memory. When KYNA levels were elevated in the brain, total REM duration was reduced and total wake duration was increased. REM and wake architecture, assessed as number of vigilance state bouts and average duration of each bout, and theta power during REM were significantly impacted. Kynurenine challenge impaired performance in the hippocampal-dependent contextual memory task. Our results introduce kynurenine pathway metabolism and formation of KYNA as a novel molecular target contributing to sleep disruptions and cognitive impairments. © Sleep Research Society 2017. Published by Oxford University Press on behalf of the Sleep Research Society. All rights reserved. For permissions, please e-mail journals.permissions@oup.com.

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

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. © Copyright 2017 Physicians Postgraduate Press, Inc.

Acute Effects of Zolpidem Extended-Release on Cognitive Performance and Sleep in Healthy Males After Repeated Nightly Use

PubMed Central

Kleykamp, Bethea A.; Griffiths, Roland R.; McCann, Una D.; Smith, Michael T.; Mintzer, Miriam Z.

2012-01-01

The extended-release formulation of zolpidem (Ambien CR®) is approved for the treatment of insomnia without a treatment duration limit. Acutely zolpidem impairs performance, and no research to date has examined whether tolerance develops to these performance impairments during nighttime awakening. The present double-blind, placebo-controlled study examined whether tolerance develops to zolpidem-induced acute performance impairment after repeated (22–30 days) nightly use. Effects of bedtime administration of zolpidem extended-release (ZOL; 12.5 mg) were tested on a battery of performance measures assessed during a forced nighttime awakening in 15 healthy male volunteers who completed overnight polysomnographic recording sessions in our laboratory at baseline and after approximately a month of at-home ZOL. As expected, bedtime ZOL administration was associated with changes in sleep architecture and impairments across all performance domains during nighttime testing (psychomotor function, attention, working memory, episodic memory, metacognition) with no residual next morning impairment. Tolerance did not develop to the observed ZOL-related impairments on any outcome. Possible evidence of acute abstinence effects following discontinuation of ZOL was observed on some performance and sleep outcomes. Overall, these findings suggest that performance is significantly impaired during nighttime awakening even after a month of nightly ZOL administration and these impairments could significantly impact safety should nighttime awakening require unimpaired functioning (e.g., driving; combat-related activities in the military). PMID:21928913

The Effects of Sleep Continuity Disruption on Positive Mood and Sleep Architecture in Healthy Adults.

PubMed

Finan, Patrick H; Quartana, Phillip J; Smith, Michael T

2015-11-01

The purpose of this study was to test an experimental model of the effects of sleep continuity disturbance on sleep architecture and positive mood in order to better understand the mechanisms linking insomnia and depression. Participants were randomized to receive 3 consecutive nights of sleep continuity disruption via forced nocturnal awakenings (FA, n = 21), or one of two control conditions: restricted sleep opportunity (RSO, n = 17) or uninterrupted sleep (US, n = 24). The study was set in an inpatient clinical research suite. Healthy, good-sleeping men and women were included. Polysomnography was used to measure sleep architecture, and mood was assessed via self-report each day. Compared to restricted sleep opportunity controls, forced awakenings subjects had significantly less slow wave sleep (P < 0.05) after the first night of sleep deprivation, and significantly lower positive mood (P < 0.05) after the second night of sleep deprivation. The differential change in slow wave sleep statistically mediated the observed group differences in positive mood (P = 0.002). To our knowledge, this is the first human experimental study to demonstrate that, despite comparable reductions in total sleep time, partial sleep loss from sleep continuity disruption is more detrimental to positive mood than partial sleep loss from delaying bedtime, even when controlling for concomitant increases in negative mood. With these findings, we provide temporal evidence in support of a putative biologic mechanism (slow wave sleep deficit) that could help explain the strong comorbidity between insomnia and depression. © 2015 Associated Professional Sleep Societies, LLC.

Sleep interacts with aβ to modulate intrinsic neuronal excitability.

PubMed

Tabuchi, Masashi; Lone, Shahnaz R; Liu, Sha; Liu, Qili; Zhang, Julia; Spira, Adam P; Wu, Mark N

2015-03-16

Emerging data suggest an important relationship between sleep and Alzheimer's disease (AD), but how poor sleep promotes the development of AD remains unclear. Here, using a Drosophila model of AD, we provide evidence suggesting that changes in neuronal excitability underlie the effects of sleep loss on AD pathogenesis. β-amyloid (Aβ) accumulation leads to reduced and fragmented sleep, while chronic sleep deprivation increases Aβ burden. Moreover, enhancing sleep reduces Aβ deposition. Increasing neuronal excitability phenocopies the effects of reducing sleep on Aβ, and decreasing neuronal activity blocks the elevated Aβ accumulation induced by sleep deprivation. At the single neuron level, we find that chronic sleep deprivation, as well as Aβ expression, enhances intrinsic neuronal excitability. Importantly, these data reveal that sleep loss exacerbates Aβ-induced hyperexcitability and suggest that defects in specific K(+) currents underlie the hyperexcitability caused by sleep loss and Aβ expression. Finally, we show that feeding levetiracetam, an anti-epileptic medication, to Aβ-expressing flies suppresses neuronal excitability and significantly prolongs their lifespan. Our findings directly link sleep loss to changes in neuronal excitability and Aβ accumulation and further suggest that neuronal hyperexcitability is an important mediator of Aβ toxicity. Taken together, these data provide a mechanistic framework for a positive feedback loop, whereby sleep loss and neuronal excitation accelerate the accumulation of Aβ, a key pathogenic step in the development of AD. Copyright © 2015 Elsevier Ltd. All rights reserved.

Frontal predominance of a relative increase in sleep delta and theta EEG activity after sleep loss in humans

NASA Technical Reports Server (NTRS)

Cajochen, C.; Foy, R.; Dijk, D. J.; Czeisler, C. A. (Principal Investigator)

1999-01-01

The effect of sleep deprivation (40 h) on topographic and temporal aspects of electroencephalographic (EEG) activity during sleep was investigated by all night spectral analysis in six young volunteers. The sleep-deprivation-induced increase of EEG power density in the delta and theta frequencies (1-7 Hz) during nonREM sleep, assessed along the antero-posterior axis (midline: Fz, Cz, Pz, Oz), was significantly larger in the more frontal derivations (Fz, Cz) than in the more parietal derivations (Pz, Oz). This frequency-specific frontal predominance was already present in the first 30 min of recovery sleep, and dissipated in the course of the 8-h sleep episode. The data demonstrate that the enhancement of slow wave EEG activity during sleep following extended wakefulness is most pronounced in frontal cortical areas.

Can standardized sleep questionnaires be used to identify excessive daytime sleeping in older post-acute rehabilitation patients?

PubMed

Skibitsky, Megan; Edelen, Maria Orlando; Martin, Jennifer L; Harker, Judith; Alessi, Cathy; Saliba, Debra

2012-02-01

Excessive daytime sleeping is associated with poorer functional outcomes in rehabilitation populations and may be improved with targeted interventions. The purpose of this study was to test simple methods of screening for excessive daytime sleeping among older adults admitted for postacute rehabilitation. Secondary analysis of data from 2 clinical samples. Two postacute rehabilitation (PAR) units in southern California. Two hundred twenty-six patients older than 65 years with Mini-Mental State Examination (MMSE) score higher than 11 undergoing rehabilitation. The primary outcome was excessive daytime sleeping, defined as greater than 15% (1.8 hours) of daytime hours (8 am to 8 pm) sleeping as measured by actigraphy. Participants spent, on average, 16.2% (SD 12.5%) of daytime hours sleeping as measured by actigraphy. Thirty-nine percent of participants had excessive daytime sleeping. The Pittsburgh Sleep Quality Index (PSQI) was significantly associated with actigraphically measured daytime sleeping (P = .0038), but the Epworth Sleepiness Scale (ESS) was not (P = .49). Neither the ESS nor the PSQI achieved sufficient sensitivity and specificity to be used as a screening tool for excessive daytime sleeping. Two additional models using items from these questionnaires were not significantly associated with the outcome. In an older PAR population, self-report items from existing sleep questionnaires do not identify excessive daytime sleeping. Therefore we recommend objective measures for the evaluation of excessive daytime sleeping as well as further research to identify new self-report items that may be more applicable in PAR populations. Copyright © 2012 American Medical Directors Association, Inc. Published by Elsevier Inc. All rights reserved.

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

The relevance of sleep abnormalities to chronic inflammatory conditions.

PubMed

Ranjbaran, Z; Keefer, L; Stepanski, E; Farhadi, A; Keshavarzian, A

2007-02-01

Sleep is vital to health and quality of life while sleep abnormalities are associated with adverse health consequences. Nevertheless, sleep problems are not generally considered by clinicians in the management of chronic inflammatory conditions (CIC) such as asthma, RA, SLE and IBD. To determine whether this practice is justified, we reviewed the literature on sleep and chronic inflammatory diseases, including effects of sleep on immune system and inflammation. We found that a change in the sleep-wake cycle is often one of the first responses to acute inflammation and infection and that the reciprocal effect of sleep on the immune system in acute states is often protective and restorative. For example, slow wave sleep can attenuate proinflammatory immune responses while sleep deprivation can aggravate those responses. The role of sleep in CIC is not well explored. We found a substantial body of published evidence that sleep disturbances can worsen the course of CIC, aggravate disease symptoms such as pain and fatigue, and increase disease activity and lower quality of life. The mechanism underlying these effects probably involves dysregulation of the immune system. All this suggests that managing sleep disturbances should be considered as an important factor in the overall management of CIC.

Exercise and sleep in aging: emphasis on serotonin.

PubMed

Melancon, M O; Lorrain, D; Dionne, I J

2014-10-01

Reductions in central serotonin activity with aging might be involved in sleep-related disorders in later life. Although the beneficial effects of aerobic exercise on sleep are not new, sleep represents a complex recurring state of unconsciousness involving many lines of transmitters which remains only partly clear despite intense ongoing research. It is known that serotonin released into diencephalon and cerebrum might play a key inhibitory role to help promote sleep, likely through an active inhibition of supraspinal neural networks. Several lines of evidence support the stimulatory effects of exercise on higher serotonergic pathways. Hence, exercise has proved to elicit acute elevations in forebrain serotonin concentrations, an effect that waned upon cessation of exercise. While adequate exercise training might lead to adaptations in higher serotonergic networks (desensitization of forebrain receptors), excessive training has been linked to serious brain serotonergic maladaptations accompanied by insomnia. Dietary supplementation of tryptophan (the only serotonin precursor) is known to stimulate serotonergic activity and promote sleep, whereas acute tryptophan depletion causes deleterious effects on sleep. Regarding sleep-wake regulation, exercise has proved to accelerate resynchronization of the biological clock to new light-dark cycles following imposition of phase shifts in laboratory animals. Noteworthy, the effect of increased serotonergic transmission on wake state appears to be biphasic, i.e. promote wake and thereafter drowsiness. Therefore, it might be possible that acute aerobic exercise would act on sleep by increasing activity of ascending brain serotonergic projections, though additional work is warranted to better understand the implication of serotonin in the exercise-sleep axis. Copyright © 2014 Elsevier Masson SAS. All rights reserved.

Neural Consequences of Chronic Short Sleep: Reversible or Lasting?

PubMed Central

Zhao, Zhengqing; Zhao, Xiangxiang; Veasey, Sigrid C.

2017-01-01

Approximately one-third of adolescents and adults in developed countries regularly experience insufficient sleep across the school and/or work week interspersed with weekend catch up sleep. This common practice of weekend recovery sleep reduces subjective sleepiness, yet recent studies demonstrate that one weekend of recovery sleep may not be sufficient in all persons to fully reverse all neurobehavioral impairments observed with chronic sleep loss, particularly vigilance. Moreover, recent studies in animal models demonstrate persistent injury to and loss of specific neuron types in response to chronic short sleep (CSS) with lasting effects on sleep/wake patterns. Here, we provide a comprehensive review of the effects of chronic sleep disruption on neurobehavioral performance and injury to neurons, astrocytes, microglia, and oligodendrocytes and discuss what is known and what is not yet established for reversibility of neural injury. Recent neurobehavioral findings in humans are integrated with animal model research examining long-term consequences of sleep loss on neurobehavioral performance, brain development, neurogenesis, neurodegeneration, and connectivity. While it is now clear that recovery of vigilance following short sleep requires longer than one weekend, less is known of the impact of CSS on cognitive function, mood, and brain health long term. From work performed in animal models, CSS in the young adult and short-term sleep loss in critical developmental windows can have lasting detrimental effects on neurobehavioral performance. PMID:28620347

Neural Consequences of Chronic Short Sleep: Reversible or Lasting?

PubMed

Zhao, Zhengqing; Zhao, Xiangxiang; Veasey, Sigrid C

2017-01-01

Approximately one-third of adolescents and adults in developed countries regularly experience insufficient sleep across the school and/or work week interspersed with weekend catch up sleep. This common practice of weekend recovery sleep reduces subjective sleepiness, yet recent studies demonstrate that one weekend of recovery sleep may not be sufficient in all persons to fully reverse all neurobehavioral impairments observed with chronic sleep loss, particularly vigilance. Moreover, recent studies in animal models demonstrate persistent injury to and loss of specific neuron types in response to chronic short sleep (CSS) with lasting effects on sleep/wake patterns. Here, we provide a comprehensive review of the effects of chronic sleep disruption on neurobehavioral performance and injury to neurons, astrocytes, microglia, and oligodendrocytes and discuss what is known and what is not yet established for reversibility of neural injury. Recent neurobehavioral findings in humans are integrated with animal model research examining long-term consequences of sleep loss on neurobehavioral performance, brain development, neurogenesis, neurodegeneration, and connectivity. While it is now clear that recovery of vigilance following short sleep requires longer than one weekend, less is known of the impact of CSS on cognitive function, mood, and brain health long term. From work performed in animal models, CSS in the young adult and short-term sleep loss in critical developmental windows can have lasting detrimental effects on neurobehavioral performance.

Impact of a Mindfulness-Based Weight-Loss Intervention on Sleep Quality Among Adults with Obesity: Data from the SHINE Randomized Controlled Trial.

PubMed

Adler, Elizabeth; Dhruva, Anand; Moran, Patricia J; Daubenmier, Jennifer; Acree, Michael; Epel, Elissa S; Bacchetti, Peter; Prather, Aric A; Mason, Ashley; Hecht, Frederick M

2017-03-01

Sleep disturbance is a common problem among adults with obesity. Mindfulness interventions have been shown to improve sleep quality in various populations but have not been investigated in adults with obesity. The aim of this study was to compare the effects of a mindfulness-based weight-loss intervention with an active control on self-reported sleep quality among adults with obesity. This study was a secondary analysis of a randomized controlled trial and included 194 adults with a body mass index in the range 30-45 kg/m 2 . The treatment intervention included mindfulness-based eating and stress-management practices, and the active control intervention included training in progressive muscle relaxation (PMR). Both groups received identical diet and exercise guidelines in 17 group sessions conducted over 5.5 months that were matched for time, attention, and social support. The primary outcome of this analysis was between-group change in self-reported sleep quality, which was assessed using the Pittsburgh Sleep Quality Index (PSQI) global score at baseline and at 6, 12, and 18 months. Between-group differences in mean PSQI change scores in the mindfulness group (n = 100) compared to the control group (n = 94) were -0.27 (-0.68, 1.22; p = 0.58) at 6 months, -0.57 (-0.35, 1.50; p = 0.22) at 12 months, and -0.50 (-0.53, 1.53; p = 0.34) at 18 months, all in the direction of more sleep improvement in the mindfulness group but none reaching statistical significance. In the mindfulness group, average weekly minutes of meditation practice time was associated with improved sleep quality from baseline to 6 months. No statistically significant evidence was found that a weight-loss program that incorporates mindfulness improves self-reported sleep quality compared to a control diet/exercise intervention that included PMR. Within the mindfulness group, average weekly minutes of mindfulness practice was associated with improved sleep quality.

Sleep Deprivation and the Epigenome.

PubMed

Gaine, Marie E; Chatterjee, Snehajyoti; Abel, Ted

2018-01-01

Sleep deprivation disrupts the lives of millions of people every day and has a profound impact on the molecular biology of the brain. These effects begin as changes within a neuron, at the DNA and RNA level, and result in alterations in neuronal plasticity and dysregulation of many cognitive functions including learning and memory. The epigenome plays a critical role in regulating gene expression in the context of memory storage. In this review article, we begin by describing the effects of epigenetic alterations on the regulation of gene expression, focusing on the most common epigenetic mechanisms: (i) DNA methylation; (ii) histone modifications; and (iii) non-coding RNAs. We then discuss evidence suggesting that sleep loss impacts the epigenome and that these epigenetic alterations might mediate the changes in cognition seen following disruption of sleep. The link between sleep and the epigenome is only beginning to be elucidated, but clear evidence exists that epigenetic alterations occur following sleep deprivation. In the future, these changes to the epigenome could be utilized as biomarkers of sleep loss or as therapeutic targets for sleep-related disorders.

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

Sleep apnoea is a risk factor for acute kidney injury after coronary artery bypass grafting.

PubMed

Kua, Jieli; Zhao, Liang-Ping; Kofidis, Theodoros; Chan, Siew-Pang; Yeo, Tiong-Cheng; Tan, Huay-Cheem; Lee, Chi-Hang

2016-04-01

Acute kidney injury (AKI) is a common complication in patients who undergo coronary artery bypass grafting (CABG). Sleep apnoea is associated with sympathetic activation, inflammatory reaction and plaque burden. The possible status of sleep apnoea as a risk factor for AKI after CABG has not been studied. We recruited 169 patients for an overnight sleep study using a Food and Drug Administration-approved portable device before they underwent elective CABG. AKI after CABG was defined as a relative increase of greater than 25% or an absolute increase of greater than 0.5 mg/dl in the serum creatinine level from baseline within 5 days after CABG. A generalized structural equation model (gSEM) was then applied to ascertain whether sleep apnoea, defined as an Apnoea-Hypopnoea index (AHI) of 15 or higher, was associated with AKI after CABG after adjusting for the effects of confounding variables. Of the 150 patients (88.8%) who completed the study, the incidence of AKI after CABG was 22.7%. The mean AHI was higher in the AKI group (27.4 ± 19.8) than that in the non-AKI group (18.3 ± 16.5; P < 0.01). The prevalence of sleep apnoea was higher in the AKI group (64.7%) than that in the non-AKI group (45.7%; P = 0.05). The patients in the AKI group were older (P < 0.01) and shorter (P = 0.03) and had higher systolic blood pressures (P = 0.01), greater waist circumferences (P = 0.04) and larger left atrial diameters (P < 0.01) than those in the non-AKI group. The patients in the AKI group had higher serum haemoglobin levels (P = 0.04) and lower glucose levels (P < 0.01) than those in the non-AKI group. A gSEM based on binomial distributions showed that sleep apnoea was an independent predictor of AKI after CABG (adjusted odds ratio, 2.89; confidence interval, 1.09-7.09; P = 0.03) after adjustment for the effects of haemoglobin, glucose levels, the left atrial diameter and systolic blood pressure. Sleep apnoea is prevalent and is associated with AKI after CABG. The data

The Effects of Sleep Continuity Disruption on Positive Mood and Sleep Architecture in Healthy Adults

PubMed Central

Finan, Patrick H.; Quartana, Phillip J.; Smith, Michael T.

2015-01-01

Objective: The purpose of this study was to test an experimental model of the effects of sleep continuity disturbance on sleep architecture and positive mood in order to better understand the mechanisms linking insomnia and depression. Design: Participants were randomized to receive 3 consecutive nights of sleep continuity disruption via forced nocturnal awakenings (FA, n = 21), or one of two control conditions: restricted sleep opportunity (RSO, n = 17) or uninterrupted sleep (US, n = 24). Setting: The study was set in an inpatient clinical research suite. Participants: Healthy, good-sleeping men and women were included. Measurement and Results: Polysomnography was used to measure sleep architecture, and mood was assessed via self-report each day. Compared to restricted sleep opportunity controls, forced awakenings subjects had significantly less slow wave sleep (P < 0.05) after the first night of sleep deprivation, and significantly lower positive mood (P < 0.05) after the second night of sleep deprivation. The differential change in slow wave sleep statistically mediated the observed group differences in positive mood (P = 0.002). Conclusions: To our knowledge, this is the first human experimental study to demonstrate that, despite comparable reductions in total sleep time, partial sleep loss from sleep continuity disruption is more detrimental to positive mood than partial sleep loss from delaying bedtime, even when controlling for concomitant increases in negative mood. With these findings, we provide temporal evidence in support of a putative biologic mechanism (slow wave sleep deficit) that could help explain the strong comorbidity between insomnia and depression. Citation: Finan PH, Quartana PJ, Smith MT. The effects of sleep continuity disruption on positive mood and sleep architecture in healthy adults. SLEEP 2015;38(11):1735–1742. PMID:26085289

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

Differential modulation of global and local neural oscillations in REM sleep by homeostatic sleep regulation.

PubMed

Kim, Bowon; Kocsis, Bernat; Hwang, Eunjin; Kim, Youngsoo; Strecker, Robert E; McCarley, Robert W; Choi, Jee Hyun

2017-02-28

Homeostatic rebound in rapid eye movement (REM) sleep normally occurs after acute sleep deprivation, but REM sleep rebound settles on a persistently elevated level despite continued accumulation of REM sleep debt during chronic sleep restriction (CSR). Using high-density EEG in mice, we studied how this pattern of global regulation is implemented in cortical regions with different functions and network architectures. We found that across all areas, slow oscillations repeated the behavioral pattern of persistent enhancement during CSR, whereas high-frequency oscillations showed progressive increases. This pattern followed a common rule despite marked topographic differences. The findings suggest that REM sleep slow oscillations may translate top-down homeostatic control to widely separated brain regions whereas fast oscillations synchronizing local neuronal ensembles escape this global command. These patterns of EEG oscillation changes are interpreted to reconcile two prevailing theories of the function of sleep, synaptic homeostasis and sleep dependent memory consolidation.

Sleep deprivation: a mind-body approach.

PubMed

Aguirre, Claudia C

2016-11-01

The purpose of this review is to summarize recent advances in our understanding of the impact sleep disturbances have on our health, with particular focus on the brain. The present review considers the influence of sleep disturbance on the neurovascular unit; the role of sleep disturbance in neurodegenerative diseases; and relevant strategies of neuro-immuno-endocrine interactions that likely contribute to the restorative power of sleep. Given the latest discoveries about the brain's waste clearance system and its relationship to neurodegenerative diseases like Alzheimer's disease, this review gives a brief overview on the molecular mechanisms behind sleep loss-related impairments. Recent evidence indicates that sleep plays a vital role in neuro-immuno-endocrine homeostasis. Sleep loss has been linked to elevated risks for cognitive and mood disorders, underscored by impaired synaptic transmission. The glymphatic system has been shown to be modulated by sleep and implicated in neurodegenerative disorders. Interactions between sleep quality, the immune system, and neurodegenerative disease are complex and a challenge to distil. These interactions are frequently bidirectional, because of sleep's characterization as an early symptom and as a potential factor contributing to the development and progression of mood and cognitive disorders. VIDEO ABSTRACT.

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

Working Memory, Sleep, and Hearing Problems in Patients with Tinnitus and Hearing Loss Fitted with Hearing Aids.

PubMed

Zarenoe, Reza; Hällgren, Mathias; Andersson, Gerhard; Ledin, Torbjörn

2017-02-01

Tinnitus is a common condition and there is a need to evaluate effects of tinnitus management in relation to moderating factors such as degree of hearing loss. As it is possible that tinnitus influences concentration, and thus is likely to disturb cognitive processing, the role of cognitive functioning also needs to be investigated. To compare a group of patients with sensorineural hearing loss and tinnitus to a control group with only sensorineural hearing loss (and no tinnitus). To investigate working memory, sleep, and hearing problems measured before and after hearing rehabilitation. A prospective study. The sample consisted of 100 patients, 50 with hearing loss and tinnitus, and 50 controls with hearing loss but no tinnitus. All patients were between 40 and 82 yr old and had a pure-tone average (PTA; average of 0.5, 1, 2, and 4 kHz) <70 dB HL. Patients were tested before and after rehabilitation with hearing aids with regard to their working memory capacity, sleep quality, hearing problems, speech recognition, and tinnitus annoyance. Eight patients dropped out of the study. Thus, a total of 92 patients were included for analysis, with 46 in each group. As a consequence of unplanned age and PTA differences between the groups, an age-matched subsample (n = 30 + 30) was selected for further analysis. Tests including the Reading Span, Hearing-in-Noise Test (HINT), Tinnitus Handicap Inventory (THI), Hearing Handicap Inventory for the Elderly (HHIE), and Pittsburgh Sleep Quality Index (PSQI) were administered before and after hearing aid rehabilitation. There were no between-group differences at baseline in the full sample (n = 92), with the exception of the THI (p < 0.001) and the PSQI (p < 0.002), on which the hearing loss and tinnitus group had significantly higher scores. Pre/post changes were significant for both groups on the Reading Span, and HHIE. However, these improvements were significantly larger for the patients in the hearing loss and tinnitus group on

Auto-titrating continuous positive airway pressure treatment for obstructive sleep apnoea after acute quadriplegia (COSAQ): study protocol for a randomized controlled trial.

PubMed

Berlowitz, David J; Ayas, Najib; Barnes, Maree; Brown, Douglas J; Cistulli, Peter A; Geraghty, Tim; Graham, Alison; Lee, Bonsan Bonne; Morris, Meg; O'Donoghue, Fergal; Rochford, Peter D; Ross, Jack; Singhal, Balraj; Spong, Jo; Wadsworth, Brooke; Pierce, Robert J

2013-06-19

Quadriplegia is a severe, catastrophic injury that predominantly affects people early in life, resulting in lifelong physical disability. Obstructive sleep apnoea is a direct consequence of quadriplegia and is associated with neurocognitive deficits, sleepiness and reduced quality of life. The usual treatment for sleep apnoea is nasal continuous positive airway pressure (CPAP); however, this is poorly tolerated in quadriplegia. To encourage patients to use this therapy, we have to demonstrate that the benefits outweigh the inconvenience. We therefore propose a prospective, multinational randomized controlled trial of three months of CPAP for obstructive sleep apnoea after acute quadriplegia. Specialist spinal cord injury centres across Australia, New Zealand, the UK and Canada will recruit medically stable individuals who have sustained a (new) traumatic quadriplegia (complete or incomplete second cervical to first thoracic level lesions). Participants will be screened for obstructive sleep apnoea using full, portable sleep studies. Those with an apnoea hypopnoea index greater than 10 per hour will proceed to an initial three-night trial of CPAP. Those who can tolerate CPAP for at least 4 hours on at least one night of the initial trial will be randomized to either usual care or a 3-month period of auto-titrating CPAP. The primary hypothesis is that nocturnal CPAP will improve neuropsychological functioning more than usual care alone. The secondary hypothesis is that the magnitude of improvement of neuropsychological function will be predicted by the severity of baseline sleepiness measures, sleep fragmentation and sleep apnoea. Neuropsychological tests and full polysomnography will be performed at baseline and 3 months with interim measures of sleepiness and symptoms of autonomic dysfunction measured weekly. Spirometry will be performed monthly. Neuropsychological tests will be administered by blinded assessors. Recruitment commenced in July 2009. The results of

Auto-titrating continuous positive airway pressure treatment for obstructive sleep apnoea after acute quadriplegia (COSAQ): study protocol for a randomized controlled trial

PubMed Central

2013-01-01

Background Quadriplegia is a severe, catastrophic injury that predominantly affects people early in life, resulting in lifelong physical disability. Obstructive sleep apnoea is a direct consequence of quadriplegia and is associated with neurocognitive deficits, sleepiness and reduced quality of life. The usual treatment for sleep apnoea is nasal continuous positive airway pressure (CPAP); however, this is poorly tolerated in quadriplegia. To encourage patients to use this therapy, we have to demonstrate that the benefits outweigh the inconvenience. We therefore propose a prospective, multinational randomized controlled trial of three months of CPAP for obstructive sleep apnoea after acute quadriplegia. Methods/design Specialist spinal cord injury centres across Australia, New Zealand, the UK and Canada will recruit medically stable individuals who have sustained a (new) traumatic quadriplegia (complete or incomplete second cervical to first thoracic level lesions). Participants will be screened for obstructive sleep apnoea using full, portable sleep studies. Those with an apnoea hypopnoea index greater than 10 per hour will proceed to an initial three-night trial of CPAP. Those who can tolerate CPAP for at least 4 hours on at least one night of the initial trial will be randomized to either usual care or a 3-month period of auto-titrating CPAP. The primary hypothesis is that nocturnal CPAP will improve neuropsychological functioning more than usual care alone. The secondary hypothesis is that the magnitude of improvement of neuropsychological function will be predicted by the severity of baseline sleepiness measures, sleep fragmentation and sleep apnoea. Neuropsychological tests and full polysomnography will be performed at baseline and 3 months with interim measures of sleepiness and symptoms of autonomic dysfunction measured weekly. Spirometry will be performed monthly. Neuropsychological tests will be administered by blinded assessors. Recruitment commenced in

What may cause fetus loss from acute pancreatitis in pregnancy: Analysis of 54 cases.

PubMed

Tang, Min; Xu, Jian-Ming; Song, Sha-Sha; Mei, Qiao; Zhang, Li-Jiu

2018-02-01

Acute pancreatitis in pregnancy (APIP) poses a serious threat to the mother and her fetus, and might lead to fetal loss including miscarriage and stillbirth in certain patients. We sought to identify possible factors that affect fetal distress and evaluated outcomes of patients with APIP.We retrospectively reviewed clinical records of 54 pregnant women with APIP, who were treated at 2 tertiary clinical centers over a 6-year period. Clinical characteristics including etiology and severity of APIP, fetal monitoring data, and maternofetal outcomes were analyzed.Etiology of APIP included acute biliary pancreatitis (ABP, n = 14), hyperlipidemic pancreatitis (HLP, n = 22), and other etiologies (n = 18). Severity was classified as mild acute pancreatitis (MAP, n = 23), moderately severe acute pancreatitis (MSAP, n = 24), and severe acute pancreatitis (SAP, n = 7). The incidence of preterm delivery, fetal distress, and fetal loss increased with the progression of severity of APIP (P < .05). The severity of HLP was significantly higher than that of ABP and APIP of other etiology (P < .01). HLP was more likely to lead to fetal distress than other APs (P < .01). Only 12 (22.2%) patients had fetal monitoring including non-stress test (NST); 1 case of SAP (14.3%) and 15 cases of MSAP (62.5%) were not transferred to intensive care unit for intensive monitoring.The incidence of fetal distress and fetal loss increased with worsening of APIP severity. HLP tends to result in worse fetal outcomes. The deficiencies of fetal state monitoring, lack of assessment, and management of pregnant women might increase the fetal loss in APIP.