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Abstract: Sleep has been found to have wide-ranging effects on sports performance and overall well-being. Recent research has found evidence relating chronic suboptimal sleep with the risk of musculoskeletal pain and sports injury. The amount of sleep that consistently has been found to be associated with increased risk of injury is ≤7 h of sleep, which when sustained for periods of at least 14 d has been associated with 1.7 times greater risk of musculoskeletal injury. However, it is unknown if sleep loss predisposes the athlete to specific types of musculoskeletal injuries. The role of sleep on musculoskeletal pain is important to understand as studies in both children and adults have found that suboptimal sleep more consistently predicts next-day pain as compared with pain predicting subsequent sleep loss. Despite the evidence that certain aspects of sleep behavior seem to increase the risk of musculoskeletal injury and pain, sleep should be considered as only a part of the athlete's overall health and well-being when assessing the athlete for risk of injury. [ABSTRACT FROM AUTHOR]

The sleep-wake cycle regulates interstitial fluid (ISF) and cerebrospinal fluid (CSF) levels of b-amyloid (Ab) that accumulates in Alzheimer’s disease (AD). Furthermore, chronic sleep deprivation (SD) increases Ab plaques. However, tau, not Ab, accumulation appears to drive AD neurodegeneration. We tested whether ISF/CSF tau and tau seeding and spreading were influenced by the sleep-wake cycle and SD. Mouse ISF tau was increased ~90% during normal wakefulness versus sleep and ~100% during SD. Human CSF tau also increased more than 50% during SD. In a tau seeding-and-spreading model, chronic SD increased tau pathology spreading. Chemogenetically driven wakefulness in mice also significantly increased both ISF Ab and tau. Thus, the sleep-wake cycle regulates ISF tau, and SD increases ISF and CSF tau as well as tau pathology spreading. [ABSTRACT FROM AUTHOR]

The main objective of the study was to analyze the impact of sleep deprivation upon hemodynamic and autonomic parameters in subjects with normal blood pressure (BP) compared to prehypertension and hypertension at 24, 28, and 32 h of total sleep deprivation (TSD). Thirty volunteers, healthy men with current medical tests indicating the absence of disease took part in the study. After physical examination (basic neurological, clinical examination, echocardiography and doppler ultrasound of the renal arteries, evaluation of the autonomic nervous system) subjects were divided into three groups: I – normotensive, II – pre-hypertensive, III – hypertensive (age: 31.2 ± 2.1 vs. 33.5 ± 2.7 vs. 36.8 ± 2.7 years, p > 0.05; BMI: 25.2 ± 0.8 vs. 29.0 ± 1.5 vs. 26.4 ± 1.0 kg/m2, p > 0.05). Hemodynamic and autonomic parameters were automatically measured at rest and in a tilted position with a Task Force Monitor. The Task Force Monitor consists of electrocardiography, impedance cardiography, oscillometric, and continuous BP measurement. Mixed models with random effects was applied in order to analyze the parameters' dependence on the time and the group of patients. One-way ANOVA or Kruskal–Wallis test were used to detect differences between normotensive, pre-hypertensive and hypertensive groups in each time point. In the pre-hypertensive group 28-h TSD resulted in increased vagal outflow [changes in high frequency heart rate (HR) variability, p = 0.0189], as evidenced by decreased HR (p = 0.0293). Moreover after 24-h TSD and 28-h TSD we observed changes in BP parameters. In hypertensive group, the most important changes in hemodynamic parameters: systolic blood pressure (sBP, p = 0.0031), diastolic blood pressure (dBP, p = 0.0136), cardiac output (CO, p = 0.0439) and changes in HR (p = 0.0063) after tilt test were observed after 32-h TSD. In conclusion, our results show that changes in hemodynamic parameters during sleep deprivation depend on the baseline BP and duration of TSD. What is important, both groups reported a decrease of sBP and dBP during the TSD (pre-hypertensive group after 24, 28-h TSD; hypertensive group after 32-h TSD. In our opinion, this is the first study which considers three homogenous groups in terms of gender: only men, during different points of acute TSD: 24, 28, and 32 h of TSD in laboratory condition. [ABSTRACT FROM AUTHOR]

Stress, a ubiquitous part of daily human life, has varied biological effects which are increasingly recognized as including modulation of commensal microorganisms residing in the gastrointestinal tract, the gut microbiota. In turn, the gut microbiota influences the host stress response and associated sequelae, thereby implicating the gut microbiota as an important mediator of host health. This narrative review aims to summarize evidence concerning the impact of psychological, environmental, and physical stressors on gut microbiota composition and function. The stressors reviewed include psychological stress, circadian disruption, sleep deprivation, environmental extremes (high altitude, heat, and cold), environmental pathogens, toxicants, pollutants, and noise, physical activity, and diet (nutrient composition and food restriction). Stressors were selected for their direct relevance to military personnel, a population that is commonly exposed to these stressors, often at extremes, and in combination. However, the selected stressors are also common, alone or in combination, in some civilian populations. Evidence from preclinical studies collectively indicates that the reviewed stressors alter the composition, function and metabolic activity of the gut microbiota, but that effects vary across stressors, and can include effects that may be beneficial or detrimental to host health. Translation of these findings to humans is largely lacking at present. This gap precludes concluding with certainty that transient or cumulative exposures to psychological, environmental, and physical stressors have any consistent, meaningful impact on the human gut microbiota. However, provocative preclinical evidence highlights a need for translational research aiming to elucidate the impact of stressors on the human gut microbiota, and how the gut microbiota can be manipulated, for example by using nutrition, to mitigate adverse stress responses. [ABSTRACT FROM AUTHOR]

Objectives To our knowledge, the influence of sleep deprivation on hearing levels has yet to be assessed in animals. Therefore, we evaluated whether auditory function was affected by sleep deprivation in rats. Methods Male Wistar rats (aged 9 weeks, weighing 300–400 g) were used for the study and were randomly assigned to a control (n = 15) or sleep deprivation group (n = 12). Hearing levels were evaluated at baseline and 9 days after sleep deprivation using auditory evoked brainstem responses (ABRs) and distortion product otoacoustic emission (DPOAE) measurements. Blood was collected for the measurement of interleukin-1β and corticosterone levels. Results The ABR thresholds (at 8, 16, and 32 kHz) at 9 days were significantly elevated in the sleep deprivation group compared to the control group ( p  < 0.05, respectively). The sleep deprivation group showed a defect in the function of outer hair cells, as evidenced by decreased levels of distortion product otoacoustic emission. IL-1β was significantly increased in the sleep deprivation group. Sleep-deprived rats exhibited rupture of Reissner's membrane and morphological damage to stereocilia. Conclusion These results suggest that sleep deprivation induces damage to the cochlea and results in hearing loss in Wistar rats. [ABSTRACT FROM AUTHOR]

Lack of sleep has a considerable impact on vigilance: we perform worse, we make more errors, particularly at night, when we should be sleeping. Measures of brain functional connectivity suggest that decrease in vigilance during sleep loss is associated with an impaired cross-talk within the fronto-parietal cortex. However, fronto-parietal effective connectivity, which is more closely related to the causal cross-talk between brain regions, remains unexplored during prolonged wakefulness. In addition, no study has simultaneously investigated brain effective connectivity and wake-related changes in vigilance, preventing the concurrent incorporation of the two aspects. Here, we used electroencephalography (EEG) to record responses evoked by Transcranial Magnetic Stimulation (TMS) applied over the frontal lobe in 23 healthy young men (18–30 yr.), while they simultaneously performed a vigilance task, during 8 sessions spread over 29 h of sustained wakefulness. We assessed Response Scattering (ReSc), an estimate of effective connectivity, as the propagation of TMS-evoked EEG responses over the fronto-parietal cortex. Results disclose a significant change in fronto-parietal ReSc with time spent awake. When focusing on the night-time period, when one should be sleeping, participants with lower fronto-parietal ReSc performed worse on the vigilance task. Conversely, no association was detected during the well-rested, daytime period. Night-time fronto-parietal ReSc also correlated with objective EEG measures of sleepiness and alertness. These changes were not accompanied by variations in fronto-parietal response complexity. These results suggest that decreased brain response propagation within the fronto-parietal cortex is associated to increased vigilance failure during night-time prolonged wakefulness. This study reveals a novel facet of the detrimental effect on brain function of extended night-time waking hours, which is increasingly common in our societies. [ABSTRACT FROM AUTHOR]

INTRODUCTION: Sleep loss can result in cognitive, motor, and neurobehavioral impairments. In an aviation context, this can cause a serious threat to flight safety. Therefore, the study aimed to investigate the effects of 24-h sleep deprivation on mood, fatigue, and airline pilot competencies. METHODS: Seven subjects attended two 24-h testing periods, one with an 8-h sleep opportunity, and the other with no sleep opportunity (i.e., sleep deprivation). Subjects were required to complete a battery of mood, fatigue, and analogue measures of pilot competency tasks every 8 h (0 h, 8 h, 16 h, 24 h) throughout each testing period. RESULTS: While total mood disturbance was found to significantly increase (83.42, SD = 25.7), both objective (352.71, SD = 42.00) and subjective (34.85, SD = 8.82) fatigue were found to significantly decrease following 24-h sleep deprivation. Cognitive flexibility (757.45, SD = 58.48) and hand-eye coordination (dominant hand only) (60.28, SD = 3.86) were also negatively impacted following 24-h sleep deprivation. However, working memory and situation awareness were not significantly negatively impacted by the bout of sleep deprivation. DISCUSSION: Some pilot-specific task-related factors such as subjective fatigue, cognitive flexibility, and working memory were found to be particularly susceptible to sleep loss, with significant declines in performance observed following 16-h continuous wakefulness, suggesting reductions in optimal functioning following this period of wakefulness. Further investigation using more regular testing time points, employing additional pilot competencies, and using more aviation-specific tasks is warranted. [ABSTRACT FROM AUTHOR]

Background: Sleep deprivation is known to diminish postural control.Research Question: We investigated whether sleep deprivation affects sensory reweighting for postural control due to loss of visual and proprioceptive cues.Methods: Two cohorts of cadet pilots were deprived of sleep for 40 h. Variabilty in force-platform center of pressure was analyzed based on the whole path length (WPL); circumference area (CA); mean of displacement along x and y axes and corresponding standard deviations (SDx, SDy); and frequency of body-sway intensity, all of which were recorded while the cadets stood with eyes open (NEO), eyes closed (NEC), and eyes closed on a foam platform base (FEC) A sleepiness index (SUBI) based on principal component analysis of selected Cohort 1 data (n = 37) was used to compare Cohort 2 data (n = 29) with scores for the Stanford Sleepiness Scale (SSS) and Pittsburg Sleep Quality Index (PSQI).Results: Balance began to deteriorate at 16 h for NEO and at 28 h for NEC and FEC (p < 0.05). At 40 h, WPL, CA, and SDy of COP for NEO indicated balance deteriorated further while WPL and SDy for NEC and WPL, CA, SDx, and SDy for FEC indicated balance incrementally improved. Frequency bias of body-sway differed between NEO, NEC, and FEC. In Cohort 2, the SUBI correlated significantly with SSS (p < 0.05), but not with PSQI.Significance: Effects of sleep deprivation were mitigated over time, suggesting that compensatory mechanisms influenced sensory reweighting for NEC and FEC between 28 and 40 h of sleep deprivation, but not for NEO. Frequency bias of body-sway suggested that sensory reweighting in the absence of visual cues differed from that in the absence of both visual and proprioceptive cues. [ABSTRACT FROM AUTHOR]

Many studies have shown the effects of sleep deprivation in several aspects of health and disease. However, little is known about how mitochondrial bioenergetics function is affected under this condition. To clarify this, we developed a simple model of short-term sleep deprivation, in which fruit-flies were submitted to a nocturnal light condition and then mitochondrial parameters were assessed by high resolution respirometry (HRR). Exposure of flies to constant light was able to alter sleep patterns, causing locomotor deficits, increasing ROS production and lipid peroxidation, affecting mitochondrial activity, antioxidant defense enzymes and caspase activity. HRR analysis showed that sleep deprivation affected mitochondrial bioenergetics capacity, decreasing respiration at oxidative phosphorylation (OXPHOS) and electron transport system (ETS). In addition, the expression of genes involved in the response to oxidative stress and apoptosis were increased. Thus, our results suggest a connection between sleep deprivation and oxidative stress, pointing to mitochondria as a possible target of this relationship. [ABSTRACT FROM AUTHOR]

Sleep deprivation (SD) and amphetamine use are commonly associated conditions. SD shares similar neurobiological effects with psychostimulants, playing an important role in drug addiction, especially through conditioning manipulations. The aim of the present study was to investigate the effects of SD on the development of amphetamine-induced conditioned place preference (CPP) in a protocol with a reduced number of conditioning sessions. Male adult Wistar rats were submitted to 4 conditioning sessions (2 sessions/day) in the CPP apparatus, half with saline (non-drug-paired compartment) and half with 2 mg/kg amphetamine (drug-paired compartment) after control (home-cage maintained) or SD (6 h gentle handling method) conditions. Control animals did not express a preference for the amphetamine-paired compartment, showing that 2 conditioning sessions with the drug were not sufficient to establish CPP. On the other hand, animals submitted to SD during the conditioning sessions expressed a preference for the amphetamine-paired compartment, which was maintained across the entire test session. SD precipitated the development of CPP to amphetamine, showing that lack of sleep can contribute to the establishment of a conditioning between the drug effect and environmental cues. [ABSTRACT FROM AUTHOR]

The article focuses on the role of sleep for learning, memory consolidation and information processing in adolescence focusing on the impact of sleep disruption on their learning. Topics include circadian rhythms of sleep and sleep/wake cycle, changes in human chronotype during adolescence, and the impact of the social jet on the academic performance of undergraduates.

Sleep deprivation has severe consequences for higher nervous functions. Its effects on neuronal excitability may be one of the most important factors underlying functional deterioration caused by sleep loss. In the present work, excitability changes were studied using two complementary in vivo and ex viv o models. Auditory evoked potentials were recorded from freely-moving animals in vivo. Amplitude of evoked responses showed a near-continuous decrease during deprivation. Prevention of sleep also reduced synaptic efficacy ex vivo , measured from brain slices derived from rats that underwent sleep deprivation. While seizure susceptibility was not affected significantly by sleep deprivation in these preparations, the pattern of spontaneous seizure activity was altered. If seizures developed, they lasted longer and tended to contain more spikes in slices obtained from sleep-deprived than from control rats. Current-source density analysis revealed that location and sequence of activation of local cortical networks recruited by seizures did not change by sleep deprivation. Moderate differences seen in the amplitude of individual sinks and sources might be explained by smaller net transmembrane currents as a consequence of decreased excitability. These findings contradict the widely accepted conception of synaptic homeostasis suggesting gradual increase of excitability during wakefulness. Our results also indicate that decreased neuronal excitability caused by sleep deprivation is preserved in slices prepared from rats immediately after deprivation. This observation might mean new opportunities to explore the effects of sleep deprivation in ex vivo preparations that allow a wider range of experimental manipulations and more sophisticated methods of analysis than in vivo preparations. [ABSTRACT FROM AUTHOR]

Lack of adequate sleep has become increasingly common in our 24/7 society. Unfortunately diminished sleep has significant health consequences including metabolic and cardiovascular disease and mental disorders including depression. The pathways by which reduced sleep adversely affects physiology and behavior are unknown. We found that 6 h of sleep deprivation in adult male rats induces changes in neuronal activity in the lateral hypothalamus, the paraventricular nucleus, the arcuate nucleus and the mammillary bodies. Surprisingly, these alterations last for up to 48 h. The data show that sleep loss has prolonged effects on the activity of multiple hypothalamic areas. Our data indicate also that measuring electroencephalographic slow wave activity underestimates the amount of time that the hypothalamus requires to recover from episodes of sleep deprivation. We propose that these hypothalamic changes underlie the well-established relationship between sleep loss and several diseases such as metabolic disorders, stress and depression and that sufficient sleep is vital for autonomic functions controlled by the hypothalamus. [ABSTRACT FROM AUTHOR]

Sleep is essential for proper brain function in mammals and insects. During sleep, animals are disconnected from the external world; they show high arousal thresholds and changed brain activity. Sleep deprivation results in a sleep rebound. Research using the fruit fly, Drosophila melanogaster, has helped us understand the genetic and neuronal control of sleep. Genes involved in sleep control code for ion channels, factors influencing neurotransmission and neuromodulation, and proteins involved in the circadian clock. The neurotransmitters/neuromodulators involved in sleep control are GABA, dopamine, acetylcholine, serotonin, and several neuropeptides. Sleep is controlled by the interplay between sleep homeostasis and the circadian clock. Putative sleep-wake centers are located in higher-order brain centers that are indirectly connected to the circadian clock network. The primary function of sleep appears to be the downscaling of synapses that have been built up during wakefulness. Thus, brain homeostasis is maintained and learning and memory are assured. [ABSTRACT FROM AUTHOR]

The aim of this study was to explore the association between sleep-related problems with the occurrence of minor psychiatric disorders in shift workers of southern Brazil. A cross-sectional study with 1202 workers (785 females) aged 18–50 years was carried out. Minor psychiatric disorders were assessed using the Self-Reporting Questionnaire (SRQ-20), and four sleep problems were collected and analyzed: sleep deprivation (≤ 5 h), difficulty falling asleep, waking up during sleep, and sleep medication use. Results show that the overall prevalence of minor psychiatric disorders was 26.8%, but it was more prevalent among females than males (30.2% vs. 20.4%). Nightshift work was significantly associated with the occurrence of sleep-related problems. After adjusting for confounding factors, the number of sleep-related problems showed a positive linear trend with psychiatric disorders in both sexes. Having two or more sleep-related problems was associated with increased probability of psychiatric disorders approximately three-fold among males and two-fold among females, when compared with those without sleep problems. In conclusion, this study demonstrated that sleep-related problems have a strong and independent association with psychiatric disorders among shift workers. Furthermore, the prevalence of both conditions was higher among females than males; however, the strength of these associations was higher in males. [ABSTRACT FROM AUTHOR]

Objectives Aircraft, road, and rail traffic noise can cause sleep disturbances. Since night work and shorter sleep durations have been linked to increased risks of breast cancer, we examined if 24-hour, or day- or night-time traffic noise exposure may also increase the risk of breast cancer. Methods To investigate the noise-related risks of breast cancer, the pseudonymized insurance records of three large statutory health companies (2005-2010) for women aged ≥40 years living in the region surrounding the Frankfurt international airport were analyzed with address-specific acoustic data representing aircraft, road, and rail-traffic noise. Noise exposure among women with incident breast cancer (N=6643) were compared with that of control subjects (N=471 596) using logistic regression and adjusting for age, hormone replacement therapy, education and occupation (only available for 27.9%), and a regional proportion of persons receiving long-term unemployment benefits as an ecological indicator of socioeconomic level. Analyses were also stratified according to estrogen receptor (ER) status. Results An increased odds ratio (OR) was observed for ER negative (ER-) tumors at 24-hour aircraft noise levels 55-59 dB [OR 55-59 dB 1.41, 95% confidence interval (CI) 1.04-1.90] but not for ER positive (ER+) breast cancers (OR 55-59 dB 0.95, 95% CI 0.75-1.20). Clear associations between road and rail traffic noise were not observed. Conclusions The results indicate increased aircraft noise may be an etiologic factor for ER-breast cancers. However, information regarding potential confounding factors was largely unattainable. Further research is required to understand how environmental noise may be involved in the pathogenesis of ER-breast cancers. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

Background and aims Habitual short nightly sleep duration is associated with increased atherosclerotic cardiovascular disease risk and morbidity. Vascular endothelial dysfunction represents an important mechanism that may underlie this heightened cardiovascular risk. Impaired endothelium-dependent vasodilation, particularly NO-mediated vasodilation, contributes to the development and progression of atherosclerotic vascular disease and acute vascular events. We tested the hypothesis that chronic insufficient sleep is associated with impaired NO-mediated endothelium-dependent vasodilation in middle-aged adults. Methods Thirty adult men were studied: 15 with normal nightly sleep duration (age: 58 ± 2 y; sleep duration: 7.7 ± 0.2 h/night) and 15 with short nightly sleep duration (55 ± 2 y; 6.1 ± 0.2 h/night). Forearm blood flow (FBF) responses to intra-arterial infusion of acetylcholine, in the absence and presence of the endothelial NO synthase inhibitor N G -monomethyl-L-arginine (L-NMMA), as well as responses to sodium nitroprusside, were determined by strain-gauge venous occlusion plethysmography. Results The FBF response to acetylcholine was lower (∼20%; p <0.05) in the short sleep duration group (from 4.6 ± 0.3 to 11.7 ± 1.0 ml/100 ml tissue/min) compared with normal sleep duration group (from 4.4 ± 0.3 to 14.5 ± 0.5 ml/100 ml tissue/min). L-NMMA significantly reduced the FBF response to acetylcholine in the normal sleep duration group (∼40%), but not the short sleep duration group. There were no group differences in the vasodilator response to sodium nitroprusside. Conclusions These data indicate that short nightly sleep duration is associated with endothelial-dependent vasodilator dysfunction due, in part, to diminished NO bioavailability. Impaired NO-mediated endothelium-dependent vasodilation may contribute to the increased cardiovascular risk with insufficient sleep. [ABSTRACT FROM AUTHOR]

We examined whether a process common to anxiety, labeled the cognitive attentional syndrome (CAS), is also associated with sleep disturbances. The CAS represents the sustained use of self-regulating strategies, such as rumination and worry, and beliefs individuals hold about such strategies. Using a sample of community adults located in the United States (N = 226), we found that the CAS was positively associated with sleep difficulties. The association remained intact after controlling for demographic variables, physical health, and negative affect. We further found that self-regulating strategies may be the component of the CAS that is most important to sleep disturbances. Future experimental studies are needed to elucidate whether there exists a causal, and potentially bidirectional, link between the CAS and sleep difficulties. [ABSTRACT FROM AUTHOR]

Empirical evidence supports an intimate link between sleep and affective functioning. While the bidirectional relationship between sleep duration and mood is well documented, limited research targets other aspects of affective functioning, such as emotion and emotion regulation, or considers their interrelationships. The present review summarizes research examining the relationship between sleep and emotion, emotion regulation, and mood, and presents a theoretical model representing the relationships between these constructs. Disruptions to sleep and mood may trigger and maintain a negative cascade, leading to more entrenched sleep problems and psychopathology. Given that insufficient sleep is a widespread phenomenon, understanding the interrelationships between sleep and affective functioning has implications for both public health and clinical practice. [ABSTRACT FROM PUBLISHER]

BackgroundSleep loss may trigger mood episodes in people with bipolar disorder but individual differences could influence vulnerability to this trigger.AimsTo 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.MethodDuring 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.ResultsSleep 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.ConclusionsGender 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. [ABSTRACT FROM AUTHOR]

Study Objective: Medical residents working overnight call shifts experience sleep deprivation and circadian clock disruption. This leads to deficits in sensorimotor function and increases in workplace accidents. Using quick tablet-based tasks, we investigate whether measureable executive function differences exist following a single overnight call versus routine shift, and whether factors like stress, rest and caffeine affect these measures.Design: A prospective, observational, longitudinal, comparison study was conducted.Setting: An academic tertiary hospital's main operating room suite staffed by attending anesthesiologists, anesthesiology residents, anesthesiologist assistants and nurse anesthetists.Patients: Subjects were 30 anesthesiology residents working daytime shifts and 30 peers working overnight call shifts from the University of Texas Health Science Center at Houston.Interventions: Before and after their respective work shifts, residents completed the Stanford Sleepiness Scale (SSS) and the ProPoint and AntiPoint tablet-based tasks. These latter tasks are designed to measure sensorimotor and executive functions, respectively.Measurements: The SSS is a self-reported measure of sleepiness. Response times (RTs) are measured in the pointing tasks.Main Results: Call residents exhibited increased RTs across their shifts (post-pre) on both ProPoint (p=0.002) and AntiPoint (p<0.002) tasks, when compared to Routine residents. Increased stress was associated with decreases in AntiPoint RT for Routine (p=0.007), but with greater increases in sleepiness for Call residents (p<0.001). Further, whether or not a Call resident consumed caffeine habitually was associated with ProPoint RT changes; with Call residents who habitually drink caffeine having a greater Pre-Post difference (i.e., more slowing, p<0.001) in ProPoint RT.Conclusions: These results indicate that (1) overnight Call residents demonstrate both sensorimotor and cognitive slowing compared to routine daytime shift residents, (2) sensorimotor slowing is greater in overnight Call residents who drink caffeine habitually, and (3) increased stress during a shift reduces (improves) cognitive RTs during routine daytime but not overnight call shifts. [ABSTRACT FROM AUTHOR]

Background: Sleep problems, especially in the adolescent stage of development, may be associated with excessive daytime sleepiness, impaired neurocognitive function, and a host of others leading to suboptimal performance. Objectives: To determine the pattern of sleep problems in school-going adolescents based on the bedtime problems; excessive daytime sleepiness; awakenings during the night and problems falling back asleep; regularity and duration of sleep; sleep-disordered breathing (BEARS) sleep screening algorithm. Materials and Methods: This is a cross-sectional descriptive study involving 353 secondary school-going adolescents in Kano metropolis. Subjects were selected for the study using multistage sampling technique. The study lasted from March 2015 to July 2015. Sleep problems were screened for using the BEARS sleep screening algorithm. Tables were used to present the qualitative data. The various BEARS sleep patterns were assessed, and comparison between stages of adolescence was done using Chi-square test (and Fisher's exact test where necessary). A significant association was considered at P < 0.05. Results: Of the 353 adolescents studied, 61.8% were males while 38.2% were females with male, female ratio of 1.6:1. Early, middle, and late adolescents constituted 13.9%, 39.9%, 46.2% respectively. BEARS sleep screening revealed awakenings during the night (34.6%) as the most common sleep-related problem reported, and this was followed by excessive daytime sleepiness (21.0%). Age-group dependent sleep duration was 7.19 ± 1.26, 7.13 ± 1.13, 7.16 ± 1.28, with P > 0.05. Although 62.9% of all the adolescents watched TV/play video games until 1 h before going to bed and this was highest in late adolescence, it was not statistically significantly associated with any of the sleep problems. Conclusion: Both the quality and quantity of sleep in Nigerian adolescents in Kano is suboptimal. Adolescent and sleep medicine should receive more attention in our environment. [ABSTRACT FROM AUTHOR]

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

Hypersomnolence plays an important role in the presentation, treatment and course of mood disorders. However, there has been relatively little research that examines objective measures of sleep duration and continuity in patients with depression and hypersomnolence, despite the use of these factors in sleep medicine nosological systems. This study compared total sleep time and efficiency measured by naturalistic actigraphic recordings followed by ad libitum polysomnography ( PSG; without prescribed wake time) in 22 patients with major depressive disorder and co-occurring hypersomnolence against age- and sex-matched healthy sleeper controls. The major depressive disorder and co-occurring hypersomnolence group demonstrated significantly longer sleep duration compared with healthy sleeper controls quantified by sleep diaries, actigraphy and ad libitum PSG. No between-group differences in sleep efficiency ( SE), latency to sleep or wake after sleep onset were observed when assessed using objective measures. To further contextualize these findings within the broader scientific literature, a systematic review was performed to identify other comparable investigations. A meta-analysis of pooled data demonstrated patients with mood disorders and co-occurring hypersomnolence have significantly greater sleep duration and similar SE compared with healthy controls when assessed using ad libitum PSG. These results suggest current sleep medicine nosology that distinguishes hypersomnia associated with psychiatric disorders primarily as a construct characterized by low SE and increased time in bed may not be accurate. Future studies that establish the biological bases hypersomnolence in mood disorders, as well as clarify the accuracy of nosological thresholds to define excessive sleep duration, are needed to refine the diagnosis and treatment of these disorders. [ABSTRACT FROM AUTHOR]

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

Purpose: Neighborhood-level socioeconomic disadvantage and lower individual-level socioeconomic status are associated with poorer sleep health in adults. However, few studies have examined the association between neighborhood-level disadvantage and sleep in adolescents, a population at high-risk for sleep disturbances.Methods: The current study is the first to examine how objective (i.e. via census tract-level data) and subjective measures of neighborhood disadvantage are associated with sleep in a racially/ ethnically and socioeconomically diverse sample of 2493 youth [Non-Hispanic White (20%), Hispanic (46%), Asian (21%), and Multiracial/ Other (13%)].Results: Findings indicated that greater perceived neighborhood-level social cohesion and lower neighborhood-level poverty were associated with better sleep outcomes in adolescents. However, there was some evidence that the magnitude of the associations differed according to family-level socioeconomic status and race/ ethnicity.Conclusions: Findings suggest that subjective and objective neighborhood characteristics may affect the sleep health of older adolescents, with certain demographic subgroups being particularly vulnerable. [ABSTRACT FROM AUTHOR]

This paper evaluates the relative contribution of vibration and noise from railway on physiological sleep outcomes. Vibration from railway freight often accompanies airborne noise, yet is almost totally absent in the existing literature. In an experimental investigation, 23 participants, each sleeping for six nights in the laboratory, were exposed to 36 simulated railway freight pass-bys per night with vibration alone (aWd,max=0.0204 ms-2), noise alone (LAF,max=49.8 dB), or both vibration and noise simultaneously. A fourth exposure night involved 52 pass-bys with concurrent vibration and noise. Sleep was measured with polysomnography. Cardiac activity was measured with electrocardiography. The probability of cortical arousals or awakenings was greater following all exposures, including vibration alone, than spontaneous reaction probability (p<0.05). The effects of vibration exposure and noise exposure on changes of sleep stage and arousals were directly additive. Vibration and noise exposure both induced heart rate acceleration above spontaneously expected fluctuations at baseline. The results indicate that vibration and noise are processed in the brain separately yet in parallel, with both contributing towards the likelihood of sleep disruption. The findings show that vibration is of importance when considering the impact of railway freight on sleep. [ABSTRACT FROM AUTHOR]

Purpose: The effects of sleep deprivation on physical performance are well documented, but data on the consequence of sleep deprivation on recovery from exercise are limited. The aim was to compare cyclists' recovery from a single bout of high-intensity interval training (HIIT) after which they were given either a normal night of sleep (CON, 7.56 ± 0.63 h) or half of their usual time in bed (DEP, 3.83 ± 0.33 h).Methods: In this randomized cross-over intervention study, 16 trained male cyclists (age 32 ± 7 years), relative peak power output (PPO 4.6 ± 0.7 W kg-1) performed a HIIT session at ±18:00 followed by either the CON or DEP sleep condition. Recovery from the HIIT session was assessed the following day by comparing pre-HIIT variables to those measured 12 and 24 h after the session. Following a 2-week washout, cyclists repeated the trial, but under the alternate sleep condition.Results: PPO was reduced more 24 h after the HIIT session in the DEP (ΔPPO -0.22 ± 0.22 W kg-1; range -0.75 to 0.1 W kg-1) compared to the CON condition (ΔPPO -0.05 ± 0.09 W kg-1, range -0.19 to 0.17 W kg-1, p = 0.008, d = -2.16). Cyclists were sleepier (12 h: p = 0.002, d = 1.90; 24 h: p = 0.001, d = 1.41) and felt less motivated to train (12 h, p = 0.012, d = -0.89) during the 24 h recovery phase when the HIIT session was followed by the DEP condition. The exercise-induced 24 h reduction in systolic blood pressure observed in the CON condition was absent in the DEP condition (p = 0.039, d = 0.75).Conclusions: One night of partial sleep deprivation impairs recovery from a single HIIT session in cyclists. Further research is needed to understand the mechanisms behind this observation. [ABSTRACT FROM AUTHOR]

Current antipsychotic medications fail to satisfactorily reduce negative and cognitive symptoms and produce many unwanted side effects, necessitating the development of new compounds. Cross-species, experimental behavioural model systems can be valuable to inform the development of such drugs. The aim of the current study was to further test the hypothesis that controlled sleep deprivation is a safe and effective model system for psychosis when combined with oculomotor biomarkers of schizophrenia. Using a randomized counterbalanced within-subjects design, we investigated the effects of 1 night of total sleep deprivation in 32 healthy participants on smooth pursuit eye movements (SPEM), prosaccades (PS), antisaccades (AS), and self-ratings of psychosis-like states. Compared with a normal sleep control night, sleep deprivation was associated with reduced SPEM velocity gain, higher saccadic frequency at 0.2 Hz, elevated PS spatial error, and an increase in AS direction errors. Sleep deprivation also increased intra-individual variability of SPEM, PS, and AS measures. In addition, sleep deprivation induced psychosis-like experiences mimicking hallucinations, cognitive disorganization, and negative symptoms, which in turn had moderate associations with AS direction errors. Taken together, sleep deprivation resulted in psychosis-like impairments in SPEM and AS performance. However, diverging somewhat from the schizophrenia literature, sleep deprivation additionally disrupted PS control. Sleep deprivation thus represents a promising but possibly unspecific experimental model that may be helpful to further improve our understanding of the underlying mechanisms in the pathophysiology of psychosis and aid the development of antipsychotic and pro-cognitive drugs. [ABSTRACT FROM AUTHOR]

Summary The purpose of this investigation was to determine the effects of one night of sleep deprivation on the waking and diurnal cycles of cortisol, dehydroepiandrosterone (DHEA) and testosterone. Saliva samples were collected every 3 hours from 0600 to 2100 hours on 2 separate days [after 1 night of 8 hours in bed; after 1 night with complete sleep deprivation] in 9 recreationally trained soccer players. Diurnal decline for all steroids was observed under both conditions. There was, however, a significant increase in cortisol concentrations on the 2 nd part of the day (i.e., 1800 and 2100 hours, P < 0.05) after sleep deprivation vs. the control night. The results of this investigation indicate that one night of sleep deprivation does not affect the circadian pattern of saliva adrenal and gonadal steroids in recreationally trained athletes over a 15-hour waking period, despite higher end-afternoon and evening cortisol levels. Further studies are needed to determine the potential impact of these increased catabolic hormone concentrations induced by one night of sleep deprivation on cognitive and physiological performance capacity involved in soccer match or training. [ABSTRACT FROM AUTHOR]

Short sleep duration has been associated with obesity in numerous epidemiological studies. However, such association studies cannot establish evidence of causality. Clinical intervention studies, on the other hand, can provide information on a causal effect of sleep duration on markers of weight gain: energy intake and energy expenditure. Herein is an overview of the science related to the impact of sleep restriction, in the context of clinical intervention studies, on energy intake, energy expenditure and body weight. Additionally, studies that evaluate the impact of sleep restriction on weight loss and the impact of sleep extension on appetite are discussed. Information to date suggests that weight management is hindered when attempted in the context of sleep restriction, and the public should be made aware of the negative consequences of sleep restriction for weight regulation. [ABSTRACT FROM AUTHOR]

Weight gain, obesity and diabetes have reached alarming levels in the developed world. Traditional risk factors such as over-eating, poor nutritional choices and lack of exercise cannot fully account for the high prevalence of metabolic disease. This review paper examines the scientific evidence on two novel risk factors that contribute to dys-regulated metabolic physiology: sleep disruption and circadian misalignment. Specifically, fundamental relationships between energy metabolism and sleep and circadian rhythms and the impact of sleep and circadian disruption on metabolic physiology are examined. Millions of individuals worldwide do not obtain sufficient sleep for healthy metabolic function, and many participate in shift work and social activities at times when the internal physiological clock is promoting sleep. These behaviours predispose an individual for poor metabolic health by promoting excess caloric intake in response to reduced sleep, food intake at internal biological times when metabolic physiology is not prepared, decreased energy expenditure when wakefulness and sleep are initiated at incorrect internal biological times, and disrupted glucose metabolism during short sleep and circadian misalignment. In addition to the traditional risk factors of poor diet and exercise, disturbed sleep and circadian rhythms represent modifiable risk factors for prevention and treatment of metabolic disease and for promotion of healthy metabolism. [ABSTRACT FROM AUTHOR]

The degree of punishment assigned to criminals is of pivotal importance for the maintenance of social order and cooperation. Nonetheless, the amount of punishment assigned to transgressors can be affected by factors other than the content of the transgressions. We propose that sleep deprivation in judges increases the severity of their sentences. We took advantage of the natural quasi-manipulation of sleep deprivation during the shift to daylight saving time in the spring and analyzed archival data from judicial punishment handed out in the U.S. federal courts. The results supported our hypothesis: Judges doled out longer sentences when they were sleep deprived. [ABSTRACT FROM AUTHOR]

What effects do factors that impair or enhance performance in individuals have when these individuals act in groups? We provide a framework, called the GIE ("Effects of Grouping on Impairments and Enhancements”) framework, for investigating this question. As prominent examples for individual-level impairments and enhancements, we discuss sleep deprivation and caffeine. Based on previous research, we derive hypotheses on how they influence performance in groups, specifically process gains and losses in motivation, individual capability, and coordination. We conclude that the effect an impairment or enhancement has on individual-level performance is not necessarily mirrored in group performance: grouping can help or hurt. We provide recommendations on how to estimate empirically the effects individual-level performance impairments and enhancements have in groups. By comparing sleep deprivation to stress and caffeine to pharmacological cognitive enhancement, we illustrate that we cannot readily generalize from group results on one impairment or enhancement to another, even if they have similar effects on individual-level performance. [ABSTRACT FROM AUTHOR]

Sleep disturbances are common in multiple sclerosis (MS), but its impact on cognition and functional connectivity (FC) of the hippocampus and thalamus is unknown. Therefore, we investigated the relationship between sleep disturbances, cognitive functioning and resting-state (RS) FC of the hippocampus and thalamus in MS. 71 MS patients and 40 healthy controls underwent neuropsychological testing and filled out self-report questionnaires (anxiety, depression, fatigue, and subjective cognitive problems). Sleep disturbances were assed with the five-item version of the Athens Insomnia Scale. Hippocampal and thalamic volume and RS FC of these regions were determined. Twenty-three patients were categorized as sleep disturbed and 48 as normal sleeping. No differences were found between disturbed and normal sleeping patients concerning cognition and structural MRI. Sleep disturbed patients reported more subjective cognitive problems, and displayed decreased FC between the thalamus and middle and superior frontal gyrus, inferior frontal operculum, anterior cingulate cortex, inferior parietal gyrus, precuneus, and angular gyrus compared to normal sleeping patients. We conclude that sleep disturbances in MS are not (directly) related to objective cognitive functioning, but rather to subjective cognitive problems. In addition, sleep disturbances in MS seem to coincide with a specific pattern of decreased thalamic FC. [ABSTRACT FROM AUTHOR]

Objective: Chronic partial sleep deprivation (SD) by environmental noise exposure increases weight gain and feeding in rodents, which contrasts weight loss after acute SD by physical methods. This study tested whether acute environmental noise exposure reduced sleep and its effect on weight gain, food intake, physical activity, and energy expenditure (EE). It was hypothesized that acute exposure would (1) increase weight gain and feeding and (2) reduce sleep, physical activity, and EE (total and individual components); and (3) behavioral changes would persist throughout recovery from SD.Methods: Three-month old male Sprague-Dawley rats slept ad libitum, were noise exposed (12-h light cycle), and allowed to recover (36 h). Weight gain, food intake, sleep/wake, physical activity, and EE were measured.Results: Acute environmental noise exposure had no effect on feeding, increased weight gain (P < 0.01), and reduced sleep (P < 0.02), physical activity (P < 0.03), total EE (P < 0.05), and several components (P < 0.05). Reductions in EE and physical activity persisted during recovery.Conclusions: Reductions in EE during sleep, rest, and physical activity reduce total EE and contribute to weight gain during acute SD and recovery from SD. These data emphasize the importance of increasing physical activity after SD to prevent obesity. [ABSTRACT FROM AUTHOR]

Sleep deprivation may lead to increased impulsivity, however, previous literature has focused on examining effects of total sleep deprivation (TSD) rather than the more common condition, partial sleep deprivation (PSD) or ‘short sleep’. Moreover, it has been unclear whether PSD impacts impulse-related cognitive processes, and specifically if it differentially affects impulsive action versus impulsive decision-making. We sought to determine if short compared to long sleep (6 vs. 9 h/night) impacts impulsive action via behavioral inhibition (Go/No-Go), and/or impulsive decision-making processes of risk taking (Balloon Analogue Risk Task [BART]) and preferences for immediate over delayed rewards (Delay Discounting). In a within-subject design, 34 participants (71% female, mean age = 37.0 years, SD = 10.54) were assigned to four consecutive nights of 6 h/night (short sleep) and 9 h/night (long sleep) in their own home in random counterbalanced order. Sleep was measured via wrist-worn actigraphs to confirm adherence to the sleep schedules (mean short sleep = 5.9 h, SD = 0.3; mean long sleep = 8.6 h, SD = 0.3, p < 0.001). The Go/No-Go, BART, and Delay Discounting tasks were completed following both sleep conditions. Participants had more inhibition errors on the Go/No-Go task after short (mean false alarms = 19.79%, SD = 14.51) versus long sleep (mean = 15.97%, SD = 9.51, p = 0.039). This effect was strongest in participants reporting longer habitual time in bed (p = 0.04). There were no differences in performance following long- versus short-sleep for either delay discounting or the BART (p's > 0.4). Overall, these results indicate that four days of PSD diminishes behavioral inhibition abilities, but may not alter impulsive decision-making. These findings contribute to the emerging understanding of how partial sleep deprivation, currently an epidemic, impacts cognitive ability. Future research should continue to explore the connection between PSD and cognitive functions, and ways to minimize the occurrence and negative consequences of short sleep. [ABSTRACT FROM AUTHOR]

Background: Many herbal medicines are traditionally used as anti-fatigue agents in east Asian countries; however, there is a dearth of clinical evidence supporting the anti-fatigue effects of such medicines and their mechanisms. This study is a feasibility trial to assess the clinical efficacy of Gongjin-dan (GJD) and verify its mechanisms by exploring fatigue outcomes, including endocrine and immunological biomarkers in humans.Methods/design: To investigate the anti-fatigue effects of GJD and the mechanism underlying these effects, a randomised, double-blind, placebo-controlled crossover clinical trial was designed. Participants (24 healthy male volunteers) will be hospitalised for 4 days (3 nights), during which acute fatigue and stress conditions will be induced by sleep deprivation, and GJD or a placebo will be administered (twice daily). The primary outcome will be changes in serum cortisol levels, measured in the morning, as an objective biomarker of sleep deprivation-induced fatigue and stress. The secondary outcomes will include: the Fatigue Severity Scale; the Brief Fatigue Inventory, and the Leeds Sleep Evaluation Questionnaire scores; levels of salivary cortisol, epinephrine, norepinephrine, oxidative stress-related biomarkers, homocysteine, and immunological factors; and heart rate variability. After a washout period of more than 4 weeks, a second treatment phase will commence in which participants who were previously administered the placebo will receive the drug and vice versa, following the same treatment regime as in the first phase.Discussion: This study protocol provides a unique opportunity to enhance our understanding of fatigue and the effects of GJD on fatigue in terms of endocrine and immunological mechanisms by validating the study design and determining feasibility. Findings from this trial will help researchers to design a pilot or definitive clinical trial of traditional herbal medicine for chronic fatigue.Trial Registration: Korean National Clinical Trial Registry CRIS; KCT0001681 , registered on 29 October 2015. [ABSTRACT FROM AUTHOR]

The influence of sleep restriction ( SR) during pregnancy on blood pressure and renal function among female adult offspring was investigated. Pregnant Wistar rats were distributed into control and SR groups. The SR was performed between the 14th and 20th days of pregnancy (multiple platforms method for 20 h/day). At 2 months of age, half of the offspring from both groups were subjected to an ovariectomy (ovx), and the other half underwent sham surgery. The groups were as follows: control sham (Csham), control ovx (Covx), SR sham ( SRsham), and SR ovx ( SRovx). Renal function markers and systolic blood pressure ( BPi, indirect method) were evaluated at 4, 6, and 8 months. Subsequently, the rats were euthanized, kidneys were removed, and processed for morphological analyses of glomerular area ( GA), number of glomeruli per mm3 ( NG), and kidney mass ( KM). Increased BPi was observed in the Covx, SRsham, and SRovx groups compared to Csham at all ages. Increased plasma creatinine concentration and decreased creatinine clearance were observed in the SRsham and SRovx groups compared to the Csham and Covx groups. The SRovx group showed higher BPi and reduced creatinine clearance compared to all other groups. The SRovx group showed reduced values of GA and KM, as well as increased NG, macrophage infiltration, collagen deposit, and ACE1 expression at the renal cortex. Therefore, SR during pregnancy might be an additional risk factor for developing renal dysfunction and increasing BP in female adult offspring. The absence of female hormones exacerbates the changes caused by SR. [ABSTRACT FROM AUTHOR]

Background: Sleep disturbance is a common complaint in patients with chronic obstructive lung disease (COPD). However, the factors resulting in sleep disturbance remain unclear. This retrospective, observational, multicenter study aimed to identify the factors associated with sleep disturbance in patients with COPD.Methods: The study was a retrospective, observational, and multicenter research. Data including age, sex, body mass index, smoking status, COPD inhaler prescribed, clinical symptoms, pulmonary function tests, medical history of comorbidities, and questionnaires were collected. Parameters including demographics, symptoms, medication, severity, functional classification, and comorbidities were correlated with sleep quality scores.Results: Among 377 patients with COPD, 200 (53 %) patients experienced poor sleep quality (Pittsburg Sleep Quality Index scores > 5). A significant difference in sleep quality, as measured by PSQI scores, was noted between groups based on the 2011 Global Initiatives for Chronic Obstructive Lung Disease (GOLD) classification system. The most common sleep disturbances included "getting up to use the bathroom" (70.3 %), "wake up at night or early morning" (40.3 %), and "cough and snore loudly at night" (15.9 %). The use of inhaled corticosteroids, the presence of wheezing, COPD Assessment Test (CAT) scores, and Modified Medical Research Council (mMRC) dyspnea scale scores positively correlated with poor sleep quality (odds ratio: 1.51, 1.66, 1.09, and 1.30, respectively). Upon multivariate analysis, the CAT score was an independent factor for poor sleep quality in these patients. With the exception of sleep problem items, based on the CAT questionnaire, phlegm was significantly higher in COPD patients with poor sleep quality.Conclusions: Poor sleep quality is common among patients with COPD and symptoms including wheeze, phlegm, and inhaled corticosteroid use may contribute to poor sleep quality. The CAT score is a good indicator of poor sleep quality in patients with COPD. [ABSTRACT FROM AUTHOR]

The extent to which the diurnal fluctuations of different cognitive processes could be affected by sleep loss may be explored to predict performance decrements observed in the real world. Twenty healthy male subjects voluntarily took part in 8 test sessions at 06:00, 10:00, 14:00, and 18:00 h, following either a night with or without sleep in random order. Measurements included oral temperature, simple reaction time, sign cancelation, Go/NoGo, and the Purdue pegboard test. The results indicate that simple reaction time and motor coordination had morning–afternoon variations closely following the rhythms of temperature and vigilance. Inhibitory attention (Go/NoGo) presented no morning–afternoon variations. Sleep deprivation may affect the profiles of cognitive performance depending on the processes solicited. Sustained and inhibitory attention are particularly affected in the morning (after 24 and 28 waking hours), while a complex task (visuo-motor coordination) would be affected after 32 waking hours only. [ABSTRACT FROM AUTHOR]

Neurodegenerative changes following sleep deprivation (SD) result in debilitating behavioral and cognitive dysfunction. SD causes gradual cognitive impairment and later results in neurodegeneration. These changes are thought to be the consequences of cellular disorganization and degeneration in selected brain areas – the hippocampus, prefrontal cortex, amygdala, and hypothalamus. We investigated the histological changes in mice exposed to 6 days SD and to the effects of 2 days of recovery sleep in the brain regions listed above. Cytological changes, total viable cell count in hippocampal subregions, Bcl-2 expression, and degenerative changes like cell morphology and membrane integrity of neurons were evaluated. Results demonstrated that prolonged SD decreased the count of viable and healthy cells and caused a decrease in Bcl-2 positive cells and an increase in degenerated cells with pyknotic morphology, chromatolysis and darkly stained cytoplasm. Degenerative changes were ameliorated by 2 days of recovery sleep or rehabilitation after SD. Data suggest that chronic SD constitutes a severe threat to the brain and leads to neurodegeneration, while rehabilitation or recovery sleep ameliorates or protects the brain from neurodegenerative challenges. [ABSTRACT FROM AUTHOR]